Handbook of Interventional Radiologic Procedures

Editors
Krishna Kandarpa MD, PhD

Director, Research Sciences and Strategic Directions, National Institute of Biomedical
Imaging and Bioengineering, National Institutes of Health, Bethesda,
Maryland. Previously, he served as Chief Medical and Scientific Officer, Delcath
Systems, Inc., New York, New York; Professor and Chair of Radiology at the University
of Massachusetts Medical School and Radiologist-in-chief, UMass Memorial
Medical Center, Worcester, Massachusetts; Professor of Radiology, Cornell Medical
School, and Chief of Service, Cardiovascular & Interventional Radiology, New York-Presbyterian
Hospital, New York, New York; Associate Professor of Radiology, Harvard
Medical School; and co-Director, Cardiovascular & Interventional Radiology,
Brigham and Women's Hospital, Boston, Massachusetts. He received a doctorate in
Engineering Science from Pennsylvania State University, State College, Pennsylvania,
and a doctorate in medicine from the University of Miami, Miami, Florida. He
was past President and Chair of the SIR Research & Education Foundation and on
the Board of Directors, Academy of Radiology Research.
Lindsay Machan MD
Associate Professor of Radiology, University of British Columbia and Interventional
Radiologist, Vancouver Hospital, Vancouver, Canada. Previously served as
regional lead, Interventional Radiology Vancouver Coastal Health, and interventional
radiologist at the Hammersmith Hospital in London, United Kingdom, and
the Hospital of the University of Pennsylvania in Philadelphia, Pennsylvania. He
received his MD from the University of Alberta, Edmonton, Canada. Diagnostic
Radiology residency and Interventional fellowship were completed at the University
of British Columbia. He is a past President of the Western Angiographic and
Interventional Society and a founding member of the Canadian Interventional Radiology
Association. He was a co-founder of Angiotech Pharmaceuticals, Inc., and
Ikomed Medical, Vancouver, Canada, both medical device companies.
Janette D. Durham MD
Professor of Radiology, University of Colorado School of Medicine, Aurora, Colorado.
Previously served as Medical Director for Interventional Radiology, co-Director
of the Cardiac and Vascular Center, and President of the Medical Staff,
University of Colorado Hospital, Aurora, Colorado. She received an MD from the
Indiana University School of Medicine, Indianapolis, Indiana, and an MBA from
the University of Denver, Denver, Colorado. Diagnostic Radiology residency was
completed at Indiana University, Indianapolis, Indiana, and Vascular fellowship at
Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts.
She is a past President of the Society of Interventional Radiology (SIR).
Contributing Authors
Hani H. Abujudeh, MD, MBA
Associate Professor of Radiology
Massachusetts General Hospital/Harvard
Medical School
Boston, Massachusetts
Sun Ho Ahn, MD, FSIR

Assistant Professor of Radiology
Alpert Medical School of Brown
University
Providence, Rhode Island
Mohammed T. Alshammari, MD
Consultant Interventional Radiologist
Security Forces Hospital Program
Riyadh, Saudi Arabia
Parag Amin, MD
Loyola University Medical Center
Maywood, Illinois
Ronald S. Arellano, MD, FSIR

Medical School
Jamie B. Arton, MHS, PA-C

Instructor of Radiology
University of Colorado School of Medicine
Aurora, Colorado
James F. Benenati, MD
Clinical Professor of Radiology
Miami Cardiac and Vascular Institute
Florida International University Herbert
Wertheim College of Medicine
Miami, Florida
Susan Benveniste, BSN, RN, CRN

Division of Interventional Radiology
Brigham and Woman's Hospital
Michael A. Bettmann, MD, FACR, FSIR

Professor of Radiology Emeritus
Wake Forest University School of
Medicine
Winston-Salem, North Carolina
Allison Borowski, MD
Radiologist
Lenox Hill Hospital
New York, New York
Ugur Bozlar, MD
Gulhane Military Medical Academy
Ankara, Turkey
Daniel B. Brown, MD, FSIR

Professor of Radiology
Vanderbilt University School of Medicine
Nashville, Tennessee
Michael A. Bruno, MS, MD, FACR

Professor of Radiology and Medicine
Penn State College of Medicine
Hershey, Pennsylvania
Francisco Cesar Carnevale, MD, PhD

University of São Paulo Medical School
São Paulo, Brazil
Matthew D. Cham, MD
Icahn School of Medicine at Mount Sinai
New York, New York
Daniel Chan, MD
Precision Vascular and Interventional
Dallas, Texas
Maye M. Chan, PA-C

Division of Abdominal Imaging and
Intervention
Brigham and Women's Hospital
Danny Cheng, MD
Assistant Clinical Professor of
Radiology
UC Davis Medical Center
Sacramento, California
Jared D. Christensen, MD
Duke University Medical Center
Durham, North Carolina
John Chung, MD, FRCPC

Clinical Instructor of Radiology
University of British Columbia
Vancouver, British Columbia, Canada
Petra Clark, MS, CNS-AG, RN, CRN

Timothy W.I. Clark, MD, FSIR

Associate Professor of Clinical
Radiology and Surgery
University of Pennsylvania Perelman
School of Medicine
Philadelphia, Pennsylvania
Sarah D. Cohn, RN, JD, FACNM

General Counsel
Medical College of Wisconsin
Milwaukee, Wisconsin
Anne M. Covey, MD, FSIR

Memorial Sloan-Kettering Cancer Center/Weill Cornell Medical Center
New York, New York
Laura Crocetti, MD, PhD, EBIR

Cisanello Hospital/Pisa University
School of Medicine
Pisa, Italy
Michael D. Dake, MD
Thelma and Henry Doelger Professor
Department of Cardiothoracic Surgery
Stanford University School of Medicine
Stanford, California
Michael D. Darcy, MD
Washington University School of Medicine
St. Louis, Missouri
André Moreira de Assis, MD

Interventional Radiology
São Paulo, Brazil
Olga Duran-Castro, MD
and Vascular Medicine
University of Minnesota
Minneapolis, Minnesota
Jeremy J. Erasmus, MD
Professor of Diagnostic Radiology
MD Anderson Cancer Center
Houston, Texas
Joseph P. Erinjeri, MD, PhD

Associate Member
Memorial Sloan Kettering Cancer
Center/Weill Cornell Medical
Center
New York, New York
Khashayar Farsad, MD, PhD

Assistant Professor
Dotter Interventional Institute
Oregon Health and Science University
Portland, Oregon
Siobhan M. Flanagan, MD
and Vascular Medicine
Michael G. Flater, RN
Territory Manager
ZOLL LifeVest
Pittsburgh, Pennsylvania
Richard Foley, MS, RN
Radiology and IV Therapy
Brian Funaki, MD
University of Chicago
Chicago, Illinois
Ripal T. Gandhi, MD, FSVM

Associate Clinical Professor
Florida International University
Herbert Wertheim College of
Medicine
Miami, Florida
Christos S. Georgiades, MD, PhD, FSIR

FCIRSE Associate Professor of Radiology and
Surgery
Johns Hopkins University
Baltimore, Maryland
Jean-Francois H. Geschwind, MD
Professor of Radiology and Oncology
Yale University School of Medicine
New Haven, Connecticut
Matthew G. Gipson, MD
Aurora, Colorado
Jafar Golzarian, MD, FSIR

Professor of Radiology and Surgery
Roy L. Gordon, MD
Professor Emeritus of Radiology
University of California
San Francisco, California
Rajan K. Gupta, MD
Aurora, Colorado
Klaus D. Hagspiel, MD
Professor of Radiology, Medicine
(Cardiology) and Pediatrics
University of Virginia
Charlottesville, Virginia
Michael J. Hallisey, MD
Department of Radiology
Hartford Hospital
Hartford, Connecticut
Rulon L. Hardman, MD, PhD

University of Utah
Salt Lake City, Utah
Ziv J. Haskal, MD, FSIR, FAHA, FACR

FCIRSE Professor of Radiology
University of Virginia School of Medicine
Peter B. Hathaway, MD
Utah Imaging Associates
Utah Vascular Clinic
Salt Lake City, Utah
Nicholas J. Hendricks, MD
Virginia Hospital Center
Arlington, Virginia
Claudia I. Henschke, PhD, MD

Icahn School of Medicine at Mount Sinai
New York, New York
Manraj K.S. Heran, MD, FRCPC

Mikhail C.S.S. Higgins, MD, MPH

Fellow, Division of Interventional Radiology
Hospital of the University of Pennsylvania
Stephen G.F. Ho, MD, FRCPC

David M. Hovsepian, MD
David W. Hunter, MD, FSIR, FACR

Professor Emeritus of Radiology
Jonathan J. Iglesias, MD
Miami, Florida
Maxim Itkin, MD
Associate Professor of Radiology and
Surgery
University of Pennsylvania Medical Center
M. Fuad Jan, MBBS, MD, FACC, FACCP

Aurora Cardiovascular Services
Aurora Health Care
D. Thor Johnson, MD, PhD

Aurora, Colorado
Michele H. Johnson, MD, FACR

Professor, Diagnostic Radiology, Surgery
(Otolaryngology) and Neurosurgery
Rathachai Kaewlai, MD
Department of Diagnostic and
Therapeutic Radiology
Mahidol University
Bangkok, Thailand
S. Lowell Kahn, MD, MBA

Assistant Professor, Surgery and
Tufts University School of Medicine
Springfield, Massachusetts
John A. Kaufman, MD, MS, FSIR

Frederick S. Keller Professor of
Portland, Oregon
Frederick S. Keller, MD
Professor of Interventional Radiology
Portland, Oregon
Neil M. Khilnani, MD
Radiology
Weill Cornell Medicine
New York, New York
Jin Hyoung Kim, MD, PhD

University of Ulsan College of Medicine
Seoul, South Korea
K. Pallav Kolli, MD
Assistant Professor of Clinical
Radiology
University of California, San Francisco
California, San Francisco
Sebastian Kos, EBIR, FCIRSE

Chairman, Institute of Radiology and
Nuclear Medicine
Hirslanden Klinik St. Anna
Luzern, Switzerland
Joshua D. Kuban, MD
Fellow, Vascular and Interventional
Radiology
Alpert Medical School of Brown University
David A. Kumpe, MD, FSIR

Professor of Radiology, Surgery, and
Neurosurgery
Aurora, Colorado
Marcus A. Lehman, MD
Assistant Professor of Anesthesiology
University of Cincinnati
Cincinnati, Ohio
Evan Lehrman, MD
Assistant Professor of Radiology and
Biomedical Imaging
University of California, San Francisco
San Francisco, California
Riccardo Lencioni, MD, FSIR, EBIR

Pisa University School of Medicine
Pisa, Italy
Robert J. Lewandowski, MD, FSIR

Northwestern University
Chicago, Illinois
David Li, MD, PhD

New York-Presbyterian Hospital/Weill
Cornell Medical Center
New York, New York
Leonard J. Lind, MD, FCCM

Professor of Clinical Anesthesiology
University of Cincinnati College of
Medicine
Cincinnati, Ohio
Andrew J. Lipnik, MD
Assistant Professor of Clinical Radiology
and Radiological Sciences
Vanderbilt University Medical Center
Nashville, Tennessee
David M. Liu, MD, FRCPC, FSIR

Clinical Associate Professor of Radiology
Robert A. Lookstein, MD, FSIR, FAHA

Mount Sinai Health System
New York, New York
J. Diego Lozano, MD
Fellow, Interventional Neuroradiology
University of Massachusetts Medical
School
Worcester, Massachusetts
David C. Madoff, MD
New York, New York
Mohammad Mansouri, MD
Massachusetts General Hospital
Karen Marshall, RN, BSN

Northwestern Memorial Hospital
Chicago, Illinois
Michael L. Martin, MD
Clinical Associate Professor of Radiology
Alan H. Matsumoto, MD, FACR, FSIR, FAHA

Chair and Theodore E. Keats Professor
of Radiology
University of Virginia Health System
Ellen McKeon-Levine, RN, BSN

DéAnn O. McNamara, MS, ACNP-BC, CRN

Clinical Educator
Mark W. Mewissen, MD
Clinical Adjunct Professor of Medicine
University of Wisconsin
Madison, Wisconsin
Donald L. Miller, MD, FSIR, FACR

Chief Medical Officer for Radiological
Health
Office of In Vitro Diagnostics and
Radiological Health
Center for Devices and Radiological
Health
Food and Drug Administration
Silver Spring, Maryland
Robert J. Min, MD, MBA

Professor & Chairman of Radiology
New York, New York
Jennifer P. Montgomery, MD, PhD

Dotter Interventional Institute
Portland, Oregon
Airton Mota Moreira, MD, PhD

Specialist in Vascular and Interventional
Radiology
São Paulo, Brazil
Peter L. Munk, MDCM, FRCPC, FSIR

Professor of Radiology and Orthopedics
Timothy P. Murphy, MD
Alpert Medical School of Brown University
Kieran Murphy, MB, FRCPC, FSIR

University of Toronto
Toronto, Ontario, Canada
Susan Kiernan O'Horo, MD, MPH, FSIR

Sanjay K. Paidisetty, MD
Radiology
Aneeta Parthipun, MBBS, BSc (Hons), FRCR

Fellow, Interventional Radiology
Guy's and St. Thomas' NHS Foundation
Trust
London, United Kingdom
Aalpen A. Patel, MD, FSIR

Fellowship Director, Vascular and
Geisinger Health System
Danville, Pennsylvania
Parag J. Patel, MD, MS

Surgery
Edward F. Patz Jr., MD

James and Alice Chen Professor of
Radiology, Professor of Pharmacology
and Cancer Biology
Duke University Medical Center
Durham, North Carolina
Joseph F. Polak, MD, MPH

Tufts University School of Medicine
Jeffrey S. Pollak, MD
The Robert I. White, Jr. Professor of
Martin R. Prince, MD, PhD, FACR

Cornell and Columbia Universities
New York, New York
Bradley B. Pua, MD
Cornell Medical College
New York, New York
Ajit S. Puri, MD
Neurosurgery
University of Massachusetts Medical
School
Martin G. Radvany, MD, FSIR

Chief, Interventional Neuroradiology
WellSpan Neurosciences & Radiology
York, Pennsylvania
Mahmood K. Razavi, MD, FSIR, FSVM

Director, Center for Clinical Trials and
Research
St. Joseph Heart and Vascular Center
Orange, California
Sidney Regalado, MD
Clinical Assistant Professor of Radiology
NorthShore University Health System/University of Chicago Hospitals
Evanston, Illinois
Eric H. Reiner, DO
Robert J. Rosen, MD
Director of Peripheral Vascular
Intervention
Director, AVM Center of New York
Lenox Hill Heart and Vascular Institute
New York, New York
David A. Rosenthal, MHP, PA-C

Chief Physician Assistant
Wael E.A. Saad, MD, FSIR

University of Michigan Medical Center
Ann Arbor, Michigan
Tarun Sabharwal, MBBcH, FRCSI, FRCR

FSIR, FCIRSE, EBIR Consultant Interventional Radiologist
Department of Interventional Radiology
Guy's and St. Thomas' Hospitals
London, United Kingdom
Nisha I. Sainani, MD
Staff Radiologist
Harvard Medical School
Gloria M. Salazar, MD
Medical School
Riad Salem, MD, MBA

Professor of Radiology, Medicine, and
Surgery
Northwestern University
Chicago, Illinois
J. Anthony Seibert, PhD, FAAPM, FACR

Professor, Department of Radiology
University of California Davis Health
System
Sacramento, California
Raj P. Shah, MD, MBA

Resident, Department of Radiology
Hartford Hospital
Hartford, Connecticut
Ji Hoon Shin, MD, PhD

University of Ulsan College of Medicine
Asan Medical Center
Seoul, South Korea
Stuart G. Silverman, MD, FACR

Brigham and Women's Hospital/Harvard
Medical School
Jennifer R. Simpson, MD
Assistant Professor of Neurology
University of Colorado School of
Medicine
Aurora, Colorado
Ajay K. Singh, MD
Medical School
Mitchell Smith, MD, MS

Aurora, Colorado
Stephen B. Solomon, MD
Memorial Sloan Kettering Cancer
Center/Weill Cornell Medical College
New York, New York
Ho-Young Song, MD, PhD

Asan Medical Center/University of
Ulsan College of Medicine
Seoul, Republic of Korea
Thomas A. Sos, MD, FSIR, FACR, FAHA

Professor and Vice Chair of Radiology
New York, New York
Michael C. Soulen, MD, FSIR, FCIRSE

University of Pennsylvania
James B. Spies, MD, MPH

Georgetown University School of
Medicine
Washington, DC
Brian F. Stainken, MD
Chairman, Radiology
The Stamford Hospital
Stamford, Connecticut
Keith J. Strauss, MSc, FAAPM, FACR

University of Cincinnati School of
Medicine
Cincinnati, Ohio
Nathaniel C. Swinburne, MD
Resident, Department of Radiology
Icahn School of Medicine at
Mount Sinai
New York, New York
Ashraf Thabet, MD
Diagnostic Radiologist
Massachusetts General Hospital
Nanda Deepa Thimmappa, MD
Fellow, Body MRI
New York, New York
Scott O. Trerotola, MD
Stanley Baum Professor of Radiology
and Professor of Surgery
University of Pennsylvania Perelman
School of Medicine
David W. Trost, MD
Radiology
NewYork-Presbyterian Hospital/Weill
New York, New York
Maria Tsitskari, MD
Vascular and Interventional Radiologist
American Medical Center
Nicosia, Cyprus
Sabah S. Tumeh, MD, FACR

Medical Director
Piedmont Atlanta Hospital
Atlanta, Georgia
Ulku C. Turba, MD
Rush University Medical Center
Chicago, Illinois
Thuong G. Van Ha, MD

University of Chicago Medicine
Chicago, Illinois
Suresh Vedantham, MD
Washington University School of
Medicine
St. Louis, Missouri
Thomas M. Vesely, MD, FSIR
Interventional Radiologist
Vascular Access Services, LLC
St. Louis, Missouri
Ajay K. Wakhloo, MD, PhD, FAHA

Professor of Radiology, Neurosurgery, and Neurology
University of Massachusetts
David S. Wang, MD
Clinical Assistant Professor of Radiology
Joshua L. Weintraub, MD, FSIR

NewYork-Presbyterian Hospital/Columbia
University Medical Center
New York, New York
Evelyn P. Wempe, MBA, MSN, ARNP, ACNP-BC, AOCNP, CRN

Director of Nursing, Interventional
Radiology
University of Miami Miller School of
Medicine
Miami, Florida
Luke R. Wilkins, MD
University of Virginia
Ronald S. Winokur, MD
Weill Cornell Medicine
New York, New York
David F. Yankelevitz, MD
Icahn School of Medicine at Mount
Sinai
New York, New York
Don C. Yoo, MD
(Clinical) The Warren Alpert Medical School of
Brown University
Chang Jin Yoon, MD, PhD

Seoul National University Bundang
Hospital
Seongnam, Gyeonggi-do, South Korea
Dedication
“Dedicated to the innovative spirit of interventional radiologists.”
Foreword
The field of interventional radiology continues to grow and to change. The scope of care provided by this critical
medical discipline has advanced rapidly over the quarter of a century since the very first edition of this Handbook
in 1989. There are few other disciplines that have changed so much in this brief amount of time. The scope of
this change is represented by the table of contents that has expanded to over 100 chapters, and more important,
the Handbook continues to emphasize not only procedures that have been described in previous editions but
also the important expanding roles of endovascular and nonvascular interventional therapies for a multitude of
disease states. Reflecting changes in the health care system, important chapters on quality assurance and
improvement, risk management, as well as safety—including radiation and infection control—have been
included.
More important, discussions on the clinical practice of interventional radiology are addressed, including
organizational and operational issues, nursing management, and the practical use and management of
pharmacologic therapies.
It is hard to imagine how the Handbook of Interventional Radiologic Procedures could possibly improve over
prior editions. Since its initial publication, this Handbook has become an essential reference for interventionalists
at all levels of experience. It will undoubtedly be essential for residents and fellows during their training and
should remain an important reference for practitioners who will benefit from the valuable practical information
contained in this volume.
The field of interventional radiology continues to evolve as both a clinical and a procedural discipline. The
challenges of creating a comprehensive handbook of practical information in a volume that can actually be
carried around has become more difficult. Yet the editors and authors have amassed a volume that is brisk and
focused in style, extremely well organized and catalogued to make it easy for the reader to get critical information
when necessary in the treatment of specific patients. This handbook is a tool in the hands of interventionalists
which is as helpful as any of the devices that may be used in specific procedures. In keeping with the times, an
updated electronic version for handheld devices is once again provided.
I'm certain that the fifth edition of the Handbook of Interventional Radiologic Procedures will become an
indispensable tool and resource in the lab coat of all interventional radiologists and staff performing these
procedures. I know it will for me.
Barry T. Katzen, MD
Preface
From inability to let well alone; from too much zeal for the new and contempt for what is old; from putting
knowledge before wisdom, science before art, and cleverness before common sense, from treating patients as
cases, and from making the cure of the disease more grievous than the endurance of the same, Good Lord,
deliver us.
Sir Robert Hutchinson
Correspondence regarding modern treatment in the British Medical Journal , March 12, 1953, p. 671.
Interventional radiology remains a vibrant field with evolving and rapidly growing applications due in large part of
the ingenuity and creativity of its practitioners. Although it is true that medical necessity may have mothered
many inventions, scientific advances and competitive pressures have also done much to motivate this
innovational spirit. Future success will depend not only on a continued proactive “innovational” attitude but, more
importantly, also on embracing the clinical management of patients, and staying ahead of unrelenting
competition. Fortunately, the pace of innovations and the specialty's acquisition of clinical management skills
have necessitated a fifth edition of Handbook of Interventional Radiologic Procedures.
This book should be useful not only for practicing interventional radiologists but also for fellows and residents in
training, and for those seasoned general radiologists who are several years out from formal training but have
retained the skills required for performing interventional procedures. This book will also help interventional
nurses and special procedure technologists in performing their own vital tasks more efficiently by enhancing
medical knowledge specific to each procedure.
We realize that there is no single way to perform a procedure and do not mean to imply that the descriptions here
are the only appropriate ones. The intent is to provide a framework that the interventionalist can use and build on
as more experience is gained. As in prior editions, each chapter on procedures has been organized in a
consistent outline format to facilitate easy access to specific sections on indications and contraindications,
preprocedure preparation, procedural protocol, postprocedure care, and expected outcomes—all toward
improving patient safety by preventing complications or managing them appropriately when they do occur. This
latter information is especially useful while the procedure is being discussed with the patient before obtaining
informed consent. We have—to the best of our ability—corrected mistakes and oversights from prior editions.
We are eternally grateful to the contributors worldwide for their painstaking efforts in creating what we hope will
be another successful handbook. We thank Dr. Barry Katzen for kindly writing the foreword. We thank Ryan
Shaw and Rebeca Barroso of Wolters Kluwer for guiding us through the process, and most of all for their
patience.
K. K.
L. M.
J. D.
Abbreviations
0-9
18F-FDG
18F-fluorodeoxyglucose
2D
Two-dimensional
3D
Three-dimensional
A
A
Ankle
AAA
Abdominal aortic aneurysm
AASLD
American Association for the Study of Liver Diseases
ABI
Ankle-brachial index
ACA
Anterior cerebral artery
ACAS
Asymptomatic Carotid Atherosclerosis Trial
ACD
Advance care directives
ACE
Angiotensin-converting enzyme
ACLS
Advanced cardiac life support
ACR
American College of Radiology
ACT
Activated clotting time
ADC
Analog-to-digital converter
ADH
Antidiuretic hormone
ADP
Adenosine diphosphate
AE
Adverse events
AECD
Automatic external cardioverter-defibrillator
AF
Atrial fibrillation
AFB
Acid-fast bacilli
AFP
α-Fetoprotein
AGIH
Acute gastrointestinal hemorrhage
AHRQ
Agency for Healthcare Research and Quality
AK
Above-knee
ALS
Amyotrophic lateral sclerosis
AMFPI
Active matrix flat-panel imager
AMI
Acute mesenteric ischemia
AML
Angiomyolipoma
Ao
Aorta
AP
Anteroposterior
APD
All-purpose drainage
APF
Arterioportal fistula
APTT
Activated partial thromboplastin time
ARDS
Adult respiratory distress syndrome
ARNP
Advanced registered nurse practitioner
ASA
Acetylsalicylic acid
ASA
American Society of Anesthesiologists
ASD
Atrial septal defect
ASPECTS
Alberta Stroke Program early computed tomography scan
AT
Anterior tibial
ATIII
Antithrombin III
ATM
Atmospheres
AV
Arteriovenous
A-V
Atrioventricular
AVF
Arteriovenous fistula
AVG
Arteriovenous graft
AVM
Arteriovenous malformation
AVP
Amplatzer Vascular Plug
B
BAC
Bronchioloalveolar carcinoma
BAE
Bronchial artery embolization
BCLC
Barcelona Clinic Liver Cancer
BE
Balloon expandable
β hCG
Beta human chorionic gonadotropin hormone
BGC
Balloon-guiding catheter
bid
Two times per day
BIPAP
Bi-level positive airway pressure
BLS
Basic life support
BMI
Body mass index
BMS
Bare-metal stents
P.xxvi
BMT
Bone marrow transplant
BOT
Balloon occlusion tolerance
BP
Blood pressure
BPH
Benign prostatic hyperplasia
BRTO
Balloon-occluded retrograde transvenous obliteration
BTK
Below-the-knee
BUN
Blood urea nitrogen
BW
Bandwidth
C
CABG
Coronary artery bypass graft
CAD
Coronary artery disease
CAS
Carotid artery stenting
CASH
Chemotherapy-associated steatohepatitis
CAVATAS
Carotid and Vertebral Artery Transluminal Angioplasty Study
CaVenT
Catheter-directed Venous Thrombolysis
CBC
Complete blood count
CBCT
Cone-beam computed tomography
CBF
Cerebral blood flow
CBV
Cerebral blood volume
CC
Cisterna chyli
CCA
Common carotid artery
CCD
Charge-coupled device
CCS
Canadian Cardiovascular Society
CDC
Centers for Disease Control and Prevention
CDT
Catheter-directed thrombolysis
CEA
Carcinoembryonic antigen; carotid endarterectomy
CFA
Common femoral artery
CFV
Common femoral vein
CHA
Common hepatic artery
CHF
Congestive heart failure
CIA
Common iliac artery
CIN
Contrast-induced nephropathy
CIWA
Clinical Institute Withdrawal Assessment
CKD
Chronic kidney disease
CLABSI
Central line-associated bloodstream infection
CLI
Critical limb ischemia
CMS
Centers for Medicare and Medicaid Services
CNS
Central nervous system
COPD
Chronic obstructive pulmonary disease
COX
Cyclooxygenase
CP
Cerebral protection
CPAP
Continuous positive airway pressure
CPAS
Congenital pulmonary artery stenosis
CPOE
Computerized physician order entry
CPR
Cardiopulmonary resuscitation
CPRF
Curved planar reformats
CPT
Current Procedural Terminology
Cr
Creatinine (serum)
CQI
Continuous quality improvement
CR-BSI
Catheter-related bloodstream infections
CRC
Colorectal cancer
CREST
Carotid Revascularization Endarterectomy versus Stenting Trial
CRP
C-reactive protein
CSF
Cerebrospinal fluid CsI Cesium iodide
CT
Computed tomography
CTA
Computed tomographic angiography
cTACE
Conventional transarterial chemoembolization
CTO
Chronic total occlusion
CTP
CT perfusion
CTV
Computed tomography venography
CV
Central venous
CVA
Cerebral vascular accident
CVC
Central venous catheter
CVD
Chronic venous disease
P.xxvii
CXR
Chest radiograph; chest xray
D
D5½NS
5% dextrose, half-normal saline solution
D5W
5% Dextrose solution
DAP
Dose-area product
DAVF
Dural arteriovenous fistula
DCI
Delayed cerebral ischemia
DEB
Drug-eluting bead; drugeluting balloon
DER
Dual energy radiography
DES
Drug-eluting stent
DH
Degree of hypertrophy
DIC
Disseminated intravascular coagulopathy
DICOM
Digital imaging and communication in medicine
DIPS
Direct intrahepatic portosystemic shunt
DLGJ
Double lumen gastrojejunostomy
DIR
Dose Index Registry; double inversion recovery
DM
Diabetes mellitus
DMSO
Dimethyl sulfoxide
DNI
Do not intubate
DNR
Do not resuscitate
DOQI
Disease Outcomes Quality Initiative
DQE
Detective quantum efficiency
DSA
Digital subtraction angiography
DTPA
Diethylenetriamine pentaacetic acid
DUS
Doppler ultrasound; duplex ultrasound
DVT
Deep vein thrombosis
E
E&M
Evaluation and Management
EASL
European Association for the Study of the Liver
ECG
Electrocardiogram
ECOG
Eastern Cooperative Oncology Group
ECST
European Carotid Surgery Trial
ED
Emergency department
EDV
End-diastolic velocity
EGFR
Epidermal growth factor receptor
eGFR
Estimated GFR
EIA
External iliac artery
ENT
Ear, nose, and throat
EPD
Embolic protection device
ERCP
Endoscopic retrograde cholangiopancreatography
ERF
Esophagorespiratory fistula
ESBL
Extended-spectrum betalactamase
ESCAPE
Endovascular Treatment for Small Core and Anterior Circulation Proximal Occlusion with Emphasis on
Minimizing CT to Recanalization Times
ESI
Epidural steroid injection
ESWL
Extracorporeal shock wave lithotripsy
EUS
Endoscopic ultrasound
EVA-3S
Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis
EVAR
Endovascular aortic aneurysm repair
EVLT
Endovenous laser treatment
EVOH
Ethylene vinyl alcohol
EXTENDIA
Extending the Time for Thrombolysis in Emergency Neurological Deficits-Intra-arterial
F
FB
Foreign body
FDA
U.S. Food and Drug Administration
FDG-PET
Positron emission tomography
FFP
Fresh frozen plasma
FHVP
Free hepatic venous pressure
FLR
Future liver remnant
FNA
Fine needle aspiration
FNH
Focal nodular hyperplasia
FOV
Field-of-view
P.xxviii
G
GA
General anesthesia
GABA
γ-Aminobutyric acid
Gd
Gadolinium
GDA
Gastroduodenal artery
GDC
Gugliemi detachable coil
Gd-MRA
Gadolinium enhanced MRA
GFR
Glomerular filtration rate
GI
Gastrointestinal
GJ
Gastrojejunostomy
GP
Glycoprotein
GSV
Greater saphenous vein
GU
Genitourinary
GW
Guidewire
H
HA
Hepatic artery
HAP
Hepatic artery pseudoaneurysm
HAS
Hepatic artery stenosis
HASTE
Half-Fourier acquisitions with single-shot turbospin echo
HAT
Hepatic artery thrombosis
HCC
Hepatocellular carcinoma
HCFMEA
Health Care Failure Mode and Effects Analysis
hCG
Human chorionic gonadotropin
HCl
Hydrochloride
Hct
Hematocrit
HD
Hemodialysis
Hgb
Hemoglobin
HHT
Hereditary hemorrhagic telangiectasia
HIFU
High-intensity focused ultrasound
HIT
Heparin-induced thrombocytopenia
HITT
Heparin-induced thrombocytopenia with thrombosis syndrome
HMPAO
Hexamethylpropyleneamine oxime
HMW
High-molecular-weight
HOCA
High-osmolality contrast agents
HPS
Hepatopulmonary syndrome
HR
Hazard ratio; heart rate
HSG
Hysterosalpingogram
HT
High thigh
HTN
Hypertension
HU
Hounsfield unit
HV
Hepatic venous
HVPG
Hepatic venous pressure gradient
I
IA
Intra-arterial
IC
Intracranial
ICA
Internal carotid artery
ICBT
Intercostobronchial trunk
ICD-10
International Classification of Diseases, 10th revision
ICH
Intracerebral hemorrhage
ICP
Intracranial pressure
ICSS
International Carotid Stenting Study
ICU
Intensive care unit
ID
Internal diameter
IFU
Instructions for use
IHI
Institute for Healthcare Improvement
IHSS
Idiopathic hypertrophic subaortic stenosis
II
Image intensifier
IIA
Internal iliac artery
IIEF
International Index of Erectile Function
IJ
Internal jugular
IJV
Internal jugular vein
IM
Intramuscular
IMA
Inferior mesenteric artery; internal mammary artery
IMS III
Interventional Management of Stroke III
IMV
Inferior mesenteric vein
INR
International normalized ratio
IO
Interventional oncology
IOM
Institute of Medicine
IPSS
International Prostate Symptom Score
IQR
Interquartile range
IR
Interventional radiology; interventional radiologist
P.xxix
IRE
Irreversible electroporation
ISAT
International Subarachnoid Aneurysm Trial
ISV
Internal spermatic vein
ITT
Intention to treat
IV
Intravenous; intravenously
IVA
Inferior vesical artery
IVC
Inferior vena cava
IVUS
Intravascular ultrasound
J
J-tube
Jejunostomy
K
KAP
Kerma-area product
KGR
Kinetic growth rate
KP
Kyphoplasty
K-RAS
Kirsten Rat Sarcoma Viral Oncogene Homolog
KTS
Klippel-Trenaunay syndrome
kVp
Kilovolt peak
KVO
Keep vein open
L
LA
Left atrial; left atrium
LAD
Left anterior descending
LAO
Left anterior oblique
LCD
Liquid crystal display
LDCT
Low-dose CT
LDH
Lactate dehydrogenase
LDL
Low-density lipoprotein
LFT
Liver function test
LGIB
Lower GI bleeding
LM
Lymphatic malformations
LMA
Laryngeal mask airway
LMWH
Low-molecular-weight heparin
LOCA
Low-osmolality contrast agents
LOCM
Low osmolar contrast medium
LSCA
Left subclavian artery
LSF
Lung shunt fraction
LSN
Last seen normal
LUTS
Lower urinary tract symptoms
LV
Left ventricle; left ventricular
LVEDP
Left ventricular enddiastolic pressure
LVEDV
Left ventricular enddiastolic volume
LVO
Large vessel occlusion
M
MAA
Macroaggregated albumin
MAC
Monitored anesthesia care
MAO
Monoamine oxidase
MAP
Mean arterial pressure
MBB
Medial branch block
MC
Manual compression
MCA
Middle cerebral artery
mCRC
Metastatic colon cancer
mCTA
Multiphase CTA
MD
Medical doctor
MI
Myocardial infarction
MIP
Maximum intensity projection
MODS
Multiple organ dysfunction syndrome
MPA
Multipurpose shape
MPR
Multiplanar reformations
MR
Magnetic resonance
MRA
Magnetic resonance angiography
MR CLEAN
Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute Ischemic Stroke in the Netherlands
MRCP
Magnetic resonance cholangiopancreatography
MRDSA
Magnetic resonance digital subtraction angiography
mRECIST
Modified Response Evaluation Criteria in Solid Tumors
MR RESCUE
Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy
MRI
Magnetic resonance imaging
MRV
Magnetic resonance venogram; magnetic resonance venography
P.xxx
mTICI
Modified thrombolysis in cerebral infarction
MTT
Mean transit time
MWA
Microwave ablation
N
nAC
n-Acetyl cysteine
NaHCO3
Sodium bicarbonate
NASCET
North American Symptomatic Carotid Endarterectomy Trial
nBCA
n-Butyl cyanoacrylate
NCCT
Noncontrast computed tomography
NG
Nasogastric
NG-tube
Nasogastric tube
NIH
National Institutes of Health
NIHSS
National Institutes of Health Stroke Scale
NINDS
National Institute of Neurological Disorders and Stroke
NKF-KDOQI
Kidney Disease Outcomes Quality Initiative
NLST
National Lung Screening Trial
NOHAH
Nonocclusive hepatic artery hypoperfusion syndrome
NOMI
Nonocclusive mesenteric ischemia
NPH
Neutral protamine Hagedorn
NPO
Nil per os
NS
Normal saline
NSAID
Nonsteroidal antiinflammatory drug
NSCLC
Non-small cell lung cancer
NSF
Nephrogenic systemic fibrosis
NTG
Nitroglycerin
NYHA
New York Heart Association
O
OD
Outer diameter
OP
Outpatient
OPSI
Overwhelming postsplenectomy infection
OR
Operating room
OSA
Obstructive sleep apnea
P
PA
Physician's assistant; pulmonary artery
PACS
Picture archiving and communication system
PAD
Peripheral arterial disease; pulmonary artery diastolic
PAE
Prostate artery embolization
PAP
Pulmonary arterial pressure
PARTO
Plug-assisted retrograde transvenous obliteration
PAVM
Pulmonary arteriovenous malformation
PBD
Percutaneous biliary drainage
PCA
Patient-controlled analgesia; posterior cerebral artery
PCC
Prothrombin complex concentrate
PCDT
Pharmacomechanical catheter-directed thrombolysis
PCI
Percutaneous coronary intervention
PC-MRA
Phase contrast-MRA
PCN
Percutaneous nephrostomy
PCORI
Patient-Centered Outcomes Research Institute
PCSA
Patient-controlled sedation
PCW
Pulmonary capillary wedge
PCWP
Pulmonary capillary wedge pressure
PD
Peritoneal dialysis
PDCA
Plan-Do-Check-Act
PE
Peroneal; pulmonary embolism/embolus
PEEP
Positive end-expiratory pressure
PEG
Polyethylene glycol
PEM
Polidocanol endovenous microfoam
P.xxxi
PERP
Patient entrance reference point
PET
Positron emission tomography
PFO
Patent foramen ovale
PGA
Polyglycolic acid
PGJ
Percutaneous gastrojejunostomy
PIAA
Physicians Insurers Association of America
PICC
Peripherally inserted central catheter
PIOPED
Prospective Investigation of Pulmonary Embolism Diagnosis
PJ
Percutaneous jejunostomy
PMMA
Polymethylmethacrylate
PMT
Percutaneous mechanical thrombectomy
PO
By mouth
PPH
Postpartum hemorrhage
P-PS
Power-pulse spray
pr
Per rectum
PRBC
Packed red blood cell
PRG
Percutaneous radiologic gastrostomy
PSA
Pseudoaneurysm
PSA
Prostate specific antigen
PSD
Peak skin dose
PSV
Peak systolic velocity
PT
Prothrombin time; posterior tibial
PTA
Percutaneous transluminal (balloon) angioplasty
PTC
Percutaneous transhepatic cholangiography
PTD
Percutaneous thrombolytic device
PTFE
Polytetrafluoroethylene
PTRA
Percutaneous transluminal renal angioplasty
PTS
Postthrombotic syndrome
PTT
Partial thromboplastin time
PTX
Pneumothorax
PV
Percutaneous vertebroplasty; portal vein/venous
PVA
Polyvinyl alcohol
PVC
Premature ventricular contraction
PVE
Portal vein embolization
PVR
Pulmonary vascular resistance; pulse volume recording
PVS
Portal vein stenosis
PVT
Portal vein thrombosis
Q
QA
Quality assurance
qEASL
Quantitative European Association for the Study of the Liver
qid
Four times per day
QISS
Quiescent interval single shot
QOL
Quality of life
R
RA
Right atrium
RAO
Right anterior oblique
RAPTURE
Radiofrequency Ablation of Pulmonary Tumors Response Evaluation
RAS
Renal artery stenosis
RBBB
Right bundle branch block
RBC
Red blood cell
RCA
Root cause analysis
RCC
Renal cell carcinoma
RCT
Randomized controlled trial
RF
Radiofrequency
RFA
Radiofrequency ablation
RHV
Right hepatic vein
RI
Renal insufficiency; resistive index
RIJ
Right internal jugular
RIM
Rösch inferior mesenteric
RN
Registered nurse
ROBOT
Rotational bidirectional thrombectomy
ROI
Region of interest
ROSE
Rapid on site evaluation
RPO
Right posterior oblique
RR
Respiratory rate
RT
Respiratory therapist
rt-PA
Recombinant tissue plasminogen activator
RV
Right ventricle
P.xxxii
RVEDP
Right ventricular enddiastolic pressure
RVR
Renal vein renin
S
SAH
Subarachnoid hemorrhage
SAP
Superabsorbent polymer
SBP
Systolic blood pressure
SBRT
Stereotactic body radiotherapy
SC
Subcutaneous; subclavian
SEER
Surveillance, Epidemiology, and End Results
SEMS
Self-expanding metallic stents
SEV
Superficial epigastric vein
SFA
Superficial femoral artery
sFLR
Standardized future liver remnant
SI
Sacroiliac
SICH
Symptomatic intracranial hemorrhage
SIN
Salpingitis isthmica nodosa
SIR
Society of Interventional Radiology
SIRS
Systemic inflammatory response syndrome
SK
Streptokinase
SMA
Superior mesenteric artery
SMV
Superior mesenteric vein
SNMMI
Society of Nuclear Medicine and Molecular Imaging
SNR
Signal-to-noise ratio
SNRB
Selective nerve root block
SPACE
Stent-supported Percutaneous Angioplasty of the Carotid Artery versus Endarterectomy
SPECT
Single-photon emission computed tomography
SPGR
Spoiled gradient echo
SPN
Solitary pulmonary nodules
SQ
Subcutaneous
SSFP
Steady state free precession
SSFSE
Single-shot fast spin echo
SSI
Surgical site infection
SSV
Short saphenous vein
STIR
Short T1 inversion recovery
STS
Sodium tetradecyl sulfate
SUV
Standardized uptake value
SVC
Superior vena cava
SVR
Systemic vascular resistance
SVS
Society of Vascular Surgery
SVT
Superfical venous thrombosis
SWIFT PRIME
Solitaire with the Intention for Thrombectomy as Primary Endovascular Treatment
T
TA
Tumescent anesthesia
TAA
Thoracic aortic aneurysm
TACE
Transarterial chemoembolization
TAE
Transarterial embolization
TCD
Transcranial Doppler
TcPO2
Transcutaneous oxygen pressure
TD
Thoracic duct
TDE
Thoracic duct embolization
TEE
Transesophageal echo
TELV
Total estimated liver volume
TEVAR
Thoracic endovascular aortic repair
TFT
Thin-film transistor
TIA
Transient ischemic attack
TIPS
Transjugular intrahepatic portosystemic shunt
TLR
Target lesion revascularization
TLV
Total liver volume
TNB
Transthoracic needle biopsy
TNK
Tenecteplase
TNM
Tumor, node, metastasis
TOF
Time-of-flight
TOPAS
Thrombolysis or Peripheral Arterial Surgery
TPN
Total parenteral nutrition
TR
Repetition time
TRICKS
Time Resolved Imaging of Contrast Kinetics
P.xxxii
TTP
Thrombotic thrombocytopenic purpura; time to peak
TTS
Time to start
TURP
Transurethral resection of prostate
U
UAE
Uterine artery embolization
UFE
Uterine fibroid embolization
UK
Urokinase
UR
Urinary retention
US
Ultrasound
UTI
Urinary tract infection
V
VAA
Visceral arterial aneurysms
VB
Vertebral body
VCD
Vascular closure device
VEGF
Vascular endothelial growth factor
VENC
Velocity encoding value
VIP
V-Twist Integrated Platform
VIPR
Vastly undersampled Isotropic Projection Reconstruction
VM
Venous malformations
[V with dot above]/[Q with dot above]
Ventilation/perfusion
VS
Vital signs
VT
Ventricular tachycardia
VTE
Venous thromboembolism
W
WBC
White blood cell
WHO
World Health Organization
WHOL
Worst headache of life
WHVP
Wedged hepatic venous pressure
1
Vascular Access and Catheter-Directed Angiography
Khashayar Farsad
Frederick S. Keller
Krishna Kandarpa
Indications
Catheter-based diagnostic angiography is most commonly performed either when there is intention to
proceed to endovascular intervention or when computed tomography (CTA) or magnetic resonance
angiography (MRA) is nondiagnostic or not possible. Indications include:
1. As part of percutaneous endovascular procedures (e.g., thrombolysis, balloon angioplasty, atherectomy,
thrombectomy, stenting, embolization, infusion of pharmaceuticals)
2. Diagnosis of primary vascular disease (e.g., vascular occlusive disease, vasculitis, vasospastic
disorders, aneurysms, arteriovenous [AV] malformations, AV fistulas)
3. Vascular complications of trauma, surgery, or disease
4. Preprocedural definition of vascular anatomy (e.g., for revascularization procedures, local tumor
resection, organ transplantation, complex embolization, assessment of arterial hemorrhage)
5. Diagnosis and localization of vascular tumors (e.g., parathyroid adenomas, pancreatic neuroendocrine
tumors)
Contraindications
Absolute
Medically unstable patient with multisystem dysfunction (If angiography is absolutely necessary, underlying
abnormalities should be corrected and preventive measures against anticipated complications should be
taken.)
Relative
1. Recent myocardial infarction, serious arrhythmia, and substantial serum electrolyte imbalance
2. Serious documented past contrast reaction (see Chapter 64)
3. Impaired renal status (see Chapter 65). Consider prehydration or CO2 angiography.
4. Uncooperative patient (consider general anesthesia)
5. Coagulopathies or seriously altered coagulation profile
6. Inability to lie flat on angiography table due to congestive heart failure or compromised respiratory status
7. Residual barium in abdomen from recent examination (will obscure details of visceral angiography)
8. Pregnancy, because of risk of exposure of fetus to ionizing radiation
9. Ehlers-Danlos syndrome (high risk of arterial injury, dissection)
Preprocedure Preparation
1. Evaluate and document the patient's chief complaint, brief medical history, significant past medical history,
allergies, previous surgical procedures, and
P.2
current medications (Fig. 1.1). Explain the procedure to the patient and perform a targeted physical examination
including peripheral pulses. All prior imaging studies and physiologic tests (e.g., noninvasive vascular tests,
magnetic resonance angiograms, computed tomograms, and radionuclide scans) should be available for review
at the time of the study.
FIGURE 1.1 • Patient data sheet.
2. Obtain informed consent (see Chapter e-95).

3. Check laboratory results including estimated glomerular filtration rate (eGFR), hemoglobin, international
normalized ratio (INR), partial thromboplastin time (PTT), and platelet count. Routine evaluation of coagulation
parameters prior to transfemoral angiography may not be needed in everyone, and limiting evaluation of the
coagulation profile to patients who have clinical evidence of a bleeding disorder or liver disease and to those
who are anticoagulated may avoid unnecessary testing and delay.
P.3
4. Preprocedure hospital fasting guidelines should be followed due to the possible need to administer conscious
sedation (e.g., solids and nonclear liquids 6 to 8 hours, clear liquids 2 to 4 hours) (1). Oral medications may be
taken with small quantities of water.
5. See Chapter 65 for a detailed approach to the hydration of a patient with underlying renal disease.
6. Patient must void urine before leaving for the angiography suite (unless the bladder is catheterized).
7. Considerations for patients with specific diseases or conditions: Consult with referring or managing clinician,
or both, on all items listed below (for more specific details, see the appropriate cited chapters).
a. Heparinized patient: Stop heparin infusion 2 hours prior to the arterial puncture in order to normalize the
coagulation status. A PTT of 1.2 times control is acceptable, in the absence of other bleeding abnormalities.
Alternatively, activated clotting time (ACT) may be followed. Because this test can be performed at the bedside,
the timing of catheter removal and reinstitution of heparin can be more accurately determined. Heparin may be
restarted within 2 to 4 hours after removal of the catheter for manual puncture-site compression or sooner in
selected cases (e.g., patients for whom an arterial puncture closure device was used or venous
catheterizations). For patients getting therapeutic dose injections of low-molecular-weight heparin, the dose prior
to the procedure is held (2).
b. Warfarinized patient: Stop warfarin (Coumadin) 3 to 5 days prior to arterial puncture if possible. For
hospitalized patients with persistently elevated INR and nonurgent indications for angiography, vitamin K (2 to 10
mg) may be administered either orally 24 to 48 hours preprocedure or intravenously (IV) 12 to 24 hours
preprocedure with serial monitoring of the INR for reversal (3). Patients who require procedures on an urgent or
emergent basis should be treated with short-acting products to reverse anticoagulation, such as fresh frozen
plasma (FFP), prothrombin complex concentrate (PCC), recombinant factor VIIa, or activated PCC. The goal is to
achieve an INR of 1.5 or less. For patients in whom discontinuation of anticoagulation is unacceptable (e.g.,
metal prosthetic heart valve), warfarin can be stopped and anticoagulation may be transitioned with low-
molecular-weight heparin as an outpatient, or the patient may be admitted for transition with IV heparin.
c. Oral anticoagulants: Three newer oral anticoagulant medications include the direct thrombin inhibitor,
dabigatran, and two direct factor Xa inhibitors, rivaroxaban and apixaban. These medicines have relatively short
halflives (<14 hours). As such, discontinuation for 1 to 2 days prior to arterial puncture is usually sufficient
(longer in patients with renal disease because these drugs are cleared by the kidneys) (4,5). Recently, a
monoclonal antibody fragment, idarucizumab, has been approved by the U.S. Food and Drug Administration to
neutralize the effects of dabigatran in the event of a bleeding emergency.
d. Antiplatelet agents: These include aspirin, clopidogrel, and glycoprotein (GP) IIb/IIIa inhibitors. Guidelines
recommend discontinuation of the latter two until cleared (5 to 7 days for clopidogrel, 8 to 48 hours for GP IIb/IIIa
inhibitors) or potential platelet transfusion for emergency cases (2,5).
e. Thrombocytopenic patient: For transfemoral or transaxillary punctures, the functional platelet count should
be greater than 50,000 per μL (2).
f. Insulin-dependent diabetic patient: In consultation with the referring physician, cut the morning insulin dose
by half and schedule the procedure for the morning if possible. A slow infusion of 5% dextrose may be started
prior to the procedure, and volume expansion with IV fluids is indicated to prevent contrast-induced nephropathy.
Blood glucose levels should be monitored during prolonged procedures; insulin dose may need to be titrated
before
P.4
resumption of usual regimen. If a diabetic patient on neutral protamine Hagedorn (NPH) insulin receives heparin
during the procedure, do not reverse the heparin with protamine sulfate because this may cause a fatal
anaphylactic reaction (6). Restart normal insulin schedule after the procedure once the patient has resumed oral
intake.
g. Renal dysfunction (see Chapter 65)
h. Prior documented reaction to iodinated contrast media: Use measures described in Chapters 64 and e-
89. Alternatively, consider gadolinium-enhanced MRA for patients without severe renal insufficiency. Carbon
dioxide arteriography, intra-arterial pressure measurements, and duplex scan (infrainguinal) arterial mapping may
aid diagnosis in selected patients. (See appropriate chapters.)
i. Precautionary measures: The patient’s chart should list the precautions necessary to protect both the
patient (especially if immunocompromised) and the personnel who may come in contact with a patient with an
infectious disease (e.g., HIV, infectious hepatitis, drug-resistant bacteria, Clostridium difficile).
j. Lidocaine hypersensitivity (local infiltration) (see Chapter 62). Consider:
(1) Local skin test, and if negative, proceed with local infiltration, or
(2) Procaine hydrochloride (or an aminoester local anesthetic rather than an aminoamide)
8. Medication precautions (see Chapters 62, 63, and e-94)
a. Sedation and analgesia: Most angiography and interventional procedures can be completed safely and
expeditiously with a judicious combination of midazolam and fentanyl, which provide adequate conscious
sedation and analgesia (7).
b. Age: Reduce medication doses by 30% to 50% for elderly patients.
c. Severe coronary artery or cerebrovascular disease: Avoid drugs that cause excessive drop in blood
pressure or cardiac output.
d. Seizures: Avoid drugs that lower seizure threshold (e.g., meperidine, phenothiazines).
e. Hepatic dysfunction: Avoid drugs such as barbiturates, which are metabolized by the liver. Reduce initial
doses of sedatives and analgesics.
f. Renal dysfunction: Extreme caution should be used in administering meperidine. Accumulation of its
metabolite in these patients may lead to central nervous system excitation and seizures.
g. Pheochromocytoma: Patients with labile blood pressure need α blockade (e.g., phenoxybenzamine) (8).
Consider consulting an anesthesiologist for the procedure. Short-acting agents, such as sodium nitroprusside,
should be available for treating potential hypertensive crisis. Avoid the use of glucagon in patients with
suspected pheochromocytoma.
h. Multiple myeloma: As with patients with diabetic nephropathy, these patients should be well hydrated in
order to prevent acute tubular necrosis.
i. Sickle cell anemia and polycythemia vera: Patients may suffer thromboembolic complications following
angiography (9).
j. Neuroendocrine tumors: Carcinoid crisis can be stimulated by angiography on patients with neuroendocrine
metastases to the liver. Consider pretreatment with intramuscular (IM) octreotide and have an octreotide drip
available (10).
Procedure
Retrograde Femoral Artery Catheterization, Seldinger Technique
1. Preparation
a. Sterile puncture-site preparation (iodine or chlorhexidine solution scrub following groin shave) and
draping of patient. The patient must be in a comfortable position that can be tolerated for the duration of the
procedure prior to preparation.
P.5
b. All patients subjected to any angiographic or interventional procedure under conscious sedation should
have continuous physiologic monitoring (see Chapters 62 and 63).
c. Induce local anesthesia with 1% or 2% lidocaine (without epinephrine). Consider the addition of 1 mL
sodium bicarbonate 8.4% in the syringe with each 10 mL of lidocaine to minimize the burning sensation
during injection.
(1) Skin wheal at the entry site (using 25-gauge, 5/8-in. needle) and deep on each side of the artery in an
inverted cone distribution (using 22- to 25-gauge, 1.5-in. needle).
(2) Avoid entering the artery or vein and injecting lidocaine into the vessel wall by gentle aspiration as the
needle is advanced, and injection of anesthetic upon needle withdrawal. Slow, gentle injection will save the
patient considerable discomfort. Wait 1 to 2 minutes after injection before making a superficial skin incision
(3 mm long × 3 mm deep) with a no. 11 blade scalpel.
(3) Use a curved 5-in. mosquito forceps to spread the subcutaneous tissues; avoid spreading down to the
artery. Adequate dissection of subcutaneous tissues in this manner facilitates subsequent passage of
catheters and sheaths, enables egress of blood at the skin rather than internally, and is also important
when considering use of an arterial closure device to allow the device to track easily to the arteriotomy site.
d. Check that fluoroscopy is working before the artery is punctured.
2. Femoral artery puncture (Fig. 1.2)
a. Locate the femoral artery and inguinal ligament (which runs from the anterior superior iliac spine to the
pubic tubercle) by palpation (Fig. 1.3). Th e true position of the inguinal ligament is about 1 to 2 cm below
the location estimated by palpation or fluoroscopy (11).
b. Localizing the puncture site by fluoroscopy over the femoral head or with specific palpation techniques
for anatomical localization is important to
(1) Prevent high arterial entry that cannot be adequately compressed and may lead to uncontrollable
internal bleeding
(2) Prevent low arterial entry that may result in pseudoaneurysm of the superficial femoral artery
c. The artery should be entered over the middle of the medial third of the femoral head; the skin entry site
should be over the inferior femoral head so that the arterial puncture is directly over the femoral head after
the needle has passed through the subcutaneous tissues. This puncture location enables adequate
compression of the artery against the femoral head at the end of the procedure. A window of only 3 to 5 cm
is available for safe common femoral artery puncture (Fig. 1.4).
d. Ultrasound guidance: Routine use has demonstrated decreased frequency of access site-related
complications in large retrospective and prospective series (12,13) and should be considered for all
punctures. This technique allows precise identification of the common femoral artery and allows for direct
single-pass puncture. Ultrasound guidance is ideal for patients with poorly palpable pulses and patients
who are obese or who have higher bleeding risks. The technique is as follows (Fig. 1.5):
(1) Localize the femoral head under fluoroscopy as described earlier.
(2) Use a high-frequency linear transducer draped with a sterile probe cover.
(3) Identify the common femoral artery and vein. The common femoral vein is identified by the confluence
with the great saphenous vein and will be easily compressible in the absence of thrombus. The common
femoral artery is directly lateral to the common femoral vein and will be pulsatile and not easily
compressible. The common femoral artery bifurcation should be identified by grayscale or color Doppler to
confirm a common femoral artery puncture above the bifurcation. Acoustic shadowing from calcified plaque
may obscure the artery lumen. Color
P.6
Doppler can be used in this instance to confirm patency and target for puncture if needed.
FIGURE 1.2 • Schematic of the Seldinger puncture technique using a needle covered by a plastic sheath.
Top to bottom: (1) Needle and stylet are introduced as a unit into the artery; (2) stylet is removed and
needle is withdrawn until brisk pulsatile backflow of blood is noted; (3) inner metallic cannula is removed; (4)
a wire is introduced through the plastic sheath; (5) wire is fixed and sheath is removed with compression
over the puncture site; (6) the track is dilated; and (7) a catheter is placed over the wire. (From Johnsrude
IS, Jackson DS, Dunnick NR. A Practical Approach to Angiography. 2nd ed. Boston, MA: Little, Brown;
1987:36, reprinted with permission.)
(4) Puncture the artery with the ultrasound probe in transverse orientation and the needle positioned along
the middle of the transducer. Standard or echogenic Seldinger needles (thin-walled, 18-gauge, 2.75-in.
long) or micropuncture needles can be used. Care should be taken to puncture the anterior arterial wall and
not the side of the artery due to poor visualization of the needle trajectory by ultrasound.
(5) After confirmation of arterial puncture by blood return and, ideally, by visualization of the needle tip in the
artery, a guidewire is advanced through the needle.
e. Puncture guided by palpation
(1) Instructions for a right-handed physician puncturing a right femoral artery: Place the left middle and
index fingers above and below the skin incision, respectively, to palpate the artery. Advance the access
needle with the right hand, parallel to the course of the femoral artery and at approximately 45 degrees with
respect to the skin, until the arterial pulsations
P.7
are felt or are transmitted through the needle. Enter the artery with a steady forward thrust.
FIGURE 1.3 • Anatomical relationships of the femoral artery. A: Shows the common femoral artery crossing
over the medial third of the femoral head. The vein (not shown) is approximately 0.5 to 1.5 cm medial to the
femoral artery. Arterial and venous puncture sites should be over the femoral head and well below the
inguinal ligament, which is shown crossing diagonally from the anterior superior iliac spine to the superior
pubic tubercle. (continued)
(2) In obese patients and in those with prior local surgery, the anatomical landmarks may be markedly
different from those expected.
(3) If difficulty is encountered in puncturing the artery, fluoroscopy may be used to direct the needle.
Alternatively, use ultrasound guidance.
(4) Arterial wall calcification will occasionally provide a target by fluoroscopy.
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FIGURE 1.3 • (Continued) B: A lateral view of the same region illustrates how the external iliac artery and
vein (not shown) dive deep into the pelvis above the inguinal ligament. A puncture site above the ligament
cannot be compressed and could result in a large pelvic hemorrhage.
f. Double- or single-wall entry is an acceptable technique. Single-wall punctures are useful when directly
accessing grafts, when the patient has abnormal clotting parameters, or when prevention of any puncture-
site bleeding is mandatory. Careful single-wall, single-stick entry is also important if one is considering using
a percutaneous arterial closure device. Improper technique can result in vessel wall trauma regardless of
the type of needle used. (For available needles, see Chapter e-92.)
g. Once there is good pulsatile blood return through the needle, a guidewire should be gently advanced up
the femoral artery, through the iliac arteries, and into the aorta under fluoroscopic guidance.
(1) Assessment if the blood return is nonpulsatile: venous puncture (puncture more laterally if necessary),
needle partially intramural (reposition), and severe occlusive disease (check with small hand injection of
contrast before proceeding).
(2) If difficulty is experienced in passing the wire out the tip of the needle, do not force the wire. Gentle
manipulation is permissible, but it is better to pull the wire out, hold pressure on the puncture site for 3 to 5
minutes, and start again.
(3) If the guidewire cannot be advanced through the iliac arteries, a 5 Fr. dilator can be introduced into the
femoral artery over the wire, and if brisk backbleeding is noted, contrast may be gently injected by hand to
evaluate the problem.
(4) Knowledge of the wires available and their uses will be helpful in negotiating tortuous or difficult iliac
arteries (see Chapter e-92).
3. Catheterization
a. Once the wire is advanced into the aorta, an appropriate dilator may be introduced over the wire, and the
dilator subsequently exchanged for the desired catheter.
(1) Advancing the catheter may be difficult if the entry route is too vertical or if subcutaneous tissues have
not been adequately spread.
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FIGURE 1.4 • Localization of femoral artery puncture site. A: Frontal view showing palpation by hand below
inguinal ligament. (continued)
(2) In obese patients, use a stiff wire (extrastiff, if necessary) to avoid subcutaneous buckling. A guidewire
with a diameter matching the inner lumen diameter of the angiographic catheter often works best due to a
smoother transition between the wire and catheter. Taping the lower abdominal pannus back away from the
groin is also useful.
(3) An appropriately sized introducer sheath may be used for patient comfort and to minimize risk of arterial
trauma, especially if multiple catheter exchanges are anticipated. If a sheath is used, it is important to
frequently flush the sheath or connect it to a pressure bag with heparinized saline to prevent thrombus from
forming within the sheath.
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FIGURE 1.4 • (Continued) B: A hemostat is placed, and proper position is checked fluoroscopically
(optional, but can also serve to test fluoroscopy before puncture). (continued)
b. Always confirm the position of the tip of the catheter fluoroscopically prior to power injection.
(1) Check for free backflow, aspirate, and flush.
(2) Inject a small amount of contrast by hand to confirm vessel location.
(3) Avoid power injection into the intercostal and lumbar arteries.
4. Injection and imaging: Inform technologist of desired contrast, volume, and flow rate based on catheter
location and determine the desired filming sequence and positions (see subsequent tables for suggested
angiography protocols).
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FIGURE 1.4 • (Continued) C: Lateral view showing relationship of skin incision site to vessel-wall puncture
site. (continued)
Other Arterial and Venous Accesses

1. Antegrade femoral artery puncture (Fig. 1.6): The skin incision (not the arterial puncture site) may
have to be above the inguinal ligament in some patients. Just as in retrograde puncture, the goal is to have
the arteriotomy directly over the femoral head after passing through the subcutaneous tissues. A good
landmark for the skin incision is the acetabulum. Arterial puncture site, angle of entry, and technique are
otherwise similar to the retrograde approach. In obese patients, the pannus should be upwardly retracted
and secured; however, an antegrade approach may prove impractical in many obese patients due to the
challenge of passing through the lower abdominal pannus to appropriately access the artery over the
femoral head.
2. Converting a retrograde to an antegrade femoral artery puncture: A reverse-curve or “shepherd’s
crook”-shaped catheter-guidewire combination can be used to pass the guidewire antegrade past the
ipsilateral puncture site, followed by catheter advancement over the guidewire. If this technique is
anticipated, a more vertical puncture through the subcutaneous tissues directly over the femoral head may
be considered to facilitate catheterization in both retrograde and antegrade fashion.
3. Left axillary artery or brachial artery puncture: used when there is no femoral artery access, if there
is no evidence of stenosis in the subclavian or axillary arteries (14), and when radial access is not
appropriate
a. Abduct the left arm and place the hand under the patient’s head.
b. Obtain baseline axillary, brachial, radial, and ulnar pulses.
c. Locate the puncture site of the axillary artery along the lateral axillary fold over the proximal humerus
(neck) so that the underlying bone provides support during compression (Fig. 1.7). A high brachial artery
puncture site would be over the proximal humeral shaft. A low brachial artery puncture would
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be close to the distal humerus, where it may be easier to compress over the humeral shaft by the elbow.
FIGURE 1.4 • (Continued) D: Seldinger needle in the vessel. (continued)
d. Administer local anesthesia carefully and avoid deep penetration because of the proximity of the brachial
plexus. One of the complications of an axillary artery puncture is a hematoma causing compression of the
brachial plexus, which is why a brachial artery puncture is often preferred.
e. Ultrasound guidance is highly recommended for upper extremity arterial access. The artery is again
identified by its relative noncompressibility compared to the vein or the presence of pulsatile Doppler flow.
f. The axillary and brachial arteries are easily displaced sideways. Therefore, fix the artery firmly at the
intended puncture site with your (left) index and
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middle fingers on either side. Use of an intra-arterial sheath with brachial artery access is recommended to
facilitate catheter exchanges and provide a means for infusion of vasodilators and calcium channel blockers
if needed.
FIGURE 1.4 • (Continued) E: Frontal view showing needle tip within lumen and stylet removed. (continued)
g. The Potts-Cournand needle, which has a sharp stylet with a perforated hub, will allow easy single-wall
entry.
h. A micropuncture set may be less traumatic.
i. Angle the needle at 45 degrees with respect to the skin and gently advance it as a unit. When arterial
blood is seen exiting from the hub, place the catheter with the usual Seldinger exchange technique.
4. Radial artery puncture: used when there is aortoiliac occlusive disease, anatomy difficult to cannulate
from the femoral route, desire for early ambulation, need for anticoagulation and antiplatelet agents, or a
patient who cannot safely discontinue anticoagulation
a. Radial artery access kits are commercially available. This typically includes a short 1.5 cm 21-gauge
access needle, a 0.018- to 0.025-in. microwire, and 4 to 6 Fr. hydrophilic introducer sheaths with a tapered
transition between the introducer and sheath (15).
b. Optimal patients—strong radial pulse, normal Allen’s or Barbeau test, no vasospasm (e.g., Raynaud),
and no present or planned same arm AV fistula for dialysis. The ulnar artery may be used, but achieving
adequate hemostasis with compression may be trickier due to the relationship of the ulnar artery to the
carpal bones.
c. Allen’s test is performed by manual compression of both radial and ulnar arteries while the patient
clenches his or her fist until the hand becomes blanched (Fig. 1.8). The hand is opened and compression of
the ulnar artery released, observing for the presence of capillary refill in the hand. A normal Allen’s test
demonstrates reperfusion within 7 seconds, whereas an abnormal test takes over 15 seconds. Waveform
plethysmography with a pulse oximeter on the thumb (Barbeau test) is a more sensitive method to monitor
reperfusion. Abnormal Allen’s test is a relative contraindication for transradial access due to the risk of radial
artery occlusion.
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FIGURE 1.4 • (Continued) F: Guidewire is passed through needle into vessel and up into the aorta. Wire is
used to dilate the tract and place the catheter (not shown).
d. The hand is placed supine on an arm board and taped in a dorsiflexed position with a rolled towel or
dedicated support under the wrist (Fig. 1.9). Access is achieved using either palpation or ultrasound
guidance. Some physicians use a steeper angle of access (60 to 70 degrees) for ease of compression post
procedure. A cocktail of a calcium channel blocker (e.g., verapamil 2.5 mg), vasodilator (e.g., nitroglycerine
0.25 mg), and heparin (e.g., 2,500 to 5,000 IU) is administered immediately via the radial artery sheath to
minimize vasospasm and vessel thrombosis. The cocktail is typically mixed with blood or saline to minimize
pain from vessel irritation.
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FIGURE 1.5 • A: Transverse grayscale ultrasound view of the common femoral artery (Art) and vein (Vn)
using a linear transducer. B: Color Doppler view of the artery and vein in the same orientation. (continued)
e. The sheath can be promptly removed, even with the patient fully anticoagulated. Radial compression
devices with an inflatable bladder are designed to maintain hemostasis without obliterating blood flow (Fig.
1.10). The compression devices restrict wrist flexion and are worn between 1 hour and 4 hours, during
which the patient may sit up or ambulate.
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FIGURE 1.5 • (Continued) C: Orientation of the transducer and needle during ultrasound-guided puncture.
D: Needle tip (arrow) seen in the artery after passing through the subcutaneous tissues (dashed line).
f. Complications are rare but include spasm, dissection, radial artery occlusion, digital ischemia, traumatic
AV fistula, hematoma, and compartment syndrome. Complications are more frequent when there are
anatomical variations.
5. Femoral vein puncture
a. The femoral vein is located about 0.5 to 1.5 cm medial to the femoral artery (see Fig. 1.3). Preparation is
similar to arterial puncture described earlier.
b. Single-wall needle technique: Using ultrasound guidance makes puncture far easier and minimizes the
chance of arterial trauma. An 18-gauge single-wall bevel-tipped needle (no inner stylet) or micropuncture
needle is attached to a 5-mL syringe filled with approximately 1 mL of heparinized
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saline. The femoral vein is located as previously described, and the patient is asked to perform a Valsalva
maneuver to distend the vein during which time the needle-syringe assembly is advanced toward the
femoral vein with gentle intermittent suction. When the anterior wall of the vein has been crossed, dark
venous blood will be noted in the syringe with aspiration. Gently detach the syringe while keeping the
position of the needle firmly fixed. If nonpulsatile venous blood is noted exiting from the needle hub, the
appropriately
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sized wire is advanced into the femoral vein. Subsequent dilation and catheter placement is similar to the
arterial technique described earlier.
FIGURE 1.6 • Proper needle position for an antegrade femoral puncture in lateral view.
FIGURE 1.7 • Anatomic relationship of the axillary artery to the humeral head and location of axillary and
high brachial artery puncture sites.
FIGURE 1.8 • Allen’s test. Compression over both radial and ulnar arteries is performed while the hand is
clenched in a fist, causing blanching of the skin. The hand is then opened, and compression over the ulnar
artery is released to see whether ulnar arterial flow is sufficient to reperfuse the hand.
c. Seldinger needle technique

(1) A Seldinger needle (18 gauge) is used to obtain access to the vein. It is useful to have the patient
perform the Valsalva maneuver while you are trying to puncture it. Skin entry site and venous puncture site
should be medial to the artery by about 1 cm and below by about 1 cm.
FIGURE 1.9 • Radial artery puncture. A: The hand is placed supine and in slight dorsiflexion with a towel or
dedicated splint. Palpation or ultrasound guidance is then used to get micropuncture access to the radial
artery. (continued)
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FIGURE 1.9 • (Continued) B: Using the Seldinger technique, a sheath is advanced over the wire for stable
access into the artery.
(2) Once the needle is down to the periosteum of the femoral head, the inner stylus is removed and a 20-mL
syringe is attached to the needle. The needle is then slowly withdrawn with gentle intermittent aspiration.
When free nonpulsatile flow of dark blood is seen, the needle tip is in the vein. A wire may then be
advanced through the needle and into the vein. Subsequent dilation and catheter placement is similar to the
arterial technique described earlier.
(3) A drawback to the Seldinger technique for femoral vein puncture is that if the artery is more superficial
than the vein, it may be unknowingly traversed by the needle causing arterial injury or the creation of an AV
fistula.
d. Postprocedure manual compression for 5 to 10 minutes is usually sufficient.
Postprocedure Management (1)

1. Compression of arterial puncture (15 minutes): If the patient has been heparinized during the procedure,
make sure the coagulation parameters have normalized (PTT close to control value or ACT of approximately 150
seconds) before the catheter is removed and the puncture site is compressed.
FIGURE 1.10 • Radial artery compression. A soft air-filled bladder provides compression when inflated to the
mean arterial blood pressure to provide hemostasis while preserving blood flow.
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a. Make sure the patient is comfortable because cooperation is essential during compression. Administer
additional lidocaine around the puncture site as needed.
b. Remove the catheter as you are about to compress the artery. A wire should be placed to straighten the curl
of a pigtail catheter before it is removed to reduce risk of vessel injury.
c. Use impermeable gloves during compression. No sponges or towels should be used. Any bleeding should be
visible. Remove drapes from the patient’s inguinal area to make sure no hematoma is forming that would
otherwise be obscured.
d. Compress the actual puncture site with the middle finger. Compress above the site with the index finger and
below it with the ring finger (Fig. 1.11).
e. Do not obliterate the pulse. Distal pulses should be faintly palpable.
f. Apply steady moderate pressure for 10 minutes. Then gently reduce pressure over the next 5 minutes. Never
remove compression abruptly.
g. If rebleeding occurs, repeat compression for 15 minutes.
h. Devices for unattended prolonged groin compression (e.g., C-clamp, pneumatic compression cuffs) are labor-
saving for selected cooperative patients but require familiarity by personnel. Utilize a protocol for man agement.
i. At termination of compression, palpate all distal pulses and compare with baseline examination.
j. Bed rest with legs extended should be ordered for 4 to 6 hours (the head of the bed may be elevated slightly
using power controls); patient may be allowed to “log roll” with assistance.
2. Arterial puncture closure devices: See Chapter 3.
3. Compression of venous puncture (5 to 10 minutes): Apply steady pressure as described earlier, easing off
gently toward the end. For uncomplicated, small French-size venous punctures, bed rest may be limited to 2 to 3
hours.
4. Check groin for bleeding or hematoma every 15 minutes for 1 hour, then every 30 minutes for 1 hour, and then
every hour for 4 hours.
FIGURE 1.11 • Lateral view of a right hand compressing a right femoral artery against the femoral head. The
middle finger rests over the arterial puncture site, the index finger is above, and the ring finger is below.
Compression should not obliterate the vessel lumen.
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5. Check blood pressure and pulse every 30 minutes for 2 hours and then every hour for 4 hours.
6. IV fluids: 1,000 mL 5% dextrose, half-normal saline solution (D5½NS) at 125 to 250 mL per hour and then
1,000 mL D5½NS at 75 to 150 mL per hour or until the patient can take oral food and liquid. Adjust fluid
administration according to patient’s cardiopulmonary and renal status.
7. If the patient is unable to void and is in urinary distress, a urinary catheter may be placed until the patient is
able to ambulate.
8. Resume diet and previous orders.
9. If heparinization is needed, and there are no puncture site-related problems, restart IV infusion in about 2
hours.
10. Postprocedure check is performed on all inpatients on the evening of and the day after the procedure in
order to assess and manage any untoward effects of the procedure.
Prevention and Management of Complications

1. The incidence of complications (Table 1.1) may increase with the severity of the underlying clinical status
of the patient and the duration of the procedure; therefore, expeditious procedures are the goal.
2. Thrombosis
a. Catheter factors include size (relative to arterial lumen), type of material, and length of time catheter is
exposed to blood.
b. Patient factors include extent of intimal vessel damage, vasospasm, and coagulation status.
c. Systemic heparinization reduces risk of thrombosis.
3. Hemorrhage (puncture-site hematoma)
a. Locate puncture site accurately over the femoral head because compression of the artery is best at that
site; arterial punctures above and below the femoral head are difficult to compress adequately.
b. Always compress above skin entry site (gentle, nonocclusive compression with one finger above, one
finger at, and one finger below skin entry site is best).
c. If the angle of the needle is too flat, puncture of the posterior wall may be above the inguinal ligament;
this will predispose to retroperitoneal hematoma.
d. Using smaller sized catheters (5 Fr. and below) may reduce the degree of hemorrhage.
e. Reversal of anticoagulation to baseline status by monitoring ACT can minimize risk of hemorrhage.
f. Management of puncture-site hematoma or uncontrollable bleeding
(1) If a groin hematoma is present, trace its margins with unwashable ink and follow any increase in size.
(2) Notify a vascular surgeon in cases of uncontrollable puncture-site bleeding, diminution or loss of pulses,
neurologic symptoms in the extremity, or suspicion of a retroperitoneal hematoma (in this case, obtain an
abdominal CT scan to confirm or rule out the diagnosis quickly).
4. Pseudoaneurysm: Avoid superficial femoral artery puncture (low puncture); adequate groin compression
becomes difficult without support of the femur underneath. See Chapter 4 for treatment.
5. Embolization: To prevent sequelae of distal embolization, consider:
a. Immediate percutaneous or surgical thrombectomy
b. Selective catheter-directed thrombolysis, depending on the severity and progression of symptoms
6. Contrast-induced nephropathy: See Chapter 65.
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Table 1.1 Complications of Angiography—Types and Incidence (%)

Site
Complication Femoral Axillary
Overall incidence 1.73 3.29
Deatha 0.03 0.09
Systemic
Cardiac 0.29 0.26
Cardiovascular collapse 0.03 0.04
Neurologic (overall) 0.17 0.46
Seizures 0.06 0.15
Renal failure 0.01 0.01
Fever/chills 0.004 0.004
Puncture site
Hemorrhageb 0.26 0.68
Thrombosis/obstructionc 0.14 0.76
Pseudoaneurysm 0.05 0.22
Arteriovenous fistula 0.01 0.02
Limb amputation 0.01 0.02
Total 0.47 1.7
Catheter- and guidewire-related
Perforation/contrast extravasation 0.44 0.37
Distal embolism 0.10 0.07
Breakage 0.10 0.02

Idiosyncratic contrast reaction
Overall incidence 4.0
Requiring hospitalization 0.1
Fatal outcome (1/20,000) 0.006
aAbout 25% of deaths are due to aortic dissection or rupture; 18% are due to cardiac
complications.
bComprises about 25% of complications requiring surgery. Hemorrhage is also the most common
complication not requiring surgery.
cComprises about 50% of complications requiring surgery. The incidence of asymptomatic

thromboembolism is higher.
Injection Rates and Image-Acquisition Programs

Catheter Angiography
Injection rates and image-acquisition programs should be tailored for the patient when indicated; however, for the
vast majority of studies, routine programs are useful (Tables 1.2, 1.3, 1.4, 1.5). The suggested injection volumes
and rates are applicable for digital angiography if sufficiently diluted contrast medium is used. When using
nondiluted contrast, both rates and volumes may be adjusted down significantly, especially for selective
injections into smaller vessels (e.g., visceral, renal, and extremity arteries). One should inject at a sufficient rate
and volume to adequately visualize the segment of interest (usually the length of the vessel included within the
acquisition frame) while accounting for washout and dilution by the incoming blood.
Cone-Beam CT
Cone beam can be used for rotational angiography to define vascular supply and anatomy as well as for soft
tissue tomography to assess tissue perfusion and efficacy of embolization (16,17). Applications include
identification of arterial supply
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and assessment of tumor embolization during transarterial chemoembolization, identification of arterial supply to
aneurysms or vascular malformations, identification of the adrenal vein during adrenal vein sampling, and
identification and treatment of endoleaks related to endovascular abdominal aortic aneurysm repair (16). After
catheterization, the patient and C-arm are appropriately positioned for acquiring cone-beam CT (CBCT). Often,
power injection is used with nondiluted versus diluted contrast depending on the indication and manufacturer
recommendations. Depending on catheter location, injection rates are between 1 mL and 12 mL per second, and
an initial 2- to 10-second acquisition delay is selected for the arteriographic phase, followed by various delayed
phases to highlight parenchymal and venous structures. A sample protocol for imaging the liver during
transarterial chemoembolization is provided in Table 1.6 (17). Once the images are acquired, dedicated software
processes the imaging data from the various projections on a reconstruction workstation to provide multiplanar
and three-dimensional (3D) rendered images. The technology for this application continues to evolve to improve
soft tissue contrast resolution, greater field of view, faster acquisition, and decreased radiation.
Table 1.2 Visceral and Peripheral Angiography (General Guidelines)
Total
Volume and
Study (Injection Site) Ratea Image-Acquisition Programb
Abdominal aortogram (above celiac 40 mL at 20 3/s × 2 s 1/s × 3 s

axis) mL/s
Arch aortogram 50 mL at 25 3/s × 3 s 1/s × 3s

mL/s
Bilateral lower extremity runoff (distal 96 mL at 8 1/s × 3 s = pelvis 1/s × 2 s = thigh 1/s ×
aorta) mL/s 4 s = knee Delays = calf/foot
Pelvic arteriogram (distal aorta) 30 mL at 15 2/s × 3 s 1/s × 3 s

mL/s
Unilateral lower extremity runoff 60 mL at 6 1/s × 3 s = pelvis 1/s × 2 s = thigh 1/s ×

(ipsilateral common iliac artery) mL/s 3 s = knee Delays = calf/foot
Renal transplant (iliac fossa; ipsilateral 12 mL at 6 3/s × 2 s 2/s × 2 s Delays as needed

common iliac artery) mL/s
Renal transplant (iliac fossa; selective 10 mL at 4 3/s × 2 s 2/s × 2 s Delays as needed

ipsilateral hypogastric artery) mL/s
Unilateral renal arteriogram (proximal 12 mL at 6 3/s × 2 s 1/s × 2 s Delays as needed

ipsilateral renal artery) mL/s
Celiac arteriogram (selective) 30 mL at 6 2/s × 3 s Delays for portal venous phase

mL/s
Hepatic arteriogram (selective) 20 mL at 4 2/s × 3 s 1/s × 3 s Delays as needed

mL/s
Gastroduodenal arteriogram (selective) 15 mL at 3 2/s × 2 s 1/s × 3 s Delays as needed

mL/s
Splenic arteriogram (selective) 20 mL at 4 1/s × 3 s Delays as needed

mL/s
Left gastric arteriogram (selective) 15 mL at 3 1/s × 4 s Delays as needed

mL/s
Superior mesenteric arteriogram 30 mL at 6 1/s × 4 s Delays for portal venous phase

(selective) mL/s
Inferior mesenteric arteriogram 15 mL at 3 2/s × 2 s 1/s × 3 s Delays as needed

(selective) mL/s
Lumbar arteriogram (selective) 6 mL hand 1/s
Inferior phrenic arteriogram (selective) 12 mL at 3 1/s × 8 s

mL/s
Subclavian arteriogram (distal to 18 mL at 6 1/s stations to hand

cephalic arteries) mL/s
Hand arteriogram (midbrachial artery) 16 mL at 4 1/s until venous phase

mL/s
aBased on digital subtraction angiography (DSA) with isosmolar contrast.
bDelays = one image every second or every other second for parenchymal and venous phases.
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Table 1.3 Venography
Image-
Acquisition
Study (Injection Site) Total Volume and Rate Program
Inferior venacavogram (from iliac vein 40 mL at 20 mL/s 4/s × 4 s

confluence)
Common femoral vein 24 mL at 6 mL/s 2/s × 4 s
Renal venogram (selective) 25 mL at 10 mL/s after injecting 2/s × 4 s 1/s × 2 s

epinephrine into renal artery
Adrenal venogram (selective) Left: 8 mL by hand Right: 5 mL by 2/s 2/s

hand
Superior venacavogram (unilateral or 30 mL at 15 mL/s 0 × 3 s 1/s × 12 s

bilateral antecubital vein)
Wedge hepatic venogram 5 mL by hand 2/s
Table 1.4 Pulmonary Angiography
Study (Injection Site) Total Volume and Rate Image-Acquisition Program
Unilateral pulmonary arteriogram 50 mL at 25 mL/s 4/s × 3 s 1/s × 3 s
Lobar pulmonary arteriogram 18 mL at 6 mL/s 4/s × 3 s 1/s × 3 s
Right ventriculogram (intracavitary) 50 mL at 15 mL/s Cine
Right atriogram (intracavitary) 50 mL at 25 mL/s Cine
Table 1.5 Useful Obliquities for Peripheral Angiography
Anatomy of Interest Projection
Carotid bifurcation Lateral and AP (with head turned opposite)
Carotid siphon Lateral
Circle of Willis Variable AP views in different craniocaudal projections
Aortic arch (to open arch) AP and steep (70 degrees) LAO
Aortic arch (for brachiocephalic 45-degree LAO with head true lateral, chin raised, and shoulders
vessels) dropped down
Selective pulmonary artery AP and lateral; left 45-60 degrees LAO; right 45-60 degrees RAO
Opposite obliques for lower lobe branches
Origins of mesenteric vessels Lateral aorta
Hepatic artery branches Left: RAO 30-45 degrees Right: LAO 30-45 degrees
Origin of renal arteries 10-15 degrees LAO
Common iliac bifurcation Contralateral oblique 45 degrees

Common femoral bifurcation Ipsilateral oblique 45 degrees
AP, anteroposterior; LAO, left anterior oblique; RAO, right anterior oblique.
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Table 1.6 Sample Cone-Beam CT Protocol for Hepatic Angiography (17)
Catheter Contrast Injection Scan

Location Volume Rate Dilution Time Acquisition Delay Findings
Proper or 12-64 1-3 mL/s 100-370 5-10 2-10 s arterial phase Tumor supply
selective mL mg s followed by 20-40 s in first phase;
hepatic iodine/mL parenchymal/venous parenchymal
artery phase enhancement
or
pseudocapsule
in delayed
phases
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complications. Clin Radiol . 1992;45:390-394.
15. Caputo RP, Tremmel JA, Rao S, et al. Transradial arterial access for coronary and peripheral
procedures: executive summary by the Transradial Committee of the SCAI. Catheter Cardiovasc Interv.
2011;78:823-839.
16. Angle JF. Cone-beam CT: vascular applications. Tech Vasc Interv Radiol . 2013;16:144-149.
17. Tacher V, Radaelli A, Lin M, et al. How I do it: cone-beam CT during transarterial chemoembolization for
liver cancer. Radiology. 2015;274:320-334.
2
Diagnostic Venography
Rulon L. Hardman
Krishna Kandarpa
Diagnostic venography is performed only when noninvasive imaging is nondiagnostic or prior to a contemplated
intervention. It is an infrequent first-line modality because of the accuracy of noninvasive imaging—both for
peripheral (Doppler ultrasound) and central (computed tomography venography [CTV]/magnetic resonance
venography [MRV]) veins. Preintervention venography is discussed in the appropriate chapters. The discussion
here is restricted to the careful technique required for performing high-quality, diagnostic venography.
Indications
Lower Extremity Venography
1. Diagnosis of deep vein thrombosis (DVT) following nondiagnostic or incomplete ultrasound examination;
also, when there is a high clinical suspicion for DVT but an extremity ultrasound study is negative
2. Planning for catheter-directed venous thrombolysis
3. Evaluation of venous malformations
4. Evaluation of venous encasement by tumor
5. Evaluation of venous reflux and valvular incompetency by descending lower extremity venography
Upper Extremity Venography
1. Diagnosis of superficial thrombosis or DVT following nondiagnostic or incomplete ultrasound examination
2. Evaluation of superior vena cava (SVC) or subclavian vein obstruction or stenosis (1)
3. Evaluation for external compression of the axillary-subclavian vein secondary to clavicular fracture,
thoracic outlet syndrome, or neoplastic compression
4. Presurgical mapping for hemodialysis access (2)
5. Planning for complicated central venous access or evaluation following a complication of central venous
access
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Contraindications
Relative
1. Previous contrast reaction (premedicate if necessary)
2. Renal insufficiency
3. Pregnancy—complement venography with duplex ultrasound and MRV to minimize radiation to the fetus.
Use lead shielding over pelvis during fluoroscopy.
4. Severely compromised cardiopulmonary status
1. Clarify the indication for the procedure.
2. Review all prior ultrasounds, venous plethysmography, and available crosssectional imaging.
3. Restrict oral intake to clear liquids; nil per os (NPO) if planning conscious sedation (as guided by hospital
policy).
4. Evaluate recent creatinine and hydration status, especially in patients with diabetes.
a. If a large contrast volume is anticipated, intravenous (IV) hydration may be appropriate.
b. Hold metformin in patients with diabetes and/or compromised renal function; restart following creatinine
evaluation in 48 hours.
5. Obtain informed consent.
Procedure
Lower Extremity Ascending Venography (3,4)
Of the several variations of ascending lower extremity venography reported, the two most commonly cited
are the Greitz technique (as modified by Rabinov and Paulin) and the Thomas technique (5,6). A
combination of these methods, which were developed with overhead filming incorporated for conventional
fluoroscopic rooms, is described. Tilting fluoroscopic tables now have integrated digital subtraction imaging,
which permits further modification of these techniques.
1. Patient is positioned on a fluoroscopic tilt table, preferable with integrated digital subtraction angiography
(DSA) capability. A 6-in. or 12-in. footrest is used to support the contralateral leg. The knee of the extremity
being studied can be supported in 30 degrees of flexion with a foam pad to improve flow through the
popliteal vein. Avoid excessive external compression, which can obstruct the popliteal vein.
2. Access a peripheral vein on the dorsum of the foot with a 20-gauge or 21-gauge butterfly needle or small
peripheral IV catheter. Direct the needle toward the toes if possible to aid in filling the deep veins. If
extravasation is seen, leave the catheter in place and select another location for access.
a. A swollen foot can lead to compression of the superficial veins.
(1) Elevate the extremity for several hours prior to the procedure, and/or
(2) Wrap the foot in elastic bandage for 30 to 60 minutes or longer, as necessary.
b. Collapsed, poorly visible veins
(1) Keep the extremity in a dependent position, and/or
(2) Apply warm compresses to the dorsum of the foot.
(3) Ultrasound guidance is now routinely used to aid difficult access.
3. Infusion setup. Attach a three-way stopcock, with inputs for a contrast syringe and heparinized saline
syringe or bag.
4. Venography is performed with nonionic, low-osmolar or iso-osmolar contrast with concentration between
200 mg per mL and 300 mg per mL. High concentration (350 mg per mL) contrast may not mix as well with
blood as a lower concentration. Routine venography usually requires between 50 mL and 100 mL of
contrast.
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FIGURE 2.1 • Tilt table ascending leg venography. Spot images are obtained as follows. A: Below the knee
with table tilted 45 to 60 degrees: AP and lateral projections. B: Over the knee with table tilted 30 to 45
degrees: AP and lateral projections. C: Over the thigh and groin with table tilted 15 to 30 degrees: AP
projection. D: Supine frontal overhead image of pelvis and lower abdomen. A Valsalva maneuver,
performed during elevation of the examined leg, facilitates opacification of the iliac veins and inferior vena
cava. (From Kim DS, Orron DE. Peripheral Vascular Imaging and Intervention. St. Louis, MO: Mosby Year
Book; 1992:284, with permission.)
5. Standard views (Fig. 2.1)

a. With the table upright at 45 to 60 degrees, gently inject contrast by hand and periodically assess the vein
puncture site for extravasation. Barring none, follow the IV contrast column intermittently with fluoroscopy
until contrast reaches the popliteal vein (about 50 mL).
b. Obtain anteroposterior (AP) and lateral spot views of the lower leg (anterior tibial, posterior tibial, and
peroneal veins) by manually rotating the extremity or the C-arm. Magnified views are obtained at any area
of discontinuous or clot-filed vein.
c. AP spot views of the popliteal vein are obtained with the table at 30 to 45 degrees. Bilateral oblique views
are recommended.
d. AP views of the thigh are obtained with a decrease tilt to 15 to 30 degrees. Flow may be brisk through
the thigh and digital imaging at one or two frames per second may be required.
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e. Continue venography through the pelvic veins, to the confluence at the inferior vena cava. An AP view is
taken of the pelvis. Bilateral obliques are recommended to evaluate the internal iliac veins. If a positive
diagnosis of thrombus is made at a lower level, especially in pregnant patients, a limited exam is appropriate
and examination of the pelvis is not necessary.
f. To improve visualization of the iliac veins and inferior vena cava (IVC), DSA runs with imaging at two or
three frames per second are used in combination with one of the following techniques:
(1) Have patient compress his or her femoral vein below the inguinal ligament during contrast injection to fill
the extremity veins. Release compression just prior to radiographic exposure of the pelvis.
(2) Manually compress the calf and thigh veins (if no large clots are seen in large veins on fluoroscopy)
while imaging the upstream veins.
(3) Raise leg or tilt table to horizontal position prior to quickly imaging pelvic veins.
6. Preferential filling of superficial veins
a. Placement of both an above ankle and above knee tourniquet improves deep venous filling. Using
tourniquets may cause venous spasm or artifact at the tourniquet site. Imaging can be performed with and
without tourniquets in place.
b. A blood pressure cuff inflated to 50 mm Hg just above the ankle may afford uniform compression and
avoid the artifacts associated with tourniquets.
7. Interpretation
a. Normal lower extremity venous anatomy (Figs. 2.2 and 2.3). Interpretation should include assessment of
the deep veins of the calf, thigh, and pelvis; filling of incompetent perforating veins (deep to superficial
filling) is noted.
FIGURE 2.2 • Lower extremity veins. The lower extremity is composed of superficial, deep, and perforating
veins. The calf veins are paired. The paired anterior tibial veins arise from the venous plexus at the dorsum
of the foot. The peroneal veins join with the posterior tibial veins—both are paired. The posterior tibial veins
arise from the ventral foot veins. The greater saphenous is the dominant superficial vein, which arises at the
medial foot and continues along the medial calf and medial thigh. The lesser saphenous vein courses along
the lateral ankle and to the lateral calf. The lesser saphenous may empty into the popliteal vein or greater
saphenous. Perforating branches are not named but can be seen along the thigh and calf. EI, external iliac;
CF, common femoral; GS, greater saphenous; SF, superficial femoral; PF, profunda femoral; P, popliteal; G,
gastrocnemius veins; AT, anterior tibial; PE, peroneal; PT, posterior tibial. (From Dyer R. Handbook of
Basic Vascular and Interventional Radiology. New York, NY: Churchill Livingstone; 1993:188, with
permission.)
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FIGURE 2.3 • Deep pelvic and abdominal veins. The left gonadal vein has confluence with the left renal
vein. The right gonadal vein usually drains into the IVC directly. The internal iliac vein arises from the
confluence of the superior gluteal, inferior gluteal, pudendal, obturator, lateral sacral, middle hemorrhoidal,
vesical, uterine, and vaginal veins. IVC, inferior vena cava; LR, left renal; RR, right renal; LG, left gonadal;
RG, right gonadal; EI, external iliac; CF, common femoral; II, internal iliac. (Figure art by Sharon A. Vogl.)
b. Visualization of thrombus as a filling defect within the vein is diagnostic of acute DVT. Outlining thrombus
with contrast passage along the vein wall is referred to as “tram-tracking.”
c. Quantitative estimation of clot burden and its change following thrombolytic infusions can be described by
the use of multiple grading systems beyond the scope of this chapter.
Lower Extremity Descending Venography (7)
1. Patient is positioned supine on a fluoroscopic tilt table. After femoral accesses (for bilateral injections) are
obtained, the table is tilted to 60 degrees semiupright position.
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2. Access the common femoral vein in an antegrade direction using a 21-gauge IV catheter. Alternatively,
access the femoral vein with a 21-gauge micropuncture needle and exchange over a 0.018-in. wire for a 4
Fr. or 5 Fr. catheter.
3. Venography is performed with nonionic, low-osmolar or iso-osmolar contrast with concentrations of 300
mg per mL. Inject 15 mL of contrast under fluoroscopic guidance.
4. Standard views
a. Bilateral injections of contrast are usually performed simultaneously through both needles in order to
demonstrate antegrade filling of the iliac veins and lower IVC.
b. Obtain an AP digital run to document the degree of reflux as the contrast is slowly injected.
c. Repeat the procedure with the patient performing the Valsalva maneuver.
5. Image interpretation. Valvular incompetence is classified below. Grades 0 and 1 are considered normal.
Valsalva prompts some degree of reflux even in normal patients.
a. Grade 0: competence, no reflux of contrast material
b. Grade 1: minimal incompetence, reflux of contrast beyond the uppermost valve in the femoral vein but not
beyond the proximal aspect of the thigh
c. Grade 2: mild incompetence, reflux into the femoral vein to the level of the knee
d. Grade 3: moderate incompetence, reflux to a level just below the knee
e. Grade 4: severe incompetence, reflux into the paired calf veins at the level of the ankle
Upper Extremity Venography (8)
1. Patient is positioned supine on the fluoroscopic table. Position the upper extremity palm up (anatomic
position) on an arm extension board.
a. Cushion the arm and hand with towels. Keep arm extended, approximately 70 degrees from the body.
Ninety-degree or greater angulation of the arm relative to the body can cause compression of the axillary
vein.
b. A small pillow or roll behind the shoulder may facilitate contrast opacification of the central veins.
2. Place a 22-gauge or 25-gauge butterfly needle or 21-gauge IV catheter into a dorsal hand vein. Confirm
access by injecting saline and evaluating for extravasation.
3. Venography is performed with dilute nonionic, iso-osmolar or low-osmolar contrast with concentrations
between 200 mg per mL and 300 mg per mL. Hand injection usually consists of 2 to 4 mL per second, for a
total injection volume of 8 to 20 mL. Power injection can be used if access is suitable. Extravasation is
evaluated between runs.
4. Inflating an upper arm blood pressure cuff to 50 mm Hg facilitates filling of the deep venous system. The
forearm veins can be filled with contrast and spot images obtained.
a. Avoid use of a tourniquet because this can lead to vasospasm or artifact.
5. Standard views
a. Obtain AP (palm up) and lateral views of the hand and forearm, including paired ulnar, interosseous, and
radial veins. The patient can hold a bag of saline or tape the hand to an arm support to maintain a palm-up
position. Spot images are usually sufficient for diagnosis.
b. Obtain an AP view of the upper arm, including paired brachial, basilic, and cephalic veins. A spot image
may be possible, but flow can be brisk. DSA at one or two frames per second can capture the best vein
opacification. Images should document an opacified basilic and cephalic vein.
c. A central venogram is obtained documenting the axillary vein, subclavian vein, and SVC. Obtain upper
extremity and central venous images as you slowly deflate the blood pressure cuff and/or reduce arm
elevation.
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FIGURE 2.4 • Upper extremity veins. The upper extremity veins are paired into deep and superficial
drainage. The superficial veins tend to be larger and the dominant system of the upper extremity. The
superficial system comprises the cephalic and basilic veins at the forearm. The cephalic vein extends along
the lateral forearm. The cephalic vein joins the axillary vein at the humeral head or clavicle. The cephalic
vein can be paired. The basilic vein runs through the medial forearm and continues to the upper arm. The
basilic vein joins the brachial vein at the mid-upper arm to form the axillary vein. The median antebrachial
vein runs on the ventral forearm and drains the palmar venous plexus. The deep veins (radial and ulnar
veins) are small, paired, communicate with each other, and accompany the forearm arteries. SC,
subclavian; C, cephalic; A, axillary; BR, brachial; B, basilic; R, radial; I, interosseous; U, ulnar. (From Dyer
R. Handbook of Basic Vascular and Interventional Radiology. New York, NY: Churchill Livingstone;
1993:160, with permission.)
d. Place a 4 Fr. or 5 Fr. catheter into an upper extremity vein if venography of the central veins is too dilute
following hand injection. Following contrast injection with a 20-mL saline “chaser” may also facilitate central
opacification. DSA at two or three frames per second is utilized.
e. In patients being evaluated for thoracic outlet syndrome, images should also be obtained with the arm in
abduction and external rotation (ABER) positioning.
6. Interpretation
a. Note status of upper extremity venous anatomy (Fig. 2.4). Comment on both the deep and superficial
veins of the forearm, arm, and chest.
b. Hemodialysis access planning (mapping): Assess the superficial veins including the condition and size of
the cephalic vein in both the forearm and arm and the basilic vein in the arm. Comment on any
discontinuous segments. Note central venous stenoses.
c. Evaluation for superficial thrombosis or DVT: An intraluminal defect within the vein confirms acute venous
thrombosis similarly to lower extremity findings. Well-formed collaterals around the obstruction are more
common in chronic venous thrombosis.
d. Thoracic outlet obstruction: Evaluate the length and location of venous stenosis/occlusion when
assessing central obstruction. Note anatomic variants
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that can be seen on a radiograph, for example, cervical ribs. Note venous collaterals around the
obstruction.
CO2 Venography
CO2 venography is a reasonable alternative to contrast venography in patients with contrast allergy or renal
insufficiency. Patients with renal insufficiency but not yet on dialysis may be best imaged for dialysis access
planning with CO2.
1. CO2 is an endogenously produced, low-viscosity gas, that is nonallergenic, non-nephrotoxic, and highly
soluble.
a. Because it is a gas, the viscosity of CO2—at 1/400 that of liquid contrast —is negligible, allowing it to be
injected through small needles (27 gauge).
b. High solubility allows the gas to diffuse into blood and be cleared from the lungs.
2. Care must be taken to use a self-contained (airtight) system while administering CO2. Various CO2 tank
options are available. Research grade tanks are usually more pure than medical grade. The CO2 must be
exchanged periodically to avoid rust and contaminants that build up in the tanks. No matter which system is
used, exquisite care must be taken to avoid injecting room air or other gases at all costs. Three delivery
systems are described:
a. 60-mL syringe. Attach a 60-mL syringe with a one-way valve and a three-way stopcock to the line from a
CO2 canister. Fill the syringe with CO2 and briskly clear the syringe three times. Lock CO2 into the syringe
with the one-way stopcock. Attach the stopcock to catheter’s Luer lock.
b. Reservoir bag with one-way valve (Merit Medical, South Jordan, UT). Fill the reservoir bag and clear
three times. The syringe is filled from the bag, avoiding over compression of the CO2 within the syringe.
c. Disposable canisters with a K-Valve switch (AngioAdvancements, LLC, Ft. Myers, FL). A K-Valve switch
is closed system allowing for flow of CO2 from a small disposable cartridge into a “reservoir” syringe (Fig.
2.5). The gas is then pushed from the reservoir syringe into the “administration” syringe. Oneway valves
between the connections allow for a continuous closed airtight system.
FIGURE 2.5 • K-Valve switch (AngioAdvancements, LLC, Ft. Myers, FL). The K-Valve switch allows for flow
of CO2 from the source into a 60-mL “reservoir” syringe. The design allows for “airtight” gas exchange
between syringes.
P.34
3. Venography
a. DSA images are acquired at high imaging rates—six frames per second. Most digital angiography
systems have CO2-imaging software that permits sequential images to be stacked (summed) to enhance
image contrast.
(1) Injection of 5 to 20 mL in the forearm and lower leg usually is usually sufficient for imaging.
(2) Injection of 10 to 30 mL is usually needed at the upper arm and thigh.
(3) Injection of 30 to 40 mL is needed to evaluate the IVC.
b. Wait 30 to 60 seconds between injections to allow absorption of the injected gas.
c. CO2 displaces the gas blood to give a negative contrast image (white veins on grayscale background).
4. Imaging considerations
a. CO2 is buoyant and will rise to the nondependent part of the vessel, unless the gas displaces the entire
blood volume in the vessel. This principle should be considered if there is a dependent thrombus or vessel
abnormality. A 90-degree obliquity will demonstrate if the entire vessel area is being imaged.
b. CO2 is best seen in small vessels.
c. CO2 gas defects should disappear within 30 seconds. If gas persists, there is likely room air
contamination of the CO2.
5. Safety
a. A total dose of up to 1.6 mL per kg of CO2 can be administered safely during a study (9).
b. “Air lock.” Gas can be trapped in a nondependent branch vessel, blocking blood flow and causing
ischemia. Avoid air lock by waiting at least 60 seconds between injections for the gas to wash away.
c. Unlike contrast, CO2 is a compressible gas. A 20-mL syringe can hold up to 200 mL of gas through
compression. A highly pressurized injection can cause pain. This can be avoided by using a large syringe to
avoid excessive compression (60 mL).
d. Contamination. CO2 can be easily contaminated. Do not leave CO2-filled syringes sitting for long
because the CO2 will slowly be replaced with room air. Exchange CO2 tanks/reservoirs regularly.
e. Do not use CO2 in the coronary arteries, thoracic aorta, or cerebral vessels due to risk of stroke.
Postprocedure Management
1. Usually, postprocedure observation is not required following upper and lower extremity venography performed
without sedation.
2. Postprocedure hydration is important following large volumes of contrast to avoid renal toxicity. Encourage
oral fluid intake for patients who can drink; IV fluids may be considered in hospitalized patients or those
recovering from sedation.
3. Wash out contrast from extremity veins at end of the study by infusion of heparinized saline (1,000 units per L)
for several minutes.
4. Patients with cardiovascular compromise or previous episodes of congestive heart failure (CHF) may need
diuretic management after large volumes of contrast.
Results
1. In extremity evaluation for DVT, sensitivity is 100% for clots larger than 0.5 cm. Specificity is 95% using
the strict criteria of a filling defect noted on more than one view (4).
a. False-positive exams can occur as a result of:
(1) Underfilling of a vein, creating a pseudothrombus
(2) Inadvertent injection of air
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(3) Extrinsic defects that may be due to compression by adjacent muscles or positional entrapment
2. CO2 has been shown to have sensitivity and specificity of 97% and 85%, respectively, compared to
contrast venography (10).
Complications
1. Post-venography thrombophlebitis (incidence <3% with nonionic, iso-osmolar, or low osmolar contrast
agents)
a. Occurs 24 hours following venography and most often resolves without sequelae
b. Using nonionic contrast, reducing contact time between contrast and endothelium, and flushing veins
with heparin following contrast exposure reduces the incidence.
2. Extravasation of contrast into subcutaneous tissue
a. Stop infusion immediately.
b. Assess size of extravasation: Less than 10 mL in a patient without peripheral arterial or venous disease is
considered clinically insignificant.
c. Treat significant extravasation with analgesic and warm compresses for 24 hours.
d. Surgical consultation is warranted if there is neurologic or vascular compromise.
3. Adverse contrast reactions (see Table 64.1)
References
1. Desjardins B, Rybicki FJ, Kim HS, et al. ACR Appropriateness Criteria® suspected upper extremity deep
vein thrombosis. J Am Coll Radiol . 2012;9:613-619.
2. The Vascular Access Work Group. III. NKF-K/DOQI clinical practice guidelines for vascular access: update
2000. Am J Kidney Dis. 2001;37:S137-S181.
3. Weinmann EE, Salzman EW. Deep-vein thrombosis. N Engl J Med. 1994;331:1630-1641.
4. Bettmann MA, Robbins A, Braun SD, et al. Contrast venography of the leg: diagnostic efficacy, tolerance,
and complication rates with ionic and nonionic contrast media. Radiology. 1987;165:113-116.
5. Rabinov K, Paulin S. Roentgen diagnosis of venous thrombosis in the leg. Arch Surg. 1972;104:134-144.
6. Thomas ML. Phlebography. Arch Surg. 1972;104:145-151.
7. Herman, RJ, Neiman HL, Yao JS, et al. Descending venography: a method of evaluating lower extremity
venous valvular function. Radiology. 1980;137:63-69.
8. Andrews RT. Contrast peripheral phlebography and pulmonary angiography for diagnosis of
thromboembolism. Circulation. 2004;109:I22-I27.
9. Hawkins IF, Cho KJ, Caridi JG. Carbon dioxide in angiography to reduce the risk of contrast-induced
nephropathy. Radiol Clin North Am. 2009;47:813-825.
10. Heye S, Maleux G, Marchal GJ. Upper-extremity venography: CO2 versus iodinated contrast material.
Radiology. 2006;241:291-297.
3
Vascular Closure Devices
Evan Lehrman
Joshua L. Weintraub
Safe and effective arterial access closure and hemostasis continue to present a challenge for interventional
radiologists. Arterial access is required for a wide range of procedures ranging from interventional oncology and
peripheral arterial disease to aneurysm repair and trauma. Arterial access sheaths range from 4 Fr. for diagnostic
angiography to 12 to 25 Fr. for endograft delivery. Although manual compression (MC) has been the gold
standard for achieving hemostasis for smaller arteriotomies since the inception of interventional radiology,
vascular closure devices (VCDs) were introduced in the early 1990s, and a large body of evidence and
experience has accumulated to support their use. Advantages and disadvantages exist for both methods of
arteriotomy closure (Table 3.1).
Table 3.1 Advantages and Disadvantages of Manual Compression and Vascular Closure
Devices
Method Advantages Disadvantages
Manual -Gold standard -Patient discomfort

compression -Limited learning curve -Delayed time to hemostasis
-No device cost -Delayed time to ambulation
-Anticoagulation must be reversed (ACT
<180)
-Decreased workflow
Vascular closure -Immediate hemostasis -Device cost

devices -Hemostasis possible with -Learning curve for each device
anticoagulation -Immediate repuncture not recommended
-Decreased time to ambulation for all devices
-Improved patient comfort -Potential for severe complications
-Improved workflow may offset
device costs
Indications
VCD can be used without reservation when the following criteria are met:
1. Common femoral artery (CFA) puncture
a. Between the inferior epigastric artery takeoff (below the inguinal ligament) and the femoral bifurcation
(see Figure 3.1)
b. If there is a high femoral bifurcation (above the femoral head), consider ipsilateral superficial femoral
artery (SFA) puncture or contralateral access.
2. Retrograde access
3. Artery diameter 5 mm or larger
4. No large atherosclerotic plaque on the anterior wall of the access site
a. Consider using ultrasound-guided puncture technique to avoid plaque.
Off-label Uses for Vascular Closure Device
Many VCD instructions for use manuals will not include these situations, but there is an improving evidence
base for use outside of retrograde CFA access.
1. Low puncture—SFA
a. SFA puncture closure okay if >5 mm (1)
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2. Antegrade puncture
a. Several reports support VCDs after antegrade puncture (CFA or SFA) (2)
3. Nonfemoral artery puncture closure using VCDs has been described.
a. Brachial artery (3)
b. Popliteal artery (4)
c. Axillary artery (5)
4. High puncture—external iliac artery
a. MC likely to be ineffective—risk for retroperitoneal hematoma that can be life-threatening
b. Reports of using Angio-Seal in this clinical scenario when patient characteristics are favorable (1)
c. Surgical treatment may be necessary.
FIGURE 3.1 • Common femoral angiogram, performed through the indwelling sheath. The puncture (black
circle) is appropriate for device closure, between the takeoff of the inferior epigastric artery (asterisk) and
the femoral bifurcation (<), in a vessel >5 mm in caliber. Please note this puncture could also be closed with
MC as it enters the CFA directly over the femoral head. (Angiogram courtesy of San Francisco General
Hospital, San Francisco, CA.)
Contraindications
There are no absolute contraindications to VCD use. If any of the below conditions exist, consider an
alternate hemostasis strategy such as MC:
1. Contaminated field
a. Infected VCD needs to be treated surgically with high morbidity and not insignificant mortality.
2. Severe calcified atherosclerotic peripheral artery disease in the CFA
a. MC may be more appropriate.
b. Recent reports suggest VCD use may be safe in this population (6).
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3. Small CFA, less than 5 mm
4. Multiple puncture attempts required for initial access
5. Back wall puncture
6. Prior angioplasty, stent or bypass graft in the CFA
7. Uncontrolled hypertension systolic blood pressure (SBP) >180 mm Hg
8. Morbid obesity—body mass index (BMI) >40
Procedure
The following general steps should be taken prior to device delivery as part of the VCD procedure:
1. Perform an ipsilateral CFA angiogram to assess puncture site location and vessel caliber (Fig. 3.1).
a. 5 to 10 mL contrast hand injection through the sheath
b. Can be documented at the start of the case through a micropuncture sheath prior to upsizing to the
procedural sheath
c. Oblique projections often necessary to separate sheath and CFA for clear identification of the access
entry site
2. Consider re-prepping the groin with a ChloraPrep and fresh sterile towels.
3. Consider glove change or removal of outer gloves if double gloved.
4. Bluntly dissect the soft tissue tract between the skin and the arteriotomy.
a. Crucial for successful delivery of several of the VCDs
b. Helps alert operator to incomplete hemostasis, readily seen as bleeding from the puncture site
5. Readminister subcutaneous lidocaine into the soft tissues for anesthesia.
6. Exchange the existing sheath over a wire for the VCD or insert the VCD into the sheath depending on the
device being used.
7. Deploy the device—see following sections for specific instructions and diagrams for several of the
commonly used devices from each category.
8. Bed rest for 1 to 2 hours, followed by ambulation trial
9. Assess groin for evidence of delayed hematoma or pseudoaneurysm (PSA) prior to discharge.
Types of Devices
Several categories of VCD are currently manufactured, each with their own mechanism of action, applications,
and learning curves.
1. Active approximators (Table 3.2)
These devices mechanically close the arteriotomy as material is fixed to the vessel wall. With Angio-Seal, the
arteriotomy is sandwiched between an intravascular footplate and collagen plug. With suture- and clip-mediated
devices, the arteriotomy itself is cinched closed. Active approximators are considered the most secure form of
VCD but carry the highest risk of serious complication.
2. Passive approximators (Table 3.3)
These devices deploy a sealant, gel, or plug at the extravascular aspect of the arteriotomy to achieve
hemostasis. Adjunctive MC is often held for 1 to 3 minutes. These devices have the highest risk of incomplete
hemostasis.
3. Nondepositional hemostasis aids (Table 3.4)
This is a heterogeneous group of devices that do not leave any material behind at the end of the procedure.
4. Hemostatic patches (Table 3.5)
These patches are placed externally over the dermatotomy prior to MC. Substances interact with blood products
to aid in hemostasis.
5. Mechanical compression aids (Table 3.6)
These devices allow MC to be performed by the device rather than an operator.
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Table 3.2 Active Approximators
Sheath
Size
Device Manufacturer Mechanism (Fr.) Comments
StarClose SE Abbott Clip 5, 6 Extravascular clip cinches

Vascular arteriotomy closed
Angio-Seal St. Jude Footplate/plug 6, 8 Arteriotomy sandwiched between

Medical footplate and collagen plug
-VIP
-
Evolution
Perclose Abbott Suture 5-8 Braided polyester or monofilament

Vascular sutures
-ProGlide
-A-T
Prostar XL Abbott Suture 8.5-10 Braided polyester suture, used for

Vascular larger sheaths
FemoSeal St. Jude Intra- and 7 Biodegradable polymer discs

Medical extravascular
discs
Table 3.3 Passive Approximators
Sheath
Size
Mynx Access Sealant 5-7 Polyethylene glycol deployed while

Closure intravascular balloon creates temporary
-Grip hemostasis
-Ace
FISH Morris Sealant 5-8 Extracellular matrix closure patch

Innovative premounted on procedural sheath
EXOSEAL Cordis Sealant 5-8 Polyglycolic acid deployed through

existing sheath
FastSeal Vascular Bioabsorbable 6, 8 Plug deployed through existing sheath.

Closure plug Safety tether allows removal if
Systems malpositioned.
VASCADE Cardiva Collagen plug 5-7 Collagen plug deployed while

intravascular mesh disc creates
temporary hemostasis
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Table 3.4 Nondepositional Hemostasis Aids
Sheath
Size
CATALYST Cardiva Disc 5-7 Intravascular nitinol mesh disc left in

Medical place under tension until hemostasis
- achieved and then disc removed.
CATALYST CATALYST II coated in
II kaolin/chitosan. CATALYST III
coated in kaolin/chitosan and
protamine.
-
CATALYST
III
Axera Arstasis Long 5, 6 Conventional micropuncture access

intramural converted to long shallow intramural
arteriotomy course. Only brief MC required.
Table 3.5 Hemostatic Patches
Sheath
Size
Syvek Marine Polymer Patch N/A Poly-N-acetyl glucosamine activates

Excel Technologies platelets
MPatch Medafor Patch N/A Porous microspheres dehydrate blood,

concentrating clotting factors
Clo-Sur Medtronic Patch N/A Positively charged polyprolate acetate

PAD Vascular biopolymer attracts RBCs
D-Stat Vascular Patch N/A Thrombin activates clotting factors and

Dry Solutions platelets
Chito- Abbott Vascular Patch N/A Positively charged chitosan molecules

Seal attract RBC and platelets
Neptune Biotronik Patch N/A Calcium alginate wound dressing

Pad facilitates hemostasis
RBCs, red blood cells.
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Table 3.6 Mechanical Compression Aids
Sheath
Size
FemoStop St. Jude Balloon N/A Device strapped around patient and
Medical compression then balloon inflated at groin site
CompressAR Advanced Disc N/A Metallic stand slid under patient and
Vascular compression disc tightened onto groin
Dynamics
ExpressAR Advanced Disc N/A Device strapped around patient,

Vascular compression then disc tightened onto groin
Dynamics
Selected Device Profiles

1. Angio-Seal (St. Jude Medical, St. Paul, MN) active approximator
a. Mechanism: An intravascular footplate and extravascular collagen plug are sandwiched around the
arteriotomy and cinched tight with a suture.
b. Features
(1) Considered an extremely secure form of closure with consistent hemostasis
(2) The Evolution model (eighth generation) utilizes an innovative deployment mechanism that allows for one-
handed deployment with decreased variability with the collagen compaction step occurring automatically during
device retraction.
(3) V-twist collagen folding pattern creates a larger footprint at the arteriotomy.
(4) Bondek coated suture facilitates smoother, more consistent collagen compaction.
(5) All components, including the intravascular anchor, are fully absorbed at 60 to 90 days.
(6) If re-entry is necessary within 90 days, access is recommended to be at least 1 cm from the previous site.
c. Angio-Seal deployment (V-Twist Integrated Platform [VIP] model) (Fig. 3.2)
(1) The procedural sheath is exchanged over a guidewire for the Angio-Seal sheath.
(2) It is advanced until blood flows out through the exit hole in the dilator, then withdrawn until flow ceases, and
subsequently readvanced until flow restarts.
(3) The dilator and wire are removed with careful attention to keeping the sheath stable and at a similar angle to
the initial access.
(4) The Angio-Seal is inserted into the sheath and advanced until a click is heard as the barrel meets the sheath.
(5) The footplate is deployed as the barrel is pulled back and another click is heard.
(6) The device and sheath are then retracted with the anchor held in place by gentle traction until a tamper
becomes visible.
(7) The tamper is then advanced forward to tie a knot over the collagen plug, compressing it against the
arteriotomy site.
(8) The tamper is removed and the suture is cut close to the skin.
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FIGURE 3.2 • Angio-Seal deployment—see section 1.c for detailed instructions. (Courtesy of St. Jude Medical.)
2. StarClose SE (Abbott Vascular, Abbott Park, IL) active approximator

a. Mechanism: A nitinol clip is deployed around the arteriotomy, cinching it closed.
b. Manual release: If the device cannot be retracted after clip deployment, a manual release will need to be
performed. A small dilator is inserted into the manual release hole on the side of the device (see the instructions
for use [IFU] for exact location).
c. Features
(1) Secure mechanical closure
(2) Immediate reaccess possible
d. StarClose deployment (Fig. 3.3)
(1) Exchange the procedural sheath for a StarClose sheath over a .035-in. guidewire.
(2) Remove the inner dilator and wire.
FIGURE 3.3 • StarClose deployment—see section 2.d for detailed instructions. (Courtesy of Abbott Vascular. ©
2010 Abbott Laboratories. All rights reserved.)
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(3) Insert the StarClose device until it clicks into the sheath.
(4) Deploy the locator wing by pressing down on the blue plunger at the back of the device—a click will be
heard.
(5) Pull the device back until resistance is met at the vessel wall.
(6) Shuttle the thumb advancer forward splitting the sheath—a click will be heard.
(7) Deploy the clip by increasing the angle of the device and pressing the blue button—a click will be heard.
3. Perclose (Abbott Vascular, Abbott Park, IL) active approximator
a. Mechanism: Sutures are deployed on either side of the arteriotomy site with a preformed knot. The knot is
tightened then locked using the provided knot pusher. ProGlide and Auto Tie models are available.
b. Features
(1) Wire access can be maintained throughout the entire deployment. If hemostasis is not achieved, another
Perclose or different device can be deployed.
(3) Can be utilized for preclosure of large arteriotomies
(5) Simplified knot delivery with pre-tied knot
c. Perclose ProGlide deployment (Fig. 3.4)
(1) Exchange the procedural sheath for a Perclose device over a .035-in. guidewire.
(2) When the wire exit hole nears the dermatotomy, remove the wire.
(3) Advance the device until pulsatile blood flow is seen from the marker lumen.
(4) Deploy the footplate and pull pack until resistance is met.
(5) Depress the plunger until a click is heard, deploying the needles (Fig. 3.4A,B).
(6) Pull back on the plunger until the suture exiting the back of the device is taut.
(7) Cut the suture using the trimming tool on the front of the device.
(8) Collapse the footplate.
(9) Retract the device (optional: reinsert the wire through the wire exit hole).
(10) Use the knot pusher to advance the knot along the blue suture as the device is removed.
(11) Lock the knot by pulling on the white suture.
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FIGURE 3.4 • Perclose deployment—see section 3.c for detailed instructions. (Courtesy of Abbott Vascular. ©
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4. Prostar XL (Abbott Vascular, Abbott Park, IL) active approximator
a. Mechanism: Two braided polyester sutures and four nitinol needles are deployed from the arterial lumen and
pulled out through the tissue tract then tied by hand.
b. Features
(1) Can be used to close large arteriotomies—IFU up to 10 Fr.
(2) Can be used to preclose very large arteriotomies up to 25 Fr.
(3) Sutures can be tied with wire in place—if hemostasis not achieved, second Prostar or other device can be
deployed.
(5) Requires the most experience
(6) Steepest learning curve
c. Prostar XL deployment (Fig. 3.5)
(1) Slightly extend the skin incision and blunt dissect the tissue tract.
(2) Exchange the sheath for a Prostar XL device over a .035-in. guidewire.
(3) Advance the device until the wire exit port reaches the dermatotomy and then remove the wire and advance
the device to the skin.
(4) Squeeze the white interlocks together with thumb and forefinger unlocking the barrel.
(5) Advance the barrel while rotating back and forth until pulsatile blood returns.
(6) Turn the ring-shaped handle 90 degrees clockwise and then pull it out of the back hub of the barrel—this
deploys the needles.
(7) Retrieve the four needles/suture tails from the back of the device using a Kelly clamp.
(8) Cut the needles off the end of each suture tail and discard.
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(9) Retract the device until the sutures can be seen along the device shaft and harvest the suture tails from the
device hub.
(10) Pair up the suture tails across from each other (green with green and white with white).
(11) Tie a sliding self-locking knot with one suture and set it to the side.
(12) Tie a sliding self-locking knot with the second suture and advance it to the arteriotomy while removing the
Prostar device from the vessel then tighten the suture.
(13) Advance and tighten the knot that was previously tied and set to the side.
FIGURE 3.5 • Prostar XL deployment—see section 4.c for detailed instructions. (Courtesy of Abbott Vascular. ©
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5. Mynx (AccessClosure/Cardinal Health, Dublin, OH) passive approximator
a. Mechanism: With a semicompliant intravascular balloon inflated for temporary hemostasis, a polyethylene
glycol (PEG) sealant plug is delivered to the extravascular surface of the artery. Grip technology at the tip of the
plug facilitates adherence to the vessel wall. Blood products and extracellular fluids cause the plug to swell to
three to four times its original size. The balloon is deflated and removed. Two models are available—MynxAce
and MynxGrip.
b. Features
(1) Grip technology—PEG tip adheres to outer surface of vessel wall.
(2) MynxAce is introduced through a proprietary sheath and includes a mechanism that compresses the swelling
plug down onto the outer vessel wall.
(3) MynxGrip is used through the indwelling procedural sheath.
(4) Completely resorbed at 30 days
(6) Balloon can be inflated with contrast for fluoroscopic visualization during SFA and antegrade puncture
closures.
c. MynxGrip deployment (Fig. 3.6)
(1) Insert the device through the indwelling sheath up to the white shaft marker.
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(2) Inflate the balloon and close the stopcock; check the inflation indicator.
(3) Retract the device until the balloon is against the arteriotomy (Fig. 3.6A).
(4) Open the stopcock on the procedural sheath to confirm temporary hemostasis.
(5) Advance the green shuttle delivering the PEG to the arteriotomy (Fig. 3.6B).
(6) Withdraw the sheath and green shuttle to the back of the device.
(7) Move the advancer tube forward two notches.
(8) Lay the device down for a moment.
(9) Deflate the balloon and remove it through the advancer tube (Fig. 3.6C).
(10) Remove the advancer tube and apply light pressure for 2 minutes (Fig. 3.6D).
FIGURE 3.6 • Mynx deployment—see section 5.c for detailed instructions. (Courtesy of AccessClosure.)
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6. EXOSEAL (Cordis/Cardinal Health, Dublin, OH) passive approximator
a. Mechanism: A bioabsorbable polyglycolic acid (PGA) plug is deployed into the extravascular tract overlying
the arteriotomy. The plug is held in place within the tract by the overlying fascia.
b. Features
(1) Used through indwelling sheath
(2) Bioabsorbable material completely resorbed at 60 to 90 days
(3) Lockout mechanism prevents intravascular deployment
(4) Sheath must be 12 cm in length or less.
c. Deployment (Fig. 3.7)
(1) The device is inserted through the indwelling procedural sheath (Fig. 3.7A) until pulsatile blood return is
visualized from the indicator port (Fig. 3.7B).
(2) The sheath and device are retracted together until the pulsatility of blood diminishes (Fig. 3.7C,D).
(3) The indicator window is then checked (Fig. 3.7E)—the device is in proper extravascular position at the
Radiology Books
arterial surface when the indicator switches from black/white to black/black.
(4) If the indicator switches to black/red, it has been retracted too far and tension should be released.
FIGURE 3.7 • EXOSEAL deployment—see section 6.c for detailed instructions. (© 2013 Springer-Verlag Berlin,
Germany.)
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(5) With a black/black indicator window, the plug is deployed by pressing the green switch on the handle (Fig.
3.7F).
(6) The device and sheath are removed and MC is held for 2 minutes.
7. Axera 2 (Arstasis, Fremont, CA) nondepositional compression aids
a. Mechanism: The device converts standard percutaneous femoral artery access to a longer, shallower
intramural course before the procedural sheath is placed. After the procedure, the sheath is removed and light
MC is only required for a few minutes to achieve “self-sealing” hemostasis.
b. Features
(1) Long, shallow arteriotomy creates significant tissue overlap within the vessel wall.
(2) The access is self-sealing with minimal compression needed for hemostasis.
(3) No deposition of material eliminates implant-related complications.
(4) Immediate reaccess is possible.
c. Axera 2 deployment (Fig. 3.8)
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(1) Achieve CFA access using the supplied 19-gauge needle.
(2) Insert the latch wire and remove the needle.
(3) Attach the latch wire to the front end of the device.
(4) Insert the device into the artery until flash is seen in the marker port.
(5) Deploy the intravascular heel by pulling back on the actuator.
(6) Apply gentle upward traction and confirm that the flash in the marker port has stopped or is significantly
reduced.
(7) Advance the integrated micropuncture needle through the arterial wall by pressing the plunger (Fig. 3.8A).
(8) Confirm intraluminal location by resumption of blood flow from the marker port.
(9) Insert and advance the guidewire through the plunger port and into the artery.
(10) Remove the device and insert the procedural sheath (Fig. 3.8B).
(11) When the procedure is over, the sheath is removed and light compression is held for a few minutes.
FIGURE 3.8 • Axera deployment—see section 7.c for detailed instructions. (© 2015 Arstasis. All rights reserved.)
Advanced Techniques
1. Preclose technique for large arteriotomies (7)
a. Suture-mediated VCD used to close large arteriotomies
(1) Two Perclose devices or one Prostar XL device
b. Used for percutaneous endovascular aneurysm repair
c. Access initially obtained with 6 Fr. sheath and .035-in. guidewire.
d. Two Perclose ProGlide devices are deployed in succession each rotated 30 degrees in opposite directions
(10 o’clock and 2 o’clock) or one Prostar XL device is deployed.
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e. Sutures left untightened and secured to the side.
f. Serial dilatation of the arteriotomy and completion of the repair
g. The sheath is removed over a stiff .035-in. guidewire with MC and the preformed knots are cinched tight
(Perclose) or knots tied and cinched tight (Prostar).
h. MC released
(1) If hemostasis confirmed—remove guidewire.
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(2) If pulsatile blood flow persists—deploy another Perclose, Prostar, or Angio-Seal.
(3) If hemostasis still not achieved, reinsert sheath; surgical repair needed.
i. MC reapplied for 5 to 10 minutes after hemostasis confirmed.
j. Bed rest for 6 hours
2. Double Angio-Seal technique for large arteriotomies (8)
a. Two .035-in. guidewires are inserted through an 8 to 10 Fr. sheath at the completion of the procedure.
b. An 8 Fr. Angio-Seal is deployed over the first wire.
c. The collagen plug is tamped into place, but the suture is not cut.
d. If there is adequate hemostasis, the remaining wire can be removed.
e. If hemostasis is not achieved, a second 8 Fr. Angio-Seal is deployed over the remaining wire.
f. Once both devices are securely deployed and hemostasis achieved, the sutures are cut.
3. Inadvertent subclavian artery catheter placement (9)
a. Case reports during attempted central venous access
b. Angio-Seal, StarClose, Mynx, and Perclose use reported for arterial closure after catheter removal over a wire
c. An arterial occlusion balloon can be inserted from groin access and used adjunctively while the indwelling
catheter is exchanged for the VCD.
4. Treatment of CFA PSA (10)
a. Percutaneously access PSA with a micropuncture needle and navigate the mandril wire through neck into the
parent artery.
b. Exchange for .035-in. guidewire and deploy active approximator VCD.
c. Consider in patients with coagulopathy who fail thrombin injection.
5. Venous closure (11)
a. Angio-Seal and Perclose have been used for venous closure both at completion or as preclosure before
dilation to a large sheath size.
Complications (Table 3.7)

1. Access-site complications can occasionally be life-threatening, but even minor complications may result in
longer hospital stays and increased 1-year mortality rates (12). Complications are often multifactorial with
potential contributions from:
a. Initial access quality/location/size
b. Anticoagulant/antiplatelet/thrombolytic medications
c. Choice of device and technique used for deployment or MC
Table 3.7 Major and Minor Complications of Vascular Closure Device Deployment
Major Complications Minor Complications
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Femoral artery occlusion Hematoma
Device embolization Pseudoaneurysm
Arterial laceration Arteriovenous fistula
Retroperitoneal hematoma Nerve injury
Limb ischemia
Access site infection
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2. Major complications
a. Result from damage to the vessel during device deployment, dislodgment of plaque during deployment, or
device embolization
b. Vessel damage is most likely to occur with use of active approximator devices that mechanically cinch the
arteriotomy closed, but device embolization can occur with active or passive approximators.
c. Major complications usually require open surgical or endovascular repair.
d. Overall, these complications are quite rare with decreased incidence after evolution of devices and cumulative
operator experience.
3. Minor complications
a. Other than nerve injury, minor complications usually result from device failure or ineffective MC.
b. Hematomas are usually managed conservatively but may require transfusion.
c. PSA is usually managed with thrombin injection or compression with stent graft coverage or VCD closure
reserved for refractory cases.
d. Injury to superficial cutaneous branches of the femoral nerve with otherwise unremarkable Angio-Seal
deployment has been reported.
Results
1. Many very concerning case reports of serious complications related to VCD use in the late 1990s and
early 2000s (12).
2. Meta-analyses and randomized controlled trials of coronary catheterization patients in the mid to late
2000s raised concern for overall increased rates of complications with use of VCD (13,14).
3. Only one meta-analysis specific to interventional radiology use of VCDs did not show any statistically
significant differences between pooled VCD and MC (15). There were trends toward decreased
complications with Angio-Seal and increased complications with Perclose.
4. Multiple reports of using StarClose specifically in interventional oncology patients with good safety
profiles even with elevated international normalized ratio (INR) and decreased platelet count (16,17)
5. Randomized controlled trials from the last few years ISAR-CLOSURE and CLOSE UP showed
noninferiority of VCD to MC with decreased rates of hematoma in the VCD groups versus MC (18,19).
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Key Take-Home Points
1. The literature has firmly established that closure devices decrease time to hemostasis, ambulation, and to
discharge when compared to the gold standard of MC.
2. As a whole, VCD safety remains controversial. After 20 years of device evolution and collective operator
experience, data now suggests that the devices are not different from MC in terms of serious complications. The
rate of less severe but potentially morbid complications of hematoma and PSA may be decreased in patients that
receive VCDs.
3. With dozens of devices to choose from, the key to successful VCD deployment is familiarity with the concept,
mechanism, and instructions for each device used in one’s practice. Knowing the steps of deployment is
insufficient; the operator must be able to visualize what is happening inside and around the artery as each button
is pushed and each plunger depressed.
4. Some devices are better suited than others for certain clinical applications and patient populations. The key is
to become comfortable with multiple devices that can be deployed with confidence in a predictable fashion.
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References
1. Bose R, Schussler JM. Use of Angio-Seal closure device when the arteriotomy is above or below the
common femoral artery. Clin Cardiol . 2011;34(11):700-702.
2. Lupattelli T, Tannouri F, Garaci FG, et al. Efficacy and safety of antegrade common femoral artery access
closure using the Angio-Seal device: experience with 1889 interventions for critical limb ischemia in diabetic
patients. J Endovasc Ther. 2010;17(3):366-375.
3. Lupattelli T, Clerissi J, Clerici G, et al. The efficacy and safety of closure of brachial access using the
AngioSeal closure device: experience with 161 interventions in diabetic patients with critical limb ischemia. J
Vasc Surg. 2008;47(4):782-788.
4. Noory E, Rastan A, Sixt S, et al. Arterial puncture closure using a clip device after transpopliteal retrograde
approach for recanalization of the superficial femoral artery. J Endovasc Ther. 2008;15(3):310-314.
5. Gonen KA, Erdoğakan C, Hakyemez B. Closure of the axillary artery puncture site with StarClose system
after endovascular interventions. J Vasc Interv Radiol . 2014;25(4): 640-645.
6. Kara K, Kahlert P, Mahabadi AA, et al. Comparison of collagen-based vascular closure devices in patients
with vs. without severe peripheral artery disease. J Endovasc Ther. 2014;21(1):79-84.
7. Lee WA, Brown MP, Nelson PR, et al. Total percutaneous access for endovascular aortic aneurysm repair
(“Preclose” technique). J Vasc Surg. 2007;45(6):1095-1101.
8. Bui QT, Kolansky DM, Bannan A, et al. “Double wire” angio-seal closure technique after balloon aortic
valvuloplasty. Catheter Cardiovasc Interv. 2010;75(4):488-492.
Radiology Books
9. Mousa AY, Abu-Halimah S, Nanjundappa A, et al. Inadvertent subclavian artery cannulation and options
for management. Vascular. 2015;23(2):132-137.
10. Xiang DC, Hillegass WB, Luo GX, et al. Treatment of refractory iatrogenic femoral artery
pseudoaneurysm with a vascular closure device. J Vasc Interv Radiol . 2009;20(12):1639-1640.
11. Mylonas I, Sakata Y, Salinger M, et al. The use of percutaneous suture-mediated closure for the
management of 14 French femoral venous access. J Invasive Cardiol . 2006;18(7):299-302.
12. Ortiz D, Jahangir A, Singh M, et al. Access site complications after peripheral vascular interventions:
incidence, predictors, and outcomes. Circ Cardiovasc Interv. 2014;7(6):821-828.
13. Koreny M, Riedmüller E, Nikfardjam M, et al. Arterial puncture closing devices compared with standard
manual compression after cardiac catheterization: systematic review and meta-analysis. JAMA.
2004;291(3):350-357.
14. Biancari F, D’Andrea V, Di Marco C, et al. Meta-analysis of randomized trials on the efficacy of vascular
closure devices after diagnostic angiography and angioplasty. Am Heart J. 2010;159(4):518-531.
15. Das R, Ahmed K, Athanasiou T, et al. Arterial closure devices versus manual compression for femoral
haemostasis in interventional radiological procedures: a systematic review and meta-analysis. Cardiovasc
Intervent Radiol . 2011;34(4):723-738.
16. Prajapati HJ, Rafi S, Edalat F, et al. Safety and efficacy of a circumferential clip-based vascular closure
device in cirrhotic and coagulopathic patients with hepatocellular carcinoma after doxorubicin drug-eluting
beads transarterial chemoembolization. Cardiovasc Intervent Radiol . 2014;37(3):664-670.
17. Wang Z, Li X, Chen J, et al. Safety and effectiveness of repeat arterial closure using the StarClose
vascular closure device in patients with hepatic malignancy. Clin Radiol . 2013;68(9):e498-e501.
18. Schulz-Schüpke S, Helde S, Gewalt S, et al. Comparison of vascular closure devices vs manual
compression after femoral artery puncture: the ISAR-CLOSURE randomized clinical trial. JAMA.
2014;312(19):1981-1987.
19. Holm NR, Sindberg B, Schou M, et al; for CLOSE-UP study group. Randomised comparison of manual
compression and FemoSeal™ vascular closure device for closure after femoral artery access coronary
angiography: the CLOSure dEvices Used in everyday Practice (CLOSE-UP) study. EuroIntervention.
2014;10(2):183-190.
Radiology Books
4
Management of Vascular Complications
John Chung
Lindsay Machan
Access site complications are relatively rare, ranging from small groin hematomas to transection of the access
artery with exsanguination (1,2,3). Common complications and their occurrence rates are listed in Table 4.1.
Pseudoaneurysms
The most common vascular access site complication requiring intervention is pseudoaneurysm formation.
Surgical repair has surprisingly high complication rates, from 19% to 32% (4), including inadequate wound
healing, femoral neuralgias, and lymphatic leaks; thus, ultrasound-guided procedures have revolutionized their
treatment (5).
Indication
1. Identification of an arterial access site pseudoaneurysm. Conservative, observational management has
largely been abandoned.
Contraindications
Absolute
1. Hemodynamically unstable patient
2. Active hemorrhage (retroperitoneal or percutaneous); expanding hematoma
3. Impending skin necrosis due to size of hematoma/pseudoaneurysm
4. Acute distal limb ischemia due to compression effects of hematoma/pseudoaneurysm
5. Active infection at the site of percutaneous access
Relative
1. Width of pseudoaneurysm neck >8 mm
2. Lack of any discernible pseudoaneurysm neck
3. Pseudoaneurysm sac diameter <10 mm (increased risk of arterial thrombosis)
1. Detailed imaging, most commonly with ultrasound, or alternatively computed tomographic angiography (CTA)
or magnetic resonance angiography (MRA). The extent and morphology of the pseudoaneurysm should be
identified, including the number of lobes the pseudoaneurysm has as well as the width and length of its neck. If
performing ultrasound, the Doppler waveform pattern of the outflow artery should also be assessed.
Table 4.1 Common Complications Following Percutaneous Arterial Access
Complication Incidence (%)

Radiology Books
Hematoma 5-23
Pseudoaneurysm 0.2-9
Arteriovenous fistula 0.1-2.1
Hemorrhage 0.15-0.44
Dissection/occlusion <0.5
Neuropathy 0.21
Infection <0.1
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2. Recent laboratory data should be obtained, including complete blood count (CBC), platelets, and international
normalized ratio (INR).
3. Doppler or palpation assessment of ipsilateral foot arteries (dorsalis pedis, tibialis posterior) immediately prior
to percutaneous therapy
Procedure
Ultrasound-Guided Compression
1. The first described ultrasound-guided management of iatrogenic pseudoaneurysms (5). It remains the
preferred treatment option for pseudoaneurysms <1 cm and is still an acceptable therapy when thrombin is
not available.
2. Inject copious amounts of local anesthetic. Consider intravenous sedation. Due to extensive bruising,
these patients are often exquisitely tender.
3. A linear array (4 to 7 MHz) ultrasound transducer is placed on the affected groin with direct visualization
of the pseudoaneurysm neck and body (or lobe closest to the neck in a multilobed, complex
pseudoaneurysm) as well as the artery from which the pseudoaneurysm arises.
4. With real-time color Doppler sonographic guidance, pressure is applied on the pseudoaneurysm via the
probe to eliminate flow through the pseudoaneurysm while maintaining flow through the parent artery.
5. Pressure is slowly alleviated at 10-minute intervals to assess for any persistent flow through the
pseudoaneurysm.
6. At the first instance persistent flow is identified, step 4 is repeated until the pseudoaneurysm internal flow
remains obliterated when transducer pressure is fully released.
7. Limitations of this technique include the relatively long time required, patient discomfort with possible
need for sedation, and higher failure rates relative to other ultrasound-guided treatment methods.
Ultrasound-Guided Thrombin Injection
1. This method is the standard of care in most institutions.
2. Standard sterile preparation and draping of the affected site and a sterile cover is applied to an
ultrasound transducer (most commonly a 4 to 7 MHz linear array probe).
Radiology Books
3. Subcutaneous local anesthesia is administered as needed. Due to extensive bruising, these patients are
often exquisitely tender.
4. Preparation of thrombin solution. Multiple thrombin formulations are available. Typically, it is reconstituted
with sterile saline. Use of bovine or human thrombin in concentrations of 100 to 1,000 IU per mL have been
described, all with equal efficacy.
a. In some institutions, thrombin is only available as part of a kit (e.g., Tisseel [Baxter, Deerfield, IL])
containing various doses of dehydrated human thrombin. The provided 2-mL calcium chloride solution is
injected into a 1,000 IU thrombin vial. The mixture is vigorously swirled to reconstitute the thrombin into
solution. The resultant 2-mL thrombin solution is further added to a 10-mL syringe containing 8 mL of sterile
saline, resulting in a 10-mL solution with a concentration of 100 IU per mL.
5. Ultrasound-guided insertion of a 21- or 22-gauge needle into the pseudoaneurysm is performed,
preferentially into the proximal most lobe in direct communication with the pseudoaneurysm neck in complex
pseudoaneurysms.
6. The thrombin solution is injected slowly in increments of 0.1 to 0.2 mL (10 to 20 IU) under real-time
sonographic color Doppler visualization of the pseudoaneurysm, only until there is complete cessation of
internal color Doppler flow.
7. Sonographic grayscale and color Doppler assessment of the pseudoaneurysm is performed 10 minutes
after thrombin injection to ensure it remains thrombosed; if any residual flow has returned, additional
thrombin is injected as per steps 4 and 5.
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1. Doppler or palpation assessment of ipsilateral foot circulation immediately after percutaneous therapy
2. Bed rest for a minimum of 2 hours after ultrasound-guided therapy
3. Follow-up ultrasound Doppler assessment of the pseudoaneurysm in 24 hours is essential.
Results
1. Ultrasound-guided compression (5,6)
a. Technical success ranges from 63% to 88%.
b. Mean compression times are 30 to 44 minutes; thus patient discomfort and need for sedation/analgesia
are frequent.
c. Failure rates increase significantly if the patient is anticoagulated (≤70%) or if the pseudoaneurysm size
is >4 cm.
2. Ultrasound-guided thrombin injection (4,5,7,8)
a. Primary technical success rates 90% to 94%, with overall success rates ranging from 93% to 100%.
Mean injected thrombin dose ranges from 225 to 425 IU.
b. Procedural times are significantly shorter than ultrasound-guided compression. Patient sedation is
typically not necessary.
c. Failures usually in pseudoaneurysms >6 cm in diameter
Complications (1,4,5)
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1. Groin pain (41%)
2. Pseudoaneurysm reperfusion (2.1%)
3. Thromboembolism (0.8%)
4. Allergic reaction, if bovine thrombin is used
5. Blood-borne infections, if human thrombin is used
6. Acute expansion and/or rupture of the pseudoaneurysm after therapy necessitating emergency surgery
(2.1%); this has only been described with ultrasound-guided compression.
Management of Complications (1,5)

1. Groin pain—analgesia is typically sufficient.
2. Pseudoaneurysm reperfusion—repeat ultrasound-guided therapy is the first recourse in most cases.
3. Thromboembolism—management depends on severity. If nonocclusive, it can be managed with systemic
anticoagulation. If occlusive and/or extensive, surgical thrombectomy or endovascular pharmacomechanical
thrombolysis should be performed.
4. Allergic reaction—avoid use of bovine-derived thrombin in patients with allergy to bovine products. If allergic
reaction occurs, start standard treatment of anaphylaxis.
5. Acute pseudoaneurysm expansion/rupture—limit use of the ultrasound-guided compression technique to
pseudoaneurysms <4 cm in size and in patients who are not actively anticoagulated.
Other Access Site Complications

1. Hematoma—this is the most common minor complication.
a. Typically managed conservatively. The hematoma can be outlined with a marking pen and inspected at
regular intervals (such as when vital signs are taken) to ensure no expansion.
b. If the hematoma is massive and symptomatic, (e.g., causing femoral neuralgia or acute limb ischemia),
surgical evacuation may be required (1,5).
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2. Arteriovenous fistula—the use of ultrasound guidance to ensure single wall arterial access greatly
minimizes this complication (9).
a. Surgical repair is usually necessary.
b. If asymptomatic, it can be initially managed conservatively as up to one third will spontaneously resolve
(10).
c. Endovascular treatment could be considered if the patient is not a surgical candidate. If the fistulous tract
is of sufficient length, it can be embolized with coils. Fistula occlusion with a nitinol-covered stent within the
arterial segment is possible but not considered ideal given the downsides of stenting across a moving joint
(1,5).
3. Arterial dissection—treatment depends on the severity.
a. If focal and non-flow-limiting, it could be managed conservatively with imaging surveillance, typically via
CTA.
b. If flow-limiting, prolonged endovascular balloon inflation across the dissection should be performed to
reappose the dissected intima with the vessel media.
c. If the dissection extends into the iliac arteries, placement of self-expanding nitinol stents within the iliac
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arteries may be necessary to maintain luminal patency (1).
4. Arterial thrombosis—therapy depends on the extent of thrombus.
a. Thrombosis is not complicated by dissection, if nonocclusive can be managed medically with systemic
anticoagulation.
b. If occlusive, surgical thrombectomy is the treatment of choice because the arteriotomy can be repaired at
the same time. If thrombosis was induced by a vascular closure device, any intravascular component can be
definitively removed.
c. If the patient is not a surgical candidate, endovascular access can be achieved from a second arterial
access site (typically the contralateral common femoral artery), and endovascular pharmacomechanical
thrombolysis can be performed (1,5).
5. Retroperitoneal hematoma/uncontrollable puncture site bleeding—may result from a high arterial
puncture above the inguinal ligament with retroperitoneal bleeding, or failure to achieve primary hemostasis
after appropriately placed puncture
a. Retroperitoneal bleeding is usually not immediately clinically obvious and can be devastating. Early clues
before pain or hypotension can be decreased urine output or tachycardia. Urgent noncontrast pelvic
computed tomography (CT) is the diagnostic method of choice and is recommended even when there is
slight suspicion.
b. The standard of therapy is urgent surgical repair.
(1) If there is intra-arterial access when discovered, angioplasty balloon can be inflated at, or a temporary
occlusion balloon proximal to, the site of injury while the patient awaits surgery.
c. If vascular surgery is not readily available or the patient is not a surgical candidate, placement of a
covered stent across the vascular injury can be performed. The stent graft should be nitinol-based, sized 1
mm larger than the vessel diameter in which it is to be placed (remember that the artery may be contracted
if the patient is hypotensive), be as short as possible, and should not be landed across the common femoral
bifurcation if possible (1).
References
1. Tsetis D. Endovascular treatment of complications of femoral arterial access. Cardiovasc Intervent Radiol .
2010;33(3):457-468.
2. Fruhwirth J, Pascher O, Hauser H, et al. Local vascular complications after iatrogenic femoral artery
puncture. Wien Klin Wochenschr. 1996;108(7):196-200.
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3. Nasser TK, Mohler ER III, Wilensky RL, et al. Peripheral vascular complications following coronary
interventional procedures. Clin Cardiol . 1995;18(11):609-614.
4. Krueger K, Zaehringer M, Strohe D, et al. Postcatheterization pseudoaneurysm: results of US-guided

percutaneous thrombin injection in 240 patients. Radiology. 2005;236(3):1104-1110.
5. Morgan R, Belli AM. Current treatment methods for postcatheterization pseudoaneurysms. J Vasc Interv
Radiol . 2003;14(6):697-710.
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6. Stone PA, Campbell JE, AbuRahma AF. Femoral pseudoaneurysms after percutaneous access. J Vasc
Surg. 2014;60(5):1359-1366.
7. Luedde M, Krumsdorf U, Zehelein J, et al. Treatment of iatrogenic femoral pseudoaneurysm by

ultrasound-guided compression therapy and thrombin injection. Angiology. 2007;58(4):435-439.
8. Vlachou PA, Karkos CD, Bains S, et al. Percutaneous ultrasound-guided thrombin injection for the
treatment of iatrogenic femoral artery pseudoaneurysms. Eur J Radiol . 2011;77(1):172-174.
9. Lo RC, Fokkema MT, Curran T, et al. Routine use of ultrasound-guided access reduces access site-
related complications after lower extremity percutaneous revascularization. J Vasc Surg. 2015;61(2):405-412.
10. Kelm M, Perings SM, Jax T, et al. Incidence and clinical outcome of iatrogenic femoral arteriovenous
fistulas: implications for risk stratification and treatment. J Am Coll Cardiol . 2002;40(2):291-297.
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5
Acute Ischemic Stroke: Endovascular Management
Rajan K. Gupta
Jennifer R. Simpson
David A. Kumpe
Stroke is the number one cause of severe disability and number four cause of death in the United States with an enormous cost to the medical care system. The ultimate goal of
acute stroke treatment is to limit disability and return the patient to functional independent living. This is accomplished by rapid reperfusion of ischemic tissue at risk for progression
to infarction. Intravenous (IV) tissue plasminogen activator (tPA) is a proven medical revascularization therapy for acute ischemic stroke indicated in selected patients up to 4.5 hours
after symptom onset. Unfortunately, IV tPA is often ineffective in large vessel occlusion (LVO) stroke that carries a high morbidity and mortality. Multiple prospective randomized
controlled trials have demonstrated that endovascular thrombectomy is highly effective in reducing disability in selected patients with acute LVO anterior circulation stroke
(1,2,3,4,5). The statement that “time is brain” cannot be overemphasized when treating stroke. An estimated 1.9 million neurons are lost per minute in untreated acute LVO strokes
(6). Every 30-minute delay is associated with a 10% decrease in function outcome at 90 days (7,8,9). Time can be saved across every level of stroke care from prehospital care to
intraprocedural technique. Identification of appropriate patients with noninvasive imaging, an emphasis on rapid and complete revascularization with modern thrombectomy devices,
and a multidisciplinary commitment to process improvement are critical factors for improving patient outcomes.
Indications
Patient selection for endovascular therapy is based on the location of the occlusion, time from symptom onset, and imaging findings that estimate the completed core infarct and
the ischemic penumbra. Imaging strategies will be discussed in depth in the “Preprocedure Preparation” section. The strongest data for endovascular therapy is in patients who
are eligible for and receive full-dose (0.9 mg per kg) IV tPA. Subgroup analysis of randomized trials suggests that the benefit of thrombectomy persists in patients who are not
eligible for IV tPA, and endovascular therapy should not be withheld in this population (1,3,4).
1. Acute symptomatic ischemic stroke from documented LVO
a. Anterior circulation
(1) The strongest data for endovascular thrombectomy is in patients with occlusions of the intracranial internal carotid artery and/or proximal middle cerebral artery (M1). Subset
analyses of randomized trials demonstrate a benefit when extracranial carotid occlusion is present (1,3). Less data is present for treatment of occlusion of proximal anterior
cerebral artery (A1) and proximal middle cerebral artery branches (M2).
(2) The strongest data is for patients who can start endovascular therapy by 6 hours after last seen normal (LSN). The evidence of benefit at time windows beyond 6 hours is
less robust but appears promising with strict patient selection (3,10). Selection criteria should be defined at each individual institution.
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b. Posterior circulation
(1) Occlusion of the basilar artery is a reasonable target due to the dismal prognosis of large vessel posterior circulation stroke.
(2) Time windows for treatment are often extended up to 24 to 48 hours.
Contraindications
Contraindications to endovascular therapy, particularly now that mechanical thrombectomy can be performed with little or no fibrinolytics, are not uniformly agreed upon and
should be institutionally defined or discussed on a case-by-case basis.
Absolute
1. Anaphylactic reaction to contrast
2. Hemorrhagic conversion of stroke or midline shift
3. Large core infarct with expected futile revascularization. These contraindications will depend on the imaging strategy used (see “Preprocedure Preparation” section and
discussion on imaging).
a. MRI diffusion-weighted imaging (DWI) core infarct >70 mL
b. Hypodensity >1/3 middle cerebral artery (MCA) territory or Alberta Stroke Program Early Computed Tomography Scan (ASPECTS) <6 on noncontrast computed tomography
(CT)
c. Matched defect or <20% penumbra with perfusion imaging
d. <50% filling of MCA collaterals on multiphase computed tomographic angiography (CTA) (correlates well with ASPECTS ≤5)
Relative
Lack of appropriate vascular access
1. Although direct carotid and upper extremity access have been described for stroke intervention, the majority of stroke interventions are performed from a femoral approach
and lack of appropriate femoral access precludes safe and timely therapy for most operators not skilled with more advanced techniques.
2. Minimal clinical deficit or rapidly improving stroke symptoms after IV tPA
3. Poor baseline functional status All recent randomized trails excluded patients with poor baseline functional status. Clinical judgment should guide decision making because
some patients who are high functioning may not be independent at baseline (such as those with lower extremity amputations) and may benefit substantially from reperfusion
therapy.
4. Limited life expectancy or other severe medical comorbidities
5. Medical factors that increase bleeding risks and represent contraindications to IV tPA administration (Table 5.1) are also relative contraindications when intraarterial (IA)
fibrinolytics are contemplated, although these risks are substantially reduced with mechanical thrombectomy when fibrinolytics can be avoided.
1. History, physical examination, National Institutes of Health stroke scale (NIHSS), and consultation with a neurologist
a. Patients with acute ischemic stroke should be rapidly evaluated in the emergency room in consultation with a neurologist. The primary objective is to establish a correct diagnosis
of acute ischemic stroke. The NIHSS should be calculated, as it is a standardized method of determining stroke severity and monitoring changes over time. Large vessel anterior or
posterior stroke syndromes (Table 5.2) should be differentiated from lacunar stroke syndromes (Table 5.3) and can be utilized to help guide clinical localization of a clot.
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Table 5.1 Inclusion/Exclusion Criteria for Intravenous Tissue Plasminogen Activator (13)
Inclusion Criteria: Arrival within 4.5 h of onset or “last known well”
Ischemic stroke causing a measurable neurologic deficit

Onset <4.5 h before beginning treatment
Age >18 y
Exclusion Criteria: Arrival within 3 h of onset or “last known well”
Head trauma or prior stroke within the last 3 mo

Symptoms suggestive of intracranial hemorrhage
Arterial puncture in noncompressible site in last 7 d
History of previous intracerebral hemorrhage
Recent intracranial or intraspinal surgery
Blood pressure >185 mm Hg systolic or 110 mm Hg diastolic
Blood glucose <50 mg/dL
CT demonstrates multilobar infarction (hypodensity >1/3 of cerebral hemisphere)
Acute bleeding diathesis, including, but not limited to
Platelets less than 100,000/μL
Anticoagulant use with INR >1.7 or PT >15
Current use of direct thrombin or Xa inhibitors with elevated sensitive laboratory tests
Heparin use within 48 h, with elevated APTT above the upper limit of normal
Active internal bleeding
Relative Exclusion Criteria for patients arriving within 3 h of onset or “last known well.” Under some circumstances, patients can receive tPA despite one or
more relative contraindications. Careful weighing of risks and benefits is required.
Minor or rapidly improving symptoms

Pregnancy
Seizure at the onset with residual neurologic deficits
Major surgery or trauma within previous 14 d
GU or GI tract hemorrhage within the last 21 d
Acute MI within last 3 mo
Additional Exclusion Criteria for patients presenting within 3-4.5 h
Age older than 80 y

Severe stroke, that is NIHSS >25
Taking an oral anticoagulant regardless of INR
History of both diabetes and a previous stroke
PT, prothrombin time; APTT, activated partial thromboplastin time; GU, genitourinary; GI, gastrointestinal; MI, myocardial infarction.
b. Establishing the correct time of onset of symptoms is critical to establish if the patient is in an acceptable time window for therapy. If the exact time of onset is unknown, the last
time the patient was seen normal is used as the onset.
c. Review of medications, allergies, and comorbidities should be performed.
d. Pulse exam is important in patient assessment because most stroke interventions are performed from a femoral approach.
2. Laboratory evaluation
a. Evaluation includes complete blood count; international normalized ratio (INR); and serum electrolytes including creatinine, fingerstick glucose, and troponin. These labs should
not delay the administration of endovascular therapy but are important for overall care of the acute stroke patient. Correction is tailored to the overall patient condition and
anticipated method
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of treatment. For example, a mild elevation of INR may not be corrected if thrombectomy is anticipated but corrected when IA tPA is planned.
Table 5.2 Large Vessel Stroke Patterns
Anterior Circulation
ACA occlusion Contralateral hemiparesis: leg > arm

Contralateral sensory loss: leg > arm
Confusion, personality changes
MCA occlusion Contralateral hemiparesis: arm/face > leg

Contralateral sensory loss: arm/face > leg
Aphasia
Spatial neglect
Homonymous hemianopia on opposite side of the infarct
Gaze deviation toward side of stroke
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Posterior Circulation
PCA occlusion Contralateral homonymous hemianopia
Contralateral sensory loss
Possible aphasia
Disconjugate gaze (uncommon)
Vertebrobasilar occlusion Ataxia, vertigo, diplopia, dysarthria, hiccups, nausea, vomiting

Disconjugate gaze
Crossed signs
Decreased level of consciousness
ACA, anterior cerebral artery; MCA, middle cerebral artery; PCA, posterior cerebral artery.
b. Electrocardiogram. Cardiac abnormalities often coexist with stroke and have important implications on patient treatment and outcome.
3. Imaging evaluation
Urgent imaging should occur for patient triage. Guidelines suggest that radiologic imaging should begin within 25 minutes and be interpreted within 45 minutes of arrival in at least
80% of cases (11). During acute stroke, perfusion to the brain distal to the clot is dependent on collateral flow. The ideal revascularization candidate has relatively little irreversibly
injured brain (core infarct) and a relatively large area of brain at risk for progression to complete infarction (ischemic penumbra). If no revascularization is performed, then the core
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infarct will grow over time leading to greater disability. Recent randomized trials have strongly emphasized CT protocols to promote rapid triage of patients to thrombectomy. Multiple
imaging techniques have been demonstrated to lead to effective patient selection including CTA alone, multiphase CTA (mCTA), and perfusion imaging with CT or MRI. Use of
advanced imaging is likely more important in late time windows (>6 hours). Institutional protocols should be developed based on evidence, local factors, and operator preferences.
Table 5.3 Lacunar Stroke Syndromes
Pure motor Equal weakness in the contralateral face, arm, and leg
Pure sensory Equal numbness or paresthesia in the contralateral face, arm, and leg
Mixed sensory-motor Numbness and weakness equally distributed in the contralateral face, arm, and leg
Clumsy hand-dysarthria Incoordination and weakness of one hand with slurred speech and facial weakness
Ataxic hemiparesis Cerebellar ataxia and weakness on the same side of the body, with the ataxia out of proportion to weakness
a. Noncontrast computed tomography (NCCT) NCCT is fast, has no contraindications, and has 24/7/365 availability at most institutions, making it perfect for exclusion of
hemorrhage and triage to IV tPA. The ASPECTS is a 10-point scale for defining early ischemic changes on NCCT. A normal NCCT scan yields a score of 10 with 1-point deducted
for every area of ischemic change in a defined segment. Patients with a large ischemic core (ASPECTS <6) should be excluded from endovascular therapy. Further vascular
imaging should be utilized to document an LVO before proceeding to endovascular therapy.
b. Computed tomographic angiography (CTA)
CTA can be rapidly acquired in nearly all patients. It is highly accurate at identification of vascular occlusion, easy to read, and information obtained about the aortic arch and neck
vasculature is useful for planning endovascular interventions. Of recent randomized trials, Multicenter Randomized Clinical Trial of Endovascular Treatment for Acute Ischemic
Stroke in the Netherlands (MR CLEAN) predominantly used NCCT and CTA alone for endovascular triage (1). Use of CTA alone, however, may select some patients with larger
core infarcts or minimal penumbra who may not benefit from endovascular therapy.
c. Multiphase CTA (mCTA)
mCTA utilizes additional venous phases to assess collaterals and exclude patients with a large core infarct who may not benefit from endovascular therapy. A standard CTA is
performed in late arterial phase from the aortic arch through the vertex, and then two additional acquisitions are immediately performed in venous and late venous phases through
the brain only. This strategy was utilized in the Endovascular Treatment for Small Core and Anterior Circulation Proximal Occlusion with Emphasis on Minimizing CT to
Recanalization Times (ESCAPE) trial where collateral filling of <50% of the MCA territory was used to exclude patients with a large core infarct and correlated well with ASPECTS of
≤5 (3). Advantages of this approach include low cost, minimal additional radiation, and fast post-processing times.
d. CT perfusion (CTP)
CTP involves an additional contrast bolus with continuous scanning of either a segment of brain or more recently whole brain imaging where software can then be used to calculate
various parameters such as time to start (TTS), time to peak (TTP), mean transit time (MTT), cerebral blood volume (CBV), and cerebral blood flow (CBF). Color-coded maps are
generated. Brain at risk is best quantified by areas where TTP is >6 seconds although areas of increased MTT and TTS roughly approximate penumbra as well. Areas where CBV
or CBF falls below specified thresholds are used to estimate the core infarct.
Significant controversy exists in the literature about use of CTP for estimation of core infarct and penumbra for endovascular patient selection. Evaluation of the same source data
on different vendor software packages leads to differing estimations of core infarct and penumbra potentially making CTP unreliable for patient selection (12). Radiation concerns
also exist with use of CTP. Nevertheless, the Solitaire with the Intention for Thrombectomy as Primary Endovascular Treatment (SWIFT PRIME) and Extending the Time for
Thrombolysis in Emergency Neurological Deficits-Intra-arterial
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(EXTEND-IA) trials demonstrated that CTP with automated reconstruction software (RAPID, iSchemaView) led to appropriate patient selection for endovascular therapy (2,5). In
these trials, patients with large core infarcts of >50 to 70 mL were excluded, and patients were required to have a penumbra at least 20% to 80% larger than the core. It is possible
that use of more strict eligibility criteria with CTP in these trials selected out some patients who would otherwise benefit from therapy as up to 25% of patients excluded from
EXTEND-IA would have been eligible in other trials.
e. Magnetic resonance imaging (MRI)
Diffusion-weighted restriction on MRI is the most sensitive modality for early detection of irreversibly injured brain. MRI alone is also highly sensitive for blood products. The
disadvantages of MRI mainly involve lack of 24/7/365 availability, slower acquisition times, additional time required to screen patients for implants and metallic foreign bodies,
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increased sensitivity to patient motion, and patient claustrophobia. MR perfusion-weighted images can be used to determine the ischemic penumbra of brain at risk similar to CTP. At
the authors' institution, MRI is mainly used in patients with unknown time of onset, for reimaging of patients who were transferred from another institution who already had an outside
CTA documenting LVO, and when endovascular therapy is being considered in later time windows.
4. All patients who are eligible should receive full-dose (0.9 mg per kg) IV tPA. Bridging strategies are no longer recommended.
5. In acute stroke intervention, consent is not practically obtained from the patient. Consent should be expeditiously obtained from family when practical. Emergency consent may be
required and should be a consensus decision with the consulting neurologist. Institutional preprinted consents are recommended to save time and standardize risk and benefit
discussion.
6. IV access is critical for administration of IV fibrinolytics and medications for blood pressure control. At least two large-bore IVs should be placed. IV fluids can be administered to
decrease risks of contrast.
7. Invasive pressure monitoring is important in acute stroke therapy. Collateral circulation maintains perfusion to the ischemic penumbra through leptomeningeal collaterals. Prior to
revascularization, permissive hypertension is acceptable. If the patient has not received IV tPA, a pressure of up to 220/110 mm Hg is acceptable unless there are signs of end-organ
injury (13). If IV tPA has been administered, the pressure should be brought to less than 180/105 mm Hg for 24 hours (13). If radial arterial line placement is feasible in the
emergency department (ED) prior to transport to angiography, it should be performed. Given the ability to rapidly gain groin arterial access for arterial pressure monitoring in the
angiography suite, this should not delay transport to the angiography suite. Use of a femoral sheath 1 Fr. larger than the balloon guide allows anesthesia the ability to immediately
have invasive arterial pressure monitoring without multiple arterial access points.
8. When time allows, Foley catheter placement in the ED is helpful. It should not delay the procedure.
9. Groin preparation. If additional time is available in the ED, then shaving the groin and preparation for angiography may save minimal time.
Procedure
1. General considerations
a. Airway protection and anesthesia considerations Intubation may be required for airway protection but should not be routinely performed. Several retrospective studies have
demonstrated improved clinical outcome with conscious sedation as compared with general anesthetic. These analyses are inherently flawed as patients with more severe
strokes,
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and left hemispheric strokes are more likely to require intubation and likely will have worse outcome. Despite these limitations, general anesthesia is associated with
hypotension, which may compromise perfusion through collateral vessels and also adds time to the procedure. The majority of stroke interventions are now performed with
conscious sedation with anesthesia present to provide airway support and blood pressure control. Recent randomized trials utilized general anesthesia in 7% to 38% of
patients. Although an intermittently moving patient is not ideal, the majority of stroke intervention with modern mechanical devices can be safely performed with conscious
sedation. Conversion to general anesthetic can be performed for airway protection or with an uncooperative patient.
b. Angiographic equipment
Stroke intervention is ideally performed with biplane angiography. This allows for easier identification of emboli, increased safety navigating intracranial anatomy, and lower
contrast use.
c. Vascular access
Access can be obtained in standard fashion, although patients are often actively receiving IV tPA and are at higher risk for bleeding complications. Ultrasound-guided
micropuncture access can mitigate many of these complications and requires little extra time when used routinely.
2. Mechanical thrombectomy
The two dominant techniques for mechanical thrombectomy include stent retrievers and aspiration thrombectomy. The mechanical systems and medical therapies each have
advantages and disadvantages and may be used in concert with one another. The main advantage of mechanical devices is the improved ability to remove large clots rapidly
and avoid the use of fibrinolytics.
a. Stent retrievers
Solitaire (Covidien, Minneapolis, MN) and Trevo (Stryker Neurovascular, Fremont, CA) stent retrievers were both approved by the U.S. Food and Drug Administration (FDA) for
use in the United States in 2012. They represent a remarkable advance in stroke therapy and are generally used in the same fashion. All recent positive randomized trials
utilized stent retrievers as the dominant endovascular strategy, and these devices carry the highest level of evidence for efficacy. The Solitaire stent retriever is available in 4
mm and 6 mm diameters in varying lengths. The 4-mm device is delivered through a 0.021-in. internal diameter (ID) microcatheter, whereas the 6-mm device is delivered
through a 0.027-in. ID microcatheter. The Solitaire stent has an overlapping stent design, is not packaged with a microcatheter, and only has radiopaque markers at the ends of
the stent. The Trevo ProVue stent retriever comes in 4-mm and 6-mm diameters and is packaged with its own delivery catheter. It is composed of a single circular stent and is
radiopaque.
(1) Place a vascular sheath to accommodate the appropriate balloon-guiding catheter (BGC), most commonly 8 Fr. or 9 Fr.
(2) Manufacturer guidelines suggest using the stent retrievers with flow reversal. To effectively accomplish flow reversal, a BGC must be placed into the internal carotid artery
(ICA). Balloon placement in the common carotid artery (CCA) will not effectively accomplish flow reversal as occlusion of the CCA will lead to flow reversal in the ipsilateral
external carotid, which may continue to supply antegrade flow in the ICA. The larger the ID of the balloon guide, the more effectively that aspiration from the guiding catheter
can reverse flow and the less likely that the clot will shear off and become embolic debris. Experimental models have demonstrated that BGCs can reverse flow and result in
fewer distal emboli when compared to similar-sized guiding catheters without balloons, and clinical studies have demonstrated improved outcomes with BGC utilization (14,15).
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(a) The balloon guide is prepared on the back table with either dilute (50%) contrast or lower density contrast such as Isovue-200 (Bracco, Monroe Township, NJ). Aspiration of
air is ideal in the event a balloon ruptures to prevent intracranial air embolus. The balloon guide is delivered into the descending thoracic aorta, flushed, and connected to a
heparinized saline drip with a rotating hemostatic valve.
(b) Given the importance of time to revascularization, diagnostic cerebral arteriography of nontarget vasculature is of little value. The decision for thrombectomy should have
been made prior to angiography, and the goal is minimizing time to revascularization. The ICA is then catheterized with a 125-cm 5 Fr. catheter with a 180-cm Glidewire
(Terumo, Somerset, NJ), preferably under road map technique. A Berenstein-or Davis-shaped catheter can typically be used to rapidly catheterize a Type I or Type II arch. An
alternative approach is initial catheterization of the ICA with a diagnostic catheter of choice and wire exchange over a 260-cm stiff steel wire. In a difficult Type II or Type III arch,
reverse curved slip catheters (5 Fr. or 5.5 Fr. depending on balloon guide ID) such as a Vitek (VTK) or Simmons 2 (SIM 2) along with a 180-cm stiff Glidewire (Terumo,
Somerset, NJ) are particularly helpful. The balloon guide is then delivered into the ICA over the catheter.
(c) A small contrast injection can then be performed to look for spasm or flow occlusion from the guiding catheter. If there is flow arrest due to spasm, slowly withdraw the
guiding catheter until antegrade flow is restored. Significant spasm may be treated with small doses (50 to 100 μg) of IA nitroglycerin if the blood pressure permits.
(3) Perform a diagnostic angiogram to evaluate the level of occlusion. Allow the angiogram to run into the venous phase to evaluate leptomeningeal collaterals and potentially
identify the distal aspect of the occlusion.
(4) Cross the occlusion. Use a microcatheter appropriately sized to the stent retriever with a soft-tipped microwire to cross the occlusion. Creation of J-shaped curve can
increase safety of intracranial wire manipulation and prevent inadvertent catheterization of smaller branch or perforating vessels such as lenticulostriates. If the J-shaped tip
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does not cross the occlusion, reduce the J and cross with the leading wire tip. Deliver the microcatheter past the occlusion and remove the wire. Aspiration should yield blood if
the clot has been successfully crossed, and the catheter is intravascular.
(5) Perform a gentle angiogram with dilute contrast. Contrast has been demonstrated to stain injured brain when the blood-brain barrier is disrupted and may worsen outcome.
Dilute contrast with saline (1:3) for intracranial injections. This injection can then be used to determine clot length and optimize planning of stent retriever placement.
(6) Backflush the stent retriever in the rotating hemostatic valve in a similar manner to coil preparation to remove any air.
(7) Deliver the stent retriever across the clot and uncover it. This will temporarily establish antegrade flow. The authors prefer to place a moderate amount of stent distal to the
clot in M2 branches so that if the clot slips or migrates on retrieval there is more distal stent to continue to engage the clot (Fig. 5.1). Perform an angiogram through the guiding
catheter to assess flow. Typically, flow will now be antegrade through the clot.
(8) Allow for clot incorporation. Wait at least 5 minutes for the stent to incorporate into the clot. Flow may occlude through the stent after the clot has sufficiently incorporated.
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FIGURE 5.1 • Endovascular thrombectomy with Solitaire. An 81-year-old woman found down with left hemiparesis and neglect. NIHSS of 20. She received full-dose IV tPA. A:
CTA demonstrates right M1 cutoff (white arrow). B: CTP TTP demonstrate a large ischemic penumbra (white outline). C: CTP CBV map shows a small core infarct (white
outline). D: PA angiogram demonstrates right M1 cutoff (white arrow) distal to the anterior temporal artery. Note the corrugation/spasm of the internal carotid artery with balloon
guide catheter placement (red arrow). E: Lateral angiogram shows absence of filling in the right MCA territory. F,G: PA and lateral still shots showing placement of a 6 mm × 30
mm Solitaire stent retriever. The distal end (white arrow) is placed with a moderate amount of stent distal to the clot (red arrow). The clot was retrieved with a single pass under
flow reversal. H,I: Post-thrombectomy PA and lateral angiograms show thrombolysis in cerebral infarction (TICI) 3 reperfusion. The patient rapidly improved to a stroke scale of
5.
(9) Inflate the BGC. Inflation should be performed until the edges of the balloon begin to achieve a rectangular shape with rounded edges.
(10) Begin aspirating on the sidearm of the balloon catheter with a 60-mL syringe. It is helpful to have an assistant perform this task. Alternatively, the Penumbra aspiration
pump (Penumbra Inc, Alameda, CA) can be used for aspiration with a single operator. A very tortuous carotid with the balloon guide positioned at a turn may limit aspiration
efficacy, and placement of the BGC in a straight segment of vessel is preferred to optimize flow reversal.
(11) Retrieve the stent and clot into the BGC with a slow smooth pulling motion. This can be painful, particularly in the awake patient.
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(12) Vigorously aspirate the BGC to remove embolic debris and waste the blood.
(13) Deflate the BGC and perform a diagnostic angiogram.
(14) If spasm is present, administer IA verapamil (2.5 to 5 mg) or nitroglycerine (50 to 100 μg) if the blood pressure permits.
(15) When revascularization is obtained, reduction in the blood pressure may help mitigate risks of reperfusion hemorrhage. Although guidelines have not been established,
reducing systolic pressures to less than 140 to 160 mm Hg is reasonable.
(16) End points. Revascularization is most commonly measured with the modified thrombolysis in cerebral infarction (mTICI) score (Table 5.4). The angiographic goal is mTICI
2B or 3 revascularization, which represents reperfusion ≥50% of the affected vascular territory. Other end points include dramatic clinical improvement, wire perforation,
hemorrhagic transformation, or failed reperfusion after multiple attempts.
b. Penumbra aspiration catheter
The Penumbra Aspiration System (Penumbra, Inc, Alameda, CA) was FDA-approved in 2008. It is a system composed of a reperfusion catheter, a suction pump, suction tubing,
and a diamond-tipped separator. The system was initially designed so that the separator could be used to fragment clot into the aspiration catheter with a back-and-forth
motion, but with the larger aspiration catheters such as the 5 MAX ACE and 5 MAX ACE 064, the separators are rarely used because the clot is more likely to be ingested as a
whole fragment. There is less data using the Penumbra system as compared to stent retrievers, but efficacy in clinical practice seems similar when appropriately used. There
are no direct comparisons between the Penumbra system and the stent retrievers at the time of this manuscript creation.
(1) Place a long 6 Fr. sheath such as a Shuttle (Cook, Bloomington, IN) into the descending thoracic aorta. A 9 Fr. BCG with a 6 Fr. inner lumen may be used as well, which
carries the advantage of allowing for use of a stent retriever if the aspiration strategy fails. If a stent retriever is required due to failure of an aspiration technique, it can be
utilized through the 5 MAX ACE or 5 MAX ACE 064 catheter providing local aspiration at the clot face without use of a balloon guide (Fig. 5.2). Flush the sheath and connect it
to a rotating hemostatic valve and heparinized saline drip.
(2) Deliver the sheath into the CCA or ICA with a 125-cm catheter and 180-cm glidewire. Because direct aspiration will be utilized, flow reversal is not required and sheath
placement in the CCA is preferred when the ICA is small or tortuous.
(3) Inject contrast to ensure there is antegrade flow.
(4) Perform a diagnostic angiogram.
(5) Use the largest aspiration catheter that is reasonable for the vessel size (typically 5 MAX ACE or 5 MAX ACE 064 for ICA or M1 occlusion). This is delivered coaxially with a
medium-sized microcatheter (3 MAX or 0.027-in. microcatheter) and soft-tipped microwire. The aspiration
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catheter may get caught at branch points, most commonly at the ophthalmic artery and A1 origin.
Table 5.4 Modified Thrombolysis in Cerebral Infarction Score (mTICI)
0 No perfusion
1 Minimal filling past occlusion without distal branch filling
2A Perfusion of <50% of the vascular distribution
2B Perfusion of ≥50% of the vascular distribution
3 Complete reperfusion
FIGURE 5.2 • Endovascular thrombectomy with Penumbra and Solitaire. A 52-year-old man with acute MI who underwent coronary catheterization and drug-eluting stent
placement for complete right coronary occlusion. The patient became unresponsive. CT showed a hyperdense basilar suspicious for thrombosis. He was not a candidate for IV
tPA due to a recent procedure and hematemesis with IV Integrilin. NIHSS on admission was 22. A: Coronal CTA demonstrates clot at the basilar tip (white arrow). B,C: PA and
lateral angiographic views showing a filling defect at the basilar tip (white arrow). The left posterior cerebral artery and thalamoperforators do not fill. D: Lateral road map
demonstrating placement of Penumbra 5 MAX ACE catheter (white arrow) to basilar clot. Aspiration alone was unsuccessful in clot removal. E,F: PA and lateral still shots
showing deployment of a Solitaire 6 mm × 30 mm stent retriever ( red arrow is distal stent) into the right posterior cerebral artery deployed through the Penumbra catheter
(white arrow) in the basilar. A moderate amount of stent was placed distal to the clot. The clot was retrieved under direct aspiration with the Penumbra after two passes. G:
Post-thrombectomy PA view demonstrates TICI 3 recanalization with spasm in the left P1 (white arrow) treated with IA Verapamil. H: Post-thrombectomy lateral view
demonstrates reperfusion of the thalamoperforators (white arrow). I: Post-thrombectomy MRI shows left greater than right thalamic infarcts (white arrows). The patient regained
consciousness and was discharged with an NIHSS of 3.
(6) Deliver the Penumbra aspiration catheter to the face of the clot under road map technique. Remove the inner catheter and wire.
(7) Start the pump and connect the Penumbra aspiration catheter to the pump. Watch blood flow in the tubing as a guide to what is occurring
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inside the body. As the clot is engaged, flow should cease or dramatically slow. If the clot is aspirated into the pump, flow will rapidly restore. Allow at least 3 minutes for the clot
to aspirate into the catheter. Alternatively, suction with a 60-mL syringe can be utilized.
(8) If flow has not restored and the clot has not been ejected into the pump after 2 to 3 minutes, slowly withdraw the aspiration catheter. The clot will commonly be “corked” in
the aspiration catheter and removed as a large fragment. This technique of “a direct aspiration” first strategy has been termed ADAPT (16).
(9) Aspirate the sheath or BCG vigorously and discard the blood.
(10) Perform an angiogram.
(11) Repeat aspiration or change to a stent retriever as required.
(12) Once reperfusion is obtained, then lowering of the blood pressure is as described earlier.
3. Intra-arterial fibrinolysis
IA fibrinolytics are now most commonly used when mechanical methods fail, in smaller distal vessels where mechanical devices cannot be safely delivered, or to treat distal
embolic complications of mechanical embolectomy. IA fibrinolysis can use both tPA (Genentech, South San Francisco, CA) and glycoprotein IIb/IIa inhibitors such as abciximab
(Janssen Biotech, Horsham, PA).
a. A 0.021-in. or smaller soft-tipped neuromicrocatheter is delivered through the clot, preferably under road map technique. A soft 0.014-in. microwire with a J shape can be
utilized to cross the lesion as described earlier.
b. Most US physicians now use IA tPA as the fibrinolytic of choice. Typically, several milligrams of tPA are laced through the clot as the microcatheter is withdrawn. The
microcatheter is then advanced into the clot for a local infusion. The infusion can be performed with hand injection or a dilute solution (50-mg tPA in 250-mg normal saline) can
be connected to an infusion pump. The appropriate IA infusion dose is likely between 5 mg and 10 mg per hour. The total dose of IA tPA for most interventions is typically 10 to
20 mg when systemic IV tPA has not been administered.
c. Checkup arteriography should be performed through the base guiding catheter in the neck every 10 to 15 minutes.
d. Abciximab can additionally be administered in 1-mg aliquots up to approximately 5 mg. Abciximab is particularly effective in dissolving hyperacute platelet plugs.
e. End points of clot resolution, clinical improvement, or hemorrhage are similar to with mechanical techniques.
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4. Sheath management
After thrombectomy, the groin sheath can be sutured in and left in place overnight or a closure device may be utilized. A common femoral arteriogram should be performed to
ensure that the sheath is not occlusive or anatomy is appropriate for a closure device. If the sheath is left in place, it should be connected to a heparinized saline transducer.
1. Patients are managed in the intensive care unit (ICU) with close observation by the nursing staff and ICU physician.
2. Frequent reassessment of the patient should occur after ischemic stroke to evaluate for clinical worsening, which may be a sign of symptomatic intracranial hemorrhage (SICH).
Neurovascular checks are performed every 15 minutes for the first hour and at least every hour subsequently for the first 24 hours. An increase of the NIHSS by greater than or
equal to 4 points is a sign that SICH has occurred and should prompt an emergent CT to evaluate for hemorrhage.
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3. The femoral artery puncture site and distal pulses should be monitored per institutional guidelines. Groin hematoma is the most common complication at the puncture site.
4. No guidelines for blood pressure management after endovascular revascularization have been established. Maintaining systolic blood pressure less than 140 to 160 mm Hg is
prudent to reduce the risk of reperfusion hemorrhage. IV antihypertensive medications may include labetalol, nicardipine, or nitroprusside.
5. An NCCT is typically obtained within the first 24 hours to evaluate for hemorrhage and swelling. Early CT may demonstrate parenchymal contrast staining, which is due to
breakdown of the blood-brain barrier and will typically clear after 1 to 2 days. Guidelines suggest that 90% of patients should have a CT scan within 36 hours after the procedure
(11).
6. Workup for etiology may include carotid ultrasound, cardiac echocardiography with bubble study, lipid panel, and hemoglobin A1C.
7. The patient should remain nil per os (NPO) until a formal swallow evaluation to prevent aspiration.
Results/Outcomes
Before 2013, evidence for mechanical thrombectomy had been from trials performed without a noninterventional control arm. In January of 2013, three randomized studies were
published (Interventional Management of Stroke III [IMS III], A Randomized Controlled Trial on Intra-Arterial Versus Intravenous Thrombolysis in Acute Ischemic Stroke
[SYNTHESIS Expansion], Mechanical Retrieval and Recanalization of Stroke Clots Using Embolectomy [MR RESCUE]) that failed to show improved results with endovascular
therapy as compared to best medical therapy raising the doubt of efficacy of endovascular techniques (7,17,18). The negative result of these trials has largely been attributed
to poor patient selection with lack of documentation of LVO prior to randomization, use of older mechanical devices, poor revascularization rates, and slower times to
revascularization.
Recently, five randomized trials (MR CLEAN, ESCAPE, EXTEND-IA, SWIFT PRIME, and REVASCAT) comparing endovascular therapy plus best medical therapy to best
medical therapy alone in anterior circulation acute LVO stroke have been published, all of which demonstrated a dramatic benefit of endovascular therapy (1,2,3,4,5). These
results were obtained in patients with moderate to severe clinical deficits. Imaging was used to document large vessel anterior circulation occlusion. Modern thrombectomy
devices dominated by stent retrievers were used achieving high revascularization rates. Patients with large core infarcts were excluded. Most patients received full-dose IV tPA
when indicated. Groin puncture was generally achieved by 6 hours. In this context, a 14% to 31% improvement in functional independence at 90 days was seen in the
endovascular group as compared to best medical therapy as a control. This corresponds to a number needed to treat of approximately four to prevent disability in a single
patient. Additionally, there was a trend to decreased mortality and no statistical difference in symptomatic intracranial hemorrhage. A summary of patient characteristics and
major outcome measures of these trials are listed in Table 5.5.
With further improvements in devices and technique, we can expect incremental improvement in degree of recanalization to >90% and a reduction in intraoperative
recanalization time to less than 40 minutes. However, more effectiveness may be gained by streamlining the process from onset of symptoms to getting patients to the
interventional suite. This includes public education for awareness of the urgency of stroke symptoms, transportation of patients to an appropriate facility, and improved times for
patient evaluation and initiating appropriate IV treatment while arranging the transfer of appropriately selected patients to the interventional suite. Although infrequently studied
at present, it is likely that the
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quality of post-thrombectomy acute ICU management and follow-up rehabilitation therapy affect long-term outcome as well.
Table 5.5 Randomized Trials for Endovascular Therapy of Large Vessel Anterior Circulation S
Trial MR CLEAN (1) ESCAPE (2) EXTEND IA (3)
Treatment Endo Control Endo Control Endo Control

Arm
No. of 233 267 165 150 35 35

Patients
Median 17 18 (14- 16 17 17 13
NIHSS (14- 21) (13,14,15,16,17,18,19,20) (12,13,14,15,16,17,18,19,20) (13,14,15,16,17,18,19,20) (9,10,11,12,13,14,15,16,17,18,19) (13,14,
(IQR) 22)
IV tPA 87% 91% 73% 79% 100% 100%
LSN to 260 — NR — 210 —

Groin
(min)a
mTICI 59% — 72% — 86% —

2B/3
Stent 97% — 86% — 100% —

Retrieverb
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mRS 0-2 33% 19% 53% 29% 71% 40%
at 90 d
Mortality 21% 22% 10% 19% 9% 20%

at 90 d
Endo, endovascular therapy; IQR, interquartile range; LSN, last seen normal; mTICI 2B/3, mTICI score (2B/3 is considered good revascularization); mRS, modified Rankin score (0-2 is c
aMedian times reported.
bWhen a device used for revascularization, percentage usage of stent retrievers.
Complications/Management
Recent trials emphasizing mechanical thrombectomy with current stent retrievers demonstrate excellent safety.
1. Symptomatic intracranial hemorrhage (SICH), 0% to 8% (1,2,3,4,5) Type II parenchymal hematoma (space occupying hematoma of >30% of the infarct zone with substantial mass
effect) or subarachnoid hemorrhage associated with neurologic deterioration (decline in NIHSS of >4 or death within 36 hours of therapy) occurred in recent trials in 0% to 8% of
patients and was not statistically different from patients receiving medical management only (1,2,3,4,5). SICH can occur from reperfusion hemorrhage or procedure related
complications such as wire perforation. Management of SICH may include correction of coagulopathy, strict blood pressure management, intubation for airway management,
invasive monitoring of intracranial pressure, possible medical therapy of elevated intracranial pressure (ICP) with mannitol or hyperventilation, and possibly decompressive
craniotomy.
2. Dissection or wire perforation, 1% to 6% (19,20)
Recognized intraprocedural wire perforation with active extravasation is an emergent life-threatening situation and should be treated with IV protamine to reverse any heparin,
immediate lowering of the blood pressure, and possible use of temporary balloon occlusion. Intraprocedural cone-beam CT can be utilized to detect midline shift or growing
hemorrhage that may require immediate neurosurgical consultation.
3. Groin complications, 1% to 8% (19,20)
Most common is a groin hematoma exacerbated by concurrent IV tPA administration, although pseudoaneurysm, retroperitoneal hemorrhage, arteriovenous (AV) fistula, thrombosis,
and infection have all been reported. Ultrasound-guided micropuncture access to limit the number of access attempts and reduce overall risks is recommended. Management of a
hematoma begins with compression to stop the bleeding and diffuse the blood into soft tissues limiting formation of solid hematoma. Vascular surgical consultation may be required if
there are loss of signals in the foot or the hematoma appears to be causing skin necrosis.
4. Embolization, 5% to 9% (1,2,4)
An important risk of mechanical stroke intervention is dislodging clots and causing embolic occlusion in new territories (ENT). Prevention of ENT is best done with flow reversal with
larger inner lumen BGCs when using stent retrievers and is discussed in the procedure section. Depending on where the embolic debris is, further endovascular therapy may be
performed. Distal emboli are often not treated due to the increased risk of distal navigation of intracranial vessels and frequent concomitant use of IV tPA, which may dissolve distal
clots.
References
1. Berkhemer OA, Fransen PS, Beumer D, et al. A randomized trial of intraarterial treatment for acute ischemic stroke. N Engl J Med. 2015;372(1):11-20.
2. Campbell BC, Mitchell PJ, Kleinig TJ, et al. Endovascular therapy for ischemic stroke with perfusion-imaging selection. N Engl J Med. 2015;372(11):1009-1018.
3. Goyal M, Demchuk AM, Menon BK, et al. Randomized assessment of rapid endovascular treatment of ischemic stroke. N Engl J Med. 2015;372(11):1019-1030.
4. Jovin TG, Chamorro A, Cobo E, et al. Thrombectomy within 8 hours after symptom onset in ischemic stroke. N Engl J Med. 2015;372:2296-2306.
5. Saver JL, Goyal M, Bonafe A, et al. Stent-retriever thrombectomy after intravenous t-PA vs. t-PA alone in stroke. N Engl J Med. 2015;372:2285-2295.
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6. Saver JL. Time is brain—quantified. Stroke. 2006;37(1):263-266.
7. Broderick JP, Palesch YY, Demchuk AM, et al. Endovascular therapy after intravenous t-PA versus t-PA alone for stroke. N Engl J Med. 2013;368(10):893-903.
8. Khatri P, Abruzzo T, Yeatts SD, et al. Good clinical outcome after ischemic stroke with successful revascularization is time-dependent. Neurology. 2009;73(13):1066-1072.
9. Shi ZS, Liebeskind DS, Xiang B, et al. Predictors of functional dependence despite successful revascularization in large-vessel occlusion strokes. Stroke. 2014;45(7):1977-
1984.
10. Turk AS, Magarick JA, Frei D, et al. CT perfusion-guided patient selection for endovascular recanalization in acute ischemic stroke: a multicenter study. J Neurointerv Surg.
2013;5(6):523-527.
11. Sacks D, Black CM, Cognard C, et al. Multisociety consensus quality improvement guidelines for intraarterial catheter-directed treatment of acute ischemic stroke, from the
American Society of Neuroradiology, Canadian Interventional Radiology Association, Cardiovascular and Interventional Radiological Society of Europe, Society for
Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society of NeuroInterventional Surgery, European Society of Minimally Invasive Neurological
Therapy, and Society of Vascular and Interventional Neurology. J Vasc Interv Radiol . 2013;24(2):151-163.
12. Fahmi F, Marguering HA, Streekstra GJ, et al. Differences in CT perfusion summary maps for patients with acute ischemic stroke generated by 2 software packages. AJNR
Am J Neuroradiol . 2012;33(11):2074-2080.
13. Jauch EC, Saver JL, Adams HP Jr, et al. Guidelines for the early management of patients with acute ischemic stroke: a guideline for healthcare professionals from the
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American Heart Association/American Stroke Association. Stroke. 2013;44(3):870-947.
14. Chueh JY, Kühn AL, Puri AS, et al. Reduction in distal emboli with proximal flow control during mechanical thrombectomy: a quantitative in vitro study. Stroke.
2013;44(5):1396-1401.
15. Nguyen TN, Malisch T, Castonguay AC, et al. Balloon guide catheter improves revascularization and clinical outcomes with the Solitaire device: analysis of the North
American Solitaire Acute Stroke Registry. Stroke. 2014;45(1):141-145.
16. Turk AS, Spiotta A, Frei D, et al. Initial clinical experience with the ADAPT technique: a direct aspiration first pass technique for stroke thrombectomy. J Neurointerv Surg.
2014;6(3):231-237.
17. Ciccone A, Valvassori L. Endovascular treatment for acute ischemic stroke. N Engl J Med. 2013;368(10):904-913.
18. Kidwell CS, Jahan R, Gornbein J, et al. A trial of imaging selection and endovascular treatment for ischemic stroke. N Engl J Med. 2013;368(10):914-923.
19. Akins PT, Amar AP, Pakbaz RS, et al. Complications of endovascular treatment for acute stroke in the SWIFT trial with solitaire and Merci devices. AJNR Am J Neuroradiol .
2014;35(3):524-528.
20. Gill HL, Siracuse JJ, Parrack IK, et al. Complications of the endovascular management of acute ischemic stroke. Vasc Health Risk Manag. 2014;10:675-681.
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6
Carotid Artery Stenoses
J. Diego Lozano
Ajit S. Puri
Ajay K. Wakhloo
Approximately 87% of all new strokes are ischemic in nature, of which an estimated 20% to 30% are due to
atherosclerotic disease of the extracranial internal carotid artery (ICA). The primary mechanism of stroke in
patients with atherosclerotic disease and stenosis of the ICA (or common carotid artery) is the embolization of
atherosclerotic debris or thrombotic material from plaque into the more distal cerebral vasculature. There also
seems to be a synergistic effect between thromboembolism to the cerebral vasculature and diminished
downstream flow to the ipsilateral brain from concomitant significant carotid stenosis.
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It was early in the 1900s when observations of the relationship between stroke and extracranial ICA were made.
However, it took almost another 50 years for the understanding of this relationship to lead to the development of
carotid endarterectomy (CEA). CEA is now a widely available, broadly accepted therapy for carotid
revascularization with proven efficacy and low procedural morbidity. Carotid balloon angioplasty was first
performed in 1980, and a stent in the carotid artery was first used in 1989 to treat an intimal flap after
angioplasty. Since those early days, carotid artery stenting (CAS) has become a widely accepted minimally
invasive alternative to CEA with similar benefits and a lower procedural risk, as indicated by a number of
largescale randomized controlled trials comparing these two techniques. Carotid stenting is now seen as an
alternative to CEA with a similar periprocedural risk profile for symptomatic patients with stenosis greater than
70% on duplex ultrasonography (1). As technology and techniques for CAS evolve, indications for CAS may
expand to a broader subset of patients requiring carotid artery revascularization.
Indications
According to the 2011 guideline on the management of patients with extracranial carotid and vertebral artery
disease, patients meeting the following criteria are candidates for carotid revascularization (1).
1. Patients at average or low surgical risk who experience nondisabling ischemic stroke or transient cerebral
ischemic symptoms, including hemispheric events or amaurosis fugax, within 6 months (symptomatic
patients) should undergo CEA if the diameter of the lumen of the ipsilateral ICA is reduced more than 70%
as documented by noninvasive imaging or more than 50% as documented by catheter angiography and the
anticipated rate of perioperative stroke or mortality is less than 6%.
2. CAS is indicated as an alternative to CEA for symptomatic patients at average or low risk of complications
associated with endovascular intervention when the diameter of the lumen of the ICA is reduced by more
than 70% as documented by noninvasive imaging or more than 50% as documented by catheter
angiography and the anticipated rate of periprocedural stroke is less than or equivalent to CEA.
3. Patients who are at high risk for CEA are considered to benefit particularly from the reduced procedural
risks of CAS. Current practice advocates for the use of an embolic protection device when performing
carotid stenting; with this in mind, the risks associated with CAS are perhaps even lower than those
associated with CEA, particularly in this group of high-risk patients (2). Patients have been considered
“high-risk” when they have the following major comorbidities and/or anatomic conditions (or two minor
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criteria in some investigations) (3,4,5,6,7,8,9):
a. High-risk comorbidities
(1) Major criteria
(a) Congestive heart failure (New York Heart Association [NYHA] functional class III/IV)
(b) Left ventricular ejection fraction <30%
(c) Chronic obstructive pulmonary disease (COPD) manifested with forced expired volume <30%
(d) Recent open-heart surgery (within 6 weeks)
(e) Dialysis-dependent renal failure
(f) Uncontrolled diabetes (fasting glucose >400 mg per dL, urine ketones >2)
(g) Patients under evaluation for or awaiting major organ transplantation
(2) Minor criteria
(a) Age >75 years
(b) Unstable angina (Canadian Cardiovascular Society [CCS] class III/IV)
(c) Recent myocardial infarction (MI) (<30 days)
(d) Major diseased coronary arteries (>2) with > 70% stenosis (patients with angina)
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(e) Planned peripheral vascular surgery, or other major surgeries postcarotid intervention
b. Anatomic high-risk conditions
(1) Major criteria
(a) Tandem stenosis (hemodynamically significant carotid artery stenosis with one or more ipsilateral
intracranial stenosis)
(b) Carotid dissection
(c) Previous neck or head radiation therapy/surgery including area of stenosis
(d) Surgically inaccessible lesions at or above C2 or below clavicle
(e) Spinal immobility of the neck
(f) Laryngeal palsy or laryngectomy
(g) Tracheostoma
(h) Tumor-encased carotid arteries
(i) Markedly irregular, ulcerated plaque
(2) Minor criteria
(a) Contralateral total occlusion, contralateral carotid disease requiring revascularization, or other limitation
of cross-flow circulation
(b) Restenosis post-carotid endarterectomy or attempted CEA with arteriotomy, at least 31 days prior
(c) Planned coronary artery bypass graft (CABG) or valve replacement post-carotid revascularization
procedure
Contraindications
In addition to absolute and relative contraindications applicable to all angiographic and interventional
procedures, the following considerations apply to CAS:
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Absolute
1. Chronic carotid artery occlusion
2. Allergy to antiplatelet medication
3. Allergy to metals in the stent (nickel, titanium, cobalt, chromium, and others depending on the stent
chosen)
4. Uncorrectable bleeding diathesis
5. Anatomic configurations that prohibit navigation of the devices to their target locations
Relative
1. Fresh clot within stenosis
2. Recent stroke (<4 to 6 weeks old) or prior disabling stroke (modified Rankin scale >3)
3. Recent intracranial hemorrhage
4. Positive blood cultures/sepsis
5. Immunologically compromised state
6. Circumferential or near circumferential calcification
1. Baseline history and physical examination
a. Consider obtaining consultation for cardiac and/or pulmonary risk assessment prior to procedure.
b. Patients with any potential impairment of renal function should be assessed for the risk of contrast-induced
nephropathy. Dialysis should be coordinated as necessary for patients with end-stage renal disease.
2. Comprehensive neurologic evaluation by an independent neurologist, including assessment with the National
Institutes of Health (NIH) Stroke Scale, modified Rankin scale, and Barthel index of activities of daily living
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3. 12-lead electrocardiogram (ECG)
4. Serum electrolytes including blood urea nitrogen (BUN) and creatinine, complete blood count (CBC),
prothrombin time (PT)/international normalized ratio (INR)/partial thromboplastin time (PTT)
5. Urine human chorionic gonadotropin (hCG) in women of childbearing age
6. Imaging
a. Ultrasonography (B-mode and Doppler) is the mainstay of screening for carotid stenosis. This is the
recommended initial diagnostic test to detect hemodynamically significant carotid stenosis. It is widely available
and shown to accurately depict a flow-limiting stenosis in the carotid arteries. A qualified technologist in a
certified laboratory should perform the examination.
(1) Primary parameters: peak systolic velocity (PSV) and direct estimation of plaque thickness
(2) Secondary parameters: end-diastolic velocity (EDV) and ICA/common carotid artery (CCA) ratio (ratio of PSV
in the ICA to PSV in the ipsilateral common carotid artery)
(3) May provide for evaluation of plaque composition and surface characteristics (stable vs. vulnerable plaque).
Ultrasound, however, is an operatordependent modality and sensitivity and specificity may vary greatly for the
detection of features of a vulnerable plaque. The mean sensitivity across several studies for the detection of
plaque ulcerations has been estimated to be close to 60% with a specificity of 74%.
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(4) Complementary to magnetic resonance angiography (MRA)/computed tomographic angiography (CTA), which
can evaluate for other carotid, vertebral, and intracranial abnormalities including tandem lesions, dissection,
thrombus, plaque border irregularity
b. MRA can be used to exclude stenosis but is limited in quantifying the degree of stenosis and is susceptible to
a wide variety of artifacts. Multiple techniques are available:
(1) Time of flight—does not require intravenous (IV) contrast
(2) Phase contrast-MRA—allows quantification of blood flow, flow velocity, and blood volume
(3) Contrast enhanced—improves image quality and lowers artifacts related to nonlaminar flow
c. Magnetic resonance imaging (MRI) for plaque morphology. Multiple studies have investigated the association
between MRI and histologic morphologic measurements. These morphologic measurements of the carotid vessel
wall made with MRI have shown a strong correlation with histology (10). Data from these and other studies
support the notion that features of plaque composition alone may provide value in the assessment of risk of
future events; still considered by some of limited value for the characterization of plaque calcification.
d. CTA is useful for evaluating the degree of stenosis and calcifications of the aortic arch and carotid arteries. An
accurate evaluation of the type of aortic arch, tortuosity of the common carotid artery, and course and caliber of
the vessel proximal and distal to the stenosis can also be obtained via this method. Other uses:
(1) As the resolution of newer generation of multiple detector computed tomography (MDCT) improves, so does
the detection of ulceration in an atherosclerotic plaque in the carotid arteries. This information is useful in
planning the procedural approach and in device selection.
(2) Although digital subtraction angiography (DSA) remains the gold standard, CTA has a high sensitivity and
specificity to diagnose intracranial stenosis, which can be very relevant when planning an intervention on a
patient with extracranial carotid stenosis.
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(3) CTA is also useful if ultrasound (US)/MRA results are discordant, or if MRA is contraindicated.
(4) MDCT angiography of the craniocervical carotid arteries is continuously evolving with the development of
newer bone subtraction algorithms which allow for much improved visualization of the ICA at the skull
base/clinoidal region.
e. DSA remains the gold standard for the evaluation of carotid and intracranial atherosclerosis. A complete four-
vessel angiogram should be performed to assess for intracranial atherosclerosis, aneurysms, and other vascular
abnormalities that may affect the approach to treatment. This can be performed at the time of a planned CAS.
7. CAS may be performed under moderate sedation, monitored anesthesia care (MAC), or general anesthesia
(GA), with continuous monitoring during the procedure of the electrocardiogram (ECG), blood pressure (BP), and
pulse oximetry. An arterial line for continuous BP measurement is recommended, especially when a carotid lesion
is located at the carotid bifurcation.
8. Correct hypo-/hyperglycemia preprocedurally and monitor intraprocedurally.
9. Correct INR to <1.7. Utilize a bridging strategy with unfractionated heparin when medically indicated and keep
the PTT 2 to 3 times baseline.
10. Medication management
a. Outpatient medications. Patients should continue their home medications except for β-blockers (due to
potential bradycardia during manipulation near the carotid bulb) and metformin. Metformin should be halted 24
hours prior to and 48 hours after the procedure. The American College of Radiology (ACR) has adopted a more
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relaxed policy for metformin management that varies according to renal dysfunction and presence of
comorbidities. Given the substantial complexity and challenges in implementing the new guidelines, the authors
consider continuing with the standard protocol of suspending metformin, as highlighted earlier, as a more
practical approach with little to no significant impact on patients.
b. Premedications (1,11)
(1) Elective cases. Start premedication at least 5 days prior to procedure.
(a) Antiplatelet therapy. Before and for a minimum of 30 days after CAS, dual-antiplatelet therapy with aspirin (81
to 325 mg daily) plus clopidogrel (75 mg daily) is recommended. Clopidogrel (Plavix) is usually continued for a
minimum of 6 weeks to 12 months following the procedure. Aspirin is continued indefinitely after the procedure.
(b) Antihypertensive therapy. Administration of antihypertensive medication is recommended to control BP before
and after CAS.
(c) Statins. Treatment with a statin medication is recommended for all patients with extracranial carotid
atherosclerosis to reduce lowdensity lipoprotein (LDL) cholesterol below 100 mg per dL or below 70 mg per dL
when there is a history of associated ischemic stroke and/or diabetes mellitus. Statin therapy should be
continued indefinitely.
(2) Emergent cases (less than 72 hours from onset of ischemic stroke). At present, there is no consensus on
medical or endovascular management of patients with acute ischemic stroke presenting with severe clinical
symptoms due to atherosclerotic stenosis/occlusion of the extracranial ICA (12,13). The authors recommend a
loading dose 3 to 4 hours prior to procedure of clopidogrel 300 mg by mouth (PO) and aspirin 650 mg PO or PR.
In patients unable to take clopidogrel, ticlopidine (Ticlid) 250 mg PO two times per day (bid) can be substituted.
The patient should receive at least two doses of ticlopidine (500 mg) prior to an emergent procedure.
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Procedure
1. Intraprocedural medication management
a. Anticoagulation. The procedure is performed with anticoagulation for all indications using either
unfractionated heparin or a direct thrombin inhibitor.
(1) Unfractionated heparin with a target activated clotting time (ACT) of 250 to 300 seconds. Start with a 50
to 70 IU per kg IV bolus and titrate appropriately.
(2) Direct thrombin inhibitors particularly for patients with heparin-induced thrombocytopenia. Standardized
regimens of bivalirudin and argatroban are yet to be established.
(a) Suggested dosing regimen for argatroban is 15 to 30 μg/kg/min IV infusion that can be achieved with a
350 μg per kg IV bolus, followed by 25 μg/kg/min IV infusion.
(b) Suggested dose regimen for bivalirudin is 0.75 mg per kg IV bolus, followed by infusion at 1.75 mg/kg/h
IV × 4 hours. ACT should be monitored 5 minutes after bolus and may give an additional 0.3 mg per kg IV
bolus if needed.
b. Glycoprotein (GP) IIb/IIIa blockers in case of in-stent platelet-rich clot formation
(1) Baseline ACT should be lower than 200 seconds prior to administration to reduce risk of intracranial
hemorrhage. This can be achieved by blocking part of the heparin activity with IV infusion of protamine.
(2) Eptifibatide (Integrilin)—2 μg/kg/min IV. Start with 180 μg per kg bolus (up to 22.6 mg total), with a
maximum maintenance infusion of 15 mg per hour.
(3) Abciximab (ReoPro)—0.125 μg/kg/min IV × 12 hours. Start 0.25 mg per kg IV bolus 10 to 60 minutes prior
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the start of the procedure. Maximum infusion dose is 10 μg per minute.
c. Management of intraprocedural bradycardia
(1) Glycopyrrolate—0.2 to 0.4 mg IV. This drug is administered prophylactically in cases where the target
lesion is close to the carotid bulb, as pressure on the baroreceptors during percutaneous transluminal
angioplasty (PTA) or stent placement may trigger bradycardia; may repeat dose if there is a long interval
before angioplasty.
(2) Atropine—0.6 to 1.0 mg IV bolus
(3) Rarely, dopamine is used.
d. Intra-arterial (IA) antihypertensive medications and vasospasm treatment
(1) Nicardipine is useful in the treatment (and prevention if used prior to endovascular intervention) of
vasospasm related to cerebral protection device placement, angioplasty, and stent placement. The dose is 2
to 10 mg IV bolus at a slow rate of approximately 1 mg per minute. Monitor BP closely.
(2) Verapamil has the same benefits, dose, and administration rate as nicardipine.
e. Management of hypotension. Colloid (20% albumin) solution can be useful in managing periprocedural
hypotension by expanding intravascular volume. Additionally, albumin is considered beneficial for improving
cerebral microcirculation independent of increase in BP. Albumin should be administered slowly, 50 mL over
20 minutes and may be repeated every 4 to 6 hours.
2. Access. CAS is typically performed via common femoral artery access. Radial, brachial, axillary, or direct
carotid punctures may also be used.
3. Diagnostic angiography
a. Establish access using modified Seldinger technique and a micropuncture system.
b. Place a 6 Fr. long flexible sheath. The sheath should be connected to a pressurized bag of heparinized
saline (1 drop per second continuous infusion).
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c. Aortic arch aortography using a 5 Fr. pigtail catheter is optional to analyze access and other
atherosclerotic lesions.
d. Using a 4 to 5 Fr. diagnostic catheter and hydrophilic guidewire, perform selective catheterization of
bilateral carotid and vertebral arteries. Angiographic runs should include frontal, oblique, and lateral views of
the neck, frontal and lateral views of the intracranial circulation, and any additional projections. Three-
dimensional (3D) rotation angiography of the carotid bulb may be helpful in evaluating high-grade stenosis
and calcified lesions. 3D can also be helpful to illustrate the best projection for navigation across the
stenosis and optimal projection for stent deployment.
e. Key points for assessment
(1) Assess collateral blood supply through external carotid arteries and the posterior circulation.
(2) Identify potential dangerous anastomoses to the internal carotid circulation from the external circulation
and the vertebrobasilar system.
(3) Assess the circle of Willis and intracranial collateral blood supply.
(4) Define the lesion extent (length, degree of stenosis) and regional anatomy (landing zone diameters,
relationships of the lesion to the carotid bulb, degree of calcification, tortuosity, ulceration, and thrombus).
4. Equipment
a. Guidewires
(1) A torqueable, hydrophilic 0.035-in. guidewire with a shapeable tip is used to facilitate selective
catheterization of the common carotid artery (e.g., Glide Wire, Terumo Medical Corp, Somerset, NJ).
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(2) A stiff, exchange-length 0.035-in. wire is used whenever needed to exchange the diagnostic catheter for
the guide catheter (e.g., Amplatz Extra Stiff 260 cm or 300 cm, Cook Medical Inc, Bloomington, IN).
(3) In cases where a cerebral protection device cannot be used, an exchange length 0.014-in. or 0.018-in.
wire is navigated beyond the stenotic lesion to support positioning of a PTA balloon for predilatation.
b. Catheters
(1) A 4 Fr. or 5 Fr. diagnostic catheter is used to perform preprocedure angiography (e.g., Bernstein II,
Sidewinder II, Multipurpose, Vertebral, Headhunter).
(2) A 6 Fr., or occasionally 7 Fr., guide catheter is used during the procedure (e.g., Envoy, Codman
Neurovascular, Raynham, MA, or Shuttle, Cook Medical Inc, Bloomington, IN).
c. Cerebral protection (CP) devices
(1) Filter devices are the most commonly used CP devices (Table 6.1). These consist of collapsible filters
mounted at the end of a 0.014-in. guidewire. The guidewire is navigated beyond the stenosis and the filter is
deployed. The filter traps embolic debris, which is removed along with the device after stent placement and
PTA.
(2) The MO.MA Ultra Device (Medtronic Vascular Inc, Santa Rosa, CA) is a proximal protection device that
consists of a catheter exchanged over a stiff 0.035-in. wire in the external carotid artery. The distal balloon
is inflated in the external carotid artery, the stiff guidewire is retracted, and the proximal balloon is inflated in
the common carotid artery. While on flow arrest through the ICA, the 0.014-in. guidewire is navigated across
the stenosis. The stent delivery system is advanced over the 0.014-in. wire and the self-expandable carotid
stent is deployed. The delivery system is removed and the balloon for angioplasty is advanced and inflated
across the stented stenotic segment. The angioplasty balloon is removed and aspiration through the MO.MA
Ultra device is performed, retrieving debris. The distal and proximal balloons are then deflated and
antegrade flow is restored. The MO.MA Ultra device is withdrawn. The distal tip profile is 5 Fr. and requires
an introducer sheath of at least 9 Fr.
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Table 6.1 Carotid Stents and Cerebral Embolic Protection Devices
Manufacturer Stent System Filter Device
Abbott Vascular (Santa Clara, CA) RX Acculink AccuNet
Abbott Vascular (Santa Clara, CA) xACT Emboshield BareWire
Boston Scientific Corp (Natick, MA) WALLSTENT FilterWire EZ
Cordis Corp (Miami, FL) Precise RX Angioguard RX
Covidien (Plymouth, MN) PROTÉGÉ RX SpiderFX
d. PTA balloons
(1) For predilatation (if required prior to stent placement), choose a 3.0 to 4.0 mm × 20 mm noncompliant
PTA balloon. If unable to navigate the lesion, predilatation using a low-profile cerebral angioplasty balloon
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such as the Gateway (Stryker Neurovascular, Fremont, CA) or Maverick (Boston Scientific Corp, Natick,
MA) can be performed.
(2) For dilatation after stent placement, choose a 4.0 to 7.0 mm × 20 mm noncompliant PTA balloon. The
diameter should match that of the normal artery distal to the target lesion.
e. Stents
(1) Self-expandable stents are used for the majority of CAS due to their superior crush resistance and their
ability to regain their shape when deformed (see Table 6.1). These advantages are important due to the
mobility of the neck. Balloon expandable stents offer more precise placement and still have a role in the
treatment of common carotid artery ostial lesions, where the segment of artery being treated remains
protected by the thoracic cage.
(2) Landing zones should be at least 5 to 10 mm distal and proximal to the atherosclerotic plaque. It is
preferable to cover the entire target lesion using a single stent. Lesions located in tortuous carotid segments
may be treated by overlapping two shorter stents, which avoids the arterial kinking and pseudo-occlusion
that generally occurs distal to a stented segment due to straightening of the ICA.
(3) Stents should be oversized 1 to 2 mm above the diameter of the vessel in the landing zones. In
contradistinction to PTA balloons, stents are sized with references to the larger, more proximal host vessel.
Tapered stents are available and may be useful in cases where there is a particularly large discrepancy
between proximal and distal landing zone diameters.
5. Carotid stenting procedure
a. After placement of the femoral sheath (and an arterial line, if needed) and after completion of the
diagnostic study, initiate heparinization and ensure an ACT of 250 to 300 seconds.
b. Under road map, place the diagnostic catheter over a hydrophilic guidewire into the ipsilateral external
carotid artery, if patent.
c. Remove the hydrophilic guidewire and replace with a stiff 300-cm exchange wire.
d. Over the stiff exchange wire, replace the diagnostic catheter with a 6 Fr. or 7 Fr. guide catheter. Place the
guide catheter approximately 20 mm proximal to the target lesion. The guide catheter is connected to a
pressurized bag of heparinized saline (1 drop per second continuous infusion). Confirm the inner diameter of
the guide catheter is sufficient as per the stent's instructions for use (IFU).
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e. Using road map, navigate the cerebral distal protection device through the lesion and deploy it,
preferentially in a straight segment of the ICA (Fig. 6.1, step 1).
f. Obtain a follow-up angiogram of the common carotid artery (working projections should open up the
carotid bifurcation).
g. Position the PTA balloon and perform angioplasty, if needed (<2 mm residual lumen) (Fig. 6.1, steps 2 to
4).
h. Remove the PTA balloon and obtain follow-up angiograms of the common carotid artery.
i. Position the stent delivery system and place the stent to cover the entire target lesion, including plaque
adjacent to the stenotic segment. Frequently, bony features serve well to landmark the extent of the lesion
and guide the stent placement prior to deployment (Fig. 6.1, steps 5 to 7).
j. Remove the stent delivery catheter.
k. Obtain a follow-up angiogram and assess for residual stenosis.
l. Perform poststent PTA if needed (residual stenosis >10% to 15%). Balloon size should match the distal
normal artery diameter (Fig. 6.1, steps 8 and 9).
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m. Remove the PTA balloon.
n. Obtain a follow-up angiogram of the common carotid artery in multiple views.
o. Remove the cerebral protection device over the provided resheathing catheter as per the IFU (Fig. 6.1,
step 10).
p. Obtain follow-up angiograms of the common carotid artery and the intracranial circulation. Assess for
vasospasm, dissection, and distal emboli.
q. Remove the guide catheter.
r. Discontinue heparin.
s. The femoral sheath should be removed in accordance with the access closure method selected.
FIGURE 6.1 • The carotid stenting procedure step-by-step.
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1. If the patient is stable, admit to a step-down unit for 24-hour (overnight) observation.
a. Check vital signs and neurologic examination every hour.
b. Keep systolic BP between 100 mm Hg and 160 mm Hg.
c. If placed, keep the Foley catheter to gravity until a few hours before discharge.
d. Start PO fluids and advance to regular diet as tolerated.
e. Hydrate the patient with normal saline solution (NS) at 150 mL per hour for a total of 400 mL.
f. Initiate deep vein thrombosis (DVT) prophylaxis.
g. Maintain bed rest until the following morning.
2. Follow-up
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a. Continue clopidogrel 75 mg PO daily and aspirin 325 mg PO daily for 6 weeks. After 6 weeks, patients remain
on aspirin 81 mg PO daily for life.
b. Obtain a duplex ultrasound at 6 months and 1 year postprocedure.
Results
The North American Symptomatic Carotid Endarterectomy Trial (NASCET) was the first to demonstrate that
symptomatic patients with carotid stenosis benefited from surgical revascularization over medical therapy,
with significant reduction in the rates of stroke and mortality in populations with stenosis ≥50% (14). These
findings were corroborated by the European Carotid Surgery Trial (ECST) (15). The results of the
Asymptomatic Carotid Atherosclerosis Trial (ACAS) showed that CEA is superior to medical management for
asymptomatic patients with ≥60% stenosis and serve as the basis for performing revascularization
procedures in this population (16).
The Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS) was the first large randomized
study to demonstrate the feasibility and safety of endovascular carotid interventions (17). Despite the use of
stents in only 26% of the patients in the endovascular arm, and the absence of CP devices, the CAVATAS
study showed similar major risks and effectiveness between surgical and endovascular intervention at 3
years. The subsequent proliferation of CAS devices was accompanied by the enrollment of patients into a
number of manufacturer-supported trials.
The Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial
was a randomized controlled trial comparing CAS versus CEA in high-risk patients who had symptomatic or
asymptomatic carotid artery disease (2,8). SAPPHIRE showed that, in a population at high risk for CEA,
CAS was noninferior to CEA in the 30-day risk of stroke, death, or MI. Furthermore, SAPPHIRE showed that
CAS was noninferior to CEA in the risk of reaching a composite end point at 3 years. The results of several
manufacturer supported trials then showed that, in patients at high risk for CEA, CAS was noninferior to
objective performance criteria derived from historical CEA studies. The results of these trials supported the
U.S. Food and Drug Administration (FDA) approval of the variety of devices now available and have
supported the continued use of CAS in the high-risk population.
The results of two more randomized controlled trial (RCTs) casted doubt over the safety of CAS. The
Endarterectomy versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S) and
Stent-supported Percutaneous Angioplasty of the Carotid Artery versus Endarterectomy (SPACE) trials were
both terminated early after failing to prove the noninferiority of CAS to CEA for periprocedural complications
(18,19). It is important however to highlight that these studies had concerns about operator inexperience in
the CAS arm and nonuniform use of cerebral embolism protection devices. The EVA-3S trial was a
multicenter study that required only limited operator experience (five prior CAS procedures, or no CAS
procedures, if supervised). The SPACE trial was conducted without the now mandatory use of CP devices,
which were employed in only 27% of the cases. These
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factors likely resulted in a higher periprocedural event rate, leading to premature study termination due to
safety and futility issues.
The initial early results of the International Carotid Stenting Study (ICSS) suggested that CEA was superior
to CAS—at 120 days follow-up, the risk of stroke, death, or procedural MI was 8.5% in the CAS group
versus 5.2% in the CEA group ( P = .006) (20). The initial conclusion was that CEA should remain the
treatment of choice for patients requiring carotid revascularization. However, the results of the long-term
data from this same study have recently been made available (21). Regarding these long-term outcomes of
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the ICSS study, 1,713 patients were assigned to stenting ( n = 855) or endarterectomy ( n = 858) and
followed up for a median of 4.2 years (interquartile range [IQR] 3.0-5.2, maximum 10.0). Three patients
withdrew immediately, and therefore, the intention to treat (ITT) population comprised 1,710 patients. The
number of fatal or disabling strokes (52 vs. 49) and cumulative 5-year risk did not differ significantly between
the stenting and endarterectomy groups (6.4% vs. 6.5%; hazard ratio [HR] 1.06, 95% CI 0.72—1.57, P =
.77). Strokes were more frequent in the stenting group than in the endarterectomy group but were mainly
nondisabling. As a result, the ICSS long-term functional outcome and risk of fatal or disabling stroke were
ultimately found to be similar for stenting and endarterectomy for symptomatic carotid stenosis.
The largest randomized trial comparing CAS versus CEA for the treatment of carotid artery stenosis and for
the prevention of stroke was an NIH-sponsored Carotid Revascularization Endarterectomy versus Stenting
Trial (CREST) study (22). This study included low- and medium-risk patients. The primary end point in
CREST was a composite including any stroke, MI, or death in the periprocedural period, and all ipsilateral
strokes thereafter. In 2,502 patients followed for up to 4 years, there was no significant difference between
the rates of reaching the primary endpoint in the CAS and CEA groups (7.2% vs. 6.8%, P = .51). CAS was
associated with a higher risk of periprocedural stroke (4.3% vs. 2.3%, P = .01); however, CEA was
associated with a higher risk of periprocedural MI (1.1% vs. 2.3%, P = .03). The risk of major periprocedural
stroke was not significantly different (0.9% vs. 0.7%, P = .52), indicating that the excess strokes attributable
to CAS were nondisabling or minor. In CREST, age was the only patient variable that determined the
primary outcome and differential primary outcomes, CEA versus CAS. In those patients undergoing CAS,
four angiographic variables were associated with more periprocedural strokes: severe distal tortuosity,
sequential lesions, lesion length greater than 20 mm, and a narrow mouth ulcer in the carotid plaque.
Overall, these characteristics may help in patient selection.
The CREST-2 trial will be headed by University of Maryland Medical Center (UMMC) and the Mayo Clinic
and run at 120 clinical centers across the United States and Canada. The study is funded by the NIH
National Institute of Neurological Disorders and Stroke (NINDS) and was fundamentally designed to be two
parallel, randomized trials that build on the data collected by the CREST team but veers off in one crucial
way. Instead of comparing one procedure to the other (CEA vs. CAS), CREST-2 compares a combination of
CEA and intensive medical management to intensive medical management alone, and CAS combined with
intensive medical management to intensive medical management alone, in two separate arms. Both arms
will randomize 600 patients to each group for a total of 2,400 patients, all of whom have at least 70% or
higher blockage of one of their carotid arteries but have not suffered a stroke from it (23). The research
team began enrolling patients in early 2014, with UMMC running the imaging core facility that processes all
imaging scans used in the research. The results of this study will attempt to elucidate a more definitive
answer for the controversy of CEA versus CAS.
The results of RCTs comparing endarterectomy with stenting in symptomatic patients with carotid stenosis
are summarized in Table 6.2. Trials comparing endarterectomy with stenting in asymptomatic patients with
carotid stenosis are summarized in Table 6.3.
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Table 6.2 Randomized Trials Comparing Endarterectomy with Stenting in Symptomatic

Patients with Carotid Stenosis
Trial, Year Patients Key Features Death or Any OR (95% CI) Comments
(Reference) Stroke
CAVATAS- 504 Multicenter; CEA: 25/253 P = NS in Follow-up to 3

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CEA, 2001 patients of any (9.9%) original article; y; relatively low-
(17) age with CAS: 25/251 OR not stent use (26%)
symptomatic or (10.0%) reported in CAS group
asymptomatic
carotid
stenosis
suitable for
CEA or CAS
SAPPHIRE, 334 Multicenter CEA: 9.3% P = .18 Terminated

2004 (2) randomized symptomatic prematurely
trial of patients patients because of a
with ≥80% CAS: 2.1% drop in
asymptomatic symptomatic randomization
carotid patients
stenosis (70%)
and ≥50%
symptomatic
carotid
stenosis (30%)
EVS-3S, 527 Multicenter; CEA: 10/259 RR = 2.5 (1.2- Study

2006 (24) patients with (3.9%) 5.1), P = .01 terminated
symptomatic CAS: 25/262 prematurely
carotid (9.6%) because of
stenosis >60% safety and
within 120 d futility issues;
before concerns about
enrollment operator
suitable for inexperience in
CEA or CAS the CAS arm
and nonuniform
use of embolism
protection
devices
SPACE, 1,183 Multicenter; Primary end 1.19 (0.75- Study

2006 (19) patients >50 point of 1.92) terminated
years old with ipsilateral prematurely
symptomatic ischemic after futility
carotid stroke or analysis;
stenosis >70% death from “concerns
in the 180 d time of about operator
before randomization inexperience in
enrollment to 300 d after the CAS arm
the procedure; and nonuniform
CEA: 37/584 use of embolism
(6.3%) protection
CAS: 41/599 devices.”
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(6.8%)
EVA-3S, 4- 527 Multicenter, Major outcome HR for any A hazard

y follow-up, randomized, events up to 4 stroke or function
2008 (18) open, y for any periprocedural analysis
assessor- periprocedural death 1.77 showed 4-y
blinded, stroke or (1.03-3.02) differences in
noninferiority death: CEA: P =.04 cumulative
trial 6.2% CAS: HR for any probabilities of
Compared 11.1% stroke or outcomes
outcome after death 1.39 between CAS
CAS with (0.96-2.00) and CEA were
outcome after P =.08 largely
CEA in 527 R for CAS accounted for
patients who versus CEA by the higher
had carotid 1.97 (1.06- periprocedural
stenosis of at 3.67) (within 30 d of
least 60% that P =.03 the procedure)
had recently risk of stenting
become compared with
symptomatic endarterectomy.
After the
periprocedural
period, the risk
of ipsilateral
stroke was low
and similar in
the two
treatment
groups.
SPACE 2-y 1,214 Patients with Intention-to- Intention-to- In both the

follow-up, symptomatic, treat treat intention-to-
2008 (25) severe carotid population: population: treat and per-
artery stenosis Ipsilateral Ipsilateral protocol
(70%) were ischemic ischemic populations,
recruited to this strokes within strokes within recurrent
noninferiority 2 y, including 2 y, including stenosis of 70%
trial and any any was
randomly periprocedural periprocedural significantly
assigned with a strokes or strokes or more frequent
block deaths: CAS: deaths: HR = in the CAS
randomization 56 (9.5%) 1.10 (0.75- group than the
design to CEA: 50 1.61) CEA group, with
undergo CAS (8.8%) Any deaths a life table
or CEA. Any deaths between estimate of
between randomization 10.7% vs. 4.6%
randomization and 2 y: HR = (P = .0009) and
and 2 y: CAS: 1.11 (0.67- 11.1% vs. 4.6%
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32 (6.3%) 1.85) (P = .0007),
CEA: 28 Any strokes respectively.
(5.0%) between
Any strokes randomization
between and 2 y: HR =
randomization 1.10 (0.77-
and 2 y: CAS: 1.57)
64 (10.9%) Ipsilateral
CEA: 57 ischemic
(10.1%) stroke within
Ipsilateral 31 d and 2 y:
ischemic HR = 1.17
stroke within (0.51-2.70)
31 d and 2 y: Per-protocol
CAS: 12 population:
(2.2%) CEA: Ipsilateral
10 (1.9%) ischemic
Per-protocol strokes within
population: 2 y, including
Ipsilateral any
ischemic periprocedural
strokes within strokes or
2 y, including deaths: HR =
any 1.23 (0.82-
periprocedural 1.83)
strokes or Any deaths
deaths: CAS: between
53 (9.4%) randomization
CEA: 43 and 2 y: HR =
(7.8%) 1.19 (0.83-
Any deaths 1.73)
between Ipsilateral
randomization ischemic
and 2 y: CAS: stroke within
29 (6.2%) 31 d and 2 y:
CEA: 25 HR = 1.18
(4.9%) (0.51-2.73)
Any strokes
between
randomization
and 2 y: CAS:
61 (11.5%)
CEA: 51
(9.8%)
Ipsilateral
ischemic
stroke within
31 d and 2 y:
CAS: 12
(2.3%) CEA:
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10 (2.0%)
SAPPHIRE 260 Long-term data Stroke: CAS: Stroke: P =
3-y follow- were collected 15 (9.0%) .99 (-6.1-6.1)
up, 2008 for 260 CEA: 15 Death: P =.68
(26) individuals; (9.0%) (-10.9-6.1)
included Ipsilateral
symptomatic stroke: CAS:
carotid artery 11 (7.0%)
stenosis of at CEA: 9 (5.4%)
least 50% of Death: CAS:
the luminal 31 (18.6%)
diameter or an CEA: 35 (21%)
asymptomatic Note: Data
stenosis of at were
least 80%. calculated
using n = 167
for both
groups
because
breakdowns of
CAS and CEA
for n = 260
were not
given.
ICSS, 2010 1,713 Multicenter 120-d follow- OR not Primary

(20) study. In the up data: CAS: available outcome was 3-
study, the 72/853 (8.5%) HR = 1.86 y rate of fatal or
degree of CEA: 40/857 (1.26-2.74) disabling stroke
carotid (4.7%) P = .001 in any territory;
stenosis was interim results
70%-99% in have been
89% of stent provided for
patients and in 120-d rate of
91% of stroke, death,
endarterectomy or procedural
patients. Study MI.
patients had
>50% carotid
artery stenosis
measured by
the NASCET
criteria.
CREST, 2,502 The study Any Any The risk of

2010 (22) included 1,321 periprocedural periprocedural composite
symptomatic stroke or stroke or primary
patients and postprocedural postprocedural outcome of
1,181 ipsilateral ipsilateral stroke, MI, or
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asymptomatic stroke: stroke: death did not
patients. Symptomatic: Symptomatic: differ
Symptomatic CAS: 37 (5.5 ± P =.04 significantly
patients in the 0.9 SE) CEA: Any among
study had 21 (3.2 ± 0.7 periprocedural symptomatic
≥50% carotid SE) stroke or and
stenosis by Any death or asymptomatic
angiography, periprocedural postprocedural patients
≥70% by stroke or ipsilateral between CAS
ultrasound, or death or stroke: and CEA.
≥70% by CTA postprocedural Symptomatic:
or MRA. ipsilateral P =.02
Asymptomatic stroke:
patients had Symptomatic:
carotid CAS: 40 (6.0 ±
stenosis 0.9 SE) CEA:
(patients with 21 (3.2 ± 0.7
symptoms SE)
beyond 180 d
were
considered
asymptomatic)
≥60% by
angiography,
≥70% by
ultrasound, or
≥80% by CTA
or MRA.
ICSS, 2014 1,713 Multicenter Median of 4.3- 5-y cumulative Any stroke was
(21) study. In the y follow-up. risk HR = more frequent
study, the Events: 1.71, 95% CI in the CAS
degree of Fatal or 1.28-2.30, P < group than in
carotid disabling .001; per- the CEA group
stenosis was strokes: protocol were mainly
70%-99% in CAS: 52/853 population, 5-y nondisabling
89% of stent (6.1%) cumulative risk strokes. The
patients and in CEA: 49/857 8.9% vs. distribution of
91% of (5.7%) 5.8%, 1.53, modified Rankin
endarterectomy Any stroke: 1.02-2.31, P = scale scores at
patients. Study CAS: 119/853 .04 1 y, 5 y, or final
patients had (13.9%) follow-up did
>50% carotid CEA: 72/857 not differ
artery stenosis (8.4%) significantly
measured by between
the NASCET treatment
criteria. groups.
Longterm
functional
outcome and
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risk of fatal or
disabling stroke
are similar for
stenting and
endarterectomy
for symptomatic
carotid
stenosis.
CI, confidence interval; OR, odds ratio; RR, risk reduction; SE, standard error.
Adapted from Brott, TG, Halperin JL, Abbara S. et al. 2011
ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the
management of patients with extracranial carotid and vertebral artery disease: executive summary: a
report of the American College of Cardiology Foundation/American Heart Association Task Force on
Practice Guidelines, and the American Stroke Association, American Association of Neuroscience
Nurses, American Association of Neurological Surgeons, American College of Radiology, American
Society of Neuroradiology, Congress of Neurological Surgeons, Society of Atherosclerosis Imaging
and Prevention, Society for Cardiovascular Angiography and Interventions, Society of Interventional
Radiology, Society of NeuroInterventional Surgery, Society for Vascular Medicine, and Society for
Vascular Surgery. Developed in collaboration with the American Academy of Neurology and Society of
Cardiovascular Computed Tomography. J Am Coll Cardiol . 57(8):1002-1044.
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Table 6.3 Trials Comparing Endarterectomy with Stenting in Asymptomatic Patients with
Carotid Stenosis
Trial, Year Patients Key Features Death or Any P Value Comments

(Reference) Stroke
SAPPHIRE, 334 Multicenter Asymptomatic: .2 Terminated

2004 (2) randomized CEA: 10.2%b prematurely
trial of patients because of a
CAS: 5.4%b
with >50% drop in
Combined:
symptomatic randomization
carotid CEA: 9.8%b
stenosis (58%) CAS: 4.8%b
or >80%
asymptomatic
carotid
stenosis (42%)
with one or
more
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comorbidity
criteriaa (high-
surgical risk
group)
SAPPHIRE, 334 Multicenter SAPPHIRE 3-y Stroke: .99 No significant

2008 (8) randomized data Death: .68 (or difference
trial of patients Stroke: CEA: not reported) could be
with >80% 15/167 CAS: shown in
asymptomatic 15/197 long-term
carotid Death: CEA: outcomes
stenosis (70%) 35/167 CAS: between
and ≥50% 31/167 patients who
symptomatic underwent
carotid CAS with an
stenosis (30%) EPD and
those who
underwent
CEA.
CREST, 2,502 The study Any Any The risk of

2010 (22) included 1,321 periprocedural periprocedural the composite
symptomatic stroke or stroke or primary
patients and postprocedural postprocedural outcome of
1,181 ipsilateral ipsilateral stroke, MI, or
asymptomatic stroke: stroke: death did not
patients. Asymptomatic: Asymptomatic: differ
Symptomatic CAS: 15 (2.5 ± .15 significantly
patients in the 0.6 SE) CEA: Any among
study had 8 (1.4 ± 0.5 periprocedural symptomatic
≥50% carotid SE) stroke or and
stenosis by Any death or asymptomatic
angiography, periprocedural postprocedural patients
≥70% by stroke or ipsilateral between CAS
ultrasound, or death or stroke: and CEA.
≥70% by CTA postprocedural Asymptomatic:
or MRA. ipsilateral .15
Asymptomatic stroke:
patients in the Asymptomatic:
study had CAS: 15 (2.5 ±
carotid 0.6 SE)
stenosis CEA: 8 (1.4 ±
(patients with 0.5 SE)
symptoms
beyond 180 d
were
considered
asymptomatic)
≥60% by
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angiography,
≥70% by
ultrasound, or
≥80% by CTA
or MRA.
EPD, embolic protection device; OR, odds ratio; SE, standard error.
aCriteria for high risk as discussed previously.
bDeath, stroke, and MI.

Adapted from Brott, TG, Halperin JL, Abbara S. et al. 2011
ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the
management of patients with extracranial carotid and vertebral artery disease: executive summary:
a report of the American College of Cardiology Foundation/American Heart Association Task Force
on Practice Guidelines, and the American Stroke Association, American Association of
Neuroscience Nurses, American Association of Neurological Surgeons, American College of
Radiology, American Society of Neuroradiology, Congress of Neurological Surgeons, Society of
Atherosclerosis Imaging and Prevention, Society for Cardiovascular Angiography and Interventions,
Society of Interventional Radiology, Society of NeuroInterventional Surgery, Society for Vascular
Medicine, and Society for Vascular Surgery Developed in collaboration with the American Academy
of Neurology and Society of Cardiovascular Computed Tomography. J Am Coll Cardiol .
57(8):1002-1044.
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Complications and Management
1. Complications of CAS including allergic contrast reaction, groin hematoma, and retroperitoneal hematoma are
managed similarly to any other angiographic examination. Anticoagulation and antiplatelet therapy may increase
the frequency and severity of bleeding complications.
2. Bradycardia. Infrequently observed if the target lesion is calcified, and in the proximity of the carotid bulb,
bradycardia is usually transient and resolves spontaneously. Bradycardia can be avoided by slow inflation of the
PTA balloon under ECG monitoring and/or pretreatment with glycopyrrolate. Atropine may be needed, albeit
infrequently, as discussed previously. Rarely, the patient may require a temporary transvenous ventricular
pacemaker.
3. Arterial hypotension. Manage with colloid infusion, dopamine, or Neo-Synephrine as necessary.
4. Arterial vasospasm. Generally resolves spontaneously; otherwise, treat with nicardipine or verapamil as
discussed previously.
5. Arterial dissection. Treat with acute stenting or terminate the PTA/CAS procedure and manage medically. If
medical management is opted, continue heparin as a bridge to Coumadin therapy. Maintain anticoagulation with
Coumadin for 6 months postprocedure.
6. Acute thromboembolism. Consult a neurointerventionalist. A number of treatments are available to manage
acute thromboembolism, including intra-arterial ReoPro (abciximab) or Integrilin (eptifibatide), intra-arterial tPA,
thrombectomy with a stent retriever, aspiration thrombectomy, with ancillary treatments like colloid infusion, and
induction of arterial hypertension.
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7. Plaque rupture with immediate vessel occlusion. Proceed with CAS.
8. Incomplete coverage of the target lesion. Place a second stent.
9. Neck hematoma. May occur during PTA/CAS due to venous or arterial rupture; generally occurs in patients
who have undergone prior CEA and usually self-containing. Reverse heparinization with Protamine (Protamine
IV, 10 mg per 1,000 units of heparin administered). If there is major vessel rupture, immediately occlude the
vessel with a balloon catheter. Reconstructive methods could include emergent placement of a covered stent
(currently off-label use). Safe, permanent endovascular occlusion of the entire carotid artery with coils should be
considered. Transfer patient for emergency surgery if needed.
10. Reperfusion brain edema. Can be managed with mannitol and corticosteroids.
11. Intracerebral hemorrhage (ICH). Consult neurosurgery. ICH may be reperfusionrelated or due to delayed
transformation of a small ischemic insult.
12. Myocardial infarction. A rare complication during PTA/CAS; consult a cardiologist.
References
1. Brott TG, Halperin JL, Abbara S, et al.
ASA/ACCF/AHA/AANN/AANS/ACR/ASNR/CNS/SAIP/SCAI/SIR/SNIS/SVM/SVS guideline on the management
of patients with extracranial carotid and vertebral artery disease: executive summary: a report of the American
College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, and the
American Stroke Association, American Association of Neuroscience Nurses, American Association of
Neurological Surgeons, American College of Radiology, American Society of Neuroradiology, Congress of
Neurological Surgeons, Society of Atherosclerosis Imaging and Prevention, Society for Cardiovascular
Angiography and Interventions, Society of Interventional Radiology, Society of NeuroInterventional Surgery,
Society for Vascular Medicine, and Society for Vascular Surgery. Developed in collaboration with the
American Academy of Neurology and Society of Cardiovascular Computed Tomography. J Am Coll Cardiol .
2011;57(8):1002-1044.
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2. Yadav JS, Wholey MH, Kuntz RE, et al. Protected carotid-artery stenting versus endarterectomy in high-
risk patients. N Engl J Med. 2004;351(15):1493-1501.
3. National Coverage Analysis (NCA) for Percutaneous Transluminal Angioplasty (PTA) of the Carotid
Artery Concurrent with Stenting (CAG-00085R7). Baltimore, MD: Centers for Medicare & Medicaid Services;
2009.
4. Gray WA, Hopkins LN, Yadav S, et al. Protected carotid stenting in high-surgical-risk patients: the
ARCHeR results. J Vasc Surg. 2006;44(2):258-268.
5. Hopkins LN, Myla SV, Grube E, et al. Carotid artery revascularisation in high-surgicalrisk patients with the
NexStent and the FilterWire EX/EZ: 3-year results from the CABERNET trial. EuroIntervention.
2010;5(8):917-924.
6. Safian RD, Bresnahan JF, Jaff MR, et al. Protected carotid stenting in high-risk patients with severe carotid
artery stenosis. J Am Coll Cardiol . 2006;47(12):2384-2389.
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7. White CJ, Iyer SS, Hopkins LN, et al. Carotid stenting with distal protection in high surgical risk patients:
the BEACH trial 30 day results. Catheter Cardiovasc Interv. 2006;67(4):503-512.
8. Massop D, Dave R, Metzger C, et al. Stenting and angioplasty with protection in patients at high-risk for
endarterectomy: SAPPHIRE Worldwide Registry first 2,001 patients. Catheter Cardiovasc Interv.
2009;73(2):129-136.
9. Higashida RT, Popma JJ, Apruzzese P, et al. Evaluation of the medtronic exponent self-expanding carotid
stent system with the medtronic guardwire temporary occlusion and aspiration system in the treatment of
carotid stenosis: combined from the MAV-ErIC (Medtronic AVE Self-expanding CaRotid Stent System with
distal protection In the treatment of Carotid stenosis) I and MAVErIC II trials. Stroke. 2010;41(2):e102-e109.
10. Cai J, Hatsukami TS, Ferguson MS, et al. In vivo quantitative measurement of intact fibrous cap and lipid-
rich necrotic core size in atherosclerotic carotid plaque: comparison of high-resolution, contrast-enhanced
magnetic resonance imaging and histology. Circulation. 2005;112(22):3437-3444.
11. Amarenco P, Bogousslavsky J, Callahan A III, et al. High-dose atorvastatin after stroke or transient
ischemic attack. N Engl J Med. 2006;355(6):549-559.
12. Papanagiotou P, Roth C, Walter S, et al. Carotid artery stenting in acute stroke. J Am Coll Cardiol .
2011;58(23):2363-2369.
13. Puri AS, Kühn AL, Kwon HJ, et al. Endovascular treatment of tandem vascular occlusions in acute
ischemic stroke. J Neurointerv Surg. 2015;7(3)158-163.
14. Barnett HJ, Taylor DW, Eliasziw M, et al. Benefit of carotid endarterectomy in patients with symptomatic
moderate or severe stenosis. N Engl J Med. 1998;339:1415-1425.
15. European Carotid Surgery Trialists' Collaborative Group. Randomised trial of endarterectomy for recently
symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet.
1998;351:1379-1387.
16. Walker MD, Marler JR, Goldstein M, et al. Endarterectomy for asymptomatic carotid artery stenosis.
Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA. 1995;273:1421-1428.
17. Ederle J, Bonati LH, Dobson J, et al. Endovascular treatment with angioplasty or stenting versus
endarterectomy in patients with carotid artery stenosis in the carotid and vertebral artery transluminal
angioplasty study (CAVATAS): long-term follow-up of a randomised trial. Lancet Neurol . 2009;8(10):898-907.
18. Mas JL, Trinquart L, Leys D, et al. Endarterectomy versus angioplasty in patients with symptomatic
severe carotid stenosis (EVA-3S) trial: results up to 4 years from a randomised, multicentre trial. Lancet
Neurol . 2008;7(10):885-892.
19. Ringleb PA, Allenberg J, Brückmann H, et al. 30 Day results from the SPACE trial of stent-protected
angioplasty versus carotid endarterectomy in symptomatic patients: a randomised non-inferiority trial. Lancet.
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2006;368(9543):1239-1247.
20. Ederle J, Dobson J, Featherstone RL, et al. Carotid artery stenting compared with endarterectomy in
patients with symptomatic carotid stenosis (International Carotid Stenting Study): an interim analysis of a
randomised controlled trial. Lancet. 2010;375(9719):985-997.
21. Bonati LH, Dobson J, Featherstone RL, et al. Long-term outcomes after stenting versus endarterectomy
for treatment of symptomatic carotid stenosis: the International Carotid Stenting Study (ICSS) randomised
trial. Lancet. 2015;385(9967):529-538.
22. Brott TG, Hobson RW II, Howard G, et al. Stenting versus endarterectomy for treatment of carotid-artery
stenosis. N Engl J Med. 2010;363(1):11-23.
23. Suissa S. Calculation of number needed to treat. N Engl J Med. 2009;361(4):424-425.
24. Mas JL, Chatellier G, Beyssen B, et al. Endarterectomy versus stenting in patients with symptomatic
severe carotid stenosis. N Engl J Med. 2006;355(16):1660-1671.
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25. Eckstein HH, Ringleb P, Allenberg JR, et al. Results of the stent-protected angioplasty versus carotid
endarterectomy (SPACE) study to treat symptomatic stenoses at 2 years: a multinational, prospective,
randomised trial. Lancet Neurol . 2008;7(10):893-902.
26. Gurm HS, Yadav JS, Fayad P, et al. Long-term results of carotid stenting versus endarterectomy in high-
risk patients. N Engl J Med. 2008;358(15):1572-1579.
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7
Vascular Emergencies of the Head and Neck
Michele H. Johnson
Vascular emergencies can generally be divided into those with neurologic/neurosurgical implications (head,
cervical spine, and brain) and those with otorhinolaryngologic (ear, nose, and throat [ENT]) considerations. As
one would expect, there can be considerable overlap, such as in those patients with facial and skull base trauma
and those with carotid blowout syndrome. Emergent intervention for stroke is discussed in a separate chapter.
Diagnostic angiographic protocols vary with the indication for intervention. As in other areas of the vascular
system, selectivity is the key to safe and successful diagnostic angiography and intervention.
Neurologic and Neurosurgical Disorders

Intracranial Subarachnoid Hemorrhage
Etiology and Diagnosis (1,2)
1. Trauma is the most common cause of subarachnoid hemorrhage and is not usually associated with major
vascular injury. Identification of the distribution of the blood and the presence of associated intracranial and soft
tissue injury permits differentiation from aneurysmal subarachnoid hemorrhage in most cases.
2. Ruptured saccular (“berry aneurysm”) is the second most common cause of subarachnoid hemorrhage. Giant,
fusiform and dissecting intracranial aneurysms represent the smaller subset of aneurysm pathologies. Other
causes of subarachnoid hemorrhage include pial and mixed pial-dural arteriovenous malformation (AVM), dural
arteriovenous fistula (DAVF), vasculitis, and moyamoya disease. The incidence of ruptured aneurysm varies by
location (Table 7.1).
3. Clinical presentation: headache (worst headache of life [WHOL]), nausea, vomiting, stiff neck, photophobia.
The presentation is usually acute, although some may present subacutely with a few days of intractable
headache.
4. Noncontrast computed tomography (CT) demonstrates blood within the subarachnoid spaces in the basal
cisterns, sulci, and ventricles; the distribution of blood varies with the location of the aneurysm (Table 7.2).
5. Computed tomographic angiography (CTA) at the time of initial CT often permits identification of the aneurysm
and characterization sufficient for triage to open surgery or endovascular treatment. CTA may circumvent the
need for digital subtraction angiography (DSA) or may reduce the number of injections required for evaluation
with DSA (3,4).
Indications for Cerebral Angiography (1,2,3,4,5)

1. Clinical and imaging (noncontrast CT) criteria for suspect nontraumatic subarachnoid hemorrhage
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Table 7.1 Incidence of Ruptured Aneurysms by Location
Location Incidence (%)
Anterior communicating artery 30.3

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Posterior communicating artery 25.0
Middle cerebral artery bifurcation 13.1
Internal carotid artery bifurcation 4.5
Anterior choroidal artery 4.3
M1 segment of middle cerebral artery 3.9
Basilar bifurcation 2.0
A1 segment of anterior cerebral artery 1.5
Distal middle cerebral artery 1.4
Distal posterior cerebral artery 0.9
Vertebrobasilar junction 0.9
Midbasilar artery 0.8
Posterior inferior cerebral artery 0.8
2. CTA is usually performed following the noncontrast CT in patients with subarachnoid hemorrhage in order to
define the source of the subarachnoid hemorrhage and inform triage to surgical or endovascular treatment.
3. Cerebral angiography is performed following CTA when needed to clarify uncertain findings on CTA, in lieu of
CTA when renal function is limited requiring contrast limitations and for endovascular treatment.
Contraindications to Cerebral Angiography

1. Stabilization of the patient's clinical condition should precede angiography.
2. Relative contraindications to cerebral angiography include renal failure, uncontrolled hypertension, and clinical
instability.
3. Standard renal protection measures should precede contrast administration when possible.
4. Standard premedication for contrast allergy should be employed in appropriate patients.
Standard preangiographic workup, preparation, and monitoring are used in addition to intracranial pressure (ICP)
monitoring and central venous lines and/or arterial lines and Swan-Ganz catheters as dictated by the patient's
clinical condition.
Table 7.2 Distribution of Subarachnoid Hemorrhage (SAH) by Aneurysm Location

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Anterior communicating artery SAH in anterior interhemispheric fissure or septum pellucidum
Hematoma in anteromedial frontal lobe
Posterior communicating artery SAH in suprasellar cistern, ambient (perimesencephalic) cistern

Hematoma in anteromedial frontal lobe, basal ganglia
Middle cerebral artery SAH in ipsilateral sylvian fissure

Hematoma in temporal lobe
Basilar artery SAH in interpeduncular cistern

Hematoma in midbrain
Posterior inferior cerebellar artery SAH in prepontine cistern, fourth ventricle

Cerebellar hematoma
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Procedure (1,2,5)
1. Standard heparin bolus is often administered at the time of angiography (approximately 2,000 units
intravenously [IV] for an average adult vs. a weightbased dose to achieve an activated clotting time or ACT of
200 to 250 seconds).
2. Bilateral common, internal and external carotid injections or bilateral common carotid injections (when
catheterization is difficult or when significant common carotid bifurcation disease precludes safe catheterization)
3. Bilateral vertebral injections or one vertebral injection with reflux into the contralateral vertebral artery proximal
to the posterior inferior cerebellar artery origin
4. Angiography should include anteroposterior (AP), lateral, and at least one oblique view of the intracranial
circulation in order to facilitate visualization of the branching points where aneurysms usually arise (1,2).
5. Digital rotational angiography with three-dimensional (3D) reconstruction images may be performed in addition
to the above or in lieu of oblique images and can provide multiple projection images with reduction of contrast
and radiation as compared to conventional orthogonal imaging. It is important to survey these rotational images
carefully to avoid missing tandem lesions (6).
6. Adjunctive maneuvers to improve visualization of communicating arteries
a. Multiple projections, rotational angiography, rapid frame rates, and increasing injection volumes are simple
tools to improve communicating artery and aneurysm visualization.
b. Carotid cross-compression—manual compression of the contralateral carotid in the neck during injection and
filming to increase flow through the anterior communicating artery to improve visualization
c. Alcock's test—bilateral manual carotid compression during vertebral injection and filming to increase flow
through the posterior communicating arteries to improve visualization
d. Negative cerebral angiography: In order to exclude the possibility that a ruptured aneurysm is obscured by
spasm or thrombus, a follow-up angiogram has traditionally been performed in 7 to 10 days following the initial
examination. More recently, this follow-up has been performed using CTA within 1 week and prior to discharge.
Magnetic resonance imaging (MRI) with magnetic resonance angiography (MRA) may also be performed (7,8).
Radiology Books
e. Intraoperative and/or postoperative angiography is often performed in order to optimize clip placement and
assess patency of adjacent vessels. Sheaths are placed in the operating room (OR) and sterile access to the
sheath established. Rapid recognition and revision of clip placement, when needed, may improve outcome.
7. Spinal subarachnoid hemorrhage
a. Spinal subarachnoid hemorrhage often presents with headache or cervical pain. Blood may be demonstrated
at the skull base and in the upper cervical region.
b. Cross-sectional imaging with MRI +/- MRA should be performed prior to spinal arteriography. Spinal CTA may
be useful when MRI is contraindicated. Cross-sectional imaging may allow for more limited spinal angiography.
c. Additions to the cerebral angiographic protocol include both cervical vertebral arteries, and bilateral ascending
cervical, costocervical, and thyrocervical trunks should be examined.
d. Spinal radicular arteries must be selectively catheterized in turn, in order to exclude a spinal source for
subarachnoid hemorrhage. When the cerebral arteriogram is negative and a spinal source is suspected,
complete spinal angiography is often done in a separate session due to contrast considerations.
1. Hemostasis achieved at the puncture site in standard fashion with manual compression or vascular closure
device.
2. Neurologic checks are included in the postprocedural nursing order set.
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Results (1,2,3,5,8)
1. CTA demonstrates cerebral aneurysm in the majority of cases and aids in triage of patients to surgical clipping
or endovascular treatment (1,2,3).
2. DSA is performed for CTA negative subarachnoid hemorrhage, for those patients triaged for endovascular
therapy, and for intraoperative or postoperative assessment (5).
3. Diagnostic arteriography demonstrates cerebral aneurysm in the majority of circumstances (>85%). Repeat
angiography (DSA, CTA) improves the yield to greater than 95% (8).
4. MRI +/- MRA of the brain and spine may be adjunctive in the diagnosis, particularly when initial arterial
imaging is negative for aneurysm.
Complications (9,10,11,12,13)
Complications of diagnostic cerebral angiography include contrast allergy, transient ischemic attack (TIA), stroke
(0.5% to 2%), hematoma, and dissection.
Treatment for Ruptured Intracranial Saccular Aneurysm (5)

Surgical Clipping
1. Intraoperative angiography is adjunctive to confirm clip placement and patency of adjacent vessels.
2. Proximal control with surgical access to the carotid in the neck is sometimes utilized for temporarily reducing
the flow in the internal carotid artery at the time of clip placement for treatment of large paraclinoid or
supraclinoid aneurysms.
3. Balloon suction decompression (rarely performed today): A nondetachable balloon catheter is inserted
into the internal carotid artery in the operating room and inflated at the time of clip placement. Gentle suction is
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applied on the catheter through the central lumen during occlusion, which serves to decompress the aneurysm
and facilitate clip placement.
Endovascular Aneurysm Treatment by Detachable Platinum Coil Embolization
Indications
1. Anatomical criteria that favor successful coil placement
a. Aneurysm morphology; shape size relationship to adjacent branches, relationship to critical structures,
that is, cranial nerves
b. Small neck of the aneurysm compared to the dome; aneurysms with neck to dome ratio >0.5, or neck of 4
mm, will likely require balloon or stent assist for endovascular management.
c. Absence of perforators or branches arising from the aneurysm
2. Posterior circulation aneurysms such as basilar summit, superior cerebellar and posterior inferior
cerebellar artery aneurysms
3. Balloon-assisted techniques and stent-assisted coiling have expanded the range of aneurysms that can
be successfully treated by endovascular means.
Contraindications and Relative Contraindications

1. Severely tortuous atherosclerotic vessels with inadequate access to the aneurysm may require open
surgery.
2. Fusiform or dissecting aneurysms: may require stent assist or flow diversion (see the following
discussion)
3. Vasospasm that inhibits adequate catheterization and deployment of the coils may require endovascular
treatment of vasospasm and the aneurysm in the same session.
1. General anesthesia, arterial line, ventriculostomy, and central venous catheters as needed for patient care
2. Preparation similar to diagnostic cerebral angiography
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Procedure
1. Detachable coil systems for endovascular treatment of aneurysms (available through multiple vendors)
2. Coils are available in a wide variety of diameters, lengths, shapes, and degrees of softness. New
technologies include stretch resistance.
3. Platinum microcoils are introduced through a microcatheter placed into the aneurysm using at least a 5
Fr. or 6 Fr. guiding catheter platform.
4. For balloon-assisted coiling, larger internal diameter (ID) guiding catheters are needed, and the balloon is
inflated across the neck of the aneurysm to protect the parent artery during coil placement. The balloon is
deflated just prior to coil detachment in order to look for coil prolapse, although the coil can still be removed.
A balloon can also provide some protection in the case of intraprocedural rupture and may be lifesaving.
5. Heparin administration is titrated to an ACT level of approximately 200 to 300 seconds, following the
standard heparin bolus administered at initiation of angiography (2,000 U IV for an average 70-kg adult).
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6. Stent-assisted coiling is reserved for unruptured aneurysm patients who can be electively treated with
antiplatelet agents prior to treatment. The stent is placed crossing the aneurysm neck and the aneurysm
accessed through the stent mesh. Alternatively, the aneurysm can be catheterized and the catheter “jailed”
by the stent. The aneurysm is coiled, and the microcatheter removed.
1. Intensive care unit (ICU) management, vasospasm monitoring
2. Systemic heparinization (partial thromboplastin time [PTT] 40 to 60 seconds) is maintained for at least 48
hours. Antiplatelet therapy, usually aspirin, is added after 24 hours.
3. Follow-up CTA to assess for vasospasm and coil stability
Results (14,15)
1. With endovascular coil techniques, the International Subarachnoid Aneurysm Trial (ISAT) study of treatment
for ruptured saccular aneurysms demonstrated an absolute risk reduction for endovascular versus surgery of
7.4%. The metric was death and disability at 1 year. Although there are many criticisms of the study, the basic
conclusion has been supported by extended ISAT follow-up and other studies.
2. Aneurysms with smaller sacs will have a higher rate of total occlusion.
Complications (9,10,11,12,13)
1. Complications of diagnostic cerebral angiography include contrast allergy, TIA, stroke (0.5% to 2%),
hematoma, and dissection.
2. Risk of aneurysm rupture is low during diagnostic angiography and approximately 1% to 3% during
endovascular coiling.
3. Risk of TIA/stroke during endovascular coiling (thromboembolic complications) is 3% to 5% depending on the
series. Some authors feel the risk of stroke during diagnostic or endovascular procedures is reduced by the
administration of heparin during the procedure and for 48 hours following endovascular coiling.
4. Compaction of coils within the aneurysm may result in aneurysm recurrence requiring placement of additional
coils, stent, or flow diverter treatment, or surgical clipping.
5. Perforation or vascular injury with hemorrhage; compromise of adjacent or parent vessel by thrombus or due
to compression by the coil mass
Endovascular Aneurysm Treatment: Parent Vessel Occlusion
Indications
Parent vessel occlusion remains viable as a treatment alternative for certain surgically or endovascularly
inaccessible and/or giant aneurysms (16).
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1. Permanent occlusion of a parent artery should be preceded by diagnostic arteriography to visualize the
aneurysm and assess the circle of Willis.
2. Balloon occlusion tolerance (BOT) test is performed in order to assess the patient's ability to tolerate
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permanent occlusion.
3. The predictive value of BOT is enhanced by the use of controlled hypotension during occlusion and cerebral
blood flow testing using hexamethylpropyleneamine oxime (HMPAO) single-photon emission computed
tomography (SPECT) at the time of occlusion (see “Balloon Occlusion Tolerance Test” for technique).
Procedure
1. Internal carotid or vertebral occlusion can be safely accomplished using surgical clipping, platinum
microcoils, or more recently AMPLATZER plugs. Detachable balloons are no longer available in the United
States (17).
2. Proximal occlusion is sufficient in most cases to induce thrombosis without the need for trapping of the
aneurysm.
Complications (16)
1. Complications of diagnostic cerebral angiography include contrast allergy, TIA, stroke (0.5% to 2%),
hematoma, and dissection.
2. Risk of stroke, immediate or delayed, is the most worrisome complication. Clinical, anatomic, and physiologic
passing of a carotid BOT test is greater than 85% predictive of a good outcome. ICU management is important to
ensure maintenance of cerebral perfusion pressure following carotid occlusion.
Nonruptured Intracranial Aneurysms: Flow Diverting Stents for Endovascular Repair (18)
1. This new technology deploys a low-porosity, self-expanding stent (braided platinum and nickel-cobalt
chromium alloy), designed to divert flow from the aneurysm and reconstruct the parent vessel lumen, thereby
excluding the aneurysm from the circulation. The only one approved for use in the United States is the Pipeline
Embolization Device (2011; PED eV3, Irvine, CA).
2. Current indications are for nonruptured wide-necked aneurysms of the internal carotid artery from the
petrous internal carotid to the superior hypophyseal segment. These aneurysms are not amenable to coiling or
clipping.
3. Antiplatelet therapy is required to prevent in-stent thrombosis.
4. Complications include delayed thrombosis and delayed aneurysm rupture in addition to the risks of diagnostic
angiography.
Treatment of Cerebral Vasospasm (19,20)

Cerebral vasospasm usually results from subarachnoid hemorrhage where blood in the subarachnoid space
causes local irritation of the vessels at the level of the circle of Willis. Loss of autoregulation, narrowing, and flow
limitation may result in parenchymal ischemia and clinical deterioration. Angiographic vasospasm occurs in 30%
to 70% of patients, but delayed cerebral ischemia (DCI) occurs in 20% to 30% and half of those patients will
require endovascular therapy.
Vasospasm peaks at 7 to 10 days postsubarachnoid hemorrhage. Spasm results in ischemia to the territories
supplied by the involved vessels. Clinical symptoms vary with the territory of involvement and include depressed
consciousness and focal neurologic deficits. Serial transcranial Doppler (TCD) evaluation may be of value in
demonstrating early evidence of cerebral vasospasm. CTA and MRA may demonstrate vessel narrowing and
diffusion MR can identify associated cerebral ischemia.
Triple-H therapy to include hypervolemia, hypertension, and hemodilution is utilized in order to maintain
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pressure and blood supply through the vessels. These methods are implemented at the point of neurologic
deterioration. Endovascular treatment should commence if there is no response to medical management.
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Indications (19,20)
1. The primary indication for angiography is for diagnosis and endovascular treatment in the setting of suspected
vasospasm (focal or global neurologic deterioration, not responding to medical treatment).
2. Endovascular treatment should be initiated early after the onset of symptoms and after failure of initial medical
therapy in order to maximize the opportunity for clinical improvement.
3. CT examination (noncontrast) is performed prior to angiography in order to ascertain areas of parenchymal
ischemic injury and to exclude other (nonvasospastic) causes of neurologic deterioration, such as hydrocephalus
or rebleeding. TCD and CTA may show direct evidence of vasospasm. CTA can identify proximal and peripheral
vessel spasm.
Contraindications
1. Relative contraindications to cerebral angiography include renal failure and uncontrolled hypertension.
2. Relative contraindications to vasospasm treatment include ischemic or hemorrhagic infarction in the
involved territory. Revascularization can lead to hemorrhage in severely ischemic and/or infarcted
territories.
1. Standard preangiography assessment of bleeding parameters (prothrombin time [PT], PTT, and international
normalized ratio [INR]) and renal function (blood urea nitrogen [BUN] and creatinine) is performed.
2. Patient must be monitored as in the ICU, that is, ICP monitoring, arterial and central lines. Anesthesia support
with intubation, sedation, and paralysis are needed for the majority of patients, especially those undergoing
angioplasty.
Cerebral Angiography of Vasospasm

1. Standard heparin bolus is administered at the time of angiography (2,000 U IV for an average adult),
approximately 1,000 U per hour additional is given during the procedure to maintain the ACT between 200
seconds and 250 seconds.
2. Diagnostic angiographic protocol includes both the carotid and vertebral territories with a focus on the vessel
supplying the clinically suspected ischemic territory.
3. Angiographic criteria for diagnosis of vasospasm
a. Narrowing of vessels: proximal vessel narrowing or sometimes areas of narrowing and dilatation in late stages
of vasospasm
b. Delayed transit time
c. Parenchymal staining
d. Comparison with initial CTA and/or initial diagnostic arteriogram when available
Procedure (19,20)
1. Endovascular treatment for vasospasm: vasodilator infusion
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a. Using a 5 Fr. or 6-Fr. guide catheter platform, a microcatheter (10 or 18 system) is advanced into the involved
internal carotid artery, vertebral artery, or proximal branches and control angiography performed. Vasospasm is
confirmed and a stable catheter position achieved.
b. Papaverine, a phosphodiesterase inhibitor, is no longer recommended for treatment of vasospasm. It can be
neurotoxic, increase ICP, and lead to monocular blindness if administered below the ophthalmic artery.
c. Calcium-channel blockers such as nicardipine and verapamil have replaced papaverine for infusion
vasospasm therapy. Nicardipine is given as an infusion at 0.5 to 0.6 mg per vessel and is a more potent
vasodilator than verapamil. Verapamil is given as a bolus of 5 mg in 5 ml normal saline administered over
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5 minutes for a maximum dose of 15 mg per vessel. Class IIb recommendation, American Heart Association
(AHA).
d. Intermittent control arteriography is obtained to document angiographic response. The minimum dose
necessary to provide a resumption of good cerebral blood flow is utilized.
e. Complications of endovascular treatment for vasospasm
(1) Increased ICP was a problem with papaverine administration, which is no longer recommended.
(2) Hypotension, in response to vasodilator infusion, may lead to decreased cerebral perfusion pressure. Arterial
line monitoring is critical during these infusion procedures.
(3) Respiratory arrest (basilar artery infusion) may lead to heart block in the elderly.
(4) Retinal hemorrhage was reported with infusion of papaverine below the ophthalmic artery.
(5) Hemorrhage into territories infarcted secondary to vasospasm following vasodilator infusion has been
reported (hemorrhagic infarct).
2. Transluminal balloon angioplasty for vasospasm (19,20)
a. Established vasospasm may not respond to vasodilator therapy and may require angioplasty for treatment.
This may be related to the degree of spasm and the timing of therapy.
b. The distal internal carotid artery, the M1 segment of the middle cerebral artery, the A1 segment of the anterior
cerebral artery, the vertebrobasilar junction, the basilar artery, and sometimes the P1 segment of the posterior
cerebral artery may be amenable to angioplasty for vasospasm.
c. The angioplasty technique is most successful for treatment of vasospasm in the distal internal carotid artery
and the A1 and M1 segments of the anterior and middle cerebral arteries, respectively. The vertebrobasilar
system may also respond to angioplasty, but risks are greater in the basilar artery and the P1 segment of the
posterior cerebral artery due to the presence of perforating branches (see below).
d. Angioplasty for vasospasm is performed with a soft, nondetachable silicone microballoon inflated with gentle
intermittent inflation pressures in order to mechanically expand the vessel and improve flow.
e. Complications of angioplasty for vasospasm
(1) Higher risk than vasodilator infusion
(2) Arterial dissection
(3) Arterial rupture
(4) Arterial thrombosis/occlusion
(5) Secondary embolic sequelae
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Postprocedure Management (After Vasodilator or Angioplasty Treatment)
1. Maintenance of triple-H therapy and close neurologic monitoring for signs of recurrent vasospasm
2. Daily angiography and vasodilator infusion therapy may be needed in intractable cases of vasospasm.
3. TCD is a useful method to follow the recurrence of vasospasm. CTA is adjunctive.
Results (20)
1. About 66% of patients respond to treatment of vasospasm with vasodilator therapy alone (nicardipine >
verapamil).
2. About 54% of the remainder will respond to a combination of papaverine and angioplasty.
3. The response to therapy is best when treatment is initiated within 2 hours of symptom onset. Few patients will
demonstrate clinical improvement following endovascular treatment with stable clinical symptoms of greater than
48-hour duration.
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Cerebral Parenchymal Hemorrhage (21,22)
Etiology and Diagnosis

1. Intraparenchymal hemorrhage can be in any location, some typical of distinct clinical syndromes and
some associated with underlying pathology. Recognition of key anatomic findings can help to determine the
need for cerebral angiography.
2. The spot sign on CT imaging is defined as a tiny (1 to 2 mm) focus (foci) of enhancement within acute
primary intraparenchymal hematoma and is a manifestation of contrast extravasation within the hematoma.
Several authors have stressed the importance of looking for this sign as it appears to predict hematoma
expansion in the setting of acute intracranial hemorrhage. The finding is not associated with any specific
pathologic entity.
3. Basal ganglia hematoma: Focal hemorrhages in the basal ganglia are thought to be due to
microaneurysms from the lenticulostriate vessels (Charcot aneurysm). These are not amenable to
intervention and generally do not require arteriography. CTA is performed, and if no underlying lesion is
identified, angiography is not indicated.
4. Lesions that may result in parenchymal hemorrhage not typical for the pattern of basal ganglia
hemorrhage
a. AVMs, DAVFs, cavernous malformations, capillary telangiectasia, and other angiographically occult
vascular malformations
b. Amyloid angiopathy: lobar hemorrhages, microbleeds are seen on MRI; rebleeds common.
c. Tumors: metastases; melanoma, thyroid, choriocarcinoma, and primary tumors
d. Venous infarction and hemorrhage secondary to cortical vein or dural venous sinus thrombosis
e. Note that aneurysmal rupture may also result in intraparenchymal hematoma, usually associated with
subarachnoid or intraventricular hemorrhage.
(1) Middle cerebral artery aneurysms may rupture into the adjacent temporal lobe.
(2) Anterior communicating artery aneurysms may rupture into the medial frontal lobe.
f. Nontraumatic extra-axial hematomas may occasionally result from aneurysm, AVM, or DAVF. They are
often associated with either subarachnoid or parenchymal hemorrhage. Criteria for angiography are similar
to those for the assessment of other intraparenchymal hematoma.
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Indications
1. Angiography may be indicated when the hemorrhage is not confined to the basal ganglia region, is not
associated with hypertension, or is not in a typical location for amyloid angiography.
2. Patients in need of emergent decompression of the parenchymal hematoma due to mass effect may not
undergo angiography until after surgical decompression. This has the side benefit of reducing the mass
effect potentially compressing the underlying vascular pathology.
1. Noninvasive imaging, including CTA (performed at the time of the initial noncontrast CT) and/or cerebral
MRI/MRA imaging for evaluation of underlying vascular pathology, precedes catheter angiography in the majority
of these patients.
2. Routine preparation for cerebral angiography to include assessment of bleeding parameters (PT, PTT, INR)
and renal function (BUN, creatinine)
Procedure
1. Heparin bolus may be administered at the time of angiography (2,000 U IV for an average adult)
dependent on coagulation factors and the timing of surgery.
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2. Angiographic protocol should include examination of the internal and external carotid arteries, or
alternatively, both common carotid arteries and both vertebral arteries.
3. Criteria for emergent endovascular intervention for AVM or DAVF
a. Embolization of AVM and DAVF are usually performed in the nonacute stage; however, if urgent surgery
is planned, early targeted embolization may be initiated.
b. Embolic agents vary with the nature of the malformation and include onyx and n-butyl cyanoacrylate;
platinum microcoils may be employed for associated aneurysms.
c. The risk of rebleeding during or following embolization is higher in the acute period following hemorrhage.
This is due in part to the fragility of the recently ruptured vasculature.
4. Criteria for emergent endovascular intervention for ruptured cerebral aneurysm associated with
parenchymal hematoma:
a. Endovascular coil treatment may be possible under many circumstances, depending on the need for
urgent surgical decompression of the parenchymal hematoma (7).
b. Treatment triage usually made based on the configuration of the aneurysm and the need for hematoma
decompression.
c. Regarding the aneurysms commonly associated with parenchymal hematoma
(1) Middle cerebral aneurysms at the M1 bifurcation generally require remodeling at the bifurcation and may
not be amenable to simple coiling as a primary form of treatment. Partial coiling is sometimes employed for
stabilization prior to definitive treatment. Balloon assistance may increase the types of aneurysms amenable
to endovascular coil treatment.
(2) Anterior communicating and pericallosal aneurysms may be coiled under many circumstances despite
the presence of hematoma.
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Includes puncture site hemostasis and the postprocedure management as with any intervention
Results and Complications

1. The yield of emergent angiography for intracerebral hematoma is highly variable and dependent on the
noninvasive imaging findings regarding the location and character of the hematoma.
2. Noninvasive imaging sensitivity can be increased by the addition of contrast enhancement and/or CTA
prior to triage to angiography.
3. Complications include the standard risks of diagnostic cerebral angiography and the relative risks of any
intervention previously described.
Otolaryngologic (ENT) Emergencies

Epistaxis (23,24,25)
Etiology and Diagnosis

1. Hereditary vascular dysplasia: Prototype: hereditary hemorrhagic telangiectasia (HHT) autosomal
dominant vascular dysplasia with telangiectasias involving the nasal mucosa, skin, and airway. Hepatic and
pulmonary AVMs are common.
2. Tumor: Primary or metastatic tumors involving the nasal cavity and/or paranasal sinuses may present
with intractable epistaxis. CT can define the location and extent of the mass and may suggest diagnosis.
3. Trauma to the nose and face, both penetrating and blunt, may result in vascular injury, including
laceration, occlusion, pseudoaneurysm, and arteriovenous fistula. CT defines the extent of bony injury and
demonstrates proximity of the
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fracture fragments, foreign body, or projectile track to the major vessels of the head and neck. The addition
of CTA to the initial CT has the added benefit of defining vascular patency prior to determining the need for
catheter angiography.
4. Intracranial source for epistaxis
a. Rupture of aneurysms of the petrous or cavernous carotid may occasionally present with epistaxis.
Traumatic pseudoaneurysms in this location include iatrogenic injury to the internal carotid artery during
pituitary or sphenoid surgery (24,25).
b. Dural arteriovenous fistula may also be a source of epistaxis.
5. Idiopathic epistaxis
a. No underlying source of bleeding; may be associated with bleeding diathesis, anticoagulation, including
aspirin, often seen at start of heating season—dry nasal mucosa
b. Conservative, particulate embolization is indicated when posterior packs fail to control bleeding.
Indications (23,24,25)
Angiographic indications include intractable epistaxis, not responsive to anterior and posterior packs, often
associated with significant blood loss, requiring transfusion.
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2. Airway control is paramount in a patient who may hemorrhage while supine on the angiography table.
Anesthesia support is preferred with intubation and general anesthesia.
Procedure
1. Standard heparin bolus is administered at the time of angiography (2,000 U IV for an average adult).
2. Angiographic protocol should include examination of the internal and external carotid arteries or, when
significant internal carotid occlusive disease precludes safe selective catheterization, both common carotid
arteries.
3. Vascular supply to the nasal mucosa must be assessed:
a. Both the distal internal maxillary and the distal facial arteries supply the nasal mucosa.
b. The ophthalmic artery may provide a major supply to the nasal mucosa via ethmoidal branches.
c. Other contributions from the internal carotid artery include the inferolateral trunk, the artery of the
foramen rotundum, or other petrous or cavernous branches.
4. Angiographic protocol
a. Internal carotid arteries (bilateral)
b. External carotid arteries (bilateral)
c. Internal maxillary arteries (bilateral)
d. Facial arteries (bilateral)
5. Embolization protocol
a. The distal nasal mucosal branches should be embolized via three of the four major external carotid nasal
feeding arteries, leaving the main trunks intact.
b. At least one of the major feeding artery's distal territories remains untouched in order to provide collateral
flow to the remaining mucosa and prevent necrosis.
c. Embolic agents include the following:
(1) Polyvinyl alcohol (PVA) foam particles measuring 150 to 250 or 250 to 355 μm, in order to avoid necrosis
(2) Gelfoam pledgets and platinum microcoils may be adjunctive in certain settings; however, one should
avoid proximal occlusions and address the
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bleeding site primarily. This will allow for repeat embolization in the future, as needed.
(3) Embospheres and other newer embolic agents are becoming available as potential alternatives to PVA.
Complications
Complications include the routine risks of cerebral arteriography as well as the risk of local vascular injury
and the possibility of skin or nasal mucosal sloughing if the particle size is too small or the collateral
circulation is compromised.
1. Puncture site hemostasis
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2. ICU or step-down unit management
3. Nasal packs are removed when the coagulation parameters have returned to normal following angiography
with heparin bolus (often packs are removed the following day).
Traumatic Vascular Injuries (26,27,28)

Etiology
1. Blunt trauma
a. Fractures involving the face, skull base, or cervical spine may result in injury to major vessels.
b. CT/CTA is useful for determining the location of fracture fragments in relation to the location of normal arterial
structures. 2. Penetrating trauma
a. With or without an expanding hematoma, penetrating trauma may require catheter angiography to evaluate for
vascular injury and to potentially treat sites of direct vascular injury.
b. CT and/or CTA may demonstrate the path of the projectile or demonstrate a vessel injury.
c. Vascular laceration, occlusion, pseudoaneurysm formation (± hematoma) and vasospasm (often the site of
dissection or pseudoaneurysm development) may be identified angiographically.
2. Generally, angiographic protocols for traumatic injury should include examination of the aortic arch, both
common carotid arteries, the internal and external carotid arteries, and both vertebral arteries. Modification of this
protocol should be made based on the mechanism and nature of the injury.
3. Standard heparin bolus is administered at the time of angiography (1,000 to 2,000 U IV for an average adult).
This should be modified according to additional injuries and the timing of surgery.
Procedure: Selected Angiographic Protocols

1. Facial fractures with oral or nasal bleeding (27)
a. Angiographic protocol would be similar to that for idiopathic epistaxis.
b. Embolization of bleeding source, usually an external carotid artery branch injury, is useful to provide
immediate hemostasis and to allow healing. Often temporary embolic agents, such as gelfoam pledgets, or larger
PVA foam particles may be sufficient for small vessels (300 to 500 μm or larger). Liquid embolic agents such as
n-butyl cyanoacrylate or onyx can be used for pseudoaneurysm or fistulas. Microcoils can be used but beware
too proximal occlusions. The rich collateral network of the face may recanalize fistulas or pseudoaneurysms if
their entry points are not occluded.
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2. Carotid artery injuries (26,27,28)
a. Angiographic protocol requires evaluation of both carotid arteries and at least one vertebral artery in order to
look for vascular injury and to assess collateral flow through the circle of Willis.
b. Carotid injury in the neck most commonly occurs from direct blunt or penetrating trauma. The carotid may also
be injured at fixed points, such as at the level of the skull base where the carotid pierces the dura, at the level of
the supraclinoid internal carotid artery, and within the cavernous sinus.
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c. The carotid artery may be lacerated or ruptured with resultant occlusion or carotid cavernous fistula formation.
d. Treatment for carotid artery occlusion is expectant in the setting of trauma. Revascularization by surgical
bypass is usually not possible.
e. Pseudoaneurysms may arise in the internal carotid artery following penetrating trauma.
f. Pseudoaneurysm may be treated by parent artery occlusion, if adequate collateral vascular supply can be
demonstrated. Endovascular treatment can be accomplished with stents, or covered stents, or conventional
stents plus platinum detachable coils placed through the stent mesh into the pseudoaneurysm. Surgical repair
may be possible depending on the location.
g. TIAs or hemiparesis following carotid endarterectomy may result from carotid occlusion, often requiring
reoperation. CTA is performed for assessment and DSA may be added depending on whether re-exploration or
endovascular management is planned. Emergent angiography is often performed in order to establish the
etiology of the symptomatology and the nature of the vascular compromise prior to re-exploration.
3. Traumatic carotid cavernous fistula (26)
a. May arise acutely or delayed developing over time following a severe head injury
b. Clinical symptoms relate to the pattern of venous drainage.
(1) Anterior venous drainage into the superior and/or inferior ophthalmic veins leads to ocular symptoms such as
chemosis, proptosis, and increased intraocular pressure.
(2) Posterior venous drainage into the superior and/or inferior petrosal sinuses with increased jugular venous
drainage and tinnitus
(3) Cortical venous drainage (cortical venous reflux via the greater Sylvian vein or other cortical vein) with
venous hypertension and intraparenchymal hemorrhage
(4) Transcavernous collateral venous egress may result in bilateral symptomatology with a unilateral fistula.
c. Does not require emergency treatment unless the vision is threatened
d. Treatment of carotid cavernous fistula may involve closure of the fistula from an arterial approach versus
closure of the fistula via a venous approach depending on the location of the fistulous opening and the pattern of
venous drainage.
e. Parent artery occlusion must be performed in some traumatic carotid cavernous fistulas, particularly if the
underlying carotid injury is severe.
4. Vertebral artery injury
a. Angiographic protocol requires evaluation of both carotid arteries and at least one vertebral artery in order to
look for vascular injury and to assess collateral flow through the circle of Willis.
b. Vertebral artery injury may also result from blunt or penetrating injury. Points of fixation, such as the entrance
into the foramen transversarium at C5-C6, the C1-C2 junction, and between the arch of C1 and the foramen
magnum, are potential sites of injury.
c. Cervical spine fractures, particularly those that extend through the foramen transversarium, are commonly
associated with vertebral artery injury (dissection, occlusion pseudoaneurysm, fistula).
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d. CT examination of the spine without contrast can demonstrate the loss of integrity of the foramen
transversarium. Contrast CTA can be most useful in defining the patency of the vertebral artery acutely at the
time of initial imaging.
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e. Recanalization of lacerated or dissected vertebral arteries may lead to distal embolization and stroke.
f. Endovascular treatment when needed may include vertebral artery sacrifice, following demonstration of
adequate collateral flow. Platinum microcoils may be used for embolization in this setting.
5. Vertebrojugular fistulas
a. More commonly seen with penetrating trauma
b. May also steal blood from the brain and/or the arm and may cause hemodynamic instability when large
c. Can be occluded from the arterial side using platinum coils with or without sacrifice of the proximal vertebral
artery. A venous endovascular approach can sometimes be used with preservation of the vertebral artery
patency. A surgical approach is uncommonly required.
Complications
These include the routine risks of cerebral arteriography as well as the risk of local vascular injury and
stroke. Risks vary according to the therapeutic technique applied.
1. Puncture site hemostasis
2. ICU neurologic monitoring, particularly when vertebral or internal carotid vessels were compromised
3. Hemodynamic support if major vessel sacrifice was required for treatment
Malignant Disease of the Head and Neck (27,28)

Emergent intervention in malignant disease is usually required when intractable oronasal bleeding develops in a
patient with underlying head and neck cancer. Assessment of the distribution of the residual tumor by CT or MRI
is useful in planning the endovascular therapy.
Endovascular treatment usually consists of occlusion of tumoral neovascularity derived from the external carotid
arterial branches or occlusion of a major branch, common carotid, or internal carotid artery.
Provocative testing using the BOT test is a critical part of the management of these patients (see the following
discussion).
2. Airway control is paramount in a patient who may hemorrhage while supine on the angiography table.
Anesthesia support is preferred, with intubation and local standby anesthesia when possible, in order to permit
clinical testing.
Diagnostic Arteriography
1. Generally, angiographic protocols should include examination of both common carotid arteries and the internal
and external carotid arteries. Intracranial as well as extracranial vessels should be studied.
2. The vertebral artery circulation should be assessed if carotid occlusion is contemplated. The circle of Willis
and the patency of the anterior and posterior communicating arteries should be assessed.
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Balloon Occlusion Tolerance Test
1. A clinical and angiographic test for tolerance of carotid occlusion performed prior to possible surgical or
endovascular occlusion of the internal carotid artery.
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2. Components include diagnostic arteriography for collateral assessment, clinical testing during occlusion, and
HMPAO SPECT evaluation of cerebral blood flow at the time of the temporary occlusion.
Procedure
1. BOT test is performed with placement of a nondetachable balloon catheter into the internal or common
carotid artery. A microballoon or a conventional 8.5-mm occlusion balloon may be used for the occlusion.
2. The patient is systemically heparinized during the temporary occlusion (ACT 250 to 300 seconds).
3. Neurologic testing is ongoing during the period of temporary occlusion.
4. Systemic hypotension is induced with reduction of mean arterial pressure to two-thirds normal using a
sodium nitroprusside (Nipride) or other pharmacologic intervention. During this period of pressure reduction,
the patient is injected with HMPAO for a first-pass assessment of cerebral blood flow.
5. The balloon is deflated and withdrawn. The patient is taken to the nuclear medicine department for
SPECT imaging, leaving the sheath sutured in place.
6. If the patient tolerates the clinical examination and the SPECT demonstrates no focal abnormalities, the
patient returns to angiography for the permanent occlusion (see “Permanent Carotid Sacrifice”).
Permanent Carotid Sacrifice (16)

1. Emergent carotid sacrifice is performed when no option is available to salvage the carotid using stent
techniques. 2. Elective carotid sacrifice
a. Patients with local recurrence of head and neck carcinoma in the neck following surgical and/or radiation
treatment may be eligible for radical surgical options, often requiring resection of the carotid artery within the
surgical block.
b. Sacrifice of the carotid artery at the time of surgery is associated with a higher risk of perioperative stroke than
with elective carotid sacrifice several weeks prior to the definitive surgical procedure.
Preprocedural Preparation and Procedure

1. Routine preparation for cerebral angiography to include assessment of bleeding parameters (PT, PTT,
INR) and renal function (BUN, creatinine)
2. Prior to endovascular occlusion, the patient undergoes placement of a central line. (This is done prior to
the administration of heparin; thus, when permanent occlusion is contemplated, the central line is placed
before the diagnostic angiogram and BOT test.)
3. Diagnostic cerebral arteriography is performed with particular attention to the circle of Willis and the
patency of the anterior communicating and posterior communicating arteries. The common carotid arteries
in the neck are also examined (see earlier discussion).
4. BOT test of the carotid artery is performed prior to permanent occlusion. If tolerance is demonstrated,
permanent occlusion follows.
5. Endovascular carotid occlusion is performed using detachable platinum coils with or without an
AMPLATZER plug or like closure device.
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Carotid Blowout Syndrome
1. Carotid blowout syndrome is a syndrome of acute oral, nasal, or paratracheal bleeding originating from the
vasculature of the head and neck secondary to erosion from adjacent malignant tumor.
2. A subset of the carotid blowout patients would represent those with more chronic or intermittent hemorrhage.
Sentinel hemorrhage is not uncommon.
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Preprocedure Preparation and Procedure

1. Routine preparation for cerebral angiography to include assessment of bleeding parameters (PT, PTT,
INR) and renal function (BUN, creatinine)
2. Protocols for evaluation of this population of patients must include airway management. We perform the
procedures with the patient intubated and with anesthesia for airway control. A central line is important for
evaluation for patient monitoring, particularly in the situation where carotid sacrifice may be imminent.
3. Angiographic protocol includes bilateral common carotid arteries, both internal carotid arteries, and both
vertebral arteries for establishment of the integrity of the circle of Willis as well as to establish the lesion
itself.
4. When time permits, temporary BOT test is performed with HMPAO injected in order to ascertain stability
of the intracranial circulation and tolerance of carotid occlusion.
5. Subsequent to this, the carotid is occluded using detachable balloons or, in certain circumstances, a
combination of Guglielmi detachable coil (GDC) and complex helical coils.
6. When the carotid sacrifice cannot be performed due to incomplete circle of Willis or lack of collateral flow,
or a lack of tolerance of temporary balloon occlusion, covered stents have had limited use to stabilize the
patient prior to permanent carotid occlusion. Rarely extracranial-to-intracranial bypass may be considered
but these have distinct limitations in the setting of the malignant postradiation neck.
7. On occasion, the carotid blowout manifests as uncontrollable hemorrhage, and carotid sacrifice must be
performed without preocclusion testing in order to be lifesaving. Risk of stroke may be considerably higher
in such patients. In this situation, HMPAO SPECT may be performed following occlusion in order to plan for
aggressive hypertensive and hypervolemic management.
Postprocedure Management: Major Vessel Sacrifice

1. Neurointensive ICU management, including hypertensive and hypervolemic therapy, is critical to maintain
cerebral perfusion and allow the patient to equilibrate and adjust to the changes in cerebral perfusion.
2. Systemic heparinization (PTT 60 to 80 seconds) is maintained for at least 48 hours; antiplatelet therapy,
usually aspirin, is added.
3. The femoral access may be maintained for 24 to 48 hours. Alternatively, percutaneous closure devices are
utilized to obtain hemostasis in order to allow for the maintenance of systemic heparinization and antiplatelet
therapy for several days.
Results and Complications: Major Vessel Sacrifice

1. Carotid and/or vertebral artery sacrifice may be well tolerated in the patient with good collateral circulation and
a good clinical and HMPAO SPECT response to test occlusion.
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2. Aggressive ICU management designed to maximize cerebral perfusion, coupled with anticoagulation, is
necessary for success.
3. Risks include hypoperfusion stroke and focal infarction during the procedure and during the first week of the
postocclusion period.
4. Risks are increased in those patients with poor collateral circulation, poor response to test occlusion,
hypoperfusion on HMPAO SPECT, and/or exsanguinating bleeding necessitating emergent carotid sacrifice.
Tumoral Hemorrhage
1. Oral, nasal, or paratracheal bleeding may result from tumoral neovascularity, or erosion through the wall of a
small vessel rather than a major vessel erosion.
2. Vascular lacerations or pseudoaneurysms may be encountered and are treated directly with embolization to
address the specific site of bleeding.
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3. In many of these patients, subacute assessment of the tolerance for carotid occlusion may be necessary and
subsequent carotid sacrifice performed.
4. Preprocedure and angiographic protocols are analogous to those used for epistaxis.
5. Complications include the routine risks of cerebral arteriography as well as the risk of local vascular injury and
stroke. Risks vary according to the therapeutic technique applied; in general, the risks are similar to those for
epistaxis management.
6. Careful diagnostic angiography and controlled embolization of tumoral bleeding sites are greater than 95%
effective in bleeding control.
7. Postprocedural management
a. Puncture site hemostasis
b. ICU or step-down management to follow bleeding; packing removed when bleeding parameters stabilize
c. Neurologic monitoring and hemodynamic therapy (hypervolemia, hypertension) when carotid occlusion has
been performed
References
1. Bagley LJ. Aneurysms—all you need to know. Appl Radiol . 2009;38(1):6-18.
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2006;16(3):371-382.
3. Dehdashti AR, Rufenacht DA, Delavelle J, et al. Therapeutic decision and management of aneurysmal
subarachnoid haemorrhage based on computed tomographic angiography. Br J Neurosurg. 2003;17(1):46-
53.
4. Edlow JA. What are the unintended consequences of changing the diagnostic paradigm for subarachnoid
hemorrhage after brain computed tomography to computed tomographic angiography in place of lumbar
puncture? Acad Emerg Med. 2010;17(9): 991-995.
5. Connolly ES Jr, Rabinstein AA, Carhuapoma JR, et al. Guidelines for the management of aneurysmal
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subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart
Association/American Stroke Association. Stroke. 2012;43(6):1711-1737.
6. Tonkopi E, Al-Habsi AH, Shankar JJ. Radiation dose from 3d rotational vs. conventional 2d digital
subtraction angiography in intracranial aneurysm coiling. Can J Neurol Sci . 2015;42(3):176-180.
7. Kim YW, Lawson MF, Hoh BL. Nonaneurysmal subarachnoid hemorrhage: an update. Curr Atheroscler
Rep. 2012;14(4):328-334.
8. Inamasu J, Nakamura Y, Saito R, et al. “Occult” ruptured cerebral aneurysms revealed by repeat
angiography: result from a large retrospective study. Clin Neurol Neurosurg. 2003;106(1):33-37.
9. Thiex R, Norbash AM, Frerichs KU. The safety of dedicated-team catheter-based diagnostic cerebral
angiography in the era of advanced noninvasive imaging. AJNR Am J Neuroradiol . 2010;31(2):230-234.
10. FifiJT, Meyers PM, Lavine SD, et al. Complications of modern diagnostic cerebral angiography in an
academic medical center. J Vasc Interv Radiol . 2009;20(4):442-447.
11. Geyik S, Yavuz K, Akgoz A, et al. The safety and efficacy of the Angio-Seal closure device in diagnostic
and interventional neuroangiography setting: a single-center experience with 1,443 closures.
Neuroradiology. 2007;49(9):739-746.
12. Klisch J, Weyerbrock A, Spetzger U, et al. Active bleeding from ruptured cerebral aneurysms during
diagnostic angiography: emergency treatment. AJNR Am J Neuroradiol . 2003;24(10):2062-2065.
13. Paramasivam S, Leesch W, FifiJ, et al. Iatrogenic dissection during neurointerventional procedures: a
retrospective analysis. J Neurointerv Surg. 2012;4(5):331-335.
14. Molyneux AJ, Birks J, Clarke A, et al. The durability of endovascular coiling versus neurosurgical clipping
of ruptured cerebral aneurysms: 18 year follow-up of the UK cohort of the International Subarachnoid
Aneurysm Trial (ISAT). Lancet. 2015;385(9969): 691-697.
15. Piotin M, Blanc R. Balloons and stents in the endovascular treatment of cerebral aneurysms: vascular
anatomy remodeled. Front Neurol . 2014;5:41.
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16. Cui L, Peng Q, Ha W, et al. Parent artery occlusion for intracranial aneurysms. Interv Neuroradiol .
2009;15(3):309-315.
17. Ong CK, Lam DV, Ong MT, et al. Neuroapplication of Amplatzer vascular plug for therapeutic sacrifice of
major craniocerebral arteries: an initial clinical experience. Ann Acad Med Singapore. 2009;38(9):763-768.
18. Alderazi YJ, Shastri D, Kass-Hout T, et al. Flow diverters for intracranial aneurysms. Stroke Res Treat.
2014;2014:415653.
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19. Malhotra A, Johnson MH. Imaging vasospasm: CT, CTA and CTP correlated with digital subtracted
angiography in cerebral vasospasm. In: Bulsara KR, Gilmore E, eds. Contemporary Understanding and
Management of Cerebral Vasospasm: A Practical Guide. New Delhi, India: Jaypee; 2015:32-42.
20. Grant RA, Bulsara KR, Matouk CC. Practical microsurgical and endovascular management of
vasospasm. In: Bulsara KR, Gilmore E, eds. Contemporary Understanding and Management of Cerebral
Vasospasm: A Practical Guide. New Delhi, India: Jaypee; 2015:75-84.
21. Smith SD, Eskey CJ. Hemorrhagic stroke. Radiol Clin North Am. 2011;49(1):27-45.
22. Barnes B, Cawley CM, Barrow DL. Intracerebral hemorrhage secondary to vascular lesions. Neurosurg
Clin N Am. 2002;13(3):289-297.
23. Krajina A, Chrobok V. Radiological diagnosis and management of epistaxis. Cardiovasc Intervent Radiol .
2014;37(1):26-36.
24. Shukla PA, Chan N, Duffis EJ, et al. Current treatment strategies for epistaxis: a multidisciplinary
approach. J Neurointerv Surg. 2013;5(2):151-156.
25. Villwock JA, Jones K. Recent trends in epistaxis management in the United States: 2008-2010. JAMA
Otolaryngol Head Neck Surg. 2013;139(12):1279-1284.
26. Luo CB, Teng MM, Chang FC, et al. Endovascular management of the traumatic cerebral aneurysms
associated with traumatic carotid cavernous fistulas. AJNR Am J Neuroradiol . 2004;25(3):501-505.
27. Zhao LB, Shi HB, Park S, et al. Acute bleeding in the head and neck: angiographic findings and
endovascular management. AJNR Am J Neuroradiol . 2014;35(2):360-366.
28. Wan WS, Lai V, Lau HY, et al. Endovascular treatment paradigm of carotid blowout syndrome: review of
8-years experience. Eur J Radiol . 2013;82(1):95-99.
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8
Renovascular Hypertension: Endovascular Management
Thomas A. Sos
David W. Trost
Revascularization of renal artery stenosis (RAS) is indicated in the treatment of renovascular hypertension (RVH) and renal
insufficiency (RI) due to ischemic nephropathy (IN); RVH and IN frequently coexist but may be present independently of
each other. Hemodynamically significant RAS is one of the few potentially reversible causes of RI due to IN and
hypertension. Recent multicenter prospective randomized trials, STAR (1), ASTRAL (2), and CORAL (3), have not shown
any additional benefit for renal artery stenting in atheromatous disease over optimal medical therapy. The negative results
of these trials have been criticized as being based on faulty methodology and statistics (4). The challenge for physicians is
to identify patients with RAS who would benefit from renal revascularization, whether by interventional techniques or open
surgery. In order to do so, RAS must first be clinically suspected and anatomically identified, and its hemodynamic
significance and causal relationship to hypertension or RI must be documented. The risks and benefits of alternative
medical and invasive therapies must be compared to each other and to the natural history of the disease.
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Renovascular Hypertension
RVH accounts for about 5% of all hypertensive patients (5,6,7) and is usually due to atherosclerosis (75% of patients with
RVH) or fibromuscular dysplasia (FMD) in the renal artery.
Indications for Revascularization (6,7,8,9,10,11)

Angiographically documented RAS, greater than 70% diameter, and a history of sustained hypertension (140/95 mm Hg) in
the setting of
1. Failed optimal medical therapy
2. Multiple antihypertensive agents required for blood pressure (BP) control (with an aim toward reducing, if not eliminating,
the number of medications needed)
3. A strong clinical suspicion for RVH and at least one of the following:
a. A positive “Captopril Challenge Test” (plasma renin activity with angiotensinconverting enzyme inhibitor [ACEI])
b. A positive radionuclide renogram with ACEI (captopril or enalapril) challenge
c. Renal vein renin (RVR) secretion that lateralizes to one side with associated suppression of renin secretion from the
uninvolved side (see “Renal Vein Renin Sampling”)
4. A mean arterial pressure gradient greater than 10% of the systemic BP across the stenotic segment of the renal artery
(12). Areas of web-like stenosis that appear noncritical on angiography but have a significant systolic pressure gradient
occur more often with FMD than with atherosclerosis. To measure gradients accurately in FMD, especially in the “string of
beads” medial form, a pressure wire or a very flexible microcatheter is often necessary—a stiff angiographic catheter may
“stent open” the soft fibrotic flaps responsible for the narrowing.
Note: Indications 1 through 3 may not be present in every case. Indication 4 must be present in every case.
Ischemic Nephropathy
IN usually results from bilateral atheromatous RAS; FMD virtually never produces IN. Many patients with IN have coexistent
RVH. Revascularization may, especially in recent onset IN, reverse the process or prevent further decline of renal function.
Indications for Revascularization (7,8,11,13,14,15,16,17,18)

Angiographically documented RAS greater than 70% in diameter and recent onset or deteriorating renal function while on
optimal medical management and
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1. A mean arterial pressure gradient greater than 10% of the systemic BP across the stenosis (12)
2. Loss of renal mass demonstrated on serial imaging. A kidney length of 8 cm is considered by some to be the lower limit at
which function is likely to be restored (15,16).
Renovascular Hypertension, Ischemic Nephropathy, or Both, with Any of the

Following Conditions
Indications (7,8,9,10,11,12,13,14,15,16,17,18,19)
1. Renal transplant arterial stenosis: Most transplant renal artery stenoses are due to neointimal hyperplasia,
accelerated atherosclerosis, clamp, or other iatrogenic injury usually at the perianastomotic area (9).
2. Renal artery venous, arterial, or synthetic bypass graft stenosis: These lesions occur most often at or adjacent to
anastomoses and are due to perianastomotic fibrosis or clamp injury. Anastomoses must be examined in multiple
projections to identify and quantify stenosis severity.
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3. Recurrent flash pulmonary edema: These patients with RVH and/or azotemia usually have severe bilateral RAS
rendering their kidneys unable to excrete sodium and water; they often do not have severe coronary artery disease (19).
4. Unstable angina: Some patients with unstable angina and RAS experience improvement in their coronary symptoms
following renal revascularization (20).
Contraindications to Renal Revascularization (7,8,9,10,11,12,13,14,15,16,17,18,19)

Absolute
1. Medically unstable patient
2. Hemodynamically nonsignificant stenosis (12)
Relative
1. Long-segment total occlusion (16)
2. Severely diseased aorta predisposing to increased risk of embolization of atheroma
Renal Artery Balloon Angioplasty

1. Discontinue long-acting antihypertensive medications prior to procedure, if possible; manage BP with short-acting drugs
as necessary (in consultation with managing physician).
2. In patients who already have RI or in those at increased risk such as diabetes, multiple myeloma, renal disease, and
dehydration, hydrate overnight using 0.45% saline with sodium bicarbonate at a rate of 100 to 150 mL per hour for 4 to 12
hours prior to the procedure. If overnight hydration is not possible, at least 1 hour of hydration and N-acetylcysteine (600 mg
twice daily on the day before and day of intervention) are also recommended (21,22,23). Consider using 50% or 30% dilute
iodinated contrast or alternative contrast agents such as CO2. (For an in-depth discussion of periprocedural renal function
management, see Chapter 65.)
4. Standard preangiography preparation
5. Review prior imaging studies (computed tomographic angiography [CTA], magnetic resonance angiography [MRA],
duplex ultrasound [US], radionuclide studies, angiograms, and RVR assays).
Procedure (Fig. 8.1)

1. Access to the (right preferred) common femoral artery: Almost all renal interventions can be performed from a
femoral access. Place an arterial sheath (with a side arm for flushing). Patients who have significant iliofemoral
atherosclerosis have a higher chance of distal cholesterol embolization. In this case, use a long (20 to 30 cm) arterial
sheath, which reaches into the distal abdominal aorta, to minimize disruption of plaque during catheter exchanges and
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manipulations; in any case, a 40-cm long Flexor Ansel Sheath (Cook Medical Inc, Bloomington, IN) will usually be necessary
later for intervention. Left brachial access can be used for patients with distal aortic occlusion or for those few patients who
have a very unfavorable caudal renal artery angle for a femoral approach.
2. Diagnostic angiography: This should begin with a flush aortogram. Imaging needs to be performed in the proper
oblique views to best visualize the lesion(s). Atherosclerotic patients have predominantly proximal and ostial disease, which
are best imaged in 5- to 10-degree left anterior oblique (LAO) for the left renal artery and 20- to 30-degree LAO for the right
renal artery (24). When no prior noninvasive imaging is available and both sides need to be evaluated, a compromise 20-
degree LAO projection is preferred. Children or patients with suspected FMD should have selective magnification renal
arteriography in at least two oblique views per side. When patients have significant bilateral stenoses, attempt angioplasty
on the side with the larger kidney first
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(usually also technically easier because disease tends to be less severe); if this goes well, and if the patient and operator
can tolerate a prolonged procedure, attempt the other side.
FIGURE 8.1 • Technique of renal angioplasty using shepherd's crook (recurved) catheter. After selection of an appropriate
renal artery (A), a flexible-tipped guidewire is advanced through the lesion under fluoroscopic control (B). The catheter is
advanced across the stenosis by withdrawing the catheter at the puncture site (C). The guidewire is then exchanged for a
heavy-duty, tight J-wire (D), and an appropriate balloon catheter is inserted to dilate the lesion (E). (Redrawn from
Tegtmeyer CJ, Selby JB. Percutaneous transluminal angioplasty of the renal arteries. In: Castañeda-Zúñiga WP,
Tadavarthy TM, eds. Interventional Radiology, Vol 2. 2nd ed. Baltimore, MD: Williams & Wilkins; 1992:370.)
3. Crossing the lesion: In general, the stenosis should be crossed with a soft, atraumatic guidewire, such as a Bentson,
and a recurved catheter such as a 4 Fr. Sos Omni Selective (AngioDynamics, Queensbury, NY) or a Simmons (Fig. 8.1).
Aggressive/excessive catheter manipulation while finding the renal artery and crossing the stenosis can be the cause of
cholesterol or macroparticle embolization. There are several published techniques to minimize this. The “no touch”
technique described by Feldman et al. (25) minimizes the contact between the guiding catheter and the aortic wall, as does
the “Sos flick” technique (26). Once the wire is across the lesion, the Sos Omni Selective catheter can be pulled down
across the lesion. Hydrophilic guidewires should only be used as a last resort because they may cause inadvertent
perforation or dissection and exchanged out as soon as practical. In most cases, 0.018 in. and 0.014 in. wire diameter and
monorail/rapid exchange type designs are used. Frequently, after the 0.035 in. Bentson-type wire and Sos Omni Selective
catheter have crossed, they are exchanged for a smaller diameter wire for intervention. Nitroglycerin (NTG) 100 to 200 μg
intra-arterial (IA) into the renal artery can be given through the selective catheter before any guidewire insertion to
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prevent spasm. If the wire advances with difficulty or the tip curves and is unable to be straightened, stop all wire
manipulations. Assess whether the wire has passed subintimally or perforated. If occlusive dissection is present, prolonged
(few minutes) under inflation with a balloon 1 mm lesser in diameter may restore the lumen. If occlusive dissection persists
or perforation has occurred, a stent or covered stent may be necessary to complete the procedure. If the RAS is difficult to
cross with the earlier techniques, consider using a different catheter/guidewire combination. If the renal artery has an
extreme caudal angulation, consider an upper extremity approach. Once the catheter is safely across the stenosis,
administer 5,000 U of heparin intravenously (IV) (70 U per kg).
4. Pressure gradient across stenosis: A pressure gradient is considered to be significant if it is greater than 10% of the
mean systemic arterial pressure (12). If there is not a significant gradient, then revascularization should not be continued.
NTG 100 to 200 μg IA into the renal artery may provoke a gradient. Gradients should be measured with the lowest profile
device to avoid inadvertently enhancing the severity of a stenosis. A 0.014 in. pressure wire is ideal; a 4 Fr. catheter clearly
contributes more to an existing stenosis, but it is very useful in excluding unnecessary intervention in those patients who do
not meet even this minimal threshold.
5. Balloon angioplasty (percutaneous transluminal renal angioplasty [PTRA]) (7,8,26,27,28,29) or stent placement
(30,31,32,33,34,35,36,37,38): For ostial atherosclerotic stenosis, primary stent placement is indicated. If the lesion is non-
ostial (greater than 1 cm from the origin), whether atherosclerotic or FMD, balloon angioplasty should be primarily
performed. Primary stenting of FMD is contraindicated.
6. Renal artery balloon angioplasty (26,27)
a. Choose a balloon diameter approximately 10% larger than the estimated “normal” diameter of the vessel based on the
arteriogram. Do not be fooled by poststenotic dilation into choosing too large balloon size. If in doubt, use a smaller balloon,
at least initially.
b. Some practitioners still use 5 Fr. balloon systems over a 0.035 in. guidewire; however, smaller sub-4 Fr. coronary-type
balloon systems with 0.014 in. to 0.018 in. guidewires are being used with increasing frequency.
c. Guiding catheters or sheaths (5 to 8 Fr.) are used to provide support for crossing severe calcific stenosis and better
seating within the ostium. They have a soft, blunt distal end, which minimizes arterial trauma but are almost as stiff as
guiding catheters. The Flexor Ansel Sheath (Cook Medical Inc, Bloomington, IN) is supplied with two dilators: one tapered to
a 0.035 in. guidewire and the other tapered to a 0.018 in. guidewire.
7. Dilation (see Fig. 8.1): Place a soft tip, stiff shaft guidewire into a distal branch for the intervention. Exchange the
diagnostic catheter for the sheath/guide or directly for the balloon catheter. Prevent motion of the distal wire tip by firmly
fixing it; otherwise, spasm may be provoked in the distal smaller vessels. Perforations can also occur if the guidewire is
allowed to go too peripherally. Place the balloon markers across lesion.
8. Inflate the balloon slowly until the balloon is fully inflated or has reached its rated maximum pressure; for angioplasty,
inflate for a minute, and for stenting, until stent is fully expanded. Discontinue balloon inflation if the patient experiences
severe pain.
9. Deflate the balloon immediately and completely to avoid thrombus formation on balloon surface and possible vessel
occlusion.
10. Remove the balloon catheter over the wire; prior to removal, it may be necessary to partially “refold” the deflated balloon
by gently advancing the sheath/guide over its back end.
11. It is generally best to avoid recrossing the site of angioplasty after the vessel has been dilated. Do a completion
angiogram using a technique that preserves wire position across the lesion. If a guide/sheath is present, the angiogram
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can be obtained through the sheath. If there is no guide/sheath, the injection can be performed by using a 5 Fr. multi-side-
hole catheter over the guidewire with the tip just into the renal artery and injecting through a side-arm adapter. A
postangioplasty cleft is often seen and usually resolves in about 3 months (8).
12. If the angiographic result and post-PTRA pressure gradient are acceptable, the procedure is terminated; otherwise,
usually, a balloon of 1-mm greater diameter than the one previously used is reintroduced into the stenotic segment over the
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wire, and the angioplasty is repeated until a satisfactory result is obtained.
13. Remember, if PTRA/stenting has failed or if the patient is to undergo surgical revascularization without attempted
angioplasty, the angiographer must evaluate the donor or source vessels most likely to be used for the reconstruction. A
good-quality lateral angiogram of the celiac axis and a pressure measurement in the presence of median artery ligament
compression should be obtained. The splenic artery may be used to revascularize the left kidney (28), and the hepatic and
gastroduodenal arteries to reconstruct the right renal circulation (29).
14. Prior to removing the balloon catheter from the stented or dilated artery, apply suction to the balloon to maximally
collapse it, but after evacuating the balloon, release the vacuum to avoid formation of sharp “wings.” During withdrawal, the
catheter can be rotated in the direction in which the balloon wings tend to collapse. The maneuver of gently partially
advancing the guide/sheath over the deflated balloon prior to withdrawing it (described earlier) can be very useful,
especially if the balloon is “entrapped” by the stent struts.
Renal Artery Stenting

Indications (30,31,32,33,34,35,36,37,38,39,40)
Renal artery stenting may be considered for the following specific indications:
1. Ostial atheromatous RAS (within 1 cm of the aortic lumen). For renal artery less than 4 mm diameter, coronary drug-
eluting stent should be used.
2. Restenosis after previous PTRA or stenting. For in-stent restenosis, drug-eluting (4,41) or “covered” stents (42) within
the stent are used.
3. Postoperative stenosis (renal artery bypass and transplant renal arteries)
4. Highly eccentric renal artery stenosis
5. Acute failure or complication of PTRA due to:
a. Vessel recoil with threatened closure
b. Complex dissections, which do not respond to prolonged reinflation
c. Residual stenosis greater than 30% or residual pressure gradient greater than 10% of mean arterial pressure
d. Rupture or perforation. These may require use of a “covered” stent to repair.
Contraindications (30,31,32,33,34,35,36,37,38,39,40)
Relative
1. Branch vessel disease
2. Lesion length exceeding 2 cm
3. Renal artery diameter less than 4 mm (consider coronary size or drug-eluting stent)
4. Unfavorable renal artery anatomy, not permitting sufficient distal vessel length to allow surgical bypass, if needed
5. Diffuse intrarenal vascular disease
6. Noncompliant lesion
7. Kidney size less than 7 cm
Equipment Suggestions
1. Stents: Balloon expandable metallic stents are preferred. Typical stent lengths range from 1 to 2 cm in length and 4 to 8
mm in diameter. They are mounted on 0.014 in. (coronary) and 0.018 in. monorail/rapid-exchange type and over the wire
and 0.035 in. over the wire systems.
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2. Guidewires: Initial guidewire introduction should be with a soft atraumatic wire as described in the section on “Renal
Artery Balloon Angioplasty.” The initial wire should be exchanged for a firmer wire for stent introduction. Currently, renal
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balloons and stents are very soft-tipped, but stiff shaft 0.018 in. guidewires are used; if working through a sheath or guiding
catheter, 0.014 in. diameter coronary type guidewires such as the Grand Slam and Ironman (Abbott Vascular Solutions,
Santa Clara, CA) may also be used. Hydrophilic wires, especially the stiff-tipped V-18 (Boston Scientific/Medi-Tech, Natick,
MA) should only be used as a last resort because they can easily dissect or perforate; if used, they should be exchanged
out as soon as practical. For 0.035 in. systems, suitable wires include the TAD-II and standard Rosen wire (various
manufacturers).
3. Angiographic catheters: Catheters for initial diagnostic angiography and selective renal artery catheterization are
chosen by the same criteria as for renal angioplasty.
4. Guiding catheters/sheaths: Guiding catheters and guide sheaths are always used for stent delivery. The frequently
used Flexor Ansel Sheath (Cook Medical Inc, Bloomington, IN) comes with two dilators: one tapered to a 0.035 in. guidewire
and the other tapered to a 0.018 in. guidewire.
Preparation for renal artery stenting is the same as for balloon PTRA described earlier.
Procedure
1. Perform standard diagnostic angiography to evaluate the lesions. Be sure to image the arteries in an oblique view
that adequately shows the renal ostium. The best views are usually 5- to 10-degree LAO for the left renal artery and
20- to 30-degree LAO for the right renal artery ostia.
2. Document pressure gradients across the lesion. A resting pressure gradient greater than 10% of the peak systolic
BP is hemodynamically significant.
3. Cross the lesion with a catheter and wire as with balloon angioplasty. Administer an IV heparin bolus of 3,000 to
5,000 U, followed by an infusion of 750 to 1,000 U per hour. Target activated clotting time (ACT) should be about 2.5
times baseline.
4. Selective intrarenal artery NTG in 100-μg boluses may be given to prevent or reverse spasm.
5. There are several techniques for stent deployment; almost all use 0.018 in. or lower profile systems. Predilation with
a relatively small, ≤3-mm diameter balloon is no longer routinely used. A long 5 Fr. diameter “guide sheath” with a
tapered dilator may be initially advanced through the stenosis over the 0.018 in. or 0.014 in. wire for assured stent
delivery, especially if the stenosis is heavily calcified and eccentric. The “bare back” technique utilizes a guide sheath
or catheter that never crosses the lesion. All 0.035 in. and many 0.014 in. to 0.018 in. compatible balloon catheters and
stents are available in over-thewire configuration; 0.018 in. and smaller devices are available in monorail-type rapid-
exchange designs. Monorail-type rapid-exchange balloon catheters are easier and quicker to insert and exchange (Fig.
8.1). A major disadvantage of the monorail system is the lack of a full-length wire lumen—making it impossible to (a)
inject contrast, (b) obtain pressure measurements, and (c) exchange wires during intervention. Many operators still
favor using a 0.035 in. system and predilating with a 35- to 65-cm long, 6 Fr. sheath with a tapered tip introducer. If
primary stent placement is desired, the stent delivery sheath can be placed immediately after the lesion is crossed.
6. Choose a stent and dilating balloon that will adequately cover the lesion and expand the stent to equal to the normal
vessel diameter. Do not let the poststenotic dilation fool you into using too large a balloon. If there is any doubt, use
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a smaller one and postdilate it to a larger diameter, if necessary. If the lesion is ostial, then the stent length should be
sized to ensure that it extends approximately 1 to 2 mm into the aortic lumen and past the stenosis.
7. Carefully introduce the stent across the hemostatic system of the delivery sheath. If a standard vascular sheath is
used, be careful that the stent is not displaced from the balloon during passage through the hemostatic membrane.
8. Keeping the sheath immobile, observe fluoroscopically as the stent is advanced through the sheath to the site of the
lesion.
9. After initial stent positioning, hold the stent immobile and retract the sheath to uncover the stent. Once the stent is
completely uncovered, do not try to re-sheath it because the stent may slide off the balloon. When using the “bare
back” technique, the stent system should be carefully advanced through the lesion making sure that the stent does not
catch on the stenosis.
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10. Angiography (always limit contrast use) must be performed through the sheath prior to stent deployment to confirm
positioning. Be sure to image the artery in the oblique view that best shows the lesion. This is most important for
optimal positioning of a stent at ostial lesions.
11. Using an inflating device, steadily inflate the balloon under fluoroscopic monitoring until fully expanded. Do not
inflate the balloon above its rated burst pressure.
12. Deflate the balloon completely and aspirate with a 50-mL syringe, if necessary. Retract balloon, keeping the wire
fixed, and remove through the sheath. If the stent moves during balloon removal, the sheath can be used to hold it in
place or even to begin to enfold the balloon as described earlier to keep the stent from becoming displaced.
13. Perform a repeat angiogram, either through the sheath or through a catheter (advanced over the wire) proximal to
the stent. Preserve the wire position across the stent if possible. Angiographically evaluate wall contact and any
residual stenosis.
14. If necessary, use a larger balloon and expand the stent further.
15. If more than one stent is necessary, extra care must be used when advancing a wire, a sheath, or a new stent to
avoid displacing or deforming the previously deployed stent — a very soft-tipped wire should be used to avoid
passing under or through the stent struts. A sheath (with its introducer in place) may be necessary to traverse the first
stent.
16. When stenting in series, approximately 2 mm of stent overlap is advised. Avoid gaps as well as excessive overlap
because this may contribute to local formation of intimal hyperplasia.
17. After deployment of stents to their final desirable diameter, perform a repeat arteriogram, measure pressure
gradients across the stented segment and, if necessary, evaluate with intravascular US to assess proper wall
apposition and full stent expansion in any region.
18. Remove femoral sheath when the ACT is less than 180 seconds, down from 300+ seconds during the procedure.
Obtain puncture site hemostasis by groin compression or alternatively with a closure device.
Percutaneous Renal Revascularization by PTRA and/or Stent
1. Monitor renal function (serum creatinine [SCr] and blood urea nitrogen [BUN]) as appropriate for at least the first 24
hours.
2. Monitor BP for 24 to 48 hours (8).
a. If BP drops significantly below normal levels, administer normal saline by IV infusion.
b. If BP increases during or after procedure, consider captopril (8) (an ACEI) or short-acting medication (if BP >100 mm Hg).
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3. Postprocedure, continue aspirin 81 mg by mouth (PO) and/or a stronger antiplatelet agent for up to 6 months only if a
drug-eluting stent was used.
4. Standard postangiography management must be followed.
5. Follow BP and renal function at frequent intervals for the first few months. Most recurrences of hypertension tend to
occur within 8 months.
Results—Percutaneous Revascularization
(7,8,9,10,11,12,13,14,15,16,17,18,19,20,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51)
1. Initial technical success rate: 80% to 90% (7,8,9,10)
2. Immediate therapeutic success rate
a. Hypertension: favorable (improved or cured) BP response as percentage of technical successes
(1) Fibromuscular dysplasia: 90% to 100% (7,8,18)
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(2) Atherosclerosis: 50% to 90% (7,8,17)
(3) Transplant renal artery: 70% to 100% (9)
b. Azotemia: Improvement or stabilization of renal function was seen in 81% of patients (13,14,15,16,17).
3. Restenosis: In one study (7,11), about 13% of stenoses needed redilation. Technical success was about 90%. The
most important factor determining recurrence was a postangioplasty residual diameter stenosis of 30% or greater.
4. Definitions for evaluating of BP after revascularization
a. Cured—BP of 140/90 mm Hg or less without medication
b. Improved—Decrease in diastolic BP of 15 mm Hg or greater on same or less medicines OR decrease in diastolic BP
less than 15 mm Hg but normal BP on medicines
c. Stable—Diastolic BP ± 15 mm Hg on same or less medicines
d. Failure—Diastolic BP greater than 15 mm Hg on same or less medicines
5. A similar scale exists to grade success with renal dysfunction:
a. Improved—Decrease in SCr of 20% or more over baseline
b. Stable—SCr of within 20% of baseline
c. Failure—Elevation in SCr of 20% or more over baseline
Complications
1. Overall incidence of complications: 13% (7,8,18,52,53,54)
2. Incidence of major complications (i.e., those requiring surgical intervention or having an altered hospital course): 3%
to 11% (7,8,52) versus 20% for surgical bypass (7)
3. Thirty-day mortality: less than 1% (7,8,11,17,18,43,44,45,46,47,50,51,52). Previously reported surgical mortality
was 5.9% (9); more recently, surgical mortality is reported as 0% to 5.4% (45,46).
4. Angioplasty-site complications
a. Local thrombus: 1% (7,52,53,54)
b. Angioplasty-related nonocclusive dissection: 2% to 4% (8,52). When necessary, most of these patients have
successful surgical bypass (8).
c. Arterial rupture: 1% to 2% (7,52,53,54)
d. Peripheral renal embolism: 2% (52)
e. Guidewire-related dissection: 4% (52)
5. Angioplasty-related complications
a. Renal failure: Acute renal failure or acute exacerbation of chronic renal failure: 1.5% to 6.0% (7,8,52,53,54). This
may be due to many factors; contrastinduced nephropathy and microcholesterol embolization, being the most common.
Approximately 1% may go onto chronic dialysis (54).
b. Nephrectomy: 1% (8) versus 15% for surgical bypass (7,8)
c. Segmental renal infarction and perinephric hematoma without treatment or sequelae, with therapeutic success: 3%
(7,52)
6. Other complications
a. Emboli to extremities: 1.5% to 2.0% (7)
b. Cholesterol microemboli: 1% (16)
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c. Puncture-site trauma requiring surgery: 1% to 3% (8,26)
d. Myocardial infarction: 1% (16)
7. Management of complications
Radiology Books
a. If local thrombus occurs without significant dissection or vessel perforation, a trial of local IA thrombolysis may be
useful: 5-mg tissue plasminogen activator (tPA) over 30 minutes, followed by 0.5 mg per hour for up to 24 hours.
b. If arterial rupture occurs, retroperitoneal hemorrhage may be prevented or slowed by gently reinflating the balloon
across the tear. A “covered” stent may be utilized to seal the leak.
c. If the balloon ruptures and no arterial damage is present, exchange the balloon catheter for a new one and proceed
with angioplasty.
d. Dissections: Angioplasty is always accompanied by minor dissections that heal within months. Non-flow-limiting
dissections may be managed conservatively even if they are severe in appearance (8,18,52,53). Flow-limiting
dissection should be treated by prolonged reinflation of a 1-mm undersized balloon or a “covered” stent.
e. Chronic steroid therapy: Extra caution is urged when contemplating angioplasty in patients on chronic steroid
therapy because they tend to be more prone to vessel rupture (54).
f. Patients with untreated hyperlipidemia and those who continue to smoke may also have increased risk for
complications and restenosis.
Renal Vein Renin Sampling

The usefulness of RVR activity to predict which patients will respond to revascularization remains controversial
(5,55,56,57,58,59,60). A review of 143 consecutive patients of whom 20 had RVH resulted in a sensitivity of 65%, a positive
predictive value of 18.6%, and a negative predictive value of 89.3%. The authors concluded that the results were neither
sensitive nor specific enough to exclude patients who do not have RVH (59). Another study (60) of elderly patients (mean
age of 60 years) found a very low specificity (21%) and negative predictive value (16%) of RVR analysis, limiting its use in
this population. This same study also found that performing angioplasty without prior RVR analysis did not significantly
affect clinical outcome. Most likely, abnormal renal function and bilateral renal artery disease render this physiologic
evaluation less useful; in younger patients with unilateral FMD and lack of essential hypertension, it is far more sensitive
and specific.
When RVR secretion lateralizes to the affected side, it has a significant positive predictive value for curable hypertension
and can influence decisions in the planning of revascularization.
Indications
1. To determine which patients with RVH may benefit from revascularization by either angioplasty or surgery
2. To determine the physiologic significance of RAS documented by imaging
Contraindications
1. Patients who are not candidates for revascularization will not benefit from selective RVR determination.
2. Lack of adequate access to the renal veins or inferior vena cava (IVC) (e.g., venous occlusions or IVC filters that
impede safe access)
1. Same as for renal angiography
2. Patients should ideally be off all antihypertensive medications for 2 weeks prior to sampling. (This is seldom achieved
unless patients are hospitalized.) However, patients can usually be taken off β-blockers and ACEIs for just several
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days prior to renin determination. The predictive value of RVR sampling is poor when plasma renin is stimulated by chronic
administration of ACEIs.
3. Captopril (1 mg per kg of body weight) administered 60 to 90 minutes before selective renal vein blood sampling
increases the diagnostic accuracy of renal vein sampling by increasing the renin secretion on the side of the stenotic
Radiology Books
kidney, especially in unilateral renal artery lesions. Captopril stimulation (57) and sodium depletion (58) enhance the
sensitivity of lateralization.
Procedure
1. Venous puncture: Access, optionally under US guidance, with 19-gauge singlewall or micropuncture needle (with
patient performing a Valsalva maneuver to distend the vein). Avoid inadvertent puncture of the artery and creation of
an arteriovenous fistula.
2. Selective catheterization
a. Insert a 5 Fr. Cobra 2 with a side-hole made at the distal tip approximately 2 to 3 mm from the end hole.
b. Sometimes, a sidewinder or other recurve catheter will be needed to access the renal veins.
3. The catheter must be advanced beyond the orifice of the left gonadal vein that empties most commonly into the
proximal to middle third of the left renal vein. The right renal vein can be sampled closer to the cava because the right
gonadal vein enters directly into the IVC.
4. Catheterize the veins without the use of contrast, which affects the production of renin. Obtain an image with the
catheter in each renal vein to document position. Search the IVC throughout its entire length to identify anomalous
renal veins.
5. Obtain control samples from the infrarenal IVC. Discard at least 2 mL of blood before collecting each sample.
6. Samples should be obtained as closely in time together as possible (within 20 minutes). Samples must be sent on
ice to the laboratory for processing. Check with your own special chemistry laboratory as to how they wish to handle
the samples.
Interpretation of Results of Renal Vein Renin

Results are commonly interpreted in one of two ways (6):
1. Simple ratio method: The ratio of the RVR activity on the involved side divided by the activity in the other kidney. Many
“thresholds” have been proposed, but 1.5:1.0 is the ratio that most investigators regard as being positive (sensitivity 62%,
specificity 60% [57]).
2. Incremental ratio method: proposed by Vaughn et al. (59) because of the poor performance of the simple ratio method:
where Vis the right or left RVR activity and A is the arterial renin activity, which is equal to the infrarenal IVC renin activity.
An abnormally increased RVR relative to arterial renin from the suspect kidney (step-up) can be used to reflect the degree
of renal ischemia, this is especially significant if there is associated suppression of renin secretion from the contralateral
uninvolved kidney. A ratio greater than 0.48 that lateralizes to one side and has associated contralateral RVR activity
suppression is considered a positive result for the presence of renin secretion from an ischemic kidney and suggests
curability of the hypertension with surgical revascularization (59) or percutaneous intervention (8).
Pitfalls in Renal Vein Renin Sampling

1. Patients on chronic ACEIs or β-blockers, and unable to safely be taken off medication for any period of time, will have
RVRs with poor predictive values.
2. Failure to identify venous anatomic variants
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3. Failure to identify segmental renal artery stenosis (SRAS). SRAS produces renin step-up in the corresponding draining
segmental vein, and it may not be detected when it is unsuspected, and blood samples are obtained from the main renal
vein or from an unrelated segmental vein.
4. Samples obtained from the left renal vein proximal to the inflow from the left gonadal vein or samples inadvertently
obtained from a low hepatic vein on the right.
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5. Failure to handle blood samples in an appropriate fashion, including delay in transporting samples to the laboratory for
processing
References
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8. Sos TA, Pickering TG, Sniderman K, et al. Percutaneous transluminal renal angioplasty in renovascular hypertension
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angioplasty. AJR Am J Roentgenol . 1988;150:839-844.
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hypertension. J Hypertens. 1986;4:S667-S669.
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benefits justify the risks? J Vasc Surg. 1987;5:622-627.
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18. Tegtmeyer CJ, Selby JB, Hartwell GD, et al. Results and complications of angioplasty in fibromuscular disease.
Circulation. 1991;83(suppl 2):I155-I161.
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artery stenosis: treatment by angioplasty or surgical revascularisation. Lancet. 1988;2:551-552.
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Cardiovasc Diagn. 1995;35:252-256.
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randomized controlled trial. JAMA. 2004;291(19):2328-2334.
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renal function by acetylcysteine. N Engl J Med. 2000;343(3):180-184.
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23. Kay J, Chow WH, Chan TM, et al. Acetylcysteine for prevention of acute deterioration of renal function following
elective coronary angiography and intervention: a randomized controlled trial. JAMA. 2003;289(5):553-558.
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J Vasc Interv Radiol . 1999;10:37-39.
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Catheter Cardiovasc Interv. 1999;46(2):245-248.
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Philadelphia, PA: Lippincott Williams & Wilkins; 2008:287-314.
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28. Moncure AC, Brewster DC, Darling RC, et al. Use of the splenic and hepatic arteries for renal revascularization. J
Vasc Surg. 1986;3:196-203.
29. Moncure AC, Brewster DC, Darling RC, et al. Use of the gastroduodenal artery in right renal artery
revascularization. J Vasc Surg. 1988;8:154-159.
30. Palmaz JC. Balloon-expandable intravascular stent. AJR Am J Roentgenol . 1988;150:1263-1269.
31. Burket MW, Cooper CJ, Kennedy DJ, et al. Renal artery angioplasty and stent placement: predictors of a favorable
outcome. Am Heart J. 2000;139(1 pt 1):64-71.
32. van de Ven PJ, Kaatee R, Beutler JJ, et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic
renovascular disease: a randomised trial. Lancet. 1999;353: 282-286.
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33. Iannone LA, Underwood PL, Nath A, et al. Effect of primary balloon expandable renal artery stents on long-term
patency, renal function, and blood pressure in hypertensive and renal insufficient patients with renal artery stenosis.
Cathet Cardiovasc Diagn. 1996;37:243-250.
34. Blum U, Krumme B, Flügel P, et al. Treatment of ostial renal-artery stenoses with vascular endoprostheses after
unsuccessful balloon angioplasty. N Engl J Med. 1997;336: 459-465.
35. White CJ, Ramee SR, Collins TJ, et al. Renal artery stent placement: utility in lesions difficult to treat with balloon
angioplasty. J Am Coll Cardiol . 1997;30:1445-1450.
36. Rundback JH, Gray RJ, Rozenblit G, et al. Renal artery stent placement for the management of ischemic
nephropathy. J Vasc Interv Radiol . 1998;9:413-420.
37. Rodriguez-Lopez JA, Werner A, Ray LI, et al. Renal artery stenosis treated with stent deployment: indications,
technique, and outcome for 108 patients. J Vasc Surg. 1999;29:617-624.
38. Rees CR. Stents for atherosclerotic renovascular disease. J Vasc Interv Radiol . 1999;10:689-705.
39. Bloch MJ, Trost DW, Pickering TG, et al. Prevention of recurrent pulmonary edema in patients with bilateral
renovascular disease through renal artery stent placement. Am J Hypertens. 1999;12:1-7.
40. Khosla S, White CJ, Collins TJ, et al. Effects of renal artery stent implantation in patients with renovascular
hypertension presenting with unstable angina or congestive heart failure. Am J Cardiol . 1997;80:363-366.
41. Zeller T, Rastan A, Schwarzwälder U, et al. Treatment of instent restenosis following stent-supported renal artery
angioplasty. Catheter Cardiovasc Interv. 2007;70(3):454-459.
42. Zeller T, Sixt S, Rastan A, et al. Treatment of reoccurring instent restenosis following reintervention after stent-
supported renal artery angioplasty. Catheter Cardiovasc Interv. 2007;70(2):296-300.
43. Martin LG, Cork RD, Kaufman SL. Long-term results of angioplasty in 110 patients with renal artery stenosis. J Vasc
Interv Radiol . 1992;3:619-626.
44. van Jaarsveld BC, Krijnen P, Pieterman H, et al. The effect of balloon angioplasty on hypertension in atherosclerotic
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2000;342(14):1007-1014.
45. Karagiannis A, Douma S, Voyiatzis K, et al. Percutaneous transluminal renal angioplasty in patients with
renovascular hypertension: long-term results. Hypertens Res. 1995;18:27-31.
46. Jensen G, Zachrisson BF, Delin K, et al. Treatment of renovascular hypertension: one year results of renal
angioplasty. Kidney Int. 1995;48:1936-1945.
47. Kløw NE, Paulsen D, Vatne K, et al. Percutaneous transluminal renal artery angioplasty using the coaxial technique.
Ten years of experience from 591 procedures in 419 patients. Acta Radiol . 1998;39:594-603.
48. Bloch MJ, Trost DA, Whitmer J, et al. Ostial renal artery stent placement in patients 75 years of age or older. Am J
Hypertens. 2001;14(10):983-988.
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49. Harden PN, MacLeod MJ, Rodger RS, et al. Effect of renal-artery stenting on progression of renovascular renal
failure. Lancet. 1997;349(9059):1133-1136.
50. Gill KS, Fowler RC. Atherosclerotic renal arterial stenosis: clinical outcomes of stent placement for hypertension and
renal failure. Radiology. 2003;226(3):821-826.
51. Lederman RJ, Mendelsohn FO, Santos R, et al. Primary renal artery stenting: characteristics and outcomes after
363 procedures. Am Heart J. 2001;142(2):314-323.
52. Trost DW, Sos TA. Complications of renal angioplasty and stenting. Semin Interv Radiol . 1994;11:150-160.
53. Dixon GD, Anderson S, Crouch TT. Renal arterial rupture secondary to percutaneous transluminal angioplasty
treated without surgical intervention. Cardiovasc Intervent Radiol . 1986;9:83-85.
54. Lois JF, Takiff H, Schechter MS, et al. Vessel rupture by balloon catheters complicating chronic steroid therapy.
55. Pickering TG, Sos TA, Vaughan ED Jr, et al. Predictive value and changes of renin secretion in hypertensive
patients with unilateral renovascular disease undergoing successful renal angioplasty. Am J Med. 1984;76:398-404.
56. Martin LG, Cork RD, Wells JO. Renal vein renin analysis: limitations of its use in predicting benefit from
percutaneous angioplasty. Cardiovasc Intervent Radiol . 1993;16:76-80.
57. Thibonnier M, Joseph A, Sassano P, et al. Improved diagnosis of unilateral renal artery lesions after captopril
administration. JAMA. 1984;251:56-60.
58. Strong CG, Hunt JC, Sheps SG, et al. Renal venous renin activity. Enhancement of sensitivity of lateralization by
sodium depletion. Am J Cardiol . 1971;27:602-611.
59. Vaughan ED Jr, Bühler FR, Laragh JH, et al. Renovascular hypertension: renin measurements to indicate
hypersecretion and contralateral suppression, estimate renal plasma flow, and score for surgical curability. Am J Med.
1973;55:402-414.
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1975;231:1043-1048.
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9
Acute Mesenteric Ischemia
S. Lowell Kahn
Luke R. Wilkins
Alan H. Matsumoto
Acute mesenteric ischemia (AMI) is a therapeutic emergency, requiring prompt intervention to attain a favorable
outcome (1,2,3). Despite modern diagnostic and interventional advancements, the mortality associated with AMI
remains high, historically between 60% and 80% (4), with more recent reports yielding a range of 52% to 70%
(5,6). However, the reported high mortality rates are likely confounded by the associated comorbidities in this
patient population.
The critical nature of this entity warrants a high index of clinical suspicion, particularly in elderly patients with
cardiovascular disease or embolic or thrombotic risk factors. Risk factors for AMI vary depending on the
underlying etiology. Common risk factors for thromboembolic causes of AMI include older age, atherosclerosis,
cardiac arrhythmias, dilated cardiomyopathies, severe cardiac valvular disease, recent myocardial infarction,
hypercoagulability, and intra-abdominal malignancy (1). Risk factors for AMI attributable to venous thrombosis
include dehydration, hypotension, portal hypertension, hypercoagulability, abdominal infection, abdominal
malignancy, pancreatitis, trauma, and splenectomy (7). Predisposing factors associated with the development of
nonocclusive AMI include a low flow state, prolonged hypotension, older age with cardiovascular disease, and
medications such as vasopressors or digitalis.
The clinical presentation of AMI is classically described as acute, severe, periumbilical abdominal pain that is out
of proportion to physical exam findings,
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with up to 25% of patients manifesting peritoneal signs (8). The presence of peritoneal signs raises concern that
the bowel ischemia has progressed to infarction. Anorexia, nausea, vomiting, diarrhea, and hematochezia are
common. Unfortunately, the clinical manifestations of AMI overlap with other, more common clinical entities, such
as bowel obstruction, pancreatitis, diverticulitis, and peritonitis. Therefore, the clinical presentation must be
considered in the context of the clinical history and patient-specific risk factors, physical examination, and
laboratory and radiographic findings.
Although grouped as a common disease process, AMI reflects a heterogeneous group of entities, which include
occlusive and nonocclusive etiologies that involve the arterial or venous systems. Occlusive causes of AMI
consist of superior mesenteric artery (SMA) embolus, SMA thrombosis, mesenteric venous thrombosis, and less
common entities such as trauma, strangulated hernias, adhesions, intestinal obstruction, cholesterol emboli, and
aortic dissection. Nonocclusive etiologies for AMI include mesenteric arterial vasoconstriction, also known as
nonocclusive mesenteric ischemia (NOMI), which is usually precipitated by a hypotensive event and/or use of
vasopressors. Despite resolution of the hypotension or discontinuation of the vasopressors, persistent
mesenteric arterial vasoconstriction (diffuse vasospasm) persists, causing bowel hypoperfusion and intestinal
ischemia. Other causes of NOMI include drugs (i.e., cocaine) and vasculitides. NOMI can also be seen in
association with mesenteric venous thrombosis or distal to an SMA embolus.
Accurate diagnosis of the cause for AMI is essential because the presentation, management, and prognosis are
influenced by the etiology. To illustrate this point, it is well known that AMI secondary to mesenteric vein
thrombosis often has a relatively insidious onset, whereas a patient with an SMA embolus usually presents with
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an abrupt and distinct onset of symptoms. Treatment will radically differ in these two comparative examples as
well.
Historically, surgery represented the mainstay of therapy for AMI, but the treatment algorithm is rapidly evolving
into an “endovascular-first” approach at many institutions in an effort to improve patient outcomes (9). A recent
paper showed that the use of endovascular therapy for AMI has more than doubled from 11.9% in 2005 to 30%
in 2009 (9). There are potential benefits to an endovascular-first approach, including decreased morbidity and
mortality, avoidance of general anesthesia and open surgery, more targeted and limited bowel resections,
decreased times for revascularization, a reduced need for parenteral nutrition, shortened lengths of stay, and
fewer postoperative complications (2,9,10,11). Table 9.1 summarizes the differences between the etiologies for
AMI and their management (8,7,12). A treatment algorithm employed at our institutions is demonstrated in Figure
9.1.
Indications
1. Diagnosis of AMI and determination of etiology
a. Although angiography remains the gold standard in the diagnosis of AMI, its diagnostic role has largely
been replaced by computed tomographic angiography (CTA) and magnetic resonance angiography (MRA)
(13).
(1) CTA and MRA generate high-resolution two- and three-dimensional images of the mesenteric arterial
and venous anatomy facilitating accurate diagnosis and treatment planning for occlusive AMI while also
providing suggestive findings of NOMI.
(2) Secondary and associated findings of bowel ischemia seen with CTA and MRA
(a) Ileus and bowel distention
(b) Bowel wall thickening/thumbprinting
(c) Intramural or portal venous gas and/or pneumoperitoneum
(d) Abnormal bowel wall enhancement
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Table 9.1 Etiologies and Treatment of Acute Mesenteric Ischemia
Etiology General Imaging Features Treatment
SMA 40%-50% of cases Filling defect Endovascular therapy (direct

embolus Frequent outlined by intrathrombus infusion) may be
association with contrast, convex considered first-line in cases
cardiac disease meniscus, and with short occlusion, adequate
(e.g., atrial location that is distal collateral circulation, and
fibrillation) typically at least no peritoneal signs or elevation
Abrupt presentation 3 cm beyond of lactic acid.
with severe origin of SMA. Intraoperative thrombectomy or
abdominal pain and Lack of thrombolytic therapy may be
diarrhea collaterals considered in a hybrid OR
(hematochezia) Poor distal flow setting, if available.
20% with 15% found in Papaverine administered when
simultaneous proximal SMA; arterial vasoconstriction
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peripheral arterial 50% found at present
embolus; 33% with middle colic Systemic anticoagulation
history of prior artery
embolic event bifurcation, 25%
at the ileocolic
branch, and
10% in the distal
small bowel
branches of the
SMA
Ileus, mucosal
edema, bowel
infarction
NOMI 10%-15% of cases Diffuse arterial Papaverine infusion directly

Typically occurs in vasospasm with into the SMA at 1 mg/min is the
patients with a prior segmental, mainstay of therapy and is
hypotensive event, sausage-like continued until the symptoms
even if resolved narrowing or resolve (typically within 12-36
Associated with low diffuse h). If peritoneal signs develop,
cardiac output, narrowing of surgery is indicated to explore
hypovolemia, vessels for dead bowel while
hypotension, and commonly continuing papaverine infusion.
splanchnic identified near
vasoconstriction. branch points
Also affiliated with Delayed filling of
vasoactive drugs distal arterial
(e.g., cocaine, and intramural
vasopressin, α- branches
agonists, and Delayed bowel
digoxin) wall staining
May be an insidious and/or venous
onset filling
Improved flow at
angiography
after
administration of
60 mg
papaverine into
the SMA.
Ileus, mucosal
edema, bowel
infarction
Acute 25% of cases Occlusive lesion With elevated lactic acid or

SMA Typically occurs in commonly peritoneal signs, surgery may
thrombosis patients with located 1-2 cm be warranted with an
underlying from the origin aortomesenteric bypass and/or
atherosclerotic of the SMA thromboendarterectomy.
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lesions Collateral Alternatively, preoperative
50%-75% of vessels may be thrombectomy or thrombolysis
patients with history present may be considered with
of intestinal angina suggesting coordination of surgery in a
May have acute or underlying hybrid setting.
chronic symptoms chronic ± Preoperative papaverine
occlusive (may not be feasible
disease. because of proximal nature
Ileus; mucosal of these lesions)
edema; bowel Second-look operation 24-
infarction 48 h later
Postoperative vasodilators
as warranted
Endovascular management if
no peritoneal signs or lactic
acidosis
May perform primary
stenting ± filter wire ± lytics
Because lesions often
represent acute clot
superimposed on underlying
chronic lesion, thrombolytics
may be administered prior to
stenting to reduce the risk of
distal embolization.
SMV Accounts for less Intraluminal Hydrate patient and correct

thrombosis than 5% of all acute filling defect in predisposing factors.
mesenteric ischemia the mesenteric Anticoagulate
Predisposing factors veins with If bowel infarction, surgery is
include portal venous warranted.
hypertension, congestion and Pre- and postoperative
abdominal mucosal edema. anticoagulation
inflammatory Secondary Intra-arterial (IA) papaverine
disease, oral arterial if coexistent mesenteric
contraceptives, prior vasospasm and arterial vasoconstriction
surgery on the diminished If no peritoneal signs or lactic
portal venous perfusion acidosis, endovascular options
system, trauma, and Prolonged include transarterial, systemic,
hypercoagulable mucosal and direct transhepatic or
states. enhancement transjugular access for
Mesenteric venous Lack of or delay intrathrombus thrombolysis,
thrombosis causes in opacification mechanical thrombectomy,
mucosal edema of the angioplasty, and stent
leading to arterial mesenteric placement.
hypoperfusion. veins Most patients can be managed
Prolonged conservatively with supportive
opacification of care and anticoagulation.
venules or
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larger regional
veins
Ileus, mucosal
edema, bowel
infarction
Aortic 5% of all cases of Identification of Operative mortality is high.

dissection acute mesenteric true and false Endovascular— intravascular
ischemia lumens with ultrasound (IVUS) helpful
High (90%) possible Endograft therapy to cover
operative mortality visualization of a primary aortic fenestration
in this cohort dissection flap Creation of de novo
Mesenteric extending into fenestrations to equalize
vasculature can be the SMA or pressures between the true
supplied from true compromise of and false lumens
or false lumen. the lumen Use of stents in the SMA to
Inadequate flow perfusing the tack down the dissection flap
results when blood SMA
flow fails to meet the Ileus, mucosal
metabolic needs of edema, bowel
the bowel. infarction
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FIGURE 9.1 • Treatment algorithm for acute mesenteric ischemia.
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FIGURE 9.1 • (Continued)
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(e) Visualization of infarctions in other organs suggesting embolic disease
(f) Small-caliber branches of the SMA with delayed venous filling and poor mucosal staining with contrast
(3) Availability and rapidity of CTA allows its use as an emergent modality.
b. Angiography has diagnostic utility in cases with equivocal findings by CTA or MRA or in patients in whom
endovascular intervention is likely.
(1) Angiography may reduce contrast load and potential renal injury by bypassing the CTA examination in
select patients.
(2) Angiography is usually now performed in anticipation of an endovascular treatment solution.
2. Treatment of AMI
a. For patients with acute bowel ischemia without evidence of bowel infarction or for patients that are poor
surgical candidates, endovascular management alone is an acceptable therapeutic option (2,3,9,10,11).
b. Catheter-based techniques can provide a potential therapeutic role for AMI, regardless of the underlying
etiology. However, the first-line choice of treatment varies depending on the underlying cause (see Table
9.1).
(1) Treatment options include vasodilator infusion, thrombolysis, and mechanical thrombectomy with or
without use of a filter wire, angioplasty, and stenting.
c. Because of the high mortality associated with surgery (14), some authors advocate a broader use of
endovascular therapy, both alone and in combination with surgery for AMI, including patients with evidence
of bowel infarction (peritoneal signs and lactic acidosis) (2,9,10,11).
d. There is growing interest in hybrid operative and endovascular procedures of various forms. The broader
use of hybrid operating and interventional suites allows endovascular revascularization in the same setting
as surgical removal of bowel. Alternatively, in the case of difficult or failed antegrade endovascular
revascularization, exposure of the mesenteric root with retrograde SMA revascularization has been
described (15).
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Contraindications
1. Renal insufficiency is a relative contraindication for contrast administration, thereby compromising the
ability to perform a diagnostic CTA or an endovascular intervention. However, contrast-induced renal failure
may be a less of a risk for a patient than delaying the diagnosis and treatment of a highly lethal disease.
2. Performance of a diagnostic CTA or endovascular intervention in a patient with a severe contrast allergy
history is typically contraindicated. In patients in whom the diagnosis of AMI is highly suspected, the use of
contrast premedication and general anesthesia may obviate the concerns about the contrast allergy risks.
MRA may be an acceptable alternative diagnostic modality.
3. Evidence of bowel infarction may mandate emergent surgical exploration and resection of dead bowel.
Use of an endovascular solution alone may not be appropriate. However, adjunctive endovascular therapy
is known to improve surgical outcomes while also helping to minimize the amount of bowel resected (2,9).
Catheter-based interventions also provide the opportunity to relieve mesenteric vasospasm by pre-, intra-,
and/or postoperative catheterdirected IA infusion of papaverine.
4. Relative contraindications to angiography and an endovascular intervention include uncontrolled
bacteremia and an uncorrectable bleeding diathesis.
5. Other contraindications will be guided by the specifics of the intended therapy:
a. Papaverine is contraindicated in patients with complete heart block and papaverine allergies. Other
relative contraindications exist as well (Table 9.2).
b. Thrombolytics are relatively contraindicated in patients with active bleeding or hemorrhagic disorders,
recent trauma, uncontrolled hypertension, recent
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gastrointestinal (GI) or genitourinary bleeding, hemoptysis, epistaxis, pregnancy, recent surgery, retinal
detachment, a recent cerebrovascular accident, or an acute or recent (less than 3 months) intracranial or
intraspinal process.
Table 9.2 Papaverine Administration
Indications Primary therapy for NOMI or adjunctive therapy for acute mesenteric
ischemia regardless of the cause
Can also be used pre- and postoperatively in those patients requiring
surgical revascularization
Contraindications Absolute
Complete arteriovenous (AV) heart block
Relative
Simultaneous administration of alkaline substances through the same
catheter, including Lactated Ringer's, urokinase, heparin, etc. (can
cause precipitation)
Narrow-angle glaucoma
Severe cardiac disease (particularly with bradyarrhythmias)
Severe liver dysfunction
Dose IA bolus of 45-60 mg followed by steady infusion of 0.5-1.0 mg/min. Initial

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treatment period of 12-24 h prior to reevaluation.
Optional Nifedipine 10-20 mg by mouth (PO) q6h can be given as an adjunct to

papaverine and may confer some beneficial vasodilatory effect but may
worsen hypotension.
Risk for inducing reflex tachycardia and cardiac ischemia
Common Systemic vasodilatation/hypotension, but >90% of the drug is metabolized

complications on first pass through the liver.
Diarrhea and abdominal pain are common after reestablishing flow to the
bowel.
Preprocedure Evaluation and Preparation

1. Pathophysiology of AMI
a. AMI manifests a complex pathophysiology, an understanding of which is imperative for successful
management. A common pathway with associated severe morbidity and mortality is a systemic inflammatory
response syndrome (SIRS), multiple organ dysfunction syndrome (MODS), and acute respiratory distress
syndrome (ARDS). These clinical entities can be exacerbated by reperfusion of infarcted bowel.
b. Vascular occlusive disease produces splanchnic-mesenteric hypoperfusion and mesenteric vascular
vasoconstriction (16). Hypoxia, acidosis, and epithelial permeability develop which allows for bacterial
transgression of the mucosal barrier and subjects the immune system to massive stimulation from bacterial
antigens, stimulating the proinflammatory pathways (2,17). Enteric decontamination has been shown to improve
survival in intensive care unit (ICU) patients (2,18).
2. Once the diagnosis of AMI is entertained, a review of the history, serial clinical exams, laboratory data, and
available imaging studies are requisite (8).
a. Laboratory assays of serum L-lactate levels remain the most common marker of bowel ischemia and infarction,
but it is a nonspecific marker of tissue hypoperfusion and may become elevated even in the absence of bowel
infarction. However, the higher the L-lactate levels, in general the worse the patient prognosis. More specific
markers such as D-lactate or intestinal fatty
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acid-binding protein (which are assays that are not routinely available) may gain wider acceptance in the future
(19).
3. Medical optimization/preparation (2)
a. Blood volume resuscitation to achieve a mean arterial pressure (MAP) >65 mm Hg and urine output >0.5
mL/kg/h
b. Systemic heparinization +/- acetylsalicylic acid (ASA) for embolic or thrombotic events
c. Broad-spectrum enteric decontamination with PO and/or intravenous (IV) antibiotics (see specific
recommendations in “Postprocedure Management” section)
d. IV proton pump inhibitors
e. Supplemental O2 as needed
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f. Bowel rest with nil per os for >5 days +/- nasogastric tube (NG-tube) if ileus with total parenteral nutrition
(TPN) as needed.
g. Transfusion as needed for hemoglobin (Hgb) <9 g per dL
4. If bowel infarction is present, the patient will require surgery. Depending on the operator and institutional
capabilities, endovascular revascularization can be attempted first to allow better definition of the ischemic
versus infarcted bowel segments at the time of surgery. However, a delay for surgery should be minimized to
reduce the risk for developing a reperfusion syndrome. Hybrid ORs or endovascular suites equipped to do open
surgery confer the advantage of allowing operative and endovascular intervention in a single session.
5. Assess the patient for the appropriateness for the intended procedure (e.g., papaverine and/or thrombolytic
infusion, or a direct transhepatic or transjugular approach for mesenteric venous thrombosis). If NOMI is present,
strongly consider pre- and perioperative IA papaverine infusion because there is usually no fixed obstruction to
fix with balloon angioplasty, stenting, or surgery.
6. Consider using general anesthesia for the uncooperative patient or for whom a bowel exploration is planned.
With a combative or disoriented patient, the patient should remain intubated until treatment is complete.
7. Maintain large-bore IV access and administer fluid resuscitation as tolerated.
8. Correct underlying hypotension, coagulopathy, and electrolyte imbalances as soon as possible while initiating
definitive treatment.
9. Continue physiologic monitoring (pulse oximetry, blood pressure [BP], pulse, and electrocardiogram [ECG])
periprocedurally and until treatment is complete, employing ICU monitoring until the patient is stabilized.
Procedure
1. Arterial access: Access may be obtained via either the femoral artery or the left brachial or radial artery
for arterial interventions. Regardless of the chosen access site, an appropriately sized sheath should be
placed and secured.
a. Although advances in catheter and sheath technology have reduced the need for brachial arterial access,
certain clinical situations mandate use of the brachial or radial artery, including inaccessible groin access
(i.e., total aortic or iliac artery occlusions, active groin infections, and flexion contractures) and mesenteric
anatomic factors (when the mesenteric vessels have a very sharp caudal angle relative to the aorta). In
these situations, catheter access and intervention may be more favorable from a brachial or radial artery
approach.
b. The brachial artery is a second-line approach because it is associated with a higher rate of complications
relative to a femoral access (20). The risk of stroke is decreased using a left brachial arterial access in lieu
of a right brachial access because this approach avoids manipulation of catheters and wires across the
origins of the cerebral vessels (except the left vertebral artery). Use of the radial artery reduces the risk of
brachial nerve injury, but there is a defined risk for radial artery thrombosis. Therefore, an Allen's test
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should be performed to insure an intact palmar arch. Having devices of appropriate lengths to perform the
necessary interventions may be more challenging with a radial artery approach.
c. If use of thrombolytics is under consideration, arterial access should be obtained with ultrasound (US)
guidance to ensure atraumatic single-wall entry into the artery.
2. Preliminary imaging
a. Using a pigtail catheter, obtain a lateral and anteroposterior (AP) abdominal aortogram, preferably
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simultaneously (biplane). These images can be eliminated to minimize contrast load and expedite the
procedure if a prior CTA or MRA defined the mesenteric vascular anatomy well enough to allow a more
targeted approach to treatment.
(1) The AP aortogram is particularly useful in the assessment of aortic disease, collateral vascularization,
and the overall perfusion of the bowel. Additionally, although most occlusive pathology involves the proximal
main and first-order branch vessels of the mesenteric circulation, the more distal arterial anatomy is better
appreciated on the AP projection.
(2) Delayed imaging on the AP projection allows visualization of the SMV, inferior mesenteric vein (IMV),
and portal vein (PV) to assess for mesenteric venous patency.
(3) The lateral aortogram should define the origins and the patency of the proximal celiac artery, SMA, and
inferior mesenteric artery (IMA).
3. Catheterization of the SMA
a. A variety of commercially available 4 Fr. and 5 Fr. catheters (AngioDynamics, Queensbury, NY; Boston
Scientific, Natick, MA; Cook Medical, Bloomington, IN) will readily engage the SMA. Although the RC1,
RC2, and C2 Cobra catheters are commonly used to select the SMA, reverse curve catheters such as the
Sos 1 and Sos 2 and the Simmons 1 and Simmons 2 catheters confer better catheter stability for further
intervention (e.g., papaverine infusion).
(1) The RC1 or RC2 and C2 Cobra catheters are placed above the vessel of interest and retracted slowly in
order to engage the target vessel. A softtipped wire can then be advanced through the catheter more
distally into the SMA over which the catheter is subsequently maneuvered to obtain a more stable catheter
position.
(2) Once formed, reverse curve catheters (Sos and Simmons) are advanced cranially from an inferior
position until the catheter tip selects the target vessel. A soft-tipped wire is then advanced into the target
vessel and the catheter is gently retracted over the wire to seat the catheter into the SMA in a more stable
position.
b. Use of a long sheath (e.g., Flexor Ansel 2, Cook Medical, Bloomington, IN) advanced over a support wire
with the inner dilator or alone over a catheter to the origin of the SMA may be helpful if additional
interventions (i.e., stenting, mechanical thrombectomy, and/or suction embolectomy) are intended.
4. SMA angiography
a. The diagnosis of AMI and the ascertainment of its etiology are often made from a previous CTA or MRA
but can readily be made with a combination of aortography and/or selective SMA angiography as well. The
angiographic findings of the various etiologies for AMI are outlined in Table 9.1.
(1) The selective AP SMA injection of contrast should be at a rate of 4 to 6 mL per second for a 10-second
duration (40 to 60 mL total volume). Filming should be carried out for at least 30 to 40 seconds to allow
visualization of the mesenteric veins. Selective SMA angiography is specifically helpful in making the
diagnosis of NOMI, especially if there is significant improvement in the flow characteristics and visualization
of the vasa recta with repeat angiography after IA administration of 60 mg of papaverine directly
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into the SMA. Additionally, mesenteric ischemia due to vasculopathies, volvulus, hernias, distal emboli, and
mesenteric venous thrombosis can be detected with selective SMA arteriography.
5. Treatment (see Table 9.1 and Fig. 9.1)
a. The specifics of treatment are dictated by the underlying pathology (see Table 9.1).
b. SMA embolus
(1) Endovascular options
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(a) Depending on the clinical scenario, endovascular treatment may be used in lieu of or as adjunct to open
surgery. It is accepted first-line therapy for nonoperative patients or patients with short occlusions, adequate
distal collateralization, absent peritoneal signs, minimal lactic acidosis, and less than 12 hours of symptoms.
(b) On occasion, an SMA embolus can be managed by exclusion with a covered stent and with use of an
embolic protection device (EPD). More commonly, catheter-directed mechanical thrombectomy, suction
embolectomy with a non-tapered guide catheter, or intrathrombus infusion of a thrombolytic agent may be
performed (9). Recombinant tissue plasminogen activator (rt-PA; Genentech, South San Francisco, CA) is
the most commonly used lytic agent in the United States. Its use is an off-U.S. Food and Drug
Administration (FDA) label application of an FDA-approved drug. It is administered as a drip infusion of rt-PA
through an infusion catheter positioned in direct contact with the clot, at a rate of 1 mg per hour with or
without a prior bolus. Short-term (e.g., every 4 to 8 hours) angiographic reassessment, frequent serum
lactate levels, and monitoring for the development of peritoneal signs for response to therapy are
necessary. Concomitant use of heparin is variable depending on the institutional preference. However, we
prefer to administer heparin systemically to keep the patient fully anticoagulated, if the patient is at risk for
further embolization or vessel thrombosis. The development of peritoneal signs or imaging findings
suggesting dead bowel in a patient undergoing thrombolysis may warrant emergent open surgery.
(c) Papaverine infusion can also be used to reduce the ischemia from diffuse vasospasm that frequently
occurs distal to the embolus. A coaxial infusion system is usually used. Papaverine should not be infused
via the same catheter as heparin because the two agents will precipitate if mixed together.
(d) Underlying occlusive lesions may be treated with angioplasty and/or stenting as necessary.
(2) Surgery remains an important component of therapy, especially in the presence of bowel infarction. The
goal of surgery is to resect irreversibly infarcted bowel, to preserve as much bowel as possible, and to
perform a surgical or hybrid revascularization in the setting of endovascular therapy. Adjunctive peri- and
postoperative papaverine infusion into the SMA can help to enhance perfusion to residual ischemic bowel
segments in order to preserve as much bowel as possible.
(a) Second-look operations may be necessary at 24 to 48 hours to evaluate for additional bowel necrosis.
c. NOMI
(1) Vasodilators administered intra-arterially are the mainstay of therapy. Surgery is indicated only if
peritoneal signs or bowel infarction develops.
(a) Papaverine is administered into the SMA as a 45- to 60-mg bolus followed by a continuous infusion at a
rate of 30 to 60 mg per hour (0.5 to 1 mg per minute—most often 1 mg per minute). Typically, it is titrated for
effect for an initial 12- to 24-hour period. After 12 to 24 hours, if the
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symptoms of ischemia have resolved, the papaverine is stopped and replaced with heparinized saline. If the
patient remains asymptomatic for 6 to 12 hours and is hemodynamically stable (no longer hypotensive or on
vasopressors), the catheter is removed. Repeat angiography is only performed if there is a question about
the mesenteric vascular anatomy relative to the patient's symptoms (7).
i. Papaverine may have an adjunctive role with surgery as described earlier and is administered before and
12 to 24 hours after surgery.
ii. Papaverine is usually administered through the 4 Fr. or 5 Fr. catheter positioned in the SMA. More
superselective administration is possible with the use of microcatheters.
iii. More information about papaverine is detailed in Table 9.2.
(b) The use of other IA vasodilators including tolazoline and alprostadil (Prostavasin) has also been
described (21).
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(c) Nifedipine 10 to 20 mg PO q6h may have an additive vasodilatory effect (optional).
(d) As with all types of AMI, surgery is indicated for the resection of infarcted bowel.
d. SMA thrombosis
(1) Endovascular management alone or as an adjunct to surgery is acceptable in most patients and consists
of primary stent placement with or without use of an EPD (to prevent distal clot migration) or thrombolysis of
any underlying acute thrombus prior to stent placement (2,9,10). A balloon expandable covered stent
(iCAST, Atrium Medical, Hudson, NH) or self-expanding covered stent (Viabahn, Gore Medical, Flagstaff,
AZ) may help to trap any acute clot between the stent and vessel wall and prevent herniation and distal
embolization of thrombotic material through the cells of a bare-metal stent.
(2) Surgery is indicated in the presence of peritoneal signs or severe lactic acidosis, which are indicative of
bowel infarction. Surgical revascularization options include aortomesenteric bypass and/or
thromboendarterectomy with resection of nonviable bowel. These occlusions usually are due to thrombosis
of an underlying chronic atherosclerotic SMA stenosis.
(a) As with surgery for SMA emboli, a second-look operation may be necessary at 24 to 48 hours to
evaluate for further bowel necrosis.
(b) Adjunctive IA vasodilator administration is more difficult in these patients because the occlusion of the
SMA is often at its origin and stable positioning of the infusion catheter can be problematic.
e. SMV thrombosis
(1) The initial goal is to hydrate the patient, stabilize the cardiovascular status, and correct the precipitating
event(s).
(2) As with all cases of AMI, signs of peritoneal irritation or elevated lactic acid indicative of bowel infarction
may warrant emergent surgical exploration.
(3) Anticoagulation is a critical facet of management because these patients are highly prone to recurrent
thrombosis.
(4) Most of these patients do well with supportive care, hydration, and meticulous anticoagulation. However,
in some patients, symptoms progress or do not improve despite these measures, so endovascular therapy
is implemented. Thrombolytics with or without mechanical thrombectomy are the mainstay of endovascular
therapy and are given intra-arterially via a catheter positioned in the SMA or directly into the thrombosed
SMV or PV via a transhepatic or transjugular access. Mechanical thrombectomy, angioplasty, and stent
placement are performed as needed (22). Successful mesenteric venous recanalization has been
demonstrated with all methods but appears to be most effective, as with other catheter-directed
thrombolysis (CDT), when the catheter is directly positioned within the
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clot. However, a transhepatic (either direct or via the internal jugular vein) approach is associated with a
significant risk for bleeding. Therefore, the treatment should be tailored to the patient and the risks and
benefits of aggressive therapy versus less invasive therapy.
f. Aortic dissection
(1) Mesenteric ischemia secondary to an aortic dissection can be the result of direct extension of the
dissection flap into the SMA or due to the false lumen compressing the true lumen, causing diminished
perfusion pressures in the SMA. Open surgical repair in a patient with mesenteric ischemia in the setting of
an acute aortic dissection is associated with mortality rates approaching 90%. Therefore, endovascular
solutions are being used more frequently to address this clinical problem.
(a) The goal of aortic endografting is to exclude the primary fenestration(s) with a stent graft to decrease the
perfusion pressure in the false lumen, induce false lumen collapse, and allow better perfusion of the SMA
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via the true lumen. In cases in which the dissection flap extends directly into the SMA, use of a self-
expanding uncovered stent may result in reapproximation of the dissection flap against the SMA wall to
allow better mesenteric perfusion. Intravascular ultrasound (IVUS) is critical in helping to determine the true
versus false lumens and to insure that the stent or endograft deployment will be in the true lumen.
(b) When an endograft or stent solution is not feasible, creation of de novo fenestrations to facilitate
equalization of perfusion to both the true and false lumens can be beneficial. The ability to measure
simultaneous pressures in both lumens is very helpful so that the size of the fenestrations can be increased
by using larger balloons.
1. All patients treated for AMI should be admitted to the ICU regardless of the underlying etiology. The goals of
therapy in the perioperative or periprocedural period are rehydration, resuscitation, avoidance of reperfusion
injury, prevention of clot propagation, prevention of sepsis, and minimizing the extent of bowel injury.
a. Aggressive monitoring of vital signs and central venous pressures may be necessary. Close monitoring for the
development of hypotension with use of vasodilators is mandatory, although this occurrence is rare because
>90% of papaverine administered into the SMA is metabolized on first pass through the liver. If necessary,
vasopressors or cardiotonic agents including dopamine (2 to 5 μg/kg/min) or dobutamine (0.5 to 1.0 μg/kg/min
titrated to 2.5 to 20 μg/kg/min), respectively, may be used, but their use should be limited when possible.
Vasopressin and α-agonists should be avoided because of the concern for worsening mesenteric
vasoconstriction.
b. Correction of fluid and electrolyte disturbances is necessary in order to minimize the risk for arrhythmias or
further hypotension.
c. Anticoagulation with IV heparin is recommended. The initial heparin bolus should be 70 to 100 U per kg,
unless a major intervention (i.e., transhepatic puncture) is planned and then titrated to maintain a partial
thromboplastin time (PTT) of 60 to 80 seconds. Use of low-molecular-weight heparin (LMWH) should be
discouraged if endovascular therapy is contemplated because LMWHs have long half-lives and their excretion is
affected by changes in renal function. In addition, there is no easy test to monitor their activity (i.e., PTT) without
doing factor Xa assays.
d. Mesenteric venous thrombosis can lead to edema and/or breakdown of the intestinal mucosa, with secondary
seeding of the clot by GI bacteria. Therefore, these patients are at risk of developing septic thrombophlebitis
from
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gram-negative and anaerobic organisms, so broad-spectrum antibiotic therapy is recommended for these
patients.
(1) Piperacillin/tazobactam (Zosyn): given intravenously every 6 hours (typical IV dose is 3.375 g)
(2) Metronidazole (Flagyl): loaded at a dose of 15 mg per kg given over 1 hour and then continued at a dose of
7.5 mg per kg every 6 to 8 hours
(3) Levofloxacin (Levaquin): provided in conjunction with Zosyn or Flagyl at a dose of 500 mg every 24 hours
e. Prevention of reperfusion injury
(1) Glucagon may be used as an adjunct for patients undergoing papaverine therapy. Glucagon causes intestinal
vasodilatation and hypotonicity, reducing the demand for oxygen. The dose is 1 μg/kg/min titrated up to 10
μg/kg/min as tolerated; however, nausea and vomiting are frequent with this medication, so its use in this setting
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is infrequent.
(2) Other agents such as allopurinol and enalapril that act as free-radical scavengers may decrease the risk of
reperfusion injury, but there is limited experience with the use of these medications (4).
2. Patients undergoing papaverine or other vasodilator therapy should be monitored for signs or symptoms
indicative of bowel infarction.
a. Worsening lactic acidosis (normal = 0.5 to 2.2 mmol per L) is an indicator of advancing ischemia and possible
bowel infarction and although nonspecific may be very helpful in patients with an altered mental status or those
on steroids or analgesics where assessment for peritoneal signs and serosal irritation may not be helpful. Based
on our experience, lactic acid values above 6.0 mmol per L portend a bad prognosis. As mentioned earlier, high
lactic acid levels are associated with advanced ischemic injury (19).
b. Papaverine treatment can be continued for up to 5 days if the patient remains stable, but most often, if NOMI
is the etiology and the cause for hypotension has been reversed, papaverine infusions greater than 36 hours are
unusual (8).
3. Patients undergoing thrombolysis are reevaluated angiographically at frequent intervals (e.g., ˜4 to 8 hours).
Plasma fibrinogen levels are concurrently monitored to assess for a systemic lytic effect. The infusion dose may
be reduced in order to maintain fibrinogen levels above 100 g per L. Fresh frozen plasma (FFP) is transfused in
select cases in which fibrinogen levels decrease to below 100 g per L.
4. The development of peritoneal signs and worsening lactic acidosis is suggestive of bowel infarction and
requires prompt surgical exploration (8).
a. Patients who have undergone extensive bowel resection are at risk for developing short-gut syndrome (4), and
appropriate diet modifications in consultation with a gastroenterologist and nutrition specialist are necessary.
5. Follow-up CTA can be performed at 1 month if a proximal occlusion has been treated. If stents are placed, a
follow-up CTA or duplex US at 6 to 12 months to evaluate for in-stent restenosis is warranted (7).
6. Patients with stents should be placed on clopidogrel (Plavix, Bristol-Myers Squibb, New York, NY) using a
300-mg loading dose and 75 mg per day thereafter, for 3 to 6 months and ASA at 81 to 325 mg per day for life.
Results
1. Optimal results are attained with early and rapid diagnosis and intervention (1,2,3):
a. Despite advances in treatment, mortality has not improved much in the last 70 years secondary to the
difficulty in making a rapid diagnosis (4). There are isolated reports of mortality rates as low as 24% (23),
but most estimates range between 52% and 70% (5,6).
b. Predictors of increased mortality in the setting of AMI include an elevated Society of Vascular Surgery
(SVS) comorbidity score, the presence of
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congestive heart failure (CHF), chronic kidney disease, cerebrovascular disease, bowel resection,
peripheral vascular disease, coronary artery disease, lactate > 2.2 mmol per L, advanced age, and the
presence of connective tissue disease. Conversely, the presence of chronic mesenteric ischemia appears
protective, likely from the development of collateral blood flow (3,9).
c. Higher rates of survival are attainable with a multimodal, multispecialty strategy. As an example, Corcos
et al. (2) report a 95% 30-day and 89% 2-year survival for patients with AMI referred to their Intestinal
Stroke Center. This is achieved by prompt recognition, a specific medical protocol, and rapid
revascularization (2).
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2. Although surgery remains an essential component in the management of AMI, there is growing evidence
for early endovascular intervention, and some practitioners advocate for an “endo-first” approach, even in
the setting of infarcted bowel (2,9,10,11,24).
a. Benefits of endovascular therapy include a reduced need for anesthesia and an urgent laparotomy, less
bowel resection, decreased need for TPN, the potential for more rapid revascularization, lower morbidity,
and possibly improved mortality. In a retrospective study, Arthurs et al. (9) reported that 31% of patients with
AMI avoided laparotomy altogether, and in comparison with the traditional surgery, patients who underwent
endovascular therapy first had a mean of 52 cm of bowel resected compared to 160 cm in the surgeryfirst
group. Mortality for the endovascular group was 36% compared with 50% for the surgical group (9). Other
groups have confirmed marked reduction in bowel resection, decreased hospital stays, and decreased
mortality using an endovascular-first approach (10). However, the nature of these studies remains subject
to considerable selection bias, and there remains a lack of prospective randomized trials comparing surgical
and endovascular outcomes, likely in part because of the logistical and ethical challenges inherent with
such a study.
3. The authors advocate a multidisciplinary approach to AMI with a team composed of vascular surgery,
interventional and diagnostic radiology, gastroenterology, and intensive care specialists. In the setting of
bowel necrosis, endovascular therapy is not a substitute for surgical therapy, but an adjunct that can
improve subsequent surgical outcomes (2,9,10). In the acute setting, the decision between surgery and
endovascular as first-line therapy is made on an individual patient basis and should incorporate the specific
resources and expertise available to the institution. An endo-first approach should not be embraced if this
approach substantially delays surgical resection of necrotic bowel.
4. The results of endovascular therapy are also influenced by the specific etiology of AMI.
a. Use of vasodilators has a high reported efficacy for AMI due to NOMI (7).
b. Thrombolysis for SMA emboli is also effective. The largest reported series (10 patients) found 90%
achieved angiographic success, and 70% had resolution of symptoms following IA thrombolysis of the SMA
(24). Another study found 62.5% of patients with AMI achieved clinical success after thrombolysis (25).
c. In select patients with SMA thrombosis, use of angioplasty and/or stenting with thrombolysis is beneficial.
One report showed technical success in 71% of patients with AMI. Of those successfully treated, 80%
experienced clinical success with improvement in their symptoms (25). One series reported a good clinical
outcome in 81% (17 of 21) of patients presenting with either acute SMA thrombosis or an SMA embolus with
aggressive endovascular therapy, sometimes combined with surgery, even in patients presenting with
bowel infarction (26).
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Complications
1. Access site
a. Hematoma or pseudoaneurysm formation
(1) Increased risk with thrombolysis and anticoagulation
2. Papaverine (or other vasodilator) associated hypotension
a. More commonly occurs if catheter inadvertently disengages SMA and direct infusion into the aorta occurs
3. Contrast-related complications
a. Renal toxicity: increased risk with dehydration, renal insufficiency, and associated renal emboli
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b. Allergic reactions
4. Thrombolysis-associated complications
a. Access site or distant site bleeding, embolization, stroke, and intraperitoneal bleeding with transhepatic
approaches for mesenteric venous thrombosis
5. Angioplasty-associated complications
a. Vessel injury: dissection, rupture
b. Distal embolization
6. Reperfusion injury manifested as a systemic inflammatory response or ARDS
7. Cardiac arrhythmias (8)
References
1. Oldenburg WA, Lau LL, Rodenberg TJ, et al. Acute mesenteric ischemia: a clinical review. Arch Intern
Med. 2004;164:1054-1062.
2. Corcos O, Castier Y, Sibert A, et al. Effects of a multimodal management strategy for acute mesenteric
ischemia on survival and intestinal failure. Clin Gastroenterol Hepatol . 2013;11:158-165.
3. Ryer EJ, Kalra M, Oderich GS, et al. Revascularization for acute mesenteric ischemia. J Vasc Surg.
2012;55:1682-1689.
4. Berland T, Oldenburg WA. Acute mesenteric ischemia. Curr Gastroenterol Rep. 2008;10(3):341-346.
5. Kassahun WT, Schulz T, Richter O, et al. Unchanged high mortality rates from acute occlusive intestinal
ischemia: six year review. Langenbecks Arch Surg. 2008;393:163-171.
6. Cho JS, Carr JA, Jacobsen G, et al. Long-term outcome after mesenteric artery reconstruction: a 37-year
experience. J Vasc Surg. 2002;35:453-460.
7. Leung DA, Matsumoto AH, Hagspiel KD, et al. Endovascular interventions for acute and chronic
mesenteric ischemia. In: Baum S, Pentecost MJ, eds. Abrams' Angiography: Interventional Radiology. 2nd
ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2006:398-414.
8. Kandarpa K. Acute mesenteric ischemia. In: Kandarpa K, Aruny J, eds. Handbook of Interventional
Radiologic Procedures. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2002:211-217.
9. Arthurs Z, Titus J, Bannazadeh M, et al. A comparison of endovascular revascularization with traditional

therapy for the treatment of acute mesenteric ischemia. J Vasc Surg. 2011;53(3):698-704.
10. Beaulieu RJ, Arnaoutakis KD, Abularrage CJ, et al. Comparison of open and endovascular treatment of
acute mesenteric ischemia. J Vasc Surg. 2014;59(1):159-164.
11. Gagnière J, Favrolt G, Alfidja A, et al. Acute thrombotic mesenteric ischemia: primary endovascular
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treatment in eight patients. Cardiovasc Intervent Radiol . 2011;34(5): 942-948.
12. Matsumoto AH, Angle JF, Spinosa DJ, et al. Percutaneous transluminal angioplasty and stenting in the
treatment of chronic mesenteric ischemia: results and long-term followup. J Am Coll Surg. 2002;194:S22-
S31.
13. Shih MC, Hagspiel KD. CTA and MRA in mesenteric ischemia: part 1. Role in diagnosis and differential
diagnosis. AJR Am J Roentgenol . 2007;188:452-461.
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14. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with
peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary: a
collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery,
Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology,
Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee
to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the
American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood
Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease
Foundation. J Am Coll Cardiol . 2006;47:1239-1312.
15. Wyers MC, Powell RJ, Nolan BW, et al. Retrograde mesenteric stenting during laparotomy for acute
occlusive mesenteric ischemia. J Vasc Surg. 2007;45:269-275.
16. Dhindsa M, Sommerlad SM, DeVan AE, et al. Interrelationships among noninvasive measures of
postischemic macro- and microvascular reactivity. J Appl Physiol (1985). 2008;105:427-432.
17. Eltzschig HK, Carmeliet P. Hypoxia and inflammation. N Engl J Med. 2011;364:656-665.
18. de Smet AM, Kluytmans JA, Blok HE, et al. Selective digestive tract decontamination and selective
oropharyngeal decontamination and antibiotic resistance in patients in intensive-care units: an open-label,
clustered group-randomised, crossover study. Lancet Infect Dis. 2011;11:372-380.
19. Demir IE, Ceyhan GO, Friess H. Beyond lactate: is there a role for serum lactate measurement in
diagnosing acute mesenteric ischemia? Dig Surg. 2012;29:226-235.
20. Kaufman JA. Invasive vascular diagnosis. In: Mauro MA, Murphy KPJ, Thomson KR, et al, eds. Image-
Guided Interventions. Philadelphia, PA: Saunders; 2008:39-61.
21. Huwer H, Winning J, Straub U, et al. Clinically diagnosed nonocclusive mesenteric ischemia after
cardiopulmonary bypass: retrospective study. Vascular. 2004;12:114-120.
22. Jun KW, Kim MH, Park KM, et al. Mechanical thrombectomy-assisted thrombolysis for acute symptomatic
portal and superior mesenteric venous thrombosis. Ann Surg Treat Res. 2014;86(6):334-341.
23. Foley MI, Moneta GL, Abou-Zamzam AM Jr, et al. Revascularization of the superior mesenteric artery
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alone for treatment of intestinal ischemia. J Vasc Surg. 2000;32:37-47.
24. Simó G, Echenagusia AJ, Camúñez F, et al. Superior mesenteric arterial embolism: local fibrinolytic
treatment with urokinase. Radiology. 1997;204:775-782.
25. Simonetti G, Lupattelli L, Urigo F, et al. Interventional radiology in the treatment of acute and chronic
mesenteric ischemia. Radiol Med. 1992;84:98-105.
26. Acosta S, Sonesson B, Resch T. Endovascular therapeutic approaches for acute superior mesenteric
artery occlusion. Cardiovasc Intervent Radiol . 2009;32:896-905.
Radiology Books
10
Acute Gastrointestinal Hemorrhage
Michael D. Darcy
Angiography and embolization are a critical component of the modern management of gastrointestinal (GI)
bleeding, not only providing important diagnostic information but also potential lifesaving therapy. Generally,
these procedures can be performed with high level of success and low complication rates.
Indications
1. For upper GI bleeding (UGIB), endoscopy is usually the first approach because a diagnosis can be made
in the majority of cases and the bleeding can be treated at the same time by injection, heater probe
coagulation, etc. Angiography is usually not used for diagnosis but instead is used to manage ongoing
hemorrhage (usually with embolization). Indications include the following:
a. Bleeding too vigorous for the endoscopist to be able to define the source
b. Bleeding not controllable by endoscopic therapy
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c. Inability of the patient to undergo endoscopy for medical or anatomic reasons
d. Lack of availability of a qualified endoscopist
2. For lower GI bleeding (LGIB), endoscopy is much more difficult and less often used as the initial
approach. Angiography can be used to identify the source of bleeding in planning for surgery, but most
often, the intent of angiography is to localize and stop the bleeding. Situations in which angiography, with
planned embolization, is indicated include the following:
a. Ongoing bleeding documented by tagged red blood cell (RBC) scan or computed tomography (CT) scan.
Because these studies have better sensitivity for detecting bleeding, angiography is usually not indicated if
these studies are negative. These procedures can detect bleeding at rates of 0.1 mL per minute for tagged
RBC scan, 0.3 mL per minute for CT (1), and 0.5 to 1.0 mL per minute for angiography.
b. For massive LGIB, one may proceed to angiography without waiting for a scan to confirm bleeding.
c. Angiography can be indicated to look for a structural lesion in patients with intermittent chronic LGIB.
Contraindications
Absolute
1. Given that angiography and embolization may be needed as lifesaving procedures, there are no absolute
contraindications.
2. History of life-threatening contrast reaction is a serious contraindication, but rapid steroid preparation can
be given if angiography is required to stop critical hemorrhage.
Relative
1. There are several relative contraindications that may help you to decide not to do an arteriogram
especially if the indications are marginal in the first place.
a. Renal insufficiency
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b. Contrast allergy
c. Uncorrectable coagulopathy
d. If the rate of bleeding is massive, surgery may be preferable to angiography because angiography may
not be able to control the bleeding as quickly as surgery.
1. History and physical exam
a. Adequate history may provide clues as to the source of bleeding. For example, history of recent polypectomy
in a patient with LGIB would point to post polypectomy bleeding, but significant recent vomiting in a person with
UGIB would suggest a Mallory-Weiss tear.
b. Other medical conditions (especially cardiac and pulmonary conditions and allergies) that might increase the
risk of angiography should be assessed.
2. Ensure adequate monitoring.
a. Automated BP is essential because UGIB patients can become hypotensive.
b. Electrocardiogram (ECG), pulse oximetry, and capnography—loss of blood and dilution of the blood pool by
crystalloid infusion decreases the oxygencarrying capacity of the blood, increasing the potential for cardiac
ischemia, and possibly arrhythmias or infarcts.
c. Body temperature—patients can get hypothermic due to transfusion of large amounts of fluid. Hypothermia
can induce coagulopathy by reducing the effectiveness of various clotting factors. Keep patients covered, use
blood warmers, and consider use of warming blankets.
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3. Resuscitation efforts—although resuscitation is critical, it cannot be performed as an isolated event prior to
angiography. Some patients cannot be stabilized until the bleeding is actually stopped. Thus, angiographic
therapy needs to be undertaken quickly, and resuscitation should be an ongoing process that continues into the
angiography suite.
a. Ensure adequate intravenous (IV) access for infusion of boluses of saline or transfusion of blood. Typically,
two large-gauge (16 gauge) IVs are recommended.
b. Correct hypotension—initially, saline bolus infusion is used, but blood transfusions may also be needed in
order to maintain hemoglobin content and enhance the oxygen-carrying capacity of the blood.
c. Correct coagulopathy—embolization is much less effective when done in a coagulopathic patient because the
embolic agents often only initiate clot formation.
Procedure
a. A sheath must be placed in the artery to avoid losing access if the angiographic catheter becomes
occluded during embolization. A femoral artery approach is used in most cases, barring more proximal
occlusions.
b. Aortograms are usually not performed because visualization of contrast extravasation into the GI tract
requires more selective injection.
c. The vessel selected first should be based on suspicion of the likely source of bleeding according to
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history, clinical signs, as well as localization provided by tagged RBC scans or CT scans. If there is no good
clue as to the source, some prefer to select the inferior mesenteric artery (IMA) first to study the rectum
before the overlying bladder fills with contrast. For suspected UGIB, the celiac and superior mesenteric
arteries (SMA) are the primary targets. For LGIB, the IMA and SMA need to be studied first. However, if
these runs are negative, the celiac artery (e.g., gastroduodenal artery [GDA]) should be injected because
rapid distal duodenal bleeding can present as LGIB. If extravasation is not seen on injection of the main
trunks, more subselective injection may be needed. For duodenal or gastric fundus bleeding, the GDA, or
left gastric arteries, respectively, should be studied. Choice of subselective injections can be guided by
localization provided by tagged RBC scan, CT, or endoscopic findings.
d. Contrast injections are at a rate of 5 to 6 mL per second for celiac and SMA, and 2 to 3 mL per second
for the IMA. Four- to five-second long injections help maximize visualization of contrast extravasation while
avoiding overlap between the arterial injection and the venous phase.
e. Filming should be continued until the venous phase has cleared out to help distinguish contrast
extravasation from persistent venous opacification. Although digital subtraction angiography (DSA) is the
standard technique, viewing the images in nonsubtracted mode is important to distinguish true extravasation
from misregistration artifacts caused by respiratory or peristaltic motion. Use of glucagon before the
angiogram can help reduce artifacts from bowel motion.
f. Unfortunately, GI bleeding is often intermittent and an angiogram may be negative even after positive
tagged RBC scans. If a bleeding source is not identified, some authors (2,3) advocate using provocative
maneuvers such as infusion of vasodilators, heparin, or even thrombolytics like tissue plasminogen activator
(tPA). The goal is to stimulate bleeding to allow the pathology to be localized, which will then allow
treatment. In a recent series, these infusions helped identify the bleeding site in 37.5% of cases without
causing any hemodynamic instability (2).
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2. Vasopressin infusion to stop bleeding
a. Vasopressin works by constricting the mesenteric vessels, thus reducing the blood flow to the site of
bleeding. This allows stable clot to form at the bleed site.
b. Compared to embolization, it has several disadvantages (4) so it is rarely used except when the patients
are not a candidate of embolization, that is, diffuse bleeding or bleeding site is inaccessible for embolization.
c. Patient should be on continuous cardiac monitoring because vasopressin can induce coronary
vasoconstriction.
d. The angiographic catheter is positioned in the main trunk of the artery supplying the bleed. It should not
be advanced selectively. Infusion is started at 0.1 units per minute.
e. Repeat angiography is performed after 15 to 20 minutes to ensure that bleeding has stopped and that the
vessels are not excessively constricted. If bleeding persists, dose is increased to 0.2 units per minute.
Repeat the process and increase up to a maximum of 0.4 units per minute. DSA runs are repeated after
each increment to see if the bleeding has stopped and to ensure that the vessels have not been
overconstricted. On the DSA runs, contrast should flow though the vessels all the way to the antimesenteric
wall of the bowel. If contrast does not flow to the bowel wall, stop or decrease the infusion and repeat the
arteriogram in 10 minutes to assess for excessive vasoconstriction. Excessive vasoconstriction can lead to
bowel infarction.
3. Upper GI embolization
a. The vessel supplying the bleed (usually GDA or left gastric arteries) should be subselectively
catheterized. For left gastric bleeds, a common technique is embolization with Gelfoam (Pharmacia and
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Upjohn Co, Kalamazoo, MI), allowing blood flow to carry the particles to peripheral branches. For GDA
bleeding, a microcatheter is usually advanced beyond the site of bleeding and the vessel is occluded there
with either coils or Gelfoam to prevent backflow to the bleeding site. The catheter is then withdrawn
depositing more emboli until the GDA is occluded back to its origin. Care must be taken when depositing the
final emboli to avoid having coils or Gelfoam move in a retrograde manner into the GDA causing nontarget
embolization of the hepatic artery. In patients with coagulopathy, n-butyl cyanoacrylate (NBCA) glue can
also be effectively used because it is occlusive and does not rely on the patient's ability to form stable clot
(5); however, considerable technical expertise is required to be able to use this and avoid nontarget
embolization.
b. Just placing coils at the vessel origin should be avoided because collaterals will rapidly reconstitute flow
to the bleeding site beyond the coils.
c. After GDA embolization, it is essential to do an SMA arteriogram to make sure there is no collateral flow
to the bleeding via the pancreaticoduodenal arcade.
d. Empiric embolization (embolizing a suspected target vessel even though extravasation was not seen on
angiography) may be indicated if the site of bleeding is well localized by endoscopy. For example, the GDA
may be embolized for a duodenal ulcer or the left gastric artery may be embolized if bleeding is localized to
the fundus or gastroesophageal junction region.
4. Lower GI embolization
a. Avoiding ischemic complications in lower GI embolization requires superselective catheterization. After
engaging the origin of the parent vessel with a 5 Fr. angiographic catheter, a 3 Fr. microcatheter is
advanced coaxially through the 5 Fr. catheter. The 3 Fr. microcatheter should be advanced as close as
possible to the point of extravasation. For colonic bleeds, it is often possible to advance all the way into the
vasa recta in the bowel wall.
b. If the catheter can be advanced right up to the site of bleeding, a 0.018-in. microcoil can be pushed
through the microcatheter. Usually, only one or two
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microcoils are needed, and they should be short in length to avoid embolizing too large of a vascular
territory.
c. If the bleeding site is more diffuse (as from an angiodysplasia) or if the microcatheter can be advanced
close to but not right next to the bleed, then injection of flow-directed polyvinyl alcohol (PVA) particles can
be done. Care must be taken to inject only a very small amount of particles to avoid embolizing an
excessive arterial territory. Particles should be larger than 300 microns because smaller particles may travel
too peripherally and are associated with a higher rate of infarction.
d. NBCA glue has been gaining increasing acceptance as an embolic agent for LGIB. NBCA has
advantages of being a fluoroscopically visible, flow-directed agent that is more permanent than flow-
directed particles. In addition, because it is occlusive without having to rely on thrombus formation, it works
better in coagulopathic patients (6).
1. Routine postangiography orders/puncture site management
a. Vital signs (VS) need to be taken frequently to look for any signs of new bleeding, such as a retroperitoneal
hematoma that may be caused by an inadvertent puncture above the inguinal ligament.
b. The access site should be inspected for a hematoma, with each VS check.
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c. Neurovascular checks of the extremity distal to the puncture site should be done to assess for arterial
occlusion or distal embolization.
2. Assess if the GI bleeding has stopped or not.
a. Follow VS looking for hemodynamic stability. Persistent hypotension or tachycardia could be signs of ongoing
hemorrhage.
b. Check serial hemoglobin and hematocrit levels.
c. Follow the nature and volume of bloody output from GI tract, either nasogastric (NG) aspirates for UGIB or
degree of hematochezia/melena for LGIB. Realize that the colon is a large reservoir and has the capacity to hold
a lot of blood. Thus, passage of blood per rectum may occur for some time after the bleeding has actually been
controlled. This clinical finding must be taken in context. Continued active bleeding is unlikely if passage of dark
blood occurs in a patient with stable VS and stable hematocrit.
3. Vasopressin infusion
a. If a vasopressin infusion was started, the patient must be monitored in an intensive care unit (ICU) on
continuous cardiac monitoring.
b. The infusion should be continued in the ICU at the final starting rate for approximately 12 hours. At that point,
the infusion rate is decreased by 0.1 units per minute every 12 hours. After being at 0.1 units per minute for 12
hours, the vasopressin infusion is replaced with a saline infusion for several more hours. If there is no further
evidence of bleeding, the catheter may be removed.
Results
1. Vasopressin
a. Although vasopressin effectively stops bleeding in over 85% of cases of diverticular bleeding, the
constrictive effect stops after the infusion is terminated. Thus, rebleeding is seen in as many as 50% of
cases in which it is used (4). This, plus the necessity for prolonged catheterization, is why vasopressin
infusions are rarely used.
2. Upper GI embolization
a. Technical success is defined as the ability to deliver the embolic agent to the desired spot with
termination of active bleeding. This is distinguished from
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clinical success because some patients have continued bleeding despite a technically successful
embolization. This can be due to a diffuse source of bleeding (such as angiodysplasia), collateral flow
around the therapeutic emboli, or coagulopathy preventing stable clot formation.
b. Clinical success is considerably lower than technical success because of the multitude of collaterals in
the celiac arterial system and because UGIB often arises from more diffuses processes such as gastritis.
Control of bleeding without further interventions is achieved in 56% to 88% of cases (7,8,9). Two studies
(10,11) compared embolization to surgery for management of UGIB refractory to endoscopic treatment and
found comparable results in terms of durable hemostasis (in the 75% to 88% range) and mortality rates. A
recent systematic review of 711 patients from nine studies found that patients referred for embolization
tended to have worse comorbidities, but although surgery was associated with lower rebleeding rates, there
were no differences in mortality between the two treatments (12).
c. Success after empiric embolization has been reported to be as good as embolization done after
identification of extravasation. Although several studies have shown rebleeding rates to be comparable after
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empiric and targeted embolization, one study (8) reported comparable mortality in the two groups, whereas
another study (13) reported that patients undergoing empiric embolization had higher mortality than those
undergoing targeted embolization.
3. Lower GI embolization
a. Technical success for lower GI embolization is high, usually around 90% to 100% (14,15,16). This is
made possible by the use of microcatheters that allow the catheter to be advanced close to the bleed.
Technical failure is most often due to vessel tortuosity or spasm preventing advancing the catheter to the
desired point of embolization.
b. Clinical success is lower at 84% to 92%, meaning that 8% to 16% of patients rebleed soon after
embolization (14,15,16,17). Rebleeding after embolization is more common in the small bowel than in the
colon (18). This is likely because there are more collateral vessels in the small bowel mesentery than in the
colonic mesentery. Success also varies with the type of lesion being treated. In one series, rebleeding
occurred in only 15% of patients with diverticular bleeds but in 45% of patients who bled from
angiodysplasias and other pathology (19). This is because diverticular bleeds usually have a simple single
vasa recta arterial source, whereas angiodysplasias have multiple feeding arteries.
Complications
1. Standard complications common to all angiograms
a. Puncture site bleeding or occlusion, and dissection of vessels, can occur but are rare.
b. Contrast reactions
2. Vasopressin complications
a. Bowel infarction can occur but is rare.
b. Cardiovascular complications including myocardial infarction (MI), arrhythmia, and hypertension (HTN)
are most common and occur at a rate of 4.2%.
3. Embolization complications
a. Nontarget embolization involves embolic material inadvertently passing into a vascular bed that was not
the intended target. This may result from excessive pressure when injecting flow-directed particles or from
buckling of the delivery catheter out of the target vessel during coil deployment. This complication is rare.
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b. End-organ ischemia as a result of embolization
(1) This is extremely rare for UGIB embolizations due to the rich collateral network around the stomach and
duodenum. The potential for ischemia is increased if the patient has had prior upper GI surgery because
collateral pathways may be disrupted.
(2) After superselective embolization for LGIB, minor ischemic complications occur at a rate of 2% to 20%
but include self-limited abdominal pain, asymptomatic elevation of serum lactic acid levels, or asymptomatic
mucosal changes discovered at follow-up endoscopy, most of which require no therapy. Major ischemic
complications such as bowel infarction or ischemic strictures are uncommon occurring at a rate of 0% to 6%
(4,14,15,16,17).
c. Coil erosion through the bowel wall has been reported once after an upper GI embolization, and in that
case, it led to fatal recurrent hemorrhage (20).
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Management of Complications
1. Puncture site complications
a. Hematomas are usually self-limited and require no treatment.
b. Retroperitoneal hematoma with ongoing bleeding can be life-threatening and may require surgical repair
of the puncture site. Surgery consult is indicated.
c. Pseudoaneurysm of the puncture site can often be closed by ultrasoundguided compression or injection
of thrombin.
2. Contrast reactions (see Chapter 64)
3. Arterial dissection
a. If a larger artery (such as an iliac artery) was dissected, it may be possible to place an intravascular stent
to restore a patent lumen.
b. For smaller vessels (<5 mm in diameter) stents are not a good choice because of limited patency.
Balloon angioplasty can be attempted to tack the dissection flap against the vessel wall but may also extend
the dissection.
4. Nontarget embolization
a. The need to treat the nontarget embolization depends on whether the errant emboli are lodged in a
critical vessel or one that can be sacrificed. If noncritical (like a peripheral branch of the profunda femoris),
the emboli should be left in place.
b. If the nontarget embolic blocks a critical vessel, removal should be carefully attempted. Suction with a
catheter can be used for some particulate emboli, but errant coils need to be retrieved with snares. If NBCA
glue gets into nontarget vessels, it cannot be removed. Thus, NBCA should only be used by those with
considerable expertise.
5. Ischemic complications
a. Temporary changes such as self-limited abdominal pain or asymptomatic serum lactic acid elevation
require no therapy.
b. If true bowel infarction occurs, surgical resection is generally required.
c. For more chronic ischemic complications such as bowel stricture, balloon dilation may be possible, but
resection of the strictured bowel segment may be required if there is symptomatic obstruction.
References
1. Kuhle WG, Sheiman RG. Detection of active colonic hemorrhage with use of helical CT: findings in a
swine model. Radiology. 2003;228(3):743-752.
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2. Ryan JM, Key SM, Dumbleton SA, et al. Nonlocalized lower gastrointestinal bleeding: provocative bleeding
studies with intraarterial tPA, heparin, and tolazoline. J Vasc Interv Radiol . 2001;12(11):1273-1277.
3. Kim CY, Suhocki PV, Miller MJ Jr, et al. Provocative mesenteric angiography for lower gastrointestinal
hemorrhage: results from a single-institution study. J Vasc Interv Radiol . 2010;21(4):477-483.
4. Darcy M. Treatment of lower gastrointestinal bleeding: vasopressin infusion versus embolization. J Vasc
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Interv Radiol . 2003;14(5):535-543.
5. Yata S, Ihaya T, Kaminou T, et al. Transcatheter arterial embolization of acute arterial bleeding in the
upper and lower gastrointestinal tract with N-butyl-2-cyanoacrylate. J Vasc Interv Radiol . 2013;24(3):422-
431.
6. Hur S, Jae HJ, Lee M, et al. Safety and efficacy of transcatheter arterial embolization for lower
gastrointestinal bleeding: a single-center experience with 112 patients. J Vasc Interv Radiol . 2014;25(1):10-
19.
7. Larssen L, Moger T, Bjørnbeth BA, et al. Transcatheter arterial embolization in the management of
bleeding duodenal ulcers: a 5.5-year retrospective study of treatment and outcome. Scand J Gastroenterol .
2008;43(2):217-222.
8. Padia SA, Geisinger MA, Newman JS, et al. Effectiveness of coil embolization in angiographically
detectable versus non-detectable sources of upper gastrointestinal hemorrhage. J Vasc Interv Radiol .
2009;20(4):461-466.
9. Poultsides GA, Kim CJ, Orlando R III, et al. Angiographic embolization for gastroduodenal hemorrhage:
safety, efficacy, and predictors of outcome. Arch Surg. 2008;143(5): 457-461.
10. Defreyne L, De Schrijver I, Decruyenaere J, et al. Therapeutic decision-making in endoscopically

unmanageable nonvariceal upper gastrointestinal hemorrhage. Cardiovasc Intervent Radiol . 2008;31(5):897-
905.
11. Eriksson LG, Ljungdahl M, Sundbom M, et al. Transcatheter arterial embolization versus surgery in the
treatment of upper gastrointestinal bleeding after therapeutic endoscopy failure. J Vasc Interv Radiol .
2008;19(10):1413-1418.
12. Beggs AD, Dilworth MP, Powell SL, et al. A systematic review of transarterial embolization versus
emergency surgery in treatment of major nonvariceal upper gastrointestinal bleeding. Clin Exp
Gastroenterol . 2014;7:93-104.
13. Yap FY, Omene BO, Patel MN, et al. Transcatheter embolotherapy for gastrointestinal bleeding: a single
center review of safety, efficacy, and clinical outcomes. Dig Dis Sci . 2013;58(7):1976-1984.
14. Funaki B, Kostelic JK, Lorenz J, et al. Superselective microcoil embolization of colonic hemorrhage. AJR
Am J Roentgenol . 2001;177(4):829-836.
15. Kickuth R, Rattunde H, Gschossmann J, et al. Acute lower gastrointestinal hemorrhage: minimally
invasive management with microcatheter embolization. J Vasc Interv Radiol . 2008;19(9):1289.e2-1296.e2.
16. Lipof T, Sardella WV, Bartus CM, et al. The efficacy and durability of super-selective embolization in the
treatment of lower gastrointestinal bleeding. Dis Colon Rectum. 2008;51(3):301-305.
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17. Koh DC, Luchtefeld MA, Kim DG, et al. Efficacy of transarterial embolization as definitive treatment in
lower gastrointestinal bleeding. Colorectal Dis. 2009;11(1):53-59.
18. Tan KK, Wong D, Sim R. Superselective embolization for lower gastrointestinal hemorrhage: an
institutional review over 7 years. World J Surg. 2008;32(12):2707-2715.
19. Khanna A, Ognibene SJ, Koniaris LG. Embolization as first-line therapy for diverticulosis-related massive
lower gastrointestinal bleeding: evidence from a metaanalysis. J Gastrointest Surg. 2005;9(3):343-352.
20. Ooishi T, Nishikawa J, Satake M, et al. Ulceration after arterial microcoil embolization. Gastrointest
Endosc. 2008;67(4):724.
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11
Aortoiliac Interventions
Joshua D. Kuban
Sun Ho Ahn
Timothy P. Murphy
Peripheral arterial disease (PAD) is a progressive common medical disease with a presentation that can vary
from asymptomatic to extremity gangrene. Since the first percutaneous transluminal revascularization was
performed by Dotter and Judkins in 1964, revolutionary changes have occurred in management of PAD. With
advances in angioplasty and stents, endovascular management has become the mainstay therapy for aortoiliac
arterial obstructive disease.
Indications
1. Disabling or lifestyle altering intermittent claudication—defined as reproducible pain or symptoms in the
buttocks, thighs, or calves with exertion, which subsides with rest—that is refractory to medical therapy and
lifestyle modifications
2. Critical limb ischemia: rest pain and/or tissue loss
3. The TransAtlantic Inter-Society Consensus (TASC) provides a general algorithm for surgical versus
endovascular management of aortoiliac disease (TASC II) based on lesion morphology and location (Table
11.1). Routine use of TASC II classification has fallen out of favor as emerging data supports endovascular
management of TASC C and D lesions. First-line endovascular treatment is indicated in nearly all cases of
aortoiliac disease with surgery indicated for those who fail endovascular treatment.
4. Angioplasty is indicated for concentric, noncalcified, short (<3 cm) lesions.
5. Primary stent placement is recommended for complex stenosis and chronic total occlusions (CTOs).
6. Secondary stent placement is indicated for technically unsuccessful angioplasty (residual gradient ≥5 mm
Hg or greater than 30% residual stenosis) and complications, including flow-limiting dissection and vessel
perforation.
Contraindications
There are no absolute contraindications. Relative contraindications to arteriography apply to aortoiliac
endovascular interventions.
1. Uncorrectable coagulopathy
2. History of life-threatening iodinated contrast allergy/reaction
3. Severe non-dialysis-dependent renal insufficiency
1. History and physical exam should be performed, with a focus on the vascular system. The operator should
perform the peripheral vascular exam and document locations and quality of pulses in the bilateral extremities.
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2. Pertinent noninvasive imaging (pulse volume recording [PVR], multilevel segmental lower extremity brachial
indices, computed tomographic angiography [CTA], or magnetic resonance angiography [MRA]) should be
reviewed or obtained if necessary.
3. Preprocedure laboratory evaluations should include platelet count, creatinine/glomerular filtration rate (GFR),
and coagulation profile.
4. Baseline ankle-brachial index (ABI) should be obtained prior to procedure.
5. Evaluation of acetylsalicylic acid (ASA) status for conscious sedation should be performed.
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Table 11.1 TASC II Classification for Aortoiliac Disease (19)
1. Type A—Endovascular treatment is the treatment of choice.
a. Unilateral or bilateral stenosis of common iliac artery (CIA)

b. Unilateral or bilateral single short stenosis of external iliac artery (EIA) (<3 cm)
2. Type B—Endovascular treatment is preferred.
a. Short (<3 cm) stenosis of infrarenal aorta

b. Unilateral CIA occlusion
c. Single or multiple stenoses up to 3-10 cm of EIA not extending into common femoral artery (CFA)
d. Unilateral EIA occlusion not involving the origins of internal iliac artery (IIA) or CFA
3. Type C
a. Bilateral CIA occlusions

b. Bilateral EIA stenosis, 3-10 cm long not extending into CFA
c. Unilateral EIA stenosis extending into CFA
d. Unilateral EIA occlusion involving the origins of IIA and/or CFA
e. Heavily calcified unilateral EIA occlusion with or without involvement of origins of IIA and/or CFA
4. Type D—Primary treatment traditionally is surgical repair.
a. Infrarenal aortoiliac occlusion

b. Diffuse disease of aorta and both iliac arteries requiring treatment
c. Diffuse multiple stenoses involving unilateral CIA, EIA, CFA
d. Unilateral occlusions of both CIA and EIA
e. Bilateral occlusions of EIA
f. Iliac stenosis in patients with abdominal aortic aneurysm (AAA) requiring treatment not amenable
to endograft or other lesions requiring open aortic or iliac surgery
6. Patients should halt oral intake as per institutional protocol.

7. Morning insulin dose should be reduced to half for patients for whom food is withheld.
8. If a contrast allergy exists—steroid pretreatment should be given (see Chapter 64).
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9. For non-dialysis-dependent renal insufficiency, hydration with 0.9% saline at 1 mg/kg/h for 24 hours beginning
at 2 to 12 hours prior to the procedure is recommended for patients without congestive heart failure. Although not
routinely used in our practice, sodium bicarbonate and N-acetylcysteine may be helpful, but the data are
equivocal (1). See Chapter 65.
10. Patients are started on dual antiplatelet therapy 1 week prior to intervention with 325 mg of aspirin and 75 mg
of clopidogrel daily. Otherwise, 325 mg of aspirin and 300 mg of clopidogrel (loading dose) are administered prior
to the procedure. Individual patient response to clopidogrel is not routinely evaluated.
11. Urinary bladder catheter is usually placed prior to the procedure.
12. Sterile preparation, including surgical clipping, of both inguinal regions and/or arm is performed.
13. Procedures are performed under conscious sedation with incremental intravenous aliquots of midazolam and
fentanyl with hemodynamic and respiratory monitoring.
14. Prophylactic antibiotics are not routinely administered for aortoiliac interventions performed under sterile
conditions, even for those with cardiac valve prostheses, or mitral valve prolapse or other valvulopathy.
Procedure
Diagnostic Arteriogram
1. CFA access is preferred. Left arm access may be required on occasion. For diagnostic portion of the
exam, initial contralateral CFA access is usually preferred,
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unless a CIA intervention is planned. Contralateral access allows complete imaging of the aorta, the iliac
arteries, and the distal arteries and permits precise localization of the causative lesion(s). In addition,
contralateral approach maintains the potential to intervene above or below the inguinal ligament on the
symptomatic side without performing an additional puncture. For intervention, a second or ipsilateral CFA
access may be required, especially in the case of ostial CIA lesions. When a palpable pulse is absent,
fluoroscopically guided puncture of CFA using landmarks and/or vessel calcifications can be performed.
Ultrasound is helpful for difficult cases but should be used in conjunction with fluoroscopy to avoid
inadvertent external iliac access. Preprocedure CTA or MRA can assist in determining optimal access.
2. A diagnostic arteriogram of the infrarenal aorta and lower extremity(ies) should be performed. The
diagnostic arteriogram may be tailored depending on preoperative CTA or MRA findings and/or in the
presence of renal insufficiency to reduce contrast load.
3. Lesion significance can be determined by hemodynamic gradient measurements or diameter reduction
measurement. Generally, a resting mean trans-stenotic gradient ≥5 mm Hg or a systolic gradient >10 mm
Hg is considered significant. Following augmentation by a vasodilator (e.g., 100 μg nitroglycerin given intra-
arterially), a mean gradient >10 mm Hg or systolic gradient >20 mm Hg is significant. Diameter reduction
>50% is considered significant. Hemodynamic measurements across total occlusions are unnecessary.
4. Pressure gradients are considered the gold standard and can be measured by several methods.
a. Double access simultaneous measurement above and below the lesion is most accurate.
b. Coaxial simultaneous measurement requires a 2-Fr.-sized difference between the sheath and the
catheter.
c. Pullback pressures may be unreliable and affected by temporal variation in blood pressure.
d. Pressure wires may be more accurate in smaller sized arteries due to less flow reduction by the catheter
or the sheath but add to the cost and procedure time.
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Techniques General to All Interventions
1. Once the determination to intervene has been made, systemic anticoagulation is achieved with
intravenous heparin unless contraindicated. Activated clotting time (ACT) during the procedure can be
done with a working goal of 250 seconds.
2. Intervention should be performed through an appropriately sized sheath. A 6 Fr. sheath can
accommodate most stents and balloons used in the iliac system. For contralateral intervention, a long
braided sheath (e.g., Pinnacle Destination, Terumo Medical, Somerset, NJ; or BRITE TIP, Cordis,
Bridgewater, NJ) should be advanced over the bifurcation.
3. The lesion must be crossed. Most stenoses can be negotiated with a long taper (LT) straight
guidewire and an angled-tip catheter. More complex stenoses may require a steerable hydrophilic
guidewire (e.g., Glidewire, Terumo Medical, Somerset, NJ) with a directable catheter (e.g., Kumpe,
Cook Medical, Bloomington, IN).
4. CIA lesions, especially ostial, are best treated by an ipsilateral approach, whereas EIA lesions are
best treated by a contralateral approach.
5. After lesion traversal, an appropriate-sized sheath should be placed across the lesion over an
exchange guidewire. An angioplasty balloon or stent is then positioned at the lesion and the sheath is
retracted. Angioplasty or stent placement is then performed.
6. After an intervention, an arteriogram is performed to determine technical success (<30% residual
stenosis) and to exclude complications (i.e., arterial rupture, dissection, distal embolization, etc.).
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7. Postprocedure pressure gradient may be performed. Less than 5 mm Hg mean gradient after
intervention defines technical success.
8. Puncture site hemostasis, with manual compression or a closure device, is achieved after the effects
of anticoagulation have expired (1 to 2 hours, partial thromboplastin time [PTT] <1.5 times normal, or
ACT <160 seconds).
9. Pearls
a. Always maintain guidewire purchase across the treated lesion until completion angiogram. This will
preserve treatment options in case of complication such as dissection or rupture.
b. Minimize the number of lesion traversals with wires and catheters to avoid potential distal
embolization.
Angioplasty Technique
1. Angioplasty balloon is positioned to cover the lesion. Appropriate placement of the balloon usually can be
confirmed with contrast injection via the sheath just prior to deployment, but fluoroscopic landmarks or
digital road mapping can also be done.
2. Angioplasty balloon is inflated with an inflation device until the waist is resolved. In general, 8 atm is
sufficient; however, if greater than 10 atm is required, beware of potential arterial rupture especially if the
patient reports significant pain during balloon inflation. Persistent pain after balloon deflation can be
indicative of arterial rupture, and if present, an immediate angiogram of the angioplasty site is warranted.
3. Postangioplasty arteriogram is performed to assess technical success, failure, and complications. If a
residual stenosis (>30%) or flow-limiting dissection is present, a repeat prolonged dilation or stent
placement may be required.
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Stent Placement Technique (Fig. 11.1)
1. Stent diameter should be chosen with consideration for intimal hyperplasia, which may narrow the lumen
by, on average, a millimeter. Stent length should be sufficient to cover the entire lesion. Care must be taken
when using selfexpanding stents, which tend to foreshorten after deployment. Measurements can be
obtained from a prior CTA or by using digital angiography software calibrated to an internal standard or
marker catheters.
2. Stent positioning can be confirmed with road mapping or contrast injection. The vascular sheath is
retracted and stent is deployed. For balloon-mounted stents, care should be given to ensure that stent does
not become dislodged when traversing the lesion or aortic bifurcation. Minimize this risk by crossing the
lesion with a vascular sheath that has an adequate inner diameter to ensure the safe passage of the stent.
3. Traversal of the lesion with the sheath “dotters” the stenosis and thus balloon predilation is rarely
required.
4. Balloon-mounted stents are expanded with the provided balloon, using an inflator that has a pressure
gauge. For self-expanding stents, withdrawing the outer sleeve covering the collapsed stent on the delivery
catheter initiates deployment. When unsheathing the self-expanding stent, the hand holding the inner
catheter should be stationary to avoid the tendency to advance the stent during deployment. Newer self-
expanding stents may have measured incremental retraction systems such as a wheel. Some nitinol stents
are known to “lurch” forward if redundancy isn't removed from the introducer catheter prior to unsheathing,
so it is recommended with these devices to advance the catheter beyond the desired location and then
retract the entire device into position prior to unsheathing.
5. Self-expanding stents usually require postdeployment dilation with a balloon.
6. As with angioplasty, a poststent arteriogram is mandatory.
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FIGURE 11.1 • A 55-year-old female smoker with lifestyle altering bilateral buttock and thigh claudication.
A: Digital subtraction angiogram shows a high-grade stenosis in the distal aorta with a mean gradient of 25
mm Hg. B: Balloon-expandable stent is delivered with a 12-mm scratch-resistant angioplasty balloon
(arrow), after the sheath has been retracted. C: Poststent aortogram with technical success. Patient is
symptom-free at 3 years.
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7. Lower extremity run-off or in-suite peripheral vascular clinical exam should be performed to assess for
distal thromboembolic complications.
Available Stents
1. There is a myriad of available stents for use in the aortoiliac disease and a detailed analysis is beyond
the scope of this chapter. The general categories of stents are self-expanding (SE), balloon expandable
(BE), and stent grafts (SGs).
2. Self-expanding stents are composed of nitinol or Elgiloy and possess shape memory. They are
compressed into a delivery catheter that is unjacketed at placement.
a. Advantages: SE stents generally possess greater flexibility, conformability, and trackability. Their elastic
capability allows them to be placed in segments that experience external compression.
b. Disadvantages: SE stents generally have lower hoop strength and due to foreshortening are more
difficult to precisely place, for example, bifurcation or ostial locations.
c. Examples of SE stents (selective list and not exhaustive): Zilver (Cook, Bloomington, IN) (Fig. 11.2A),
WALLSTENT (Boston Scientific, Natick, MA),
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Absolute (Guidant, Santa Clara, CA), Luminexx (C.R. Bard, Covington, GA), SMART (Cordis
Endovascular/Johnson & Johnson, Warren, NJ)
FIGURE 11.2 • A: Zilver SE stent. B: Atrium iCAST stent.
d. The Zilver PTX (Cook, Bloomington, IN) is an SE drug (paclitaxel)-eluting stent (DES) that has shown to
be effective in the femoropopliteal system but is not routinely used in the aortoiliac system (2).
3. Balloon expandable stents are typically manufactured premounted on a balloon. Larger sizes (>14 mm),
which still need hand mounting, should be placed on an appropriate-sized scratch-resistant balloon using a
crimper or by hand.
a. Advantages: BE stents possess stronger radial force, the ability for precise placement, and superior
radiopacity.
b. Disadvantages: BE stents have the potential for dislodgment from the balloon, are more rigid, and
possess plastic deformity. Use of a sheath as suggested earlier should minimize stent dislodgment. Rigidity
may be detrimental in tortuous arteries. Finally, BE stents have no elastic memory that precludes utilization
in areas of potential external compression, that is, across the inguinal ligament.
c. Examples of BE stents (selective list and not exhaustive): PALMAZ (Cordis Endovascular/Johnson &
Johnson, Warren, NJ), PALMAZ GENESIS (Cordis Endovascular/Johnson & Johnson, Warren, NJ),
Express (Boston Scientific, Natick, MA), Bridge Assurant (Medtronic, Minneapolis, MN)
4. Stent grafts (covered stents) are generally composed of synthetic material such as polyethylene
terephthalate (e.g., Dacron) or extruded polytetrafluoroethylene (PTFE) covering or lining a stent. They may
be SE or BE depending on the properties of the stent scaffold.
a. Advantages: SGs are theorized to limit restenosis by their barrier effect and are essential for the
treatment of arterial rupture or aneurysms.
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b. Disadvantages: There are limited data for SGs in aortoiliac disease, they require a larger delivery
system, and cost.
c. Examples (selective list and not exhaustive): iCAST (BE) (Atrium Medical, Hudson, NH) (Fig. 11.2B),
Fluency (SE) (C.R. Bard, Covington, GA), VIABAHN (SE) (W.L. GORE, Flagstaff, AZ), Wallgraft (SE)
(Boston Scientific, Natick, MA)
Stent Selection
Choose an appropriate stent based on lesion characteristics (diameter, location, length, calcification, and
eccentricity).
1. Diameter—Usually, stent diameters of 10 to 15 mm in the aorta (although in some cases, an 8-mm
diameter is satisfactory, e.g., small, elderly person with critical limb ischemia and severe aortic stenosis), 8
to 10 mm in the CIA, and 7 to 9 mm in the EIA are desirable. The lumen diameter achieved after stent
placement will be reduced by 0.5 to 1 mm by the development of neointimal hyperplasia within the stent,
and this must be considered when sizing stents. After the stent is incorporated into the arterial wall, a
luminal diameter of at least 6 mm is desirable. To achieve this, a minimum stent diameter of 7 mm is
preferred if the caliber of the patient's artery will accommodate.
2. Location—For ostial and aortic bifurcation lesions, BE stents may be preferred for their superior radial
strength and precise placement ability.
3. Length—Short, focal lesions are ideal for BE stents. Longer lesions or occlusions are better treated by
SE stents. Although multiple BE stents can be overlapped to treat diffuse iliac artery stenoses, their
inelasticity prevents motion in the stented artery. Pulsatile wall motion produces strains within the stents,
which may result in stent fracture due to metal fatigue. Alternatively, if the stents are not overlapped but are
placed contiguously, stent motion may result in shearing of the artery and pseudoaneurysm formation in the
gaps between stents.
4. Calcification and eccentricity—Calcified and/or eccentric atherosclerotic plaques generally require a stent
with higher radial force, that is, BE stents.
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Special Situations
1. CTOs (Fig. 11.3)
a. Most CTOs can be successfully treated with endovascular methods. Most occlusions are traversed using
an angled-tip hydrophilic guidewire and a directable catheter. Excimer laser can be used when a pilot
channel cannot be created but is rarely required.
b. In long occlusions, a trial of thrombolysis may reduce the length of occlusion, reveal stenosis, reduce
potential for emboli, and improve stent wall apposition. Disadvantages include increase in procedure time,
prolonged hospitalization, presence of chronic thrombus resistant to thrombolysis, and risks of bleeding.
Because of the chronic nature of CTOs, routine prestent thrombolysis has fallen out of favor.
c. Subintimal wire passage may be unavoidable in some cases. This is acceptable as long as re-entry into
the true lumen is gained. This may require approaching the occlusion simultaneously from both anterograde
and retrograde directions.
(1) Modified “wire-loop” technique—If a wire but not a catheter can be passed, the wire can be snared from
a contralateral approach and be tightly fixed from both ends to pass a catheter.
(2) Sharp needle recanalization may be required in certain situations when a wire cannot be passed into the
true lumen. When attempting sharp needle recanalization, (a) a compliant balloon is inflated as a target, (b)
the distance between the target balloon and the sharp needle should be minimized, (c) indentation effect on
the balloon should be confirmed and viewed on multiple projections, and (d) contrast should be injected in
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the tract prior to stent placement to ensure that the location is subintimal and has not perforated the artery.
(3) Re-entry devices (e.g., Outback Ltd, Cordis Endovascular/Johnson & Johnson, Warren, NJ) or
intravascular ultrasound (IVUS) may be useful.
2. Aortic bifurcation lesions
a. These include stenosis and/or occlusion involving the origin(s) of the CIA(s) and a distal abdominal aortic
plaque extending to the ostia of the CIA(s). A supporting stent may be required in the contralateral CIA even
if there is no hemodynamically significant stenosis there. In this case, the contralateral stent protects the
contralateral ostium from compression by the ipsilateral therapeutic stent and may also minimize turbulent
flow. Alternatively, a low compliance angioplasty balloon can be inflated in the nonstenotic CIA to stabilize
the stent placement and protect the ostium.
b. Technique—Stent placement in the distal abdominal aorta should be done only after consideration of the
origin of the inferior mesenteric artery and the status of the superior mesenteric, celiac, and hypogastric
arteries. Ideally, the intervention should preserve the inferior mesenteric artery (IMA) origin; however, this is
not always possible. An appropriate length vascular sheath should be inserted via each CFA. Digital road
mapping or real-time hand injection through one of the sheaths is critical for precise deployment of stents at
the aortic bifurcation. Ideal positioning of stents is less than 5 mm cephalad to the aortic bifurcation.
Extension of stents into the aorta should be limited as durability of the procedural result will be reduced.
Stents should be deployed using a “kissing stent technique,” that is, simultaneous balloon inflation while
attempting to keep inflation pressures equal during deployment.
3. Coexistent CFA stenosis—In cases with CFA stenosis, in addition to ipsilateral iliac artery disease, CFA
endarterectomy should be considered to preserve durability of the iliac intervention. Surgery should ideally
be done at the time of, or at the least during the same hospital admission as, the aortoiliac intervention
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to reduce the risk of stent thrombosis. Alternatively, percutaneous transluminal (balloon) angioplasty (PTA)
or atherectomy may be considered for CFA lesions.
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FIGURE 11.3 • A 58-year-old man with Leriche syndrome. A: Digital subtraction arteriogram shows distal
aortic occlusion. Delayed images (not shown) showed concomitant bilateral common iliac occlusions with
right EIA stenosis. More importantly, common femoral arteries were preserved as were infrainguinal arteries.
B: Although wire (from right) and catheter (left) appear to be touching, oblique views (not shown) showed
that they were in different planes. True lumen re-entry was not possible for the right common iliac occlusion
from a right retrograde approach. C: After a wire was passed from the contralateral approach from the left, it
was snared from the right side access and pulled out of the right sheath. (continued)
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FIGURE 11.3 • (Continued) D: After catheters were advanced into the aorta via each end of the wire, stents
were deployed over wires advanced into the aorta from both accesses. Poststent angiogram shows
successful endovascular recanalization.
1. Selected patients with uncomplicated interventions may be safely discharged the same day of the procedure,
although most may require overnight observation.
2. Serial vascular exams and ABI are performed in the recovery area.
3. In the presence of renal insufficiency, the authors perform overnight hydration.
4. Patients are seen in follow-up in the office within 1 to 4 weeks and then longitudinally.
5. There is controversy regarding use and duration of single and dual antiplatelet administration after stent
placement (3). After stent placement, the authors routinely continue 75 mg of clopidogrel for 1 to 3 months and
81 mg or 325 mg of aspirin indefinitely.
6. Smoking cessation, lipid optimization, and blood pressure reduction should be aggressively pursued, either by
the treating interventionist or in conjunction with the primary care physician (4).
7. All patients with PAD should be on a statin, regardless of lipid profile, with few exceptions (e.g., chronic liver
disease, statin-induced myopathies).
8. If patient was on cilostazol preprocedure, this should be continued (5).
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Results
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Intervention, Medical Therapy, and Exercise
1. Stenting technical success and patency
a. Overall high technical success varying somewhat with lesion type (6)
(1) TASC A to C, 94% to 100%; TASC D, 85% to 90%
b. Primary patency rates vary between reports but overall are 90%, 75%, 70%, and 50% at 1, 3, 5, and
10 years, respectively. Long-term secondary patency rates are substantially higher—90%, 80%, and
65% at 3, 5, and 10 years, respectively (7,8,9).
c. Traditionally complex lesions (TASC C/D) have a 10% lower patency rate; more recent studies
suggest similar patency rates.
d. Balloon angioplasty alone has lower patency rates compared with stenting with 75%, 60%, and 50%
primary patency at 1, 3, and 5 years (10).
2. Claudication: Exercise versus Endoluminal Revascularization (CLEVER) prospective randomized
trial (11)
a. There were 111 patients randomly assigned to optimal medical care (OMC group), supervised
exercise plus optimal medical care (SE group), or stent revascularization plus optimal medical care (ST
group).
b. Change in peak walking time for SE was significantly greater than ST. Both were significantly
greater than OMC.
c. Quality of life measurements and validated walking scores greater for ST than SE.
d. Supervised exercise programs are few in number and usually not covered by insurance, limiting
generalizability of results.
3. Meta-analysis has shown improved ABI and treadmill walking times when stenting is added to
medical therapy and supervised exercise. However, there was no significant difference between
stenting alone and supervised exercise alone (12).
Stenting versus Angioplasty

1. The Dutch Iliac Stent Trial (DIST) randomized patients to primary angioplasty with secondary stent
placement, or primary stent placement for iliac disease (13).
a. There was no significant difference in short-term or long-term patency.
b. However, the primary PTA with selective stent group had a high number of secondary stent placement
(43%) and higher complication rates (4% vs. 7%).
2. Meta-analysis of 14 series (6 angioplasty and 8 stent) of 2,116 patients showed better results with stent
placement compared with angioplasty (14).
a. Technical success rate was higher for stent group: 96% versus 91%.
b. Four-year patency rate was higher for stent group: 77% versus 64%.
c. Complications and mortality rates were not significantly different.
Stent Grafts versus Bare-Metal Stents
1. Retrospective study of iCAST (Atrium Medical, Hudson, NH) SG versus baremetal stent (BMS) (15).
a. Improved 1- and 2-year primary patency for SG versus BMS (92% and 92% vs. 78% and 62%,
respectively)
b. Sustained positive clinical outcome in 85% of patients treated with SG at 21 months compared with 54%
treated with BMS
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2. Prospective, randomized trial comparing covered BE stent graft versus BMS (Covered Versus Balloon
Expandable Stent Trial [COBEST]) (16)
a. Freedom from restenosis greater with SG than BMS at 18 months (95.4% vs. 82.2%)
b. SG resulted in lower amputation and complication rate than BMS (1.2% vs. 3.6% and 4.8% vs. 10.7%,
respectively)
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FIGURE 11.4 • Left EIA rupture. A: Poststent placement angiogram reveals brisk extravasation of contrast
from the EIA (arrow). B: Balloon was immediately placed for tamponade (arrow). Contrast injection from
above and below confirming correct placement and adequate tamponade. C: No further extravasation after
stent-graft placement. Patient recovered well and is without claudication at 2 years.
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c. Subgroup analysis revealed significant advantages for TASC C and D lesions but not for TASC B
lesions.
3. Conversely, a retrospective study compared SG and BE BMS in 162 patients (17).
a. Three-year primary patency (89% vs. 72%), assisted primary patency (98% vs. 90%), and secondary
patency (98% vs 92%) all significantly better in the BMS group.
b. SG 2.5 times more likely to require repeat intervention.

1. Society of Interventional Radiology (SIR) definition of major complications— those complications requiring
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therapy or minor hospitalization (<48 hours); require major therapy, unexpected increase in level of care, or
prolonged hospitalization; result in permanent sequelae or death
2. A meta-analysis of 1,300 iliac PTA and 816 iliac stent patients showed all-inclusive 30-day mortality rates of
1% and 0.8%, respectively. The rates of major complications requiring therapy for PTA and stent groups were
4.3% and 5.2% (14).
3. Major complications include arterial rupture, dissection, thromboses, distal embolization, access site
hematoma and pseudoaneurysm, and stent infections.
a. Arterial ruptures (Fig. 11.4):
(1) Aortoiliac interventions are rarely complicated by arterial ruptures. Rates between 0.8% and 0.9% have been
reported.
(2) Usually diagnosed during the procedure as patients may report persistent pain after intervention, or
extravasation of contrast may be seen. Patient resuscitation should be begun immediately with intravenous
fluids, pressure support medications, reversal of anticoagulation with protamine sulfate, and transfusions as
required. A balloon should be immediately inflated to a low pressure (3 to 4 atm) covering the rupture site, and
contrast should be injected above and below to ensure appropriate seal. An SG may be required to exclude the
rupture. Emergent surgical management may be needed, if the above fails.
b. Dissections: may occur during catheterization, PTA, or stenting. If a flow limitation is seen, the flap may be
sealed with PTA or a stent.
c. Distal embolization: Most emboli may be resolved with catheter suction, aspiration devices (e.g., AngioJet,
[Boston Scientific, Natick, MA] and Indigo System, [Penumbra Medical, Alameda, CA]), and thrombolytics.
Traditional surgical open thrombectomy may be required in severe rare cases.
d. Access site pseudoaneurysm and hematoma: See Chapter 4.
e. Stent infections: occur rarely but may have devastating results including limb loss or death. Darcy reported
eight documented cases in his review, but this is likely an underestimate (18). Fever, pain, and positive blood
cultures are clues for stent infection. Pseudoaneurysm formation and sepsis may ensue. Aggressive antibiotic
administration is imperative, and surgical exploration may be warranted.
References
1. Barrett BJ, Parfrey PS. Clinical practice. Preventing nephropathy induced by contrast medium. N Engl J
Med. 2006;354(4):379-386.
2. Dake MD, Ansel GM, Jaff MR, et al. Sustained safety and effectiveness of paclitaxeleluting stents for
femoropopliteal lesions: 2-year follow-up from the Zilver PTX randomized and single-arm clinical studies. J
Am Coll Cardiol . 2013;61(24):2417-2427.
3. Allemang MT, Rajani RR, Nelson PR, et al. Prescribing patterns of antiplatelet agents are highly variable
after lower extremity endovascular procedures. Ann Vasc Surg. 2013;27(1):62-67.
4. Westin GG, Armstrong EJ, Bang H, et al. Association between statin medications and mortality, major
adverse cardiovascular event, and amputation-free survival in patients with critical limb ischemia. J Am Coll
Cardiol . 2014;63(7):682-690.
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5. Warner CJ, Greaves SW, Larson RJ, et al. Cilostazol is associated with improved outcomes after
peripheral endovascular interventions. J Vasc Surg. 2014;59(6):1607-1614.
6. Ye W, Liu CW, Ricco JB, et al. Early and late outcomes of percutaneous treatment of TransAtlantic Inter-
Society Consensus class C and D aorto-iliac lesions. J Vasc Surg. 2011;53(6):1728-1737.
7. Schürmann K, Mahnken A, Meyer J, et al. Long-term results 10 years after iliac arterial stent placement.
Radiology. 2002;224(3):731-738.
8. Timaran CH, Prault TL, Steven SL, et al. Iliac artery stenting versus surgical reconstruction for TASC
(TransAtlantic Inter-Society Consensus) type B and type C iliac lesions. J Vasc Surg. 2003;38(2):272-278.
9. Ye K, Lu X, Yin M, et al. Midterm outcomes of stent placement for long-segment iliac artery chronic total
occlusions: a retrospective evaluation in a single institution. J Vasc Interv Radiol . 2013;24(6):859-864.
10. Kudo T, Chandra FA, Ahn SS. Long-term outcomes and predictors of iliac angioplasty with selective
stenting. J Vasc Surg. 2005;42(3):466-475.
11. Murphy TP, Cutlip DE, Regensteiner JG, et al. Supervised exercise versus primary stenting for
claudication resulting from aortoiliac peripheral artery disease: six-month outcomes from the claudication:
exercise versus endoluminal revascularization (CLEVER) study. Circulation. 2012;125(1):130-139.
12. Ahimastos AA, Pappas EP, Buttner PG, et al. A meta-analysis of the outcome of endovascular and
noninvasive therapies in the treatment of intermittent claudication. J Vasc Surg. 2011;54(5):1511-1521.
13. Tetteroo E, van der Graaf Y, Bosch JL, et al. Randomised comparison of primary stent placement versus
primary angioplasty followed by selective stent placement in patients with iliac-artery occlusive disease.
Dutch Iliac Stent Trial Study Group. Lancet. 1998;351(9110):1153-1159.
14. Bosch JL, Hunink MG. Meta-analysis of the results of percutaneous transluminal angioplasty and stent
placement for aortoiliac occlusive disease. Radiology. 1997;204(1):87-96.
15. Sabri SS, Choudhri A, Orgera G, et al. Outcomes of covered kissing stent placement compared with bare
metal stent placement in the treatment of atherosclerotic occlusive disease at the aortic bifurcation. J Vasc
Interv Radiol . 2010;21(7):995-1003.
16. Mwipatayi B, Thomas S, Wong J, et al. A comparison of covered vs bare expandable stents for the
treatment of aortoiliac occlusive disease. J Vasc Surg. 2011;54(6):1561-1570.
17. Humphries MD, Armstrong E, Laird J, et al. Outcomes of covered versus baremetal balloon-expandable
stents for aortoiliac occlusive disease. J Vasc Surg. 2014;60(2):337-343.
18. Darcy M. Complications of iliac angioplasty and stenting. Tech Vasc Interv Radiol . 2000;3(4):226-239.
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19. Jaff MR, White CJ, Hiatt WA, et al. An update on methods for revascularization and expansion of the
TASC lesion classification to include below-the-knee arteries: a supplement to the inter-society consensus
for the management of peripheral arterial disease (TASC II). Catheter Cardiovasc Interv. 2015;86(4):611-
625.
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12
Superficial Femoral Artery Interventions
Ripal T. Gandhi
Jonathan J. Iglesias
James F. Benenati
Technology has rapidly advanced in the last several years, and the endovascular options available to treat
superficial femoral artery (SEA) disease have markedly increased. Although percutaneous transluminal (balloon)
angioplasty (PTA) was previously considered the initial therapy for treatment of femoropopliteal disease, this
therapy is being replaced with bare-metal stents, covered stents, drug-eluting stents, and drug-eluting balloons,
which have shown improved patency rates and outcomes. Atherectomy can be performed as an adjunct and may
be valuable in
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the treatment of in-stent restenosis. As new clinical trials emerge, the precise role of each of these new
technologies in the ever-expanding SFA endovascular landscape continues to evolve.
Indications
1. Lifestyle-limiting moderate to severe claudication (Fontaine category IIb, Rutherford stages 2 and 3) in
patients who have failed medical management (i.e., cilostazol and/or exercise program)
2. Critical limb ischemia (CLI) characterized by rest pain, nonhealing ulcerations, or gangrene
3. Pre- or post-bypass surgery to increase inflow or outflow
4. Salvage of failing bypass graft with significant flow-limiting stenosis of the anastomosis or outflow vessels
Contraindications
There are no absolute contraindications to endovascular therapy for the SFA. Most of the contraindications
listed below are relative.
2. Severe renal insufficiency (glomerular filtration rate [GFR] <30) in the absence of hemodialysis. Patient
should be hydrated, contrast use minimized, and carbon dioxide angiography should be considered.
3. Active phase of vasculitis
4. Nonambulatory critically ill patients with limited life expectancy and/or dementia
5. Patients who have mild claudication symptoms
6. Unfavorable anatomy
a. SFA occlusion with involvement of the popliteal artery and trifurcation vessels
b. Hemodynamically significant common femoral artery (CFA) disease. A combined femoral endarterectomy
with endovascular treatment of the SFA or femoropopliteal bypass is recommended. Common femoral
angioplasty and/or atherectomy may be considered in patients who are not surgical candidates. Stenting of
the CFA is not desirable and may preclude future surgical options.
c. Significant calcification involving a long SFA segment, especially “coral reef” calcification
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d. Absent runoff via at least one vessel to the foot
e. Presence of hemodynamically significant inflow disease, which cannot be corrected by endovascular or
surgical means
f. Severe aneurysmal disease at intended access site
1. Obtain preprocedure physiologic studies with an arterial noninvasive examination with and without exercise
(exercise exam not performed in patients with critical limb ischemia) including baseline ankle-brachial index (ABI)
values, segmental plethysmography with pulse volume recordings, and toe pressures when appropriate.
a. Preprocedural imaging with computed tomography (CTA) or magnetic resonance angiography (MRA) can be
utilized to develop a patient-specific course of treatment. Cross-sectional imaging is valuable in determining
access site and to plan the procedure, which may ultimately allow for a safer procedure with reduced contrast
and radiation exposure.
2. Preangiography preparation: Verify stable renal function relative to baseline. Emergent or nonpostponable
procedures in patients with impaired kidney
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function necessitate the use of preventative measures such as aggressive hydration with or without concomitant
acetylcysteine. Ascertain allergy history to contrast mediums and treat as needed.
3. Premedication: All patients should be on antiplatelet therapy with aspirin and/or clopidogrel.
a. Per the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial, there was a profound
superiority in patients with peripheral arterial disease (PAD) treated with clopidogrel over aspirin in the
prevention of stroke, myocardial infarction, and vascular death (1). As a result of this trial, many advocate that
clopidogrel be the antiplatelet medication of choice in the PAD population given that the safety profile of this drug
is at least as good as aspirin.
b. All patients treated with drug-eluting balloons and drug-eluting stents require dual antiplatelet therapy for a
short period of time. Per instructions for use, a minimum duration of dual antiplatelet therapy is 1 month and 2
months for Lutonix drug-eluting balloon (Bard, New Providence, NJ) and Zilver PTX drug-eluting stent (Cook
Medical, Bloomington, IN), respectively.
c. In patients who were not previously on antiplatelet mediations, a loading dose of 81 mg of aspirin and 300 mg
of clopidogrel can be given at the time of the procedure.
d. Whether all patients should be treated with dual antiplatelet therapy remains controversial and continues to
evolve; this decision should be patient-specific, and the risks of vascular occlusion must be balanced with risk of
hemorrhage.
Procedure
1. Obtain initial arterial access.
a. A contralateral common femoral approach is the norm for SFA procedures; however, this approach may
not be feasible in patients with a steep native aortic bifurcation, prior endovascular aneurysm repair, or
aortobifemoral bypass.
b. Ipsilateral antegrade access is advantageous if tibial interventions are also necessary provided the
patient's body habitus and CFA anatomy allow it.
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c. If the occlusion involves the origin of the SFA or the very proximal SFA, a contralateral approach is
generally required.
d. In patients with proximal SFA occlusion and significant disease in the contralateral CFA, a popliteal or
distal SFA access may be considered.
e. At the current time, devices are not of sufficient length to perform mid to distal SFA interventions via an
upper extremity brachial or radial access.
f. Tibiopedal arterial puncture may be used in conjunction with antegrade or contralateral common femoral
access in recanalizing complex occlusions.
2. Perform initial angiography including distal runoff.
a. Multiple views may be required to establish a vascular map exhibiting the exact location and morphology
of some lesions.
b. We generally perform both anteroposterior and lateral views of the foot in patients without renal
insufficiency prior to intervention to establish a baseline.
3. Generally, stenoses of more than 50% are considered hemodynamically significant in symptomatic
patients.
a. Orthogonal views and correlation with noninvasive imaging and physiologic studies are of paramount
importance.
b. Although pressure wires may be utilized to determine the hemodynamic significance of questionable
lesions, this is rarely performed in the femoropopliteal segment.
4. Anticoagulation during interventions
a. Patients are generally anticoagulated with either heparin or bivalirudin when performing endovascular
intervention to minimize risk of intraprocedural
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thrombus. Patients with SFA stenosis are anticoagulated prior to crossing the lesion, whereas patients with
chronic occlusions are anticoagulated immediately after successful crossing of lesion.
(1) Typically, a heparin bolus dose of 70 to 100 units per kg is given with approximately 1,000 IU per hour
subsequently.
(2) Bivalirudin dosing is as follows: initial bolus of 0.75 mg per kg followed by standard infusion of 1.75
mg/kg/h. Infusion dose is reduced to 1.0 mg/kg/h in patients with renal insufficiency (GFR 10 to 29 mL per
minute) and to 0.25 mg/kg/h in patients on dialysis.
b. Activated clotting time >250 seconds is recommended prior to SFA interventions.
c. The unpredictability associated with heparin therapy has popularized the use of direct thrombin inhibitors
(bivalirudin) in more extensive lower extremity interventions as these drugs circumvent the pitfalls
associated with heparin therapy.
(1) Unlike heparin, bivalirudin cannot be reversed with protamine; however, it does have a short half-life of
approximately 25 minutes.
(2) Because bivalirudin is excreted in the urine, it is important to note that its half-life is increased in patients
with renal insufficiency. In patients with GFR between 10 and 29, half-life is approximately 57 minutes.
5. Technique for crossing an SFA occlusion
a. Before treatment can be initiated, a guidewire must cross the lesion. In 80% to 85% of SFA occlusions,
only a catheter and guidewire are necessary to successfully recanalize the lesion.
b. Although there are a multitude of guidewires and catheters on the market and every operator has his or
her favorites, the technique described here is that preferred by the authors. A.035 system is recommended
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to cross the majority of SFA occlusions. A.035 Cerebral Newton LLT Guidewire (Cook Medical,
Bloomington, IN) in conjunction with a straight or angled catheter is our initial guidewire of choice in
crossing SFA occlusions. If this guidewire is not successful in crossing the lesion, hydrophilic guidewires
such as an angled GLIDEWIRE (Terumo, Somerset, NJ) or Roadrunner (Cook Medical, Bloomington, IN)
are employed. It is desirable to achieve an intraluminal path across the lesion (Fig. 12.1).
c. There are a variety of chronic total occlusion (CTO) crossing devices available on the market; however,
there are no randomized clinical studies assessing the safety and efficacy of these devices.
(1) Crossing devices include Viance (Covidien/Medtronic, Mansfield, MA), TruePath (Boston Scientific,
Natick, MA), Crosser (Bard, New Providence, NJ), FRONTRUNNER XP (Cordis, East Bridgewater, NJ),
Wildcat (Avinger, Redwood City, CA), and Ocelot (Avinger, Redwood City, CA). The latter device utilizes
optimal coherence tomography to help direct the device and achieve intraluminal crossing.
(2) Most of the crossing devices require that an occlusion has not been previously manipulated with a
catheter and guidewire as the devices have a tendency to follow the same path created by the guidewire.
(3) Because the majority of femoropopliteal occlusions can be crossed successfully with a guidewire and
catheter and there is an up-front cost to utilizing CTO devices, we generally do not utilize these devices. A
study comparing conventional guidewire techniques to CTO devices, focusing on end points including
crossing success, cost, time to recanalization, need for re-entry, and complications would be valuable.
d. If the lesion cannot be crossed intraluminally, a subintimal approach (Bolia technique) will be used.
(1) A guidewire loop (typically with a hydrophilic.035 guidewire) is formed and advanced subintimally with a
catheter until reaching or opposite
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a patent arterial segment. It is important to limit the extension of the subintimal dissection beyond the
occlusion because this may result in loss of important collaterals.
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FIGURE 12.1 • A: Nonselective arteriogram in a 75-year-old woman with claudication (left > right) showing
occlusion of both SFAs. B: Left SFA was recanalized advancing a wire loop through the occluded segment.
C,D: SFA was then balloon dilated and stented with good flow. (Courtesy of Razavi MK, Gilbert M, and
Razavi M)
(2) If still subintimal, attempts will be made to re-enter the true lumen with the guidewire and catheter.
(3) If this is unsuccessful, re-entry devices are extremely helpful in achieving controlled re-entry into the true
lumen. (Fig. 12.2)
(a) There are a multitude of re-entry devices available on the market including the OUTBACK (Cordis, East
Bridgewater, NJ), Pioneer (Volcano, San Diego, CA), OffRoad (Boston Scientific, Natick, MA), and Enteer
(Covidien/Medtronic, Mansfield, MA).
(b) Advantages of re-entry devices include increased technical success; ability to treat more complex
lesions (Trans-Atlantic Inter-Society Consensus [TASC] C and D); and the potential for decreased
procedure time, contrast dose, and fluoroscopy time.
(4) Patency rates after subintimal angioplasty are comparable to intraluminal angioplasty.
e. If the guidewire very easily crosses an SFA occlusion (known as the “guidewire test”), there is likely
acute thrombus, and the patient should generally be treated with thrombolysis or mechanical thrombectomy
prior to further endovascular intervention to minimize risk of distal embolization.
(1) Thrombolysis will generally uncover an underlying lesion, which is typically shorter than the initial
occlusion.
(2) Covered stents may be used in the presence of small amounts of acute thrombus; however, there is a
risk of distal embolization, and an embolic protection device should be considered if this strategy is
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entertained.
6. SFA intervention following crossing lesion/occlusion: Once the wire has been advanced across the
stenoses/occlusions, it is critical to perform an angiogram to confirm an intraluminal position.
a. For lesions <5 cm, PTA using appropriately sized balloons may be performed. For longer and more
complex lesions, we generally favor drug-eluting balloons, bare-metal stents, drug-eluting stents, or covered
stents over PTA.
b. If stenting, angioplasty with a balloon 1 mm in diameter less than the diameter of the target vessel should
be performed prior to introduction of the stent. Following placement of stent, postdilatation is performed to
the diameter of the native artery.
c. If the plan is to use a drug-eluting balloon, the vessel should initially be predilated with a conventional
balloon (PTA) matching the diameter of the artery. If there is a good angiographic result (i.e., no flow-limiting
dissection, <30% residual stenosis), the drug-eluting balloon may be subsequently advanced and dilated.
The initial angioplasty prevents loss of drug coating during advancement of the balloon.
d. If there is significant residual stenosis or dissection after PTA, the lesion should be stented.
e. For very long lesions (i.e., > 20 cm), covered stents (VIABAHN, GORE Medical, Flagstaff, AZ) are
favored.
f. If atherectomy is being considered, an embolic protection device is favored.
g. The precise algorithm and choice of device for SFA disease continues to evolve. See “Results” section
for review of the data on the various SFA endovascular technologies.
7. Final angiography must be performed after intervention to confirm there is no residual stenosis. It is
essential to perform runoffimaging as well to ensure that there has not been distal embolization from the
procedure.
8. Vasospasm
a. Vasospasm is not uncommon when performing endovascular interventions and is more likely to occur
when treating small vessels and with poor runoff.
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FIGURE 12.2 • A 78-year-old woman with severe left lower extremity claudication. Selective angiogram
confirmed occlusion of left SFA (A) with reconstitution of popliteal artery (B). Re-entry into the true lumen
was achieved by using OUTBACK (Cordis, Inc, East Bridgewater, NJ) device. OUTBACK is positioned next
to the reconstituted segment (C) and actuator applied projecting a nitinol needle into the adjacent flow
lumen (arrow) (D). (continued)
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FIGURE 12.2 • (Continued) SFA was then balloon dilated and stented (E and F). (Courtesy of Razavi MK,
Gilbert M, and Razavi M)
Nitroglycerin 100 to 300 μg, intra-arterial bolus, is our medication of choice if vasospasm is observed.
b. Blood pressure should be monitored closely when administering vasodilating medications.
1. If manual compression is used to achieve hemostasis at access site, activated clotting time (ACT) should be
less than 180 seconds to minimize risk of bleeding. We generally do not reverse heparin with protamine unless
there is a bleeding complication as there is a risk of anaphylaxis.
2. Closure devices impart a benefit in reducing the time to patient ambulation. See Chapter 3 for more
information.
3. Although there is no consensus with regard to dual antiplatelet therapy, lifelong antiplatelet therapy with
aspirin (81 mg) or clopidogrel (75 mg) is essential in all patients with PAD. As previously stated, patients who are
treated with drugeluting balloon or stents require dual antiplatelet therapy for a short period of
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time (1 month for Lutonix drug-eluting balloon, 2 months for Zilver PTX [Cook Medical, Bloomington, IN] per
instructions for use [IFU]).
4. Risk factor modification is mandatory with a focus on aggressive management of diabetes, hypertension,
hyperlipidemia, and smoking. Unless there is a contraindication or allergic reaction, all patients should be
prescribed a statin medication. Statins have been shown to decrease cardiovascular mortality in patients with
PAD.
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5. Although there are no standard guidelines, surveillance after treatment of femoropopliteal disease is advised.
A noninvasive arterial examination with measurement of the ABIs following intervention is recommended to
establish a postintervention baseline. Clinic visits with or without duplex follow-up studies should be considered
at 1, 3, 6, and 12 months, and yearly thereafter. Patient with CLI may require more frequent follow-up.
Results
SFA treatment is rapidly evolving. Although some general recommendations are provided, there is clinical
equipoise in many areas, and the interventionalist must remain up to date as new clinical data changes the
treatment approach.
1. Balloon angioplasty (PTA). According to the RESILIENT clinical trial, angioplasty and bare-metal stenting
were equivalent for lesions <5 cm in length (2). PTA alone should be reserved for these short lesions
provided that a flowlimiting dissection does not occur.
2. Bare-metal stents (BMS)
a. The RESILIENT trial compared PTA to BMS placement in the femoropopliteal segment with mean lesion
length of 64 mm and 71 mm, respectively. The 12-month primary was 36.7% in the PTA group and 81.3% in
the stent group with freedom from target lesion revascularization (TLR) of 45.1% and 87.3% (2). At 3 years,
freedom from TLR (75.5% vs. 41.8%) and clinical success (63.2% vs. 17.9%) were significantly improved in
the stent group (3). A 4.1% stent fracture rate was observed at 18 months.
b. Supera stent (Abbott Vascular) is a newer generation BMS made with a flexible and strong interwoven
wire technology utilized for the treatment of SFA and proximal popliteal disease. The Comparison of the
SUpera PERipheral System in the Superficial Femoral Artery (SUPERB) clinical trial, which evaluated this
stent in lesions with a mean length of 7.8 cm, demonstrated 1-year primary patency of 78.9%. Freedom from
TLR was 89%, 84%, and 82% at 1,2, and 3 years, respectively (4). Patency rates were decreased when
stents were inadvertently elongated beyond nominal during deployment. Stent fracture rate was 0.6% at 3
years.
3. Drug-eluting stents (Zilver PTX, Cook Medical, Bloomington, IN) have been shown to be superior to both
balloon angioplasty and provisional BMS placement. In the Zilver PTX randomized clinical trial, 5-year
freedom from TLR was 83.1% for the Zilver PTX group compared to 67.6% for the standard group, which
included optimal angioplasty and provisional stent placement (5). In addition, primary patency at 5 years
was 66.4% for the drug-eluting stent group compared to 43.4% for the standard group, representing a 41%
reduction in restenosis. Stent fracture rate was 1.9% at 5 years. At the time of this writing, this is the only
clinical trial for SFA disease with 5-year follow-up.
4. Drug-eluting balloons (DEB) have better patency than standard angioplasty balloons.
a. The IN.PACT SFA randomized clinical trial demonstrated higher 1-year patency rate of DEB (IN.PACT
Admiral, Medtronic) versus standard angioplasty (89.8% vs. 66.8%). TLR was 2.4% in the DEB arm versus
20.6% in the latter (6). Mean lesion length were similar between both groups (8.9 cm vs. 8.8 cm).
b. U.S. Food and Drug Administration (FDA) approval of the Lutonix DEB in 2014 (as the first approved
DEB in the United States) is on the basis of the
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LEVANT 2 clinical trial, which demonstrated a 29.4% improved primary patency of the Lutonix DEB (Bard)
compared to PTA (73.5% vs. 56.8%) at 1 year (7). Mean lesion length in this trial was 63 mm. DEB may
become the new standard of care in the treatment of TASC A and B lesions, which do not have significant
calcification.
c. The role of DEB in longer TASC C and D lesions remains to be seen; stenting may be necessary with
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flow-limiting dissections and significant residual stenosis (>30%) in these cases.
5. Covered stents/stent grafts. Long-segment disease (>20 cm) is best treated with a covered stent
(VIABAHN, GORE, Flagstaff, AZ) in the presence of adequate runoff.
a. According to the VIABAHN endoprosthesis with heparin bioactive surface in the treatment of superficial
femoral artery obstructive disease (VIPER) trial, which evaluated lesions with a mean length of 19 cm, there
was a 73% primary patency rate of the VIABAHN which was not affected by the diameter or length (<20 cm
vs. >20 cm) of the device. If the stent grafts were oversized greater than 20% in diameter compared to the
native vessel diameter, the patency rates were decreased (8).
b. The multicenter, prospective Viabahn endoprosthesis with PROPATEN bioactive surface versus bare
nitinol stent in the treatment of long lesions in superficial femoral artery occlusive disease (VIASTAR) trial
randomized patients to the VIABAHN versus BMS with mean lesion length of 19 cm in the former and 17.3
cm in the latter (9). The overall primary patency rate at 1-year was 78% in the VIABAHN group versus 54%
in the BMS group; for lesion length >20 cm, patency rates were 73% versus 33%, respectively. This study
provides level 1 evidence that long SFA lesions are likely best treated with a stent graft.
(1) For optimal results, predilatation should be performed prior to the deployment of this device and post
stent-graft deployment PTA requires the utilization of balloons matching the diameter of the device used.
(2) There has been some concern that coverage of collaterals from a covered stent may result in an
increased incidence of acute limb ischemia when there is occlusion of the stent. However, the incidence of
acute limb ischemia after covered stent occlusion is no higher than that observed after BMS occlusion.
6. Atherectomy
a. There are several atherectomy devices available on the market. These include SilverHawk and
TurboHawk (Covidien/Medtronic, Mansfield, MA), Diamondback (Cardiovascular System Inc, St. Paul, MN),
Jetstream (Pathway Medical, Garden Grove, CA), Turbo-Elite and Turbo-Tandem (Spectranetics Inc,
Colorado Springs, CO), Phoenix (Volcano, San Diego, CA), and Crosser (Bard, New Providence, NJ).
b. According to the DEFINITIVE LE study, directional atherectomy with the SilverHawk or TurboHawk
device is a safe and effective therapy for patients with claudication and CLI (10). The 12-month primary
patency rate was 78% with no difference between patients with diabetes and patients without diabetes.
Complications included distal embolization (3.8%), perforation (5.3%), and abrupt closure (2.0%) with a
bailout stent rate of 3.2%.
c. In the authors' institution, atherectomy is generally not used as primary therapy for SFA disease, although
debulking may be helpful for certain clinical scenarios enumerated below:
(1) Adjunctive treatment of heavily calcified disease, especially “coral reef” and eccentric calcification, which
may not be adequately treated with angioplasty or stenting alone
(2) Treatment of lesions in the CFA, profunda femoral artery, and popliteal artery where stenting is not ideal
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(3) Treatment of in-stent restenosis in conjunction with other modalities. FDA has cleared the Turbo-
Tandem and Turbo Elite laser atherectomy devices (Spectranetics Inc, Colorado Springs, CO) to be used in
conjunction with PTA. According to the EXCImer Laser Randomized Controlled Study for Treatment of
FemoropopliTEal In-Stent Restenosis (EXCITE ISR) multicenter, randomized clinical trial, laser atherectomy
with PTA demonstrated improved procedural success compared to PTA alone (93.5% vs. 82.7%). Average
lesion length was 20 cm (11).
d. Vessel perforation is a known complication of atherectomy and is often the result of aggressive cutting of
plaque. Care must be taken during debulking, and covered stent may be necessary should a significant
perforation be encountered.
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e. Distal embolization is not uncommon during atherectomy procedures. An embolic protection device is
recommended when performing atherectomy. At the time of this writing, the only FDA-approved embolic
protection device in the periphery is the SpiderFX (Covidien/Medtronic, Mansfield, MA). The authors prefer
the NAV6 Emboshield embolic protection device (Abbott Vascular, Santa Clara, CA), which must be loaded
onto a 315-cm .014 Barewire (Abbott Vascular, Santa Clara, CA) to be utilized in the periphery.
Complications
1. Interventions of the femoropopliteal vessels carry a complication rate up to 10%, with 3% to 4%
necessitating treatment.
2. Access site complications are common and include hematoma, pseudoaneurysm, arteriovenous fistula
(AVF), vascular occlusion, and retroperitoneal hemorrhage. The latter is usually due to inadvertent “high
puncture” of the external iliac artery (above the inguinal ligament). Special care must be taken when
performing antegrade common femoral puncture to avoid external iliac puncture. Ultrasound-guided arterial
access is beneficial.
3. Distal thromboembolism resulting in vascular occlusion. Factors predisposing to thromboembolism
include acute limb ischemia with thrombus, inadequate anticoagulation during intervention, treatment of long
occlusions, and atherectomy.
4. Flow-limiting dissection is more common after aggressive balloon dilatation.
5. Arterial rupture/perforation. Perforation may be due to guidewire, CTO device, atherectomy device, or
aggressive dilatation with balloon or stent. Patients with underlying collagen vascular disease, vasculitis,
and on chronic steroids are at increased risk.
6. Infection
7. Contrast-induced nephropathy (CIN), especially in patients with baseline compromised renal function.
See Chapter 65.
1. Access site including pseudoaneurysm and AVF—see Chapter 4.
a. Retroperitoneal hemorrhage due to puncture of the external iliac artery may present as a life-threatening
complication because the access site cannot be adequately compressed and closure devices typically will
not work through the inguinal ligament. Recognition of the problem followed by reversal of anticoagulation
and immediate placement of a covered stent or surgery are crucial. Volume expansion, blood transfusion,
and vasopressors may be needed if the patient becomes hemodynamically unstable.
2. Distal embolization may be treated with aspiration thrombectomy, thrombolysis, or surgical Fogarty
balloon thromboembolectomy.
a. Aspiration thrombectomy may be performed with a large profile guide catheter, specially designed
aspiration catheters, or rheolytic thrombectomy.
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b. Administration of nitroglycerin may help differentiate whether occlusion is due to embolization versus
vasospasm.
c. It is critical to ensure that the patient is adequately anticoagulated by checking the ACT.
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3. Flow-limiting dissection
a. Initially treated with prolonged low-pressure balloon angioplasty in an attempt to tack down the dissection
flap
b. Flow-limiting dissections which fail to resolve with prolonged angioplasty are treated with a stent.
4. Arterial rupture/perforation should be immediately tamponaded with a balloon, and consideration should
be given to reversing anticoagulation if the perforation is large.
a. If this strategy is not successful in resolving the bleeding, placement of a covered stent is recommended.
b. Small guidewire perforations during crossing of an occlusion are not uncommon and can be self-limited.
c. If significant bleeding occurs from a small branch or subintimal tract, coil embolization may be considered
if the occlusion has not been crossed.
References
1. CAPRIE Steering Committee. A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of
ischaemic events (CAPRIE). Lancet. 1996;348:1329-1339.
2. Laird JR, Katzen BT, Scheinert D, et al. Nitinol stent implantation versus balloon angioplasty for lesions in
the superficial femoral artery and proximal popliteal artery: twelve-month results from the RESILIENT
randomized trial. Circ Cardiovasc Interv. 2010;3:267-276.
3. Laird JR, Katzen BT, Scheinert D, et al. Nitinol stent implantation vs. balloon angioplasty for lesions in the
superficial femoral artery and proximal popliteal arteries of patients with claudication: three-year follow-up
from the RESILIENT randomized trial. J Endovasc Ther. 2012;19(1):1-9.
4. Garcia L. The SUPERB Trial: 3-year results. Paper presented at: Vascular Interventional Advances (VIVA)
Conference; November 5, 2014; Las Vegas, NV.
5. Dake M. The Zilver PTX randomized trial of paclitaxel-eluting stents for femoropopliteal artery disease: 5-
year results. Paper presented at: Vascular Interventional Advances (VIVA) Conference; November 5, 2014;
Las Vegas, NV.
6. Tepe G. 12-Month data from the randomized multicenter IN.PACT SFA Trial. Paper presented at: Charing
Cross Conference; March 2014; London, United Kingdom.
7. C.R. Bard, Inc. 1-year results of the LEVANT 2 trial. Paper presented at: FDA Circulatory System Devices
Advisory Panel; June 12, 2014; Murray Hill, NJ.
8. Saxon RR, Chervu A, Jones PA. Heparin-bonded, expanded polytetrafluoroethylenelined stent graft in the
treatment of femoropopliteal artery disease: 1-year results of the VIPER (Viabahn Endoprosthesis with
Heparin Bioactive Surface in the Treatment of Superficial Femoral Artery Obstructive Disease) trial. J Vasc
Interv Radiol . 2013;24(2): 165-173.
9. Lammer J, Zeller T, Hausegger KA, et al. Heparin-bonded covered stents versus baremetal stents for
complex femoropopliteal artery lesions: the randomized VIASTAR trial (Viabahn endoprosthesis with
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PROPATEN bioactive surface [VIA] versus bare nitinol stent in the treatment of long lesions in superficial
femoral artery occlusive disease). J Am Coll Cardiol . 2013;62:1320-1327.
10. McKinsey JF, Zeller T, Rocha-Singh KJ, et al. Lower extremity revascularization using directional
atherectomy: 12-month prospective results of the DEFINITIVE LE study. JACC Cardiovasc Interv.
2014;7(8):923-933.
11. Dippel EJ, Makam P, Kovach RC, et al. TCT-531 EXCITE ISR: A prospective, randomized controlled trial
of excimer laser atherectomy vs balloon angioplasty for the treatment of femoropopliteal in-stent restenosis. J
Am Coll Cardiol . 2014;64(11S):10.
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13
Infrapopliteal Arterial Interventions
Mahmood K. Razavi
Introduction
Below-the-knee (BTK) arterial interventions are almost exclusively performed in the setting of chronic critical limb
ischemia (CLI). Although peripheral arterial disease (PAD) is a common condition, CLI occurs in only about 10%
of patients with PAD (1). The term CLI should only be used when symptoms are caused by ischemic conditions.
Diagnosis is confirmed by measurement of ankle-brachial index (ABI), toe pressures (TP), and/or transcutaneous
oxygen pressure (TcPO2).
Definition of Critical Limb Ischemia

CLI refers to chronic rest pain requiring analgesics or opioids (Rutherford-Becker category 4) and tissue loss
resulting from severe ischemia (Rutherford-Becker categories 5 and 6). In patients with rest pain, the ankle
pressure is usually ≤50 mm Hg (TP ≤30 mm Hg). In those with tissue loss, ankle pressure should be ≤70 mm Hg
(TP ≤50 mm Hg) to be classified as CLI. Although the Rutherford-Becker classification is now known to be
insufficient to classify patients with CLI, it is used in this chapter because of its simplicity and wide recognition.
Differential Diagnosis
Pain
1. Diabetic neuropathy: often described as “burning” which is worse at night with symmetrical distribution in
feet or legs. Other signs and symptoms of neuropathy are often present.
2. Complex regional pain syndrome: formerly known as sympathetic dystrophy; patients often have normal
arterial flow.
3. Peripheral sensory neuropathy: Isolated sensory neuropathy can be caused by various conditions such
as vitamin B12 deficiency, syringomyelia, alcohol toxicity, and other toxins such as some chemotherapeutic
agents.
4. Nerve root compression: Various spinal conditions can give rise to continuous leg pain. There is usually
no evidence of ischemia.
5. Thromboangiitis obliterans (Buerger disease): usually occurs in younger smokers. The etiology is distal
ischemia due to an inflammatory vascular disease involving both arteries and vein.
Foot Ulceration
1. Venous ulcers: usually occur above the forefoot (ankle and calf) with adequate arterial flow
2. Diabetic foot ulcers: can be divided into three general categories: ischemic, neuropathic, and
neuroischemic. Neuropathic is the more common form of diabetic foot ulcers.
3. Mixed arterial and venous: The location is usually malleolar causing mild pain as opposed to purely
ischemic ulcers that are usually more distal and cause severe pain.
4. Skin infarcts: usually due to systemic disease or thromboembolism
Indications
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1. Arterial disease in the setting of rest pain or tissue loss
a. Depending on the availability of expertise, endovascular approach can be and often is the first-line
therapy for revascularization in CLI.
b. Surgical bypass can be reserved for failures of endotherapy.
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Contraindications
Absolute
1. Contraindications to angiography
Relative
1. Advanced anatomic disease such as long segment occlusion involving the trifurcation (Fig. 13.1A). The
rationale revolves more around the futility of endotherapy rather than true contraindications in such cases.
1. Similar to any other patient undergoing catheter angiography
2. Ensure adequate hydration unless presence of end-stage renal disease or congestive heart failure prevents
aggressive hydration.
3. General anesthesia can make the procedure easier. Patients with CLI often experience severe pain and
cannot hold their legs and feet in one position for prolonged periods.
4. Preprocedural antiplatelet therapy is mandatory if there are no contraindications. Dual antiplatelet therapy with
aspirin and a thienopyridine is recommended when patients can tolerate them.
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FIGURE 13.1 • Digital subtraction arteriogram in a 78-year-old man with rest pain. A: Occluded SFA, popliteal
and proximal trifurcation arteries. B: Delayed imaging demonstrates the reconstitution of peroneal and posterior
tibial arteries.
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5. Optimal medical therapy for comorbidities such as diabetes, hypertension, infection, heart failure, and pain
should continue.
6. Imaging: Noninvasive duplex examination with hemodynamic measurements is the standard preprocedural
imaging. Magnetic resonance angiography (MRA) and computed tomographic angiography (CTA) are useful
preprocedural imaging tools to better delineate BTK arterial anatomy in centers where both the technical and
diagnostic expertise exists. CTA can be limited in BTK applications due to the presence of dense calcifications in
small-caliber vessels.
Procedure
1. Arterial access: Three anatomic sites can be used. Regardless of the approach, the tip of the access
sheath/guide catheter should be placed as close to the diseased area as possible to gain maximal torque
and forward force advantage.
a. Contralateral common femoral artery (CFA): preferred in patients with hostile groins (e.g., scarring from
prior surgery), morbid obesity with large pannus, or high occlusion of the superficial femoral artery (SFA), all
of which make an antegrade ipsilateral approach difficult
b. Ipsilateral CFA: the preferred approach in most patients with BTK disease excluding the situations
described earlier. Antegrade CFA access:
(1) Allows better manipulation and improved pushability of wires/catheters/devices
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(2) Allows a shorter distance to the target lesions
(3) Below-the-ankle lesions can be treated with better advantage.
(4) In case of complications such as thromboembolism, proximity to the target site improves ability to
aspirate through shorter catheters.
c. Tibiopedal access: can be utilized if attempts at antegrade recanalization of chronic total occlusions
(CTO) fail (2). Dedicated pedal access needles and sheaths (4 Fr. or 5 Fr.) make this approach more
practical. Ultrasound-guided access is the preferred method, but direct access using fluoroscopic or
angiographic images can also be utilized (Fig. 13.1B). The author uses pedal access as the sole
interventional approach only in case of failure of antegrade approaches. Others use pedal access in
patients with severe back pain or respiratory compromise who cannot tolerate flat positions for long (3).
2. Crossing the lesions: can be difficult and time-consuming in the BTK territory. This is especially true of
long segment CTO because the vessels are often calcified, small-caliber, and effective re-entry devices for
these specific arteries do not currently exist. A variety of specialty wires and support catheters have been
developed to assist in such lesions. The optimal devices and approaches are in continuous evolution.
a. Specialty wires—have robust tips and high-performance compatible support catheters. Some operators
prefer 0.018 in. wires in combination with compatible crossing catheters. The 0.014 in. wires, however,
have emerged as the preferred choice in the majority of cases. Several companies including Abbott
Vascular, Terumo, Asahi, Boston Scientific, and Cook make wires that are particularly well suited for BTK
interventions. They have different performance characteristics, and no wire has been shown to be superior
to another. Their use remains the operator's preference. Interventionists should become familiar with these
wires to be able to choose their favorite platform.
b. Support catheters—have improved pushability, trackability, and high longitudinal support characteristics.
Current examples of dedicated BTK support catheters include Rubicon (Boston Scientific, Natick, MA),
speX (ReFlow Medical, San Clemente, CA), Seeker (Bard Peripheral Vascular, Tempe, AZ), TrailBlazer
(Covidien, Plymouth, MN), Quick-Cross (Spectranetics, Colorado Springs, CO), Minnie (Vascular Solutions,
Minneapolis, MN), CXI catheters (Cook Medical, Bloomington, IN), and Tornus (Asahi Inc, Santa Ana, CA).
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c. Crossing tools—Occasionally passage of wires through long segment occluded calcified lesions is not
possible using specialized support catheters. Hence, some manufacturers have developed BTK crossing
tools to assist with recanalization of long segment CTO. Current examples include Viance (Covidien,
Plymouth, MN), Crosser (Bard Peripheral Vascular, Tempe, AZ), TruePath (Boston Scientific, Natick, MA),
Turbo-Elite laser catheter (Spectranetics, Colorado Springs, CO), Wingman (ReFlow Medical, Mission
Viejo, CA), KittyKat (Avinger, Redwood City, CA), and PowerWire (Baylis Medical, Montréal, Quebec,
Canada).
3. Treatment tools: Once the target lesions have been crossed, the stenoses must be treated.
a. Angioplasty—the mainstay of therapy in BTK (often referred to as “plain old balloon angioplasty” or
POBA). Most manufacturers make high-performance balloons of various diameters and lengths for BTK
applications. The longest balloon that best matches the diseased segment should be used. Care should be
taken to closely match the diameter of the balloon to that of the nondiseased adjacent segment.
Undersizing balloon diameter is a common mistake that can lead to recoil or suboptimal results.
b. Debulking—for example, rotational or directional atherectomy, or laser. All current debulking systems in
the market have dedicated BTK tools. Although the author prefers “front-cutting” atherectomy devices,
experience and comfort level of the operator should determine which device is used. There is currently no
data proving the superiority of one debulking system to another in BTK interventions.
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c. Drug-coated balloons (DCB), bare-metal stents (BMS), drug-eluting stents (DES), or bioabsorbable drug-
eluting vascular scaffolds (BVS)—dedicated DES, DCB, or BVS for tibial vessels do not currently exist in
the United States. Coronary BMS and DES are used off-label when stents are needed. Another off-label
BMS is the Xpert stent (Abbott Vascular, Santa Clara, CA), which is a 4 Fr. compatible self-expanding nitinol
stent that is supplied in diameters 3 to 8 mm.
d. Specialty balloons
(1) Angioplasty-resistant lesions can be treated by either the Flextome Cutting Balloon (Boston Scientific,
Natick, MA) or AngioSculpt scoring balloon (Spectranetics, Colorado Springs, CO), which are designed to
overcome such lesions. Due to its lower profile, AngioSculpt is more suited to crossing the BTK lesions.
(2) A specialty balloon that is designed to theoretically reduce angioplasty trauma is the Chocolate Balloon
(TriReme Medical, Pleasanton, CA). Studies to investigate the long-term outcome of this technology are
currently ongoing.
4. Procedural pharmacology: Intraprocedural anticoagulation can be accomplished by heparin with a target
activated clotting time above 250 seconds. An alternative anticoagulant is bivalirudin, which is administered
intravenously at standard doses. The more precise and predictable anticoagulation properties of bivalirudin
may be preferable when treating patients with infrainguinal long segment CTO.
1. Management of patients with CLI is best done in a multispecialty setting. Optimal wound care, management of
pain and infection, and active risk factor modification are all integral parts of the optimal treatment of patients with
CLI.
2. Patients with foot ulceration should be evaluated in wound-care centers and treated accordingly before and
after the revascularization procedure.
3. Postprocedure antiplatelet therapy is continued indefinitely. Dual antiplatelet can be discontinued 3 months
after the procedure with continuation of monotherapy. It should be noted that there are no current standards for
dual antiplatelet therapy in CLI patients.
4. Follow-up imaging using duplex arterial evaluation should be done at regular intervals according to the routine
of treating physician and reimbursement
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policies of the local payers. Evaluation outside of the routine windows must be performed if there is persistence
or recurrence of symptoms.
Results
1. Limb salvage and control of pain and infection—Various studies have documented 1-year limb salvage
rate of 70% to 90% in such patients using different endo-revascularization strategies, which is similar to
surgical bypass outcomes.
a. A meta-analysis of the results of randomized trials comparing various treatments for BTK vessels showed
no significant difference in limb salvage rates and hence recommended treatment with POBA with bailout
stenting using BMS when possible (4). It should be noted that limb salvage is a relatively insensitive tool to
measure incremental differences between various technologies and techniques.
2. Patency, wound healing, improvements in Rutherford-Becker classification, and rate of target lesion
revascularization (TLR)—there are differences between different techniques and devices in BTK
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intervention.
a. Although DCB use was associated with improved patency (73% vs. 26% at 1 year) in the DEBATE-BTK
trial (5), the larger IN.PACT DEEP randomized trial failed to show any difference between the POBA and
DCB (6).
b. There are currently two ongoing international prospective randomized trials to investigate the outcome of
DCB versus POBA (Lutonix BTK and Illuminate BTK). Results of these two trials will likely determine the
utility of DCB in BTK territory.
c. Use of DES appears to improve 1-year patency, wound healing, and event-free survival as well as
reduce restenosis and need for reintervention as compared to POBA in relatively short lesions (7,8).
3. Given the current uncertainty of optimal endovascular treatment for patients with CLI, local results and
individual experiences will likely determine the strategy used. Results of ongoing trials should clarify the role
of various devices in the treatment of patients with CLI.
Complications
1. The most common complications are those related to catheter angiography such as access site
complications and kidney injury.
2. Vascular injury such as rupture is rare and can be treated by placement of stent grafts, BMS, or
prolonged balloon inflation. In case of failure or unsuitability, surgical intervention may be needed.
Embolization of the vessel can also be performed, especially if the artery was occluded to begin with.
3. Acute failures of intervention can also occur depending on the devices used and the operator experience.
a. Inability to cross an occluded segment occurs in 5% to 10% of cases (9). In this scenario, tibiopedal
access can often be successful in achieving recanalization. Technical details of instrumentation and
approaches to such are beyond the scope of this writing and can be found elsewhere (2).
b. Other causes of acute failure include thrombosis, dissection, and recoil. The latter is common in BTK
interventions, and use of debulking devices, prolonged inflation at high pressure, cutting/scoring balloons,
and placement of stents have all been shown to improve acute results (9).
References
1. Hiatt WR. Medical treatment of peripheral arterial disease and claudication. N Engl J Med.
2001;344(21):1608-1621.
2. Razavi MK, Kafai NM. Re-entry and wire snaring techniques in CLI interventions. In: Mustapha J, ed.
Critical Limb Ischemia: CLI Diagnostics and Interventions. Malvern, PA: HMP Communications, LLC; 2014:
chap 16.
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3. Mustapha JA, Saab F, McGoff T, et al. Tibio-pedal arterial minimally invasive retrograde revascularization
in patients with advanced peripheral vascular disease: the TAMI technique, original case series. Catheter
Cardiovasc Interv. 2014;83(6):987-994.
4. Jens S, Conijn AP, Koelemay MJ, et al. Randomized trials for endovascular treatment of infrainguinal
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arterial disease: systematic review and meta-analysis (Part 2: Below the knee). Eur J Vasc Endovasc Surg.
2014;47(5):536-544.
5. Liistro F, Porto I, Angioli P, et al. Drug-eluting balloon in peripheral intervention for below the knee
angioplasty evaluation (DEBATE-BTK): a randomized trial in diabetic patients with critical limb ischemia.
Circulation. 2013;128(6):615-621.
6. Zeller T, Baumgartner I, Scheinert D, et al; for IN.PACT DEEP Trial Investigators. Drug-eluting balloon
versus standard balloon angioplasty for infrapopliteal arterial revascularization in critical limb ischemia: 12-
month results from the IN.PACT DEEP randomized trial. J Am Coll Cardiol . 2014;64(15):1568-1576.
7. Fusaro M, Cassese S, Ndrepepa G, et al. Drug-eluting stents for revascularization of infrapopliteal

arteries: updated meta-analysis of randomized trials. JACC Cardiovasc Interv. 2013;6(12):1284-1293.
8. Katsanos K, Spiliopoulos S, Diamantopoulos A, et al. Systematic review of infrapopliteal drug-eluting

stents: a meta-analysis of randomized controlled trials. Cardiovasc Intervent Radiol . 2013;36(3):645-658.
9. Razavi MK, Mustapha JA, Miller LE. Contemporary systematic review and meta-analysis of early outcomes
with percutaneous treatment for infrapopliteal atherosclerotic disease. J Vasc Interv Radiol .
2014;25(10):1489-1496.
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14
Acute Limb Ischemia: Pharmacomechanical and Thrombolytic
Therapy
M. Fuad Jan
Mark W. Mewissen
Intra-arterial Catheter-Directed Thrombolytic Therapy

Pioneered by Dotter in the 1970s, intra-arterial (IA) thrombolysis has become a routine medical practice in the
emergent treatment of an acutely ischemic limb with the goal of rapidly restoring blood flow to the endangered
limb (Fig. 14.1). Prethrombolytic angiography also helps identify the underlying culprit lesion(s) for treatment by
surgery and/or percutaneous endovascular methods.
Indication
Thrombotic or embolic occlusion(s) of native arteries or bypass grafts with newonset claudication or limb-
threatening ischemia (Table 14.1) (1,2,3,4). Both acute (less than 14 days' duration) and chronic thrombi
are amenable to treatment (5).
Contraindications
Absolute (1,2,3,4)
1. Active or recent internal bleeding including gastrointestinal bleeding (within 10 days)
2. Irreversible limb ischemia with major tissue loss or permanent nerve damage (severe sensorimotor loss,
paralysis/muscle rigor)
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FIGURE 14.1 • Algorithm for the evaluation and management of acute limb ischemia (ALI). Once diagnosed,
anticoagulation is initiated with subsequent treatment depending on classification of the ALI. Initial options
include catheter-directed thrombolysis (CDT) with or without percutaneous mechanical thrombectomy
(PMT) or surgical revascularization. Clinical categories of ALI include limbs that are (a) viable, with no
immediate threat of tissue loss, intact muscle power and sensations, and audible arterial/venous Doppler
signals; (b) marginally threatened, with a threat of tissue loss, minimal or no sensory loss, intact muscle
power weak, and often inaudible arterial Doppler signals but intact venous Doppler signals (treated
promptly, these limbs are salvageable; these limbs afford time for vascular imaging); (c) immediately
threatened and need prompt attention without delay and manifest as limbs with sensory (more than the
toes) and motor loss (mild to moderate) with inaudible arterial Doppler signals but audible venous Doppler
signals; these limbs are salvageable; and (d) irreversibly ischemic or nonviable, with major tissue loss,
profound sensory and motor loss (paralysis), and inaudible arterial/venous Doppler signals.
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Table 14.1 Classification of Acute Limb Ischemia
Rutherford Category Prognosis Sensory Muscle Arterial Venous

Class Loss Weakness Doppler Doppler
I Viable limb Not None None Audible Audible

(Reversible immediately
ischemia) threatened
IIA Salvageable Salvageable if Minimal None Often Audible

(Reversible limb: promptly (toes) or inaudible
ischemia) threatened revascularized none
marginally
IIB Salvageable Salvageable if More than Mild to Usually Audible

(Reversible limb: immediately toes and moderate inaudible
ischemia) threatened revascularized associated
immediately with rest
pain
III Nonviable Limb loss or Profound Profound None None

(Irreversible limb permanent anesthetic paralysis
ischemia) damage with loss (rigor)
major tissue
loss or
permanent
nerve damage
inevitable
From Rutherford RB, Baker JD, Ernst C, et al. Recommended standards for reports dealing with
lower extremity ischemia: revised version. J Vasc Surg. 1997;26:517-538.
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3. Recent stroke (arbitrary guideline: transient ischemic attack [TIA] within 2 months or cerebrovascular
accident [CVA] within 6 months; some prefer to wait up to 12 months)
4. Intracranial neoplasm or recent neurosurgery (within 3 months)
5. Protruding mobile left heart thrombus
Relative (1,2,3,4)
Although thrombolysis is not usually considered in the following conditions, clinical decision making revolves
around the anticipated benefit and attendant risks. Careful clinical evaluation and sound judgment in patient
selection, especially elderly patients, are essential.
1. History of gastrointestinal bleeding
2. Recent major nonvascular surgery (10 days), including biopsy
3. Recent trauma
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4. Recent (10 days) episode of cardiopulmonary resuscitation (CPR)
5. Severe uncontrolled high blood pressure (BP) (systolic BP >180 mm Hg or diastolic BP >110 mm Hg)
6. Emboli from cardiac source (obtain echocardiogram if suspected)
7. Subacute bacterial endocarditis
8. Coagulopathy
9. Pregnancy and postpartum period (<10 days)
10. Severe cerebrovascular disease
11. Diabetic hemorrhagic retinopathy
1. Good-quality noninvasive imaging (color Doppler ultrasound, multidetector computerized tomography,
or magnetic resonance angiography) “may” have an important role prior to the initiation of IA thrombolysis
by defining the distribution of disease.
2. Standard laboratory evaluation includes hematocrit (Hct)/hemoglobin (Hgb) (>10 gm per dL and 30% by
volume), platelet count (>100,000 per μL), baseline blood urea nitrogen (BUN)/creatinine (Cr), prothrombin
time (PT) with international normalized ratio (INR), partial thromboplastin time (PTT) (alternatively, activated
clotting time [ACT]), and fibrinogen levels (optional).
3. Access site selection: Review of previous angiograms is useful for planning the access site. Occlusive
disease can be approached from either the contralateral or the ipsilateral side. An ipsilateral antegrade
approach may avoid catheter manipulation, facilitating complementary techniques like aspiration
thromboembolectomy and balloon dilation. Careful direct puncture of a graft is usually risk-free; an axillary
artery puncture should be avoided when thrombolytic therapy is anticipated.
Procedure
1. After obtaining the desired IA access and placing an IA sheath, a baseline arteriogram is performed
to document the extent of the thrombus and arterial disease (Fig. 14.2).
2. After identifying the occlusion and deciding on IA thrombolysis (Fig. 14.3), the 5 Fr. short sheath
(typically used initially) is replaced with a 6 Fr. crossover sheath (when possible, place tip of sheath in
the external iliac artery, in case of occlusion of all lower extremity branches).
3. Attempt is next made to traverse the occlusion (using an angled 0.035-in. hydrophilic wire with or
without the help of a smaller-size angled catheter, e.g., Bernstein/glide/Quick-Cross Support Catheter
[Spectranetics, Colorado Springs, CO]). Progress is monitored by periodic angiography, and catheter
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position is adjusted appropriately. Oblique views may help find the entry orifice of the thrombus. Once
through, the wire is advanced across the thrombus well distally, and the catheter is advanced over it in
order to allow exchange for a more sturdy wire.
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FIGURE 14.2 • Arteriographic patterns typically corresponding to clinical acute ischemia categories: (I)
Viable limbs often show a single segmental occlusion with patent collaterals and reconstitution of calf
runoff vessels; (II) threatened limbs can have tandem lesions in series or in parallel with patent
collaterals and reconstitution of calf runoff vessels; and (III) irreversibly ischemic limbs have extensive
parallel thrombotic occlusions, occluded collaterals, and no distal reconstitution of runoff vessels.
(Borrowed from McNamara TO. Thrombolysis as an alternative initial therapy for the acutely ischemic
limb. Semin Vasc Surg. 1992;5:89-98.)
4. After estimating the length of the occlusion, a thrombolytic infusion catheter is placed over the
guidewire. Typically, the infusion catheter should cover the length of the occlusion and leaving a 2- to
5-cm area at either end.
a. A thrombus that is resistant to passage of a standard guidewire (guidewire traversal test or GWTT)
is probably chronic and may be difficult to dissolve (6,7). However, this should not discourage an
attempt at thrombolysis (1,2,3,4,5). If the catheter tip cannot be successfully placed within the
thrombus, it may be placed proximal to it for a short trial of (regional) lytic therapy. This may soften the
proximal thrombus for a later attempt at intrathrombic catheter placement.
b. Failure to place the catheter within the thrombus (intrathrombic catheter position) decreases the
likelihood of a technically successful lysis (2,3).
5. Catheter selection: A variety of infusion catheters (e.g., Cragg-McNamara Valved Infusion catheter
[Covidien, Plymouth, MN] and MicroMewi infusion catheter [Covidien, Plymouth, MN]) with different
catheter and infusion lengths are available. The catheters are typically used for slow, continuous
infusion of the thrombolytic.
6. Thrombolytic agents (see Table 14.2 for dose administration): CDT relies on diffusion of the agent
into the thrombus, a slow process that requires a high concentration gradient to drive the reagent into
the clot.
a. Several thrombolytic agents have been described in the literature, and currently none has U.S. Food
and Drug Administration (FDA) approval for use in peripheral arteries or veins. Prospective randomized
trials comparing the agents directly are limited and thus do not yield a meaningful comparison.
(1) UK was the most commonly used agent in the United States, but it is no longer available. rt-PA has
been more widely used in Europe (8). The
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literature on thrombolytic therapy reflects these preference patterns (2). Reteplase (rt-PA), a
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recombinant deletion mutant of rt-PA, is currently the most widely used thrombolytic agent in the United
States for peripheral vascular applications (9).
FIGURE 14.3 • Stages of IA thrombolysis. A: An occluded segment of vessel is demonstrated

arteriographically. B: A coaxial catheter is introduced through the IA sheath and advanced into the
proximal thrombus, and a guidewire is then advanced to the distal end of the thrombus (GWTT). C: A
tip-occluded multiside-orifice catheter is advanced into the entire thrombus, which is saturated with a
lacing dose of lytic agent deposited by rapid pulse-spray infusion. (Alternatively, an end-hole catheter
or a catheter with fewer distal side-holes is advanced distally and then retracted proximally while
depositing small doses of lytic agent at each site.) D: Continuous infusion is administered with an end-
hole catheter with its tip in the proximal thrombus and a smaller side-hole catheter that is advanced
much farther into the clot. (A distal untreated segment of thrombus is shown here, but a side-hole
catheter, with its tip occluded, may be advanced so as to bathe the thrombus with lytic agent
throughout its length.) E: As thrombolysis progresses, both catheters may be advanced, but with this
configuration, the inner catheter alone may be advanced into the receding thrombus front. The process
continued until the entire thrombus is dissolved and an underlying obstructing lesion is uncovered for
treatment by angioplasty or surgery.
(2) The general consensus is that UK and rt-PA are equally efficacious and safe (2,5,8), and that both
are superior to SK for treating peripheral arterial occlusions (2,3,8). Tissue-plasminogen activator
produces more rapid early lysis than UK (4,5,10). Although experience with peripheral thrombolysis
using rt-PA is limited, the efficacy and safety profile appears to be acceptable (9).
b. Intrathrombic lacing involves depositing concentrated agent into the thrombus using multiple side-
hole catheters and the pulsed-spray technique (2,3,11,12). High-dose intrathrombic lacing of the agent
saturates the thrombus and significantly decreases treatment duration, total dose, and complication
rates (12). Lacing is started distally, and the catheter is progressively retracted proximally. Some
advocate leaving a distal plug of thrombus in place in order to avoid possible embolization caused by
the forced infusion. Others lace the entire thrombus in order to reestablish flow quickly.
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Table 14.2 Popular Dosing Schemes for Treatment of Peripheral Arterial Occlusions
with Thrombolytic Agentsa
Agent Plasma Concentration Dosing Scheme Systemic

Half- Heparin
life
(min)
Streptokinase 30 1,500 IU/mL Intrathrombic lace: 20,000- May be needed

(SK) 50,000 IU Infusion: 5,000 early; perhaps
(Kabikinase, IU/h (optional) unnecessary or
Kabi, Inc) optional
beyond 12 h
Urokinase 15 3,000 IU/mL Intrathrombic lace: Full therapeutic

(UK) 250,000-500,000 IU dose
(Abbokinase, Infusion: 4,000 IU/h × 2 h;
Abbott 2,000 IU/h × 2 h then
Laboratories) 1,000 IU/h for duration
(optional)
rt-PA 5 0.2 mg/mL Intrathrombic lace: 5-10 Subtherapeutic

(Alteplase, mg Infusion: 0.5-1.0 mg/h (2,500 U IV
Genentech, (optional) bolus + 500
Inc) U/h IV infusion);
optional
Reteplase 15 0.5 U/mL Intrathrombic lace: 2-5 U Subtherapeutic;

(Retevase, Infusion: 0.5-1.0 U/h optional
Centocor Inc) (optional)
rt-PA, recombinanttissue plasminogen activator; IV, intravenous.

aFor a more complete listing and descriptions, please see references 2, 4, and 9.
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Small distal emboli of thrombus usually dissolve with continued infusion of the lytic agent (2,3).
c. Slow continuous IA infusion, especially after significant clot resolution and restoration of flow, is
determined as required in individual cases.
7. Concomitant intravenous anticoagulation: Heparin is given as an IV bolus dose of 70 U per kg
and then as a continuous IV infusion at 600 to 1,200 U per hour (1,2,3,4) to prevent thrombus
formation around an occlusive catheter. This may be initiated as soon as the thrombus is crossed with
a guidewire.
a. Heparin should be adjusted to maintain either the PTT or ACT (1,2,3) in the therapeutic range.
However, several operators use a lower rate heparin infusion at a fixed rate of 500 U per hour (2,4,8)
to maintain PTT in the lower range (40 to 50 seconds).
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b. Interactions between heparin and lytic agents can cause precipitate formation (data from Abbott
Laboratories, Abbott Park, IL; and Genentech Inc, San Francisco, CA), and so the two drugs should
not be mixed together prior to administration (4).
8. Ultrasound-enhanced thrombolysis: It has been demonstrated that acoustic microstreaming
created by ultrasound pulses augments the transportation of the lytic agent, disseminating it
throughout the clot. Ultrasound during thrombolysis enhances the thrombolytic process by accelerating
the contact of the lytic agent with the thrombus (13). Energy transmitted by the ultrasound waves also
separates/loosens the fibrin strands, increasing the surface area of the thrombus and making more
thrombus available to the lytic agent. The EKOS infusion catheter (EKOS Corp, Bothell, WA), which is
based on these principles and FDA-approved (for peripheral pulmonary artery use), is guided over a
standard 0.035-in. wire. Once positioned within the thrombus, the guidewire is replaced by the
ultrasound core consisting of miniaturized ultrasound transducers that deliver pulsed high-frequency
(2-MHz), low-power ultrasound waves. Both the infusion catheter and the ultrasound core wire are
attached to a catheter interface cable, which in turn is connected to the system control unit, which may
be used to identify when blood flow is reestablished and thus signaling when angiographic
reassessment should be performed.
1. Pressure bandage at site of catheter entry; puncture site is checked every 30 minutes for 4 hours and then
every 2 hours during infusion.
2. Patients are usually managed in the intensive care or step-down unit and vital signs monitored frequently per
institutional thrombolysis protocol. Extremity pulses (palpation/Doppler) are checked every 4 hours or more
frequently as clinically indicated.
3. Laboratory monitoring
a. Hct, PT and PTT/ACT every 2 hours twice and then as needed
b. Desired PTT is 2.0 to 2.5 times control level (with a control level of 35 seconds, target PTT would be 70 to 90
seconds or lower as per operator preference). The ACT should be around 300 seconds during lytic therapy.
4. Fluid input/output and serum Cr are monitored closely.
5. Intramuscular injections are best avoided during this period.
6. Heparinized saline (1,500 U heparin in 500 mL normal saline solution [NS]) is used via outer coaxial catheter
(at keep vein open [KVO] rate), if this catheter is not being used for lytic agent.
7. In case of fever, acetaminophen is suggested, not aspirin.
8. The patient is usually returned to the laboratory for repeat angiogram in 4 to 12 hours to check for dissolution
of the thrombus or as deemed necessary clinically.
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9. Therapy is terminated on evidence of successful recanalization (angiographic resolution with clinical
improvement, return of Doppler signals), complication, or failure.
a. Both the lytic agent and heparin are discontinued. The infusion catheter is removed over a guidewire
(maintaining wire access across the site of occlusion). Heparinized saline infusion is continued via the IA sheath.
A check angiogram may be performed.
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b. Attempts to treat the underlying obstructing lesion(s) promptly by percutaneous endovascular methods or
surgery (1,2,3,4) should be undertaken as soon as possible.
c. Once definitive endovascular treatment has been undertaken (angioplasty/stent), the sheath can be removed,
or when ACT is <160 seconds. For earlier removal (1 to 2 hours), if PTT or ACT is elevated, protamine sulfate,
30 mg slow IV infusion, may be given, barring contraindications. Alternatively, a percutaneous puncture-site
closure device can be used.
d. IV anticoagulation can be restarted in 4 to 6 hours (after removal of IA sheath and successful groin
compression), if peripheral thrombus was from an embolic source, or if anticoagulation needs to be continued
until surgery or conversion to oral therapy or for other indications (e.g., atrial fibrillation).
Results
1. Despite widespread use, evidence for thrombolysis in ALI is limited. A review (14) found 10 randomized
controlled trials (RCTs) addressing the issue. Of those, only five compared lysis directly to surgery. In
addition to the RCTs, a large database of thrombolysis is maintained in the United Kingdom: the National
Audit of Thrombolysis in Acute Leg Ischemia (NATALI).
2. Three randomized trials—ROCHESTER, STILE, and TOPAS (5,7,15)—comparing thrombolysis to
primary surgery have largely defined the role of CDT in the treatment of ALI. Although the limb salvage rate
for CDT at 1 year in all these trials was the same as the limb salvage rate for surgical revascularization
(82% to 88%), the mortality rate at 1 year was significantly lower: 16% at 1 year in the ROCHESTER study
versus 42% for surgery, 6.5% versus 8.5% in the STILE trial, and 13.3% versus 15.7% in TOPAS. ALI,
associated with acutely occluded bypass grafts, was seen to have a better outcome than acute occlusion in
native vessels in both the TOPAS and STILE trials. Thus, the studies demonstrated a reduction in the
magnitude of interventions required and a better early survival with CDT. However, use of thrombolytic
therapy is associated with hemorrhagic complications and stroke, and there are also reports of recurrent
ischemia (1,2,3,4,5). Therefore, CDT is mainly recommended for graft thromboses or in situ thromboses of
native vessels of short duration.
3. Cumulative results (2,16) from published series on thrombolysis with UK for acutely ischemic lower limbs
reveals a positive thrombolytic outcome in 85% to 95% patients with mean duration of infusion,
approximately 24 hours. A rapid early (<2 hours) response to thrombolysis is associated with improved
initial success (1,2,3). Infusion duration is generally reported to be shorter with rt-PA (1,2,3,4,10,16) and
much longer with SK (1,2). Duration of treatment may vary with the doses and infusion rates used (2,10).
The lower success rates and higher complication rates of SK relative to UK and rt-PA are most likely related
to the greater plasminogen and fibrinogen depletion caused by the former agent (17).
4. Long-term patency is improved if the underlying lesions are treated promptly by percutaneous and/or
surgical techniques (1,2,3,4,6). Long-term patency is generally better for successfully treated suprainguinal
occlusions (vs. infrainguinal occlusions) (6) and vein grafts (vs. synthetic grafts) (1,2).
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5. When thrombolysis fails, simple thrombectomy and/or graft revision also do poorly (2).
6. Patients with acute lower limb ischemia who are initially treated by thrombolytic therapy have a
significantly higher 6-month (5) to 1-year (7) amputationfree survival rate compared to those who are
treated initially with surgery. This benefit appears to be especially significant for patients who present with
acute embolic occlusions (7,18). Patients with chronic occlusions (duration >14 days) reportedly have a
better long-term prognosis with initial surgical intervention (5), but thrombolysis remains a viable option for
them.
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7. Two prospective, randomized studies compared conventional low-dose infusion with different techniques
using high-dose thrombolysis and demonstrated contradictory results (12,19). A more recent study by Plate
and colleagues (20), however, did not demonstrate any disadvantage with high-dose, short-duration lytic
therapy (120 minutes) compared to low-dose, long-duration (24 hours) therapy, with major bleeding events
occurring in 7% of patients with high-dose versus 13% with the low-dose regimen and mortality at 1 month
being 10% and 11%, respectively.
Complications
1. The accepted overall mortality from thrombolysis in the periprocedural period is usually 3% to 5% with
stroke, myocardial infarction, or hemorrhagic complications accounting for the vast majority. Sullivan et al.
(12) showed that the probability of a major complication increased dramatically with the duration of
thrombolysis. Reported incidences of various complications are shown in Table 14.3.
2. The incidence of a major allergic reaction with SK or rt-PA is under 0.5% but is lower with UK; intracranial
hemorrhage is less than 1%, without significant differences between the agents (1,2,3,21).
3. Because many of the factors that increase hemorrhagic complications remain uncertain, it is prudent to
direct efforts toward early detection and appropriate management of hemorrhage. Patients who develop
hypofibrogenemia (fibrogen level <100) during treatment are more prone to bleeding. Also, avoidance of
arterial puncture in noncompressible anatomical areas is advisable (e.g., axillary artery).
4. Other reported incidences of complications of thrombolysis are as follows:
a. Pericatheter thrombus formation (with IV heparinization), 3% to 5% (1,2,3,21)
b. Sepsis or renal failure <1% (21)
c. Pseudoaneurysm formation at the puncture site, <1% (21)
Management of Complications during Lytic Agent Infusion

1. Severe bleeding
a. Immediate discontinuation of the thrombolytic agent and IV heparin
b. Consider transfusion of fresh whole blood, packed red blood cells, or fresh frozen plasma (2 to 4 units may be
needed).
c. For severe continuing hemorrhage, consider aminocaproic acid (Amicar 5 g by mouth [PO] or slow IV infusion
and then 1 g per hour for 2 to 4 hours).
d. Avoid dextran.
e. Meticulous search for source of internal bleeding to take specific corrective measures (e.g., computed
tomography scan for occult retroperitoneal hemorrhage)
2. Distal embolization of thrombus occurs in about 5% to 10% of cases, usually resolving with continued lytic
therapy or suction embolectomy. Surgical embolectomy is rarely needed.
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Table 14.3 Overall Incidence of Complications of Peripheral Arterial Thrombolysis
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Complication Incidence (%)
Major bleeding 6.6
Intracranial hemorrhage 0.5
Retroperitoneal hemorrhage 0.3
Minor bleeding 6.3
Limb-related complications
Distal embolization 5.2
Amputation
Due to distal embolization 0.8
Due to preexisting severe ischemia 8.0
Reperfusion syndrome 0.7
Compartment syndrome 2.0
Concurrent rethrombosis 3.0
Local arterial dissection 0.6
Systemic complications
Acute renal failure 0.3
Acute myocardial infarction 0.2
Other
Nonhemorrhagic stroke <1.0
Death 0.8
Compiled from two reviews of the literature on regional thrombolysis for peripheral arterial occlusions by
Gardiner GA and Sullivan KL (Kadir S, ed. Current Practice of Interventional Radiology. Philadelphia,
PA: CB Decker; 1991:87-91.) (n = 1,787 cases) and McNamara et al. (McNamara TO, Goodwin SC,
Kandarpa K. Complications associated with thrombolysis. Semin Interv Radiol . 1994;2:134-144.) ( n =
1,000 cases).
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3. Allergic reaction
a. Rare with UK and rt-PA; most frequently associated with SK
b. Occasional reports of chills and rigors following large rapid-bolus infusions of UK (e.g., 500,000 IU for
treatment of occluded dialysis access grafts) have been reported. Prophylactic treatment consists of
acetaminophen 1 g PO and diphenhydramine hydrochloride (Benadryl) 50 mg PO, given 30 to 60 minutes prior
to UK infusion. For reactions occurring once UK infusion has started, treat with meperidine hydrochloride
(Demerol) 50 mg IV or cimetidine 300 mg IV.
Mechanical Thrombectomy in Acute Limb Ischemia

In addition to CDT, other minimally invasive techniques, such as percutaneous aspiration thrombectomy (PAT) or
PMT, are used in the treatment of ALI (22,23,24,25). PMT allows rapid debulking of a large thrombus burden, as
a stand-alone thrombectomy therapy or as an adjunct to IA thrombolytic therapy to decrease symptomatic
ischemia time (22).
1. Several PMT catheters have been introduced and are described in detail elsewhere (23). Most of these
catheters physically remove the thrombus by a combination of localized mechanical maceration and suction (23).
Such devices have a role when thrombolytic therapy is contraindicated.
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2. Many reliable methods of percutaneous clot retrieval exist and mechanical removal of the thromboembolic
material may utilize one of several techniques:
a. Manual aspiration or PAT
b. Hydrodynamic thrombectomy
c. Rotational/oscillating thrombectomy
d. Stent placement
3. Manual aspiration, or PAT, is an inexpensive, rapid PMT technique that is often underestimated. Essential
tools involve a sheath with a removable hub, end-hole catheters of appropriate diameter, and/or hydrophilic
guidewires. When aspirating the clot, the end of the catheter is brought into contact with the proximal end of the
clot and is suction applied by use of a 20-mL or 50-mL syringe; suction is continued while the catheter is pulled
back into the sheath. Suction is stopped when easy aspiration of blood occurs indicating loss of thrombus or
successful aspiration. The Pronto extraction catheter (Vascular Solutions, Inc, Minneapolis, MN) is a low-profile,
duallumen, rapid-exchange PAT catheter compatible with a 0.014-in. wire. Although successfully used in acute
myocardial infarction during coronary interventions and for mesenteric arterial interventions, its success in ALI is
anecdotal, limiting its application in primarily managing embolization during peripheral interventions.
4. Hydrodynamic thrombectomy uses the principle of hydrodynamic recirculation. Dissolution of the thrombus
occurs within an area of continuous mixing referred to as the “hydrodynamic vortex,” where the thrombus is
trapped, dissolves, and is finally evacuated. There are three devices of this type and all utilize the Venturi
principle for thrombus removal, for example, Cordis hydrolyzer (Cordis, New Brunswick, NJ), Boston Scientific
Oasis (Boston Scientific, Natick, MA), and the Possis AngioJet system (Possis Medical Inc, Minneapolis, MN).
The essential principle involves saline solution injection through a small-bore channel that ends in a large
exhaust lumen at the tip of the catheter. At this point, a flow vortex is created removing surrounding clot material
while the fluid leaves the body through the exhaust lumen. Under ideal circumstances, the procedure is
isovolumic, avoiding fluid overload in the patient. The AngioJet Rheolytic Thrombectomy System (Possis Medical
Inc, Minneapolis, MN) is extensively used currently and is the only FDA-approved device. It is a dual-lumen
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catheter, one lumen of which accommodates either a 0.014-in. or a 0.035-in. guidewire, depending on model,
and the smaller lumen delivers a high-velocity, pulsatile saline flow to the catheter tip via a high-pressure
stainless steel hypotube connected to an external piston pump and drive unit. The hypotube forms a closed loop
at the catheter tip, which contains multiple jets aimed retrograde into the larger effluent lumen that is used for
both guidewire passage and evacuation of thrombus debris. The jets fragment and dislodge the thrombus,
creating a localized low-pressure zone (Bernoulli/Venturi effect) that draws the thrombus into the catheter tip and
then out of the vessel through the catheter's effluent lumen. The AngioJet catheter also can be used for the
power-pulse spray (P-PS) technique (25) that involves thrombolytic drug infusion through the catheter while
occluding the outflow port and is followed by thrombus aspiration.
5. Rotational/oscillating thrombectomy involves fragmenting the thrombus into small pieces that are small enough
to pass through the capillary bed.
a. The oldest of such devices is the Amplatz clot buster, while the Rotarix catheter (Straub Medical, Inc, Wangs,
Switzerland) combines thrombus destruction with suction. Such devices are usually effective in removing both
organized and fresh thrombus. However, to be safe and effective, the artery needs to be somewhat larger in
diameter than the catheter. Arterial spasm and vessel wall damage are inherent risks.
b. The Trellis Thrombectomy System (Covidien, Mansfield, MA) is a 7 Fr. drug dispersion catheter designed to
prevent distal embolization and systemic release of the infused thrombolytic agent (24). Briefly, the catheter is
passed over a 0.035-in. wire across the length of the thrombotic occlusion. Two ports
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are used to inflate a distal and a proximal balloon (diameter 3 to 10 mm), and thrombolytic agent is infused into
the isolated treatment segment (usually 10 to 30 cm) wherein a dispersion wire oscillates (500 to 3,000 rpm) in
two planes to fragment the clot and disperse the drug (typically 1 mg rt-PA per minute to a total of 10 mg). The
drug and dissolved/liquefied thrombus are then aspirated via an integral port as the proximal balloon is deflated
while the inflated distal balloon prevents distal embolization. Isolation of the treatment segment sets the Trellis
device apart from other PMTs wherein the proximal and distal occlusion balloons help circumvent the release of
embolic debris during mechanical and pharmacologic thrombus dissolution.
6. Stent placement may be used to treat soft thrombotic occlusions. Stents are able to displace a clot to the
periphery of the vessel wall and can be utilized as a last resort if mechanical clot removal fails.
7. Simultaneous angioplasty with thrombolytic irrigation (SATI) combines a lowpressure balloon angioplasty with
simultaneous in situ thrombolysis using the ClearWay irrigation balloon (Atrium Medical Corp, Hudson, NH), a
monorail 0.014-in. or 0.035-in. compatible over-the-wire device. This microporous polytetrafluoroethylene (PTFE)
balloon creates a fluid/drug layer over its surface when the thrombolytic is injected through the balloon, which
spontaneously inflates as the drug is injected (three-in-one procedure: occlusion, containment, and infusion).
The thrombolytic is infused through the balloon into the target area, allowing local delivery of thrombolytics while
a low-atmosphere angioplasty is accomplished. One drawback is that small balloon length requires several
balloon inflations in the case of large thrombus distribution; however, recent availability of 50-mm long balloons
should improve applicability.
8. Conclusion: The efficiency of PMT depends mainly on the age of the thrombus: A fresh thrombus responds
better than an older, organized clot. Current evidence suggests that mechanical devices may be used safely for
rapidly removing acute thrombi from the lower extremities (22,23,24,25). Nevertheless, adjunctive treatment with
thrombolysis may be required in about half these patients, with about 80% of them requiring additional aspiration
thrombectomy. Small series have shown that rheolytic thrombectomy (RT), with or without chemical lysis, leads
to effective thrombus removal in a short time and reduces major adverse events in ALI patients. The 30-day limb
salvage rate for ALI is about 90% using the P-PS and RT. Shammas et al. (25) studied the presence of thrombus
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using intravascular ultrasound to evaluate the feasibility of combined thrombolysis (P-PS) and RT in patients with
ALI and recent-onset (6 months) limb ischemia. They observed that the application of the P-PS/RT led to partial
or complete thrombus resolution in about two thirds of the patients treated and that the overall safety outcome
was favorable.
a. These devices perform best for treating acute emboli, an application for which thrombolytic therapy is superior
to surgery with respect to long-term, amputation-free survival (7,18).
b. Mechanical thrombectomy is a feasible concept for the acutely ischemic limb and in most instances allows
rapid removal of the clot material and rapid revascularization, avoiding lengthy procedures and repeat
angiography. A combination of PMT with IA thrombolysis may speed up clot lysis and decrease time to
revascularization.
References
1. Kandarpa K. Catheter-directed thrombolysis of peripheral arterial occlusions and deep vein thrombosis.
Thromb Haemost. 1999;82:987-996.
2. Thrombolysis in the management of lower limb peripheral arterial occlusion—a consensus document.
Working Party on Thrombolysis in the Management of Limb Ischemia. Am J Cardiol . 1998;81:207-218.
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3. Kandarpa K. Technical determinants of success in catheter-directed thrombolysis for peripheral arterial

occlusions. J Vasc Interv Radiol . 1995;6:55S-61S.
4. Valji K. Evolving strategies for thrombolytic therapy of peripheral vascular occlusions. J Vasc Interv Radiol .
2000;11:411-420.
5. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower
extremity: the STILE trial. Ann Surg. 1994;220:251-268.
6. McNamara TO, Bomberger RA. Factors affecting initial and 6 month patency rates after intraarterial
thrombolysis with high dose urokinase. Am J Surg. 1986;152:709-712.
7. Ouriel K, Shortell CK, DeWeese JA, et al. A comparison of thrombolytic therapy with operative
revascularization in the initial treatment of acute peripheral arterial ischemia. J Vasc Surg. 1994;19:1021-
1030.
8. Semba CP, Bakal CW, Calis KA, et al. Alteplase as an alternative to urokinase. Advisory Panel on
Catheter-Directed Thrombolytic Therapy. J Vasc Interv Radiol . 2000;11:279-287.
9. Ouriel K, Katzen B, Mewissen M, et al. Reteplase in the treatment of peripheral arterial and venous
occlusions: a pilot study. J Vasc Interv Radiol . 2000;11:849-854.
10. Meyerovitz MF, Goldhaber SZ, Reagan K, et al. Recombinant tissue-type plasminogen activator versus
urokinase in peripheral arterial and graft occlusions: a randomized trial. Radiology. 1990;175:75-78.
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11. Kandarpa K, Chopra PS, Aruny JE, et al. Intraarterial thrombolysis of lower extremity occlusions:
prospective, randomized comparison of forced periodic infusion and conventional slow continuous infusion.
Radiology. 1993;188:861-867.
12. Sullivan KL, Gardiner GA Jr, Shapiro MJ, et al. Acceleration of thrombolysis with a highdose
transthrombus bolus technique. Radiology. 1989;173:805-808.
13. Owens CA. Ultrasound-Enhanced Thrombolysis: EKOS EndoWave Infusion Catheter System. Semin
Intervent Radiol . 2008;25:37-41.
14. Palfreyman SJ, Booth A, Michaels J. A systematic review of intra-arterial thrombolytic therapy for lower-
limb ischaemia. Eur J Vasc Endovasc Surg. 2000;19:143-157.
15. Ouriel K, Veith FJ, Sasahara AA. A comparison of recombinant urokinase with vascular surgery as initial
treatment for acute arterial occlusion of the legs. Thrombolysis or Peripheral Arterial Surgery (TOPAS)
Investigators. N Engl J Med. 1998;338:1105-1111.
16. Graor RA, Olin J, Bartholomew JR, et al. Efficacy and safety of intraarterial local infusion of
streptokinase, urokinase, or tissue plasminogen activator for peripheral arterial occlusion: a retrospective
review. J Vasc Med Biol . 1990;2:310-315.
17. Holden RW. Plasminogen activators: pharmacology and therapy. Radiology. 1990;174:993-1001.
18. Diffin DC, Kandarpa K. Assessment of peripheral intraarterial thrombolysis versus surgical
revascularization in acute lower-limb ischemia: a review of limb-salvage and mortality statistics. J Vasc Interv
Radiol . 1996;7:57-63.
19. Braithwaite BD, Buckenham TM, Galland RB, et al. Prospective randomized trial of high-dose bolus
versus low-dose tissue plasminogen activator infusion in the management of acute limb ischaemia.
Thrombolysis Study Group. Br J Surg. 1997;84:646-650.
20. Plate G, Jansson I, Forssell C, et al. Thrombolysis for acute lower limb ischaemia—a prospective,
randomised, multicentre study comparing two strategies. Eur J Vasc Endovasc Surg. 2006;31:651-660.
21. McNamara TO, Goodwin SC, Kandarpa K. Complications associated with thrombolysis. Semin Interv
Radiol . 1994;2:134-144.
22. Ansel GM, Botti CF Jr, Silver MJ. Treatment of acute limb ischemia with a percutaneous mechanical
thrombectomy-based endovascular approach: 5-year limb salvage and survival results from a single center
series. Catheter Cardiovasc Interv. 2008;72:325-330.
23. Sharafuddin MJ, Hicks ME. Current status of percutaneous mechanical thrombectomy. Part I. General
principles. J Vasc Interv Radiol . 1997;8:911-921. Part II. Devices and mechanism of action. J Vasc Interv
Radiol . 1998;9:15-31. Part III. Present and future applications. J Vasc Interv Radiol . 1998;9;209-224.
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24. Hanna EB, Gupta R, Hennebry TA. Use of Trellis thrombectomy system in acute aortofemoral graft
occlusion. Catheter Cardiovasc Interv. 2010;75:838-842.
25. Shammas NW, Dippel EJ, Shammas G, et al. Dethrombosis of the lower extremity arteries using the
power-pulse spray technique in patients with recent onset thrombotic occlusions: results of the
DETHROMBOSIS Registry. J Endovasc Ther. 2008;15:570-579.
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15
Trauma Management
Brian F. Stainken
Worldwide, the leading cause of death in patients younger than the age of 44 years is trauma. In 2013, trauma
claimed over 2.1 million years of potential life with direct costs of over $700 billion in the United States alone.
These staggering numbers do not take into consideration the additional expense of disability or the lost financial
productivity of survivors (1). The cost to society of lost productivity alone is approximately four times the direct
medical expenses (2).
Great strides have been made toward improving trauma care in the United States. Integrated systems that initiate
resuscitation at the site and expedite transfer to specialized centers have helped save lives. And these systems
continue to evolve. In the past, the trauma patient was best cared for in a trauma operating room (OR). A primary
goal of trauma care was to expedite transfer from the field to the OR where diagnostics and definitive care could
be provided. Over the past decade however, primarily due to the deployment of helical computed tomography
(CT) in the trauma bay, the path followed by the trauma patient now detours through CT. Diagnosis and triage
have moved from the OR to the CT scanner. Following CT diagnosis, expedited directed care based on imaging
findings follows—orthopedic, neurosurgical, laparotomy, or interventional radiology (IR) embolotherapy.
Resuscitation moves with the patient. Whole-body CT scanning prior to intervention in hemodynamically
unstable patients and patients requiring emergency bleeding control is associated with significantly better
survival than direct transfer to surgery on arrival (3). Even the distance between the trauma bay and the CT
machine independently predicts survival (4).
IR has evolved in parallel since 1972 when Margolies et al. first described embolization therapy for management
of pelvic trauma. Techniques and devices to manage trauma victims nonoperatively have been validated, and
the scope of care provided has expanded. IR has become an indispensable member of the trauma team, with the
capability to rapidly address exsanguinating hemorrhage throughout the body without the inherent delay and
morbidity of open exploration. The old bromide that unstable exsanguinating trauma patients go to the OR and
the stable ones to IR no longer applies. When the IR space is appropriately configured and staffed with an
experienced, trained team, the decision for IR versus OR should be based on diagnosis, not acuity. Leading
trauma centers increasingly recognize the importance of image-guided medicine and the need to provide the
resources and expert practitioners able to effectively integrate IR in to the trauma care environment.
The initial steps of intervention for trauma are similar regardless of the location of injury. General considerations
are discussed first. The details involved in treating specific types of traumatic injury—abdominal including
splenic, hepatic, and renal; pelvic; lumbar artery; and extremity are then discussed, along with their
complications.
General Considerations in Trauma

Indications
1. Treatment of exsanguinating hemorrhage Although some trauma guidelines still recommend that
hemodynamically unstable patients go directly to surgery, it is increasingly clear that the use of helical CT
offers a major benefit for diagnosis prior to laparotomy especially in the most acute patients. As trauma
centers accept this shift, and the point of diagnosis moves from the OR suite to the CT scanner, it becomes
increasingly feasible to transfer directly from CT to IR in centers appropriately trained and
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equipped. In fact, the time to start of emergency bleeding control procedures in one center is 45 minutes for
the OR and 54 minutes for IR (3). In this changing environment, the eligibility of a patient for IR care is
driven as much by the preparation and layout of the trauma facility as it is by the procedure.
Contraindications
Relative
1. Pregnancy. A relative risk assessment may demonstrate that the morbidity of surgery exceeds the
theoretical risk of radiation exposure especially in late trimester gestation. Advanced planning for such
scenarios is paramount.
2. Renal insufficiency. Acute tubular necrosis related to prolonged hypotension is a much more common
issue in trauma patients than contrast nephropathy.
3. Allergy to contrast. Clarification of the actual history (idiosyncratic vs. anaphylactic) is important. In most
patients, this issue will be resolved at the time of CT imaging. Depending on the presentation and relative
risk, even in a known allergic patient, it may be reasonable to proceed after consultation with other
members of the trauma team.
1. Ongoing resuscitation is critical during all aspects of trauma care including endovascular intervention. This
entails ensuring an airway and appropriate ventilation as well as adequate intravenous (IV) access with large-
bore IV lines for fluid, medication, and transfusions. Warming the patient and replacement of coagulation factors
will aid in hemostasis. Other than cervical stabilization, neurologic assessment can wait in hemodynamically
labile patients. Although associated with a poorer prognosis, neurologic injury alone is not likely to cause
significant hemodynamic shock.
2. Basic laboratory studies are not a prerequisite for trauma angiography, and the procedure should not be
delayed in anticipation of complete blood count (CBC), chemistry panel, and coagulation parameters. A
worsening base deficit is the most sensitive laboratory indicator of hemodynamic shock and will precede a drop
in hematocrit.
3. Review of CT and other available imaging studies to identify all potential sites of injury and occult sources of
bleeding is essential in formulating a plan for intervention. The trauma CT is the cornerstone of initial diagnosis.
A negative CT in children is 99.6% predictive to exclude any intra-abdominal injury (5). In penetrating abdominal
trauma, CT has far greater sensitivity than focused assessment with sonography for trauma (FAST) and
emerging data suggest that its use as a primary tool (during resuscitation) saves lives (3,6).
4. Resuscitation should be continued throughout the procedure. A lifesaving procedure should not be postponed
while waiting for blood products. Safe embolization in unstable patients can be performed if the patient responds,
even transiently, to a 2-L rapid resuscitative bolus (7). Transfusions should be administered while the patient is
in the angiography suite to prevent delays.
Procedure
1. Arterial access is usually obtained via the common femoral artery. A vascular sheath is essential in all
cases. In the setting of severe hemodynamic shock, the femoral pulses may not be palpable, and ultrasound
should always be available for access. Upsize the sheath 1 to 2 Fr. beyond the planned catheter size, and
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use the side arm connected to a manometer to monitor arterial pressures. The same sheath can be used,
when warranted for resuscitation. Sew the sheath in if you expect it to be left in place after your procedure.
2. Diagnostic angiographic images have largely been supplanted by the CT scan. Treatment should not be
delayed for the purpose of angiographic documentation. If extravasation is seen on the hand-injected
fluoroscopic test imaging,
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save it and move on to treatment without a formal injector run when the situation calls for speed.
Angiographic findings for vessel disruption in the setting of trauma may include extravasation, occlusion,
arteriovenous (AV) or other fistula, intimal tear, and false aneurysm. Extravasation seen on CT and not seen
at angiography may be due to vessel spasm, slow bleeding rate (e.g., venous bleeding), changes in blood
pressure, cardiac output, or anomalous anatomy. Remember to always obtain orthogonal views when the
finding is not clear in one projection. A single angiographic projection can miss significant findings and
should not be relied on to clear a vessel of injury. Selective runs may show extravasation not visible on a
flush run.
3. Options for achieving hemostasis when faced with a traumatic vascular injury include embolization, stent
or stent-graft placement, and temporary balloon occlusion.
a. Embolization may be performed using gelfoam slurry or by selectively delivering compressed dry pledgets
aptly called torpedoes. One may employ particulate microemboli such as polyvinyl alcohol (PVA) or
spherical embolics, macroembolic metallic coils, endoluminal plugs, or any combination of these. Gelfoam is
commonly used in situations where rapid, temporary vascular occlusion is needed. It is well suited for use in
occluding small end arteries and when faced with diffuse branch bleeding as is often seen in the setting of
pelvic fractures. Coils are generally used for embolization of larger conduit vessels or to isolate arterial
fistulas. Detachable coils and plugs allow precise control over delivery.
b. Stents and stent grafts can rapidly control exsanguinating bleeding while preserving luminal continuity
when larger conduit vessels such as the aorta, carotid, hepatic, renal, iliac, and superficial femoral arteries
are disrupted.
c. Temporary balloon occlusion is an important component in the IR arsenal for hemostasis. Inflating an
appropriately sized, compliant balloon within the artery proximal to a site of extravasation may provide
immediate hemostatic control. The central lumen can then be used to better study the bleeding site and
plan care. Microcatheters can be deployed through the central lumen to deliver emboli if indicated.
Downstream pressures can be measured. Temporary balloon occlusion can achieve proximal control during
surgical exposure and preemptive balloon placement may be a useful adjunct when there is high potential
risk for bleeding (8). One example is the use of temporary balloon occlusion in penetrating subclavian artery
injury for proximal hemostatic control and repair via a clavicular resection rather than sternotomy.
4. Once stabilized, completion angiography is important to confirm hemostasis prior to removal of the
access sheath. Closure devices should be considered in this population as patients may be heavily
sedated, may proceed for additional procedures, and/or be at high risk for transfusion-related coagulopathy.
1. All trauma patients should be followed closely for signs of persistent or delayed hemorrhage with serial blood
work, physical exam, and vital sign checks. It is the responsibility of the treating physician to identify
complications and ensure that the patient has fully recovered from the intervention.
2. Adequate prophylaxis for infection and deep vein thrombosis (DVT) should be considered in trauma patients.
3. Follow-up angiography after endovascular treatment of arteriovenous fistulas (AVFs) is recommended.
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Abdominal Trauma
In order of frequency, the most commonly injured abdominal organs are the spleen, liver, and kidney. With the
widespread use of cross-sectional imaging and
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endovascular techniques, the majority of hemodynamically stable or adequately resuscitated abdominal trauma
patients, can be nonoperatively managed.
Splenic Injury
Historically, traumatic injury to the spleen was treated with splenectomy or observation. With the growing
acceptance of splenic artery embolization, most patients can safely avoid surgery (9). The immunologic benefits
of splenic preservation are accepted (10). There remains great variability in practice even between major trauma
centers. One comparative review of four level 1 trauma centers showed that centers with the highest rates of
embolization also enjoy the highest rates of splenic salvage (11). The probability of successful preservation of
the spleen is increased when embolization is used for all grade 3 and 4 lacerations (12).
Indications
1. Blunt trauma
a. Extravasation of contrast noted on arterial phase CT or on angiography. There is some debate as to the
merit of embolization over observation for stable patients presenting with a grade 1 to 3 laceration and
parenchymal contrast extravasation “blush” on CT (13).
b. Hemodynamic lability or transfusion requirements greater than 4 units packed red blood cells (PRBC)
over 24 hours. Current surgical society standards advise against embolization in the setting of
hemodynamic instability; however, larger series demonstrate clear shifts in the percentage of patients
undergoing embolization without a change in the distribution of splenic injury scores (9).
c. CT findings of splenic injury of grade 3 (laceration >3 cm or >5 cm hematoma) or vascular (involvement
of segmental or hilar vessel) laceration with or without active extravasation. Segmental infarction of the
spleen noted on CT suggests branch splenic artery injury (14).
d. Intrasplenic false aneurysm or AV fistula as demonstrated on CT. These are generally signs of ineffective
embolization or failing observational management (14).
e. Delayed bleeding as evidenced by recurrent hemodynamic lability or transfusion requirements following
initial observation or embolization for splenic trauma
2. Penetrating trauma
a. There is limited role for angiography in penetrating splenic trauma. These patients generally require
laparotomy because of the risk for coincident visceral injury.
Procedure
1. Plan your approach based on findings at CT. A celiac axis angiogram is performed through the portal
venous phase to visualize the splenic vein. The catheter is then advanced into the splenic artery, and a
dedicated splenic arteriogram in a different projection is performed.
2. Extravasation may be extremely subtle. If no extravasation or vascular injury is present at angiography,
there is a high probability that nonoperative management will be successful. Delayed rupture is rare in
these circumstances.
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3. If extravasation or vascular injury is seen, intervention may be performed as described below:
a. Intrasplenic hemorrhage. Proximal coil embolization of the splenic artery is a well-described approach for
obtaining rapid hemostasis for intrasplenic hemorrhage. Proximal coil embolization will temporarily decrease
the arterial pulp pressures such that intrasplenic hemorrhage is controlled. Because collateral circulation is
preserved, proximal splenic arterial coil embolization is associated with a low risk for splenic infarction.
Proximal embolization
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should be performed with coils sized 20% to 25% larger than the vessel diameter and positioned just distal
to the origin of the dorsal pancreatic artery. The coil should be oversized because the artery is often
vasoconstricted in the setting of hemodynamic shock. Following restoration of normal hemodynamics, the
artery may dilate and allow distal coil migration (14).
b. Intrasplenic hemorrhage can also be managed successfully with more selective embolization when the
extent of injury and the patient's presentation allow. This approach is favored by some operators, and
ultimately the choice should be made by the interventional radiologist based on the patient's stability,
experience, and pattern of splenic injury.
c. Extrasplenic hemorrhage. Selective embolization should be performed in cases of extrasplenic
hemorrhage because of the degree of hemodynamic instability and risk of continued hemorrhage. When
significant extrasplenic hemorrhage or combined intrasplenic and extracapsular bleeding is noted, a
combination of distal selective embolization and proximal splenic artery coil embolization may be used for
maximal hemostatic control (14).
d. Intraparenchymal false aneurysm or AVF. In the setting of distal false aneurysm or AVF supplied by a
discrete vessel, selective microcoil embolization of the conduit artery is warranted to minimize splenic
infarction.
e. Pseudoaneurysms or AVFs of the main splenic artery are occasionally seen in association with
penetrating trauma. They may be treated by proximal and distal splenic artery coil embolization to isolate
the site of injury. A stent graft may also be used to cover the injury and preserve flow to the spleen.
Results
Proximal splenic artery coil embolization in the setting of trauma has a technical success rate of 90% to 95%
with a similar clinical success rate in terms of avoiding splenectomy. It appears that outcomes for proximal
and distal embolization are similar as well (14,15). By requiring embolization for all hemodynamically stable
patients with grade 3 to 5 injuries, one institution increased the percentage of spleens salvaged from 52%
to 67% while reducing the rate of observation failures from 15% to 5% (12).
Complications
1. Infarct. Particularly with distal embolization, infarction to some degree is to be expected. The significance
of asymptomatic peripheral infarcts on postprocedure CT is questionable.
2. Abscess. Described in 4% of one large multi-institutional series (16). Risk may be minimized by limiting
handling and other exposure of the gelfoam prior to administration.
Hepatic Injury
The liver is a highly vascular organ with a dual blood supply provided by the hepatic artery and portal vein.
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Clinically significant traumatic hemorrhage from the liver most commonly arises from the hepatic arterial
circulation. The most devastating vascular trauma, however, is hepatic venous injury. A potential advantage of
nonoperative management of liver trauma may be avoidance of uncontrolled hemorrhage from an occult hepatic
venous laceration uncovered during liver mobilization.
Indications
1. Blunt trauma
a. Recurrent hemodynamic lability despite resuscitation or greater than 4 units of PRBC transfusion
requirements over 24 hours
b. CT findings for significant liver injury include:
(1) Laceration. American Association for the Surgery of Trauma (AAST) grade 3 or higher or extension to
involve a major hepatic vein
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(2) Focal contrast material extravasation
(3) Large subcapsular or perihepatic hematoma
c. Persistent hemobilia suggesting an arteriobiliary fistula. Recurrent biliary colic, jaundice, and melena
following trauma are other highly suggestive signs of hemobilia.
d. As a second-stage procedure following open surgical packing of a severe liver injury. The goal is to
definitively treat findings temporized by packing.
e. Repeat hemorrhage or hemodynamic lability following initial surgical management.
2. Penetrating trauma. Most patients will require laparotomy to exclude visceral injury.
a. Focal penetrating wounds isolated to the right upper quadrant may require hepatic angiography if the
patient is hemodynamically stable, and there is no CT evidence for bowel injury or clinical suggestion of
peritonitis. Proximity of the injury tract to hilar vessels particularly warrants angiographic evaluation.
b. Repeat hemorrhage or hemodynamic lability following initial surgical management.
Contraindications
Relative
1. Historically, hemodynamic lability not responsive to initial resuscitation was referred for emergent
operative management rather than angiography, but this is changing, as previously discussed. It may be
that a combination of catheter-based and open surgery will deliver the best results (17).
2. Preexisting liver disease. Embolization of multiple liver segments may place the patient at risk for liver
insufficiency, as may resection. Meticulous technique and subselective embolization are warranted in
patients with evidence of cirrhosis to minimize infarction of the liver.
3. Compromised portal vein blood supply. With portal vein thrombosis or hepatofugal portal vein flow, the
patient is at greater risk of hepatic infarct following hepatic artery embolization. However, the relative risk of
subselective embolization should be weighed against the risks of continued hemorrhage or the relative risk
of surgical management.
Procedure
1. The approach to the diagnostic angiogram should be driven by the acuity of the presentation and findings
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on CT. In the unstable patient, the speed to achieving hemostasis is all that matters. Once controlled, a full
diagnostic assessment can be completed.
2. Full assessment should include a superior mesenteric artery (SMA) angiogram through the venous phase
demonstrating portal vein patency and integrity. Because variant vascular anatomy of the liver is common,
the SMA arteriogram is important to exclude accessory or aberrant vessels such as an accessory right
hepatic artery.
3. The diagnostic catheter or a microcatheter can be advanced to the common or proper hepatic artery to
allow selective hepatic angiography. Multiple oblique views should be obtained to evaluate for arterial injury
including selective left and right hepatic arteriograms, if necessary.
4. Embolization can be performed in several ways depending on the distribution of injury and available time:
a. Multiple points of extravasation. Scatter embolization using gelfoam slurry or large (over 500 micron)
particles into the left and/or right hepatic arteries or the proper hepatic artery (with the 5 Fr. catheter).
Catheterization distal to the cystic artery is desirable to avoid nontarget embolization of the gallbladder.
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b. Single point of extravasation. Following subselective catheterization of the injured branch via a
microcatheter, focal embolization may be performed using gelfoam, particles, or microcoils.
c. Fistulas between the hepatic artery and portal vein, hepatic vein, or bile ducts. The conduit vessel should
be isolated from the fistula with coils or microcoils. For main hepatic artery fistulas, a stent graft is an
attractive treatment option.
Results
Hepatic embolization in the setting of trauma has a technical success rate ranging from 88% to 100%. The
probability of success is driven by the severity of the injury, coagulopathy, and acuity (18). In children, a
recent 5-year retrospective series reports 100% success in nonoperative management despite the fact that
46% presented with grade 4 lacerations (19). In adults presenting with grade 4 and 5 injury, embolization in
conjunction with surgery is associated with decreased mortality (20).
Complications
Differentiating complications related to the traumatic event itself from procedural complications is important.
A recent single-center review comparing operative management with embolization in 396 patients showed
equal liver-related morbidity and a reduction in mortality from 17% for surgically managed to 3% in patients
treated with embolotherapy (21). Prospective randomized trials are needed to best determine the roles of
surgical versus image-guided approaches.
1. Gallbladder injury. Rarely encountered in oncologic embolization and less likely with larger embolics used
in trauma. Nevertheless, when possible, confirm that the catheter tip is distal to the cystic artery prior to
embolization.
2. Liver necrosis or hepatic insufficiency. Review CT to assess portal venous flow prior to hepatic arterial
embolization. Avoid powders or liquid agents. Recognize that the extent of underlying parenchymal trauma
and perfusion status may influence the extent of necrosis more than the embolization procedure. The
highest risk group for liver necrosis, in fact, are patients presenting for definitive embolization after
highgrade injuries treated initially with damage control laparotomy/liver packing (18).
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Renal Injury
Most blunt renal trauma is minor, self-limiting, and requires no treatment. Patients with solitary kidneys warrant
more aggressive kidney-saving procedures. The most common cause of renal vascular injury is iatrogenic
following renal biopsy or nephrostomy placement.
Indications
1. Blunt trauma
requirements over 24 hours and CT findings of significant renal injury such as:
(1) Fractured kidney
(2) Large subcapsular hematoma, equal to or greater than 50% of the kidney volume
(3) Active extravasation
b. Evidence of renovascular injury on CT
(1) Contrast extravasation
(2) Central perinephric hematoma between the kidney and aorta or inferior vena cava (IVC) suggesting a
full-thickness injury of the renal artery
(3) Segmental infarct of the kidney suggesting embolic disease from proximal arterial injury or segmental
renal artery occlusion
(4) Complete infarct of the kidney suggesting main renal artery injury or occlusion. This is associated with a
poor prognosis for renal preservation.
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c. Abdominal bruit or thrill suggesting a renal arteriovenous fistula
d. Unrelenting gross hematuria and/or severe unremitting urinary colic suggesting an arteriocalyceal fistula
a. There is a limited role of angiography in penetrating injury to the retroperitoneum. When penetrating
injury results in concomitant intraperitoneal and retroperitoneal involvement, patients typically require
surgical intervention; however, if the injury is limited to the retroperitoneum, embolization can reduce the risk
for nephrectomy. In particular, embolization is the treatment of choice in iatrogenic renal vascular injury such
as following renal biopsy or nephrostomy placement.
b. Recurrent hemodynamic lability despite resuscitation or greater than 4 units of PRBC transfusion
requirements over 24 hours and CT findings of significant kidney injury as listed earlier without evidence for
intraperitoneal injury.
Procedure
1. If proximal renal artery injury is suspected, an aortogram should be performed to evaluate the origin of the
vessel.
2. A selective catheter is used to catheterize the renal artery, and a selective renal arteriogram performed. If
the selective arteriogram fails to enhance the entire kidney, obtain additional projections and consider a
possible accessory renal artery or thrombosed branch vessel. Review reconstructed CT images.
3. If vascular injury is seen, intervention may be performed as described below:
a. Renal artery dissection, laceration, or extravasation. A stent or endograft may be used to preserve flow to
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the kidney if the lesion can be crossed.
b. Intraparenchymal hemorrhage or false aneurysm. Subselective embolization should be performed.
Because the renal artery is an end artery, unlike the liver or spleen, there is no absolute need for
embolization distal to the site of vascular injury unless more than one renal branch is involved. In the kidney,
the goal is to minimize segments devascularized so as to maximize preservation of renal tissue.
c. Intraparenchymal arteriovenous or arteriocalyceal fistula. Embolization of the conduit vessel proximal to
the injury should be performed with microcoils. Note that arteriocalyceal fistulas may be difficult to diagnose
angiographically due to extravasation of contrast into the collecting system. Early opacification of a calyx is
highly suggestive of arteriocalyceal fistula.
4. Delayed imaging at 15 to 30 minutes should be performed to evaluate ureteral injury. The ureters should
be visualized to the level of the bladder.
Results
Multiple series of renal trauma patients have demonstrated a greater than 95% success rate of
embolotherapy in treating parenchymal renal injury as a means of obtaining hemostasis, maximizing renal
function, and avoiding nephrectomy (22). The long-term patency for stents placed in the setting of acute
trauma to the main renal artery needs further evaluation and may not offer benefit over nephrectomy (23).
The 2014 American Urological Association (AUA) Guidelines recommend surgery or embolization in
hemodynamically unstable patients with no or transient response to resuscitation (24).
Complications
Infarction of downstream renal parenchyma is a consequence of successful renal embolization. Selective
technique is important to minimize the degree of infarction. In addition, devascularization due to underlying
renal injury cannot be differentiated.
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Pelvic Trauma
Patients with pelvic fractures presenting in shock have a mortality rate ranging from 30% to 50%. Bleeding
associated with such fractures arises from small to medium size intramuscular branches that are unrecognizable
intraoperatively. The first course of action in this population is immediate stabilization of the fracture with a binder
and resuscitation. Ongoing blood loss requires aggressive management to stop continued bleeding. CT imaging
has largely supplanted peritoneal lavage and trauma emergency department (ED) ultrasound (US) for exclusion
of extrapelvic bleeding sites. Once the source is isolated to the pelvis, the next step is angiography. There are
clear data correlating time to achieving hemostasis with embolization and survival (25). Surgical options in this
population are limited, and the focus is on orthopedic external fixation and damage control packing, often
followed by embolization.
Indications
1. Blunt trauma
a. Persistent or recurrent hemodynamic shock despite resuscitation in a patient with pelvic fractures or a
retroperitoneal hematoma and no evidence for hemoperitoneum. Embolization to treat arterial hemorrhage is
the accepted treatment of choice in patients with hemorrhage associated with pelvic fractures and should
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not be delayed for operative external fixation.
b. Ongoing hemorrhage from pelvic fractures necessitating transfusion greater than 4 units of PRBC in 24
hours or 6 units of PRBC in 48 hours
c. Retroperitoneal contrast extravasation on CT evaluation of the pelvis in the setting of hemodynamic
instability or evidence for ongoing blood loss despite pelvic binding (26)
d. Large or expanding retroperitoneal hematoma identified at laparotomy
a. A penetrating pelvic injury with concern for bowel injury requires laparotomy. However, if there is no
concern for bowel injury, pelvic injury in proximity to major vessels or with imaging findings of vascular injury
may be evaluated angiographically.
b. Following laparotomy for penetrating trauma to the pelvis to exclude vascular injury or provide definitive
hemostasis
Procedure
1. At presentation, pelvic stabilization by the orthopedic trauma service to attempt limitation of pelvic volume
is first used to help control bleeding, particularly of venous origin. Many surgeons will wrap the pelvis in a
sheet for a quick means of pelvic stabilization; however, there is data suggesting that binders and C clamps
are associated with improved survival.
2. Base your initial plan and approach on the CT findings and the acuity of the case. If the patient is not
stable, don't waste time with full diagnostics; address the problem. Select the internal iliac on the side with
the most extravasation or displaced fracture and scatter embolize the posterior division of the internal iliac
with gelfoam or balloon occlude. If necessary, use a proximal occluding balloon to slow flow and a
microcatheter to select and embolize. Ultimately, the extent to which your intervention is useful to the patient
is driven by the speed with which you achieve initial hemostasis (25).
3. Initial embolization or occlusion will often produce dramatic and rapid stabilization, allowing the operator
an opportunity to assess and complete treatment in a more systematic and selective fashion.
4. Unless contraindicated, once stabilized, a flush abdominal and pelvic aortogram should be obtained due
to the association of pelvic trauma with solid organ or retroperitoneal arterial injury, particularly if lumbar
transverse process or vertebral body fractures are present.
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5. Selective bilateral internal iliac artery arteriography in two views should ultimately be performed utilizing
standard retroflexed or backward seeking catheters.
6. Pelvic fractures are most commonly associated with damage to small internal iliac artery branches. In the
setting of visualized hemorrhage, embolization may be performed as detailed below:
a. Single focus of hemorrhage. In isolated injury to a branch of the internal iliac artery, in a stable patient,
subselective embolization of the bleeding vessel may be performed via a microcatheter using gelfoam or
coils.
b. Multiple foci of hemorrhage. In the setting of massive pelvic vascular injury where distal catheterization
may be time-consuming or technically difficult, proximal internal iliac artery embolization may be performed
using a gelfoam slurry or pledgets. Exercising care to minimize refluxing emboli into the anterior division of
the internal iliac or external iliac artery is important. This is accomplished through regular contrast runs to
assess stasis and controlled administration of emboli, avoiding high-pressure or pulsed injections. Keeping
the delivery catheter flushed and limiting the concentration of emboli delivered to avoid occlusion or high
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pressure injection is advised.
7. Coil blockade may be used to prevent distal embolization to noninjured vessels. By coiling the origin of
uninjured vessels, distal flow via collateralization is preserved as is downstream tissue viability.
8. Prophylactic, nonselective embolization of the internal iliac arteries without angiographic or CT evidence
of vascular injury is not recommended.
9. Hemodynamically significant external iliac artery and branch injuries are uncommon but can be seen with
pelvic trauma. The external pudendal and external obturator branches are two sites of injury, which are
missed on selective internal iliac arteriography. While end branches of the external iliac may be embolized
with gelfoam or coils, main external iliac artery injury typically requires placement of a stent graft.
Results
Recent series of pelvic trauma patients have demonstrated technical success rates approaching 100% and
clinical success rates of 95%. In a series of 78 patients who underwent embolization for pelvic trauma, only
4 demonstrated recurrent hemorrhage, the majority of which responded to a second embolization (27). As
noted previously, there is a correlation between time to embolization and survival (25).
Complications
1. Impotence (2%). No studies have shown a causative role of internal iliac artery embolization in the setting
of trauma, however. It is unclear whether most posttraumatic impotence is due to the underlying pelvic
fracture or the embolization procedure (28).
2. Gluteal necrosis (6%). One should avoid the use of small particles and recognize that more than one
factor (e.g., hypotension, underlying muscular injury, and surgical packing) correlates with this complication.
Lumbar Artery Injury

Lumbar artery injuries can lead to significant bleeding and are associated with lumbar vertebral body and
transverse process fractures. When imaging demonstrates lumbar vertebral body injury, lumbar artery injury
should be suspected. Additionally, lumbar artery injuries may be seen in association with pelvic trauma.
Indications
1. Blunt trauma
requirements over 24 hours and lumbar vertebral body or transverse process fractures with or without pelvic
trauma (29)
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b. CT findings suggestive of lumbar artery injury such as large retroperitoneal hematoma or arterial blush
from active extravasation
Penetrating injuries of the retroperitoneum that traverse the peritoneum generally require surgical
exploration. However, CT may exclude intraperitoneal extension in focal penetrating wounds isolated to the
retroperitoneum. Endovascular management may then be considered in the setting of recurrent
hemodynamic lability or greater than 4 units of PRBC transfusion requirement in 24 hours and CT findings
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of active extravasation or large posterior pararenal hematoma.
Procedure
1. Usually, a flush aortogram is performed for initial evaluation. Correlate findings with CT reconstructions.
Typically, active extravasation will not be noted; often, the only finding of lumbar artery injury on
aortography is nonopacification of a vasoconstricted or occluded vessel.
2. Selective lumbar artery angiography is performed at the level of interest as well as levels one vertebral
body above and below to exclude collateral filling of the injured vessel. If injury (occlusion/extravasation or
spasm) is found, embolization should be performed as follows:
a. Generally, microcatheters and coils are used, and if the injured vessel can be crossed, they should be
deployed distal to proximal across the site.
b. Usually, the artery of Adamkiewicz (anterior spinal artery) arises from the left lower thoracic intercostal
arteries (75%). It can rarely arise from the lumbar arteries. If present on diagnostic examination, confirm and
proceed carefully; avoid use of small particulates or gelfoam.
Results
Angiography for retroperitoneal hemorrhage is hampered by a low sensitivity in identifying the source of
bleeding. Oftentimes, retroperitoneal hemorrhage will be self-limiting. When a vascular injury is found,
however, embolization is associated with a high technical success rate in control of hemorrhage. As noted,
lumbar artery injury can be difficult to access and manage operatively.
Extremity Trauma
Most vascular injury occurs in the extremities and acute loss of limb perfusion can be associated with
devastating consequences including exsanguination and acute limb ischemia. Although most vascular injuries
involving the extremities are a result of penetrating trauma, blunt trauma can cause significant morbidity,
especially as a result of crushing.
Predictive findings for significant vascular injury can be classified as either hard or soft (30).
The presence of hard signs is associated with a 95% positive predictive value for vascular injury. The hard signs
include:
1. Pulsatile or expanding hematoma
2. Active hemorrhage
3. Diminished or absent pulses
4. Bruit or thrill
5. Critical limb ischemia
The presence of soft signs has a 30% positive predictive value for vascular injury. The soft signs include:
1. Nonexpanding hematoma
2. History of pulsatile bleeding
3. Neurologic deficit
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4. Unexplained hypotension
5. Proximity to vascular structures
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The ankle-brachial index is also a useful tool to exclude significant arterial injury. An index of 0.9 in the absence
of symptoms excludes arterial involvement (31).
Indications
1. Blunt trauma
a. If a pulse deficit persists following reduction of the fracture, angiography is warranted.
b. Associated traumatic injuries
(1) Knee dislocation or comminuted, displaced fracture of the proximal tibia
(2) Elbow dislocation
(3) Shoulder dislocation in the elderly
(4) Scapulothoracic dissociation
a. Penetrating extremity trauma with hard signs of vascular injury warrants immediate intervention.
b. Penetration by high-velocity missiles (e.g., assault rifles) in proximity to a major vessel warrants
angiography even in the absence of hard signs of injury. The energy of the entering missile can cause
cavitation and shock wave injury many centimeters from the bullet tract. Possible resulting injuries include
vasospasm, thrombosis, intimal flap, perforation, AVF, and intramural hematoma.
Procedure
1. Opaque markers may be placed at the entrance and exit wounds to identify the injury tract.
2. Initial evaluation should begin with an angiogram in multiple obliquities centered on the site of injury.
Contrast injection should be from a sufficiently proximal location to identify potential collateral sources of
perfusion.
3. Treatment options are dependent on the location and type of injury as described below:
a. In large arteries such as the superficial femoral, popliteal, subclavian, and brachial, stent grafts have
been reported to be effective in treating false aneurysms, AVFs, dissection, and active extravasation.
b. In small arteries such as the radial, ulnar, peroneal, and tibial, expandable and coil occlusion is advised if
proximal and distal control can be accomplished. Prior to embolization, confirmation of adequate distal
circulation and patency of collaterals is required. Occlusion may be due to spasm or dissection and should
be managed with embolization if proximal and distal access can be achieved. The techniques used in such
situations are identical to those used for crossing nontraumatic occlusions. In one series, isolated anterior
tibial injuries had a higher incidence of limb loss than posterior tibial or peroneal (32).
c. Muscular arteries arising from conduit vessels such as the profunda femoral, superficial femoral, and
popliteal arteries should be treated by subselective coil or particulate embolization as close as possible to
the site of injury.
d. Management of posttraumatic AVF is deceptively complicated. All arterial inflow to the fistula must be
occluded at the time of initial embolization to permanently seal the fistula. In larger arteries, a stent graft may
be used to isolate the vessel wall injury, but if the site of fistulization is a branch vessel, crossing the ostium
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with a stent graft will be insufficient as the fistula will recruit collateral inflow. Careful angiographic
assessment of the actual site of vessel wall injury is required. In smaller vessels, coiling distally and
proximally to isolate the fistula is generally effective. Care must be exercised to prevent coil migration into
the venous system. Short fistula may require paired venous and arterial grafts. A follow-up arteriogram is
advised to confirm adequate isolation for treated AVFs.
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e. Endografts have been employed to reperfuse acutely devascularized limb in the setting of popliteal
trauma as well as other fractures, even prior to orthopedic stabilization (33). Endografts play a clear role in
the management of penetrating trauma as well (34,35).
References
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spleen salvage: a multicenter analysis. J Trauma Acute Care Surg. 2013;75(1):69-75.
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angioembolization? Am Surg. 2013;79(10):1089-1092.
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2004;56(3):542-547.
17. Stassen NA, Bhullar I, Cheng JD, et al. Nonoperative management of blunt hepatic injury: an Eastern
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18. Lee YH, Wu CH, Wang LJ, et al. Predictive factors for early failure of transarterial embolization in blunt
hepatic injury patients. Clin Radiol . 2014;69(12):e505-e511.
19. Inchingolo R, Ljutikov A, Deganello A, et al. Outcomes and indications for intervention in non-operative
management of paediatric liver trauma: a 5 year retrospective study. Clin Radiol . 2014;69(2):157-162.
20. Asensio JA, Roldán G, Petrone P, et al. Operative management and outcomes in 103 AAST-OIS grades
IV and V complex hepatic injuries: trauma surgeons still need to operate, but angioembolization helps. J
Trauma. 2003;54(4):647-654.
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21. Bertens KA, Vogt KN, Hernandez-Alejandro R, et al. Non-operative management of blunt hepatic trauma:
does angioembolization have a major impact? Eur J Trauma Emerg Surg. 2015;41(1):81-86.
22. van der Wilden GM, Velmahos GC, Joseph DK, et al. Successful nonoperative management of the most
severe blunt renal injuries: a multicenter study of the research consortium of New England Centers for
Trauma. JAMA Surg. 2013;148(10):924-931.
23. Lopera JE, Suri R, Kroma G, et al. Traumatic occlusion and dissection of the main renal artery:
endovascular treatment. J Vasc Interv Radiol . 2011;22(11):1570-1574.
24. American Urological Association. Urotrauma: AUA Guideline. Published April 2014.
http://www.auanet.org/education/guidelines/urotrauma.cfm. Accessed October 30, 2015.
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25. Tanizaki S, Maeda S, Matano H, et al. Time to pelvic embolization for hemodynamically unstable pelvic
fractures may affect the survival for delays up to 60 min. Injury. 2014;45(4):738-741.
26. Verbeek DO, Zijlstra IA, van der Leij C, et al. Management of pelvic ring fracture patients with a pelvic
“blush” on early computed tomography. J Trauma Acute Care Surg. 2014;76(2):374-379.
27. Velmahos GC, Toutouzas KG, Vassiliu P, et al. A prospective study on the safety and efficacy of
angiographic embolization for pelvic and visceral injuries. J Trauma. 2002;53(2):303-308.
28. Ramirez JI, Velmahos GC, Best CR, et al. Male sexual function after bilateral internal iliac artery
embolization for pelvic fracture. J Trauma. 2004;56(4):734-741.
29. Freezor RJ, Hess PJ Jr, Martin TD, et al. Endovascular treatment of traumatic thoracic aortic injuries. J
Am Coll Surg. 2009;208(4):510-516.
30. Modrall JG, Weaver FA, Yellin AE. Diagnosis and management of penetrating vascular trauma and the
injured extremity. Emerg Med Clin North Am. 1998;16(1):129-144.
31. Fox N, Rajani RR, Bokhari F, et al. Evaluation and management of penetrating lower extremity arterial
trauma: an Eastern Association for the Surgery of Trauma practice management guideline. J Trauma Acute
Care Surg. 2012;73(5 suppl 4):S315-S320.
32. Scalea JR, Crawford R, Scurci S, et al. Below-the-knee arterial injury: the type of vessel may be more
important than the number of vessels injured. J Trauma Acute Care Surg. 2014;77(6):920-925.
33. Simmons JD, Walker WB, Gunter JW III, et al. Role of endovascular grafts in combined vascular and
skeletal injuries of the lower extremity: a preliminary report. Arch Trauma Res. 2013;2(1):40-45.
34. Mousa A, Chong B, Aburahma AF. Endovascular repair of subclavian/axillary artery injury with a covered
stent. A case report and review of literature. Vascular. 2013; 21:400-404.
35. Worni M, Scarborough JE, Gandhi M, et al. Use of endovascular therapy for peripheral arterial lesions:
an analysis of the National Trauma Data Bank from 2007 to 2009. Ann Vasc Surg. 2013;27(3):299-305.
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16
Thoracic Aortic Aneurysms and Dissections
David S. Wang
Michael D. Dake
Introduction
Thoracic Aortic Aneurysm (1,2)
1. Localized dilatation of the thoracic aorta greater than 50% of normal. The upper limit of normal caliber for the
descending thoracic aorta is 3 to 3.5 cm.
2. Incidence—5.9 to 10.4 cases per 100,000 person-years
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3. Male-to-female ratio—1.5:1 to 1:1
4. Classification
a. Anatomic site: 30% to 40% involve the descending thoracic aorta.
b. Morphology: fusiform (80%) or saccular (20%)
5. Risk factors—Most are “degenerative,” a late stage of atherosclerosis. Other risk factors include dissection,
infection, inflammatory aortitides (e.g., Takayasu disease), connective tissue diseases (e.g., Marfan syndrome),
trauma, and iatrogenesis.
6. The natural history is progressive expansion. Risk of rupture, usually fatal, markedly increases when the
diameter exceeds 6 cm.
7. Conventional treatment is open surgical repair. With modern techniques, shortterm death rates range from 3%
to 15% for elective cases and up to 50% for emergent operations. The risk of spinal cord ischemia is 3% to 8%.
Aortic Dissection (1,2,3)

1. Begins with a tear of the aortic intima and inner layer of the media, allowing blood to cleave a longitudinal
plane within the media. The resulting dissection flap separates the aorta into true and false lumina. The false
lumen may compress the true lumen or obstruct aortic branch vessel flow, causing end-organ ischemia. The vast
majority of primary entry tears originate just distal to the left subclavian artery (LSCA) origin or within a few
centimeters of the aortic valve. Additional communications between true and false lumina may form.
2. Incidence—2 to 3.5 and 0.5 to 2.1 cases per 100,000 person-years for all dissections and those limited to the
descending thoracic aorta, respectively
3. Male-to-female ratio—2:1 to 5:1
4. Classifications
a. Anatomic site
(1) Stanford system
(a) Type A—involves the ascending aorta (60% to 70%)
(b) Type B—confined to the descending thoracic aorta (30% to 40%)
(2) DeBakey system
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(a) Type I—involves the ascending and descending aorta
(b) Type II—confined to the ascending aorta
(c) Type III—confined to the descending aorta without (IIIa) or with (IIIb) extension into the abdominal aorta
b. Time from symptom onset
(1) Acute—<2 weeks
(2) Subacute—2 to 6 weeks
(3) Chronic—>6 weeks
c. Clinical course: At initial presentation, 30% to 42% are classified as “complicated” due to aortic rupture or
impending rupture, malperfusion of visceral or peripheral arteries, rapid false lumen aneurysmal growth,
refractory hypertension, or intractable pain.
5. Risk factors—The majority of patients have hypertension (70% to 90%). Other risk factors include existing
aneurysm, connective tissue diseases (e.g., Marfan syndrome), bicuspid aortic valve, pregnancy, trauma, and
iatrogenesis.
6. The natural history is highly variable. The primary late complication is false lumen dilatation and eventual
rupture. Aneurysmal degeneration of the false lumen occurs in 20% to 50% within 4 years despite optimal
medical therapy (OMT). Predictors of degeneration include a primary entry tear ≥10 mm, total aortic diameter
≥40 mm, false lumen diameter ≥22 mm, and partial false lumen thrombosis.
7. Conventional treatment
a. Uncomplicated type B aortic dissection (AD): OMT with control of blood pressure (goal systolic blood pressure
100 to 120 mm Hg), heart rate (goal <60 beats per minute), and pain. Lifelong close surveillance is required to
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monitor for signs of disease progression, false lumen aneurysmal dilatation, and/or malperfusion.
b. Complicated type B AD: Open repair, usually performed emergently, is associated with a surgical mortality rate
of 25% to 50% with paraplegia occurring in 7% to 36%. Concomitant OMT is required. Prior to the advent of
thoracic endovascular aortic repair (TEVAR), fenestration of the dissection flap to equalize pressures in the true
and false lumina or stent placement to open obstructed branch vessels were the primary endovascular
treatments for malperfusion (4).
Stent Grafts
After the first thoracic aortic stent graft was implanted in a patient in 1992, the first commercial device was
approved by the U.S. Food and Drug Administration (FDA) in 2005. As of this writing, there are four FDA-
approved commercial thoracic endografts (Table 16.1), most of which are second-generation devices:
Conformable TAG (W.L. GORE and Associates, Flagstaff, AZ), Valiant (Medtronic, Santa Rosa, CA), Zenith TX2
Pro-Form (Cook Medical, Bloomington, IN), and RELAY (Bolton Medical, Sunrise, FL). Other commercial devices
are available outside of the United States.
Thoracic Endovascular Aortic Repair Goals

1. Aneurysms—To provide a durable conduit for aortic blood flow across the entire longitudinal extent of the
aneurysm, resulting in aneurysm sac depressurization, thrombosis formation, and eventual stabilization or
regression in size
2. ADs—Complete coverage of the primary intimal entry tear to redirect blood flow into the true lumen while
depressurizing the false lumen to promote thrombosis. Reapposition of the aortic wall layers restores true lumen
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caliber and relieves certain branch vessel obstructions. This may prevent late aneurysmal degeneration of the
aorta.
Indications (1,2)
FDA-approved indications specific to each device are listed in Table 16.2.
1. Descending thoracic aortic aneurysms (TAAs)
a. Asymptomatic with minimum orthogonal diameter of >5.5 cm or more than two times the diameter of adjacent
nonaneurysmal aorta
Table 16.1 Characteristics of FDA-Approved Thoracic Endografts
Conformable Valiant Zenith TX2 Pro-

TAG (GORE) (Medtronic) Form (Cook) RELAY (Bolton)
Stent material Nitinol Nitinol Stainless steel Nitinol
Graft material ePTFE Polyester Polyester Polyester
Diametera (mm) 21-45 22-46 28-42 22-46
Lengthsa (cm) 10, 15, 20 10, 15, 20 12.0-21.6 10, 15, 20, 25
Delivery system 18, 20, 22, 24 22, 24, 25 20, 22 22, 23, 24, 25, 26
diameter (Fr.)
Minimum neck ≥20 ≥20 ≥25 15-25 proximal,

length (mm) 25-30 distal
Minimum neck 16-42 18-44 24-38b 19-42

diameter (mm)
ePTFE, expanded polytetrafluoroethylene.
aSizes available specific to United States.
bOuter wall to outer wall diameter.
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Table 16.2 FDA-Approved On-Label Indications for Thoracic Endografts
Indication Devices
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Thoracic aortic aneurysm All FDA-approved thoracic stent grafts
Penetrating atherosclerotic ulcer All FDA-approved thoracic stent grafts
Blunt thoracic aortic injury Conformable TAG, Valiant
Type B aortic dissection Conformable TAG, Valiant
b. Asymptomatic with growth rate of >1 cm over 1 year

c. Symptomatic, regardless of aneurysm size
2. Type B ADs (3)
a. Complicated acute type B dissections: TEVAR is the treatment of choice for acute type B ADs complicated by
rupture or impending rupture, malperfusion, early aortic expansion, refractory hypertension, or intractable pain.
b. Uncomplicated acute type B dissections: Despite the completion of two randomized controlled trials (RCTs)
comparing TEVAR and medical management (see “Results” section) (5,6), the role of preemptive TEVAR
remains highly controversial. Recently, there is increased attention paid to identifying patients initially deemed
uncomplicated, who are at high risk for delayed complications. Numerous anatomic and clinical features are
being considered as high risk criteria. Proactive endovascular treatment of “uncomplicated” patients determined
to be at high risk for delayed complications is currently under active investigation.
c. Complicated subacute/chronic type B dissections: For patients who were initially uncomplicated and develop
delayed complications (i.e., aortic diameter growth >1 cm per year, false lumen aneurysm with total aortic
diameter >60 mm, malperfusion syndrome, or recurrent pain) in the subacute or early chronic phase, prompt
intervention, whether TEVAR or open surgery, is required; however, the optimal approach is unclear.
3. Other isolated thoracic aortic lesions including penetrating atherosclerotic ulcers, intramural hematomas, blunt
traumatic thoracic aortic injuries, and contained ruptures
4. Less common investigational applications include pseudoaneurysms, aortic fistulas, and mycotic aneurysms.
TEVAR is also used in hybrid surgical procedures, such as the “elephant trunk” technique (7).
Contraindications
Absolute
1. Sensitivities or allergies to device materials
2. Conditions that may increase the risk of endovascular graft infection
Relative
Exclusionary criteria from FDA clinical trials may be bypassed at the discretion of the operator, bearing in
mind that outcomes may vary.
1. Inadequate anatomy for TEVAR
a. Anatomic obstacles may be overcome with adjunctive surgical procedures (see “Special Considerations”
section).
2. Sensitivities or allergies to contrast material or renal insufficiency
3. Severe comorbidities with relatively short life expectancy
4. TEVAR is not recommended in patients with underlying connective tissue disease, except as a bailout
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procedure or adjunct to surgical therapy (1).
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Preprocedure Imaging
Imaging should be performed within 3 months of the procedure.
1. Computed tomography (CT) should be performed from the thoracic inlet to the femoral artery bifurcations.
a. Noncontrast images can be helpful for evaluation of vascular calcifications, intramural hematoma, or other
high-density lesions.
b. Computed tomographic angiography (CTA) performed during the first-pass arterial phase is the most critical
component of preprocedural imaging. Cardiac gating should be performed for lesions that may involve the
ascending aorta.
c. Reformatting in multiple planes is essential for accurate measurements.
d. For type B ADs, delayed imaging should be performed to evaluate branch vessel ischemia and other potential
complications.
2. Magnetic resonance angiography (MRA) can be used in patients with impaired renal function or intolerance to
iodinated contrast media. Evaluation of calcifications is however limited.
3. Transesophageal echo (TEE) or intravascular ultrasound (IVUS) may be useful for precise localization of the
primary entry tear in ADs.
4. If the target lesion is in close proximity to the LSCA, CT or magnetic resonance (MR) angiography of the head
and neck should be considered.
Measurement Techniques and Imaging Assessment

Measurements are made on the arterial phase images. Figure 16.1 illustrates several of the recommended
parameters for case selection and planning.
1. Descending TAAs
a. Proximal landing zone length is the distance from the LSCA (or left common carotid artery [LCCA]) to the
proximal extent of the TAA.
b. Distal landing zone length is the distance from the distal extent of the TAA to the celiac trunk.
c. Total treatment length is the sum of the length of the aneurysm and selected lengths of the proximal and distal
landing zones.
d. Landing zone diameter is generally measured from inner wall to inner wall, excluding wall calcifications but
including intraluminal thrombi and plaque.
e. Evaluation of landing zone morphology includes assessment of angulation, tortuosity, and presence of
intraluminal thrombi and calcifications.
f. Quantitative and qualitative evaluation of potential vascular access pathways are performed as done for the
landing zones. This should include the bilateral common femoral, external iliac, and common iliac arteries and the
distal infrarenal aorta.
g. The overall morphology and degree of atherosclerotic disease of the aorta should also be assessed.
2. Complicated acute type B ADs
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a. The primary intimal entry tear must be clearly identified by careful tracing of the dissecting septum.
Downstream re-entry fenestrations should also be identified.
b. Further characterization includes evaluation of the proximal and distal extents of the dissection and for
possible involvement of aortic branch vessels.
c. In the presence of branch vessel ischemia, it is important to determine if the ischemic organ is being supplied
by the true or false lumen.
Selection Criteria for Endograft Repair

Patient selection is based on:
1. Anatomic considerations. Inappropriate anatomy is one of the most common reasons for treatment failure.
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FIGURE 16.1 • Recommended aortic dimensions to be measured in evaluation of a descending thoracic aortic
aneurysm for stent-graft management.
2. Clinical considerations. The risk of TEVAR is weighed relative to that of open repair and medical management
in the context of overall life expectancy and quality of life.
Anatomic Criteria
1. Proximal and distal landing zones
a. Descending TAAs: Normal aortic segments ≥20 mm in length are required distal to either the LSCA or LCCA
and proximal to the celiac trunk.
b. Complicated acute type B ADs: No strict anatomic criteria. A proximal landing zone of ≥10 mm distal to the
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LSCA is generally sufficient.
c. Absence of significant thrombus or calcification
d. Aortic diameters that can be accommodated by available devices, generally <40 mm
e. A radius of curvature of >35 mm or aortic angulation of <60 degrees is generally preferred.
2. Iliofemoral vascular access
a. Adequate caliber to accommodate delivery systems or anatomy suitable for a surgical conduit
b. Absence of significant tortuosity, thrombus, or calcification
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Device Selection for Descending Thoracic Aortic Aneurysms
1. Device diameter: Device diameters are generally oversized 10% to 20% relative to the luminal diameter of the
native landing zones.
a. If the distal landing zone diameter is significantly smaller than the proximal, consider a tapered endograft or a
combination of devices of different diameters.
2. Device length: Longer landing zones are generally preferred when possible.
a. If multiple endografts are to be used, the devices should overlap a minimum of 5 mm.
b. If the landing zone is angulated, the treatment length may need to be elongated. Particularly important for
proximal landing zones, the leading edge of the device should not be placed in close proximity to the apex of an
acute angle. Doing so may result in malapposition of the stent graft along a tight inner curve, increasing the risk
of a type I endoleak or endograft collapse (8).
c. For a large TAA, redundancy in device length may be needed to account for potential bowing of the endograft
in the aneurysm sac.
Device Selection for Complicated Acute Type B Aortic Dissections

1. Device diameter: Endografts are oversized in the lower range of 5% to 10% over the luminal diameter of the
nondissected aorta just proximal to the primary entry tear.
2. Device length: The appropriate length remains controversial with strategies ranging from focal coverage of the
proximal tear to the less common coverage of the entire dissection. Exclusion of the mesenteric aortic branches
is not recommended. If the dissection is complicated by rupture, multiple devices are typically needed to prevent
retrograde flow into the false lumen through distal tears. The preferred sequence of multiple device implantation
is proximal to distal.
Special Considerations
1. LSCA and celiac trunk
a. For lesions that extend close to but not proximal to the LSCA, landing zone limitations are increasingly
being challenged. Intentional coverage of the LSCA is often needed to effectively extend the proximal
landing zone.
b. Although divergent opinions exist, routine preprocedural revascularization of the LSCA (e.g., left carotid
to subclavian bypass) in patients with planned LSCA exclusion is recommended, unless TEVAR is
performed emergently (9).
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c. Thoracic aortic pathologies that extend proximal to the LSCA require hybrid surgical and endovascular
treatments, such as the elephant trunk technique (7).
d. Intentional coverage of the celiac trunk without prior revascularization is not recommended. Hybrid
surgical and endovascular approaches for treatment of thoracoabdominal aneurysms are being explored.
e. Other approaches to overcome landing zone anatomic challenges include the development of branched
and fenestrated thoracic aortic endografts and percutaneous revascularization techniques (e.g., “chimney”
graft).
2. Cerebrospinal fluid (CSF) drainage (10)
a. CSF drainage can prevent and reverse spinal cord ischemia in open and endovascular procedures of the
thoracic aorta.
b. Prophylactic CSF drainage should be considered for patients with perioperative hypotension (mean
arterial pressure <70 mm Hg), aortic treatment length >20 cm, endograft coverage between the levels of T8
and L2, and prior history of AAA repair.
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Procedure
Deployment procedures are highly specific to each device. The steps described here provide a general
outline for thoracic stent-graft deployment.
Vascular Access
1. Arterial access is preferably through the common femoral artery but may be via the external iliac or
common iliac arteries or the distal infrarenal aorta. A temporary access conduit may be placed surgically to
facilitate device delivery.
2. Vascular access is typically achieved by surgical cutdown but is increasingly being done using
percutaneous approaches.
3. For ADs, select an access site that allows entrance into the true lumen.
Descending Thoracic Aortic Aneurysms
1. Continuous monitoring of vital signs, particularly arterial pressure, is mandatory.
a. If the LSCA is to be covered, the arterial line should be placed in the right radial artery.
b. Use of intraoperative somatosensory-evoked potentials and electroencephalography to detect neurologic
complications, TEE, or other invasive monitoring techniques is left to the discretion of the operator.
2. The procedure is typically performed with the patient under general or regional anesthesia.
3. With the patient supine, sterile access sites are prepared.
4. To allow for lateral angiography, patient's arms should be raised or, if brachial artery access is needed,
positioned at 90 degrees.
5. For imaging purposes, cannulate the common femoral artery contralateral to the previously determined
site for stent-graft delivery per routine techniques. The brachial artery may also be used.
6. After placement of a sheath, advance a marker pigtail catheter to the proximal aortic arch.
7. Perform an initial aortogram with the fluoroscope angled in the left anterior oblique projection,
perpendicular to the aortic arch (typically between 45 degrees and 75 degrees) as calculated from the
preprocedure CT or MR.
8. Obtain arterial access at the planned endograft insertion site.
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9. Once access is obtained, anticoagulate the patient for the duration of the procedure to achieve an
activated clotting time of 250 to 300 seconds.
10. Prepare the stent-graft delivery system according to manufacturer instructions.
11. With continuous fluoroscopic guidance angled perpendicular to the proximal landing zone, advance the
endograft delivery system to the target site over a superstiff 0.035 in. guidewire. Use the device's
radiopaque markers to confirm positioning.
12. After reconfirming positioning, deploy the device under continuous fluoroscopic visualization per
manufacturer instructions.
a. For intubated patients, transient apnea may aid in deployment accuracy.
b. Other measures to prevent device malpositioning, such as transient hypotension or adenosine-induced
cardiac asystole, are no longer necessary.
13. Carefully withdraw the delivery catheter under fluoroscopic observation.
14. Perform molding balloon angioplasty as needed.
15. Deployment of additional devices is performed in identical fashion. The order of device deployment is
dependent on the system used.
16. Completion angiogram is performed with the angiographic catheter placed proximal to the endovascular
graft.
17. As needed, deploy additional devices and/or repeat balloon dilatation to ensure adequate coverage,
device expansion, and wall apposition.
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Complicated Acute Type B Aortic Dissections
The procedure for TEVAR in complicated acute type B AD is performed in similar fashion to that of TAA with
the following key differences:
1. Blood pressure should be strictly maintained within a narrow range of normal to minimize progression of
the dissection.
2. Exclusive true lumen passage of the principal guidewire is essential as deployment of a stent graft in the
false lumen leads to catastrophic consequences.
3. TEE or IVUS may be useful for identifying the location of the primary entry tear and other intimal tears,
confirming wire passage through the true lumen, and documenting exclusion of the proximal false lumen
during deployment.
4. Once the device is deployed, balloon molding is usually not performed and further manipulation is kept to
a minimum because the dissection flap is vulnerable to additional perforations or retrograde extension into
the proximal aortic arch (11). Devices with proximal rigid or bare-metal segments are less preferred.
5. If there is persistent malperfusion after the primary entry tear is covered, deployment of bare stent(s) or
flap fenestration may be performed in the distal aspect of the dissection (4,12) and/or stents may be placed
in each obstructed aortic branch if the false lumen supplies blood to an end organ (4).
Important Tips
1. Manipulation of guidewires and the delivery system in the aortic arch should be kept to minimum.
2. Hypotension should be avoided to decrease the risk of spinal cord ischemia.
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Immediate
1. Patients are monitored in the intensive care unit for a minimum of 24 hours.
a. Mean arterial pressure should be maintained over 100 mm Hg immediately after device deployment.
b. Monitor hemodynamic function and for signs and symptoms of paraplegia or paraparesis, stroke, mesenteric
or lower extremity ischemia, and other potential immediate complications.
c. No postprocedural anticoagulation is necessary.
Follow-up Imaging Surveillance

1. Follow-up imaging and clinical evaluation are performed at 1, 6, and 12 months and then annually. More
frequent imaging is needed if an endoleak is identified.
2. CT is the default modality for postprocedural imaging.
3. MRA remains an alternative to CT. Although all of current FDA-approved devices are MR-compatible,
evaluation may be limited by compromised image quality in regions immediately adjacent to the device.
4. Chest radiograph: Frontal, lateral, and 45-degree bilateral posterior oblique views of the entire device(s) are
performed for evaluation of device integrity.
Results
Descending Thoracic Aortic Aneurysms
Clinical trial outcomes of FDA-approved devices are as follows:
1. 98% to 99.5% technical success rate (13,14,15)
2. At 1 year (13,14,15)
a. 91% to 92.9% of TAAs remain stable or decreased (>5 mm) in size.
b. ≤0.7% aneurysm rupture, ≤0.7% open conversion, and 0.7% to 3.9% stent-graft migration
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3. At 5 years (16,17)
a. Aneurysm-related mortality of 2.8% to 5.9% with TEVAR compared with 11.7% to 12% for open surgery.
b. 81% to 94.1% of TAAs remain stable or decreased in size.
Complicated Acute Type B Aortic Dissections
1. Meta-analysis of 2,531 patients who underwent TEVAR and 1,276 who underwent open surgical repair
(18)
a. Pooled 30-day/in-hospital mortality rate: 7.3% for TEVAR versus 19% for open surgery
b. Pooled cerebrovascular events and spinal cord ischemia rates: 3.9% and 3.1% for TEVAR versus 6.8%
and 3.3% for open surgery, respectively
2. Meta-analysis of 942 patients who underwent TEVAR (19)
a. Technical success: 95%
b. Complete false lumen thrombosis: 85%
c. Stroke and paraplegia: 3.1% and 1.9%
d. 30-day mortality: 9%
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e. Late mortality (mean 20 months): 3.6%
Uncomplicated Type B Aortic Dissections
Two RCTs compared TEVAR with OMT versus OMT alone
1. Investigation of Stent Grafts in Patients with Type B Aortic Dissection (INSTEAD) trial (5,20):
subacute/chronic uncomplicated type B ADs
a. Two-year follow-up (5): aortic remodelling in 91.3% of TEVAR with OMT patients versus 19.4% in OMT
only patients. However, there was no survival benefit (88.9% vs. 95.6%, respectively).
b. Five-year follow-up (20): reduced aorta-related mortality (6.9% vs. 19.3%, respectively) and disease
progression (27% vs. 46.1%, respectively) for TEVAR with OMT patients compared with OMT alone. In the
OMT-only group, 21.2% required crossover to TEVAR during follow-up due to evolving complications. After
TEVAR, complete false lumen thrombosis was found in 90.6% at 5 years.
2. Acute Dissection: Stent graft OR Best medical therapy (ADSORB) trial (6): acute uncomplicated type B
ADs
a. One-year follow-up: complete false lumen thrombosis in 63.3% of TEVAR with OMT patients versus 6.5%
in the OMT-only group with a corresponding significantly larger true lumen diameter in the combined
treatment group
Complications (8)
Early
1. Postimplantation syndrome: low-grade fever, mild leukocytosis, elevated C-reactive protein, and possible
reactive pleural effusion. This is self-limited and should resolve within a week.
2. Spinal cord ischemia (0.8% to 3%): Paraparesis or paraplegia is less common than with open surgical repair.
a. If detected early, may be reversed with prompt CSF drainage and maintaining a mean blood pressure of 80 to
90 mm Hg
b. To avoid intracranial hypotension, drainage should be performed over the first 24 to 72 hours and limited to
<15 mL per hour or <350 mL per day.
3. Cerebrovascular stroke (2.1% to 3.6%): associated with longer procedure times and extensive device
manipulation within the aortic arch
4. Aortic perforation, de novo dissection, or extension of an existing dissection. Retrograde dissection into the
ascending aorta is reported in 0.7% to 2.5% of type B AD TEVAR cases (11).
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5. Endoleaks (10% to 20%): Endoleaks and their treatment are discussed in Chapter 19.
6. Device malposition, incomplete expansion, migration, and collapse
7. Vascular access complications include thrombosis, dissection, rupture, and avulsion.
Late
1. Endoleaks
2. Spinal cord ischemia may present as late as 30 days following device implantation.
3. Device migration, collapse, component separation, or fabric tears
4. Stent fracture: Isolated fractures are often of little clinical consequence.
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5. Residual or recurrent disease and progression toward eventual rupture
References
1. Grabenwöger M, Alfonso F, Bachet J, et al. Thoracic endovascular aortic repair (TEVAR) for the treatment
of aortic diseases: a position statement from the European Association for Cardio-Thoracic Surgery (EACTS)
and the European Society of Cardiology (ESC), in collaboration with the European Association of
Percutaneous Cardiovascular Interventions (EAPCI). Eur J Cardiothorac Surg. 2012;42:17-24.
2. Hiratzka LF, Bakris GL, Beckman JA, et al. 2010 ACCF/AHA/AATS/ACR/ASA/SCA/SCAI/SIR/STS/SVM

guidelines for the diagnosis and management of patients with thoracic aortic disease. A report of the
American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines,
American Association for Thoracic Surgery, American College of Radiology, American Stroke Association,
Society of Cardiovascular Anesthesiologists, Society for Cardiovascular Angiography and Interventions,
Society of Interventional Radiology, Society of Thoracic Surgeons, and Society for Vascular Medicine. J Am
Coll Cardiol . 2010;55:e27-e129.
3. Fattori R, Cao P, De Rango P, et al. Interdisciplinary expert consensus document on management of type
B aortic dissection. J Am Coll Cardiol . 2013;61:1661-1678.
4. Williams DM, Lee DY, Hamilton BH, et al. The dissected aorta: percutaneous treatment of ischemic
complications—principles and results. J Vasc Interv Radiol . 1997;8:605-625.
5. Nienaber CA, Rousseau H, Eggebrecht H, et al. Randomized comparison of strategies for type B aortic
dissection: the INvestigation of STEnt Grafts in Aortic Dissection (INSTEAD) trial. Circulation.
2009;120:2519-2528.
6. Brunkwall J, Kasprzak P, Verhoeven E, et al. Endovascular repair of acute uncomplicated aortic type B
dissection promotes aortic remodelling: 1 year results of the ADSORB trial. Eur J Vasc Endovasc Surg.
2014;48:285-291.
7. Cao P, De Rango P, Czerny M, et al. Systematic review of clinical outcomes in hybrid procedures for aortic
arch dissections and other arch diseases. J Thorac Cardiovasc Surg. 2012;144:1286-1300.
8. Lee WA. Failure modes of thoracic endografts: prevention and management. J Vasc Surg. 2009;49:792-
799.
9. Matsumura JS, Lee WA, Mitchell RS, et al. The Society for Vascular Surgery Practice Guidelines:
management of the left subclavian artery with thoracic endovascular aortic repair. J Vasc Surg.
2009;50:1155-1158.
10. Hnath JC, Mehta M, Taggert JB, et al. Strategies to improve spinal cord ischemia in endovascular
thoracic aortic repair: outcomes of a prospective cerebrospinal fluid drainage protocol. J Vasc Surg.
2008;48:836-840.
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11. Fattori R, Lovato L, Buttazzi K, et al. Extension of dissection in stent-graft treatment of type B aortic
dissection: lessons learned from endovascular experience. J Endovasc Ther. 2005;12:306-311.
12. Canaud L, Faure EM, Ozdemir BA, et al. Systematic review of outcomes of combined proximal stent-
grafting with distal bare stenting for management of aortic dissection. Ann Cardiothorac Surg. 2014;3:223-
233.
13. Makaroun MS, Dillavou ED, Kee ST, et al. Endovascular treatment of thoracic aortic aneurysms: results
of the phase II multicenter trial of the GORE TAG thoracic endoprosthesis. J Vasc Surg. 2005;41:1-9.
14. Fairman RM, Criado F, Farber M, et al. Pivotal results of the Medtronic Vascular Talent Thoracic Stent
Graft System: the VALOR trial. J Vasc Surg. 2008;48:546-554.
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15. Matsumura JS, Cambria RP, Dake MD, et al. International controlled clinical trial of thoracic endovascular
aneurysm repair with the Zenith TX2 endovascular graft: 1-year results. J Vasc Surg. 2008;47:247-257.
16. Makaroun MS, Dillavou ED, Wheatley GH, et al. Five-year results of endovascular treatment with the
Gore TAG device compared with open repair of thoracic aortic aneurysms. J Vasc Surg. 2008;47:912-918.
17. Matsumura JS, Melissano G, Cambria RP, et al. Five-year results of thoracic endovascular aortic repair
with the Zenith TX2. J Vasc Surg. 2014;60:1-10.
18. Moulakakis KG, Mylonas SN, Dalainas I, et al. Management of complicated and uncomplicated acute
type B dissection. A systematic review and meta-analysis. Ann Cardiothorac Surg. 2014;3:234-246.
19. Parker JD, Golledge J. Outcome of endovascular treatment of acute type B aortic dissection. Ann Thorac
Surg. 2008;86:1707-1712.
20. Nienaber CA, Kische S, Rousseau H, et al. Endovascular repair of type B aortic dissection: long-term
results of the randomized investigation of stent grafts in aortic dissection trial. Circ Cardiovasc Interv.
2013;6:407-416.
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17
Pulmonary Vascular Malformations
Jeffrey S. Pollak
Pulmonary vascular malformations may involve abnormalities of the arteries, veins, communications between
these two, lymphatics, and associated lung abnormalities. This chapter will concentrate on pulmonary
arteriovenous malformation as well as acquired fistula and aneurysm, which are often amenable to interventional
radiologic management. Conditions having abnormal systemic arterial supply into abnormal or normal lung tissue
such as bronchopleural sequestration and scimitar syndrome artery are typically managed surgically or
expectantly, although embolization of arterial supply may occasionally be appropriate (1). Conditions with
abnormal venous drainage are usually also managed conservatively.
Indications
1. Pulmonary arteriovenous malformations (PAVMs): consist of a congenital connection between a
pulmonary artery and vein, without a normal capillary bed. These are the most common type of pulmonary
arteriovenous connections. They are associated with hereditary hemorrhagic telangiectasia (HHT) (Osler-
Weber-Rendu syndrome) in 56% to 97% of patients (2,3) and are more commonly multiple in that setting.
2. Acquired pulmonary arteriovenous fistula: are less commonly, clinically significant and can occur in a
variety of conditions (4):
a. Cirrhosis (hepatopulmonary syndrome): These are rarely large enough to warrant embolization.
b. Glenn or Fontan shunts for congenital heart disease
c. Infections: schistosomiasis and actinomycosis
d. Metastatic thyroid carcinoma and gestational trophoblastic disease
e. Amyloidosis
f. Fanconi syndrome
g. Erosion of an aneurysm into a vein
h. Trauma
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3. Pulmonary artery aneurysms: True and false aneurysms of the pulmonary arteries have numerous
etiologies (5):
a. Poststenotic and hyperdynamic states (such as with left-to-right shunts), usually in the setting of
congenital heart disease
b. Degenerative vascular disorders, including connective tissue diseases such as Marfan and Ehlers-
Danlos
c. Inflammatory conditions
(1) Necrotizing infections with vascular erosion (e.g., Rasmussen aneurysm of tuberculosis, fungal,
pyogenic)
(2) Mycotic aneurysms from septic emboli from right-sided endocarditis
(3) Syphilis
(4) Primary vasculitis (e.g., Behçet syndrome, Takayasu arteritis)
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d. Neoplasms, usually with erosion into a pulmonary artery
e. Pulmonary artery hypertension
f. Trauma, especially iatrogenic trauma, as from pulmonary artery catheters
g. Hughes-Stovin syndrome. A rare idiopathic condition in which patients have pulmonary artery aneurysms
and venous thromboses. Its relationship to Behçet syndrome is uncertain.
Contraindications
There are no absolute contraindications to pulmonary artery embolization; however, occlusion of a
malformation or fistula in someone with severe pulmonary hypertension should be done cautiously given the
risk of further elevation of pulmonary artery pressure and cor pulmonale.
Pulmonary Arteriovenous Malformations

Association with Hereditary Hemorrhagic Telangiectasia (3,4,6)
1. This disorder results in scattered arteriovenous malformations (AVMs), manifested primarily as
mucocutaneous telangiectases and less frequently as larger visceral AVMs. Its prevalence is estimated at 1 in
5,000 to 10,000.
2. Several different genes have been found to cause HHT, with the three identified ones coding for proteins
involved with transforming growth factor-β signal transduction. The two most common are HHT1, which results
from a defect in endoglin, and HHT2, resulting in a defect in activin receptor-like kinase 1. The third is a
combined syndrome of HHT with juvenile polyposis.
3. A definite clinical diagnosis of the heterozygous, autosomal dominant disorder depends on the presence of at
least three of the following four features. The diagnosis is possible if only two are present:
a. Multiple telangiectases of the skin and mucous membranes
b. Repeated episodes of spontaneous epistaxis, occurring in over 90% of patients
c. An autosomal dominant pattern of inheritance
d. Typical visceral malformations
(1) PAVM in approximately 20% to 70%, more common in HHT1 than HHT2
(2) Central nervous system in approximately 10%, more common in HHT1 than HHT2. Still, the most common
neurologic events in patients with HHT are due to paradoxical embolization through PAVMs.
(3) Gastrointestinal tract telangiectases and less commonly larger AVMs occur in 55% to 70% and can produce
bleeding in approximately 25%.
(4) Liver AVM occurs in 41% to 74% but are symptomatic in less than 10%, and these patients generally have
HHT2.
4. Genetic testing can identify approximately 85% of patients with HHT.
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Pathology of PAVM (4)
1. Types
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a. Simple PAVMs are fed by an artery contained within one pulmonary segment and account for 80% to 90% of
PAVMs. The artery may have more than one distal branch supplying the malformation.
b. Complex PAVMs are fed by arteries from more than one pulmonary segment and account for 10% to 20%.
c. Diffuse involvement of one or more segments or lobes, typically basilar, accounts for 5%.
d. The nidus connecting the artery(ies) and vein(s) may be a single aneurysmal sac or a plexiform, septated,
multichanneled connection, with complex PAVMs more commonly having the latter type of nidus.
e. A systemic artery will rarely be found to supply a PAVM.
2. Location
a. Lower lobes in approximately 65%
b. Upper lobes, right middle lobe, and lingula in 35%
3. Multiplicity
a. Multiple PAVMs in over 50%
b. Bilateral PAVMs in over 40%
Clinical Manifestations of PAVM and Fistulae (2,3)

1. Right-to-left shunting can result in
a. Arterial hypoxemia. Clinical manifestations include dyspnea, fatigue, cyanosis, clubbing, and rarely
polycythemia; however, patients are also often asymptomatic.
b. Paradoxical embolization. This most commonly manifests in the brain but can affect other organs.
Thromboembolic embolization can result in stroke and transient ischemic attack (TIA) in 11% to 55% of patients,
whereas bacterial embolization has been reported to result in brain abscess in 5% to 25%.
c. High-output heart failure. This is uncommon but has been reported in neonates.
2. Rupture of thin-walled PAVMs can result in hemoptysis and hemothorax in 3% to 18%.
3. Migraine headaches are more common in patients with PAVM.
4. Conditions in which the risk of PAVM complications appears greater are pregnancy and pulmonary
hypertension, during which enlargement of PAVM may occur. Preadolescent children appear to be at lower risk
for major complications, particularly with smaller lesions.
5. Symptoms can be related to associated disorders, such as other manifestations of HHT.
Embolotherapy for Pulmonary Arteriovenous Malformations

Preprocedure Evaluation: Diagnostic Evaluation for PAVM (3,7)
1. Goals
a. Detect PAVM with high sensitivity but also high specificity.
b. Characterize size, number, and location of PAVMs. This will determine whether the PAVM(s) need specific
treatment. For any one PAVM, the presence of a feeding artery of 2 to 3 mm or greater is an indication to
consider invasive treatment.
2. Who to evaluate?
a. Patients with symptoms or signs suggestive of PAVM by history, physical examination, or incidentally found on
imaging
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b. Screen all patients with HHT.
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3. Diagnostic tests for PAVM
a. Detection of right-to-left shunting. A disadvantage of these studies is the lack of morphologic detail with regard
to location, number, and size of PAVMs.
(1) Pulse oximetry may show oxygen saturation less than 97%, especially in an erect position due to the
predilection of PAVMs for the lower lobes. The sensitivity and specificity of pulse oximetry is too low for it to be
the sole diagnostic study, but due to its completely noninvasive nature, it may be acceptable in young children
because they appear to be less prone to develop complications from smaller PAVMs.
(2) Contrast echocardiography is considered the most sensitive study for detecting PAVMs, with a delay in the
appearance of left atrial echoes by 3 to 10 heartbeats enhancing specificity for intrapulmonary shunts. Stratifying
positive studies into three or four grades by the number of bubbles appearing in left cardiac chambers is of value
because those having a grade 1 study consisting of only a small number of bubbles will have no PAVMs of
sufficient size to embolize. It is even possible that this group may not have PAVM because a percentage of the
normal population can have such a low-grade positive study.
(3) Other studies that are now rarely used for specific PAVM evaluation are arterial blood gas measurements on
room air plus additionally on 100% inspired oxygen to permit shunt fraction determination and radionuclide shunt
studies.
b. Morphologic studies can provide information on the location, size, and number of lesions.
(1) Chest radiographs can show a lobular soft tissue mass with enlarged vascular structures coursing to and
from it; however, sensitivity is limited and a normal chest radiograph does not exclude PAVM.
(2) Computed tomography (CT) is highly sensitive in diagnosing and characterizing PAVM; although, false
positives can occur. Given its noninvasive nature, it has become the gold standard study. It is also very useful for
follow-up of the treated patient.
(3) Magnetic resonance imaging (MRI) holds potential for PAVM detection without ionizing radiation exposure,
but its current resolution is generally considered insufficient compared to CT.
(4) Pulmonary angiography is only performed for equivocal findings on noninvasive studies and immediately
before embolization. It can miss tiny PAVMs compared to CT. Various projections may be needed to find the
optimal one for catheterization of the supplying artery.
4. How to evaluate patients?
a. Patients with symptoms or signs indicative of PAVM by history and/or physical examination may benefit by
proceeding directly to CT.
b. Asymptomatic patients at risk for PAVM should undergo screening (see the following text). This basically
means all patients with HHT.
5. Screening for PAVM: Most HHT centers currently rely on contrast echocardiography for screening
asymptomatic patients with this condition at least once they reach adolescence. If negative, no further evaluation
is necessary. If grade 1, then microscopic or tiny PAVMs should be assumed to be present and repeat
echocardiography is performed every 5 years to assess for possible growth. Higher grades of positivity prompt
CT scanning to evaluate for PAVMs of a size requiring invasive treatment. If that is negative, currently, repeat CT
scanning at 5-year intervals, and probably before pregnancy, is recommended to look for PAVM growth.
Because asymptomatic children appear to have a very low rate of complications from PAVM, pulse oximetry
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(possibly with assessment of changes with differences in posture) is the most that is necessary. They are
rescreened in the adult fashion once they reach adolescence.
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Periprocedural Considerations
1. Light sedation—the patient should be able to hold his or her breath.
2. No air bubbles or clots in the intravenous line or the catheters because these can result in paradoxical
embolization
3. Phlebotomy if markedly polycythemic to reduce the risk of puncture site and pericatheter thrombosis.
Polycythemia is rare given the presence of HHT-related epistaxis in the majority of patients with PAVM.
4. Heparin 3,000 to 5,000 units to prevent pericatheter thrombosis that could result in paradoxical embolization
5. Antibiotic prophylaxis—typically 1 g of cefazolin
6. Elective procedures are generally performed as an outpatient.
7. If many bilateral PAVMs are present, consider treating over more than one session and embolizing in only one
lung at a time to avoid the possibility of bilateral pleurisy.
Procedure
1. Catheterization
a. Femoral vein approach with placement of a 7 Fr. sheath. Alternate sides should be used if more than one
catheterization is needed in a short time interval.
b. A 5 Fr. pigtail is used to obtain pulmonary pressures and perform pulmonary angiography. The
angiogram can be restricted to the regions of abnormality based on a prior CT scan. Pulmonary
hypertension should raise concern for hepatic AVM, primary pulmonary hypertension (which can be linked
to HHT2), or other common etiologies. When severe, embolotherapy should be performed cautiously,
especially if the PAVM is large.
c. The pigtail catheter is exchanged for an 80-cm long, 7 Fr. multipurpose guiding catheter with a 100-cm
long coaxial, 5 Fr. angled catheter (Lumax guide, Cook Medical, Bloomington, IN). The use of a guiding
catheter provides greater support and permits the coaxial use of a variety of differently shaped 5 Fr.
catheters. The pulmonary artery feeding the PAVM is then selected with the catheter(s). Steerable and
hydrophilic wires may be used to aid this. Coaxial microcatheters are occasionally necessary. Selective
angiography is performed to confirm proper positioning and determine the proper site for occlusion.
d. Strict attention is needed to avoid air entering any catheters. Guidewires should be removed while a
catheter's hub is in a basin of saline.
2. Site of occlusion (2): Feeding artery embolization is most commonly performed and should be as distal as
possible, beyond any significant supply to normal lung and as close as feasible to the arteriovenous
connection, preferably within 1 cm. Although traditionally it has not been felt to be necessary to embolize the
nidus itself, some controversy does exist over this.
3. Embolic agent: An appropriately sized mechanical agent is used, which can be placed within the feeding
artery without risk of migrating through the right-to-left shunt.
a. Embolization coils can be used for basically any PAVM. Forming a dense cross-sectional network of
metal is important for achieving long-term occlusion; one should not just rely on the promotion of thrombosis
by a looser network of fibered coils. The first coil should be either 20% or 2 mm larger than the vessel
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diameter, and additional smaller coils are typically placed within this in all but the smallest lesions. Pushable
soft platinum coils such as Nesters (Cook, Bloomington, IN) and Tornados (Cook, Bloomington, IN) are
most useful for small- and medium-sized PAVMs, and these can be nested into themselves. Higher radial
force coils (e.g., Inconel MReye coils, Cook, Bloomington, IN)
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are used for larger, high-flow fistula. Smaller, 0.018-in. microcoils are rarely needed—only if a microcatheter
was required to reach the lesion. Several techniques can permit safer deployment:
FIGURE 17.1 • Placement of the first coil during embolization of a simple PAVM with the initial part of this
coil anchored in a distal side branch. Additional coil emboli are then placed within and proximal to the first
one to achieve a dense network of metal occluding the vessel.
(1) Anchor technique (Fig. 17.1): The initial couple of centimeter of a long coil is placed within a small distal
side branch, after which the catheter is retracted to deploy the rest of the coil within the actual feeding
artery.
(2) Scaffold technique: A long, high radial force stainless steel or Inconel coil is first placed in a large, high-
flow feeding artery (preferably after anchoring its initial 1 to 2 cm in a side branch), after which additional
high and then soft platinum coils can be placed within this.
(3) An occlusion balloon is occasionally useful for high-flow arteries having significant drag or to provide
secure positioning in short feeding arteries.
(4) Intra-aneurysmal coil embolization is rarely needed when embolization of a short feeding artery is not
feasible. In this situation, 0.018-in. systems are used.
(5) Detachable coils are infrequently needed but may be useful for the first coil in situations where there is
concern over distal, transnidal migration, such as with short feeding arteries and intra-aneurysmal
embolization, and for the final coil when there is concern over proximal prolapse and nontarget embolization
of normal pulmonary vasculature.
b. AMPLATZER Vascular Plugs (St. Jude Medical, St. Paul, MN) have gained popularity particularly for
larger PAVM channels due to their relatively rapid occlusion rate and the precision conferred by the ability
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to place and retrieve them prior to detachment (2,8,9,10). Their greater expense than coils can be offset by
the need for fewer devices, typically just one. The greater rigidity of these devices can limit their use in
more tortuous and smaller feeding arteries. This is particularly true for the AMPLATZER Vascular Plug I and
II because these require a guiding catheter or sheath to be placed to the site of
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occlusion. The recanalization rate for these devices may be lower than with coils, although with the
AMPLATZER Vascular Plug I, the adjunctive use of coils appears to be helpful for reducing that risk.
c. Microvascular Plugs (Reverse Medical, Irvine, CA). There are currently two versions of the
Microvascular Plug available, one designed for 1.5 to 3 mm diameter vessels and the other for 3 to 5 mm
diameter vessels. Also, published experience now exists for their use in PAVM embolization (11).
4. Regional embolization: Diffuse segmental or multisegmental involvement may require embolization of a
region of the lung.
5. Postembolization angiography should be done to confirm occlusion and to look for accessory feeding
arteries from other nearby regions of the lung.
Postprocedure Care
1. Remove intravenous lines to prevent iatrogenic paradoxical embolization of air or thrombus through residual
PAVMs.
2. Incentive spirometry may be used to try and ameliorate atelectasis and pleurisy after embolization of larger
PAVMs.
3. Long-term follow-up after PAVM embolization
a. Follow-up is indicated to assess for the persistence or recurrence of a treated lesion and for the growth or
enlargement of other PAVMs.
b. Regimen. The following should be done at 6 to 12 months and then every 3 to 5 years:
(1) Clinical evaluation
(2) Physiologic evaluation with pulse oximetry is simple to perform. A more revealing physiologic study may be
exercise stress testing, looking for any decline in oxygen saturation as well as of the baseline value.
(3) CT scan. It is debated whether at least the first one should be done with contrast to assess for any residual
enhancement of the sac or adjacent draining vein. With regard to size, the aneurysm of a treated lesion should
shrink by typically 70% or more.
c. An abnormality should prompt pulmonary angiography.
d. Antibiotic prophylaxis is recommended prior to dental and other “dirty” procedures due to the likely presence
of residual tiny or microscopic PAVMs.
e. Management of other issues related to HHT. In particular, iron deficiency should be corrected given data
showing an increased risk of thrombosis in this population (3).
Results (2,3,9,10,12)
1. Initial complete occlusion is accomplished in over 90%.
2. Subjective improvement is seen in respiratory symptoms and performance.
3. The risks of stroke, TIA, and brain abscess are significantly reduced to no more than approximately 3% each
and even lower if all PAVMs of any size are eliminated.
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4. Migraines typically improve.
5. Persistence or recurrence rates vary.
a. With coils, this is typically 3% to 8% but occasionally higher (up to 58%). It is most commonly due to
recanalization of an embolized branch followed by the presence of an accessory branch. These can be treated
with re-embolization. A third cause is collateral reperfusion from small pulmonary artery branches (more likely in
children), and a fourth cause is collateral flow distal to the site of occlusion from bronchial or other systemic
arteries. The significance of this small left-to-left shunt is uncertain, with hemoptysis rarely reported.
b. With AMPLATZER Vascular Plugs, reported rates are typically close to zero.
6. Growth of previously tiny PAVMs to a size requiring treatment occurs in 14% to 19% and can, of course, cause
recurrent symptoms.
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Complications (3,13,14,15)
1. Paradoxical embolization of air, thrombus, or an occluding device. The rates given below are all lower in
recent series.
a. Clinically, this may result in:
(1) Angina and/or bradycardia, presumably due to air flowing into the anteriorly positioned right coronary artery in
the supine patient. This has been reported in up to 5%. It can be treated with nitroglycerine and atropine. No
adverse consequences of this have occurred.
(2) Cerebral ischemia. Transient ischemic attack has been reported in up to 2% and stroke in less than 1%.
b. Paradoxical embolization of an occluding device has occurred in less than 1% to 4%, but serious sequelae are
rare. The device may need to be retrieved if it has migrated to a critical arterial bed.
2. Rupture of the PAVM with hemorrhage is rare and managed by completion of the embolization.
3. Local venous thrombosis is quite rare.
4. Pleurisy is the most common side effect after PAVM embolization.
a. Chest pain and fever can develop several days after the procedure in 3% to 16%. It can be treated with
nonsteroidal anti-inflammatory agents.
b. Delayed pleurisy after several weeks can occur in 2% to 5%, with high fevers and infiltrates on radiography. It
is also self-limited.
5. Late hemoptysis from systemic collateral supply into a persistent or reperfused PAVM is a rare phenomenon. If
systemic embolization is performed, it must be done cautiously given the risk that any particulate agents
migrating through systemic supply could then pass through the PAVM and result in paradoxical systemic
embolization.
6. Effects of radiation exposure from multiple studies. This may foster a change in the role of late follow-up CT
scans, particularly in asymptomatic patients without hypoxemia. Improvements in MRI may permit it to play a
greater role in the future.
Pulmonary Artery Aneurysms (5)

Clinical Manifestations
1. Related to rupture, local mass effect, or peripheral emboli
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2. Manifestations include hemoptysis, dyspnea, chest pain, cough, bruit, and pulmonary hypertension.
Treatment of Pulmonary Artery Aneurysms

1. Treatment should be considered for pseudoaneurysms, symptomatic true aneurysms, and larger
asymptomatic true ones.
2. Peripheral aneurysms can be treated with embolization. This will result in the sacrifice of a small amount of
adjacent normal lung tissue. Mechanical agents are preferably placed across the origin of the aneurysm.
3. Central aneurysms are usually best treated with surgery because that permits preservation of flow.
Embolization would result in an unacceptable amount of normal lung being lost.
4. Alternative treatment methods include vascular occlusion with thrombin and glue and exclusion with a stent
graft.
References
1. Liechty KW, Flake AW. Pulmonary vascular malformations. Semin Pediatr Surg. 2008; 7(1):9-16.
2. Pollak JS, White RI Jr. Distal cross-sectional occlusion is the “key” to treating pulmonary arteriovenous
malformations. J Vasc Interv Radiol . 2012;23(12):1578-1580.
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3. Shovlin CL. Pulmonary arteriovenous malformations. Am J Respir Crit Care Med. 2014;190(11):1217-
1228.
4. Pollak JS, White RI Jr. Hereditary hemorrhagic telangiectasia. In: Mulliken JB, Burrows PE, Fishman SJ,
eds. Mulliken and Young's Vascular Anomalies: Hemangiomas and Malformations. 2nd ed. Oxford, United
Kingdom: Oxford University Press; 2013:814-838.
5. Restrepo CS, Carswell AP. Aneurysms and pseudoaneurysms of the pulmonary vasculature. Semin
Ultrasound CT MR. 2012;33(6):552-566.
6. McDonald J, Bayrak-Toydemir P, Pyeritz RE. Hereditary hemorrhagic telangiectasia: an overview of

diagnosis, management, and pathogenesis. Genet Med. 2011;13(7):607-616.
7. Velthuis S, Buscarini E, Mager JJ, et al. Predicting the size of pulmonary arteriovenous malformations on
chest computed tomography: a role for transthoracic contrast echocardiography. Eur Respir J.
2014;44(1):150-159.
8. Tapping CR, Ettles DF, Robinson GJ. Long-term follow-up of treatment of pulmonary arteriovenous
malformations with AMPLATZER Vascular plug and AMPLATZER Vascular plug II devices. J Vasc Interv
Radiol . 2011;22(12):1740-1746.
9. Rabellino M, Serra M, Peralta O, et al. Early experience with the AMPLATZER vascular plug IV for the
occlusion of pulmonary arteriovenous malformations. J Vasc Interv Radiol . 2014;25(9):1333-1337.
10. Kucukay F, Özdemir M, Şenol E, et al. Large pulmonary arteriovenous malformations: long-term results of
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embolization with AMPLATZER vascular plugs. J Vasc Interv Radiol . 2014;25(9):1327-1332.
11. Conrad MB, Ishaque BM, Surman AM, et al. Intraprocedural safety and technical success of the MVP
micro vascular plug for embolization of pulmonary arteriovenous malformations. J Vasc Interv Radiol .
2015;26(11):1735-1739.
12. Woodward CS, Pyeritz RE, Chittams JL, et al. Treated pulmonary arteriovenous malformations: patterns
of persistence and associated retreatment success. Radiology. 2013;269(3):919-926.
13. Mager JJ, Overtoom TT, Blauw H, et al. Embolotherapy of pulmonary arteriovenous malformations: long-
term results in 112 patients. J Vasc Interv Radiol . 2004; 15(5):451-456.
14. Pollak JS, Saluja S, Thabet A, et al. Clinical and anatomic outcomes after embolotherapy of pulmonary
arteriovenous malformations. J Vasc Interv Radiol . 2006;17(1):35-44.
15. Hanneman K, Faughnan ME, Prabhudesai V. Cumulative radiation dose in patients with hereditary
hemorrhagic telangiectasia and pulmonary arteriovenous malformations. Can Assoc Radiol J.
2014;65(2):135-140.
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18
Abdominal Aortic Aneurysms
Parag J. Patel
Sanjay K. Paidisetty
Introduction
1. Abdominal aortic aneurysm (AAA)—Definition:
a. An increase in diameter of 50% compared to the adjacent normal aortic segment, or
b. Sac diameter greater than 3 cm
2. Aneurysms are classified:
a. Morphologically: fusiform—affecting the entire arterial circumference, or saccular—affecting only part of the arterial circumference
b. By their relationship to the renal arteries: suprarenal, juxtarenal, or infrarenal
3. Associations include increasing age, male sex, smoking, coronary artery disease, hypercholesterolemia, peripheral vascular disease, hypertension, and
family history (higher incidence in first-degree relatives). The reported prevalence ranges from 2% to 8% in adults older than the age of 65 years (1,2).
4. The natural history of AAA is continuous expansion resulting in increased risk of rupture or distal embolization. Risk factors for AAA rupture include
aneurysm
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size, rate of expansion, poorly controlled hypertension, chronic obstructive pulmonary disease (COPD), smoking, and family history (3). Most small
aneurysms increase in size by 2.5 mm per year; 4 mm per year is maximum normal growth (4). With progressive enlargement of an AAA, there are also
changes in the aorta above and below the aneurysm. The lengths of the proximal neck and distal cuff shorten, the entire aorta lengthens and becomes
more tortuous, iliac tortuosity increases, and iliac aneurysms may form.
5. Ruptured AAA is the 10th leading cause of death in men. The annual risk of rupture for AAA (a) less than 5.5 cm: ≤1.0%, (b) 5.5 to 5.9 cm: 9.4%, (c) 6.0
to 6.9 cm: 10.2%, and (d) ≥7.0 cm: 32.5%. AAAs >5.5 cm have an annual risk of rupture exceeding the elective 30-day operative mortality; hence, this has
been the size criterion for elective repair in men (5,6).
6. The ratio of men to women with AAA is up to 6:1 (7). Women have smaller aortic diameters compared to men, and a 5.5-cm AAA represents a much
larger relative dilatation and has an increased risk of rupture. Thus, some experts have recommended elective repair at 5 cm in women (3).
7. Treatment of AAAs include endovascular aortic aneurysm repair (EVAR) and open surgical repair. The perioperative 30-day mortality rate for EVAR is
significantly lower than for open repair. However, the 1-year mortality rates are similar between the two treatments (3). At present, more than 70% of AAAs
are treated via endovascular repair (2). There are currently eight FDA-approved EVAR devices (see Table 18.1).
Goals of Stent-Graft Therapy

1. To provide a less invasive alternative for low-risk patients, lower procedural morbidity and mortality, decreased postprocedure pain, complications, and
shortened convalescence
2. To provide treatment to high-risk patients who are not surgical candidates and would otherwise have no therapeutic option for AAA repair
Indications
1. Emergent
a. Known or suspected rupture
b. Symptomatic aneurysm (tenderness, abdominal, or back pain) regardless of aneurysm diameter
c. Rapidly expanding aneurysm: >1 cm growth in 12 months (5)
2. Elective
a. Asymptomatic fusiform aneurysm: >5.5 cm in diameter for men; >5.0 cm for women (3,5)
b. Atypical (penetrating atherosclerotic ulcer, dissecting, mycotic, or saccular) aneurysm twice the diameter of normal infrarenal aorta
c. Smaller AAAs with either concomitant common iliac aneurysms requiring repair (>2.5 to 3.0 cm in diameter) or associated thrombotic/embolic
complications (8)
d. Inflammatory AAAs
Contraindications
1. Patent inferior mesenteric artery (IMA) in the setting of significant superior mesenteric artery (SMA) narrowing where the IMA is the predominant
blood supply to the bowel
2. Patients must meet anatomic criteria for successful endograft placement, including appropriate proximal and distal landing zones as well as suitable
access vessels (see Fig. 18.1).
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Table 18.1 U.S. Food and Drug Administration (FDA)-Approved Devices for Endovascular Aneurysm Repair
Neck Min. Sheath

Length OD (Fr.)
(mm)/Max. for 24-
Diameter Iliac Seal mm
(mm)/Max. Zone Proximal
FDA Stent Graft Fixation Angulation Diameter/Min. Delivery Neck
Device Manufacturer Approval Material Material Location (°) Length (mm) System Diameter
AFX Endologix 2011 Cobalt PTFE Anatomic 15/32/60 10-23/15 Separate 19

chromium at aortic sheath
alloy bifurcation
Aorfix Lombard 2013 Nitinol Woven Infrarenal 15/29/90 9-19/15 Integrated 22

polyester with hooks sheath
Endurant II Medtronic 2010 Nitinol Woven Suprarenal 10/32/60 8-25/15 Integrated 18

polyester with hooks sheath
Excluder GORE 2011 Nitinol PTFE Infrarenal 15/32/60 8-25/10 Separate 20

C3 with hooks sheath
Nellix Endologix a Cobalt chromium stents to provide 10/32/60 9-35/20 Integrated 17

blood flow from infrarenal segment to sheath
the legs surrounded by endobags
filled with polymer to seal the
aneurysm sac
Ovation TriVascular 2011 Nitinol PTFE Suprarenal 7/30/45 or 8-20/10 Integrated 14

Prime with hooks 10/30/60 sheath
and
infrarenal
polymer-
filled seal
rings
Zenith Flex Cook 2003 Stainless Woven Suprarenal 15/32/60 7.5-20/10b Integrated 21
steel polyester with hooks sheath
Zenith Cook 2012 Stainless Woven Suprarenal 4/31/45 Ipsilateral 9- Integrated 23

Fenestrated steel polyester with hooks 21/30b; sheath
Contralateral
7-21/30b
OD, outer diameter; PTFE, polytetrafluoroethylene.
aCurrently under clinical investigation with FDA investigational device exemption.
bIliac diameter measurements for the Cook Zenith devices are from outer wall to outer wall.
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FIGURE 18.1 • Aortic dimensions to be measured in evaluation of an aneurysm for endograft placement. Diameters (D) are measured from transverse
images from a CTA that are reconstructed at right angles to the long axis of the vessel being measured. D1 = lowest renal artery, D2 = 4 to 15 mm
distal to the lowest renal artery (distance depending on type of endograft chosen, see Table 18.1), D3 = aortic bifurcation, D4 = largest aneurysm sac
dimension, D5 and D6 = right and left common iliac arteries, respectively, and D7 and D8 = right and left distal landing zones, respectively. Lengths
(L) are measured from digital subtraction angiography (DSA) obtained with a calibrated catheter or from 3D reconstructions of the vessel on a CTA. L1
= neck, L2 = lowest renal artery to the aortic bifurcation, and L3 and L4 = aortic bifurcation to the right and left common iliac artery bifurcations. Angle
1 = angulation of the proximal neck obtained from DSA or CTA multiplanar reformations.
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3. Relative contraindications include severe concomitant disease with short life expectancy, renal insufficiency, and severe contrast reactions.
Endografts have been successfully implanted in patients with renal insufficiency or severe reactions to contrast using reduced amounts of diluted
contrast, alternative contrast media such as carbon dioxide, and intravascular ultrasound.
Preprocedure Imaging
As opposed to open surgical repair, endovascular repair of AAA is entirely dependent on radiologic imaging for pre-, intra-, and postprocedure
management.
Careful imaging to obtain accurate diameter and length measurements is essential to maximize the technical success of the stent-graft deployment.
Computed tomographic angiography (CTA) with three-dimensional (3D) reconstruction is the preferred imaging modality for preprocedural planning and
follow-up of EVAR.
1. CTA
a. Advantages
(1) Noninvasive
(2) High resolution; able to reveal anatomic details such as calcium and small amounts of mural thrombus
(3) Allows for postprocessing at a 3D workstation that provides multiplanar reformatted images and centerline measurements for more accurate and precise
length and diameter determination
b. Disadvantages
(1) Radiation exposure
(2) Nephrotoxic contrast
c. For CTA protocols, see Chapter e-71.
2. Angiography. Angiography has largely been replaced by CTA or magnetic resonance angiography (MRA) for the preprocedure assessment of anatomy
and suitability for EVAR, so is rarely done as a stand-alone procedure.
a. Advantages
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(1) Accurate estimation of length and size
(2) Defines aortic branch vessels, including renal arteries (main and accessory), mesenteric arteries, hypogastric arteries, and lumbar and visceral artery
collaterals
(3) Carbon dioxide (CO2) can be used to decrease contrast medium nephrotoxicity
b. Disadvantages
(1) Invasive
(2) Thrombus effect: angiography = lumenography. Only shows flow lumen; therefore, is unreliable to measure diameters; single projection may not show
true maximum cross-sectional diameter.
(3) Unable to demonstrate wall pathology such as thrombus and minimal calcifications
(4) Magnification error: Focal point-to-film distance is standard, but patient body habitus may influence magnification error. Calibrated catheters are used to
avoid magnification-related measurement errors.
(5) Foreshortening creating errors in length measurements
(6) Parallax error
(7) Contrast medium nephrotoxicity
3. Magnetic resonance imaging
a. Advantages
(1) Avoids the use of iodinated contrast agents
(2) Noninvasive
(3) No radiation exposure
(4) Excellent soft tissue visualization
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b. Disadvantages
(1) Inferior spatial resolution and may miss collateral vessels less than 2 mm in diameter
(2) Susceptible to motion artifacts
(3) Inability to assess the degree of intimal calcification. If MRA is used, then unenhanced computed tomography (CT) should be considered in conjunction.
4. Ultrasound
a. Advantages
(1) Readily available
(2) Noninvasive
(3) No radiation exposure
b. Disadvantages
(1) Diameter and length measurements are less reliable than other modalities.
(2) Operator- and patient body habitus-dependent
5. Intravascular ultrasound
a. Advantages
(1) Provides real-time 360 degrees cross-sectional view of the vessel being evaluated
(2) Used in conjunction with contrast sparing angiography or CO2 angiography to evaluate aortoiliac pathology, confirm branch vessel position, and perform
graft sizing
b. Disadvantages
(1) Operator-dependent. The catheter may not lie in a coaxial plane, which distorts the anatomy and may result in inaccurate measurements.
Selection Criteria for Endograft Repair

1. Successful endovascular repair of AAA depends on anatomic considerations and patient selection.
2. Anatomic considerations include the morphology of the aorta and access arteries. Correct measurements of the diameter and length are essential to
maximize the success of the endograft procedure.
3. Measurements required for the evaluation of an aneurysm for endograft placement are depicted in Figure 18.1. Each EVAR device has a specific
protocol for proper sizing, the majority of which are common across all devices. However, there are nuances particular to each device and familiarity with
the device is critical for correct sizing. Please refer to each device's instructions for use (IFU) for the sizing protocol.
4. Patient selection is based on elective operative risk, aneurysm rupture risk, concomitant disease, life expectancy, and patient preference.
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Anatomic Criteria
1. Proximal neck
a. Definition—the segment of aorta between the origin of the lowest renal artery and superior aspect of the aneurysm
b. Morphology is of critical importance in aneurysm evaluation and is the most common factor to exclude endovascular repair.
c. Length: Most endografts require at least 15 mm to ensure adequate proximal seal. Some devices allow for transrenal fixation of the proximal cuff, which
enables endovascular repair in patients with as short as a 4-mm neck.
d. Diameter: Requirements depend on which device is to be deployed. To correctly measure for most devices, the outer wall limits should be used. This
measures the outer media and adventitia, the layers that will support and anchor the endograft. Most proximal necks diverge caudally having a conical
shape; as a general rule, diameter should increase no more than
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10% from the proximal to the distal end of the proximal neck. The endograft should be oversized 10% to 20% larger than the neck diameter.
e. Thrombus: Thrombus greater than 2 mm in depth involving more than 25% of the proximal neck circumference is considered unfavorable, and EVAR is
contraindicated by most manufacturers' IFU (5). If EVAR is pursued in cases with appropriate neck length but significant mural thrombus, an endograft with
suprarenal active fixation could be considered. Mural thrombus may impair proximal seal and fixation. During EVAR placement, thrombus may be displaced
into or across the renal artery ostia.
f. Angulation: Angulation between the suprarenal aorta and superior portion of the aneurysm neck is common and can be measured as shown in Figure
18.1. Each endograft has a different threshold of neck angulation in the IFU. However, if it exceeds 60 degrees, the placement of most stent grafts is
contraindicated. Severe angulation may result in kinking or downward migration of the endograft during or after placement.
g. The 20% to 30% of patients will have aortic neck anatomy considered unfavorable for stent-graft placement (9). Options include:
(1) Fenestrated stent graft
(a) Approved for neck lengths >4 mm
(b) Have fenestrations and/or scallops for the ostia of the major visceral vessels to be preserved
(2) “Chimney” or “snorkel” technique—renal arteries and SMA are stented to create conduits that run parallel to the main aortic endograft (10).
2. Distal aorta
a. If an aortic tube graft is being considered, the length of the distal attachment site must be greater than 20 mm and free of significant thrombus. Infrarenal
aortic tube grafts are used only in rare instances because of a high incidence of complications.
b. If a bifurcated device is to be deployed, the diameter of the distal aorta should be evaluated. Distal aortic diameter of 18 mm will accommodate a
bifurcated aortic endograft. Distal aortic diameter less than 18 mm may complicate device delivery or result in a hemodynamically significant iliac limb
stenosis. Significant stenoses at the native aortic bifurcation may require angioplasty both before and after endograft deployment. In these situations,
consideration should also be given for the use of an EVAR device that preserves the native aortic bifurcation (Endologix AFX, Endologix Irvine, CA), or
placement of an aortouniiliac device plus a femoro-femoral bypass.
c. Evaluate the distal aorta for important branch vessels such as accessory renal arteries and the IMA.
(1) Small accessory renal arteries can be covered by an endograft. However, this increases the risk of postprocedural renal insufficiency and is a possible
source for type II endoleak.
(2) Patients with a chronically occluded SMA and IMA hypertrophy have an unfavorable situation and would be at significant clinical risk of bowel ischemia
if endovascular repair were attempted.
3. Iliac arteries
a. The length and diameter of the common iliac arteries (CIAs) must be carefully assessed because these are the target sites for distal attachment of a
bifurcated endograft. The CIA diameter should be <25 mm, and >10 mm of length is required for adequate seal.
b. Up to 20% to 30% of patients with an AAA have a concomitant iliac artery aneurysm (3).
c. Single common iliac artery aneurysm: If a single common iliac aneurysm extends to the iliac bifurcation, then the ipsilateral external iliac artery becomes
the target site for distal attachment. This would require prior coil embolization of the ipsilateral hypogastric artery to prevent a type II endoleak
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from retrograde filling. This also requires wide patency of the contralateral hypogastric artery (to prevent buttock claudication), and the patient must not rely
on hypogastric arteries for bowel perfusion.
d. Bilateral common iliac artery aneurysms: Endovascular treatment of bilateral CIA aneurysms extending to the level of the iliac bifurcation requires
embolization of the hypogastric arteries bilaterally to ensure complete exclusion of the aneurysms. Although pelvic or bowel ischemia may occur, several
studies suggest the risks associated with bilateral hypogastric artery occlusion are generally limited to buttock claudication and erectile dysfunction (3). The
risks of bilateral hypogastric artery occlusion can be mitigated by performing a staged occlusion of each hypogastric artery (procedures performed 4 to 6
weeks apart) and embolization limited to the main trunk so as to preserve pelvic collateral vessels. This may be the best option in patients who are
otherwise high-risk for operative repair. Alternatively, the “sandwich” technique, which involves the placement of two parallel endografts within an iliac limb
to create an “off-the-shelf” bifurcated iliac component, can be considered to preserve flow to the hypogastric artery (11). Branched iliac endografts are
available in some countries.
4. Vascular access
a. Common femoral and iliac arteries are the conduits for device introduction. Significant atherosclerotic changes with heavy calcification and plaque
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formation, diminutive diameter, and marked tortuosity are factors that may complicate device delivery and contraindicate endovascular repair. The most
common causes of technical failure are the inability to deliver the device through the iliac arteries or rupture of the iliac arteries during device withdrawal.
b. Women tend to have smaller caliber iliac arteries than men.
c. In the absence of heavy calcification, tortuosity can often be reduced with the introduction of a rigid guidewire such as the Amplatz Super Stiff (Boston
Scientific Marlborough, MA) or Lunderquist (Cook Medical Bloomington, IN) guidewire. Focal stenoses can often be pretreated with simple angioplasty.
d. Percutaneous versus surgical cutdown: Compared to open femoral exposure, percutaneous endovascular aneurysm repair (PEVAR) using a suture-
mediated closure device (SMCD) “preclose” technique with the Perclose ProGlide (Abbott Vascular, Inc, Redwood City, CA) is less invasive and associated
with decreased operative time and major access-related complications compared to surgical cutdown with experienced operators (12). Use of SMCD
“preclose” technique has been FDA-approved for use with up to 21 Fr. delivery sheaths. Percutaneous technique is not recommended in patients with
common femoral arteries <5 mm in diameter and/or containing calcification covering the entire anterior wall, circumferentially, and >50% of the
circumference from the posterior wall due to the increased risk for complication and conversion to cut down (12). Ultrasound access within the common
femoral artery (CFA), 1 cm proximal to the femoral bifurcation and at the 12 o'clock position is strongly recommended.
Procedure
1. Specific detailed procedural steps are unique to each device used. However, in general, some basic steps are discussed.
2. Bilateral CFA access is obtained either percutaneously or via a surgical cutdown and systemic anticoagulation achieved with intravenous heparin.
3. A pigtail marker catheter is advanced via the contralateral access to the level of the renal arteries. An abdominal aortogram can be performed to
confirm preprocedural length measurements.
4. The ipsilateral floppy guidewire access is exchanged through a diagnostic catheter for a superstiff guidewire that is positioned in the descending
thoracic aorta.
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5. The main body of the device and the introducer sheath are advanced over the superstiff guidewire so that the superior end of the endograft is at the
level of the lowest renal artery.
6. Under magnification, the superior end of the covered portion of the endograft and lowest renal artery are centered on the field so as to reduce
errors caused by parallax. Additionally, the image intensifier is angulated and/or rotated so as to best profile the lowest renal artery, as determined
from preprocedure cross-sectional imaging.
7. Intermittent angiography at this location is performed with adjustments made to position the endograft immediately distal to the lowest renal artery.
Once appropriate position is confirmed, the trunk and ipsilateral limb are deployed under fluoroscopic guidance.
8. At this time, the contralateral gate is cannulated with a guidewire. Once cannulated, a pigtail catheter is advanced over the guidewire and spun
within the main body of endograft to confirm appropriate location within the endograft rather than in the aneurysm sac.
9. A superstiff guidewire is advanced through the pigtail marker catheter, which is then positioned with a marker at the bottom of the contralateral gate.
A retrograde contralateral sheath angiogram is performed in the appropriate obliquity so as to profile the hypogastric artery origin. This will allow
correct length determination and positioning of the contralateral limb so as to preserve hypogastric artery flow.
10. The pigtail catheter is exchanged over the superstiff guidewire for the contralateral limb, which is positioned appropriately and then deployed. If an
ipsilateral iliac extension is needed, a similar technique can be used to determine length and position.
11. At this time, proximal, distal, and overlapping attachment sites are balloon dilated to achieve a maximum profile (“ironing”).
12. A pigtail catheter is reintroduced to the level of the renal arteries and a final aortogram is performed. Particular attention is made to renal and
hypogastric arterial flow as well as the presence of endoleaks. If necessary, secondary interventions can be performed as needed.
1. Immediate and in-hospital postprocedure management entails the evaluation of bilateral groin access sites for infection or hematoma, assessment of
distal perfusion and renal function, and early ambulation. Hospital stay is typically 1 to 3 days.
2. Following recovery from the initial procedure, indefinite long-term imaging surveillance is required. Particular attention is made to AAA diameter, detection
and classification of endoleaks, and evaluation of the endograft morphology.
3. Specific imaging modalities and their advantages/disadvantages were discussed previously. CTA remains the most widely used modality for follow-up
after EVAR. In patients with renal insufficiency, a noncontrast CT or color duplex ultrasound and plain radiography are performed.
4. Physical examination and imaging follow-up is recommended at 1 to 3 months and 6 months after the procedure. If no endoleak is identified, then
patients are followed at yearly intervals. If an endoleak is present, the patients are followed every 6 months for the first 2 years and yearly thereafter unless
treatment is mandated (discussed in the following discussion).
Results
1. EVAR is associated with significantly less blood loss, fewer days in intensive care, fewer hospital days, fewer systemic complications, and
decreased
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in-hospital and 30-day mortality versus open repair of AAAs. Furthermore, aneurysm-related mortality is significantly lower with EVAR compared with
open repair (3).
2. The major disadvantages to EVAR versus open repair are the necessity for lifelong imaging follow-up and need for secondary interventions,
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especially the treatment of endoleaks.
3. Results of long-term studies are still forthcoming and will help to better define EVAR's clinical efficacy, durability, and cost efficacy.
Complications
1. EVAR is less invasive than open surgery and has low annual rates of late AAA rupture. Complications include endoleak, aneurysm sac expansion,
endograft migration, stent fracture, graft stenosis, graft thrombosis, graft infection, and groin and retroperitoneal hematoma (5).
2. Approximately 30% of patients with AAA treated with EVAR may require secondary interventions, significantly higher than for open repair (13).
1. Stenosis within or immediately distal to iliac limb. This frequently is related to severely calcified arteries or orientation of the distal orifice of the limb
into the vessel wall due to vascular tortuosity or change of stent-graft position with aneurysmal remodeling. Balloon angioplasty may work, but more
often a baremetal stent or limb extension is required.
2. Limb occlusion. Options include:
a. Reopening the limb by balloon thrombectomy or thrombolysis. Once the clot is cleared, search for an underlying mechanical problem by
angiography, and if necessary, intra-arterial pressure assessment is mandatory.
b. Leaving the limb occluded and performing a femoro-femoral bypass graft
3. Endoleaks and their treatment are discussed in Chapter 19.
References
1. Kent KC. Clinical practice. Abdominal aortic aneurysms. N Engl J Med. 2014; 371(22):2101-2108.
2. Dua A, Kuy S, Lee CJ, et al. Epidemiology of aortic aneurysm repair in the United States from 2000 to 2010. J Vasc Surg. 2014;59(6):1512-1517.
3. Chaikof EL, Brewster DC, Dalman RL, et al. SVS practice guidelines for the care of patients with an abdominal aortic aneurysm: executive summary.
J Vasc Surg. 2009;50(4):880-896.
4. Dorros G, Parodi J, Schonholz C, et al. Evaluation of endovascular abdominal aortic aneurysm repair: anatomical classification, procedural success,
clinical assessment, and data collection. J Endovasc Surg. 1997;4(2):203-225.
5. Walker TG, Kalva SP, Yeddula K, et al. Clinical practice guidelines for endovascular abdominal aortic aneurysm repair: written by the Standards of
Practice Committee for the Society of Interventional Radiology and endorsed by the Cardiovascular and Interventional Radiological Society of Europe
and the Canadian Interventional Radiology Association. J Vasc Interv Radiol . 2010;21(11):1632-1655.
6. Hoornweg LL, Storm-Versloot MN, Ubbink DT, et al. Meta analysis on mortality of ruptured abdominal aortic aneurysms. Eur J Vasc Endovasc Surg.
2008;35(5):558-570.
7. Norman PE, Powell JT. Abdominal aortic aneurysm: the prognosis in women is worse than in men. Circulation. 2007;115(22):2865-2869.
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8. Rooke TW, Hirsch AT, Misra S, et al. 2011 ACCF/AHA focused update of the guideline for the management of patients with peripheral artery disease
(updating the 2005 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice
Guidelines: developed in collaboration with the Society for Cardiovascular Angiography and Interventions, Society of Interventional Radiology, Society
for Vascular Medicine, and Society for Vascular Surgery. J Vasc Surg. 2011;54(5):e32-e58.
9. Antoniou GA, Georgiadis GS, Antoniou SA, et al. A meta-analysis of outcomes of endovascular abdominal aortic aneurysm repair in patients with
hostile and friendly neck anatomy. J Vasc Surg. 2013;57(2):527-538.
10. Patel RP, Katsargyris A, Verhoeven EL, et al. Endovascular aortic aneurysm repair with chimney and snorkel grafts: indications, techniques and
results. Cardiovasc Intervent Radiol . 2013;36(6):1443-1451.
11. Smith MT, Gupta R, Jazaeri O, et al. Preservation of internal iliac arterial flow during endovascular aortic aneurysm repair using the “sandwich”
technique. Semin Intervent Radiol . 2013;30(1):82-86.
12. Nelson PR, Kracjer Z, Kansal N, et al. A multicenter, randomized, controlled trial of totally percutaneous access versus open femoral exposure for
endovascular aortic aneurysm repair (the PEVAR trial). J Vasc Surg. 2014;59(5):1181-1193.
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13. Stather PW, Sidloff D, Dattani N, et al. Systematic review and meta-analysis of the early and late outcomes of open and endovascular repair of
abdominal aortic aneurysm. Br J Surg. 2013;100(7):863-872.
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19
Management of Stent-Graft Endoleaks
Nathaniel C. Swinburne
Robert A. Lookstein
Endovascular Aortic Aneurysm Repair and Endoleaks

1. Certain anatomic considerations made before endovascular aortic aneurysm repair (EVAR) predispose to
specific types of complications, including endoleaks (1). These include proximal/distal attachment sites,
angulation, and tortuosity of the aorta, and the presence of calcification and occlusive disease in the access
arteries.
2. EVAR requires lifelong surveillance to evaluate for possible complications (2).
3. With the more frequent use of EVAR, the occurrence of complications has risen. The most common
complication is endoleak (25% to 35% of patients), which may progress to aneurysm expansion and rupture (3).
4. An endoleak is defined as persistent perfusion of the aneurysm sac outside of the stent graft.
5. A primary endoleak occurs during the first 30 days after stent-graft placement. A secondary endoleak occurs
after the first 30 days after stent-graft placement following at least one negative cross-sectional study (1).
6. There are five types of endoleaks, which are defined by the etiology of blood flow into the aneurysm sac (4).
Endoleak Classification (see Table 19.1)

1. Type I endoleak
a. Source of blood flow is a stent-graft attachment site (either proximal attachment site [type IA], distal attachment
site [type IB], or from an incompletely occluded, contralateral common iliac artery in aortouniiliac stent-grafts
[type IC]) (1,4).
b. Type I endoleaks occur more commonly in the thoracic aorta and in aortas where the attachment sites are
complicated by thrombus, short and/or angulated necks, and dilated, irregular iliac arteries (1,4).
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Table 19.1 Classification of Endoleaks
Endoleak Etiologya Incidenceb Clinical Treatment/Management

Type (%) Significance
I Source of blood flow 12.6 Must be Add proximal or distal

from the attachment treated extension pieces
sites (either proximal immediately Place a balloon-
[IA], distal [IB], or from because of expandable or bare-metal
contralateral common direct stent at the compromised
iliac artery in communication seal zone
aortouniiliac stent grafts with high- Open repair
[IC]) pressure
arterial blood,
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which
increases risk
of rupture
II Source of blood flow 25.2 Usually require Embolization with either a

from branch vessels no immediate transarterial or
(most commonly IMA, treatment percutaneous approach
lumbar artery) with because type II Open repair
retrograde flow into the endoleaks
aneurysm sac often
May involve a single spontaneously
(IIA) or multiple (IIB) thrombose
feeding vessel(s)
III Source of blood flow 1.0 Like type I, Stent-graft extension to

through a structural must be cover the separated
defect in the stent graft treated modular component or
including junctional immediately hole within the original
separations within the because of graft
modular devices (IIIA), direct Realign endograft
or stent-graft fractures communication
or fabric holes (IIIB) with high-
pressure
arterial blood,
which
increases the
risk of rupture
IV Source of blood flow is <1.0 Rarely seen Reverse anticoagulation

through porosity in the Self-limited
stent graft and and require no
manifests as a “blush” treatment
in the immediate Resolve
postimplantation spontaneously
angiogram in patients once the
who are fully patient's
anticoagulated coagulation
status is
normalized
V Continued aneurysm 2.0 All imaging Imaging (and possibly

expansion in the modalities remote pressure sensor)
absence of a confirmed must be surveillance of aneurysm
endoleak (endotension). considered sac pressure
Exact etiology is before Open repair
unknown, but type V diagnosis
endoleaks may because open
represent occult surgical repair
instances of types I, II, is the only
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or III endoleak, treatment.
ultrafiltration of blood
across the stent-graft, or
thrombus within the sac
resulting in an
ineffective barrier to
pressure transmission.
aEtiology/Endoleak type determined by demonstrating contrast within the excluded aneurysm sac.
bIncidence of endoleaks after EVAR (18).
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c. Type I endoleaks can be seen immediately after deployment as a result of incomplete expansion of the stent-
graft, aortic tortuosity, or steep aortic angulation (5).
d. Late development of type I endoleaks may be related to changes in the configuration of the aorta as the
aneurysm sac shrinks (4).
2. Type II endoleak
a. Source of blood flow is the patent aortic branch vessels (most commonly the inferior mesenteric artery [IMA]
and lumbar arteries), with retrograde flow into the aneurysm sac (5).
b. Other less common sources include the hypogastric, median sacral, accessory renal, and gonadal arteries.
c. Type II endoleaks are further classified into IIA, in which a single vessel is involved, and type IIB, in which two
or more vessels are involved (4).
d. Type II endoleaks are the most common (40%) type of endoleak (5).
3. Type III endoleak
a. Source of blood flow is through a structural defect in the stent graft including junctional separations within
modular devices (type IIIA), or stent-graft fractures or fabric holes (type IIIB) (1).
b. Type III endoleaks are likely caused by stresses from arterial pulsations or stresses resulting from aneurysm
sac shrinkage.
4. Type IV endoleak
a. Source of blood flow is through porosity in the stent graft and manifests as a “blush” in the immediate
postimplantation angiogram in patients who are fully anticoagulated (1).
b. Type IV endoleaks are a diagnosis of exclusion as other types of endoleaks can mimic type IV endoleaks.
c. Type IV endoleaks are rarely seen now due to improved stent-graft construction.
5. Type V endoleak
a. Continued aneurysm expansion in the absence of a confirmed endoleak, also referred to as endotension
b. The exact etiology is unknown, but type V endoleaks may represent occult instances of types I, II, or III
endoleak, ultrafiltration of blood across the stent graft, or a thrombus/atheroma at an attachment site resulting in
an ineffective barrier to pressure transmission (4).
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Post-EVAR Imaging Modalities
Lifelong imaging surveillance is necessary after EVAR. An ideal protocol for imaging follow-up has not been
established.
1. Radiography
a. Useful to monitor for stent migration, detect kinks in abdominal stent grafts, and evaluate conformation of
thoracic stent grafts
b. Typical projections include anteroposterior (AP) and lateral (for migration and component separation) and
oblique (to improve sensitivity for detecting stent-graft fractures).
2. Computed tomography (CT)
a. Most common modality used for surveillance imaging after EVAR
b. Highly accurate in determining aneurysm size and volume and can detect endoleaks with a higher sensitivity
than conventional angiography (6)
c. Typical protocol includes three phases: precontrast, arterial phase, and venous phase.
d. Precontrast imaging is useful for differentiating true endoleaks from high-density mimics such as calcium or
metal.
e. Arterial phase imaging is useful for detecting endoleaks and for planning translumbar embolization of
endoleaks (7).
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f. Venous phase imaging is more sensitive than arterial phase imaging for detection of endoleaks (especially
distal type I leaks) (7).
g. Radiation exposure is a concern for CT and elimination of one of the phases, particularly precontrast, is being
explored.
3. Magnetic resonance (MR)
a. Gadolinium-enhanced MR has been shown in many studies to be at least as accurate as CT angiography
(CTA) in determining aneurysm size and stent-graft position as well as being useful in detection of endoleaks in
nitinolbased stents (8).
b. Gadolinium-enhanced studies are useful for detection of small endoleaks and demonstrate superior sensitivity
for slow-flow type II leaks as compared with CT (9,10).
c. Steady state free precession (SSFP) imaging may possess superior sensitivity for diagnosing endotension
(10).
d. Time-resolved MR angiography correctly reclassified multiple type 1 endoleaks that were initially labeled type
II via CT angiography (11).
e. Patients with a long life expectancy, for whom cumulative radiation exposure is of greater concern, and those
allergic to iodinated contrast are more suitable for surveillance with MR than CT.
f. Stainless steel stents can cause extensive susceptibility artifact and Elgiloy stents can obscure the lumen of
the stent graft; therefore, these stents cannot be evaluated with MR (1).
g. MR imaging is more time-consuming and expensive than CT.
4. Ultrasound (US)
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a. Some investigators have found US to be useful in post-EVAR surveillance, specifically for further
characterization of endoleaks using spectral Doppler analysis and microbubble contrast agents (12).
b. Used by some centers in concert with abdominal radiography for first-line surveillance, with abnormalities
detected by either modality prompting confirmatory CTA (13)
c. Although US is portable, safe, and inexpensive, US is limited by its operator dependence and potential
difficulties evaluating obese patients.
5. Digital subtraction angiography (DSA)
a. The gold standard for endoleak categorization because of its ability to demonstrate flow direction as well as its
high spatial and temporal resolution (14)
b. DSA is particularly useful for detection of outflow vessels in type II endoleaks (14).
c. Long acquisitions can be used for detection of slow-flow endoleaks that may have been otherwise missed
during the delayed phase of CT.
6. Remote pressure sensors
a. A novel, noninvasive method to detect endoleaks and monitor procedural success and long-term graft stability
after EVAR, particularly with thoracic stent grafts
b. The remote pressure sensor is deployed during EVAR and either fixed to the graft or within the aneurysm sac.
These devices use wireless radiofrequency technology to transmit direct measurements of the systolic, diastolic,
mean, and pulse pressures within the residual aneurysm sac with immediate confirmation of aneurysm sac
pressure changes (15).
c. Advantages of remote pressure sensors include the ability for multiple examinations to be performed on a
given patient at any time without the use of ionizing radiation, enabling early detection of endotension and
prompt evaluation with selective imaging to confirm endoleak (15).
d. Long-term study will be needed to prove device efficacy for postoperative surveillance.
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Endoleak Treatment
Treatment depends on the type of endoleak.
1. Type I endoleak
a. Immediate treatment is necessary because of the direct communication with high-pressure arterial blood,
which puts the patient at risk for aneurysm rupture (1).
b. These endoleaks are treated with endovascular techniques by securing the attachment site with
angioplasty balloons, stents, or stent-graft extensions (1).
c. Embolization and surgery are other options.
2. Type II endoleak
a. Can be treated by embolization with either a transarterial or percutaneous translumbar approach (1). The
goal of treatment is to protect the aneurysm sac from systemic pressure by eliminating flow through branch
vessels perfusing the aneurysm sac and obliterating the nidus.
b. Transarterial treatment
(1) Retrograde embolization of feeding arteries
(a) Possible in the majority of cases, particularly if the feeding vessel is of large caliber, however technically
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challenging and time-consuming
(b) Perform an aortogram to identify the vessels supplying and draining the endoleak nidus.
(c) With a 4 Fr. or 5 Fr. catheter, engage the major vessel from which the feeding vessel arises. Internal
iliac, median sacral, and superior mesenteric artery (SMA) are the most frequent sources.
i. If the vessel arises from the opposite internal iliac artery to the side of initial vascular access, it is easier to
puncture the opposite groin than to cross the flow divider of the stent graft.
(d) Insert a coaxial microcatheter and advance as far as possible. Advancement through the nidus of the
endoleak and into the draining artery is ideal.
(e) Selectively occlude the feeding and draining arteries and the nidus, if possible.
(f) No embolic agent has been shown to be superior. The most commonly used agents are stainless steel or
platinum coils, but cyanoacrylate glue, thrombin, and Onyx (ev3/Covidien/Medtronic, Dublin, Ireland) have
also been used (9).
(g) Following embolization, inflow can shift to another artery and recanalize the endoleak. This may explain
a recurrence rate of 36% for type II endoleaks treated with transarterial embolization versus 19% for type II
endoleaks treated using a translumbar approach (16).
(2) Transarterial perigraft access to the endoleak
(a) After femoral access, an angle-tipped catheter (e.g., Kumpe or Cobra, Cook Medical, Bloomington, IN)
and hydrophilic guidewire (e.g., 0.035 in. angled Glidewire, Terumo Medical, Tokyo, Japan) are
manipulated under fluoroscopic guidance between the inferior aspect of an iliac limb and arterial wall.
(b) It is helpful to insert a stiff guidewire and manipulate a sheath with tapered central stylet into the
perigraft space.
(c) The diagnostic catheter is then advanced into the nidus of the endoleak, enabling embolization of
feeding and draining arteries, as well as the nidus.
c. Translumbar approach
(1) Using preprocedural cross-sectional imaging, estimate the location of the endoleak. Determine the most
accessible area and assess its position in relation to the stent-graft flow divider.
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(2) With the patient in prone position, a fluoroscopically guided puncture of the aneurysm sac is performed
with a 21-gauge or 22-gauge needle. The skin puncture site should be at least one handbreadth from the
midline.
(3) Once the endoleak sac is accessed, a 6 Fr. sheathed needle is inserted using the parallel needle
puncture technique. Alternatively, a long micropuncture set can be used.
(4) The needle/sheath combination is advanced just beyond the estimated endoleak site, the needle
removed, and the sheath slowly withdrawn until pulsatile blood flows from the sheath.
(5) A left-sided approach is used most commonly; however, if necessary, a transcaval right-sided puncture
can be performed.
(6) Angiography is performed through the translumbar sheath or coaxial catheter and pressures are
recorded.
(7) Depending on the anatomy of the endoleak sac, position of the puncture, and choice of embolic agent,
embolization may be performed directly through the sheath. Alternatively, a coaxial microcatheter may be
advanced through the sac into the origins of feeding and draining vessels and selective embolization
performed.
d. Open or laparoscopic surgical ligation of the inflow and outflow vessels has also been performed (9).
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e. The general recommendation is that selective intervention of type II endoleaks is a safe approach. Most
patients with type II endoleaks who are not exhibiting aneurysm sac expansion do well without intervention,
as these endoleaks often spontaneously thrombose (1). In a large single-institution study of patients with
documented type II endoleaks, approximately 75% of type II endoleaks sealed spontaneously within 5 years
when observed without intervention, approximately 80% remained free of sac enlargement greater than 5
mm during a 4-year period, and approximately 65% of patients remained free of intervention after a 4-year
period (17).
3. Type III endoleak
a. Like type I endoleaks, these endoleaks are treated immediately at diagnosis because of the direct
communication between the high-pressured systemic arterial blood and the aneurysm sac (5).
b. A stent-graft extension is typically used to cover the separated modular component or hole within the
original graft.
4. Type IV endoleak. These leaks are self-limited and require no treatment. They resolve spontaneously
once the patient's coagulation status is normalized (5).
5. Type V endoleak. Endotension is typically treated with open aneurysm repair. Therefore, all modalities
(CT, magnetic resonance imaging [MRI], and US) should be performed before this diagnosis is made (4).
Imaging and Management Strategies

Long-term (more than 10 years) standardized clinical data on stent grafts are not yet available.
1. Typical initial modalities include radiography and CT unless the patient is severely allergic to iodinated
contrast or has poor renal function. US, MRI, and DSA may be performed to further evaluate endotension or
endoleak not detected by CT.
a. One month, 6 months, 1 year, and then annual follow-up with radiography and CT may be performed after
EVAR (1).
b. There is ongoing debate regarding the optimal method and frequency of post-EVAR imaging, with many
authors following alternative guidelines.
2. If the size of the aneurysm sac is increasing (more than 5 mm in diameter), higher pressure and a relatively
higher long-term risk of rupture are suggested. More urgent treatment is required regardless of the type of
endoleak (5).
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a. High-pressure endoleaks (types I and III) are treated immediately.
b. Low-pressure endoleaks (types II and IV) are considered less urgent.
3. Evaluation by angiography or direct sac puncture is warranted if there is continued growth of the aneurysm
sac (5).
4. Delayed endoleak up to 7 years after EVAR has been reported (1).
Special Considerations
1. The number of patent aortic branches and amount of thrombus on the aneurysm sac preoperatively
correlate with the risk of endoleak development (1).
2. Contrast located in the periphery of the aneurysm sac without contact with the stent may represent a type
II endoleak. A tubular configuration abutting the aortic wall also suggests a type II endoleak. If located
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anteriorly, the most likely vessel is the IMA. If located posterolaterally, the most likely vessel is a lumbar
artery (5).
3. Contrast located centrally around the graft but not peripherally within the aneurysm sac likely represents
a type I or III endoleak and must be treated immediately (5).
4. Type II endoleaks larger than 1.5 cm have been associated with subsequent aneurysm expansion (19).
5. Nearly all endoleaks cause contrast material to appear in the inferior mesenteric or lumbar arteries at CT
angiography. This contrast material may represent outflow contrast from a type I or type III endoleak or
inflow contrast supplying a type II endoleak. Therefore, DSA is the gold standard for classification of
endoleaks. Assessment with DSA is usually performed prior to intervention (1).
References
1. Stavropoulos SW, Charagundla SR. Imaging techniques for detection and management of endoleaks after
endovascular aortic aneurysm repair. Radiology. 2007;243:641-655.
2. Alimi YS, Chakfe N, Rivoal E, et al. Rupture of an abdominal aortic aneurysm after endovascular graft
placement and aneurysm size reduction. J Vasc Surg. 1998;28:178-183.
3. Walschot LH, Laheij RJ, Verbeek AL. Outcome after endovascular abdominal aortic aneurysm repair: a
meta-analysis. J Endovasc Ther. 2002;9:82-89.
4. Veith FJ, Baum RA, Ohki T, et al. Nature and significance of endoleaks and endotension: summary of
opinions expressed at an international conference. J Vasc Surg. 2002;35:1029-1035.
5. Bashir MR, Ferral H, Jacobs C, et al. Endoleaks after endovascular abdominal aortic aneurysm repair:
management strategies according to CT findings. AJR Am J Roentgenol . 2009;192:W178-W186.
6. Armerding MD, Rubin GD, Beaulieu CF, et al. Aortic aneurysmal disease: assessment of stent-graft
treatment—CT versus conventional angiography. Radiology. 2000;215:138-146.
7. Farner MC, Insko E, Jati A, et al. Endoleak detection: CT angiography versus delayed CT. Paper
presented at: 28th Annual Scientific Meeting of the Society of Interventional Radiology; March 27-April 1,
2003; Salt Lake City, UT.
8. Cejna M, Loewe C, Schoder M, et al. MR angiography vs CT angiography in the follow-up of nitinol stent
grafts in endoluminally treated aortic aneurysms. Eur Radiol . 2002;12:2443-2450.
9. Baum RA, Carpenter JP, Stavropoulous SW, et al. Diagnosis and management of type 2 endoleaks after
endovascular aneurysm repair. Tech Vasc Interv Radiol . 2001;4(4):222-226.
10. Haulon S, Lions C, McFadden EP, et al. Prospective evaluation of magnetic resonance imaging after
endovascular treatment of infrarenal aortic aneurysms. Eur J Vasc Endovasc Surg. 2001;22(1):62-69.
11. Lookstein RA, Goldman J, Pukin L, et al. Time-resolved magnetic resonance angiography as a
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noninvasive method to characterize endoleaks: initial results compared with conventional angiography. J
Vasc Surg. 2004;39:27-33.
12. McWilliams RG, Martin J, White D, et al. Detection of endoleak with enhanced ultrasound imaging:
comparison with biphasic computed tomography. J Endovasc Ther. 2002;9:170-179.
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13. Harrison GJ, Oshin OA, Vallabhaneni SR, et al. Surveillance after EVAR based on duplex ultrasound and
abdominal radiography. Eur J Vasc Endovasc Surg. 2011;42:187-192.
14. Stavropoulos SW, Clark TW, Carpenter JP, et al. Use of CT angiography to classify endoleaks after
endovascular repair of abdominal aortic aneurysms. J Vasc Interv Radiol . 2005;16:663-667.
15. Milner R, Kasirajan K, Chaikof EL. Future of endograft surveillance. Semin Vasc Surg. 2006;19:75-82.
16. Sidloff DA, Stather PW, Choke E, et al. Type II endoleak after endovascular aneurysm repair. Br J Surg.
2013:100(10):1262-1270.
17. Silverberg D, Baril DT, Ellozy SH, et al. An 8-year experience with type II endoleaks: natural history
suggests selective intervention is a safe approach. J Vasc Surg. 2006;44:453-459.
18. Nevala T, Biancari F, Manninen H, et al. Finnish multicenter study on the midterm results of use of the
Zenith stent-graft in the treatment of an abdominal aortic aneurysm. J Vasc Interv Radiol . 2009;20:448-454.
19. Timaran CH, Ohki T, Rhee SJ, et al. Predicting aneurysm enlargement in patients with persistent type II
endoleaks. J Vasc Surg. 2004;39:1157-1162.
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20
Visceral Aneurysms
David M. Hovsepian
Sebastian Kos
Visceral arterial aneurysms (VAA) are rare entities, occurring in approximately 2% of the population, based on
autopsy series. Most commonly, VAA are discovered in asymptomatic patients during cross-sectional imaging,
suggesting that their prevalence may actually be higher than previously estimated. More importantly, 22% of
patients with VAA present with leak or rupture—true emergencies that have a mortality rate of 8.5% (1).
Criteria for intervention are based on whether all three layers of the arterial wall are involved (true aneurysms) or
not (pseudoaneurysms). True aneurysms are treated based on their size, location, and symptoms, whereas all
pseudoaneurysms require treatment due to significantly higher rates of rupture (˜25%) and mortality (˜50%) (2,3).
Etiology (4,5)
1. Idiopathic
2. Atherosclerosis
3. Hereditary disorders complicated by cystic medial necrosis (e.g., Ehlers-Danlos type IV, Marfan syndrome) or
arteriopathy (neurofibromatosis type 1 [NF-1])
4. Segmental arterial mediolysis
5. Fibromuscular dysplasia
6. Blunt or penetrating trauma—includes iatrogenic injuries
7. Inflammatory
a. Proteolytic degradation, for example, pancreatitis
8. Infection
a. Direct invasion
b. Septic emboli from intravenous (IV) drug abuse, endocarditis
9. Vasculitis
a. Polyarteritis nodosa (PAN)
b. IV amphetamine use
10. Neoplasia
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Indications
Calcification of an aneurysm wall does not reduce the risk of rupture.
1. Visceral arterial aneurysms
a. Asymptomatic: size >2.0 to 2.5 cm in nonpregnant females of childbearing age or for patients about to
undergo liver transplantation. Note: The American College of Cardiology and the American Heart
Association guidelines indicate a treatment threshold of 2.0 cm, whereas some authors have suggested a
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threshold of 2.5 cm (6).
b. Increasing size
c. Symptomatic (e.g., pain, hemorrhage, renovascular hypertension)
2. Visceral artery pseudoaneurysms
a. All, including asymptomatic patients, regardless of size
Contraindications
Absolute
None
Relative
a. Anaphylactoid reactions to iodinated contrast agents (consider carbon dioxide [CO2] angiography or
gadolinium as alternatives)
b. Uncorrectable coagulopathy
c. Renal insufficiency
2. Pregnancy
3. Acute or chronic infection in target area
4. Acute hyperthyroidism
5. Thyroid carcinoma and planned radioiodine administration
6. Solitary kidney affected by renal artery aneurysm/pseudoaneurysm
1. Imaging assessment
a. Computed tomographic angiography (CTA) or magnetic resonance angiography (MRA) should be obtained to
depict the vascular relationships, identify important congenital or postoperative variations, and define the
branching anatomy.
b. Recent laboratory data should include a complete blood count (CBC), platelet count, international normalized
ratio (INR), serum creatinine, and estimated glomerular filtration rate (eGFR). For patients on heparin, a partial
thromboplastin time (PTT) may be indicated. For suspected vasculitis or inflammatory conditions, a C-reactive
protein (CRP) should be obtained.
2. Patient preparation
a. Obtain informed consent.
b. Oral intake restrictions according to institutional guidelines (e.g., nil per os [NPO] for 6 to 8 hours for solids, 3
to 4 hours for fat-containing liquids, 1 to 2 hours for water and clear liquids). Typically, oral medications are
permitted with sips of water.
c. Secure IV access.
d. Periprocedural antibiotic guidelines have not been established.
e. Attach equipment to monitor vital signs (blood pressure, heart rate, and oxygen saturation).
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Procedure
1. Standard sterile skin cleansing and draping
2. Obtain arterial access. Often a guiding sheath or catheter provides more stable selective access to the
visceral trunks, especially if the origins are acutely angled. Alternative routes of access, such as via the
upper extremity, may also provide more favorable orientation in cases of severe downward angulation of the
aortic branches.
3. Perform an aortogram if a CTA or MRA has not been obtained or is inadequate or confusing. Some
authors advocate the use of IV agents to decrease peristalsis, such as glucagon (1 mg) or hyoscine
butylbromide (20 to 40 mg).
4. Select the parent vessel using a 4 Fr. or 5 Fr. catheter. Useful shapes include the Cobra 2 (Cook Medical
Inc, Bloomington, IN) and Sos Omni Selective (AngioDynamics, Latham, NY) catheters. Perform selective
angiography.
5. If available, cone-beam computed tomography (CT) can be a helpful tool to better define the three-
dimensional anatomy (7), especially when there are overlapping branches. General guidelines include the
following:
a. 48-cm field-of-view, position isocenter at catheter tip
b. Inject 3 mL of a 50:50 dilution of contrast and saline for 8 seconds.
c. Set a 2-second x-ray delay and a rotation rate of 30 degrees per second over the standard 200-degree
arc, imaging at 3 degrees per frame.
d. Image reconstruction is performed at a dedicated workstation and should include maximum intensity
projections (MIPs) to best plan the approach.
e. Access the branch containing the abnormality. As a rule, if it is less than twice the size of the selective
catheter being used, advance a microcatheter coaxially through it to the target. Microcatheter choice is
based on the embolic strategy, and care should be taken to size the inner lumen to embolic agent being
used. For instance, a 0.028-in. inner lumen may allow 0.018-in. detachable microcoils to jam and not deploy
properly.
f. Options for embolic agents include stainless steel coils, glue, covered and uncovered stents,
AMPLATZER Plugs (AGA Medical Corp, Plymouth, MN), or a combination of these.
Embolization Strategies
1. “Front and back door” closure involves placement of occlusion devices to block both the arterial inflow
and all outflow vessels, trapping the VAA. The outflow is addressed first. Before occluding the inflow, care
should be taken to ensure no significant branches are missed because occluding the inflow may render
them no longer accessible.
2. Covered stents may be deployed across the neck of the VAA, thereby preserving flow to the parent
vessel while excluding flow into the aneurysm sac (8). Thrombosis of the aneurysm should occur without
having to embolize the sac itself. The delivery systems for larger devices may be too stiff to track safely to
the target area, requiring a different strategy to treat the aneurysm. If the parent artery is small,
commercially available stent grafts used for neurologic or cardiovascular applications might be needed.
3. Coil packing of the aneurysm sac is a useful strategy for true aneurysms with narrow necks and
preserves flow in the parent artery. It is rarely used for pseudoaneurysms because of the risk of perforation
or rupture of the sac.
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4. Coil packing through a bare stent is a good option for true aneurysms that have wide necks. After
deployment of a self-expanding stent in the parent vessel, a microcatheter is advanced through the
interstices and microcoils are deposited in the aneurysm sac. The stent prevents prolapse of the coils into
the parent vessel.
5. Liquid embolic agents, such as n-butyl cyanoacrylate (NBCA) glue or Onyx (ethylene vinyl-alcohol
copolymer; ev3, Plymouth, MN), generally require
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greater operator experience than mechanical devices to avoid nontarget embolization (9) but offer some
advantages for challenging anatomy. They are often used in conjunction with flow arrest by balloon
occlusion or adjunctive deposit of permanent devices.
6. Thrombin injection can be performed via catheter or by direct percutaneous injection into the sac of a
pseudoaneurysm. For the direct approach, fluoroscopy, ultrasound, or CT can be used to guide
advancement of a 22-gauge needle into the sac (10). Placement should be away from the neck of the
aneurysm if possible. Confirmation of needle position by injection of contrast during fluoroscopy is ideal.
Thrombin injection of 100-unit aliquots (0.1 mL of a 1,000:1 dilution of thrombin in saline) is performed until
flow ceases. Color duplex ultrasound of a pseudoaneurysm characteristically reveals a “yin-yang” or “to-
and-fro” pattern. Ultrasound easily confirms cessation of flow and decreases the possibility of displacement
of thrombus into the parent vessel during contrast injection.
Organ-Specific Comments
1. Splenic artery aneurysms (SAA) are the most common VAA and account for nearly 60% of cases (11).
They are four times more common in females. Overall risk of rupture for SAA is 3%.
a. A 6 Fr. renal double curve (RDC) sheath (Destination, Terumo Medical Corporation, Somerset, NJ) is
recommended to stabilize access to the celiac trunk when advancing mechanical plugs or other devices into
the splenic artery.
b. Most SAA occur near the splenic hilum. Some degree of splenic infarction can occur following distal
embolization. Use of trivalent vaccine remains controversial.
c. Proximal SAA can be treated by stent-graft placement to preserve flow, or by total occlusion with coils.
Splenic infarcts are less likely in this setting but can still occur.
2. Hepatic artery aneurysms (HAA) comprise 20% of all VAA (10,12). The male-to-female ratio is 2:1.
Eighty percent occur in an extrahepatic location.
a. Anatomic variation is common. For example, “replaced” right hepatic arteries from the superior
mesenteric artery (SMA) are present in up to 15% of the population and “replaced” left hepatic arteries from
the left gastric artery in up to 10%.
b. Intrahepatic rupture may result in hemobilia, whereas extrahepatic rupture may lead to rapid onset of
shock and possible exsanguination.
c. The dual blood supply to the liver allows occlusion of hepatic artery branches with minimal risk of organ
ischemia. However, portal venous patency should be confirmed prior to arterial embolization.
d. Solitary HAA and hepatic artery pseudoaneurysms can be targeted individually. When multiple (e.g.,
traumatic), “field” embolization with gelatin sponge slurry is the most effective way to quickly and safely
resolve hemorrhage.
3. Renal artery aneurysms (RAA) (11) may cause hypertension or painless hematuria. The male-to-
female ratio is 2:3. Most (60%) occur at the main renal artery division. Aneurysms in patients with
neurofibromatosis type 1 (NF-1) most commonly involve the renal arteries.
a. Renal arteries are “end arteries,” and embolization often results in downstream ischemia or infarction.
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However, this lack of collateralization can be advantageous when the aneurysm is peripherally located, by
allowing safer use of liquid embolic agents, including ethanol.
b. When accessing from a femoral approach, a 6 Fr. guiding sheath or catheter that has an RDC-type
shape is well suited to the angles involved.
c. Frequent variation in renal orientation requires careful technique to obtain an optimal view (true coronal)
of the arterial vasculature. Cone-beam CT and/or additional orthogonal views can improve the delineation
of anatomic relationships.
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d. If RAA or pseudoaneurysm occurs in the setting of angiomyolipoma or other tumor, it should be occluded
prior to embolizing the tumor with particulate agents.
4. Mesenteric artery aneurysms account for 6% of all VAA (9,10,12,13). They frequently involve the
gastroduodenal artery (GDA) or pancreaticoduodenal arcade due to erosion from pancreatitis or a duodenal
ulcer. They can occur in any visceral territory in the setting of segmental arterial mediolysis (SAM).
a. For aneurysms occurring in the GDA or its branches, patency of the celiac axis and SMA should be
confirmed before embolization. If no stenosis is present in those collaterals, the GDA can be safely
occluded.
1. Standard postangiogram observation and management
2. Analgesics as needed
3. For symptoms of postembolization syndrome, antipyretics and antiemetics (e.g., ondansetron) can be added.
4. CTA or MRA within 1 month to assess aneurysm sac and distal organ perfusion, looking for signs of ischemia
or infarction
Results
1. No large prospective or comparative series exist—technical success for transcatheter treatment is
greater than 90% (3,4,8,11).
2. Overall mortality from ruptured SAA is 10% to 25%. When rupture occurs during pregnancy, there is a
70% risk of maternal death and a 90% risk of fetal demise (14).
Complications and Their Management

1. Angiographic (overall <3%). See Chapter 1 and Table 4.1.
2. Embolization-related
a. End-organ ischemia or infarction
(1) Consider pain management consultation if pain is severe.
b. Abscess formation (overall a rare occurrence, most common after splenic embolization)
(1) IV and/or oral antibiotic therapy, rarely percutaneous drainage is needed (large abscesses).
c. Nontarget embolization
(1) Follow-up cross-sectional imaging (CTA, MRA) if suspected; management in accordance with clinical and
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imaging findings
d. Postembolization syndrome
(1) Fever, malaise, nausea and vomiting, leukocytosis, typically 1 to 3 days postprocedure, self-limited to several
days
(2) IV analgesics, antiemetics, and pain control, as needed; continued observation
References
1. Huang YK, Hsieh HC, Tsai FC, et al. Visceral artery aneurysm: risk factor analysis and therapeutic
opinion. Eur J Vasc Endovasc Surg. 2007;33(3):293-301.
2. Lookstein RA, Guller J. Embolization of complex vascular lesions. Mt Sinai J Med. 2004;71:17-28.
3. Larson RA, Solomon J, Carpenter JP. Stent graft repair of visceral artery aneurysms. J Vasc Surg.
2002;36:1260-1263.
4. Chadha M, Ahuja C. Visceral artery aneurysms: diagnosis and percutaneous management. Semin
Intervent Radiol . 2009;26:196-206.
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5. Kos S, Liu DM, Jacob AI. Mesenteric aneurysms. In: Geschwind JH, Dake MD, eds. Abrams' Angiography.
3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2014:712-723.
6. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 guidelines for the management of patients with
peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic). J Am Coll Cardiol .
2006;47:1239-1312.
7. Orth RC, Wallace MJ, Kuo MD. C-arm cone-beam CT: general principles and technical considerations for
use in interventional radiology. J Vasc Interv Radiol . 2008;19:814-820.
8. Rossi M, Rebonato A, Greco L, et al. Endovascular exclusion of visceral artery aneurysms with stent-
grafts: technique and long-term follow-up. Cardiovasc Intervent Radiol . 2008;31:36-42.
9. Tulsyan N, Kashyap VS, Greenberg RK, et al. The endovascular management of visceral artery
aneurysms and pseudoaneurysms. J Vasc Surg. 2007;45:276-283.
10. Laganà D, Carrafiello G, Mangini M, et al. Multimodal approach to endovascular treatment of visceral
artery aneurysms and pseudoaneurysms. Eur J Radiol . 2006;59:104-111.
11. Vallina-Victorero Vazquez MJ, Vaquero Lorenzo F, Salgado AA, et al. Endovascular treatment of splenic
and renal aneurysms. Ann Vasc Surg. 2009;23:258.e13-258.e17.
12. Berceli SA. Hepatic and splenic artery aneurysms. Semin Vasc Surg. 2005;18:196-201.
13. Nosher JL, Chung J, Brevetti LS, et al. Visceral and renal artery aneurysms: a pictorial essay on
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endovascular therapy. Radiographics. 2006;26:1687-1704.
14. Sadat U, Dar O, Walsh S, et al. Splenic artery aneurysms in pregnancy—a systematic review. Int J Surg.
2008;6:261-265.
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21
Arteriovenous Malformations of the Viscera and Extremities
Robert J. Rosen
Allison Borowski
Vascular malformations include a wide range of clinical and anatomic problems, ranging from lesions of cosmetic
significance in adults to life-threatening conditions in infancy. Management of vascular anomalies represents a
long-term commitment to the patient and family, and one in which there will often be limited support from other
clinical specialists. Once treatment is undertaken, you will become the primary clinician caring for the patient.
Therefore, it is essential to make the correct diagnosis, be aware of its natural history, make an appropriate risk-
benefit analysis, choose the correct procedure, and be able and willing to deal with potential complications.
The International Society for the Study of Vascular Anomalies (ISSVA) recently devised an expansive
classification system of vascular anomalies (1). The new system uses immunohistologic data to differentiate
several types of vascular lesions into a comprehensive and detailed scheme, which is beyond the scope of this
chapter. Therefore, as in many of the previous classifications (2), the authors characterize vascular anomalies by
hemodynamic properties (slow vs. fast flow) and are subcharacterized by the type of anomalous channels
present as well as by their associated syndromes. For practical purposes, it is helpful to divide these lesions into
five main categories, each with its own distinct clinical presentation, natural history, and treatment options:
1. Hemangiomas
2. High-flow arteriovenous malformations (AVMs) and congenital fistulas
3. Low-flow venous malformations (VM)
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4. Congenital venous syndromes (Klippel-Trenaunay, Parkes-Weber, etc.)
5. Lymphatic malformations (LM)
The term “hemangioma” is widely misused and should only be applied to the specific benign vascular tumor of
infancy and childhood that is composed of endothelial cells (3). Infantile hemangiomas appear sometime after
birth, usually within the first 2 months of life. These lesions follow a distinctive course of proliferation followed by
spontaneous involution over a period of years. Most of these lesions will therefore require no specific treatment,
whereas some will require early intervention for life-threatening high output states, bleeding or ulceration,
interference with visual development, respiration, or feeding. An increasing number of these lesions are being
surgically removed or treated with laser therapy early in infancy to avoid the psychosocial trauma of a disfiguring
condition (4). Medical treatment of these lesions includes administration of propranolol, a well-tolerated,
nonselective, adrenergic receptor blocker. Studies have shown promising results with signs of regression
reported as early as the first month of treatment (5). Some lesions will leave abnormal skin or tissue even after
involution, which can be treated with plastic surgical revision.
In contrast, congenital hemangiomas are fully formed at birth and may rapidly involute (rapidly involuting
congenital hemangioma [RICH]). The rare noninvoluting congenital hemangioma (NICH) can be treated
surgically or with laser therapy and will not respond to propranolol. The management of congenital hemangiomas
and other vascular tumors of childhood is a highly complex subject and is not discussed further in this chapter.
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Indications
1. Hemorrhage
2. Pain
3. Ulceration
4. High-output cardiac state
5. Mass causing interference with normal activity
6. Lesions which interfere with normal growth and development
7. Disfiguring lesions
Contraindications
Absolute
1. Anatomy such that the embolic material cannot be contained within the target site
Relative
1. Minimal likelihood of clinical improvement—malformations are usually isolated benign lesions in otherwise
young healthy patients. Improving the angiographic picture does not always improve the patient's overall
condition.
a. Severe anaphylactic reaction to iodinated contrast
b. Acute renal failure
c. Uncorrectable coagulopathy
3. Pregnancy
4. Infection within the target vasculature
1. Preprocedural imaging
a. Ultrasound studies are easily performed in the office setting and provide valuable information on depth and
flow characteristics but do not usually provide enough detailed anatomic information to plan an intervention.
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b. Computed tomography (CT) and magnetic resonance imaging (MRI) provide detailed information on size,
location, flow characteristics, and the relationship to surrounding structures (6). MRI, including magnetic
resonance angiography (MRA) and dynamic studies, has become the mainstay in AVM imaging and is often the
only modality which clearly demonstrates slow flow malformations. It should be kept in mind that MRI studies in
pediatric patients will require sedation or anesthesia; thus, these studies should be performed only when the
findings will affect treatment decisions.
2. Routine preprocedural laboratory studies should include complete blood count (CBC), electrolytes, creatinine,
and coagulation studies. Goals for preoperative testing include an international normalized ratio (INR) <2.0 and
platelet count >50,000 per μL for both venous and arterial procedures.
3. Communication with the patient's primary physician is essential, and formal consultations with appropriate
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specialists may be required depending on the type and complexity of the malformation.
4. In preparation for sedation or general anesthesia, patients are made nil per os (NPO) for 8 hours according to
hospital guidelines. The authors perform almost all embolization procedures under general anesthesia for patient
comfort, the safety of close physiologic monitoring, and the ability to control respiration and movement during
angiography. When respiratory control is not required, as in extremity lesions, we routinely employ laryngeal
mask airway (LMA) anesthesia, which is more comfortable in the postprocedure period. Because many of these
patients will require repeat embolizations, it is important to make the treatments as psychologically atraumatic as
possible, especially in pediatric patients.
5. Once the patient has been sedated, a preprocedural dose of antibiotics (typically cefazolin) as well as steroids
(the authors use dexamethasone) are administered.
Procedure
High-Flow Malformations
By definition, high-flow malformations involve an abnormal arteriovenous connection at something larger
than capillary level. These can range from direct fistula-like connections (most commonly seen in the lung,
kidney, and carotid-cavernous lesions) to small vessel communications with a nidus, or central network, of
variable size vessels (Fig. 21.1). The treatment goal is to eliminate the abnormal shunt, which can be a
complex undertaking.
1. Perform detailed selective angiography to determine the type of malformation, feeding vessels, patterns
of venous drainage, and regional collateral pathways, which provide a safety margin to prevent ischemia
but also have the potential to resupply the malformation. Given the detailed information available from CT
and MRI, we generally do not perform diagnostic angiography until the time of planned intervention.
2. Once the anatomy has been defined, superselective coaxial catheterization of the feeding arterial vessels
is carried out. The coaxial system is essential to protect proximal vessels if the embolic material becomes
adherent to the catheter tip as well as providing secure access for repeated depositions of embolic material
without having to perform a new selective catheter placement each time.
3. The choice of embolic material is critical and depends on the vessel size and flow characteristics. The
ideal result is elimination of the nidus while preserving flow to normal vessels. Note: Proximal occlusion of
the feeding artery is ineffective because it sacrifices future transvascular access to the nidus and promotes
collateral resupply.
4. Consideration must be given to the distribution of the embolic material once it is injected because
patterns of flow may change rapidly during the embolization itself, resulting in reflux or nontarget
embolization.
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FIGURE 21.1 • High-flow AVM. Treatment must be aimed at eradicating the nidus as virtually all have
multiple feeding arteries and proximal occlusion results in recruitment of collaterals.
5. There is no ideal embolic agent for all AVMs. The agents used include:
a. Proximal occluding devices including coils, plugs (such as the AMPLATZER Vascular Plug, St. Jude
Medical, St. Paul, MN), and detachable balloons: These may be appropriate to treat fistula-like lesions
where a simple interruption of a macroscopic arteriovenous connection is required. These devices can also
be useful in protecting normal vessels from distal embolization, redirecting flow, or preventing loss of
embolic materials into the venous circulation in certain situations. They are not suitable for use as the
definitive embolic agent in complex malformations and will only hinder subsequent treatment.
b. Microspheres: These can be useful in “pruning” small vessel arteriovenous shunting, but recanalization
generally occurs with recurrence of the lesion. This agent is best used for preoperative embolization to
reduce bleeding during resection or to manage ischemic problems distal to an AVM causing a “steal”
phenomenon.
c. Liquid “casting” agents: These offer the possibility of permanently filling and occluding the nidus of the
malformation. Use of these agents requires specialized training and experience in terms of preparation and
delivery techniques.
(1) n-Butyl cyanoacrylate (NBCA) glue (Codman Neuro, Warren, NJ) is an adhesive that rapidly
polymerizes on contact with any ionic medium and is usually mixed with Ethiodol. The oil is used to slow
glue polymerization time, increase its viscosity, and provide radiopacity (7). It is best to limit oneself to a few
ratios (Ethiodol:glue) and become familiar with their behavior (the authors most commonly employ a 1:1
mixture).
(a) Glue is injected through a microcatheter either as a series of small depositions (0.2 to 0.8 mL) pushed
by dextrose 5% water in a small vessel nidus or as a “continuous column” when dealing with larger vessels
or faster flow.
(b) Flow control using balloon catheters is sometimes employed, but in most situations, it is preferable to
use forward blood flow to carry the agent deep into the nidus.
(2) Ethylene vinyl alcohol copolymer (Onyx, ev3, Plymouth, MN) is a nonadhesive polymer that is used
in combination with the solvent dimethyl sulfoxide (DMSO). Onyx has primarily been used in
neurointerventions
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where its safety profile has been well established. At present, it is only U.S. Food and Drug Administration
(FDA)-approved for neuroembolization procedures in the United States but has been used for peripheral
lesions in other countries.
(a) It is injected slowly and continuously through an Onyx-compatible microcatheter, forming a lava-like cast
of the vessels over a period of minutes. Onyx deposition does not rely on forward flow-like glue. Therefore,
it must be deposited directly in the nidus, which is often a difficult task if tortuous vessels need to be
traversed.
(b) Advantages of Onyx include no risk for catheter gluing/fracture, ability to conform to tortuous vessels,
and ease of control. Disadvantages include ischemic complications if the cast reaches very small vessels
and the fact that the marked radiopacity of the agent can obscure anatomic detail in subsequent
embolization procedures and scans. Additionally, Onyx embolization can be quite time-consuming and
costly, especially because multiple vials are usually required.
d. Absolute ethanol used intra-arterially in high-flow malformations can be highly effective by causing
rapid thrombosis and endothelial damage, resulting in permanent occlusion (8). Due to the toxicity of the
agent, it is imperative to confirm that flow will be confined to target vessels because there is a significant
risk of tissue damage, including skin sloughing and nerve injury. Escape of the agent into the central
circulation has been associated with cardiac arrhythmias, acute pulmonary vasoconstriction, and pulmonary
embolism. Some authors advocate the routine use of Swan-Ganz monitoring when this agent is used (9),
and nerve monitoring when the treatment area is within close proximity of a major nerve.
6. A more complex but highly effective approach in AVM treatment is combined arterial and venous
embolization. Occlusion of the venous drainage removes the low-pressure sump that causes collateral
recruitment and clinical recurrence. This approach is most effective when there is a large or aneurysmally
dilated draining vein that can be accessed either using a catheter from a transvenous approach or by direct
percutaneous puncture of the draining vein (Fig. 21.2). Because embolization can be performed using a
variety of materials through a 22-gauge needle (glue, microcoils, sclerosants), safe percutaneous access is
often feasible. The rapid flow in the draining vein sometimes necessitates initial placement of a filtering or
occlusion device (e.g., AMPLATZER Plug or coil) to prevent passage of embolic material into the inferior
vena cava (IVC) and pulmonary circulation. Repeated injections into the feeding artery allow progress to be
monitored during the embolization procedure.
7. Finally, if transarterial access to the nidus is not possible and the draining veins are not suitable for
occlusion, direct puncture of the nidus can allow for effective embolization. The nidus is identified initially
with a catheter angiogram, followed by direct puncture embolization carried out stepwise with monitoring by
repeated angiography (Fig. 21.3). Both glue and ethanol can be used as the embolic agent in this
technique.
Specific Anatomic Considerations
Pulmonary AVM
Pulmonary AVMs are a distinct type of lesion and are discussed in Chapter 17.
Renal AVM
Renal AVMs often consist of a simple fistula-like connection between an intrarenal artery and vein. Cure
can be achieved with macroscopic occluding devices including coils, plugs, and balloons. However, the flow
through these lesions is quite brisk, increasing the risk of loss of the embolic device into the circulation. A
combination of maneuvers may be necessary, including balloon flow control, giant framing coils, and in
some cases the use of rapidly polymerizing adhesive to
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form an instantaneous cast. Some authors have reported the use of a venous approach to these lesions.
FIGURE 21.2 • Extremity AVM. A: Angiogram demonstrated large draining vein. B: Venogram performed in
the draining vein. Coil embolization. C: Direct puncture of nidus for percutaneous sclerotherapy. D:
Postembolization angiogram demonstrating occlusion of the nidus and outflow vein.
FIGURE 21.3 • Extremity AVM. A: Angiogram via direct puncture of the nidus of a foot AVM. The needle
was inserted using arterial contrast injections for guidance. B: Angiogram via proximal arterial catheter
demonstrating that the nidus has been ablated after direct injection of NBCA through the 21-gauge needle.
Visceral AVM
AVMs can occur anywhere in the mesenteric circulation, resulting in bleeding, mesenteric ischemia due to
stealing, and portal hypertension. Depending on the specific anatomy and clinical circumstances, this lesion
can be treated surgically or by embolization. In the lower gastrointestinal (GI) tract, there is an increased
risk of bowel ischemia, but most lesions can be treated safely using selective embolization.
High-flow mesenteric AVMs with arterioportal shunting can result in severe portal hypertension. These
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lesions can be complex and difficult to cure completely; acute closure of the shunt also carries the risk of
acute portal vein thrombosis which can be fatal. It is advisable to embolize these malformations in a staged
fashion to avoid this complication.
Pelvic AVM
The pelvis is a relatively common site for high-flow AVMs. The most common pattern is a multivessel supply
from the internal iliac artery, inferior mesenteric artery (IMA), middle sacral, and common femoral branches
with drainage into the internal iliac veins. In some patients, particularly males, there is a simpler supply from
a single internal iliac branch with drainage into an aneurysmally dilated draining vein. Embolization is the
most effective treatment for the majority of these patients because they involve extensive anatomic areas
and are generally not amenable to surgical resection. The choice of embolic agent varies with operator
experience and preference, but the most commonly used are casting agents and ethanol. Absolute ethanol
has been reported to achieve a higher cure rate than the casting agents but is also associated with a higher
complication rate in most series.
1. A flush aortogram is performed initially to outline the anatomy of the malformation.
2. Selective catheterization of the major feeders is then carried out with detailed rapid-sequence imaging to
define flow patterns and identify normal branches that need to be preserved.
3. Embolization is then carried out as detailed earlier. Generally, these malformations are first embolized by
the transarterial approach, but if there is drainage into a dominant or aneurysmal outflow vein, a venous
approach may be more effective and definitive.
4. Except in the case of simple single-vessel lesions, these malformations will require multiple sessions to
achieve a successful clinical result. Overly aggressive treatment during a single session can result in
delayed rupture of a draining vein into a viscus, most commonly the urinary bladder, with uncontrolled
hematuria.
Uterine AVM
AVMs confined to the uterus generally present with menorrhagia and are almost always preceded by an
obstetric event (postpartum, postabortion, or dilation and curettage, in the presence of trophoblastic
disease). There is therefore some controversy whether these are congenital or acquired lesions. The
lesions are fed by one or both uterine arteries and are often amenable to embolization. Lesions with a small
vessel nidus may respond to embolization with microspheres, whereas higher flow lesions are best treated
with liquid casting agents (10). Not only can hysterectomy be avoided, but successful pregnancies have
been reported in several patients following embolization.
Extremity AVM
Extremity AVMs are among the most difficult lesions to treat, especially lesions of the hands and feet. It is
often difficult to define the vessels feeding the malformation
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as opposed to those necessary for perfusion of normal distal tissues. As these malformations tend to be
diffuse and cross normal tissue planes, resection or even amputation is often not feasible. Embolization,
while itself rarely curative, presents the opportunity to reduce the shunt and improve distal perfusion.
1. Careful superselective angiography is performed to identify the major feeders to the malformation and the
critical runoff vessels that must be preserved for normal distal perfusion.
2. If planning a transarterial approach, each feeding vessel is then carefully embolized using a penetrating
agent such as NBCA, Onyx, and in some cases sclerosants. Sclerosing agents must be used with caution,
as ischemic damage can occur to muscle, nerves, or skin in the event of nontarget embolization or reflux of
the agent.
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3. Because flow patterns can change virtually instantaneously during the course of embolization,
angiograms should be performed after each deposition to document the new routes of flow prior to
proceeding.
4. As in any high-flow lesion, proximal occlusion should be avoided. Again, if a transarterial approach is not
available, venous embolization or direct puncture of the nidus can be carried out.
5. Safe and effective treatment of extremity AVMs usually requires a stepwise approach over several
sessions. Treatment should be limited to only a few vessels at a time to allow for adequate perfusion of the
normal tissues to be maintained. It is nearly always preferable to err on the side of conservatism rather than
aggressiveness when treating these lesions because the risk of an ischemic complication is high.
Venous Malformations
Venous malformations are much more common than high-flow lesions, in most series by a ratio of 10:1. For
clinical purposes, the two main categories are cavernous venous lesions and venous dysplasias, with a
combination of both types in some individuals. They may present at any age and tend to grow with the
individual, in some cases showing exacerbation with activity, injury, or changes in the hormonal
environment (especially puberty and pregnancy).
Cavernous Venous Malformations
These are by far the most common type of vascular malformation and consist of spongy, low-flow venous
spaces that fill with gravity and empty on compression. In the past, they were incorrectly called cavernous
hemangiomas. They are not hemangiomas and do not follow the clinical course of involution seen in those
lesions. They can occur anywhere in the body and can cross fascial planes. They may or may not have
typical changes in the overlying skin such as birthmarks, portwine stains, or angiokeratomas. Spontaneous
thrombosis within the malformation is common and may present with pain, swelling, and inflammation, which
generally resolves spontaneously in 1 to 2 weeks and is treated symptomatically (elevation,
antiinflammatory drugs, low-dose aspirin, warm soaks).
1. Imaging studies include ultrasound, which can be performed in the office and usually demonstrates the
presence and type of malformation, and MRI with contrast, which confirms the diagnosis and provides
detailed anatomic information.
2. When the malformation appears purely venous on physical examination and imaging studies, catheter
angiography is probably not warranted. It should be noted that MRI studies often exaggerate the
microvascular shunts seen in venous malformations, leading to misinterpretation as an AVM.
3. Laboratory studies are generally within normal limits. A coagulation disorder called localized intravascular
coagulopathy (LIC) is specific to VMs and is characterized by elevated D-dimer levels and low fibrinogen
levels. There have been case reports of LIC progressing to disseminated intravascular coagulopathy
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(DIC) during or immediately after sclerotherapy (11). It has been argued that patients manifesting LIC should
be placed on prophylactic low-molecularweight heparin (LMWH) 10 days prior to and after treatment to
prevent conversion to DIC and prolonged periprocedural bleeding.
4. The mainstay of treatment is direct injection of sclerosants to produce a localized thrombosis within the
lesion, followed by fibrosis and shrinkage. A variety of agents have been used for this purpose, including
ethanol and sodium tetradecyl sulfate (Sotradecol, available in 1% to 3% concentrations). The authors most
commonly use Sotradecol 3% for deeper lesions, with 1% to 1.5% concentrations used for more superficial
lesions to reduce the risk of blistering or ulceration. Lower concentrations (0.5%) may be used in
particularly sensitive tissues such as the hand or in the thin and fragile skin of infants. The use of antibiotics
with sclerosant properties such as doxycycline, and antineoplastic agents such as Bleomycin has also been
reported, but these agents are more commonly used in the treatment of LM, discussed in the following text.
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5. Prior to induction of anesthesia, the patient (with parents, in pediatric cases) identifies the symptomatic
area and the overlying skin is marked. The patient's identification of the most symptomatic area correlates
closely with the underlying malformation in almost every case and allows the operator to prioritize the most
symptomatic part of the malformation when multiple sessions will be required.
6. In extremity lesions, a peripheral venogram is performed at the time of the initial study to confirm the
adequacy of the deep venous system and to define any major communication between the malformation
and the deep veins. The peripheral intravenous (IV) is connected to a heparinized saline infusion for the
duration of the procedure to reduce the risk of deep vein thrombosis (DVT) due either to stasis or leakage
of sclerosant into draining veins. A pressurized infusion may be required to maintain the infusion if a
tourniquet or automatic blood pressure cuff is used for outflow control. The authors use outflow control with
an automatic tourniquet system in most extremity cases, inflated to above diastolic but below systolic
pressure; this not only prevents escape of the embolic agent into the systemic veins but also distends the
malformation to create an easier target for puncture.
7. Guidance for direct puncture of the malformation may be based on a combination of the marked skin site,
palpating the mass, real-time ultrasound, or landmarks from previously performed imaging studies. On rare
occasions, CT or MRI guidance to access lesions not easily visualized with ultrasound may be necessary.
8. The skin is prepped and draped in typical sterile fashion.
9. After puncture with a small needle (typically a 7-cm micropuncture needle with echogenic tip) or needle-
sheath combination, blood return will be noted. Contrast is slowly injected that will show filling of a “fluffy”
appearing vascular space. Eventually, small draining veins will be opacified that connect the malformation
to a systemic vein at some level.
a. In infiltrating intramuscular malformations, a striated appearance may be seen that must be distinguished
from extravasation within the muscle tissue; there will not be spontaneous blood return when the needle tip
is located within normal muscle.
10. The sclerosing agent is then injected slowly under fluoroscopic monitoring.
a. Although mixing aqueous radiographic contrast at a concentration adequate to provide opacification of
the sclerosant reduces the sclerosant effect, a small amount of Ethiodol (0.5 mL per 10 mL of sclerosant)
will provide adequate opacification while maintaining the potency of the agent.
b. Injection of detergent-type agents such as Sotradecol as a foam has been shown to provide better
sclerosant effect with a smaller total volume of the liquid needed (12). There are sporadic reports of
transient neurologic
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dysfunction following use of foamed agents, presumably due to microbubbles passing into the systemic
circulation through an undiagnosed patent foramen ovale (PFO) or atrial septal defect (ASD).
c. Most authors advocate a maximum total dose of Sotradecol of not greater than 0.5 mL per kg of body
weight. Greater doses have been associated with hemolysis, hemoglobinuria, impaired renal function, and
rarely cardiopulmonary dysfunction. When a relatively high dose of sclerosant is used, a dose of IV sodium
bicarbonate has been recommended to reduce renal toxicity.
d. In areas subject to compartment syndrome (calf, forearm), much smaller doses are often used during
multiple-staged procedures. Alternatively, bleomycin can be used with minimal postprocedural swelling.
11. After each injection of the sclerosing agent, the needle or catheter is withdrawn. In order to prevent
prolonged bleeding at the puncture site, as well as avoiding backtracking of the agent to the skin with
possible ulceration, the authors inject a suspension of collagen along the entry tract during withdrawal
(Surgiflo, Ethicon, Warren, NJ; FloSeal, Baxter, Deerfield, Ill; Avitene, C.R. Bard Davol, Warwick, RI).
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12. A sterile dressing is applied, often followed by an elastic compression bandage. Outflow occlusion and
heparinized saline flush are maintained for 20 minutes following sclerosant injection. If the lesion contains
large venous channels in addition to cavernous spaces, deflation of the occlusion cuff is performed
stepwise under fluoroscopic monitoring to detect and avoid migration of the sclerosant into the systemic
circulation.
13. In extremity lesions, the limb is elevated and frequent neurovascular checks are performed over the first
24 hours.
14. Pain and tenderness are usually relatively mild, and easily controlled with oral medication, even in
children.
15. The patient and family should be instructed that the lesion will not show improvement immediately and
may in fact feel and look worse for the first 1 to 2 weeks. The result of the embolization cannot be
accurately judged until 4 to 6 weeks have elapsed.
16. When multiple-staged procedures are required, they should not be scheduled closer than 4 to 6 weeks
apart.
17. Patients with VMs involving a joint may present with recurrent hemarthrosis and eventual osteoarthritic
changes similar to those seen in hemophilia. This is most commonly seen in the knee joint, and the authors
treat lesions in this location aggressively. If hemarthrosis recurs despite several sclerotherapy sessions, a
combined orthopedic procedure utilizing both arthroscopy/synovectomy and sclerotherapy may be
performed in an effort to preserve the joint.
Venous Dysplasias
1. Congenital venous dysplasias, such as Klippel-Trenaunay Syndrome (KTS), are among the most
common vascular malformations encountered clinically. KTS is a congenital malformation generally confined
to a single extremity, most often the leg. Findings include unilateral varicose or anomalous veins (often
severe), overlying birthmarks such as port-wine stains or angiokeratomas, venous malformations, and
associated regional bone and soft tissue anomalies including overgrowth, undergrowth, and focal gigantism.
There are many variations and subtypes, the scope of which exceeds this chapter. The vast majority are
found in otherwise normal individuals with no family history of vascular malformations. Recent studies have
shown that this condition appears to be a type of mosaicism, where the involved tissues will show abnormal
genes not found in the rest of the body.
2. Treatment options are limited.
a. Mild involvement will require no treatment or simple measures such as support stockings.
b. In more symptomatic cases, the presence or absence of a normal deep venous system in the extremity is
often the determining factor in whether interventional
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treatment is feasible. It was formerly thought that a majority of these patients had an absent or hypoplastic
deep system, but recent studies using ultrasound and other modalities have shown that most of these
individuals do, in fact, have an intact deep system, thus allowing more aggressive treatment. Deep veins,
even when present and of normal caliber, may be difficult or impossible to visualize on contrast venography.
If a deep system is present, superficial symptomatic veins may be amenable to treatment by sclerotherapy,
surgical stripping, embolization, or endovenous ablation techniques (13).
3. Many patients have associated subcutaneous and/or intramuscular cavernous venous malformations
(sometimes involving the entire extremity), which can be successfully treated by the direct injection of
sclerosants as described in isolated cavernous malformations.
4. The cutaneous involvement (port-wine stain, angiokeratoma) may be the most symptomatic component in
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some patients because they often present with recurrent bleeding episodes as well as cosmetic issues.
These lesions may often be treated successfully with laser therapy.
Lymphatic Malformations
1. Lymphatic malformations are relatively uncommon and are notoriously difficult to treat, particularly the
infiltrating microcystic type.
2. Spontaneous infectious and inflammatory episodes can occur, an event rarely seen in other vascular
malformations.
3. Macrocystic lesions can be successfully treated by drainage and direct injection of sclerosants into the
cavity (see Chapter 54). Frequently, a drainage catheter is placed into the cavity, and serial instillations of
sclerosants will be performed until no further output remains. Several agents have been used, but the
mostly commonly used are doxycycline and bleomycin. A specific agent, OK-432, derived from a
streptococcal protein, has also been described for use in these lesions, causing an intense inflammatory
reaction followed by fibrosis. This agent is not currently available in the United States.
a. Doxycycline powder is reconstituted with saline to a concentration of 10 mg per 1 mL. The volume of
doxycycline used is determined by the LM size. Typically, two-thirds of its original volume is infused to a
maximum dose of 300 mg.
b. Bleomycin is a chemotherapeutic agent that can successfully treat LMs and VMs with minimal
postprocedural swelling (14). This property has proven beneficial in treating sensitive anatomic regions
such as the head and neck, airway, and regions susceptible to compartment syndrome (forearm, calf).
(1) Although pulmonary fibrosis can occur with high cumulative lifetime doses of bleomycin (>300 mg), this
toxicity is considered dose-dependent. No cases of pulmonary fibrosis have been reported following
bleomycin sclerotherapy using the accepted dose of 1 mg per kg with a maximum of 15 mg per session.
Acute bleomycin pulmonary sensitivity can occur within hours of administration. This rare event does not
appear to be dose-dependent and responds well to corticosteroids and supportive care (15).
(2) Bleomycin is most commonly used as a liquid but can also be used as a foam with Ethiodol and air.
4. Microcystic and cutaneous vesicular lesions are much more difficult to manage; in some cases,
superficial laser treatment or surgical resection with skin grafting have been effective.
1. Immediate postprocedural care includes bed rest for 6 hours following transarterial procedures, whereas
transvenous procedures require 2 hours of bed rest.
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2. A tapering dose of oral steroids is continued over 2 days following treatment of slow-flow malformations to
reduce inflammation and swelling. A tapering methylprednisolone dose pack is prescribed if the treated region is
susceptible to compartment syndrome (calf and forearm).
3. Patients are discharged with a week of prophylactic antibiotics.
4. As discussed earlier, most patients do not experience significant pain but are discharged with oral pain
medication as needed.
5. Patients are advised that normal activity postprocedure as tolerated is fine, but athletics (and gym class in
children) should not be engaged in for 10 to 14 days.
Results
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Results vary based on the type of malformation treated and its severity. As stated earlier, AVM treatments
are often performed in a staged fashion, and multiple sessions over a period of years may be necessary. In
the authors' experience, embolization and sclerotherapy have been successful in improving pain, bleeding,
and nonhealing ulcers in approximately 80% of patients. Isolated lesions may require a single treatment,
whereas patients with extensive malformations may require multiple procedures throughout their lifetime.
New Directions
Research regarding vascular anomaly development and potential pharmacologic treatment options is ongoing.
Most recently, a pathway (PI3K/mTOR pathway) responsible for regulating angiogenesis and cellular
proliferation has become an important area of interest. Although the details of the mTOR signaling pathway are
beyond the scope of this chapter, there are several components, including vascular endothelial growth factor
(VEGF) and other proteins which have been associated with vascular anomalies in animal models. Rapamycin
(sirolimus), a direct mTOR inhibitor, has been shown to effectively treat both venous and LMs. Lesions have
recurred after discontinuation of the drug, and therefore, patients require lifelong treatment. There are several
additional drugs including bevacizumab, a monoclonal antibody against VEGF, and thalidomide, which have
shown promising results (16).
Complications
High-Flow Malformations
2. Passage of embolic materials into the venous outflow and lung
3. Ischemia due to occlusion of branches supplying normal tissues
4. Local or systemic complications due to the inherent toxicity of the embolic agent
Venous Malformations
1. Skin ulceration or blistering at the injection site
2. DVT due to inadequate outflow control during sclerosant injection
3. Compartment syndrome (especially calf, forearm)
4. Cardiopulmonary complications (arrhythmia, pulmonary edema, sudden death)
1. Nontarget and ischemic complications—treatment is dependent on the vascular bed involved and the
patient's clinical status.
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2. Skin ulceration—treated with topical antiseptic cream (1% silver sulfadiazine, Silvadene), and, in some
cases, oral antibiotics. Healing generally occurs over a period of weeks with minimal sequelae.
3. DVT—treatment as in any case of DVT.
References
1. International Society for the Study of Vascular Anomalies. 2014 ISSVA Classification of Vascular
Radiology Books
Anomalies. www.issva.org/classification. Accessed December 1, 2015.
2. Mulliken JB, Young AE, eds. Vascular Birthmarks: Hemangiomas and Malformations. Philadelphia, PA:
WB Saunders; 1988.
3. Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification
based on endothelial characteristic. Plast Reconstr Surg. 1982;69:412-422.
4. Waner M, Buckmiller L, Suen J. Surgical management of hemangiomas of the head and neck. Op Techn
Otolaryng-Head Neck Surg. 2002;13:77-84.
5. Hasan M, Rahman M, Hoque S, et al. Propranolol for hemangiomas. Pediatr Surg Int. 2013;29:257-262.
6. Moukaddam H, Pollak J, Haims AH. MRI characteristics and classification of peripheral vascular
malformations and tumors. Skeletal Radiol . 2009;38:535-547.
7. Rosen RJ, Contractor S. The use of cyanoacrylate adhesives in the management of congenital vascular
malformations. Semin Intervent Radiol . 2004;21:59-66.
8. Do YS, Yakes WF, Shin SW, et al. Ethanol embolization of arteriovenous malformations: interim results.
Radiology. 2005;235:674-682.
9. Shin BS, Do YS, Lee BB, et al. Multistage ethanol sclerotherapy of soft-tissue arteriovenous
malformations: effect on pulmonary arterial pressure. Radiology. 2005; 235:1072-1077.
10. Patel S, Potti S, Jaspan D, et al. Embolization of uterine arteriovenous malformation for treatment of
menorrhagia. Arch Gynecol Obstet. 2009;279:229-232.
11. Mazoyer E, Enjolras O, Laurian C, et al. Coagulation abnormalities associated with extensive venous
malformations of the limbs: differentiation from Kasabach-Merritt syndrome. Clin Lab Haematol .
2002;24:243-251.
12. Bergan J, Pascarella L, Mekenas L. Venous disorders: treatment with sclerosant foam. J Cardiovasc
Surg (Torino). 2006;47:9-18.
13. Frasier K, Giangola G, Rosen R, et al. Endovascular radiofrequency ablation: a novel treatment of
venous insufficiency in Klippel-Trenaunay patients. J Vasc Surg. 2008;47:1339-1345.
14. Chaudry G, Guevara CJ, Rialon KL, et al. Safety and efficacy of bleomycin sclerotherapy for microcystic
lymphatic malformation. Cardiovasc Intervent Radiol . 2014; 37:1476-1481.
15. Atwa K, Abuhasna S, Shihab Z, et al. Acute pulmonary toxicity following intralesional administration of
bleomycin for a lymphovenous malformation. Pediatr Pulmonol . 2010;45:192-196.
16. Blatt J, McLean TW, Castellino SM, et al. A review of contemporary options for medical management of
Radiology Books
hemangiomas, other vascular tumors, and vascular malformations. Pharmacol Ther. 2013;139:327-333.
Radiology Books
22
Hepatic Metastases: Chemoembolization
Michael C. Soulen
Indications
1. Liver-dominant hepatic metastases. Patients with minimal or indolent extrahepatic disease may be
candidates if the liver disease is considered to be the dominant source of morbidity and mortality for that
individual.
2. In addition to primary hepatic malignancies such as hepatocellular carcinoma and cholangiocarcinoma,
tumors that typically meet these criteria include metastases from colorectal cancer, neuroendocrine tumors,
ocular melanoma, and sarcomas. Occasionally, pancreas, breast, lung, or other cancers will have liveronly
or liver-dominant metastases.
Contraindications
a. Severe anaphylactoid reactions to radiographic contrast media
c. Severe peripheral vascular disease precluding arterial access
2. Contraindications to administration of chemotherapy
a. Severe thrombocytopenia (<50,000 per μL) or leucopenia (absolute neutrophil count [ANC] <1,000 per
μL)
b. Cardiac (American Heart Association [AHA] class III to IV failure) or renal insufficiency (creatinine >2.0 mg
per dL)
3. Contraindications to hepatic artery embolization
a. The presence of hepatic encephalopathy or jaundice is an absolute contraindication to embolization.
b. Tolerance of hepatic artery occlusion is dependent on the presence of portal vein inflow. The portal vein
must be carefully assessed at the time of angiography. Compromise in portal venous blood flow is only a
relative contraindication to hepatic embolization. Chemoembolization can be performed safely despite portal
vein occlusion if hepatopetal collateral flow is present (1). In this setting, a smaller volume of the liver should
be embolized at any one time.
c. When the parenchyma is diseased, the liver becomes more dependent on the hepatic artery and less on
the portal vein. A subgroup of patients has been identified who are at high risk of acute hepatic failure
following hepatic artery embolization. They have a constellation of more than 50% of the liver volume
replaced by tumor, lactate dehydrogenase (LDH) greater than 425 IU per liter, aspartate transaminase
greater than 100 IU per liter, and total bilirubin of 2 mg per dL or greater (2).
d. Presence of a bilioenteric anastomosis, biliary stent, or prior sphincterotomy allows for colonization of the
bile ducts with enteric bacteria. Hepatic artery embolization causes microscopic bile duct injury, leading to
liver abscess formation, which can be fatal (3). This occurs almost universally even with routine antibiotic
prophylaxes. Aggressive prophylactic regimens can decrease the incidence of liver abscess to around 20%
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(4).
e. Biliary obstruction is a relative contraindication. Even with a normal serum bilirubin, the presence of
dilated intrahepatic bile ducts places the patient at high risk for bile duct necrosis and biloma formation in
the obstructed segment(s) of the liver. Presumably, the resistance to bile outflow increases pressure in the
sinusoids, which in turn decreases portal inflow and makes the liver more dependent on arterial blood.
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f. Inability to position the catheter tip selectively, so as to avoid nontarget embolization of the gut, skin, or
other vulnerable extrahepatic structures, places the patient at risk for serious injury. Coil blockade of the
nontarget vessel can be performed to allow chemoembolization to be performed safely. The cystic artery
can be chemoembolized safely, although doing so will increase the intensity and duration of
postembolization syndrome (5).
Pretreatment Assessment
1. Tissue diagnosis or convincing clinical diagnosis (e.g., liver mass with characteristic features and elevated
tumor markers)
2. Cross-sectional imaging of the abdomen and pelvis (computed tomography [CT] or magnetic resonance
imaging [MRI])
3. Exclusion of substantial extrahepatic disease (chest x-ray or CT, positron emission tomography [PET]-CT)
4. Laboratory studies including complete blood count (CBC), prothrombin time (PT), partial thromboplastin time
(PTT), creatinine, liver function tests, and tumor markers
Patient Education
Before embarking on this fairly arduous palliative regimen, patients should be thoroughly informed of the side
effects and risks (6). Eighty percent to 90% of patients suffer a postembolization syndrome, characterized by
pain, fever, and nausea and vomiting, fatigue, and anorexia. The severity of these symptoms varies from patient
to patient and can last from a few hours to a few weeks. Other significant toxicities are rare. Serious
complications occur after 5% to 7% of procedures. Given the significant discomforts, hazards, and expense of
this treatment, its palliative role should be clearly understood.
Patient Preparation
1. Patients fast overnight.
2. The patient is admitted to the hospital the morning of the procedure.
3. Vigorous hydration is instituted (normal saline solution [NS] at 200 mL per hour).
4. Prophylactic antibiotics (e.g., cefazolin [Ancef] 1 g, metronidazole [Flagyl] 500 mg) and antiemetics (e.g.,
ondansetron [Zofran] 24 mg, dexamethasone [Decadron] 10 mg, diphenhydramine [Benadryl] 50 mg) are
administered intravenously (IV). Patients with well-differentiated neuroendocrine tumors (NETs) get
subcutaneous octreotide (Sandostatin) 500 μg. Note that routine use of prophylactic antibiotics and octreotide is
common practice but not evidence-based.
Procedure
1. Diagnostic visceral arteriography (including celiac and superior mesenteric arteriography) is performed
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under conscious sedation to determine the arterial supply to the liver and confirm patency of the portal vein.
Variant hepatic artery anatomy is present in almost half of the population. The origins of vessels supplying
the gut (gastroduodenal, right gastric, supraduodenal) are carefully noted in order to avoid embolization of
the stomach or small bowel. The cystic artery should be identified. Chemoembolization of the right hepatic
artery proximal to the cystic artery is safe; however, chemoembolization of the gallbladder should be
avoided if possible in order to reduce the severity of postembolization syndrome.
2. Once the arterial anatomy is clearly understood, a catheter is advanced superselectively into the right or
left hepatic artery, depending on which lobe holds the most tumors. A power-injected superselective
angiogram with prolonged
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imaging should be performed to confirm catheter position and exclude nontarget vessels prior to injecting
any chemotherapeutic drugs. In addition, cone-beam CT should be performed routinely because this has
been shown to improve outcomes.
3. Catheters: Many chemoembolization procedures can be done with a 4 Fr. hydrophilic-coated Cobra
catheter and a long-taper hydrophilic wire. Such catheters should not be advanced into a vessel less than
twice the catheter diameter because this will cause iatrogenic stasis. When small vessels or tortuous
anatomy is encountered, a high-flow microcatheter can be advanced through a reverse-curve or Cobra
catheter into the target vessel. Median arcuate ligament compression of the celiac artery often makes
selective hepatic catheterization with a Cobra-style catheter difficult, in which case a reverse-curve catheter
(e.g., Simmons, Sos) with a coaxial microcatheter works well.
4. A variety of chemoembolic protocols exist, historically 100 to 150 mg cisplatin, 50 mg doxorubicin, and/or
10 to 20 mg mitomycin C dissolved in 10 mL of radiographic contrast and emulsified with 10 to 20 mL of
iodized oil. Powdered cisplatin has been unavailable since 2010 but may return to the market in the future.
Powdered doxorubicin has been plagued by intermittent drug shortages in the United States. Epirubicin can
be substituted but also has inconsistent availability in the United States. Alternatively, drug-eluting
microspheres allow use of doxorubicin or irinotecan in solution.
The oil:chemoemulsion ratio is adjusted by the operator based on the size and vascularity of the tumor and
typically ranges from 1:1 to 2:1. Dividing the dose into 3 to 4 aliquots allows the interventional oncologist to
adjust the emulsion ratio during the embolization to maximize drug delivery at the endpoint of near stasis.
Embolization is completed with 100 to 300 micron spherical particles mixed into the final aliquot of the
chemoembolic emulsion. All chemotherapy and associated syringes are kept on a separate tray or Mayo
stand and must be disposed of according to hospital regulations. Glass or polycarbonate syringes should
be used, along with metal or polycarbonate stopcocks. Conventional plastic syringes, stopcocks, and flow
switches will disintegrate rapidly after contact with the chemoembolic emulsion. All personnel in the room
must have eye protection and a mask on, and anyone handling the chemotherapeutic material must be fully
gowned and double-gloved.
5. The patient receives intra-arterial lidocaine (30-mg boluses prior to and between aliquots of the
chemotherapeutic emulsion, up to 200 mg total) and IV fentanyl and midazolam to alleviate pain during the
embolization.
6. For Lipiodol chemoembolization, the chemotherapeutic drugs should be dissolved in contrast in the
pharmacy and delivered in a sterile sealed bottle. The chemotherapy/contrast solution is drawn up in a 20-
mL glass or polycarbonate syringe. Iodized oil (Ethiodol), if used, is drawn up in a separate 20-mL syringe.
These serve as reservoirs during the procedure. A 5-mL or 10-mL syringe and a metal or polycarbonate
stopcock can then be used to draw off 2 mL each of chemotherapy/contrast solution and Ethiodol. A second
5- to 10-mL syringe is then used to emulsify the two by pumping vigorously back and forth through the
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stopcock 20 to 25 times. This initial 4-mL aliquot of emulsion is injected slowly through the catheter,
followed by a lidocaine flush. If a microcatheter is used, the viscous emulsion will need to be injected using
1- to 3-mL polycarbonate Luer-Lok syringes. Additional 4-mL aliquots are administered, with the addition of
one syringe of 100 to 300 micron spherical embolic to the final aliquot. The chemoembolic mixture is
injected until nearly complete stasis of blood flow is achieved. The goal is to achieve a “tree-in-winter”
appearance, with embolization of the terminal tumor-feeding branches but preservation of flow in the major
arterial trunks. By repeatedly mixing small aliquots of the emulsion, the thickness of the mix can be adjusted
to try to deliver as much of the total drug dose as possible before achieving the endpoint of 90% stasis.
Large, hypervascular
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tumors may require a thicker mix by adding more embolic particles or increasing the oil:contrast ratio.
Conversely, less vascular tumors may require thinning of the emulsion by using less oil or particles.
7. For drug-eluting beads (DEB), specific protocols exist for loading of each type of chemotherapeutic drug
(e.g., doxorubicin, irinotecan) onto each brand and size of microsphere (DC/LC Beads, Biocompatibles,
Oxford, CT; HepaSphere/QuadraSphere, Merit Medical Systems, Inc, South Jordan, UT; ONCOZENE,
CeloNova, San Antonio, TX; LifePearl/HydroPearl, Terumo, Somerset, NJ). Consult the manufacturer's
instructions for use. Currently, none of these products are approved in the United States for drug delivery.
Typically, 50 to 100 mg of drug in solution is added to a vial of microspheres a few hours before the
procedure to allow time for drug uptake. The effluent is then removed, and the drugloaded microspheres
suspended in 10 to 20 mL of nonionic contrast, which is slowly instilled into the target vessel. Because the
microspheres are not visible, extra caution is required to avoid nontarget embolization. The endpoint is drug
delivery and additional bland embolics are not required. Intra-arterial irinotecan is extremely painful and
additional analgesia is necessary.
1. Vigorous hydration (NS 3 L per 24 hours) and then 5% dextrose, half-normal saline solution (D5½NS) at 80
mL per hour until oral intake is adequate.
2. IV antibiotics until discharge (e.g., cephazolin 500 mg q8h, metronidazole 500 mg q12h)
3. IV antiemetic therapy (ondansetron and Decadron, 8 mg IV q8h)
4. Narcotics, prochlorperazine, and acetaminophen are liberally supplied for control of pain, nausea, and fever. A
patient-controlled analgesia (PCA) pump is occasionally required if pain is severe. Typical PCA doses are
morphine sulfate 1 to 2 mg per hour, 1 to 2 mg demand, with a 10- to 15-minute lockout. Alternatively,
hydromorphone (Dilaudid) can be used at a dose of 0.2 mg per hour and 0.2 mg demand.
5. The patient is discharged as soon as oral intake is adequate and parenteral narcotics are not required for pain
control. Most patients are discharged in 1 day; many insurers now only approve a 23-hour stay. The average
length of stay is 1.3 days. Oral antibiotics (amoxicillin clavulanate [Augmentin] or ciprofloxacin [Cipro], 500 mg
two times per day [bid]) are continued for another 5 days as well as antiemetics (prochlorperazine [Compazine]
10 mg by mouth [PO] q6h, or granisetron [Kytril] 1 mg PO bid, or ondansetron [Zofran] 8 mg PO bid) and oral
narcotics (acetaminophen/codeine [Tylenol with Codeine No. 3], oxycodone/acetaminophen [Percocet], or
hydromorphone [Dilaudid] 2 mg), 1 to 2 tablets q4h as needed. Patients taking narcotics should be warned about
constipation and given instructions for a concurrent laxative regimen.
6. Laboratory studies are repeated in 3 weeks. Routine liver imaging between procedures is not necessary
unless the patient develops signs or symptoms suggesting a complication.
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7. At 4 weeks, the patient returns for a second procedure directed at the other lobe of the liver. Depending on the
arterial anatomy, two to four procedures may be required to treat the entire tumor burden, after which response
is assessed by repeat imaging studies and tumor markers. Patients with tumor confined to one lobe may still
require embolization of the other lobe because intrahepatic collaterals form rapidly between the embolized and
nonembolized lobes.
Results
1. Hepatoma (7,8): Sixty percent to 80% of patients will have stabilization or regression of their hepatoma
and a decrease in α-fetoprotein level, if elevated. Median duration of response is 12 to 15 months.
Prolongation of survival has been
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demonstrated in two randomized trials. Important prognostic factors include tumor burden, stage,
macrovascular invasion, oil uptake, and severity of underlying liver disease.
2. Colon cancer (9,10): Disease control is achieved in 45% to 65%. Median survival in Phase II trials of
sequential systemic chemotherapy and chemoembolization is about 24 months from diagnosis, which is
double historical controls using systemic therapy alone, and around 12 months from time of
chemoembolization. No Phase III trials of Lipiodol chemoembolization exist to assess survival advantage.
One randomized trial adding irinotecan-loaded microspheres showed superior time to progression and
overall survival compared to irinotecan-based systemic therapy alone (11).
3. NETs (12) have a 90% response rate to either bland particle embolization or chemoembolization. The
duration of response is mostly driven by the underlying tumor grade.
4. There are limited data for metastases from ocular melanoma, sarcomas, and breast cancer.
Complications
Major complications of hepatic embolization include hepatic insufficiency or infarction (2%), hepatic abscess
(2%), biliary necrosis or stricture, tumor rupture, surgical cholecystitis, and nontarget embolization to the
gut. With careful patient selection and scrupulous technique, the incidence of these serious events
collectively is 5% to 7%. Other complications include cardiac events, renal insufficiency, and anemia
requiring transfusion, with incidences of less than 1% each. Thirty-day mortality ranges from 1% to 4%.
References
1. Pentecost MJ, Daniels JR, Teitelbaum GP, et al. Hepatic chemoembolization: safety with portal vein
thrombosis. J Vasc Interv Radiol . 1993;4:347-351.
2. Charnsangavej C. Chemoembolization of liver tumors. Semin Interv Radiol . 1993;10: 150-160.
3. Kim W, Clark TWI, Baum RA, et al. Risk factors for liver abscess formation after hepatic
chemoembolization. J Vasc Interv Radiol . 2001;12:965-968.
4. Patel S, Tuite CM, Mondschein JI, et al. Effectiveness of an aggressive antibiotic regimen for
chemoembolization in patients with previous biliary intervention. J Vasc Interv Radiol . 2006;17:1931-1934.
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5. Leung DA, Goin JE, Sickles C, et al. Determinants of postembolization syndrome after hepatic
chemoembolization. J Vasc Interv Radiol . 2001;12:321-326.
6. Tuite CM, Sun W, Soulen MC. General assessment of the patient with cancer for the interventional
oncologist. J Vasc Interv Radiol . 2006;17:753-758.
7. Lo CM, Ngan H, Tso WK, et al. Randomized controlled trial of transarterial lipiodol chemoembolization for
unresectable hepatocellular carcinoma. Hepatology. 2002; 35:1164-1171.
8. Llovet JM, Real MI, Montaña X, et al. Arterial embolisation or chemoembolisation versus symptomatic
treatment in patients with unresectable hepatocellular carcinoma: a randomised controlled trial. Lancet.
2002;359:1734-1739.
9. Vogl TJ, Gruber T, Balzer JO, et al. Repeated transarterial chemoembolization in the treatment of liver
metastases of colorectal cancer: prospective study. Radiology. 2009;250(1):281-289.
10. Albert ML, Kiefer MV, Stavropoulos SW, et al. CAM/Ethiodol/PVA chemoembolization of liver metastases
from colorectal carcinoma. J Vasc Interv Radiol . 2009;20:62.
11. Fiorentini G, Aliberti C, Tilli M, et al. Intra-arterial infusion of irinotecan-loaded drugeluting beads (DEBIRI)
versus intravenous therapy (FOLFIRI) for hepatic metastases from colorectal cancer: final results of a phase
III study. Anticancer Res. 2012;32:1387-1395.
12. Yang TX, Chua TC, Morris DL. Radioembolization and chemoembolization for unresectable
neuroendocrine liver metastases—a systematic review. Surg Oncol . 2012;21:299-308.
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23
Hepatocellular Carcinoma: Chemoembolization
Jean-Francois H. Geschwind
Maria Tsitskari
Christos S. Georgiades
It is rare in interventional radiology to have the highest level of evidence (level 1) in support of a specific
procedure. But for transarterial chemoembolization (TACE), level 1 evidence does exist thanks to two
randomized trials by Llovet et al. (1) and Lo et al. (2) and a meta-analysis by Cammà (3) in 2002. As a result,
TACE has become the standard of care for patients with unresectable hepatocellular carcinoma (HCC) and has
been included in all HCC treatment guidelines (American Association for the Study of Liver Diseases, National
Comprehensive Cancer Network, European Association for the Study of the Liver). The technique takes
advantage of the fact that whereas the liver parenchyma receives most of its blood supply (60% to 80%) from the
portal vein, liver tumors are nearly exclusively fed by hepatic artery (HA) branches. TACE preferentially deposits
the chemoembolization mixture directly in the vascular bed of the tumor while hepatic parenchymal injury is
minimized. Conventional TACE is generally composed of three ingredients: (a) chemotherapy (single, double, or
triple cocktail combination of 10 mg mitomycin C, 50 mg doxorubicin, and 100 mg cisplatin, which is the most
commonly used cocktail in the United States, or since the cisplatin shortage, doxorubicin and mitomycin C), (b)
lipiodol (a radiopaque oil carrier), and (c) embolic agent (particles or Gelfoam [Pfizer, New York, NY]) that slows
blood flow, thus prolonging the chemotherapy residence time in the tumor. The advent of drug-eluting beads
(DEB), which combine the stated three characteristics, may eclipse conventional TACE in the future, but so far,
despite some clear advantages, DEB-TACE has not been shown to be superior to conventional TACE in terms
of patient survival. DEB are polymer-based microspheres that can be loaded with a number of chemotherapeutic
agents including doxorubicin (for HCC) and irinotecan (for colorectal cancer [CRC] mets) and then delivered to
the tumor vascular bed. Selectivity, prolonged residence time within the tumor, sustained drug release, better
embolic effect, and fewer side effects are the advantages of DEB over conventional TACE (4,5).
Indications
1. The primary indication for TACE is treatment of unresectable HCC, specifically those with intermediate
stage (Barcelona Clinic Liver Cancer [BCLC] stage B) according to the Barcelona Clinic Liver Cancer
staging system.
2. Secondary indications include:
a. Bridge to transplant, especially for patients at risk of exceeding the Milan liver transplantation criteria
(one tumor less than 5 cm, or up to three tumors, each less than 3 cm) (6,7).
b. Downstage to resection or transplantation size criteria. Data are strong but not conclusive (8).
c. Aid surgery by shrinking a tumor abutting a major resection plane (i.e., right or left portal vein). Weak
supportive data and mainly surgeon's preference.
d. Palliate patients with advanced stage HCC (BCLC stage C) which includes patients with macrovascular
invasion and a weakened performance status.
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Contraindications
Absolute
1. Poorly compensated advanced liver disease. Occasionally, patients with wellcompensated Child-Pugh C
disease can be treated with TACE if it can be performed selectively.
2. Encephalopathy, refractory to medical management, unless TACE can be performed selectively
3. Poor performance status. Generally, patients with Eastern Cooperative Oncology Group (ECOG) >2 or
Karnofsky Index <70 do not benefit from TACE.
5. Large burden extrahepatic metastatic disease. If the patient's HCC is not thought to be the life-limiting
factor, then TACE will not benefit the patient.
6. Active infection
Relative
1. Total bilirubin >4. If hyperbilirubinemia is due to biliary obstruction and can be reversed with drainage,
TACE can be considered. Drainage should be external to avoid crossing the sphincter of Oddi. Violation of
the ampulla of Vater may result in bacterial colonization of the intrahepatic bile ducts which can contribute to
post-TACE intrahepatic abscess formation and/or cholangitis as a result of the profound ischemia to the
peribiliary plexus caused by TACE.
2. Anaphylactic reaction to contrast. Gadolinium can be substituted in the absence of renal failure or CO2, if
the vascular target is mapped a priori.
3. Anaphylactic reaction to chemotherapy drugs. Embolization alone may confer a benefit.
4. Portal vein occlusion. Studies have demonstrated that portal vein occlusion does not increase the risk of
complications, as long as liver reserve is within criteria (Child-Pugh A or B) and/or collateral flow to the liver
exists (9).
1. Multidisciplinary review of the patient's disease status is necessary in order to ensure that no curative options
are overlooked.
2. Clinic visit during which the patient and often family is fully informed regarding the risks and benefits and
reasonable expectation of therapy
3. Cross-sectional imaging review to plan procedure with magnetic resonance imaging (MRI) being preferred
4. Nil per os (NPO) status (except allowed medications) for at least 8 hours prior to sedation/anesthesia
5. Intravenous (IV) hydration. Dehydration from NPO status, contrast load, chemotherapy nephrotoxicity, and
possible tumor lysis syndrome increases the risk for acute renal injury. If no contraindication exists, a normal
saline bolus (i.e., 500 mL) followed by continuous IV hydration (100 mL per hour) is recommended.
6. Premedication
a. Dexamethasone 10 mg IV, diphenhydramine 50 mg IV
b. Nephroprotectants, if necessary. Most important is hydration.
c. Antiemetics. Ondansetron 8 mg IV
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Procedure
1. Moderate sedation is adequate for most patients.
2. Sterile preparation of femoral access
3. Arteriography
a. Abdominal aortogram may reveal collateral tumor supply but is not required.
b. Superior mesenteric arteriogram to identify accessory hepatic arteries and assess patency of portal vein
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c. Celiac and hepatic arteriogram for treatment planning
d. Cone-beam computed tomography (CT) imaging should be performed before treatment to ensure proper
targeting of the tumor.
5. Placement of catheter (or coaxial microcatheter, if necessary) as distal as possible to minimize collateral
liver injury but proximal enough to treat the entire targeted lesion
6. Delivery of chemotherapy/lipiodol/embolization mixture or chemotherapy loaded DEB under continuous
fluoroscopic visualization to avoid the inadvertent delivery of drugs and/or embolic agents into nontarget
vessels
a. For conventional TACE, a water-in-oil emulsion must be created, which means that the amount of lipiodol
should be slightly greater than the chemotherapy drugs. The maximum amount of lipiodol should not exceed
15 to 20 mL. The amount of lipiodol emulsion to be injected depends on the tumor size. If a visible shunt is
identified between the hepatic artery and hepatic vein or more commonly between the hepatic artery and
portal vein, complete embolization of the shunt using Gelfoam pledgets must be performed prior to the
TACE procedure. Lidocaine (up to 10 mL of 1% nonbuffered lidocaine) should be given intra-arterially after
the lipiodol-chemotherapy emulsion has been administered but before the embolization component of the
procedure. Calibrated microspheres in the 100 to 300 μm size should be used to complete the embolization.
This is important to preserve the stability of the emulsion. The angiographic end point should be 2 to 5
heartbeats to clear the contrast column.
b. For DEB-TACE, the use of 100 to 300 μm size DEB is recommended in order to achieve deeper
penetration within the tumor(s). Iodinated contrast should be mixed with the DEB in a 3 to 4:1 ratio to
maximize. Appropriate doxorubicin doses to be used in DEB-TACE range from 50 to 150 mg.
7. Cone-beam CT imaging should be performed after treatment in order to confirm appropriate tumor
targeting and assess technical success.
8. Access hemostasis
1. Symptomatic support
a. Vigorous hydration
b. Pain control. Preferably patient-controlled analgesia (PCA)
c. Antiemetics: ondansetron 8 mg IV
d. Dexamethasone 8 mg IV every 8 hours for 48 hours (or oral if discharged)
2. Discharge
a. Patient is discharged when ambulatory, demonstrates adequate by mouth (PO) intake, and produces urine. A
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23-hour or overnight stay is adequate for most patients. Occasionally, severe symptoms may require additional
hospitalization. A regular noncontrast CT on day after lipiodol embolization should be obtained to document
distribution of embolization mixture.
b. Pain medications as needed (PRN) as well as antiemetics if necessary.
c. Proton pump inhibitors and Carafate should be prescribed when there is suspicion of nontarget gastric
embolization or when treatment included a replaced left hepatic artery off the left gastric artery.
3. Follow-up
a. Imaging
(1) Post-TACE regular noncontrast CT to determine lipiodol distribution and assess adequate tumor targeting
(only for conventional TACE). Unless complications or symptoms dictate otherwise, a contrast-enhanced liver
(MRI or CT) is obtained 3 to 4 weeks after the procedure and the patient assessed in clinic to assess response
and complications.
(2) After locoregional treatments, tumor necrosis may not necessarily be accompanied by reduction in size.
Therefore, response criteria based
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purely on size have been abandoned (World Health Organization [WHO], Response Evaluation Criteria in Solid
Tumors [RECIST]). Determination of response is best obtained using modified Response Evaluation Criteria in
Solid Tumors [mRECIST] or European Association for the Study of the Liver [EASL] criteria (Fig. 23.1). Recent
research has focused on quantification of tumor response using volumetrics Quantitative EASL (qEASL) so that
the entire tumor can be evaluated (three-dimensional [3D] imaging) (10).
FIGURE 23.1 • Baseline, contrast-enhanced, portal phase CT (A) of the liver shows a minimally enhancing mass
(arrow). Right hepatic arteriogram (B) shows a slightly hypervascular lesion in the right liver lobe (arrowheads).
Contrast-enhanced CT 5 weeks post-DEB-TACE (C) shows partial central necrosis of the lesion (star). Based on
WHO or RECIST criteria, there is no response as the size of the lesion remains unchanged. However, using
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EASL and mRECIST criteria, there has been a 50% and a 60% response, respectively. EASL represents an
estimation of the percent of tumor necrosis, whereas mRECIST is calculated as 100% × (ratio of viable tumor
diameter [white double-headed arrow] over the overall tumor diameter [black double-headed arrow]). (D).
b. TACE cycle is repeated at 4- to 6-week intervals until:

(1) MRI (or CT) shows near complete tumor necrosis.
(2) Tumor does not respond after at least two TACE procedures to the same area (11).
(3) Patient develops a contraindication.
(4) Patient is downstaged into surgical/transplant criteria.
Results
1. Survival benefit has been proven in Child-Pugh A and B patients compared with supportive treatment
alone.
a. In 2002, Llovet et al. (1) published results from a randomized controlled trial, which was stopped early
because TACE provided a statistically significant
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survival benefit in the treatment group (1- and 2-year survival of 82% and 63% for TACE vs. 63% and 27%
for supportive care).
b. Two meta-analyses confirmed the survival benefit of TACE. One that included five randomized controlled
trials published in the same year concluding that TACE reduced the 2-year mortality of patients with
unresectable HCC (odds ratio 0.54, 95% CI 0.33-0.89, P =.015) (3). Another meta-analysis of randomized
controlled trials published by Llovet and Bruix (12) showed significantly decreased 2-year mortality in
patients treated with chemoembolization with an odds ratio of 0.53 (95% CI 0.32-0.89, P =.017). Lack of
imaging response to initial TACE is not predictive of subsequent TACE failure. A second TACE has been
shown to impart a significant survival benefit to patients with unresectable HCC (11), even if the first TACE
did not result in radiological response.
c. Lo et al. (2) showed statistically significant survival benefit in patients with unresectable HCC treated with
lipiodol-cisplatin chemoembolization. The 1-, 2-, and 3-year survival in TACE-treated patients was reported
by Lo et al. (2) to be 57%, 31%, and 26%, compared with 32%, 11%, and 3%, respectively, in the control
group.
d. Recent studies have confirmed the above data and life expectancy for patients with unresectable HCC
and BCLC B disease ranges between 20 and 24 months.
Complications
The expected complications related to TACE are summarized in Table 23.1. The most common side effect
of TACE is post-chemoembolization syndrome seen in up to 80% of patients. It is composed of a triad of
abdominal pain, nausea, and fever and is not indicative of a true complication.
The most serious TACE-related complications are liver failure, nontarget embolization, and liver abscess.
1. Liver failure can be avoided with proper patient selection. Advanced liver disease is indicated by Child-
Pugh C, high bilirubin, low albumin, poor performance status, or encephalopathy, which are significant
predictors of liver failure after TACE. TACE in such patients should be avoided unless a very specific goal
exists, such as superselective TACE to improve transplantation candidacy.
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Table 23.1 Complications Related to TACE
Complication Risk Factor % Risk Risk Mitigation Action
Liver failure, death, Child-Pugh C 5-10 Superselective

encephalopathy T. Bilirubin ≥4 mg/dL Unknown embolization
Albumin ≤2 mg/dL
Poor performance status
Liver abscess Compromised sphincter of Oddi 30-80 Broad-spectrum

antibiotics
Bowel preparation
Nontarget Aberrant anatomy, especially <10 Place catheter distal to

embolization left or right gastric artery origin of gastric artery
Watch for chemoreflux
Pulmonary embolism Hepatic artery to hepatic vein <1 Gelfoam embolization of

shunting shunt
Variceal bleeding Gastroesophageal varices Unknown Pre-TACE endoscopic

banding
Acute renal failure Renal insufficiency, diabetes 0.05%- Hydration,

5% renoprotection, minimize
contrast
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2. Liver abscess is a rare complication unless there is bile duct colonization by gastrointestinal flora as a
result of compromised sphincter of Oddi (biliary tube, hepaticojejunostomy). In the latter case, the risk for
liver abscess is 60% to 80% and only minimally reduced by broad-spectrum antibiotics and colonic
preparation prior to TACE. TACE may result in biliary ischemia and cause a local abscess.
3. Nontarget embolization can be catastrophic and can be avoided with intimate knowledge of vascular
anatomy, experience, and fastidious technique. High dilution of the DEB with contrast and magnified,
continuous visualization limits the chances of reflux.
1. Liver failure, encephalopathy, and death. These complications are related to poor liver function reserve
prior to TACE, and the only intervention possible is symptomatic support. IV hydration, pressure support,
and Flagyl/lactulose or rifaximin for hepatic encephalopathy may help stabilize the patient until the liver
recovers.
2. Liver abscess. Ensuing liver abscess must be drained percutaneously. Such abscesses are notoriously
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difficult to treat and may require prolonged drainage, repeat drainage, and long-term antibiotics.
a. Gastric: symptomatic support, including NPO, IV hydration, proton pump inhibitors, and gastric surface
protection. If perforation, surgery may be required.
b. Gallbladder: mostly a self-limiting situation. Pain, nausea control, NPO, and IV hydration are adequate in
most cases. Gallbladder eventually scars down and symptoms resolve.
4. Pulmonary embolism: supportive measures to resolution including anticoagulation
5. Renal failure. Dehydration, contrast nephrotoxicity, chemotherapy nephrotoxicity, and tumor lysis
increase the risk for renal injury. Aggressive IV hydration prior to TACE is the single most important
maneuver to protect the kidney. Limiting contrast load and using nephroprotectants prior to TACE may help
reduce the risk of renal failure.
6. Gastrointestinal (GI) bleeding. Two distinct complications:
a. Arterial bleeding. Nontarget embolization may result in duodenal or gastric ulceration/perforation, which
can result in arterial bleeding.
b. Variceal bleeding. Patients with portal hypertension, gastric varices, and history of variceal bleed have a
higher risk of repeat variceal bleeding. This is thought to be due to a transient increase in portal
hypertension. Treatment is symptomatic, and if unsuccessful, endoscopic banding/sclerosis is required.
References
1. Llovet JM, Real MI, Montaña X, et al. Arterial embolisation or chemoembolisation versus symptomatic
treatment in patients with unresectable hepatocellular carcinoma: a randomised controlled trial. Lancet.
2002;359:1734-1739.
2. Lo CM, Ngan H, Tso WK, et al. Randomized controlled trial of transarterial lipiodol chemoembolization for
unresectable hepatocellular carcinoma. Hepatology. 2002;35:1164-1171.
3. Cammà C, Schepis F, Orlando A, et al. Transarterial chemoembolization for unresectable hepatocellular

carcinoma: meta-analysis of randomized controlled trials. Radiology. 2002;224:47-54.
4. Malagari K, Chatzimichael K, Alexopoulou E, et al. Transarterial chemoembolization of unresectable

hepatocellular carcinoma with drug eluting beads: results of an open-label study of 62 patients. Cardiovasc
5. Poon RT, Tso WK, Pang RW, et al. A phase I/II trial of chemoembolization for hepatocellular carcinoma
using a novel intra-arterial drug-eluting bead. Clin Gastroenterol Hepatol . 2007;5(9):1100-1108.
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6. Aloia TA, Adam R, Samuel D, et al. A decision analysis model identifies the interval of efficacy for
transarterial chemoembolization (TACE) in cirrhotic patients with hepatocellular carcinoma awaiting liver
transplantation. J Gastrointest Surg. 2007;11(10): 1328-1332.
7. Frangakis C, Geschwind JF, Kim D, et al. Chemoembolization decreases drop-off risk of hepatocellular
carcinoma patients on the liver transplant list. Cardiovasc Intervent Radiol . 2011;34(6):1254-1261.
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8. Chapman WC, Majella Doyle MB, Stuart JE, et al. Outcomes of neoadjuvant transarterial
chemoembolization to downstage hepatocellular carcinoma before liver transplantation. Ann Surg.
2008;248(4):617-625.
9. Georgiades CS, Hong K, D'Angelo M, et al. Safety and efficacy of transarterial chemoembolization in
patients with unresectable hepatocellular carcinoma and portal vein thrombosis. J Vasc Interv Radiol .
2005;16(12):1653-1659.
10. Chapiro J, Wood LD, DeLin M, et al. Diffusion weighted MR imaging in patients with HCC after TACE:
diagnostic accuracy of 3D quantitative image analysis. Radiology. 2014;273(3):746-758.
11. Georgiades C, Geschwind JF, Harrison N, et al. Lack of response after initial chemoembolization for
hepatocellular carcinoma: does it predict failure of subsequent treatment? Radiology. 2012;265(1):115-123.
12. Llovet JM, Bruix J. Systematic review of randomized trials for unresectable hepatocellular carcinoma:
chemoembolization improves survival. Hepatology. 2003;37(2):429-442.
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24
Hepatic Malignancies: Radioembolization
Robert J. Lewandowski
Riad Salem
Radioembolization, a form of intra-arterial brachytherapy, is a technique where particles of glass or resin,

impregnated with the isotope yttrium-90 (90Y), are infused through a catheter directly into the hepatic arteries.
90Y is a pure beta emitter and decays to stable zirconium-90 with a physical half-life of 64.1 hours. The average
energy of the beta particles is 0.9367 MeV, has a mean tissue penetration of 2.5 mm, and a maximum
penetration of 10 mm. Once the particles are infused through the catheter into the hepatic artery, they travel to
the distal arterioles within the tumors, where the beta emissions from the isotope irradiate the tumor.
Indications
1. Glass microspheres
a. TheraSphere was approved by the U.S. Food and Drug Administration (FDA) in 1999 under a
humanitarian device exemption, defined as safe and probably beneficial for the treatment of unresectable
hepatocellular carcinoma (HCC) with or without portal vein thrombosis (PVT), or as a bridge to
transplantation in patients who could have appropriately positioned catheters. This device is also approved
for the treatment of liver neoplasia in Europe and Canada.
2. Resin microspheres
a. SIR-Spheres were granted premarket approval by the FDA in 2002, defined as safe and effective for the
treatment of metastatic colorectal cancer to the liver with concomitant use of floxuridine. This device is also
approved in Europe, Australia, and various Asian countries for the treatment of liver neoplasia.
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Contraindications
Absolute
a. Uncorrectable coagulopathy
b. Severe renal insufficiency
c. Severe anaphylactoid reaction to iodinated contrast agents
d. Severe peripheral vascular disease precluding arterial access
2. Immediate life-threatening extrahepatic disease
3. Inability to prevent 90Y delivery to the gastrointestinal (GI) tract
4. Hepatopulmonary lung shunting
a. For TheraSphere, the limitation of what can be administered to the lungs is based on the lung dose, not
lung shunt fraction (LSF) (30 Gy per infusion, 50 Gy cumulative).
b. For SIR-Spheres, infusion is limited by the LSF (20%).
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Relative
1. PVT
a. Patients with main PVT have poor prognosis; Child-Pugh A patients with main PVT may be safely
treated.
b. Radioembolization is not contraindicated in lobar or segmental PVT.
2. Poor hepatic reserve
a. Total bilirubin >2 mg per dL
b. Risks may be mitigated by selective radioembolization.
3. Poor performance status
a. Eastern Cooperative Oncology Group (ECOG) >2
4. Biliary obstruction
a. Risks of infectious complications significantly higher in the setting of compromised sphincter of Oddi
1. Patient selection
a. History, physical examination, and assessment of performance status
b. Clinical laboratory tests (complete blood count with differential, blood urea nitrogen, serum creatinine, serum
electrolytes, liver function, albumin, lactate dehydrogenase [LDH], prothrombin time [PT], tumor marker assay:
carcinoembryonic antigen [CEA], α-fetoprotein [AFP])
c. Chest computed tomography (CT) for assessment of lung metastases
d. CT/magnetic resonance imaging (MRI) scan of the abdomen and pelvis for staging with assessment of portal
vein patency
e. Arteriography/macroaggregated albumin lung shunting study
a. Patients are nil per os (NPO) 6 hours prior to procedure.
(1) Medications are allowed with sips of water.
b. Peripheral intravenous line placed prior to procedure
(1) Hydration of patients with renal insufficiency
Procedure
1. Pretreatment angiography (1): To define hepatic arterial anatomy, allow embolization of communicating
vessels that may lead to aberrant microsphere deposition, and facilitate radiation dosimetry.
a. Abdominal aorta (pigtail catheter; 15 mL per second for 30 mL)
(1) Allows for the evaluation of celiac axis, superior mesenteric artery (SMA) and renal artery patency, aortic
tortuosity, as well as guiding proper visceral catheter selection
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b. SMA (reverse curve catheter; 3 mL per second for 30 mL)
(1) Allows for the identification of a replaced right hepatic, replaced proper hepatic, replaced common
hepatic, accessory right hepatic, and patency of the portal vein as well as the rare parasitization of blood
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flow from the SMA to the liver. Retrograde flow (from tumor sumping or celiac occlusion/stenosis) into the
gastroduodenal artery (GDA) is also assessed.
c. Celiac artery (reverse curve catheter; 3 to 4 mL per second for 12 to 15 mL)
(1) Allows for the assessment of celiac anatomy and identifies the presence of any possible variants,
including a replaced left hepatic artery arising off the left gastric (gastrohepatic trunk), as well as the right
and left inferior phrenic arteries. The dorsal pancreatic artery may arise off the celiac.
d. Common hepatic artery (microcatheter; 3 mL per second for 10 to 12 mL)
(1) Arterial branches of note whose location should be identified that may require embolization arising off
the common hepatic artery (CHA) include the right gastric, dorsal pancreatic, and gastroduodenal. Other
complex variants exist:
(a) A replaced right hepatic artery off the SMA with a trifurcation from the CHA into a GDA, left hepatic, and
middle hepatic arteries. In such cases, a right gastric is often seen and unless segmental infusions of
radioembolization are planned, the GDA/right gastric should be embolized. This functionally converts the
CHA into a left hepatic artery.
(b) Trifurcation of the CHA into a GDA, right, and left hepatic arteries. Given the low margin of error if reflux
occurs from a lobar or segmental infusion, the GDA should be embolized in this case, particularly if the more
embolic resin microspheres are being administered.
(c) “Double hepatic” artery: a very early takeoff of the right hepatic artery. Unless sufficient contrast is
injected and refluxed to the origin of the celiac, this vessel may be missed.
e. GDA (microcatheter; 2 mL per second for 8 mL)
(1) Vessels sought include the accessory cystic artery, superior pancreaticoduodenal, parasitization of flow
to the liver from the GDA or from its branches (right gastroepiploic, omental/epiploic branches), as well as
accessory hepatic arteries (usually providing flow to segments 5 or 6).
(2) Routine prophylactic embolization of the GDA is no longer recommended. However, given the clinically
inconsequential effects, prophylactic embolization of the GDA should be considered when resin
microspheres are being delivered with the microcatheter positioned in close proximity to the origin of the
GDA. Settings where the GDA might not be embolized include where there is parasitization of flow to liver
that may require future catheterization and radioembolization, where there is retrograde flow from the SMA
from either hyperdynamic flow or celiac stenosis, or where a minimally embolic device is considered. In
cases of GDA parasitization, embolization of all distal vessels except the one feeding the liver tumors is
recommended if possible, essentially converting the GDA into an accessory hepatic vessel feeding the
tumor vasculature. If complete embolization of the GDA is undertaken, it should be embolized to the origin of
the vessel because small very proximal GDA branches may hypertrophy in response to incomplete
embolization.
f. Proper hepatic angiogram (microcatheter; 3 mL per second for 12 mL)
(1) Injection of this vessel at this rate will often result in supraphysiologic flow rates and reflux but will
opacify small and often overlooked vessels— the one most commonly of interest is the right gastric artery.
g. Left hepatic angiogram (microcatheter; 2 mL per second for 8 mL)
(1) Vessels of interest include the left inferior phrenic artery, accessory left gastric artery, inferior
esophageal artery, right gastric artery, and
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falciform artery. Prophylactic embolization of these vessels may decrease adverse events following
radioembolization, such as abdominal pain, gastritis, and ulceration. Furthermore, delayed imaging of the
left hepatic angiogram is recommended in order to confirm the lack of opacification of the coronary vein.
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Finally, injection of the left hepatic artery should outline where there is flow to segment 4 via the medial
branch. If the medial branch is absent, a separate middle hepatic artery should be sought, usually off the
right hepatic artery.
(2) If a gastrohepatic trunk is identified, a few vascular observations should be made. Once all of the gastric
vessels have branched off, the trunk travels in a horizontal direction. All vessels arising from the horizontal
portion of the gastrohepatic trunk are extrahepatic and provide flow to the esophagus and stomach. When
delivering glass microspheres, injection should be distal to these vessels. With resin microspheres, these
extrahepatic arteries should be embolized; otherwise, vascular redistribution could be considered.
h. Right hepatic angiogram (microcatheter; 2 to 3 mL per second for 10 to 12 mL)
(1) Vessels of interest include the middle hepatic artery, supraduodenal, and cystic artery.
i. Phrenic arteries (microcatheter; 1 to 2 mL per second for 4 to 6 mL)
(1) If a portion of the liver tumor (especially HCC) is not opacified by hepatic arteriography, interrogating
these vessels may identify the remainder of the blood supply to the tumors.
2. Macroaggregated albumin (MAA) administration
a. The LSF (fraction of Tc-99m MAA observed in the lungs relative to the total Tc-99m MAA activity
observed) can be determined by infusing 4 to 5 mCi of Tc-99m-labeled MAA particles through the catheter
into the desired liver distribution and obtaining planar imaging.
b. The Tc-99m MAA scan can also demonstrate the presence of any stomach or bowel perfusion, especially
if single-photon emission computed tomography (SPECT) imaging is performed. Thus, it is recommended
that MAA injection be performed once all vessels of concern have been embolized. The shunt evaluation
allows the physician to plan for radioembolization therapy and minimize any uncertainty in microspheres
distribution at the time of treatment.
3. Dosimetry
a. Glass microspheres
(1) As described in the product insert, TheraSphere consists of insoluble glass microspheres where 90Y is
an integral constituent of the glass. The mean sphere diameter ranges from 20 to 30 μm. Each milligram
contains between 22,000 microspheres and 73,000 microspheres. TheraSphere is supplied in 0.05 mL of
sterile, pyrogen-free water contained in a 0.3-mL vee-bottom vial secured within a 12-mm clear acrylic vial
shield. Thera-Sphere are dispensed weekly by the manufacturer (BTG, London, United Kingdom) on
Wednesdays and are calibrated for noon, Eastern Standard Time of the following Sunday and are available
in the activity sizes from 3 GBq (81 mCi) to 20 GBq (540 mCi). The activity per microsphere is approximately
2,500 Bq.
(2) The recommended activity of TheraSphere that should be delivered to a lobe of the liver containing
tumor is between 80 Gy and 150 Gy. This wide range exists to give the treating physician clinical flexibility.
(a) Patients with significant cirrhosis should be treated more conservatively (80 to 100 Gy), whereas
patients without cirrhosis may be treated more aggressively (100 to 150 Gy).
(3) Assuming TheraSphere 90Y microspheres distribute in a uniform manner throughout the liver and 90Y
undergoes complete decay in situ, radioactivity required to deliver the desired dose to the liver can be
calculated
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using the following formula: A (GBq) = [ D (Gy) × M (kg)] / 50. Given that a fraction of the microspheres will
flow into the pulmonary circulation without lodging in the arterioles, when LSF is taken into account, the
actual dose delivered to the target volume becomes D (Gy) = [ A (GBq) × 50 × (1-LSF)] / M (kg). A is the
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activity delivered to the liver, D is the absorbed delivered dose to the target liver mass, and M is the target
liver mass. Liver volume (mL) is estimated with CT, and then converted to mass using a conversion factor of
1.03 mg per mL. Note that the dosimetry for TheraSphere is independent of tumor burden.
b. Resin microspheres
(1) As described in the product insert, SIR-Spheres consist of biocompatible resin-based microspheres
containing 90Y with a size between 20 μm and 60 μm in diameter. SIR-Spheres are a permanent implant
and are provided in a vial with water for injection. Each vial contains 3 GBq of 90Y (at the time of calibration)
in a total of 5 mL water for injection. Each vial contains 40 to 80 million microspheres. Consequently, the
activity per microsphere for SIR-Spheres is much lower than that of TheraSphere (50 Bq vs. 2,500 Bq,
respectively). SIR-Spheres are dispensed three times per week by the manufacturer (Sirtex, Lane Cove,
Australia) and are calibrated for 6 PM Eastern Standard Time on the date of treatment. The shelf life is 24
hours following calibration date and time. Just as with TheraSphere, assuming SIR-Spheres 90Y
microspheres distribute in a uniform manner throughout the liver and undergo complete decay in situ,
radioactivity delivered to the liver can be calculated by incorporating the body surface area and estimate of
tumor burden as follows: A (GBq) = BSA (m2) - 0.2 + (% tumor involvement / 100), where BSA is body
surface area.
4. Radioembolization
a. The selected catheter is advanced into the treatment vessel of choice as determined by pretreatment
angiography and either the TheraSphere or SIRSpheres administration device is utilized for microsphere
infusion.
b. A treatment paradigm that parallels transarterial chemoembolization is recommended, that is, lobar or
sub/segmental infusions.
(1) If a treating physician insists on treatment to the entire liver at once, then a “bilobar lobar” infusion is
recommended. This involves placement of the catheter in the one followed by the other hepatic artery
where infusion is performed.
1. Outpatient management
a. Patients are discharged home following the appropriate management of femoral arteriotomy, 2 hours with
closure devices and 6 hours with manual compression.
b. Patients may receive 7 to 10 days of a fluoroquinolone if the entire right lobe is to be treated and the
gallbladder is present.
c. All patients are placed on a proton pump inhibitor for 7 to 10 days following treatment.
2. Follow-up
a. Clinical assessment: Patients are assessed for treatment-related side effects (e.g., fatigue, nausea, fevers,
abdominal pain) and potential complications (e.g., radiation cholecystitis, GI ulcer).
b. Laboratory: Tumor markers (AFP, CEA, CA-19-9, chromogranin A, CA-125), complete blood count, liver
function tests, and general chemistries are obtained 4 to 6 weeks postprocedure.
c. Imaging: Cross-sectional imaging (triphasic CT, dynamic gadoliniumenhanced MRI, perfusion imaging) and
functional imaging positron emission
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tomography (PET) when appropriate are obtained at that time to assess the results of therapy. The opposite
lobe is usually treated shortly following the assessment of response. Completion evaluation and assessment of
response (CT/PET/MR/tumor markers) are usually complete once both lobes have been treated and 30 to 60
days have elapsed from the last treatment.
Results
1. HCC
a. Median survival comparable to chemoembolization for intermediate stage patients (17 months; range 16.9
to 18 months) and to sorafenib for advanced stage patients (11 months; range 10 to 13.8 months) (2,3).
b. Quality of life, especially social and functional well-being, is higher with radioembolization when
compared to chemoembolization (4).
c. Treatment in patients with PVT is safe, with median survival 8 to 14 months (5). Outcomes optimized
when tumor radiation dose exceeds 205 Gy (6).
2. Metastatic colorectal disease to the liver
a. Median survival in the salvage setting (after failing at minimum second line systemic therapies)
approximately 10.5 months (7,8)
b. Novel concepts in combination with chemotherapy have been studied (9); trials combining
radioembolization with first- or second-line chemotherapy are underway.
3. Cholangiocarcinoma
a. Median survival approximately 11 months, similar to systemic therapy (gemcitabine and cisplatin) (10).
Peripheral (mass-forming) cholangiocarcinoma may respond, whereas infiltrative does not.
Complications
1. Post-radioembolization syndrome
a. Fatigue
b. Abdominal pain
c. Nausea
d. Anorexia
e. Fevers
2. Idiosyncratic reaction: During the immediate postprocedural time following radioembolization, patients
may experience a rare and unusual reaction, nearly identical to that obtained in patients receiving
urokinase, with clinical symptoms of rigors and alterations in hemodynamics.
3. Complications
a. Abscess
b. Biloma
c. Gastritis/ulceration
d. Radiation cholecystitis
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1. Post-radioembolization syndrome: The typical side effects of radioembolization are managed
conservatively. If required, over-the-counter analgesics can be utilized.
2. Idiosyncratic reaction
a. Management is supportive, including fluids if hypotensive, as well as diphenhydramine and meperidine.
b. This reaction is short-lived and usually lasts less than 1 hour.
3. Complications
a. Abscess: Pyogenic liver abscesses require antibiotic therapy directed at the causative organism(s) and,
in most cases, drainage. For a small abscess, antibiotic therapy without drainage may suffice.
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b. Biloma: Percutaneous treatments include biloma drainage, percutaneous transhepatic biliary drainage, or
biliary leak site embolization/sclerosis.
c. Gastritis/ulceration: Treatment options include acid suppression. A nonhealing ulcer may ultimately
require surgery if symptoms are severe/persistent.
d. Radiation cholecystitis: The majority of patients whose cystic artery is directly exposed to radioactive
particles recover asymptomatically or with minimal supportive care despite abnormal radiographic findings.
Antibiotics and/or cholecystectomy may be warranted in certain instances.
References
1. Lewandowski RJ, Sato KT, Atassi B, et al. Radioembolization with 90Y microspheres: angiographic and
technical considerations. Cardiovasc Intervent Radiol . 2007;30(4):571-592.
2. Salem R, Lewandowski RJ, Mulcahy MF, et al. Radioembolization for hepatocellular carcinoma using
Yttrium-90 microspheres: a comprehensive report of long-term outcomes. Gastroenterology. 2010;138(1):52-
64.
3. Mazzaferro V, Sposito C, Bhoori S, et al. Yttrium-90 radioembolization for intermediateadvanced

hepatocellular carcinoma: a phase 2 study. Hepatology. 2013;57(5):1826-1837.
4. Salem R, Gilbertsen M, Butt Z, et al. Increased quality of life among hepatocellular carcinoma patients
treated with radioembolization, compared with chemoembolization. Clin Gastroenterol Hepatol .
2013;11(10):1358.e1-1365.e1
5. Kulik LM, Carr BI, Mulcahy MF, et al. Safety and efficacy of 90Y radiotherapy for hepatocellular carcinoma
with and without portal vein thrombosis. Hepatology. 2008;47(1):71-81.
6. Garin E, Lenoir L, Edeline J, et al. Boosted selective internal radiation therapy with 90Y-loaded glass
microspheres (B-SIRT) for hepatocellular carcinoma patients: a new personalized promising concept. Eur J
Nucl Med Mol Imaging. 2013;40(7):1057-1068.
7. Kennedy AS, Coldwell D, Nutting C, et al. Resin 90Y-microsphere brachytherapy for unresectable
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colorectal liver metastases: modern USA experience. Int J Radiat Oncol Biol Phys. 2006;65(2):412-425.
8. Lewandowski RJ, Memon K, Mulcahy MF, et al. Twelve-year experience of radioembolization for colorectal
hepatic metastases in 214 patients: survival by era and chemotherapy. Eur J Nucl Med Mol Imaging.
2014;41(10):1861-1869.
9. Hendlisz A, Van den Eynde M, Peeters M, et al. Phase III trial comparing protracted intravenous
fluorouracil infusion alone or with yttrium-90 resin microspheres radioembolization for liver-limited metastatic
colorectal cancer refractory to standard chemotherapy. J Clin Oncol . 2010;28(23):3687-3694.
10. Mouli S, Memon K, Baker T, et al. Yttrium-90 radioembolization for intrahepatic cholangiocarcinoma:
safety, response, and survival analysis. J Vasc Interv Radiol . 2013;24(8):1227-1234.
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25
Uterine Fibroid Embolization
James B. Spies
Uterine fibroid embolization (UFE) was first reported in 1995 and rapidly became accepted into practice around
the world. There has been extensive study of the outcomes from embolization of fibroids, including several
randomized trials comparing UFE to surgery, with two reporting long-term outcomes (1,2). Recently, an American
College of Obstetricians and Gynecologist Practice Bulletin on Alternatives to Hysterectomy in the Management
of Leiomyomas (3) indicated that there were good and consistent data (Level A) to state “based on long- and
short-term outcomes, uterine artery embolization is a safe and effective option
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for appropriately selected women who wish to retain their uteri.” This finding was confirmed in a recent
systematic review by the Cochrane Collaborative (4).
Indications
1. Heavy menstrual bleeding
a. Fibroids typically cause heavy menstrual bleeding without interperiod bleeding. The exception is
submucosal fibroids, which may, in addition, cause interperiod bleeding and metrorrhagia. In nearly all
cases, fibroids must be deep within the uterus distorting the endometrial cavity to cause heavy bleeding. If
only serosal fibroids or small intramural fibroids are present and there is heavy menstrual bleeding, consider
other possible causes prior to proceeding with embolization.
2. Pelvic pressure
a. The most common bulk-related symptoms are pressure, heaviness, or bloating. These symptoms
typically are worse around the time of the menstrual period. They respond well to UFE. It is important to
remember that some perimenstrual bloating is normal, which will likely persist despite a successful UFE.
3. Pelvic pain
a. Fibroids usually cause menstrual cramps or low-grade aching pain. Less frequently, they may cause
shooting or severe pain. When severe pain is the predominant symptom, it is important to consider other
causes of female pelvic pain such as endometriosis. Also, patients often will experience pain or tenderness
over one particular fibroid. If the fibroids are mostly on one side of the pelvis and the patient has pain on the
other, consider other causes.
4. Urinary urgency, frequency, incontinence, retention, and hydronephrosis
a. Uterine fibroids commonly compress the urinary bladder causing urgency and frequency, which respond
well to embolization. Urinary incontinence is less common, and in women who have had prior vaginal
deliveries, the incontinence may be of multifactorial origin. Hydronephrosis may be caused by a
substantially enlarged fibroid uterus and usually resolves after UFE. However, a followup renal sonogram is
needed 3 to 6 months after treatment to ensure resolution.
Contraindications
Absolute
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1. Pregnancy
2. Suspected leiomyosarcoma or endometrial, cervical, or ovarian malignancy
a. Preoperative embolization is occasionally requested prior to surgical resection of a suspected malignancy
and this is an acceptable use of embolization, but UFE should never be considered as a sole therapy for a
suspected leiomyosarcoma.
Relative
Many of these relative contraindications are circumstances that can be managed with additional care and
should not exclude the use of embolization.
1. Coagulopathy or requirement for continuous anticoagulation
a. Similar and greater risks of bleeding are present with surgery. The risks can be reduced or eliminated
with the use of an arterial closure device at the puncture site.
a. Contrast use should be limited and the patient should be well-hydrated prior to the procedure.
3. Prior severe allergic reaction to iodinated contrast material
a. Corticosteroid premedication can ameliorate this risk. It is important that appropriate drugs and equipment
be immediately available and that there be secure intravenous (IV) access. Anesthesia support may be
helpful.
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4. Desire for pregnancy within 2 years.
a. Although patients can become pregnant and carry pregnancies to term, the relative likelihood of that
occurring after UFE may be less than with myomectomy, at least within the first 2 years after treatment (5).
However, those with prior fibroid or uterine surgery and those who are poor surgical risk or who have
declined surgery can be considered for embolization, with a clear understanding that reproductive outcomes
are uncertain.
1. Preprocedure history, physical examination, and consultation with an interventional radiologist
a. Gynecologic examination by a gynecologist within 1 year
b. Assessment of uterine size (by weeks of pregnancy) helpful during abdominal examination
2. Imaging evaluation
a. Contrast-enhanced magnetic resonance imaging (MRI) is the preferred imaging assessment because it allows
accurate assessment of fibroid number, size, and location as well as detection of adenomyosis.
b. Transabdominal and transvaginal ultrasound examination of good quality may be a suitable substitute for an
MRI in a resource-limited practice environment.
3. Laboratory evaluation
a. Current Pap smear, which should be normal
b. Endometrial biopsy when menstrual bleeding is markedly prolonged or when there is intermittent bleeding
between cycles. A useful rule of thumb is biopsy for menstrual periods that are routinely longer than 10 days or
when there is bleeding more frequent than every 21 days.
c. Complete blood count, serum electrolytes (including serum creatinine), and a urine or serum pregnancy test in
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those at risk of pregnancy before the procedure. Given the importance of excluding pregnancy, we obtain a urine
pregnancy test in all premenopausal women.
d. Coagulation panel only in patients suspected of having a coagulopathy
a. Patient should have nothing by mouth except normal medications with a sip of water for at least 6 hours prior
to the procedure.
b. Most interventionalists place a Foley catheter in the bladder prior to the procedure. This is for patient comfort
and to keep bladder empty, which will reduce fluoroscopic dose.
c. The patient should have the anticipated postprocedure recovery explained to them and they should be
instructed on the use of the patient-controlled analgesia (PCA) pump for IV narcotics.
d. Many interventionalists give a single dose of prophylactic antibiotics such as cefazolin 1 g IV, although there is
no evidence that this has any impact on infection rates postprocedure.
e. The medications needed for postprocedure management should be prepared and ready to administer
immediately at the end of the procedure.
f. An IV line should be placed and the patient should be hydrated. One approach is to infuse 500 mL of normal
saline over the 2 hours just before and during the procedure, with the rate reduced to 125 mL per hour
thereafter.
g. Patient is sedated with fentanyl and midazolam at the beginning of the procedure, with continuous monitoring
by a nurse trained in sedation.
Procedure
1. Uterine artery catheterization
a. Either unilateral or bilateral femoral puncture can be used, with a 4 Fr. or 5 Fr. sheath typically used at
each puncture site.
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b. The advantage of a bilateral puncture is that the angiographic imaging of the uterine arteries can be
done simultaneously and, if an assistant is available, the embolization of both uterine arteries can also be
done simultaneously, both of which may result in a reduction in overall radiation dose.
c. A Cobra, Rösch Inferior Mesenteric (RIM), or other curved 4 Fr. or 5 Fr. catheter is passed from the right
femoral sheath across the bifurcation of the aorta into the left hypogastric artery.
d. Either that same 4 Fr. or 5 Fr. catheter, or, more commonly, a 0.027-in. diameter microcatheter, is
advanced into the uterine artery using a digital road map for guidance. The uterine artery usually arises as
either the first branch off the inferior gluteal artery or as part of a genitourinary trunk at the level of the
bifurcation of the superior gluteal and inferior gluteal arteries. Oblique positioning of the angiographic unit is
essential for best visualization of the vessel because it is important to have good visualization of the uterine
artery origin to allow easy access. Often the left anterior oblique is used for both uterine arteries. If one
oblique does not show the origin of the vessel well, then the opposite oblique should be used.
e. A popular alternative approach is to use the Roberts Catheter (Cook Inc, Bloomington, IN) for selection of
the uterine artery. This long-armed recurved catheter is retracted at the groin entry site, which advances the
tip into the uterine artery. It may also be used with a microcatheter.
f. The uterine artery in patients with fibroids is typically tortuous, with a general U-shaped configuration. It
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descends to the level of the cardinal ligament, turns medially along that ligament, and courses to the uterine
margin where it ascends along the side of the uterus. The microcatheter (or catheter) is advanced well into
the uterine artery. Ideally, it would be advanced beyond any identifiable branches in the transverse segment
of the vessel to avoid misembolization into branches to adjacent structures (Fig. 25.1). However, due to
severe tortuosity, advancing the catheter so far into the vessel may cause spasm in many patients. Thus, a
balance between the ideal position and the avoidance of spasm is needed, and more proximal placement
may be preferred. Spasm should be avoided because it may lead to a false end point, with recanalization
shortly after catheter removal.
g. If a bilateral approach is to be used, the above process should be repeated from the opposite side into
the right uterine artery prior to filming and embolization to allow simultaneous treatment.
h. If a unilateral approach is used, uterine arteriogram and embolization are done on the left, and then a
Waltman loop is used to move the catheter into the right hypogastric artery. Alternatively, a RIM catheter
can just be pulled back until its end engages the origin of the right hypogastric artery and a microcatheter
used to cannulate the uterine artery with the same technique used on the left.
2. Embolic choice and technique
a. There are several embolic materials currently available for use in the United States and Europe. The two
best studied are particle polyvinyl alcohol (PVA) (Contour, Boston Scientific, Natick, MA; Polyvinyl Alcohol
Particles, Cook Inc, Bloomington, IN; others) and Embosphere Microspheres (Merit Medical, South Jordan,
UT) (6,7). Spherical PVA (Contour SE, Boston Scientific, Natick, MA) has been shown to be inferior in
fibroid infarction and should not be used for fibroid embolization (7,8). Acrylamide PVA hydrogel spheres
(Bead Block, Terumo, Somerset, NJ) have also been cleared for use and have been compared to
Embosphere Microspheres (9). Polyzene F-coated hydrogel spheres (Embozene Microspheres, CeloNova
Biosciences Inc, San Antonio, TX) is a newer material widely used in Europe and recently cleared by the
U.S. Food and Drug Administration (FDA) for use for fibroid embolization in the United States.
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FIGURE 25.1 • Catheter placement prior to embolization. A: Digital road map image of the uterine artery
with a microcatheter in the proximal transverse segment of the uterine artery. There is a small side branch
just beyond the tip of the microcatheter (arrow). B: To avoid the potential for embolization into the branch,
the catheter tip is advanced beyond it over a microwire. C: Final location of microcatheter prior to
embolization.
b. The embolic material is injected in small aliquots using the flow in the uterine vessels to carry the embolic
material to the fibroid arterial supply. Fibroid branches are recognized as large, generally curvilinear
branches that surround each fibroid before penetrating it. These are the targets for occlusion. The goal is
not to occlude the entire uterine artery but to leave it with slow flow or near stasis, depending on the type of
embolic material used. Supplemental gelatin sponge plugs or coils should not be used because these may
completely occlude the uterine arteries permanently. This will prevent repeat embolization if the patient
develops new fibroids.
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3. Ovarian supply and embolization
a. There is occasionally additional supply to the uterus and fibroids from the ovarian arteries. Although only
present in about 5% of patients, this can impact outcome. Routine aortography after embolization has a low
yield, but in cases where there is a disproportionately small uterine artery, when there is clearly
nonperfused tissue seen on uterine arteriography or in repeat embolization procedures, aortography should
be done to determine if there is ovarian supply.
b. Ovarian embolization is not well studied, and although there is some evidence that ovarian artery
embolization does not significantly increase the risk of ovarian injury (10), consulting with the patient about
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possible ovarian injury may be appropriate prior to proceeding.
c. Selective catheterization of the ovarian artery may be best accomplished with a Mikaelsson catheter
(AngioDynamics, Queensbury, NY). A microcatheter should be used and advanced into the vessel about
one-third the distance to the ovary to ensure no reflux occurs into the aorta.
d. Ovarian embolization is performed with particulate or spherical embolic material until the fibroid branches
are occluded. Flow is generally very sluggish because of severe spasm typically seen with ovarian
catheterization.
1. General care of the patient
a. Most interventionalists observe the patient in hospital overnight, although it is increasingly common to
discharge same day. The postprocedure treatment is usually the same for overnight or same-day patients.
b. Diet advanced slowly as tolerated. Nausea can be an issue if advanced too quickly.
c. The Foley catheter can be removed after 6 hours.
d. IV hydration should be continued until oral liquids are well tolerated.
2. Pain management
a. There is usually moderate pain for 2 to 6 hours after embolization due to transient myometrial ischemia. The
severity of pain is likely dependent on the degree of occlusion of the uterine arteries—overembolization should
be avoided.
b. In hospital, the mainstay of pain management is IV narcotics, usually administered via an IV PCA pump, and
nonsteroidal anti-inflammatory agents, initially IV ketorolac. Ketorolac is given 30 mg IV every 6 hours regardless
of pain and the PCA narcotics are used to supplement. In the first few hours, the typical PCA dose may be
inadequate, regardless of the medication used. Supplemental doses may be needed. This type of added dose
will not often be necessary but will be the difference between a tolerable procedure and one that is not. For
many years, IV acetaminophen has been a key part of pain control in Europe, at a dose of 1 g every 6 hours.
This preparation has recently been approved in the United States and is a useful adjunct to current pain
management regimens.
c. At the time of discharge, the patient is transitioned to oral medications. Typically, an oral nonsteroidal anti-
inflammatory such as ibuprofen or naproxen is used at regular interval dosing for 4 days or 5 days. This is
supplemented by oral oxycodone/acetaminophen or hydrocodone/acetaminophen for intermittent use as needed
for more severe pain. The peak pain after discharge is usually on postembolization days 2 and 3.
d. Most patients will experience intermittent cramping, fatigue, and malaise, with one-third having a low-grade
fever for several days. Usually, 7- to 10-day recovery is required to resume full activity.
3. Nausea
a. The second most common symptom needing medical management is nausea. This may be prevented to a
large degree by prophylactic doses of ondansetron (4 mg IV at the time of the procedure with an additional 4 mg
IV 6 hours
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later). Additional doses can be given, along with oral or rectal promethazine or other antiemetics.
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Results
1. Short-term outcomes
a. Both menorrhagia and bulk-related symptoms (pain, pressure, and urinary symptoms) are improved in
80% to 95% of patients, depending on the study reviewed.
b. Reintervention is needed in approximately 5% to 10% of patients within the first year due to lack of
symptom improvement.
2. Long-term outcomes
a. UFE has been demonstrated to be effective compared to surgery in randomized trials at 5 years after
treatment (11,12).
b. There are insufficient data to determine whether myomectomy or UFE is preferred for women seeking to
become pregnant, although results from one comparative trial suggest that there are better outcomes with
myomectomy in the first 2 years in women who have not had prior fibroid surgery (5).
Complications
1. Fibroid passage
a. Fibroid passage, which occurs in about 5% of cases, is the most common serious complication and
presents as severe menstrual cramping, with or without discharge, tissue passage, or heavy bleeding (13).
It may also have a more chronic presentation, with persisting vaginal discharge, often described as watery
or clear mucous, which may become superinfected. This occurs most commonly 3 weeks to 6 months after
the procedure and most frequently with large intracavitary fibroids or large fibroids with a large submucosal
interface.
b. Diagnosis may be made by vaginal exam if there is either tissue in the vagina or a dilated cervix.
Impending passage may have the same symptoms but with a negative vaginal exam. Pelvic MRI
examination will show tissue descending in the endometrial cavity, pointing to the cervix with occasional
dilation of the internal cervical os. With more advanced passage, the cervix may be dilated with tissue
extending from the endometrial cavity into the vagina.
2. Pulmonary embolus
a. The most common life-threatening complication, with an incidence of about 1 in 400
b. Transient hypercoagulability occurs after UFE (similar but to a lesser extent than surgery).
c. Use of intermittent pneumatic compression devices on the legs may reduce the risk. For high-risk
patients, low-molecular-weight heparin prophylaxis should be considered.
3. Misembolization
a. Due to embolic material occluding the vascular supply to adjacent organs. Injury to other organs (other
than the ovaries) or to the skin occurs very rarely, likely less than 1 in 1,000 patients for experienced
interventionalists.
4. Myometrial injury
a. Myometrial injury is also rare, about 1 in 500. Diagnosis should be suspected when pain is persisting and
not improving after 4 to 5 days postembolization or when pain is severe enough to require readmission.
Contrast-enhanced MRI will show nonenhancing areas of myometrium.
5. Loss of ovarian reserve/ovarian failure
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a. May occur as a result of uterine embolization and is age-dependent. Approximately 5% of women over 45
years old may have temporary or permanent amenorrhea after UFE. At age 40, the likelihood is closer to
1%.
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1. Fibroid passage: This is the most common complication requiring reintervention.
a. Can be managed with observation if uncomplicated, although if infection occurs, oral or IV antibiotics are
given
b. Dilation and curettage/hysteroscopic resection or manual extraction of the fibroid is often necessary. If
the fibroid cannot be extracted, hysterectomy may be required.
2. Misembolization
a. Management is usually conservative, with local wound care for minor skin injuries. Plastic surgery consult
can be considered for more severe injuries that result in skin ulceration.
b. Bladder injuries may require urologic evaluation and occasionally intervention.
3. Myometrial injury
a. Initial management is conservative, with re-institution of IV narcotics while assessing myometrial repair
with serial contrast-enhanced MRI studies
b. If there is severe uterine injury, hysterectomy may be needed.
4. Loss of ovarian reserve/ovarian failure
a. Treatment is conservative, with some women regaining menstrual cycles several months after
embolization.
b. For bothersome menopausal symptoms, the patient's gynecologist should be consulted to consider
managing symptoms with hormone replacement therapy.
References
1. Edwards RD, Moss JG, Lumsden MA, et al. Uterine-artery embolization versus surgery for symptomatic
uterine fibroids. N Engl J Med. 2007;356:360-370.
2. Hehenkamp WJ, Volkers NA, Birnie E, et al. Symptomatic uterine fibroids: treatment with uterine artery
embolization or hysterectomy—results from the randomized clinical Embolisation versus Hysterectomy
(EMMY) Trial. Radiology. 2008;246:823-832.
3. American College of Obstetricians and Gynecologists. ACOG practice bulletin. Alternatives to

hysterectomy in the management of leiomyomas. Obstet Gynecol . 2008;112:387-400.
4. Gupta JK, Sinha A, Lumsden MA, et al. Uterine artery embolization for symptomatic uterine fibroids.
Cochrane Database Syst Rev. 2012;(5):CD005073.
5. Mara M, Maskova J, Fucikova Z, et al. Midterm clinical and first reproductive results of a randomized
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controlled trial comparing uterine fibroid embolization and myomectomy. Cardiovasc Intervent Radiol .
2008;31:73-85.
6. Spies J, Allison S, Sterbis K, et al. Polyvinyl alcohol particles and tris-acryl gelatin microspheres for uterine
artery embolization for leiomyomas: results of a randomized comparative study. J Vasc Interv Radiol .
2004;15:793-800.
7. Spies JB, Allison S, Flick P, et al. Spherical polyvinyl alcohol versus tris-acryl gelatin microspheres for
uterine artery embolization for leiomyomas: results of a limited randomized comparative study. J Vasc Interv
Radiol . 2005;16:1431-1437.
8. Siskin GP, Beck A, Schuster M, et al. Leiomyoma infarction after uterine artery embolization: a prospective
randomized study comparing tris-acryl gelatin microspheres versus polyvinyl alcohol microspheres. J Vasc
Interv Radiol . 2008;19:58-65.
9. Worthington-Kirsch RL, Siskin GP, Hegener P, et al. Comparison of the efficacy of the embolic agents
acrylamido polyvinyl alcohol microspheres and tris-acryl gelatin microspheres for uterine artery embolization
for leiomyomas: a prospective randomized controlled trial. Cardiovasc Intevent Radiol . 2011;34:493-501.
10. Hu N, Kaw D, McCullough M, et al. Menopause and menopausal symptoms after ovarian artery
embolization: a comparison with uterine artery embolization controls. J Vasc Interv Radiol . 2011;22:710-715.
11. van der Kooij SM, Hehenkamp WJ, Volkers NA, et al. Uterine artery embolization vs hysterectomy in the
treatment of symptomatic uterine fibroids: 5-year outcome from the randomized EMMY trial. Am J Obstet
Gynecol . 2010;203:105.e1-105.e13.
12. Moss JG, Cooper KG, Khaund A, et al. Randomised comparison of uterine artery embolisation (UAE) with
surgical treatment in patients with symptomatic uterine fibroids (REST trial): 5-year results. BJOG.
2011;118:936-944.
13. Shlansky-Goldberg RD, Coryell L, Stavropoulos SW, et al. Outcomes following fibroid expulsion after
uterine artery embolization. J Vasc Interv Radiol . 2011;22:1586-1593.
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26
Splenic and Renal Embolization
Sebastian Kos
David M. Liu
Stephen G.F. Ho
Embolotherapy of solid organs in the nontrauma patient can be performed for many indications (tumor,
aneurysm, hypersplenism, and preoperative). Embolization for trauma, visceral aneurysms, and hepatic
malignancies is covered elsewhere in this book. This chapter discusses splenic embolization for hypersplenism
and renal embolization for angiomyolipoma (AML), nonfunctioning kidney/nephrotic syndrome, and prior to
surgery or renal cell carcinoma (RCC).
Indications
1. Splenic artery embolization for hypersplenism and pancytopenia
a. Hematologic disorders (idiopathic thrombocytopenic purpura, thalassemia, hereditary spherocytosis)
b. Cirrhosis with portal hypertension
c. Primary malignancies (lymphoma, leukemia)
d. Congenital disease (e.g., Gaucher disease, atresia of bile ducts)
e. Idiopathic hypersplenism
f. Chemotherapy-associated splenomegaly
2. Renal artery embolization
a. Total embolization
(1) End-stage renal failure with intractable secondary hypertension
(2) End-stage renal failure with intractable protein loss/nephrotic syndrome
(3) End-stage renal failure with hydronephrosis and intractable secondary flankpain (1)
(4) Failing kidney transplants with graft intolerance syndrome
(5) Inoperable large RCC causing paraneoplastic syndromes
(6) Preparation for surgery in patients refusing blood transfusions
(7) Intractable neoplasm-induced hematuria in the nonsurgical patient
b. Partial embolization
(1) Small RCC with hematuria or paraneoplastic syndromes in the inoperable patient
(2) Large RCC with hematuria or paraneoplastic syndromes in the inoperable patient with a single kidney
(3) AML (2)
(4) Preparation for radiofrequency or cryoablation of RCC (3)
(5) Preparation for surgery in patients refusing blood transfusions
Contraindications
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Absolute
There are no absolute contraindications for renal and splenic artery embolization. Because these
procedures usually involve other clinical disciplines, namely oncologists, nephrologists, urologists,
hematologists, etc., a multidisciplinary consensus should be obtained prior to these treatments.
Relative
a. Severe anaphylactoid reaction to iodinated contrast media (alternatives: gadolinium, CO2)
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2. Pregnancy
3. Acute or chronic infection of spleen/kidney
4. Acute hyperthyroidism
5. Thyroid carcinoma and planned radioiodine therapy
6. For renal artery embolization: solitary kidney
1. Preprocedural assessment
a. Informed consent must be obtained prior to the procedure.
b. Computed tomographic angiography (CTA) or magnetic resonance angiography (MRA) should be obtained
prior to the procedure to depict vascular anatomy, extent, and location of the disease (e.g., tumor), size of
targeted organs (spleen).
c. Recent laboratory data including partial thromboplastin time (PTT), international normalized ratio (INR),
creatinine, glomerular filtration rate (GFR), complete blood count (CBC), platelet count, and C-reactive protein
(CRP)
a. Patient preparation and preoperative management vary widely between centers and even operators. For
splenic artery embolization, in 1979, Spigos et al. (4) described a regimen, which is still accepted by some
authors (5). This includes antibiotic prophylaxis (e.g., cefazolin 1 g; 12 hours before and 1 to 2 weeks after the
procedure), additional local antibiotics (e.g., gentamicin) applied with the embolic solution. Note: Other regimens
including broadspectrum coverage (e.g., Zosyn, 3.375 mg intravenously [IV] every 12 hours × 3 days
posttreatment) and penicillin V 5 million units, coadministered with the embolic agent, have been applied but no
evidence exists for “best practice” recommendation. Strict sterility (broad surgical scrub and/or povidoneiodine
bath) is emphasized to minimize concerns relating to postembolic infection.
b. For splenic embolization, a (14-valent) pneumococcal vaccine should be given days before the procedure.
There is controversy on this subject.
c. Patient on nil per os (NPO) for at least 6 hours prior to the procedure
d. Establish IV access.
e. Supportive therapy (e.g., volume, oxygen)
f. Establish patient monitoring (electrocardiogram [ECG], respiratory rate [RR], heart rate [HR], pulse oximetry).
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g. Administer conscious sedation. Note: For total renal embolization, general anesthesia may be required
(especially when utilizing liquid embolics).
h. Administer IV antiemetics (e.g., diphenhydramine 50 mg, dexamethasone 10 mg, ondansetron 2 to 4 mg).
i. Standard sterile preparation and draping should be applied.
j. For the majority of cases, a transfemoral access should be chosen. In rare cases (e.g., pelvic artery occlusion),
upper extremity access may be used (6).
Procedure
1. Splenic artery embolization
a. Following establishment of arterial access, selective catheterization of the celiac trunk and splenic artery
is performed. For this, 5 Fr. selective catheters (e.g., Cobra, Sidewinder) are commonly used in combination
with a hydrophilic guidewire.
b. Arteriogram is performed and related to individual anatomy (anatomic variations must be considered); the
catheter is advanced such that nontarget vessels can be safely avoided (for splenic: embolization of dorsal
pancreatic, pancreatica magna and short gastric branches, or reflux into aorta; for renal : adrenal, spinal,
and lumbar collaterals). However, the selective catheter
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should not be advanced into vessels that are less than twice the catheter's diameter, to avoid stasis and
occlusion. Size of targeted vessels and splenic artery tortuosity often make usage of a coaxial system
mandatory. Coaxial microcatheters safely allow engagement of splenic arteries even distal to the hilum.
Ensure that the embolic agent and microcatheter are compatible. This includes standard as well as
controlled release coil platforms.
Off-label intra-arterial injection of lidocaine hydrochloride (50 to 100 mg) may be performed prior to
embolization (based on anecdotal evidence) to decrease patient discomfort and abdominal pain during and
after the procedure. (Slow injection and ECG monitoring are mandatory as cardiac arrhythmia may be
induced.)
c. The embolic material to be used can be chosen according to operator's experience and preference.
Different embolic agents have been described and applied for splenic artery embolization in the literature
(e.g., autologous clot, Gelfoam pledgets [Pfizer, New York, NY], polyvinyl alcohol particles, microspheres,
microcoils, ethanol, glue [isobutyl-2-cyanoacrylate]). However, no differences in complication rate, efficacy
or outcome has been demonstrated. More important than the actual choice of the embolic agent is the distal
(hilar/posthilar) deployment of the embolic agent, as central embolization may not result in sufficient
infarction due to collateral flow from pancreatic and gastric branches. (It is important to note that Gelfoam
and nonspherical particles may clog within microcatheters, resulting in uncontrolled embolization or
requirement to reselect the vessel and replace the catheter.)
d. More relevant for the procedural outcome than the actual embolic agent is the applied embolization
concept (5).
(1) Complete splenic embolization was initially described in 1973, but severe complications may occur and
this should not be performed (7).
(2) Partial splenic embolization was shown to have best results and a significantly lower complication rate.
Any embolization for hypersplenism should be performed as a partial embolization. Two major techniques
(selective vs. unselective) have been described.
(a) Using the selective technique, splenic artery branches are selectively engaged and embolized to
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complete stasis. Intermittent angiographic runs (in parenchymal phase) document the actual extent of
infarction.
(b) For the nonselective approach, the catheter is positioned in the main splenic artery distal to the
pancreatic branches and embolization is performed. As an objective end point, 50% to 80% decrease in
parenchymal blush during digital subtraction angiography (DSA) arteriography may be used.
(3) Partial sequential embolization is a concept that should be applied for embolic treatment of massive
splenomegaly, as single-step embolization may be more prone to complications (e.g., postembolic
syndrome). In these cases, some authors recommend performing stepwise partial embolization (two to three
treatments).
(4) Currently, no evidence is available regarding the optimal ratio of splenic tissue to be infarcted. Practice
suggests that embolization of 50% to 80% of splenic tissue results in better outcome than embolization of
<50% tissue and fewer complications than embolization of >80% splenic tissue.
a. Selective injection of the renal arteries is performed. For most cases, a coaxial approach using a
combination of 5 to 6 Fr. standard sheath or guide sheath of 5 to 6 Fr. internal diameter (ID) (e.g., renal
double curve), a 4 to 5 Fr. diagnostic catheter (e.g., Sos-Omni, Cobra, Vertebral, Angled taper), and a
hydrophilic guidewire should be used. Additional usage of microcatheters may be mandatory for
superselective embolization of small renal tumors.
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b. Selective angiography should be performed with gantry angulation calculated from CT or MR to obtain
optimal depiction of the renal vasculature.
c. Note: Especially in patients with RCC, if the angiogram reveals arteriovenous fistulas, these should be
embolized first, prior to any total or partial renal embolization to avoid paradoxical venous embolization and
its complications (e.g., renal vein thrombosis, pulmonary embolism, stroke).
d. Two main technical concepts have been described:
(1) Total renal embolization
(a) For total devascularization of the kidney, many therapeutic agents have been proposed and applied
(e.g., ethanol, glue, small particles, coils, AMPLATZER vascular plug [AGA Medical Corp, Plymouth, MN]).
Lacking significant evidence for a specific embolic agent to be superior, many institutions use ethanol due
to its cost-effectiveness. For ethanol embolization,
i. Proximal balloon occlusions should be performed to minimize nontargeted delivery and to maximize dwell
time.
ii. General anesthesia is essential for the management of potential hemodynamic instability resulting from
systemic release of intraarterial ethanol as well as for the management of profound pain.
iii. Following proximal occlusion, a single-contrast injection may determine the individual filling volume of the
renal arterial tree.
iv. Following deflation of the balloon, washout of the contrast media, and reinflation of the balloon, the
assessed volume of medical strength ethanol can be safely injected (<20 mL on average).
v. The balloon should remain inflated for several minutes and prior to deflation, remaining ethanol should be
aspirated through the balloon catheter.
vi. When using a technique without an occlusion balloon, 4 to 10 mL of ethanol should be slowly injected
over several minutes.
vii. Angiography should demonstrate stasis as an end point of the procedure.
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(2) Partial renal embolization
(a) Partial embolization is mostly performed for the treatment for renal tumors (RCC, AML) prior to or instead
(e.g., inoperable patient) of any surgical or locoregional therapy (e.g., radiofrequency ablation [RFA],
cryoablation).
(b) Precise depiction of vascular anatomy and tumor-feeding vessels is crucial for selective embolotherapy.
(c) For small tumors, coaxial usage of microcatheters is usually necessary to allow superselective
engagement of feeding branches, thereby sparing healthy tissue from infarction.
(d) For superselective embolization of feeding branches mostly small particles, microcoils, and glue are
used. Small, calibrated microspheres <300-μm diameter are preferred in order to assure adequate terminal
embolization.
a. IV antibiotics (cefazolin 500 mg to 1 g every 8 hours; adapted to renal function)
b. Analgesic therapy (perchlorpromazine and acetaminophen). In most cases, a patient-controlled analgesia
(PCA) pump is required.
c. Antiemetic therapy (ondansetron and dexamethasone)
d. Prior to discharge, or after 1 month, CT or MRI should be performed to assess the actual amount of infarcted
tissue.
e. The length of hospital stay depends on the underlying disease, the degree of postembolization syndrome, and
the presence of complications. In our experience, most patients can be discharged 3 to 6 days after the
procedure.
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f. Provide specific instructions to minimize the chance, in the acute and subacute phases (3 to 6 months), of
potential splenic rupture.
g. Follow-up hematologic assessment at 2 and 4 weeks
a. Severe pain may result from total renal embolization; therefore, general anesthesia and anticipated multiday
admission for management of postembolization syndrome are warranted.
b. For further postprocedural care, see recommendations for splenic embolization.
Results
1. Splenic artery embolization—the described data on clinical benefit from splenic artery embolization are
based on limited clinical trials with relatively low numbers of patients.
a. Following splenic artery embolization, increase in platelets is noted within 2 weeks of procedure in up to
90% of patients. Transient hyperthrombocythemia may occur, and normal platelet counts may even be seen
years after the procedure.
b. Lower success rates of up to 70% were noted for 35 patients with portal hypertension due to biliary
atresia, extrahepatic portal obstruction, and idiopathic cirrhosis (1,8).
c. For partial splenic embolization, Pålsson et al. (9) presented long-term results in 26 patients. In these
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patients with portal hypertension, frequency of bleeding episodes from esophageal varices was significantly
reduced and hemoglobin, leukocytes, and platelets increased (9). However, it has to be emphasized that
the data on the effect of splenic artery embolization on variceal bleeding risk are controversial.
d. In another study on partial splenic embolization, 1 of 11 complete responders and 5 of 9 partial
responders relapsed after a median period of 34 months. Repeat embolization was performed, resulting in
complete response in one patient and partial response in four patients (10).
e. Compared with surgical total splenectomy and the related risk of overwhelming post-splenectomy
infection (OPSI), even current surgical literature advocates partial splenic embolization as a safe and
efficient procedure (11).
f. No significant difference in outcome has been shown when comparing embolic agent (coils vs. gelatin
particles).
a. There is no evidence that renal embolization has a therapeutic benefit for RCC (12). However, there is
recent evidence that preoperative selective embolization may facilitate laparoscopic tumor surgery for T1
RCC (13).
b. In patients with renal pathologies (e.g., arteriovenous malformation, AML, recurrent bleed) and high
operative risk for surgical nephrectomy, clinical success with respect to management of acute bleeding
(defined as resolution of presenting symptoms without need for further interventions) is comparable
between transarterial embolization and complete nephrectomy.
c. In end-stage renal disease, secondary hypertension and nephrotic syndrome may be successfully treated
by bilateral total renal embolization (90% to 100%) (14).
d. In patients with graft intolerance, total graft embolization may be clinically successful in 50% to 90% of
patients (15,16).
e. In 64 patients with polycystic kidney disease, renal embolization resulted in decreased kidney size and
improved quality of life (1).
f. At long-term follow-up on 34 patients having undergone ethanol embolization for AML, combined clinical
and radiologic success rate was 85% (17). Other studies showed that AML embolization is efficient, safe,
and renal function may be preserved (18). With a median follow-up duration of 28 months after
embolization, mean AML volume reduction was high (>70%).
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Complications
a. Local arterial puncture site complications
b. Pain, nausea, reactive pleural effusion, atelectasis, and postembolization fever are considered side
effects of therapy rather than complications.
c. Splenic abscess (<10%) on the basis of infarcted tissue and backflow of digestive bacteria through the
flow-reversed splenic vein
d. The risk of other potential major complications (e.g., splenic perforation, necrosis of gastric wall,
pancreatitis) can be minimized by meticulous technique and selective embolization.
a. Local complications at the arterial puncture site
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b. As for splenic embolization, the risk of major complications, particularly nontarget embolization (e.g.,
aortic reflux, adrenal infarction, colonic and peripheral embolization), can be minimized by meticulous
technique and selective embolization.
c. Postembolization syndrome is commonly seen as a side effect, as described earlier.
1. Pneumonia and pleural effusion: antibiotic therapy and pleural drainage
2. Splenic/renal abscess: antibiotic therapy, percutaneous drainage, splenectomy if refractory to treatment
3. For postembolization syndrome: symptomatic treatment with hydration and antiemetic and analgesic
drugs
References
1. Ubara Y, Tagami T, Sawa N, et al. Renal contraction therapy for enlarged polycystic kidneys by
transcatheter arterial embolization in hemodialysis patients. Am J Kidney Dis. 2002;39(3):571-579.
2. Kehagias D, Mourikis D, Kousaris M, et al. Management of renal angiomyolipoma by selective arterial

embolization. Urol Int. 1998;60(2):113-117.
3. Tacke J, Mahnken A, Bücker A, et al. Nephron-sparing percutaneous ablation of a 5 cm renal cell

carcinoma by superselective embolization and percutaneous RF-ablation. Rofo. 2001;173(11):980-983.
4. Spigos DG, Jonasson O, Mozes M, et al. Partial splenic embolization in the treatment of hypersplenism.
AJR Am J Roentgenol . 1979;132(5):777-782.
5. Madoff DC, Denys A, Wallace MJ, et al. Splenic arterial interventions: anatomy, indications, technical
considerations, and potential complications. Radiographics. 2005;25(suppl 1):S191-S211.
6. Naritaka Y, Shiozawa S, Shimakawa T, et al. Transradial approach for partial splenic embolization in
patients with hypersplenism. Hepatogastroenterology. 2007;54(78):1850-1853.
7. Maddison FE. Embolic therapy of hypersplenism [abstract]. Invest Radiol . 1973;8:280-281.
8. Nio M, Hayashi Y, Sano N, et al. Long-term efficacy of partial splenic embolization in children. J Pediatr
Surg. 2003;38(12):1760-1762.
9. Pålsson B, Hallén M, Forsberg AM, et al. Partial splenic embolization: long-term outcome. Langenbecks
Arch Surg. 2003;387(11-12):421-426.
10. Kimura F, Itoh H, Ambiru S, et al. Long-term results of initial and repeated partial splenic embolization for
the treatment of chronic idiopathic thrombocytopenic purpura. AJR Am J Roentgenol . 2002;179(5):1323-
1326.
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11. Amin MA, el-Gendy MM, Dawoud IE, et al. Partial splenic embolization versus splenectomy for the
management of hypersplenism in cirrhotic patients. World J Surg. 2009;33(8):1702-1710.
12. May M, Brookman-Amissah S, Pflanz S, et al. Pre-operative renal arterial embolisation does not provide
survival benefit in patients with radical nephrectomy for renal cell carcinoma. Br J Radiol . 2009;82(981):724-
731.
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13. Simone G, Papalia R, Guaglianone S, et al. Preoperative superselective transarterial embolization in

laparoscopic partial nephrectomy: technique, oncologic, and functional outcomes. J Endourol .
2009;23(9):1473-1478.
14. Golwyn DH Jr, Routh WD, Chen MY, et al. Percutaneous transcatheter renal ablation with absolute
ethanol for uncontrolled hypertension or nephrotic syndrome: results in 11 patients with end-stage renal
disease. J Vasc Interv Radiol . 1997;8(4):527-533.
15. Delgado P, Diaz F, Gonzalez A, et al. Intolerance syndrome in failed renal allografts: incidence and
efficacy of percutaneous embolization. Am J Kidney Dis. 2005;46(2): 339-344.
16. Atar E, Belenky A, Neuman-Levin M, et al. Nonfunctioning renal allograft embolization as an alternative to
graft nephrectomy: report on seven years' experience. Cardiovasc Intervent Radiol . 2003;26(1):37-39.
17. Chick CM, Tan BS, Cheng C, et al. Long-term follow-up of the treatment of renal angiomyolipomas after
selective arterial embolization with alcohol. BJU Int. 2010;105(3): 390-394.
18. Lee SY, Hsu HH, Chen YC, et al. Embolization of renal angiomyolipomas: short-term and long-term
outcomes, complications, and tumor shrinkage. Cardiovasc Intervent Radiol . 2009;32(6):1171-1178.
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27
BPH: Prostatic Artery Embolization
André Moreira de Assis
Airton Mota Moreira
Francisco Cesar Carnevale
Benign prostatic hyperplasia (BPH) is the most common benign neoplasia in males, and moderate or severe
lower urinary tract symptoms (LUTS) will occur in approximately one-half of men in their 80s. Men with BPH can
present with prostatic enlargement, bladder outlet obstruction, or both. LUTS due to BPH, such as urinary
hesitancy, intermittency, urgency, and nocturia, can significantly impact patient quality of life and may be only
partially relieved by medical management. A large number of patients will need some invasive modality of
treatment, including transurethral resection of prostate (TURP), open prostatectomy, and laser enucleation,
procedures associated with significant morbidities (1).
Recently, prostate artery embolization (PAE) has been adopted for the treatment of LUTS due to enlarged BPH.
Previous studies have established PAE as a safe and effective treatment associated with significant prostate
volume reduction, and urodynamic, symptoms and quality of life improvements (2,3,4).
Indications
1. LUTS due to BPH with no improvement or intolerant to medical treatment (5-alpha-reductase inhibitors
and/or selective alpha-blockers)
2. LUTS due to BPH and urinary retention (UR) with indwelling catheter
3. Patients who don't want to face the risk and adverse events of surgical therapies
Contraindications (5)
Absolute
1. Active urinary tract infection (UTI)
2. Bladder atonia
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3. Neurologic bladder dysfunction or other neurologic disorder that is impacting bladder function
4. Large bladder diverticula or stones with surgical indication
5. Urethral stricture
6. Renal failure
Relative
1. Confirmed or suspected malignant neoplasm
2. Detrusor muscle hypocontractility
3. Coagulation disorders
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1. A multidisciplinary team of interventional radiologists, diagnostic radiologists, and urologists is involved in
patient selection and follow-up.
2. The International Prostate Symptom Score (IPSS; evaluated as mild, moderate, and severe) and the
International Index of Erectile Function (IIEF; evaluated as severe, moderate, mild-to-moderate, mild, and no
dysfunction) are used as assessment tools. Patients also answer a quality of life (QOL) questionnaire that
includes the question, “If you were to spend the rest of your life with your urinary condition just the way it is now,
how would you feel about that?”
3. All patients undergo digital rectal examination and prostatic specific antigen (PSA) measurement; transrectal
prostate biopsy is performed if there is suspicion of cancer.
4. A urodynamic study is performed to confirm presence of infravesical obstruction and to evaluate bladder
function. Some patients can still be obstructed on follow-up urodynamic testing, despite their LUTS improvement.
5. Pelvic magnetic resonance imaging (MRI) also plays an important role in the preprocedure evaluation. Total
prostate volume, central gland measurements, presence of BPH nodules, assessment of prostatic lobe
symmetry, median lobe protrusion, and presence of suspicious areas in the peripheral zone can all be reviewed
in detail.
a. Moreover, postcontrast sequences demonstrate prostatic parenchymal enhancement patterns and
atherosclerotic changes in pelvic arteries.
b. Bladder wall thickness and diverticula, polyps, and stones can also be assessed as well as disorders of other
pelvic structures.
c. Endorectal coils are not necessary in most cases.
Procedure
1. Intravenous antibiotic is administrated before PAE, usually ciprofloxacin or a third-generation
cephalosporin, for example, ciprofloxacin 400 mg IV preprocedure and 500 mg orally twice a day for 7 days
after PAE.
2. To provide good orientation to the prostate site and related structures in the pelvis, a Foley catheter is
introduced into the bladder in every patient and the balloon is filled with a 10% to 30% iodinated contrast
medium solution.
3. Procedure is performed under local anesthesia through unilateral femoral approach in the interventional
radiology suite.
4. PAE for BPH can be a technically challenging procedure. Identifying and catheterizing target arterial
branches are among the most technical and timeconsuming steps.
a. Atherosclerotic changes are frequent.
b. Identification of the target arteries can be difficult. Multiple origins of the inferior vesical artery and its
prostatic branches have been described, including
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the anterior trunk of internal iliac artery, obturator, internal pudendal arteries, and others (5).
5. A pelvic digital subtraction angiography (DSA) for assessment of global pelvic arterial anatomy (pigtail
catheter in distal aorta, 20 mL contrast, 10 mL per second, 600 psi) is first performed.
6. After crossing the aortic bifurcation, an internal iliac artery DSA is performed with a 5 Fr. vertebral or
cobra C2 catheter (12 mL, 4 mL per second, 300 psi).
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a. The inferior vesical artery (IVA) origin is better identified on a 30- to 50-degree ipsilateral oblique view.
b. The PROVISO acronym (internal Pudendal, middle Rectal, Obturator, Vesical Inferior and Superior under
Oblique view) is a very useful trick to remember the names of the arteries that should be investigated and
the best projection during arteriogram (Fig. 27.1).
c. In difficult cases, a three-dimensional (3D) angiography performed from the internal iliac artery can be of
help to identify the IVA and its origin, avoiding multiple DSA series and reducing radiation exposure.
7. Due to the small size of target arteries and usual tortuosity in elderly, catheterization of the IVA is
performed using a 2.4 Fr. or smaller (preference in using 2.0 Fr.) microcatheter and a high-torque 0.014-in.
or 0.016-in. guidewire. Vascular spasm can be avoided or treated using vasodilator.
8. After distal catheterization, embolization is performed slowly using a 1-mL syringe with embolic agent
(preferentially 300 to 500 μm microspheres) to total vascular stasis, avoiding embolic material reflux to
undesired branches (Fig. 27.2).
FIGURE 27.1 • The PROVISO acronym (P = Internal Pudendal; R = Middle Rectal; O = Obturator; VI =
Inferior Vesical; and S = Superior; under Oblique view).
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FIGURE 27.2 • A: DSA after distal catheterization of the left inferior vesical artery under pos-terior-anterior
view. Note the left central gland blush and its relation with the Foley catheter (F). B: Control DSA
postembolization showing devascularization of left central gland.
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9. The contralateral internal iliac artery is catheterized by Waltman loop or a Simmons-1, and embolization
is performed following the same steps.
10. The “PErFecTED technique” (6), in which embolization of prostatic branches involves a two-step
approach bilaterally, is routinely used by the authors. After standard embolization of each side of the gland
(first step), the microcatheter should be advanced distally into the intraprostatic branches in order to
continue embolization (second step), avoiding by this method early occlusion of target arteries. This two-
step technique may possibly lead to better clinical outcomes due to more ischemic areas observed.
a. The use of a 2.0 Fr. microcatheter is fully recommended when using this technique.
b. Slow injection of the microspheres is essential to achieve the goal of diffuse gland parenchymal
ischemia, and control angiography should be performed a few minutes after finishing embolization.
11. In confusing cases, cone-beam computed tomography (CT) can be used to differentiate between
prostatic and rectal or bladder branches and also to confirm that the whole prostatic lobe has been
embolized (Fig. 27.3).
12. The pelvic arterial supply is markedly interconnected by anastomosis, some of them of clinical interest,
particularly those that involve bladder, rectum, and penis. These anastomoses should probably be
selectively embolized with microcoils, reducing risk of nontarget embolization (Fig. 27.4).
a. On the other hand, migration of small amounts of microspheres through anastomosis involving the
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obturator territory or other pelvic parietal structures will not lead to a clinical relevant complication;
therefore, usually there is no need for coiling those connections. Likewise, particle reflux to seminal vesicle
branches does not seem to cause major complications.
1. The urinary catheter is removed right after the procedure, except in those patients with previous UR and
chronic use of indwelling catheters. In these cases, patients are instructed to return 1 week later for removal of
the indwelling catheter to attempt spontaneous voiding. If UR symptoms persist and the catheter cannot be
removed, another attempt is tried every week.
2. Patients are discharged from the hospital 3 to 6 hours after PAE. The use of closure devices has reduced the
recovery time.
3. Postembolization symptom control is usually achieved with nonopioid analgesics and nonsteroidal anti-
inflammatory drugs (NSAIDs). Antibiotics (ciprofloxacin 500 mg 12/12 hours) and proton-pump inhibitors are also
prescribed for a period of 1 week.
a. Dysuria, frequency, and urgency have been observed in all patients treated by PAE and are related to
ischemic prostatitis.
b. Similar to any other visceral embolization, symptoms such as nausea, fever in the absence of infection,
urethral burning, periprostatic or pelvic pain, very small amounts of blood in urine and/or mixed in the stool with
mucus for 3 to 5 days can be seen (post-PAE syndrome) (7).
4. Serum PSA is measured 24 hours after PAE and seems to correlate with clinical outcomes. Higher degrees of
PSA have been correlated to more prostate ischemia (7).
5. Patients are advised to call the interventional radiologist (IR) with any problems during the first week.
6. They return at 3 and 12 months and then annually for clinical evaluation, MRI, uroflowmetry, PSA testing, and
IPSS and QOL assessment.
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FIGURE 27.3 • Cone-beam CT in coronal view (A) and 3D reconstruction (B) showing parenchymal blush of the
left central gland of prostate (CG). F, Foley catheter.
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FIGURE 27.4 • A: DSA of the right internal iliac artery ipsilateral oblique projection showing the anterior
branches and their relationship to the balloon of the Foley catheter. SVA, superior vesical artery; IVA, inferior
vesical artery; IPA, internal pudendal artery. B: Anterior-posterior view with the microcatheter positioned at the
origin of the prostatic arteries (PAs). The right intraprostatic branches and partial left lobe opacification are
observed (arrowheads). A collateral arterial shunt (arrow) is observed vascularizing the penis. (continued)
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FIGURE 27.4 • (Continued) C: In this case, a platinum microcoil was placed occluding the shunt before
microsphere injection to avoid nontarget embolization (arrow). The prostate is not opacified and vessels
supplying the right side of the bladder are identified after prostate embolization (asterisk).
Results
1. Technical success, when defined as bilateral embolization, varies from 75% to 94.3% (7,8). When both
unilateral and bilateral embolization are considered to be technical success, published rates reach 95% to
100% (4).
2. Clinical success, including an IPSS <8 and QOL <3, varies from 80.7% to 97.1% at 3 months, 75.2% at
12 months, and 72.0% at 24 and 36 months (3,4,7,8).
a. Values of IPSS and QOL above these levels during follow-up are considered as disease recurrence
requiring therapy (medical treatment, re-embolization, or surgical resection). Recurrence rate at mean
follow-up of 20 months is 14.2% (9).
3. Prostate reduction ranges from 20% to 40% (mean of 30%) in different groups (Fig. 27.5)
(4,5,6,7,8,9,10).
a. In a study including only patients with prostates >90 g (7), clinical success was 97.1% after 3 months,
with mean reduction of prostate volume of 32.0% and increase of peak urinary flow rate of 114.1% ( P <.01
for all).
4. For patients with chronic UR, clinical success can be defined as removal of the indwelling catheter, and
varies from 91% to 100% (7,8).
5. Gao et al. (10) compared results of PAE (n = 57) and TURP (n = 57) at a mean follow-up of 22.5 months.
Clinical outcomes including IPSS and QOL values, peak urinary flow, and postvoid residual urine volume
were comparable in both groups within 12- and 24-month follow-up. The TURP group showed better results
at 1 and 3 months; however, hospital stay was significantly shorter in PAE group (2.9 vs. 4.8 days, P <
0.001).
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FIGURE 27.5 • A: MRI T2-weighted coronal view demonstrating enlarged prostate due to BPH nodules in
the central gland. B: Control MRI 3 months after PAE showing prostate volumetric reduction and low-signal
areas in central gland (arrows), corresponding to infarcted BPH nodules. (continued)
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FIGURE 27.5 • (Continued) C: Infarcted nodules (arrows) presenting as avascular areas at 3-month post-
PAE control MRI (fat-suppressed postcontrast sequence).
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The PAE procedure is considered safe, with a very low incidence of major complications. Nevertheless, there is
a potential for severe complications when the correct technique is not used.
1. In a recent study (7), the overall incidence of complications was 20.6% (17.7% minor, 2.9% major); the major
complication was related to UTI that needed hospitalization for intravenous antibiotics.
2. A mortality related to PAE has not been reported.
3. Minor complications are usually self-limited or controlled with medical treatment.
a. Postembolization syndrome is common; however, it is easily managed with antiemetics, analgesics, and
NSAIDs. Hospitalization and use of opioids are rarely necessary.
b. Other possible complications related to the procedure are access site complications such as hematoma,
urinary, rectal or seminal bleeding (usually selflimited), urinary tract infection, or infectious prostatitis.
4. Major complications are related to nontarget embolization resulting in visceral ischemia.
a. To date, at least one case of bladder wall necrosis requiring surgical resection has been reported (4).
b. Others include bladder and rectal wall ischemia, bone infarction, and radiodermatitis.
Summary
Overall, knowledge of pelvic arterial anatomy, vascular anastomosis, and familiarity with advanced
microcatheterization techniques are fundamental to optimize outcomes and avoid complications. IRs must
understand the urologic language
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and the BPH disease. Finally, working in a multidisciplinary team with urologists, diagnostic, and
interventional radiology is essential.
References
1. Oelke M, Bachmann A, Descazeaud A, et al. EAU guidelines on the treatment and follow-up of non-
neurogenic male lower urinary tract symptoms including benign prostatic obstruction. Eur Urol . 2013;64:118-
140.
2. Antunes AA, Carnevale FC, da Motta-Leal-Filho JM, et al. Clinical, laboratorial and urodynamic findings of
prostatic artery embolization for the treatment of urinary retention related to benign prostatic hyperplasia. A
prospective singe-center pilot study. Cardiovasc Intervent Radiol . 2013;36:978-986.
3. Bagla S, Martin CP, van Breda A, et al. Early results from a United States trial of prostatic artery
embolization in the treatment of benign prostatic hyperplasia. J Vasc Interv Radiol . 2014;25:47-52.
4. Pisco JM, Rio Tinto H, Campos Pinheiro L, et al. Embolisation of prostatic arteries as treatment of
moderate to severe lower urinary symptoms (LUTS) secondary to benign hyperplasia: results of short- and
mid-term follow-up. Eur Radiol . 2013;23:2561-2572.
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5. Carnevale FC, Antunes AA. Prostatic artery embolization for enlarged prostates due to benign prostatic
hyperplasia. How I do it. Cardiovasc Intervent Radiol . 2013; 36:1452-1463.
6. Carnevale FC, Moreira AM, Antunes AA. The “PErFecTED technique”: proximal embolization first, then
embolize distal for benign prostatic hyperplasia. Cardiovasc Intervent Radiol . 2014;37:1602-1605.
7. Assis AM, Rodrigues VCP, Yoshinaga EM, et al. Prostatic artery embolization (PAE) for treatment of
benign prostatic hyperplasia in patients with prostates exceeding 90 g: a prospective single center study. J
Vasc Interv Radiol . 2015;26(1):87-93.
8. Carnevale FC, da Motta-Leal-Filho JM, Antunes AA, et al. Quality of life and clinical symptom improvement
support prostatic artery embolization for patients with acute urinary retention caused by benign prostatic
hyperplasia. J Vasc Interv Radiol . 2013;24:535-542.
9. Moreira AA. Prostate artery embolization: a single center's results. Paper presented at: AIM Symposium—
Advanced Interventional Management; November 17-20, 2014; New York, NY.
10. Gao YA, Huang Y, Zhang R, et al. Benign prostatic hyperplasia: prostatic arterial embolization versus
transurethral resection of the prostate-a prospective, randomized, and controlled clinical trial. Radiology.
2014;270:920-928.
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28
Central Venous Access—Nontunneled
Sidney Regalado
Brian Funaki
Central venous (CV) access devices can be placed faster, more safely, and with fewer complications when
imaging guidance is utilized than when placed with reliance on external anatomic landmarks (1). The placement
of a nontunneled CV catheter has certain advantages over the placement of a tunneled CV catheter or
implantable subcutaneous chest port. Nontunneled CV catheters are commonly placed using local anesthesia
only, often at the bedside in an intensive care unit (ICU) setting when patients are too ill to be transported. As
these temporary catheters are placed without subcutaneous tunneling, less stringent adherence to coagulation
parameters can be observed. When the indication for these CV catheters no longer exists, these devices can be
easily removed at the bedside.
Indications (2)
1. Therapeutic indications
a. Administration of chemotherapy, total parenteral nutrition (TPN), blood products, intravenous medications, and
fluids
b. Performance of hemodialysis and plasmapheresis discussed in Chapter 33
2. Diagnostic indications
a. To confirm a diagnosis or establish a prognosis
b. To monitor response to treatment
c. For repeated blood sampling
Contraindications
Absolute
1. Cellulitis at insertion site
2. Allergy to catheter material
Relative
2. CV occlusion
3. Peripherally inserted central catheters (PICCs) are contraindicated in patients who are at risk for chronic
renal failure or who have chronic kidney disease due to concern for damage to potential future dialysis
fistula sites.
The preprocedure preparation is similar irrespective of the access device that is chosen.
1. Review of medical history to:
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a. Establish an indication
b. Obtain a history of concurrent or prior CV access devices and history of related complications, such as
extremity or facial swelling
c. Identify pertinent allergies
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2. Review of prior imaging studies to assess for anatomic variants and vessel patency. A quick ultrasound survey
is recommended.
3. Physical examination of extremities, including pulses
4. Informed consent
5. Nil per os (NPO) status is not needed as the procedure is typically performed with local anesthesia only.
6. Guidelines for coagulation parameters should be followed. PICCs and nontunneled CV access are considered
to be low risk for bleeding, which is easily detected and controllable (3).
a. International normalized ratio (INR) should be checked in patients on warfarin. INR goal is less than 2.0.
b. Partial thromboplastin time (PTT) is recommended in patients receiving intravenous unfractionated heparin.
PTT should be less than 1.5 times control.
c. Platelet count not routinely recommended, but transfusion is recommended for counts less than 50,000 per μL.
Others utilize a platelet count ≥25,000 per μL (4).
d. Plavix and aspirin do not need to be withheld.
e. Low-molecular-weight heparin (therapeutic dose) should be withheld for one dose before procedure.
7. Prophylactic antibiotics are not given before nontunneled CV catheter placement.
Procedure
a. Nontunneled CV catheters and PICCs are placed in the interventional radiology (IR) suite or at the
bedside (with or without fluoroscopic guidance) depending on operator preference and the clinical status of
the patient.
b. The skin is sterilized with a 2% chlorhexidine-based preparation. Standard surgical scrub protocol for the
operator includes hand scrubbing, gloves, mask, cap, and gown.
c. Local anesthesia with 1% lidocaine is utilized for all line placements.
d. Choice of line
(1) CV catheters differ in composition, length, number of lumens, and size. A large internal lumen is optimal
for infusions of viscous liquids, whereas multiple lumens facilitate infusion of incompatible infusates.
Generally speaking, increasing the number of lumens in the catheter will increase the size of the catheter.
For multilumen catheters, if one lumen increases in size, the other lumens may have to decrease in size to
maintain a reasonable catheter outer diameter. The choice of catheter size and number of lumens is
significant, as the risk of vessel thrombosis and infection increases as the size of the catheter and number
of lumens increase.
(2) Power injectable PICCs and nontunneled CV catheters are available and can be identified by the
catheter tubing which indicate the injection rate parameters. The Bard Power PICC (Bard Access Systems,
Salt Lake City, UT) has a maximum injection rate of 5 mL per second at 300 psi.
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e. Guidance technique
(1) Ultrasound (US) guidance is always recommended for venipunctures to avoid inadvertent arterial
puncture.
(2) When the patient can medically tolerate movement to an angiographic suite, fluoroscopic guidance is
used for visualization of guidewires, catheters, and venography. A spot fluoroscopic image at the conclusion
is used to document the catheter tip.
(3) When bedside CV lines are placed, only US guidance is used. Thus, a follow-up radiograph is obtained
to verify catheter tip position.
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f. Catheter tip position
(1) Superior vena cava-right atrial junction is ideal.
(2) Catheter tips can migrate with respirations, retraction due to pendulous breast tissue, and with
movement from the supine to upright position (1).
(3) Preexisting CV stenoses or fibrin sheaths may necessitate placement either higher in the superior vena
cava (SVC) or deeper in the right atrium.
2. PICC placement
a. Choice of vein
(1) Either arm can be used, but the nondominant arm is preferred.
(2) Some operators will choose the largest vein in the upper arm above the elbow as their access vein,
whereas others will routinely select the basilic vein, as it is not adjacent to the brachial artery and nerve.
(a) The cephalic vein may be used but is prone to spasm and thrombosis.
(b) The brachial veins travel alongside the brachial artery increasing the risk of arterial puncture.
b. A tourniquet is placed in the upper arm to distend the veins.
c. US guidance and a micropuncture needle (typically 21 gauge) are used for venous access. The access
vein can also be punctured using fluoroscopic guidance after injection of contrast medium.
d A 0.018-in., 60 cm mandril guidewire is advanced centrally under fluoroscopic guidance or until resistance
is felt, if fluoroscopy is not available.
e. A skin nick is made, and an appropriately sized peel-away sheath is placed.
f. Using fluoroscopy, the required catheter length is measured using the guidewire, and the PICC line is cut
to length. If the procedure is performed at bedside, catheter length is estimated.
g. The PICC is advanced using a stiffening stylet or a guidewire to the desired position.
h. PICC function is checked by injection of saline, and the peel-away sheath is removed.
i. A catheter is anchored to the skin with an adhesive catheter lock or nonabsorbable suture.
j. Dilute heparinized saline is instilled in the lumens, and catheter caps are placed.
k. A sterile dressing is applied.
l. Completion spot fluoroscopic image (or chest radiograph) is obtained to document catheter tip position for
future reference.
m. Tips for puncturing veins
(1) For inadvertent arterial puncture with a skinny needle, simply remove the needle and apply manual
compression to achieve hemostasis.
(2) If the wire does not advance easily through the needle, the needle tip is either against the wall or a
double-wall puncture may have occurred. Pull the wire back into the needle. Withdraw the needle into the
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lumen, and gently advance the wire with fluoroscopic guidance until the wire advances easily.
(3) If the wire tip becomes significantly deformed, consider removing the wire and needle together (as a
unit) in order to prevent shearing of the wire.
(4) If it is difficult to advance the wire further along the course of the vein, vasospasm may be present. This
can be confirmed with a gentle flush of contrast. Wait a few minutes for vasospasm to resolve
spontaneously or consider administering nitroglycerin locally (100 to 200 μg). Alternatively, choose a new
vein.
(5) Stenosis/occlusion: A tortuous vein or an anatomic variant may be present. Venography will define
anatomy. A digital road map and a properly selected wire and catheter will help in navigating past the
problem.
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3. Central venous catheter placement
a. Choice of vein
(1) The internal jugular vein (IJV) is the preferred site. Access into this vein has the lowest risk of
complications, including pneumothorax and thrombosis (5). It has a straight course toward the right atrium
simplifying catheter placement.
(2) The left IJV is a more challenging access site because it drains into the brachiocephalic vein, which may
be tortuous and enter the SVC at a right angle, necessitating additional manipulation for central access.
The wire has a natural tendency to enter the azygous arch or the right ventricle when directed from the left
side. In such situations, curved catheters (e.g., MPA, Boston Scientific, Natick, MA) and floppy-tip wires
(e.g., J-wire or a hydrophilic glidewire) are helpful to access the IVC.
(3) If internal jugular access cannot be achieved, the external jugular veins are acceptable targets (1).
(4) Subclavian veins are often targeted by nonradiologists as they can be catheterized using external
landmarks. However, subclavian vein access is associated with a higher risk of CV thrombosis and
pneumothorax (1,2,5). Given the risk of thrombosis and stenosis, subclavian vein access is contraindicated
in patients who are at risk for chronic renal failure, who have chronic kidney disease, or who are on dialysis.
(5) The femoral veins are often catheterized in patients who are uncooperative or coagulopathic, or when
access is obtained in emergency situation as these veins can be easier to cannulate. The groin is more
tolerant of complications such as bleeding when compared to the neck. Femoral veins are less optimal sites
of venous access as there is an increased risk of infection and worse patency (1).
(6) After a medical course necessitating multiple catheters, patients are predisposed to developing CV
occlusions. When conventional veins have been exhausted, unconventional venous access should be
attempted (1,6). Unconventional routes to the central veins include recanalization of collateral neck or chest
veins, translumbar access into the IVC, transhepatic venous access, or a surgically placed direct right atrial
venous access.
b. Access: Using US guidance and a micropuncture needle, the vein is accessed (Fig. 28.1).
c. The microwire (0.018 in.) is advanced centrally under fluoroscopic guidance or until resistance is felt, if
fluoroscopy is not available. A transitional dilator is placed (typically 5 Fr.).
d. A working guidewire (typically 0.035 in.) is advanced into the inferior vena cava (IVC) (Fig. 28.2).
e. Serial dilators are advanced over the wire.
f. An appropriate length catheter is advanced over the wire. A 15-cm long catheter is commonly used when
accessing the right IJV, and a 19-cm long catheter is used when accessing the left IJV. The wire is then
removed (Fig. 28.2B).
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g. Catheter tip position is assessed when possible, and function is verified (Fig. 28.2C).
h. Catheter is sutured to the skin.
i. Catheter flushing and dressings are placed per hospital protocol.
4. Device removal
a. Nontunneled central lines and PICCs can be removed at bedside or in the recovery room using local
anesthesia and manual traction.
b. If the device is removed for suspected catheter infection, the catheter tip is sent for culture.
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FIGURE 28.1 • US evaluation of the IJV. A: IJV (arrow) and carotid artery (star). B: Compression of the IJV
(arrow) shows patency of the vessel. C: Echogenic needle tip in the center of the IJV (arrow).
1. With the use of imaging guidance, catheter malposition is rare. If the catheter was not placed under
fluoroscopic guidance, a chest x-ray is obtained following the procedure to document position.
2. Patients are given written instructions that describe proper care of the catheter and catheter exit sites. Signs
and symptoms of complications are discussed, and contact information is provided.
3. The care of CV catheters is dictated by hospital protocol and includes instructions for line-flushing and
dressing changes.
Results
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Successful placement of a CV access device requires a catheter placed into the venous system with the tip
in the desired location. The catheter must also function appropriately for its intended use (i.e., medication
administration vs. dialysis) (2). The reported placement success rates are between 95% and 96%. The
threshold for successful placement in the IJV is 95% and in the subclavian or peripheral route is 90% (2).
Complications
Complications are defined as early (within 30 days of placement) or late (occurring after 30 days). Early
complications are subdivided into those within 24 hours
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(procedurally related) and those that occur beyond that time window. Imageguided insertions are associated
with lower complication rates when compared to placement using external landmarks (2,5). The overall
complication rate is 7% (2,5). The overall procedure threshold for major complications is 3% (4). Imaging-
guided placement results in fewer early complications (5% to 10%), lower infection rates (9.7 vs. 14 per
1,000 catheter-days), and fewer late complications (20% vs. 30%) when compared to surgical placement
(7). Several of the more common complications are described in the following text.
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FIGURE 28.2 • Placement of temporary CV catheter via the right IJV. A: A guidewire is placed into IVC
under fluoroscopic guidance. B: After serial dilators are advanced over the wire, a nontunneled catheter is
advanced over the guidewire. C: The guidewire is removed and catheter function verified. Catheter tip is at
the SVC/right atrium (RA) junction.
1. Malposition
a. Catheter malposition immediately after placement is rare with the use of image guidance. Tip malposition
occurs in 3% to 32% without image guidance, versus 0% to 4% with image guidance (7). Fluoroscopic
guidance is used to confirm the proper positioning of the catheter, and immediate adjustments can be made
at the time of placement. If the catheter position is uncertain, venography can also be performed. Routine
chest radiographs are not needed after image-guided catheter placement. If a PICC line is inserted at the
bedside, a follow-up chest radiograph is obtained to verify catheter tip position.
b. Catheter tips may lodge in a variety of locations due to anatomic variants including a left SVC, duplicated
SVC, anomalous pulmonary vein, a collateral vein, or retrograde within a vein.
2. Pneumothorax
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a. The incidence of pneumothorax (PTX) and accidental arterial puncture is low when US guidance is used
for IJV access (1% to 2%). The risk of PTX is higher when only external anatomic landmarks are used for
direct subclavian vein access (1). The risk is 0% for PICC placements.
b. Most PTX remain asymptomatic, especially if the visceral pleura is displaced less than 2 to 3 cm from the
parietal pleura. PTX is usually apparent immediately on postprocedure imaging. Rarely, a delayed PTX can
develop several days later (1,8,9,10).
3. Air embolus
a. Air embolus is a rare complication that occurs, if intrathoracic pressure drops, during catheter insertion
into the vein through a peel-away sheath (1%). Air entry can be minimized by having the patient maintain a
positive intrathoracic pressure by continuously humming and by manually crimping the external portion of
the sheath immediately after removing the dilator and guidewire. The sheath should remain crimped until
the catheter is advanced into it. Tiny air emboli declare themselves less frequently as patients remain
asymptomatic. Large air emboli can be symptomatic, with cough and respiratory distress, or can even be
fatal. In these cases, air lucency in the right atrium or pulmonary outflow can be seen on fluoroscopy. A
peel-away sheath with a valve can help minimize this risk (10).
4. Great vessel or cardiac perforation
a. Perforation is a rare complication (<1%) that may occur if dilator is advanced over a kinked guidewire or if
the wire is not in the IVC (1,10). Catheters placed in the right subclavian vein are more prone to this as the
vessel enters perpendicular to the SVC. Signs of hemodynamic instability, hemothorax, mediastinal
hematoma, or cardiac tamponade may be present.
5. Late complications such as infection, fibrin sheath formation, venous thrombosis, and catheter fracture
and their management will be discussed in Chapter 29. These are more often the consequence of long-term
access.
1. Malposition
a. A malpositioned catheter at the time of placement can be adjusted using fluoroscopic guidance and a
guidewire.
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b. If a catheter tip has migrated after the initial placement, many corrective options exist. For instance, if a
catheter tip has migrated into the azygous arch, the catheter can be repositioned into the SVC using a
pigtail catheter or an endovascular snare from a femoral approach. If the catheter is too short, a catheter
exchange may be indicated. If the catheter is too long, catheter can be pulled back.
c. Poor aspiration of a PICC may indicate that the catheter may be kinked. This can be corrected using a
guidewire to straighten out the catheter. If any catheter will not aspirate when the tip is central, the tip may
be against the wall of the RA. The catheter can slowly be withdrawn until free flow is achieved.
d. If a small-bore catheter is accidentally placed in the arterial system, catheter removal with manual
compression can be attempted. If a large-diameter catheter is placed in the arterial system, removal may
need to be performed in the operating room with a cut down. Other options upon removal of an arterial
catheter include balloon tamponade or deployment of a covered-stent or closure device.
2. Pneumothorax
a. Small PTXs are managed conservatively.
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b. A large or symptomatic PTX can be treated with a small-bore chest tube attached to a Heimlich valve
(Becton Dickinson, Franklin Lakes, NJ).
c. If a Heimlich valve is insufficient, the catheter can be attached to a Pleur-evac (Teleflex, Inc, Morrisville,
NC) system or wall suction.
d. Rarely would a conventional surgical large-bore chest tube need to be placed.
3. Air embolus
a. Not treated if emboli are small or patient is asymptomatic
b. If symptomatic, place patient in the left lateral decubitus position (left side down) and administer 100%
oxygen.
4. Great vessel or cardiac perforation
a. Catheter removal in the operating room, as needed
b. Catheter can be removed in the angiography suite. However, the equipment for balloon tamponade or
stenting should be readily available. A surgical team may need to stand by for high-risk cases.
References
1. Funaki B. Central venous access: a primer for the diagnostic radiologist. AJR Am J Roentgenol .
2002;179:309-318.
2. Lewis CA, Allen TE, Burke DR, et al. Quality improvement guidelines for central venous access. J Vasc
Interv Radiol . 2003;14:S231-S235.
2009;20:S240-S249.
4. O'Connor SD, Taylor AJ, Williams EC, et al. Coagulation concepts update. AJR Am J Roentgenol .
2009;193:1656-1664.
5. Silberzweig JE, Sacks D, Khorsandi AS, et al. Reporting standards for central venous access. J Vasc
6. Funaki B, Zaleski GX, Leef JA, et al. Radiologic placement of tunneled hemodialysis catheters in occluded
neck, chest, or small thyrocervical collateral veins in central venous occlusion. Radiology. 2001;218:471-
476.
7. McBride KD, Fisher R, Warnock N, et al. A comparative analysis of radiological and surgical placement of
central venous catheters. Cardiovasc Intervent Radiol . 1997;20: 17-22.
8. Tyburski JG, Joseph AL, Thomas GA, et al. Delayed pneumothorax after central venous access: a
potential hazard. Am Surg. 1993:59:587-589.
9. Vescia S, Baumgärtner AK, Jacobs VR, et al. Management of venous port systems in oncology: a review
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of current evidence. Ann Oncol . 2008;19:9-15.
10. Bhutta ST, Culp WC. Evaluation and management of central venous access complications. Tech Vasc
Interv Radiol . 2011;14:217-224.
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29
Central Venous Access—Tunneled
Sidney Regalado
Brian Funaki
Long-term central venous (CV) access devices are composed of tunneled catheters and subcutaneous chest
ports. Tunneled catheters are used for weeks to months (or even years) and are most commonly placed for
chemotherapy, total parenteral nutrition (TPN), plasmapheresis, and hemodialysis. Implantable subcutaneous
ports are used for access if the indication remains for months to years. Most commonly, ports are placed for
chemotherapy. Generally speaking, tunneled catheters are easier/quicker to place and exchange but have a
higher risk of infection and are more lifestyle-limiting (overall cosmetic appearance and ease of hygiene) when
compared to subcutaneous ports. All of these devices can be removed when they are no longer needed (1).
Indications (2)
1. Administration of chemotherapy, TPN, blood products, intravenous medications, and fluids
2. Performance of hemodialysis and plasmapheresis (Chapter 33)
Contraindications
Absolute (1)
1. Bacteremia or sepsis
2. Cellulitis at insertion site
3. Allergy to catheter material
Relative (1)
2. CV occlusion
Preprocedure preparation is similar to the placement of temporary CV access catheters described in the prior
chapter. Notable differences are described below.
1. In addition to local anesthesia, patients often require conscious sedation. Patients must remain nil per os
(NPO) for 6 hours, or per institutional protocol.
2. Guidelines to coagulation parameters should be followed to prevent bleeding complications (3). Tunneled CV
access and subcutaneous ports are considered to be procedures with moderate risk of bleeding.
a. Routine international normalized ratio (INR) should be obtained in all patients. INR goal is less than 1.5.
b. Partial thromboplastin time (PTT) is recommended in patients receiving intravenous unfractionated heparin.
Normal range is 25 to 35 seconds. PTT should be less than 1.5 times control.
c. Platelet count not routinely recommended, but transfusion is recommended for counts less than 50,000 per μL.
Others utilize a platelet count ≥25,000 per μL (4).
d. Plavix is withheld for 5 days before procedure. Aspirin not withheld.
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e. Low-molecular-weight heparin (therapeutic dose) should be withheld for one dose before procedure.
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3. Prophylactic antibiotics before central line placement is controversial because several studies support and
refute their utility (5). If prophylaxis is desired for tunneled catheter or port placement, 1 g cephazolin or 600 mg
clindamycin can be administered within 45 minutes of skin incision.
Procedure
a. All tunneled catheters and ports are placed in a fluoroscopy suite.
b. The skin is sterilized with a 2% chlorhexidine-based preparation. Standard surgical scrub protocol for the
operator includes hand scrubbing, gloves, mask, cap, and gown.
c. Local anesthesia with 1% lidocaine is used for all line placements.
d. Conscious sedation with fentanyl citrate and midazolam hydrochloride is routinely administered. The
nurse must continuously monitor vital signs.
e. Choice of device. As with temporary catheters, the smallest catheter size and minimum number of lumens
to satisfy the indication for the access is important to decrease thrombotic complications. Power injectable
devices permit their use for contrast injection during computed tomography (CT) examination.
f. Guidance technique
(1) Ultrasound (US) guidance is always recommended for venipunctures.
(2) Fluoroscopic guidance is used for visualization of guidewires, catheters, and venography.
g. Choice of vein
(1) The jugular veins are the preferred access site for tunneled catheters and subcutaneous ports.
Subcutaneous ports can be placed through an arm vein, similar to a peripherally inserted central catheter
(PICC); however, arm ports are associated with higher risk of complications such as thrombosis (1).
(2) Femoral veins are less optimal sites of venous access because there is an increased risk of infection
and worse patency (1,6).
(3) When conventional veins are exhausted, nonconventional access is considered.
2. Tunneled central venous catheters
a. For women with large breasts, the breast should be taped inferiorly to prevent excessive retraction (with
cephalad catheter-tip movement) when the patient resumes an upright posture.
b. The placement of tunneled catheters using conventional veins is essentially the same for all indications.
Access to the jugular vein is made similarly to nontunneled access (Fig. 29.1A-C).
c. A working guidewire is placed from access site to the IVC (Fig. 29.1D).
d. The intended subcutaneous path of the tunnel is anesthetized with lidocaine using a long needle and
preferably a single skin entry.
e. A skin nick is made in the chest wall at the desired catheter entry site so as to create a subcutaneous
tunnel of 8 to 10 cm in length, and a tunneling device is advanced through this nick toward the neck
venotomy site making a gentle curve in the tract (Fig. 29.1E). Some devices have a preformed curve.
f. An appropriately sized peel-away sheath is placed through the jugular access over the existing stiff 0.035-
in. wire.
g. The tunneled catheter is pulled through the tunnel so that the proximal retention cuff is at least 2 cm
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within the entry to the tunnel (Fig. 29.1F).
h. Then the catheter is briskly advanced through the jugular peel-away sheath positioning the tip at the
superior vena cava/right atrium (SVC/RA) junction (Fig. 29.1G). Avoid air embolism.
i. The neck venotomy site is closed with skin glue (Dermabond, Ethicon, Mokena, IL) or a suture.
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FIGURE 29.1 • Tunneled catheter placement. A: Transverse sonographic assessment of right internal
jugular vein (RIJV). B: Vein is compressible which suggests patency of the vessel. CA, carotid artery.
(continued)
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FIGURE 29.1 • (Continued) C: Ultrasound guidance for skinny needle puncture of RIJV. D: Guidewire is
advanced into the IVC ( solid portion is external to the vessel and long-dashed portion is intravascular).
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FIGURE 29.1 • (Continued) E: Skin incisions are made in the right chest wall and at the neck venotomy
sites (short-dashed lines). A tunneler is advanced to the puncture site in the neck (polka dot portion is
external to the skin and the solid portion is in the subcutaneous tunnel). F: Catheter is pulled through the
tunnel and the retention cuff is under the skin (polka dot portion i s external to skin, solid portion is in the
tract, and the grid pattern is going to enter the vessel through a peel-away sheath). (continued)
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FIGURE 29.1 • (Continued) G: Tip of tunneled catheter is at the SVC/RA junction ( polka dot portion is
external to skin, solid portion is in the tract, and the grid pattern is intravascular).
j. The tunneled catheter is anchored to the skin with a nonabsorbable suture.

k. Function is verified by aspiration and flushing of ports with saline.
l. Heparin is instilled in the lumens and caps are placed according to hospital policy.
m. A sterile dressing is applied.
n. A completion spot fluoroscopic image is saved to document tip position.
3. Chest port
a. After gaining access to the jugular vein, a working guidewire is placed from access site to the IVC (Fig.
29.2A).
b. The intended port placement site and the tunnel tract are generously anesthetized with lidocaine with a
minimal number of skin entries.
c. Using a no. 15 scalpel, a single 3-cm long skin incision is made in the chest wall parallel to the sensory
dermatomes. A subcutaneous pocket is made using blunt dissection. The pocket should be large enough to
contain the port without excessive skin tension. If the port is placed too deeply, access with the Huber
needle (B. Braun Medical, Inc, Bethlehem, PA) can be difficult. If the pocket is too superficial, skin erosion
and breakdown can occur. If the pocket is too capacious, the port can flip over. If pocket is too small,
excessive tension may lead to dehiscence of the wound.
d. The tunneling device is then advanced from the pocket to the neck venotomy site making a gentle curve
in the tract (Fig. 29.2B). The catheter is pulled through the subcutaneous tunnel (Fig. 29.2C).
e. An appropriate peel-away sheath is placed over the wire at the internal jugular vein (IJV) entry site.
f. The catheter tubing is advanced through the peel-away sheath and positioned at the SVC/RA junction
(Fig. 29.2D). The end hole of the catheter tubing outside of the patient must be clamped in order to prevent
air embolism and bleeding.
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FIGURE 29.2 • Placement of a subcutaneous chest port. A: A guidewire is placed into the inferior vena
cava (IVC) under fluoroscopic guidance. B: A pocket is created using blunt dissection after making a 2- to
3-cm skin incision. A subcutaneous tunnel is made using a tunneler device (arrow). C: The catheter (bent
arrow) is pulled through the tunnel to the neck venotomy site. D: The catheter is advanced through a peel-
away sheath. Most ports still have to be assembled by connecting the catheter tubing, locking hub and the
port together. Port (arrowhead) is buried in the pocket and the pocket is closed. Catheter tip at the SVC/RA
junction.
g. The catheter tubing is cut at the level of the port pocket and is then attached to the port reservoir and
secured by the hub (done in nonattached systems only). Care is required in allowing for enough catheter
length within the pocket to attach it to the port but not so much that it kinks. The port is lowered into the
pocket.
h. The pocket is closed with a two-layer closure. The deep layer is closed with 3-0 absorbable sutures
(Ethicon, Mokena, IL). A recent report suggests that barbed absorbable suture can be used for the deep
layer closure with good
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success and potentially better outcomes than traditional absorbable suture. The cutaneous layer is closed
with skin glue or a running subcuticular 4-0 absorbable suture.
i. The port is accessed with noncoring needle, aspirated, flushed with saline to check for leaks, and instilled
with heparin volume as specified.
j. The venotomy site is closed with skin glue or 4-0 absorbable suture.
k. A sterile dressing is applied.
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l. Follow-up spot fluoroscopic image is obtained to document catheter-tip position.
m. If needed, the Huber needles are placed and secured for the clinical service.
4. Device removal
a. Tunneled central lines can be removed at bedside or in the recovery room using local anesthesia and
manual traction. The retention cuff is freed from the subcutaneous tissues by using blunt and/or sharp
dissection. Tunneled catheters can break during removal. The catheters will typically break at the junction
of the catheter tubing and the cuff. If possible, the catheter is clamped to prevent air embolus and bleeding.
If this is not possible, extrinsic compression on the catheter over the clavicle is performed to prevent
bleeding and air embolus. An incision is made central to the cuff and the catheter is removed using blunt
dissection.
b. Port removal is performed in the procedure room using sterile conditions. Most port removals are
performed with local anesthesia only.
(1) An incision is made and the port is removed using blunt dissection. The port, hub, and catheter are
removed. If the pocket is clean, the pocket is closed with absorbable sutures and skin glue.
(2) If the pocket is infected, copious irrigation is performed. The pocket is packed with iodoform packing
strips and allowed to close secondarily.
(3) If the device is removed for suspected catheter infection, the catheter tip is sent for culture.
5 Exchanging a nonfunctioning tunneled catheter
a. A tunneled catheter may not be functioning due to malposition of the catheter tip, fibrin sheath formation,
or clotting of the catheter. Exchange of a tunneled catheter can be done using the same tract. Preprocedure
protocol detailed above is followed.
b. A stiff hydrophilic wire is advanced into each lumen of the old tunneled catheter and into the IVC using
fluoroscopic guidance. The old catheter is removed after dissecting the cuff out of the subcutaneous tissues
and the old catheter is removed over the wires.
c. If a pericatheter fibrin sheath is suspected, angioplasty can be performed using an 8- to 12-mm balloon to
disrupt it.
d. A new catheter is advanced over the wires.
e. The catheter is secured and function is verified.
f. Spot fluoroscopic image and sterile dressing are placed.
g. Occasionally, the new catheter may be difficult to advance through the tract, which can be due to an
immature tract or sharp angulation at the venotomy entry site. The tract and venotomy site can be stretched
with dilators or angioplasty balloons. The catheter can be advanced through a peel-away sheath placed in
the tract to provide stiffness and support while manual compression is placed over the venotomy site to help
direct the catheter inferiorly. Many catheters have either tapered distal ends or have guidewire stylets which
can help facilitate catheter exchanges.
1. With the use of imaging guidance, catheter malposition is rare. A spot radiograph is obtained to document tip
position.
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2. Patients are given written instructions that describe proper care of the catheter and wound. Signs and
symptoms of complications are discussed and contact information provided.
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3. The care of tunneled catheters and subcutaneous ports is dictated by hospital protocol and includes
instruction for line flushing and dressing changes.
4. Power injectable catheters
a. Power injectable tunneled catheters have external identifying labels on the catheter which indicate maximum
injection rates.
b. Power injectable ports have multiple safety identifiers. Certain devices can be identified by shape or palpation
points on the septum. Identifiers are also present on scout CT or plain radiographs. A special power injectable
Huber needle must be used during power injections.
c. Patients should be given written information to document the type of device that has been placed.
Results
As with temporary access, successful fluoroscopic placement of a CV access device into the venous system
with the tip in the desired location and with appropriate function for its intended use is accomplished in
nearly all cases (95%).
Complications
Early complications of CV access were described in the previous chapter and are directly applicable to
long-term CV access. Unique late complications do arise with long-term CV catheters because their
implantation time is longer than temporary catheters.
1. Infection
a. Most common complication. Coagulase-negative Staphylococcus species, Staphylococcus aureus,
aerobic gram-negative bacilli, and Candida albicans are the most common pathogens (1).
(1) In general, ports have the lowest infection rate, followed by tunneled catheters, and then nontunneled
catheters (7,8). The infection rate of ports has been reported at 0.21 per 1,000 catheter days, whereas for
tunneled lines it has been reported at 2.77 per 1,000 catheter days (1,9).
(2) Rate of catheter exit site infection is 0.26 per 1,000 catheter days. Rate of bloodstream infections is 0.19
per 1,000 catheter days (1,8,9).
(3) In cases of suspected line infection, patients are treated with broadspectrum antibiotics to cover the
most common pathogens. The antibiotic choice is tailored based on results of blood cultures, wound
cultures, or catheter-tip cultures.
2. Fibrin sheath formation
a. Most common cause of catheter dysfunction. The classic complaint is that the catheter can infuse but will
not aspirate.
b. A fibrin sheath is a proteinaceous coat of eosinophilic material and scattered inflammatory cells that
envelops the catheter tubing and tip that can be identified on venography by contrast puddling at the tip or
traveling in a retrograde direction along catheter tubing rather than flowing directly into the central veins
(1,10).
c. Fibrin sheaths form around nearly every CV catheter. Catheter dysfunction secondary to fibrin sheath can
be seen in 13% to 57% of all dialysis catheters (which can be detected early due to low flow rates).
Catheter dysfunction due to fibrin sheath is likely seen less commonly in ports and non-dialysis tunneled
lines because these catheters can function despite having low flow rates (11).
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d. Catheter dysfunction caused by a thrombus near the tip of the catheter can mimic the symptoms of a
fibrin sheath because both can cause a one-way valve disrupting proper function.
3. Catheter-related CV thrombosis
a. Manifestations of SVC syndrome such as arm swelling and face swelling can develop due to catheter-
related CV thrombosis. Often there is a preexisting stenosis which is exacerbated by superimposed acute
clot. Catheter tip malposition increases the risk of thrombosis (10).
b. Incidence is ˜4% (2).
4. Catheter pinch-off
a. Complications related to catheters passing through the subclavian vein do not occur with IJV access.
b. Catheters that are placed too medially are chronically compressed by the right rib and clavicle by the
costoclavicular ligament and subclavius muscle (1,10). Repetitive compression can lead to fatigue and
fracture. The catheter fragment may then embolize to the heart or pulmonary artery (˜1%) (10).
1. Infections
a. Not every catheter suspected of being infected should be removed immediately. Consider catheter
salvage if a patient is stable and/or lacks other sites for potential venous access.
b. Exit site or wound infections are initially treated with antibiotics.
c. Tunnel infections or port pocket infections require catheter removal and antibiotics.
d. If bacteremia is present, antibiotics are given. If blood cultures are negative for 48 hours, catheter
exchange over a guidewire can be performed for tunneled PICCs or tunneled central lines.
e. If patient is septic, emergent catheter removal is indicated.
f. Infected tunneled lines are removed by manual traction after dissection of the cuff. The catheter exit site
closes by secondary intention. The catheter tip is sent for culture and sensitivity.
g. Infected ports are excised and pocket irrigated. If the pocket is clean, it can be closed primarily. If the port
pocket is purulent, the pocket is packed with iodoform packing gauze until the pocket is clean and closes by
secondary intention. Catheter tips are sent for culture and sensitivity. Extensive port pocket infections may
require plastic surgery consultation.
2. Fibrin sheath formation
a. First-line treatment is administering tissue plasminogen activator (tPA) into the lumens (1,10). Success
rate is 87% to 93% for catheter clearance (10).
(1) Alteplase (Cathflo, Genentech, San Francisco, CA) is reconstituted by injecting 2.2 mL of sterile water
into the alteplase powder.
(2) Administer the appropriate amount of alteplase based on the specified volume of the catheter.
(3) Allow 30 minutes of dwell time and reassess for patency.
(4) If still occluded, allow an additional 90 minutes of dwell time (120 minutes total) and recheck for patency.
(5) If still occluded, re-administer a repeat dose of alteplase and repeat dwell times.
(6) An alternative protocol for pharmaceutical fibrin sheath disintegration involves administering an alteplase
drip. A sample infusion protocol is to administer 2 to 4 mg alteplase mixed with 50 mL saline and infused
over 3 to 4 hours (10).
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b. If thrombolytics fail, exchange of catheter over a guidewire, with or without balloon angioplasty, can be
performed (1,10).
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c. Exchange of a port is more involved compared to exchange of a tunneled catheter. Therefore, fibrin
sheath stripping using a loop snare is recommended. If fibrin sheath stripping fails, the port and catheter
should be exchanged.
3. Catheter-related CV thrombosis
a. Anticoagulation is the initial treatment.
b. If the catheter is no longer needed, removal is indicated.
c. If the catheter is needed, anticoagulation is continued. If anticoagulation is insufficient, thrombolytic
therapy may be instituted.
d. If a patient has an underlying SVC stenosis, angioplasty and/or stenting is needed to relieve symptoms.
e. A small amount of thrombus is often seen around catheter tips by CT. If asymptomatic and a small clot
burden, manage conservatively. If thrombus is large, consider anticoagulation.
4. Catheter pinch-off
a. A compressed, unfractured, subclavian catheter is followed with serial radiographs.
b. If the catheter is partially fractured or has embolized, removal of the device is indicated. The embolized
fragment can be retrieved using a loop snare.
c. Fragments can get chronically “endothelialized” into the right heart wall, which would preclude removal.
References
1. Funaki B. Central venous access: a primer for the diagnostic radiologist. AJR Am J Roentgenol .
2002;179:309-318.
2. Lewis CA, Allen TE, Burke DR, et al. Quality improvement guidelines for central venous access. J Vasc
2009;20:S240-S249.
2009;193:1656-1664.
5. Covey AM, Toro-Pape FW, Thornton RH, et al. Totally implantable venous access device placement by
interventional radiologists: are prophylactic antibiotics necessary? J Vasc Interv Radiol . 2012;23(3):358-362.
6. Zaleski GX, Funaki B, Lorenz JM, et al. Experience with tunneled femoral hemodialysis catheters. AJR Am
J Roentgenol . 1999;172:493-496.
7. Yip D, Funaki B. Subcutaneous chest ports via the internal jugular vein. A retrospective study of 117
oncology patients. Acta Radiol . 2002;43:371-375.
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8. Moureau N, Poole S, Murdock MA, et al. Central venous catheters in home infusion care: outcomes
analysis in 50,470 patients. J Vasc Intervent Radiol . 2002:13(10): 1009-1016.
9. Groeger JS, Lucas AB, Thaler HT, et al. Infectious morbidity associated with longterm use of venous
access devices in patients with cancer. Ann Intern Med. 1993;119: 1168-1174.
10. Bhutta ST, Culp WC. Evaluation and management of central venous access complications. Tech Vasc
Interv Radiol . 2011;14:217-224.
11. Santilli J. Fibrin sheaths and central venous catheter occlusions: diagnosis and management. Tech Vasc
Interv Radiol . 2002;5(2):89-94.
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30
Central Venous Access Management
Jamie B. Arton
Mitchell Smith
Maintaining lumen patency and preventing catheter-related bloodstream infections (CR-BSIs) or central line-
associated bloodstream infection (CLABSIs) are the goals of proper line care for both peripherally inserted
central catheters (PICC) and central venous catheters (CVCs). Vascular access devices are cited as the main
cause of health care-associated bloodstream infections. Rates of infection vary by line type, insertion location,
number of lumens, and tunneling (1).
There are approximately 15 million CVC days in United States intensive care units (ICUs) per year. The average
rate of CR-BSIs is 5.3 per 1,000 catheter days or 80,000 infections (2,3). Estimates of associated mortality range
from 0% to 35% if the study is controlled for illness severity (4,5,6). The cost of treating a CR-BSI ranges from
$34,000 to $56,000 per individual and between $296 million and $2.3 billion for the health care system (5,7,8).
In addition to the ICU setting, central venous access is also frequently used in the outpatient oncology setting,
where patients are immunosuppressed secondary to chemotherapy treatment and have a higher likelihood of
developing a central line infection. Infections of all types are a significant cause of morbidity and mortality in
oncology patients (9). One of the major risk factors determined from multivariate analysis is inflammation at CVC
insertion site (10). Gram-positive cocci are 14% more frequently isolated in the blood cultures of neutropenic
oncology patients (10).
Herein, the authors discuss the Centers for Disease Control and Prevention (CDC) guidelines for Category I (IA:
strongly recommended for implementation and strongly supported by well-designed experimental, clinical, or
epidemiologic studies; IB: strongly recommended for implementation and supported by some experimental,
clinical, or epidemiologic studies and a strong theoretical rationale, or an accepted practice [e.g., aseptic
technique] supported by limited evidence) and Category II (suggested for implementation and supported by
suggestive clinical or epidemiologic studies or a theoretical rationale) evidence for the post-insertion care of
CVCs (11).
Flushing
Anticoagulants such as heparin are used to maintain the patency of catheters by preventing intraluminal
thrombosis. There is a lack of clinical evidence for or against using heparin flushes in central lines, which is
noted by many of the evidence-based guidelines for catheter care (12). A systematic review published by
Mitchell et al. (12) found weak evidence for the use of heparin flushes in reducing the incidence of catheter
occlusion. Risks of using heparin flushes include heparin-induced thrombocytopenia (HIT), allergic reactions to
heparin, and chemical contaminants. No current studies have been done that are sufficiently powered to assess
the risk of HIT from routine central venous catheter flushing (12).
One randomized trial comparing normal saline versus heparin flushes in short-term, nontunneled, CVCs
demonstrated no difference in catheter patency and suggests that frequency of flushes and proper flushing
technique are critical in maintaining catheter patency (13). The CDC recommends against the use of
anticoagulant therapy, but the focus of their guidelines is prevention of infection and not on maintaining catheter
patency.
Institutional guidelines for line care are created, usually by dedicated central venous access committees based
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on current available evidence. An example is presented in Table 30.1.
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Table 30.1 Line Flushing Protocols
Heparin
Line Type Concentration Amount Frequency
PICC 10 units/mL 3 mL Daily
Nontunneled 10 units/mL 2 mL Daily

CVC (excluding
temporary
hemodialysis
catheters)
Nontunneled 1,000 units/mL See manufacturer After insertion and after

hemodialysis recommendations based on each hemodialysis
catheters catheter length, typically treatment (maintained by
found on each catheter trained dialysis staff)
lumen.
Tunneled CVC 10 units/mL or 100 See manufacturer Daily to weekly

(excluding units/mL recommendations based on depending on
hemodialysis depending on line catheter length, typically manufacturer
catheters) type found on each catheter recommendations and
lumen. institutional guidelines
Tunneled 1,000 units/mL See manufacturer After insertion and after

hemodialysis recommendations based on each hemodialysis
catheters catheter length, typically treatment (maintained by
found on each catheter trained dialysis staff)
lumen.
Groshong No heparin 5 mL normal saline Every 7 days or more

required due to often as needed
catheter design.
Flush with normal
saline.
Implanted port 100 units/mL 5 mL Every 30 days or more

often as needed
Access and Administration Sets

There is limited Category I evidence on the care of needleless access ports for CVCs. The use of needleless
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access is mandated to help prevent needlestick injuries. There are multiple types of stopcocks, needleless
system connectors, and Luer-activated devices currently on the market. The CDC recommends accessing these
ports with sterile devices after disinfecting the port with chlorhexidine, povidone iodine, and iodophor, or 70%
alcohol (Category IA) (11). There is growing evidence in the literature suggesting that universal disinfectant caps
placed on the end of the needleless connectors reduce CLABSI rates, and guidelines published by the Society
for Healthcare Epidemiology of America in July 2014 recommend use of disinfectant caps as Category I (14).
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Tubing used to administer fluids should be replaced routinely depending on the infusate. Propofol tubing should
be replaced every 6 to 12 hours. Tubing for blood, blood products, or fat emulsions should be replaced within 24
hours of starting the infusion (15,16,17). All other administration sets should be replaced between 4 days and 7
days of first use (11).
Site Care
Insertion
For catheter insertion as well as dressing changes, the skin should be cleaned with >0.5% chlorhexidine. If the
patient has an allergy, tincture of iodine or 70% alcohol can also be used (Category IA). When placing or
replacing PICCs or CVCs, maximum sterile barriers including hat, mask, sterile gown, sterile gloves, and full body
drape should be used (11).
Dressing
The CDC recommends using sutureless securing devices to help prevent infection (Category II) (9,11). Either
sterile transparent polyurethane dressings or sterile gauze and tape are appropriate dressings for central lines
(Category IA). There is no evidence demonstrating one dressing is superior to another in preventing infection.
Gauze is most appropriate if the catheter site is bleeding or if the patient is diaphoretic (Category II). The
dressing, regardless of what type, should be changed if it is soiled or starting to become detached from the skin
(Category IB). Depending on patient preference, transparent dressings can be changed on a weekly basis
(Category II). Gauze dressings should be changed every 2 days. Patients may be permitted to shower with the
dressing in place 48 hours after placement as long as catheter is covered with an impermeable cover (Category
II). Tunneled catheters that are well-healed may go without a dressing except in the case of immunocompromised
patients; no recommendations have been made on dressings for these catheters. A chlorhexidine impregnated
sponge dressing should be used on shortterm catheters in patients older than 2 months if the infection rate is not
decreasing (Category IB).
Infection Prevention
Additional infection prevention strategies include the use of povidone-iodine antiseptic ointment at the
hemodialysis catheter exit site after insertion and at the end of each dialysis session as long as ointment will
not interact with catheter material (Category IB). Bacitracin/gramicidin/polymyxin B ointment may be used if
it is available. If CLABSI rates are not decreasing, the CDC recommends using chlorhexidine/silver
sulfadiazine or minocycline/rifampin-impregnated CVCs in patients who need access for 5 days or longer
(Category IA). An antibiotic lock prophylaxis is recommended in patients with long-term catheters who have
had multiple line infections (Category II) (11).
References
1. Maki DG, Klueger, DM, Crinch CJ. The risk of bloodstream infection in adults with different intravascular
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devices: a systematic review of 200 published prospective studies. Mayo Clinic Proc. 2006;81(9):1159-1171.
2. Mermel LA. Prevention of intravascular catheter-related infections. Ann Intern Med. 2000;132:391-402.
3. Centers for Disease Control and Prevention. National nosocomial infections surveillance (NNIS) system
report, data summary from October 1986—April 1998, issued June 1998. Am J Infect Control . 1998;26:522-
533.
4. Digiovine B, Chenoweth C, Watts C, et al. The attributable mortality and costs of primary nosocomial
bloodstream infections in the intensive care unit. Am J Respir Crit Care Med. 1999;160:976-981.
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5. Rello J, Ochagavia A, Sabanes E, et al. Evaluation of outcome of intravenous catheter-related infections in

critically ill patients. Am J Respir Crit Care Med. 2000;162:1027-1030.
6. Soufir L, Timsit JF, Mahe C, et al. Attributable morbidity and mortality of catheterrelated septicemia in
critically ill patients: a matched, risk-adjusted, cohort study. Infect Control Hosp Epidemiol . 1999;20:396-401.
7. Dimick JB, Pelz RK, Consunji R, et al. Increased resource use associated with catheter-related
bloodstream infection in the surgical intensive care unit. Arch Surg. 2001;136:229-234.
8. Mermel LA. Correction: catheter related bloodstream-infections. Ann Intern Med. 2000;133:395.
9. Centers for Disease Control and Prevention. Basic infection control and prevention plan for outpatient
oncology settings. http://www.cdc.gov/hai/pdfs/guidelines/basic-infection-control-prevention-plan-2011.pdf.
Accessed November 2, 2015.
10. Maschmeyer G, Haas A. The epidemiology and treatment of infections in cancer patients. Int J
Antimicrob Agents. 2008;31(3):193-197.
11. Centers for Disease Control and Prevention. Guidelines for the prevention of intravascular catheter-
related infections, 2011. http://www.cdc.gov/hicpac/pdf/guidelines/bsi-guidelines-2011.pdf. Accessed
November 2, 2015.
12. Mitchell MD, Anderson BJ, Williams K, et al. Heparin flushing and other interventions to maintain patency
of central venous catheters: a systematic review. J Adv Nurs. 2009;65(10), 2007-2021.
13. Schallom ME, Prentice D, Sona C, et al. Heparin or 0.9% sodium chloride to maintain central venous
patency: a randomized trial. Crit Care Med. 2012;40(6):1820-1826.
14. Marschall J, Mermel LA, Fakih M, et al. Strategies to prevent central line-associated bloodstream
infections in acute care hospitals: 2014 update. Infect Control Hosp Epidemiol . 2014;35:753-771.
15. Melly MA, Meng HC, Schaffner W. Microbiol growth in lipid emulsions used in parenteral nutrition. Arch
Surg. 1975; 110:1479-1481.
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16. Gilbert M, Gallagher SC, Eads M, et al. Microbial growth patterns in a total parenteral nutrition
formulation containing lipid emulsion. JPEN J Parenter Enteral Nutr. 1986;10:494-497.
17. Maki DG, Martin WT. Nationwide epidemic of septicemia caused by contaminated infusion products. IV.
Growth of microbial pathogens in fluids for intravenous infusions. J Infect Dis. 1975; 131:267-272.
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31
Dialysis Fistulae
Aalpen A. Patel
Scott O. Trerotola
An estimated 2.5 million patients worldwide receive renal replacement therapy and 450,000 of those patients are
from the United States. In the mid-1990s, the National Kidney Foundation began an effort to give evidence-
based guidance to the teams caring for dialysis patients. The Disease Outcomes Quality Initiative (DOQI)
recommendation document was published in 1997. In 2000, the scope was expanded to include chronic kidney
disease even before the need for dialysis arises. This effort is now termed the Kidney Disease Outcomes Quality
Initiative (NKF-KDOQI) (1). The Vascular Access section was last updated in 2006.
Long-term dialysis access is created via the surgical construction of an arteriovenous (AV) shunt. This
connection between an artery and a vein may be created by using native conduits (native arteries and veins),
artificial conduits (grafts), or hybrid conduits. This chapter will address native arteriovenous fistulae (AVF).
The NKF-KDOQI document recommends that when possible, the order of preference for site of AVF placement
should be (a) radiocephalic (wrist), (b) brachiocephalic (elbow), and (c) transposed brachial-basilic. An
arteriovenous graft (AVG) should only be considered if AVF creation is not possible.
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Regular assessment of AVF should be performed to detect hemodynamically significant stenosis because it has
been proven in a randomized trial that treatment of hemodynamically significant anatomic stenoses in fistulae
reduces the incidence of access thrombosis and improves patency (2). The following complementary methods
may be used as part of a quality assurance program. Physical examination and evaluation for such findings as
arm swelling, development of collateral veins, prolonged bleeding, change in flaccidity of fistula, and change in
outflow vein should be performed by a qualified health care professional on a monthly basis, which is termed
monitoring. If special instrumentation is used to perform evaluation of the AVF at periodic intervals, it is termed s
urveillance. Direct flow measurements and duplex ultrasound are preferred methods of surveillance. A detailed
discussion of each method is beyond the scope of this chapter, and readers requiring more information should
refer to the NKF-KDOQI document. It is important to note that a single abnormal test result should not trigger a
response; it is an abnormal trend or persistent abnormality that should result in further steps.
Indications
1. Failure of the AVF to mature. The first access evaluation should occur 6 weeks after creation.
a. Diagnostic fistulogram, if
(1) Flow <600 mL/min
(2) Draining vein <6 mm in diameter
b. Angioplasty of stenosis anywhere in circuit up to the central veins; there is no evidence that central
venous stenosis affects maturation.
c. Embolization or ligation of “competing” veins. Th is is a controversial issue because there is little
evidence that treatment of such vessels helps with maturation (3).
2. Failing AVF. An AVF is thought to be failing when there is inflow or outflow stenosis(es) greater than 50%
associated with
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a. Decreased flow (decreased clearance)
b. Increased static venous pressure
c. Pseudoaneurysm
d. Prolonged bleeding after needle removal
e. Arm swelling
f. Recirculation
g. Abnormal physical examination
3. Clotted AVF
Contraindications
Absolute
2. Fistula infection. Note: Fistula infection is very unusual. As opposed to AVGs, erythema and warmth over
a clotted AVF nearly always represents thrombophlebitis and not an infection.
Relative
1. Right-to-left cardiopulmonary shunt (for declotting procedures due to the risk of paradoxical emboli)
2. History of contrast reaction
3. Significant cardiopulmonary disease. During declotting procedures, pulmonary emboli can occur. Most of
the time, they are without clinical consequences; however, in patients with right ventricular failure,
pulmonary hypertension, and cardiac dysrhythmias, fatal pulmonary emboli have been reported.
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4. Ischemia distal to the AV anastomosis. Increasing the flow through a fistula may further divert blood from
the ischemic area and result in worsening of the steal syndrome.
5. Systemic infection
1. Informed consent. This encounter also helps establish a rapport with the patient and helps to ease anxiety.
2. Intravenous (IV) antibiotics should be administered prior to thrombectomy/thrombolysis (cefazolin 1 to 3 g IV
[weight based] or vancomycin 0.5 to 1.5 g IV [weight based] because the contents of a clotted fistula may be
colonized) (4).
3. Obtaining a history of the current fistula (along with physical examination) is one of the most crucial steps in
preprocedure assessment. The following should be assessed and documented:
a. When the access was created
b. Type of access
c. If failure to mature (has there been any prior successful use)
d. When the dysfunction or clotting occurred
e. Presence of steal symptoms
f. Arm, face, or breast swelling
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g. Fevers or chills
h. History of prior interventions
4. Regardless of the type of access, the following should be assessed by physical exam and documented:
a. Pulses: radial, ulnar, and brachial pulses (use Doppler if not palpable)
b. Capillary refill and warmth of the arm/hand
c. Chest wall collaterals
d. Cardiac and pulmonary examination: assessment of the patient’s ability to safely tolerate moderate sedation
and the procedure. Those with pulmonary edema may require preprocedure dialysis via temporary catheter.
e. Physical evaluation of the AVF should be performed prior to each intervention.
(1) Type and condition of access (radiocephalic fistula, brachiocephalic fistula, or basilic or cephalic vein
transposition), presence of aneurysms, pseudoaneurysms, or hematoma and the location of the anastomosis.
This information helps in choice of fistula access site(s).
(2) Presence or absence of thrill/pulse
(3) Assessment whether the fistula is tense or flaccid (even with thrill)
5. Review of the images from prior interventions is critical (especially when there is early failure after a prior
procedure). In particular, determine if the previous intervention was optimal. This is a critical step and should not
be omitted.
6. Coagulation parameters (international normalized ratio [INR], partial thromboplastin time [PTT], and platelet
count) should be assessed. An INR ≤2 seconds, PTT <40 seconds, and platelets >25,000 are acceptable.
Procedure
Interventions performed in AVFs include fistulography and angioplasty in nonmaturing or failing fistulae and
clearing of clot from occluded fistulae (declotting procedures). Each will be described separately.
Fistulography and Percutaneous Transluminal (Balloon) Angioplasty for Nonmaturing
Fistulae
1. Assemble the appropriate tools and equipment prior to the procedure:
a. For fistula access: 18-gauge Angiocath or a micropuncture set
b. Guidewires: Roadrunner (Cook Medical, Bloomington, IN) (preferred), Bentson wire, or long-tapered (8-
cm taper) Glidewire.
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c. Sheaths: high-flow 6 Fr. and/or 7 Fr. short sheaths (4 to 6 cm long) with sidearm
d. Balloons: Ultrahigh-pressure balloons: High pressures are often needed for percutaneous transluminal
(balloon) angioplasty (PTA), especially in AVF. Short shaft balloons may be more convenient in fistula
intervention.
e. Inflation system (either of the following two):
(1) 1-mL polycarbonate syringe, 10-mL syringe, and a flow switch. When a high-pressure balloon is used,
this system is cost-effective and can generate more pressure than an inflator (5).
(2) Dedicated inflator
f. Other equipment as needed:
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(1) Stents (covered and uncovered, self-expanding, and balloon expandable)
(2) Catheters: Berenstein or Kumpe catheter (40 or 65 cm), Binkert, left internal mammary artery (LIMA),
Rösch inferior mesenteric (RIM), or Cobra I catheter.
2. Heparin 3,000 units is given IV at the beginning of the procedure and more as needed, guided by
activated clotting time, as nonmaturing fistulae are prone to spasm and thrombosis. Nitroglycerin (NTG, 100
μg/mL) should be available for treatment of spasm.
3. For nonmaturing fistulae, the first access should be via the brachial artery. Retrograde access is obtained
by ultrasound-guided direct puncture using the 3 Fr. inner dilator of a micropuncture set. This method
reduces the risk of venous spasm and the need for inflating a blood pressure cuff to reflux contrast across
the anastomosis, as is necessary with puncture of the venous side of the fistula. A fistulogram will
demonstrate the “true” flow dynamics of the fistula and any hemodynamically significant stenoses that might
be the reason for nonmaturation of the fistula. Venous spasm is common in a nonmaturing fistula and
responds well to NTG, although rarely will require PTA to treat it. The brachial artery access may also be
used for administration of NTG and heparin as needed in the procedure.
4. If there are stenoses requiring treatment, entry sites into the fistula from the venous side are chosen
based on the fistulogram. Angioplasty should be performed via the venous side of the fistula to avoid arterial
complications. If dilation of all stenosis is not possible via only one access, a second ultrasound or
palpation-guided access to the fistula may be performed with a micropuncture set or Angiocath.
5. Every stenosis ≥50%, potentially compromising inflow or outflow, should be treated with PTA.
a. Usually a balloon 1 mm larger than the size of the adjacent normal vein is adequate in the primary outflow
vein (7-mm and 8-mm balloons are common), with an inflation time of 90 seconds.
b. For radiocephalic anastomosis, 5- to 6-mm balloons usually suffice. The authors strive for 6 mm,
whenever possible.
c. If the initial results are not satisfactory, progressive oversizing of balloons is performed as well as
prolonged inflations of 5 minutes or more.
d. Stents and stent grafts are rarely needed for stenoses that do not respond to dilation. Most often, they
are used (stent grafts) for venous rupture refractory to prolonged PTA or for elastic recoil in locations not
easily amenable to surgical intervention.
6. A completion fistulogram should be performed by hand injection of contrast through the sidearm of the
sheath to assess residual stenoses and exclude rupture. The maximum acceptable residual stenosis is less
than 30%. Restoration of a nonpulsatile thrill is the best predictor of long-term results; this should be the
goal in all cases (6).
7. In the complete absence of significant stenoses, if veins are present that are considered to possibly be
diverting blood from the primary conduit, consideration should be given to surgical/percutaneous ligation
(preferred for cost)
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or embolization of these veins. Proof that such veins are truly competing can be done by temporarily
occluding the vein by external compression and determining if there is improvement in the physical
examination or ideally, directly measuring flow. Truly competing veins will be extremely rare, less than 1% in
most practices (3).
8. Treatment of “competing” veins should not be done at the same time as PTA of significant stenosis
because the PTA will result in maturation in the vast majority of nonmaturing fistulae (3).
9. The puncture site may be closed in several ways, taking care not to thrombose the fistula:
a. For arterial access and all punctures in nonmaturing fistulae, manual compression is recommended by
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the authors. Ultrasound-guided compression may aid in preventing hematoma in patients with large arms.
b. Manual compression with a clotting agent
c. Purse string suture, with a temporary device holding the strings or knot
Fistulography and PTA for Failing AVFs
1. Equipment: as for nonmaturing fistulae
2. For most interventions in nonoccluded mature fistulae with diminished function, heparin is not required,
unless flow is seen to be markedly reduced on fistulography.
3. The puncture site can usually be chosen based on presenting symptoms and physical exam, augmented
by ultrasound. This initial evaluation will help avoid puncturing in the wrong direction and at the wrong site.
a. If low flow is suspected and the fistula is flaccid, inflow stenosis is likely the culprit. This requires a
venous puncture directed toward the AV anastomosis.
b. If high pressure is the chief complaint and the fistula is tense, the stenosis is likely on the venous side
and the venous puncture should be made in the downstream direction.
4. A diagnostic fistulogram is critical and should opacify the anatomy from the arterial inflow to the right
atrium prior to any intervention. This will give a full dynamic evaluation of the fistula. The fistulogram
provides a picture of both static stenoses and dynamic flow diverted via collaterals.
a. The arterial inflow can be evaluated using a reflux maneuver. For forearm fistulae, an upper arm blood
pressure cuff is inflated to suprasystolic pressure to occlude the outflow veins and direct the contrast back
toward the anastomosis rather than through the venous outflow.
5. Any stenosis ≥50% that explains the presenting symptoms should be identified and treated with PTA.
a. The occlusion or stenosis is crossed with a guidewire using standard techniques.
b. Usually, a balloon 1 mm larger than the size of the vessel is adequate (typically 6 mm for a radiocephalic
anastomosis, for the remainder of the fistula 7 and 8 mm are common) with an inflation time of 90 seconds
and up to 5 minutes for prolonged PTA. A randomized trial showed that a 3-minute inflation yielded better
immediate result than a 1-minute inflation; however, this did not translate into improved long-term patency
(7).
c. The advent of ultrahigh-pressure balloons has virtually eliminated resistant stenosis.
d. If the initial result is inadequate, progressive oversizing of balloons is performed as well as prolonged
inflations of 5 minutes or more, in order to achieve a satisfactory result.
e. Stents and stent grafts are rarely used and none are U.S. Food and Drug Administration (FDA)-cleared
for use in fistulae in the United States. The most common indications are venous rupture refractory to
prolonged PTA,
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elastic stenoses in locations where surgical intervention is not easily possible, and stenoses that recur
within 3 months or less where no surgical options are available. The literature supports surgical revision of
accessible lesions when PTA fails (8,9). Whether stents or stent grafts are preferable to surgical revision
remains an unanswered question.
6. A postprocedure fistulogram should be performed to assess the effectiveness of angioplasty and to
exclude vessel rupture. After maximal treatment, there should be less than 30% residual narrowing at all
stenoses, ideally as close to 0% as possible. A continuous thrill (without significant pulsatility) is more
indicative of a satisfactory outcome than a hemodynamic end point (6).
7. Residual stenosis due to recoil (i.e., successful waist effacement with residual stenosis >30%) is
moderately common and almost always responds to prolonged PTA (two 5-minute inflations). If prolonged
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PTA fails, a stent or covered stent may be indicated. If there are no anatomic abnormalities on the
postprocedural fistulogram and there are abnormalities on the physical exam (particularly a very weak thrill),
a subclavian or innominate artery stenosis must be suspected and treated if present, working through the
dialysis access.
Clearing of Thrombus from Occluded AVFs (“Declotting Procedure”)
Equipment: as for nonmaturing fistulae
Systemic heparin is essential in declotting procedures because it helps to blunt any vasospastic or
bronchospastic response to small pulmonary emboli, in addition to its role in preventing rethrombosis during
the procedure. Prior to any declotting procedure on an AVF, heparin 3,000 units IV should be administered.
Native fistula declotting procedures may be prolonged, requiring repeated administration of heparin to
maintain the activated clotting time above 250 seconds.
1. Mechanical thrombectomy: The authors use mechanical thrombectomy almost exclusively. There are
several mechanical thrombectomy devices available for use; it is beyond the scope of this chapter to
describe them all. The technique described in the following text has steps common to all types of
mechanical devices. The steps described are in the sequence used for the majority of cases, but it may be
varied to suit a particular situation.
a. Access: As in any hemodialysis access, the entry site into the fistula depends on the physical exam.
Ultrasound findings are helpful to choose a site that is without clot or stenosis and as central as possible.
Whenever possible, puncturing into or immediately adjacent to a stenosis should be avoided. This can help
avoid the need for a second puncture. The access is made toward the anastomosis using Angiocath or a
micropuncture set. Two punctures may be required, one toward the anastomosis and the other toward the
primary venous outflow. A sufficient distance between each access site will allow the treatment of any
intervening narrowed segments and eliminates sheath overlap, which may compromise flow. The 6 Fr. or 7
Fr. sheaths are placed depending on the size of balloons or devices to be used.
b. Clot removal: After adequate heparin administration, a guidewire and catheter are used to cross the
anastomosis. Achieving this step is essential for a successful declotting procedure. Rarely, brachial artery
puncture may be required to cross the AV anastomosis; however, the authors do not advocate using
brachial artery access for intervention. Via the sheaths directed toward the anastomosis or central veins,
the thrombus is macerated with a balloon or a mechanical thrombectomy device in both directions and
aspirated manually through the large sidearm or automatically by the device itself.
c. Occasionally, an adherent chronic thrombus is difficult to fragment and remove, even with wall contact
devices. Local massage (by hand or with an ultrasound transducer to monitor progress) may loosen the
clot. If this maneuver is not successful, the clot may be loosened with a Fogarty adherent clot catheter
(Edwards Lifesciences, Irvine, CA) and/or subsequently
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fragmented with a thrombectomy device and removed. Removal of wall adherent clot may result in better
outcomes after declotting.
d. Treatment of the anastomosis/perianastomotic stenosis: Th e key to successful thrombolysis in a dialysis
access is restoration of flow. This is usually achieved by treatment of the anastomotic plug/stenosis. Initially,
this may be treated with a Fogarty balloon or a wall contact thrombectomy device, followed by PTA.
e. Treatment of significant stenoses with angioplasty and/or stents: After carefully confirming antegrade flow
in the fistula with a tiny injection of contrast, a diagnostic fistulogram can be performed. However, in order to
prevent arterial emboli, forward flow must be documented before the diagnostic study is performed. Any
stenoses identified are treated with PTA.
f. Postprocedure fistulogram: A completion fistulogram is performed from the anastomosis to right atrium
Radiology Books
including the primary venous outflow. The arterial inflow may be visualized with outflow occlusion and
contrast reflux (preferred), or by injection of contrast directly into the artery. The venous outflow may be
occluded using a balloon or by external compression (manual or with a blood pressure cuff). Manual
compression may increase the radiation dose to the operator. The same anatomic and clinical end points as
for angioplasty of failing fistulae are used.
g. Access site hemostasis: as for failing fistulae
2. Pharmaceutical thrombolysis
a. Primary thrombolysis: The use of thrombolytic agents is another way patency can be achieved. Two
catheters are placed from opposite directions without crossing the anastomosis. Lytic agents and heparin
are pulsed into the clot until the clot is cleared. Any underlying stenoses that are uncovered are then treated
in the standard fashion (10). Tissue plasminogen activator (tPA) doses vary between 3 mg and 20 mg. For
resistant clots or when there is a large clot burden, infusion thrombolysis may also be performed.
b. Adjunct thrombolysis: When there is very firm clot, large clot volumes, or in fistulae that have been clotted
for over a week, some operators will instill lytic agents into the clot prior to mechanical thrombectomy. The
lytic agent, tPA (2 to 4 mg) or reteplase (2 to 3 units), combined with heparin (3,000 to 5,000 units) is
injected into the clotted fistula 0.5 to 2 hours prior to the procedure. In order to prevent central venous and
arterial emboli due to pressurization of the fistula, both “limbs” of the fistula are occluded manually. The
theory is that partial clot lysis prior to or during mechanical thrombectomy would shorten the procedure;
however, in a prospective randomized trial this was proven not to be the case (11).
1. Postprocedure dialysis: The patient’s condition, dialysis schedule, and preprocedure potassium levels will
guide the decision to dialyze on the day of the procedure. If emergent dialysis is needed, the patient may have to
be admitted.
2. Distal pulses should be rechecked and documented.
3. For quality assurance (QA) purposes, ensure that the access is usable for dialysis.
Results
1. Outcomes for AVF angioplasty when the failing AVF has not undergone mechanical thrombectomy or
thrombolysis (12)
a. Technical success (less than 30% residual stenosis): 96%
b. Primary patency after intervention: 94% at 1 month, 82% at 3 months, 63% at 6 months, 53% at 1 year,
and 29% at 2 years (13)
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c. Secondary patency after intervention: 94% at 6 months, 84% at 1 year, and 79% at 2 years (13)
2. Outcome for AVF angioplasty when the AVF has undergone angioplasty following mechanical declotting
or thrombolysis (14)
a. Technical success: 89% to 93%
b. Primary patency after intervention (varies with clot volume) (15): 6 months—approximately 50%, 1 year—
approximately 20%
c. Secondary patency: 6 months—approximately 80%, 1 year—approximately 70%
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Complications
Major
1. Vein rupture resulting in a nonfunctioning access
2. Death related to sepsis
3. Volume overload from fluids administered during the procedure
4. Bleeding complications of thrombolysis
5. Pulmonary or extremity arterial embolization
6. Arterial emboli (can be major or minor)
Minor
1. Venous rupture has been reported in up to 10% of transposed fistulae. This usually will not result in loss
of the access if it is recognized and treated.
2. Fistula thrombosis during PTA
3. Bacteremia
4. Pseudoaneurysm formation
1. Arterial emboli
a. If symptomatic, the embolus must be removed. Initial treatments should include back bleeding, Fogarty
catheter technique, or thromboaspiration.
b. Thrombolysis may be tried next. Surgical thrombectomy is an option of last resort.
c. Puncture of the radial artery may be used to push the clot in a retrograde direction out of the artery.
d. In an asymptomatic patient, the back bleeding technique may be tried because it does not risk further
impaction of clot. For this technique to work effectively, the fistula flow must be established first. If the clot is
not cleared by this method, further treatment may not be required, particularly in light of the risk of clot
impaction or more distal embolization associated with other techniques.
2. Venous rupture
a. Approximately 70% of venous ruptures will respond to prolonged balloon tamponade (two 5-minute
inflations).
b. In the 30% of ruptures in which tamponade fails, covered stents can be used successfully to salvage the
access (9,16).
References
1. National Kidney Foundation. Clinical Practice guidelines and clinical practice recommendations. Updates:
vascular access. http://www2.kidney.org/professionals/KDOQI/guideline_upHD_PD_VA/. Accessed
November 3, 2015.
2. Tessitore N, Mansueto G, Bedogna V, et al. A prospective controlled trial on effect of percutaneous

transluminal angioplasty on functioning arteriovenous fistulae survival. J Am Soc Nephrol . 2003;14(6):1623-
Radiology Books
1627.
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3. Liang H, Fu J, Wang P, et al. Endovascular salvage of immature autogenous hemodialysis fistulas.

Cardiovas Intervent Radiol . 2014;37:671-678.
4. Ayus JC, Sheikh-Hamad D. Silent infection in clotted hemodialysis access grafts. J Am Soc Nephrol .
1998;9:1314-1317.
5. Foering K, Chittams JL, Trerotola SO. Percutaneous transluminal angioplasty balloon inflation with
syringes: who needs an inflator? J Vasc Interv Radiol . 2009;20(5):629-633.
6. Trerotola SO, Ponce P, Stavropoulos SW, et al. Physical examination versus normalized pressure ratio for
predicting outcomes of hemodialysis access interventions. J Vasc Interv Radiol . 2003;14:1387-1394.
7. Forauer AR, Hoffer EK, Homa K. Dialysis access venous stenoses: treatment with balloon angioplasty—1-
versus 3-minute inflation times. Radiology. 2008;249:375-381.
8. Quinn SF, Schuman ES, Demlow TA, et al. Percutaneous transluminal angioplasty versus endovascular
stent placement in the treatment of venous stenoses in patients undergoing hemodialysis: intermediate
results. J Vasc Interv Radiol . 1995;6:851-855.
9. Gray RJ, Horton KM, Dolmatch BL, et al. Use of Wallstents for hemodialysis accessrelated venous
stenoses and occlusions untreatable with balloon angioplasty. Radiology. 1995;195:479-484.
10. Cohen MA, Kumpe DA, Durham JD, et al. Improved treatment of thrombosed hemodialysis access sites
with thrombolysis and angioplasty. Kidney Int. 1994;46:1375-1380.
11. Vogel PM, Bansal V, Marshall MW. Thrombosed hemodialysis grafts: lyse and wait with tissue
plasminogen activator or urokinase compared to mechanical thrombolysis with the Arrow-Trerotola
percutaneous thrombolytic device. J Vasc Interv Radiol . 2001;12(10):1157-1165.
12. Maeda K, Furukawa A, Yamasaki M, et al. Percutaneous transluminal angioplasty for Brescia-Cimino
hemodialysis fistula dysfunction: technical success rate, patency rate and factors that influence the results.
Eur J Radiol . 2005;54(3):426-430.
13. Neuen BL, Gunnarsson R, Baer RA, et al. Factors associated with patency following angioplasty of
hemodialysis fistulae. J Vasc Interv Radiol . 2014;25(9):1419-1426. doi:10.1016/j.jvir.2014.05.020.
14. Turmel-Rodriques L, Raynaud A, Louail B, et al. Manual catheter-directed aspiration and other
thrombectomy techniques for declotting native fistulas for hemodialysis. J Vasc Interv Radiol . 2001;12:1365-
1371.
15. Wu CC, Wen SC, Chen MK, et al. Radial artery approach for endovascular salvage of occluded
autogenous radial-cephalic fistulae. Nephrol Dial Transplant. 2009;24: 2497-2502.
Radiology Books
16. Dale JD, Dolmatch BL, Duch JM, et al. Expanded polytetrafluoroethylene-covered stent treatment of
angioplasty-related extravasation during hemodialysis access intervention: technical and 180-day patency. J
Vasc Interv Radiol . 2010;21(3):322-326.
Radiology Books
32
Dialysis Grafts
Aalpen A. Patel
Scott O. Trerotola
Long-term dialysis access is created via the surgical construction of a connection between an artery and a vein
using only the native vessels, or non-native conduits. Non-native conduits include synthetic grafts
(polytetrafluoroethylene or polyurethane), biological grafts (bovine heterograft, bovine mesenteric vein,
cryopreserved femoral vein, or human umbilical cord vein), or hybrid grafts (with self-sealing composite material
or cryopreserved vein). Th is chapter will address the endovascular management of non-native arteriovenous
grafts (AVGs).
The Kidney Diseases Outcomes Quality Initiative (NKF-KDOQI) recommendations state that construction of an
AVG should only be considered if making a
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fistula is not possible (1). The preferred order for AVG creation is a forearm graft (loop graft preferred over
straight graft), upper arm graft, and chest wall prosthetic graft (“necklace graft”). Lower extremity AVG is an
access of last resort.
The rationale for monitoring and methods of surveillance are the same as for dialysis fistulae and are discussed
in Chapter 31.
Indications
1. Failing AVG. Clinical or hemodynamic abnormality and associated vessel/graft stenosis of greater than
50%, leading to
a. Decreased flow (decreased clearance)
b. Increased venous pressure
c. Pseudoaneurysm
d. Prolonged bleeding after needle removal
e. Arm swelling
f. Recirculation
g. Abnormal physical examination
2. Clotted AVG
Contraindications
Absolute
2. Graft infection
Relative
1. Right-to-left cardiopulmonary shunt (for declotting procedures due to risk of paradoxical emboli)
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2. History of contrast reaction
3. Systemic infection
4. Significant cardiopulmonary disease. During declotting procedures, pulmonary emboli can occur. Most of
the time, they are without clinical consequences; however, in patients with right ventricular failure,
pulmonary hypertension, or cardiac dysrhythmias, fatal pulmonary emboli have been reported.
5. Ischemia distal to the arteriovenous (AV) anastomosis. Increasing the flow through a graft may further
divert blood from the ischemic area and result in worsening of the steal syndrome.
6. AVGs inserted less than 30 days prior to intervention have not formed sufficient perigraft scar tissue and
may bleed when punctured. The resulting hematoma may lead to loss of the hemodialysis access altogether
or local infection. Patency associated with declotting in this situation is exceedingly poor.
1. A physician (preferably the one performing the procedure) or an advanced practitioner (depending on hospital
policy or state law) must obtain informed consent. This encounter also helps establish a rapport with the patient
and helps to ease anxiety.
2. Intravenous (IV) antibiotics should be administered prior to thrombectomy (cefazolin or vancomycin, based on
weight) because the contents of a clotted graft are often colonized (2).
3. Obtaining a history of the current AVG (along with physical examination) is one of the most crucial steps in
preprocedure assessment. The following should be assessed and documented:
a. When the access was created
b. Type of access
c. When the dysfunction or clotting occurred
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d. Presence of steal symptoms
e. Arm, face, or breast swelling
f. Warmth or erythema of the access site
g. Fevers or chills
h. History of prior interventions
4. Regardless of the type of access, the following should be assessed by physical exam and documented:
a. Pulses: radial, ulnar, and brachial pulses (dorsalis pedis, posterior tibial, popliteal, and femoral pulses for
lower extremity grafts). Use Doppler if the pulses are not palpable.
b. Capillary refill and warmth of the arm/hand
c. Chest wall collaterals
d. Cardiac and pulmonary examination. Assessment of the patient’s ability to safely tolerate moderate sedation
and the procedure. Patients with pulmonary edema may require preprocedure dialysis via a temporary catheter.
e. Physical evaluation of the graft should be performed prior to each intervention.
(1) Graft site: for warmth and erythema that might indicate graft infection or cellulitis. A graft infection is an
absolute contraindication to percutaneous intervention.
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(2) Type of access: straight or loop, direction of inflow and outflow, presence of aneurysmal graft degeneration,
and the location of anastomoses. Th is information helps in the determination of access site(s).
(3) Presence or absence of a thrill or pulse. Rarely, a patient may be referred with a “clotted graft” that is actually
not clotted but has very low flow. In these cases, an inflow lesion should be sought and corrected.
5. Review of the images from prior interventions is critical (especially when there is early failure after a prior
procedure). In particular, determine whether the outcome of the previous intervention was optimal.
6. Coagulation parameters (international normalized ratio [INR], partial thromboplastin time [PTT], and platelet
count) should be assessed. INR <2.0, PTT <40 seconds, and platelets >25,000 per μL are acceptable.
Procedure
Interventions performed in AVGs include fistulography and angioplasty in failing grafts and clearing of clot
from occluded grafts (“declotting procedures”).
Fistulography and Angioplasty for Failing AVGs
1. Assemble the appropriate equipment.
a. For access: 18-gauge Angiocath or micropuncture set
b. Guidewires: stiff hydrophilic wire or a Bentson wire
c. Sheaths: high-flow 6 Fr. and/or 7 Fr. short sheaths (4- to 6-cm long) with sidearm
d. Balloons: high-pressure angioplasty balloons
e. Inflation system
(1) Dedicated inflator or
(2) 1-mL polycarbonate syringe, 10-mL syringe, and a flow switch (3)
f. Other equipment as needed: stents (covered and uncovered, self-expanding, and balloon expandable)
2. The puncture site can usually be chosen based on presenting symptoms and physical exam, occasionally
augmented by ultrasound. This initial evaluation will help avoid puncturing in the wrong direction. For
example, if low flow is suspected and the graft is flaccid, the arterial limb upstream from the flaccid
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segment, or the inflow arteries, may be the culprit lesion. This would require puncture toward the arterial
anastomosis. Conversely, if high pressure is the chief complaint and the graft is tense, the puncture should
be made toward the venous anastomosis.
3. A diagnostic fistulogram is critical and should be performed from the arterial inflow to the right atrium prior
to any intervention. It alone will provide full dynamic evaluation of the graft. The fistulogram gives both a
picture of static stenoses and of dynamic flow as a result of the stenosis, diverted via the collaterals. The
arterial inflow may be evaluated with a reflux maneuver. A common technique is to compress the graft
downstream from the access to direct the contrast back toward the inflow.
4. Any stenosis ≥50% that explains the presenting symptoms should be identified and treated with
percutaneous transluminal (balloon) angioplasty (PTA).
a. The occlusion or stenosis is crossed with a guidewire using standard techniques.
b. Usually, a balloon 1 mm larger than the size of the graft is adequate, with an inflation time of 90 seconds.
c. If the initial result is inadequate, progressive oversizing of balloons is performed as well as prolonged
inflations of 5 minutes or more, in order to achieve a satisfactory result.
d. Stents are rarely used. The most common indications are venous rupture refractory to prolonged PTA,
Radiology Books
elastic stenoses in locations where surgical intervention is not easily possible, and stenoses that recur
within 3 months or less where no surgical options are available. The literature has supported surgical
revision of accessible lesions for failed PTA (4,5); however, given the favorable results of covered stents
compared to PTA at the venous anastomosis of AVGs (6), the authors place covered stents when PTA fails.
(i.e., two PTA failures in a 3-month period per NKF-KDOQI). Even with liberalization of the authors’ policy
based on emerging evidence, the authors place stents or stent grafts in fewer than 2% of dialysis
interventions.
5. A completion fistulogram (from the arterial anastomosis to right atrium including the venous outflow) is
performed to assess the effectiveness of angioplasty and to exclude vessel rupture. The arterial inflow may
be visualized with outflow occlusion and contrast reflux (preferred) or cannulating the artery (via the graft)
and performing the fistulogram from the artery. The venous outflow may be occluded by a balloon
(preferred) or manual compression.
6. After maximal treatment, there should be less than 30% residual narrowing at all stenoses (6), ideally as
close to 0% as possible. Restoration of a thrill on physical exam is the best predictor of long-term results;
thus, a thrill should be sought in all cases (7).
7. The site of puncture may be closed in several ways. Care must be taken not to thrombose the graft.
a. Manual compression
b. Manual compression with a clotting agent (8)
c. Purse-string suture (with a temporary device that holds the strings or a knot)
Clearing of Thrombus from Occluded AVGs (Declotting Procedures)
1. Equipment: same as for the treatment of failing AVGs; additional equipment as noted in the following text
2. Mechanical thrombectomy. The authors use mechanical thrombectomy almost exclusively for declotting
procedures. There are several mechanical thrombectomy devices available; it is beyond the scope of this
chapter to describe them all. The technique described in the following text has steps common to all types of
mechanical devices. The steps described are in the sequence used for
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the majority of cases, but it may be varied to suit a particular situation. If using a rheolytic device, PTA of the
outflow should be performed earlier to reduce the chance of increasing pressure in the access and the
likelihood of arterial emboli.
a. Access: The choice of access site depends on graft configuration.
(1) Loop AVG: The first puncture is made near the apex directed toward the venous anastomosis and a
second puncture (1 to 2 cm from the venous anastomosis) is directed toward the arterial anastomosis.
Choosing access in this manner allows maximum flexibility in clot access, sufficient distance between each
access site to treat any narrowed segments between them, and reduces the chances of sheath overlap that
may impede flow.
(2) Straight AVG: The first puncture is made 1 to 2 cm from the arterial anastomosis in the direction of the
venous anastomosis and the second 1 to 2 cm from the venous anastomosis directed toward the arterial
anastomosis.
b. Systemic heparin is essential in declotting procedures because it helps to blunt any physiologic response
to small pulmonary emboli, in addition to its role in preventing rethrombosis during the procedure. Prior to
any declotting procedure on an AVG, heparin 3,000 units IV should be administered.
c. An angled catheter (Berenstein or Kumpe) is advanced across the occlusion and into the central veins. A
pullback venogram is performed from the right atrium to the venous anastomosis, being careful not to inject
into the clotted graft because this may result in arterial emboli.
Radiology Books
d. A 7 Fr. short sheath (preferably 4 to 6 cm) with a radiopaque tip and largebore side arm (suitable for
aspiration) is inserted via the puncture directed toward the venous anastomosis.
e. A 6 Fr. or 7 Fr. sheath is placed at the second puncture directed toward the arterial anastomosis. The
clot is not aspirated prior to the second access because doing this may lead to the collapse of the graft,
making the second access difficult.
f. Clot removal. The thrombus is macerated with a mechanical thrombectomy device in both directions and
aspirated manually via the sheath or fragmented and aspirated automatically with a rheolytic device.
Balloon maceration may result in an unacceptable high pulmonary embolic load.
g. Treatment of the arterial plug: This can be performed with a Fogarty balloon (over the wire or non-over
the wire) or a mechanical thrombectomy device (only one device, the Arrow-Trerotola percutaneous
thrombolytic device [PTD] is U.S. Food and Drug Administration [FDA]-approved for this, however).
(1) A Fogarty balloon should be advanced beyond the arterial anastomosis; then under fluoroscopy, the
balloon should be inflated and pulled back through the anastomosis. The plug is often firm and adherent
and may require several passes for adequate treatment.
(2) If using a mechanical thrombectomy device, it is passed beyond the arterial anastomosis and deployed
in the artery. The device is pulled back until it is seen to deform the arterial plug and then activated and
mechanical thrombectomy is performed, treating the arterial plug and the arterial limb. It is important that the
device not be deployed at the anastomosis, but rather in the artery, because inadvertent forward motion of
the basket during deployment might cause an arterial embolus.
(3) Regardless of the method used to break up the clot, aspiration of the fragmented thrombus through the
sheaths is performed.
(4) Diagnostic fistulography can be performed; however, in order to prevent arterial emboli, antegrade flow
in the graft must first be documented with a tiny injection of contrast. Any residual clot must be treated.
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3. Treatment of significant stenoses with angioplasty and/or stents and postprocedure fistulogram are
performed in the same manner as described earlier for failing grafts.
4. Access site hemostasis is obtained.
5. Chemical thrombolysis. Primary and secondary thrombolysis can be performed in the same manner as
described for dialysis fistulae.
1. Postoperative dialysis: The patient’s condition, dialysis schedule, and preoperative potassium levels will guide
the decision to dialyze on the day of the procedure. If emergent dialysis is needed, the patient may have to be
admitted for dialysis.
2. Distal pulses should be rechecked and documented.
3. For quality assurance (QA) purposes, ensure the graft is usable for dialysis.
Results
1. Outcomes for graft angioplasty when the graft has not undergone mechanical thrombectomy or
thrombolysis
a. Clinical success (ability to perform dialysis for at least one session): 86% to 98% (9,10)
b. Primary patency after angioplasty: 85%, 53%, 29% at 3, 6, and 12 months, respectively (10)
Radiology Books
c. Primary assisted patency of grafts after PTA: 56% to 86% and 37% to 63% at 6 and 12 months
depending on conventional versus cutting balloon (9)
2. Mechanical declotting or thrombolysis
a. Successful clearing of thrombus: 89% to 100% (10,11,12)
b. Primary patency after intervention: 40% to 63% at 3 months and in the vicinity of 20% to 26% at 12
months (10,13)
Complications and Management of Complications

As described for dialysis fistulae.
References
1. National Kidney Foundation. Clinical practice guidelines and clinical practice recommendations: 2006.
Updates on hemodialysis adequacy, peritoneal dialysis adequacy and vascular access.
http://www2.kidney.org/professionals/KDOQI/guideline_upHD_PD_VA/va_guide2.htm. Accessed November
3, 2015.
2. Ayus JC, Sheikh-Hamad D. Silent infection in clotted hemodialysis access grafts. J Am Soc Nephrol .
1998;9:1314-1317.
3. Foering K, Chittams JL, Trerotola SO. Percutaneous transluminal angioplasty balloon inflation with
syringes: who needs an inflator? J Vasc Interv Radiol . 2009;20(5):629-633.
4. Quinn SF, Schuman ES, Demlow TA, et al. Percutaneous transluminal angioplasty versus endovascular
stent placement in the treatment of venous stenoses in patients undergoing hemodialysis: intermediate
results. J Vasc Interv Radiol . 1995;6:851-855.
5. Gray RJ, Horton KM, Dolmatch BL, et al. Use of Wallstents for hemodialysis accessrelated venous
stenoses and occlusions untreatable with balloon angioplasty. Radiolog y. 1995;195:479-484.
6. Haskal ZJ, Trerotola S, Dolmatch B, et al. Stent graft versus balloon angioplasty for failing dialysis-access
grafts. N Engl J Med. 2010;362:494-503.
7. Trerotola SO, Ponce P, Stavropoulos SW, et al. Physical examination versus normalized pressure ratio for
predicting outcomes of hemodialysis access interventions. J Vasc Interv Radiol . 2003;14:1387-1394.
8. Wang DS, Chu LF, Olson SE, et al. Comparative evaluation of noninvasive compression adjuncts for
hemostasis in percutaneous arterial, venous, and arteriovenous dialysis access procedures. J Vasc Interv
Radiol . 2008;19:72-79.
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9. Saleh HM, Gabr AK, Tawfik MM, et al. Prospective, randomized study of cutting balloon angioplasty
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versus conventional balloon angioplasty for the treatment of hemodialysis access stenoses. J Vasc Surg.
2014;60(3):735-740.
10. Turmel-Rodriques L, Pengloan J, Baudin S, et al. Treatment of stenosis and thrombosis in haemodialysis
fistulas and grafts by interventional radiology. Nephrol Dial Transplant. 2000:15;2029-2036.
11. Beathard GA, Welch BR, Maidment HJ. Mechanical thrombolysis for the treatment of thrombosed
hemodialysis access grafts. Radiology. 1996;200:711-716.
12. Uflacker R, Rajagopalan PR, Vujic I, et al. Treatment of thrombosed dialysis access grafts: randomized
trial of surgical thrombectomy versus mechanical thrombectomy with the Amplatz device. J Vasc Interv
Radiol . 1996;7(2):185-192.
13. Turmel-Rodriques L, Pengloan J, Bourquelot P. Interventional radiology in hemodialysis fistulae and

grafts: a multidisciplinary approach. Cardiovasc Intervent Radiol . 2002;25(1):3-16.
Radiology Books
33
Dialysis Catheter Management
D. Thor Johnson
Thomas M. Vesely
According to the 2006 National Kidney Foundation Guidelines for Vascular Access (Kidney Disease Outcomes
Quality Initiative [NKF-KDOQI]), an arteriovenous fistula should be created 6 months prior to requirement for
renal replacement therapy (1). Arteriovenous fistulas have lower costs, longer durability, and fewer complications
when compared to prosthetic grafts and central venous catheters. Despite these national recommendations,
nearly 80% of patients will initiate hemodialysis treatment through a central venous catheter and 25% of patients
continue hemodialysis via central venous catheter (2).
Hemodialysis catheters can be categorized by duration of use (acute or chronic catheters) and method of
insertion (tunneled or nontunneled catheters); tunneled catheters are appropriate for most clinical situations.
Nontunneled, temporary catheters are used primarily for hospitalized patients without an existing functional
access.
Central venous catheters do have several advantages when compared to arteriovenous fistulae and prosthetic
grafts. These include simplicity of insertion, immediate utility, access without needle cannulation, and ease of
replacement and removal. For these reasons, tunneled and less-often nontunneled hemodialysis catheters
continue to play an important role in renal replacement therapy.
Indications
1. A patient with urgent need of renal replacement therapy who does not have a functional hemodialysis
fistula or graft
2. Patients with stage 5 chronic kidney disease (CKD5) who require acute hemodialysis treatment but do
not have usable hemodialysis access
a. Long-term (tunneled) catheters should be used in conjunction with a plan for permanent vascular access
or peritoneal dialysis catheter placement, while awaiting placement or maturation of an arteriovenous fistula
or prosthetic graft.
b. There are few indications for use of a tunneled central venous catheter as a permanent vascular access
including patients with cardiac failure who cannot tolerate a left-to-right shunt, upper extremity vascular
anomalies or
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disease precluding placement of a graft or fistula, and patients with diffuse dermatologic conditions that
would complicate surgical placement or recurrent needle cannulation of fistula.
c. A tunneled hemodialysis catheter may also be the most appropriate access for patients with a limited
lifespan (i.e., malignancy).
3. Patients with a failed arteriovenous fistula or prosthetic graft who are awaiting surgical revision or
creation of a new vascular access
4. Patients who have exhausted all surgical options for an arteriovenous fistula or graft placement
5. Patients with a dysfunctional or infected peritoneal dialysis catheter
6. Patients without renal failure who have metabolic disturbances, uncorrectable without hemodialysis,
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undergoing plasmapheresis, or stem cell harvest
Contraindications
Absolute
1. Sepsis is an absolute contraindication to placement of a tunneled hemodialysis catheter. A nontunneled
catheter can be placed temporarily in patients who require hemodialysis.
2. Uncorrectable coagulopathy. A nontunneled catheter placed with ultrasound guidance to minimize
punctures and prevent complications may be indicated.
Relative
1. Coagulopathy. Patients with abnormal coagulation parameters or low platelet counts should be
appropriately corrected prior to access placement. Uremia also causes platelet dysfunction that can result in
bleeding, which may require therapy such as desmopressin acetate (DDAVP) administration.
2. Electrolyte abnormalities. Uremic patients may have hyperkalemia and cardiac irritability, so
measurement of serum potassium is recommended for patients with clinical signs or symptoms of acute
renal failure. Elevated potassium can induce arrhythmias manifested by peaked T-waves, flattened P-
waves, prolonged QRS, and cardiac irritability that render patients susceptible to arrhythmias. All patients
with hyperkalemia, particularly acute hyperkalemia should be assessed by electrocardiogram (ECG), and
measures should be taken to decrease serum potassium. Interventions include oral Kayexalate (sodium
polystyrene sulfonate), intravenous (IV) insulin and glucose, and inhaled albuterol.
3. Orthopnea. Patients with congestive heart failure, pulmonary edema, or sleep apnea may not be able to
maintain a supine position during an interventional procedure. Optimization of oxygenation and judicious
administration of sedation is required. A lower extremity temporary or tunneled catheter can be considered
because patients are not required to be entirely supine in femoral or saphenous vein placement.
Basic Considerations
1. A focused assessment of the patient’s current and recent medical history should be performed including:
a. Primary diagnosis and relevant medical history
b. Knowledge of prior central venous access procedures and complications
c. Drug allergies including contrast agents
2. Informed consent should be obtained and documented.
3. Light or moderate sedation is often administered for catheter insertion procedures, and qualified personnel
and physiologic monitoring equipment are required. The patient should be fasting (nil per os [NPO]) as per
hospital policy for
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sedation. Typically, solid food should be restricted for 6 hours and clear liquids for 2 hours prior to the
procedure.
4. Preprocedural laboratory studies include an international normalized ratio (INR) for all patients, an activated
partial thromboplastin time (APTT) for patients receiving heparin, and a platelet count only in patients with
specific risk factors. Patient’s coagulation profile should be corrected to an INR <1.5 and a platelet count
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>50,000 per μL. Clopidogrel should be withheld for 5 days before the procedure. An 81-mg aspirin antiplatelet
therapy does not require discontinuation.
Exchange or removal of a tunneled hemodialysis catheter is considered low risk for bleeding, and preprocedural
coagulation testing should be limited to patients with known bleeding disorders, significant liver disease, and
anticoagulated patients (3).
5. Preprocedural administration of systemic antibiotics has not been shown to decrease the incidence of
postprocedural catheter-related infections (4).
Selection of Catheter Insertion Site

1. The preferred site for insertion of a tunneled or nontunneled hemodialysis catheter is the right internal jugular
vein. If the right internal jugular vein is not usable, then the left internal jugular vein or right external jugular vein
should be used.
2. A tunneled catheter should not be inserted on the same side as a maturing hemodialysis fistula or graft. Use
the contralateral jugular vein for catheter insertion.
3. Avoid use of the subclavian (sole venous outflow of ipsilateral upper extremity) vein due to risk of central
venous stenosis and thrombosis. The subclavian vein should only be used when surgical options in the
ipsilateral upper extremity have been exhausted.
4. Femoral vein catheters
a. Catheters inserted into the femoral vein have a higher incidence of infection and shorter patency times (5).
b. Placement of a nontunneled hemodialysis catheter into the femoral vein limits mobility and should only be
used for bed-bound patients.
c. Due to the risk of iliac vein stenosis, the femoral vein should only be used after thoughtful discussion with
transplant surgery.
Evaluation of Catheter Insertion Site

1. The neck, chest wall, and shoulder region should be examined for:
a. Skin conditions or scars that may interfere with catheter insertion or creation of a subcutaneous tunnel
b. Presence of superficial collateral veins indicative of central venous obstruction
c. Presence of an implanted transvenous pacemaker or cardioverter-defibrillator devices
2. The location and patency of the access vein should be evaluated with ultrasound prior to draping the patient.
Images should be recorded to satisfy compliance requirements.
Selection of a Hemodialysis Catheter

1. Criteria for selecting a hemodialysis catheter
a. Duration of use: Nontunneled hemodialysis catheters are for short-term use (<1 week). They rarely may be
appropriate in patients not stable enough to undergo sedation or any prolonged medical procedure. A tunneled
(cuffed) hemodialysis catheter should be used when the anticipated duration of hemodialysis treatment is >1
week.
b. Catheter performance: Numerous publications have reported the performance characteristics of various
designs and features of hemodialysis catheters, but the majority of catheters provide equivalent rates of blood
flow.
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There is currently no proven advantage of one catheter design over another. Catheter choice should be based
on local experience, goals for use, and cost.
The NKF-KDOQI guidelines recommend the use of tunneled catheters that can sustain a blood flow rate of >350
mL per minute. Longer catheters (i.e., femoral) have increased resistance to blood flow but a rate of 300 mL per
minute should be achievable, although not all patients require these flow rates for adequate hemodialysis
treatment (6).
c. Catheter length: The distal tip of a hemodialysis catheter should not be cut or trimmed. Hemodialysis catheters
are available in several standard lengths, and correct catheter length is determined by patient size and the site of
insertion. Depending on the manufacturer, the length of the catheter may be measured from tip to cuff or from tip
to hub. Rigid nontunneled catheters should have the distal tip positioned at the junction of the superior vena
cava and right atrium. Soft tunneled catheters can be positioned with the catheter tip in the right atrium. Femoral
catheters should be positioned with the catheter tip in the inferior vena cava (IVC), cephalad to the confluence of
the common iliac veins.
d. Catheter construction: Acute catheters are often constructed of rigid material and have a tapered tip to allow
rapid percutaneous insertion using standard Seldinger technique. Newer generation catheters are constructed of
softer material and often have a removable plastic cannula that can be used to stiffen the catheter during
insertion. Acute hemodialysis catheters do not have a retention cuff and should not be placed in a subcutaneous
tunnel. Nontunneled catheters are available in straight or curved configurations to optimize positioning and
comfort at different insertion sites.
Tunneled or “chronic” catheters have a Dacron retention cuff that is positioned within the subcutaneous tunnel
and becomes incorporated into the surrounding tissue. The Dacron cuff provides stabilization of the catheter and
creates a fibrotic barrier to prevent bacterial migration. Tunneled hemodialysis catheters are constructed of soft
polyurethane material and are typically inserted through a peel-away introducer sheath.
Procedure
Insertion of Tunneled Hemodialysis Catheter
1. All hemodialysis catheter procedures require implementation of maximal sterile technique (1).
2. When using the internal or external jugular vein, the patient’s neck should be slightly extended and the
head should be rotated to provide optimal exposure of the insertion site.
3. Moderate sedation with IV fentanyl and midazolam is typically administered for insertion of a tunneled
hemodialysis catheter. Sedation or analgesics are not often needed for catheter exchange or catheter
removal procedures.
4. The vein entry site is identified and the surrounding tissue infiltrated with 5 to 10 mL of 1% to 2%
buffered lidocaine with or without epinephrine. The vein entry site should be located near the base of the
neck to avoid kinking of the catheter. A short dermatotomy is cut at this site prior to puncture to avoid skin
tags. A Kelly forceps can be utilized to spread the tissue in the dermatotomy down to the vein safely.
5. Ultrasound guidance should be used when inserting the needle into the vein because this decreases
complications (7).
a. A needle guide may improve accuracy of vein puncture.
b. Applying gentle aspiration when advancing the needle can help to determine when the needle tip has
entered the vein if visualization is suboptimal.
c. From a lateral approach to venipuncture, the needle should be visible in its entirety.
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6. Use of a 21-gauge needle and microintroducer set decreases the likelihood of puncture-related
complications.
7. The 21-gauge needle is inserted into the vein, and the 0.18-in. guidewire is advanced into the central
vein. The dilator from the microintroducer set is then advanced into the vein.
8. The 0.018-in. guidewire can be used to measure the intravascular distance from the venotomy site to the
right atrium.
9. The tip of a hemodialysis catheter cannot be cut and therefore the location of the catheter exit site and
the length of the subcutaneous tunnel are determined by the length of the hemodialysis catheter. The
premeasured microwire is held against the hemodialysis catheter to determine the intravascular length and
the external length of the catheter. The external length of the catheter determines the length of the
subcutaneous tunnel and the position of the catheter exit site on the chest wall.
10. The catheter exit site and course of the subcutaneous tunnel is determined and infiltrated with local
anesthetic with a minimal number of skin punctures.
11. A short (<1 cm) skin nick is made at the catheter exit site on the chest wall.
12. The tunneler is attached to the hemodialysis catheter. The tunneler is inserted into the catheter exit site
and advanced to the venotomy site to create the subcutaneous tunnel. The Dacron cuff is positioned at
least 1 cm within the subcutaneous tunnel.
13. Both lumens of the hemodialysis catheter should be filled and locked with sterile saline. Verify that both
pinch clamps are closed and the catheter can be capped as well.
14. Under fluoroscopic observation, a stiff 0.038-in. guidewire is inserted through the dilator at the
venotomy site. The tip of the guidewire should be positioned stably within the IVC.
15. The venotomy site is sequentially dilated. The tip of each dilator is advanced only 2 to 3 cm into the
central vein.
16. A peel-away introducer sheath is smoothly advanced through the venotomy site and into the central vein
with continuous fluoroscopic guidance. The guidewire and inner dilator are simultaneously removed from
the peel-away sheath; the sheath is immediately pinched if not equipped with a hemostatic valve to prevent
air embolism. Alternatively, Trendelenburg position can be utilized to increase intrathoracic pressure. The
hemodialysis catheter is quickly inserted through the introducer sheath.
17. The catheter tip should be adjusted to the level of the caval-atrial junction or into the right atrium to
ensure optimal blood flow (1). Correct orientation of the catheter tip is important for optimal performance.
The distal end hole of the arterial (red) lumen should be oriented medially, and the distal end hole of the
venous (blue) lumen should be oriented laterally.
18. The hemodialysis catheter should be held firmly at the venotomy site as the peel-away introducer
sheath is split, retracted, and removed.
19. Fluoroscopy is used to determine the position of the catheter tip and to check for kinks along the course
of the catheter.
a. The catheter can be adjusted by applying gentle traction.
b. If needed, a stiff guidewire can be inserted into one lumen to provide support for advancement of the
catheter or to remove kinks at the venotomy site.
c. A fluoroscopic image of final catheter tip position should be recorded.
20. The venotomy site at the base of the neck is closed using a 4-0 absorbable suture. A sterile adhesive
(Dermabond) can also be used at the venotomy site. Th e suture wings of the catheter are secured to the
patient’s skin using 3-0 nonabsorbable or absorbable suture. If needed, the catheter exit site can be
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cinched around the catheter with a vertical mattress stitch using an absorbable suture.
21. A sterile occlusive dressing should be applied to cover the catheter exit site. If there is bleeding at the
site, a gauze dressing can be placed under occlusive dressing.
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Removal of a Tunneled Hemodialysis Catheter
As a general guideline, the catheter can be removed when the fistula or graft has been successfully used
for three hemodialysis sessions, the peritoneal dialysis catheter is functional, or the patient no longer
requires hemodialysis.
1. The retention sutures should be cut and removed to allow more thorough cleaning of the catheter and
catheter exit site.
2. A sterile drape is placed over the catheter exit site. The catheter hub and Luer connectors are excluded
from the sterile field.
3. The catheter exit site is infiltrated with buffered lidocaine (1% to 2%). If the Dacron cuff is deep within the
subcutaneous tunnel, then additional lidocaine should be infiltrated around the cuff.
4. The ease of catheter removal is dependent on the length of time that the catheter has been in place and
the location of the Dacron cuff within the subcutaneous tunnel. The Dacron cuff becomes incorporated into
the surrounding tissue within 2 to 3 weeks after catheter insertion. If the Dacron cuff is not fully incorporated
into the tissue, then the catheter can be removed by applying firm traction. However, if the catheter has
been in place for several months, then the Dacron cuff will be fully incorporated into the subcutaneous
tunnel and is often more difficult to remove. The tip of a Kelly forceps can be inserted into the catheter exit
site and used to bluntly dissect and separate the Dacron cuff from the surrounding fibrous tissue. If the
Dacron cuff is located deep within the subcutaneous tunnel, then a separate incision adjacent to the
catheter cuff may be needed to improve exposure for blunt dissection of the Dacron cuff.
5. As the catheter is withdrawn from the catheter exit site, the operating physician should apply manual
compression on the subcutaneous tunnel to prevent air embolism and bleeding from the exit site. The tip of
the hemodialysis catheter should be inspected to verify that it is intact and has been completely removed.
6. Manual compression should be applied to the subcutaneous tunnel. Ideally, there will be some
backbleeding to occlude the subcutaneous tunnel and prevent air embolism. Manual compression is
gradually released when there is no further bleeding from the catheter exit site. If the catheter is removed
and there is no backbleeding to occlude the subcutaneous tunnel, then sterile ointment can be applied to
the catheter exit site to create an airtight seal and prevent air embolism.
7. A sterile gauze bandage and occlusive dressing should be applied to cover the catheter exit site.
Exchange of a Tunneled Hemodialysis Catheter
Exchange of a tunneled hemodialysis catheter may be necessary for improving catheter function, changing
position of the catheter tip, replacing a damaged catheter, or removing a colonized or infected catheter (8).
1. The heparin lock solution should be aspirated from both lumens of the hemodialysis catheter and
discarded. If the catheter is locked with 4% sodium citrate, then aspiration is unnecessary. The retention
sutures should be cut and removed to allow more thorough cleaning of the catheter and catheter exit site.
The length of the catheter is typically printed on the catheter hub, and this length should be considered
when selecting a replacement catheter.
2. Conscious sedation or preprocedural antibiotics are not typically necessary for catheter exchange
procedures.
3. Fluoroscopy should be performed to assess the course and tip position of the existing hemodialysis
catheter and appropriate length of catheter.
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4. Both lumens of the new catheter should be filled and locked with sterile saline. Verify that both pinch
clamps are closed.
5. The catheter exit site is infiltrated with buffered lidocaine (1% to 2%). If the Dacron cuff is deep within the
subcutaneous tunnel, then additional lidocaine should be infiltrated around the cuff. After the Dacron cuff
has been separated
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from the fibrotic tissue, the hemodialysis catheter should be moveable within the subcutaneous tunnel.
6. Under fluoroscopic observation, a 0.035-in. guidewire is advanced through the venous (blue) lumen and
the tip of the guidewire is positioned across the atrium in the IVC. If there is a difficult angle at the venotomy
site, a stiff nonkinking hydrophilic wire through each lumen can be utilized. While maintaining a stable
position of the guidewire, the hemodialysis catheter is withdrawn from the subcutaneous tunnel. As the
catheter is withdrawn from the catheter exit site, an assistant should apply manual compression on the
subcutaneous tunnel to prevent air embolism and bleeding from the exit site. The tip of the hemodialysis
catheter should be inspected to verify that it is intact and has been completely removed.
7. If desired, a venogram can be performed before insertion of the new replacement hemodialysis catheter.
The assistant should maintain manual compression of the subcutaneous tunnel to prevent air embolism or
bleeding from the exit site.
a. A 5 Fr. angiographic catheter is advanced over the guidewire and positioned within the central vein. The
guidewire is removed and x-ray contrast is injected to opacify the central veins and identify stenoses,
thrombus, or a fibrin sheath. After completion of the venogram, the guidewire is reinserted and positioned
within the IVC, and the 5 Fr. angiographic catheter is removed.
b. In certain situations, it is advantageous to maintain the intravascular position of the guidewire during the
central venogram. A 6 Fr. guiding catheter can be inserted over the guidewire and positioned within the
central vein. While maintaining the position of the guidewire the inner dilator of the guiding catheter is
removed. A sidearm adaptor (Tuohy Borst) is inserted over the guidewire and tightened onto the Luer
connection of the guiding catheter. Contrast is injected through the sidearm adaptor and venogram is
performed. After completion of the venogram, the guiding catheter is removed while maintaining position of
the guidewire.
8. The new hemodialysis catheter is inserted onto the guidewire. The majority of currently available
tunneled hemodialysis catheters have a side hole in the distal tip of the venous (blue) lumen to allow
“weaving” of the guidewire through the distal tips of both the venous and arterial lumens. Weaving the
guidewire provides increased stability of the catheter tips. The guidewire exits the catheter through the
arterial Luer connector where the operator grasps the guidewire and then advances the new hemodialysis
catheter into the subcutaneous tunnel. The guidewire is held in a stable fixed position as the new
hemodialysis catheter is advanced through the subcutaneous tunnel, into the central vein, and positioned
with the distal tip in the right atrium.
a. After removal of an infected or colonized catheter, it may be beneficial to wipe the guidewire with alcohol-
soaked gauze prior to insertion of the new hemodialysis catheter.
9. The catheter is secured and dressed in a similar manner to a newly placed line.
1. The position of the catheter tip is typically verified during the procedure using fluoroscopy. If fluoroscopic
documentation of the final catheter tip position is not possible, then a chest radiograph should be obtained.
2. Patients are given written instructions that describe proper care of the catheter and catheter exit site. Signs
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and symptoms of complications such as erythema, edema, drainage, and fever are discussed. The patient is
given emergency contact information.
3. Some patients may need oral analgesics for pain management during the 24- to 48-hour period following
insertion of a tunneled catheter.
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4. The day-to-day management of a tunneled hemodialysis catheter is the responsibility of the nursing staff at
the patient’s hemodialysis treatment center.
5. Each patient should have a plan for a permanent vascular access. Utilization of the hemodialysis catheter
should be monitored, and length of use should be minimized.
Results
1. Successful placement of a hemodialysis catheter is dependent on the skill and experience of the
operating physician, but with use of ultrasound, fluoroscopy, and venographic imaging, a catheter can be
inserted into nearly every patient. Alternative routes of venous access (translumbar, transhepatic) can be
used for patients with occluded central veins.
2. Functional success of a hemodialysis catheter is of critical importance. The National Kidney Foundation’s
NKF-KDOQI Guidelines for Vascular Access recommend catheter blood flow rates >350 mL per minute, but
a sustained highblood flow rate may not be achievable in all patients (1). Suboptimal catheter flow rates can
provide acceptable dialysis kinetics for some patients (6).
Nontunneled hemodialysis catheters have lower rates of blood flow, a higher incidence of infection, and
shortened survival when compared to tunneled hemodialysis catheters (9,10). For this reason, tunneled
catheters should be used preferentially.
3. Long-term survival of a tunneled hemodialysis catheter may be dependent on the location of the catheter
insertion site. Catheters inserted from the left internal jugular vein have a tendency to kink and exhibit
greater movement of the catheter tip when compared to catheters inserted from the right internal jugular
vein. In one study, the median survival of catheters inserted through the right internal jugular vein (633
days) was significantly longer when compared to catheters inserted through the left internal jugular vein
(430 days) or femoral vein (116 days) (5). However, other studies have failed to demonstrate any
differences between right-sided and left-sided catheters (7).
Complications/Management
Catheter-related complications are a significant cause of hospitalization, morbidity, and mortality in hemodialysis-
dependent patients, and as such, excellent technique in management of these catheters is vital (9,10).
Complications should be classified as major (requiring escalation of care) and minor (no escalation of care), and
these should be reported consistently (11).
1. Procedural related complications from a jugular or subclavian approach—overall threshold should not exceed
4% by Society Interventional Radiology (SIR) guidelines (12,13). Actual complication rates in practice are as
follows: a. Malposition (3%)
Most cases will require repositioning or exchange over a wire.
b. Pneumothorax (1% to 3%)
This can be treated with a chest tube if symptomatic.
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c. Hemothorax (1%)
This should be evaluated with contrast-enhanced computed tomography (CT) preferably with arterial phase and
delayed imaging. If active extravasation is present, open surgical or endovascular intervention is indicated. A
chest tube may be indicated in some cases.
d. Hematoma (1% to 3%)
Generally best treated with direct pressure and possibly reversal of anticoagulation. Other interventions are
generally unnecessary.
e. Venous perforation (0.5% to 1%)
Many instances of perforation are immediately fatal (usually from hemopericardium); however, nonfatal
perforation generally requires immediate surgical
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intervention. In some cases, a large balloon (e.g., a Coda balloon) can be inflated to temporize a venous
perforation until surgical intervention is possible.
f. Air embolism (<1%)
The patient should be placed left lateral decubitus on 100% oxygen to prevent embolism through a patent
foramen ovale, which is present in 25% of population (14). Cardiac defibrillator pads should be placed, and
appropriate personnel should be summoned to prepare for the possibility of cardiac arrest. Operators should also
prepare for potential intubation in the event of severe respiratory insufficiency.
g. Wound dehiscence (1%)
This generally requires removal of existing catheter and placement of catheter at a second site if infection is
suspected. Antibiotics are necessary in the majority of cases.
h. Procedure-induced sepsis (1% to 3%)
If the central catheter is tunneled, it should be removed and a temporary catheter should be placed. Sepsis
otherwise should be treated as in any other case, with appropriate escalation of clinical care depending on
degree of severity.
i. Catheter-associated venous thrombosis (4%)
Catheter-associated venous thrombosis requires removal of the existing catheter and replacement at a second
site with anticoagulation in most cases.
2. Long-term complications of hemodialysis catheters
a. Catheter occlusion related to venous thrombosis or fibrin sheath (8%) In many cases, it is preferable to
maintain access at the site of occluded catheter. This can sometimes be maintained by removal over a wire with
venoplasty and potentially stent placement if the venous access is salvageable. Simple catheter exchange is not
successful in the majority of cases because removing the catheter does not necessarily disrupt the fibrin sheath
that is present in chronic catheter placement.
b. Venous stenosis
Venous stenosis is a nearly inevitable consequence of long-term indwelling venous catheterization. This can be
treated with angioplasty and stent placement.
c. Infection
Catheter-related infection is a significant cause of hospitalization, morbidity, and mortality in hemodialysis-
dependent patients. A broad range of infection rates have been reported, and the differences may be due to
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variations in clinical practice. In the largest meta-analysis currently available, the infection rate for nontunneled
catheters ranges from 4.8 to 6.6 infections per 1,000 days and for tunneled catheters ranges from 1.2 to 1.6
infections per 1,000 days (15). Staphylococcal organisms, both Staphylococcus epidermidis and
Staphylococcus aureus, are responsible for the majority of catheter-related infections. In some cases, the
catheter should be removed and either the patient should have a line holiday with concurrent antibiotic treatment
or a temporary catheter should be placed until blood cultures are clear.
References
1. National Kidney Foundation’s Kidney Disease Outcomes Quality Initiative. Clinical practice guidelines for
vascular access. Am J Kidney Dis. 2006;48:S176-S273.
2. United States Renal Data System. United States Renal Data System 2012 annual data review.
http://usrds.org. Accessed November 11, 2015.
3. Patel IJ, Davidson JC, Nikolic B, et al. Consensus guidelines for periprocedural management of
2012;23(6):727-736.
4. O’Grady NP, Alexander M, Burns LA, et al. Guidelines for the prevention of intravascular catheter-related
infections. Am J Infect Control . 2011;39(4 suppl 1):S1-S34.
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5. Fry AC, Stratton J, Farrington K, et al. Factors affecting long-term survival of tunneled haemodialysis
catheters—a prospective audit of 812 tunneled catheters. Nephrol Dial Transplant. 2008;23:275-281.
6. Moist LM, Hemmelgarn BR, Lok CE. Relationship between blood flow in central venous catheters and
hemodialysis adequacy. Clin J Am Soc Nephrol . 2006;1:965-971.
7. Dexheimer Neto FL, Teixeira C, Oliveira RP. Ultrasound-guided central venous catheterization: what is the
evidence? Rev Bras Ter Intensiva. 2011;23(2):217-221.
8. Guttmann DM, Trerotola SO, Clark TW, et al. Malfunctioning and infected tunneled infusion catheters:
over-the-wire catheter exchange versus catheter removal and replacement. J Vasc Interv Radiol .
2011;22(5):642-646.
9. Wasse H. Catheter-related mortality among ESRD patients. Semin Dial . 2008;21: 547-549.
10. Wasse H, Speckman RA, Frankenfield DL, et al. Predictors of delayed transition from central venous
catheter use to permanent vascular access among ESRD patients. Am J Kidney Dis. 2007;49:276-283.
11. Silberzweig JE, Sacks D, Khorsandi AS, et al. Reporting standards for central venous access. J Vasc
12. Dariushnia SR, Wallace MJ, Siddigi NH, et al. Quality improvement guidelines for central venous access.
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J Vasc Interv Radiol . 2010;21(7):976-981.
13. Vesely TM, Beathard G, Ash S, et al. Classification of complications associated with hemodialysis
vascular access procedures. A position statement from the American Society of Diagnostic and Interventional
Nephrology. J Vasc Access. 2008;9(1):12-19.
14. Hara H, Virmani R, Ladich E, et al. Patent foramen ovale: current pathology, pathophysiology, and clinical
status. J Am Coll Cardiol . 2005;46(9):1768-1776.
15. Maki DG, Kluger DM, Crnich CJ. The risk of bloodstream infection in adults with different intravascular
devices: a systematic review of 200 published prospective studies. Mayo Clin Proc. 2006;81(9):1159-1171.
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34
Pulmonary Emboli: Arteriography, Thrombectomy, and
Thrombolysis
Ugur Bozlar
Ulku C. Turba
Krishna Kandarpa
Klaus D. Hagspiel
Pulmonary Arteriography
Advances in less invasive radiographic modalities, such as computed tomography pulmonary angiography
(CTPA), alone or in combination with strategies that include clinical risk scores, venous ultrasound, and
measuring serum D-dimer levels, have significantly diminished the diagnostic role of catheter-directed
arteriography in pulmonary embolism (PE). Nevertheless, arteriography remains useful for adjudication (relative
to other modalities) of suspected PE, vascular anatomic diagnosis, and treatment (1).
Indications
Diagnosis of Pulmonary Embolism
1. To reconcile a discrepancy between the clinical index of suspicion for a pulmonary embolism (PE) and
the results of a CTPA or assessment of its probability on radionuclide ventilation-perfusion ([V with dot
above]/[Q with dot above]) scan
2. Prior to inferior vena cava (IVC) filter placement, especially if extremity deep vein thrombosis (DVT) or
renal vein thrombosis could not be documented as a source for emboli (1)
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Treatment of Pulmonary Embolism
1. Anticipated interventional management (thrombolysis and/or inferior vena cava filter [IVCF] placement)
2. Knowledge or suspicion of massive PE, as a cause for hemodynamic compromise in a patient who may
benefit from emergency percutaneous or surgical thromboembolectomy. Echocardiography and intravenous
(IV) digital subtraction angiography (DSA) may have a diagnostic role in this setting.
3. Evaluation of chronic thromboembolic disease in the central pulmonary arteries causing pulmonary
hypertension in patients who are potential candidates for thromboembolectomy (2)
4. Measurement of right ventricular end-diastolic pressure to assess and minimize risk of bleeding when
anticoagulation therapy is contemplated
5. Nondiagnostic or negative CTPA despite very high clinical suspicion of PE, particularly when treatment
without definite evidence carries a high risk (i.e., when unequivocal establishment or exclusion of the
diagnosis of PE is required)
Diagnosis of Cardiopulmonary Anatomy
1. Evaluation and transcatheter treatment of congenital abnormalities
2. Evaluation and treatment of arteriovenous malformations/fistulas (acquired and congenital), and
hemoptysis with negative bronchial arteriogram
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Relative Contraindications
Cardiac evaluation may be needed in certain cases.
1. Coexistent severe pulmonary hypertension (see item 3 under “Procedure”). Noninvasive assessment of
pulmonary pressure by echocardiography or crosssectional imaging methods may be helpful.
2. Left bundle-branch block on electrocardiogram (ECG). Place a transvenous pacing catheter to break
complete heart block in the event that catheterinduced right bundle branch block (RBBB) occurs.
3. Ventricular irritability. Perform a pulmonary arteriogram only if the risk of anticoagulant or thrombolytic
therapy is high because objective evidence of PE is mandatory prior to therapy.
4. Other concomitant life-threatening illness (e.g., congestive heart failure) should be evaluated and treated
appropriately before the patient is subjected to pulmonary arteriography.
5. Severe prior documented contrast reaction
1. Perform standard preprocedure preparation for angiography (see Chapter 1). Determine if there is an
indication for filter placement, if the study is positive.
2. Check cardiopulmonary status (history, physical exam, diagnostic tests, etc.). Although individual clinical and
laboratory parameters may be nonspecific, a combination of significant manifestations suggestive of PE is
valuable in selecting patients for further diagnostic studies (3).
3. Review: Chest x-ray, ECG (rule out acute myocardial infarction, assess arrhythmias, and evaluate right
ventricular strain [P-pulmonale, right-axis deviation, RBBB, or S1Q3T3]), [V with dot above]/[Q with dot above]
scan, CTPA, venous studies, right-sided hemodynamics (if available from previously placed Swan-Ganz
catheter); pulmonary capillary wedge pressure is useful in ruling out left-sided heart failure. Right ventricular end-
diastolic pressure (RVEDP) and pulmonary artery (PA) pressure can determine the degree of pulmonary
hypertension and serve to guide a tailored pulmonary angiogram.
4. Check serum electrolytes, blood urea nitrogen (BUN)/creatinine (Cr), coagulation parameters (partial
thromboplastin time [PTT] <1.5 times control; prothrombin time [PT] <15 seconds), and platelets (>75,000 per
μL).
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5. Treat arrhythmias with prophylactic lidocaine 50 to 100 mg IV; obtain cardiology consult, if needed.
6. Study must be done with continuous cardiac monitoring in all patients. Prepare to place and activate
transvenous pacer if the patient has a left bundle-branch block.
Procedure
1. Venous access: generally into the femoral veins (preferably right) if there is no evidence of iliofemoral
thrombosis. Up to 14% of patients undergoing pulmonary angiography can have thrombus in the IVC (1). If
in doubt, perform limited ultrasound of the femoral veins prior to puncture and perform venography of pelvis
and/or IVC.
2. Catheters
a. Femoral access: Placement of a venous sheath is recommended but not necessary. Preshaped catheters
(e.g., Grollman) or pigtail catheters maneuvered with a tip-deflecting wire may be used. Higher profile
catheters are used for cut-film angiography. New lower profile catheters may be used, along with DSA, as
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long as contrast can be safely injected at the required flow rates.
b. Jugular or brachial access: Preshaped low-profile catheters are available that enter the PA without a
need for tip-deflecting wire.
c. A Swan-Ganz catheter, for pressure measurements and possible subselective balloon occlusion
injections, is suitable for introduction through all access sites. This catheter also may be exchanged over a
wire for another diagnostic catheter, if necessary. This should be done expeditiously to avoid inducing
arrhythmias when the endocardium is exposed to the bare guidewire.
3. Measure right heart pressures. About 30% of patients undergoing pulmonary angiography can have
pulmonary hypertension (3). RVEDP must be 20 mm Hg or less (and PA systolic pressure ≤70 mm Hg); if
these pressures are greater, the mortality associated with pulmonary angiography is increased
(approximately 2% to 3%) (1). In such a case, use subselective injection (with balloon occlusion technique,
if necessary) and nonionic contrast media. These safety measures are even more important if cardiac
output is determined to be below normal (1).
4. Arteriographic technique
a. Contrast agents: Nonionic low osmolality contrast agents are preferred and considered mandatory for
patients with elevated right-sided pressures. Lowcost alternative agents are acceptable when right-sided
pressures are normal.
b. Injection rates
(1) Selective arteriography: right or left PA, 30 to 50 mL at 15 to 25 mL per second
(2) Subselective arteriography: Use the CTPA or [V with dot above]/[Q with dot above] scan as guide,
especially for patients with pulmonary hypertension (RVEDP ≥20 mm Hg). Adjust the rate and volume
according to the size of the region to be studied (5 to 15 mL per second for 2 seconds; with balloon
occlusion, no more than 5 to 7 mL total volume followed by rapid deflation of the balloon) (1).
(3) Main PA injection: 70 mL at 35 mL per second, for the anatomic evaluation of central pulmonary arteries
with congenital anomalies
(4) Injection rates may be modified with DSA imaging and/or dilution of contrast agents.
c. Imaging: Use CTPA or [V with dot above]/[Q with dot above] scan as a road map; the demonstration of a
single clot is usually all that is necessary to make a therapeutic decision.
(1) Always obtain images with maximal inspiration.
(2) Begin with ipsilateral anterior and posterior oblique (45- to 60-degree) views of the side most suspected
on prior studies. Additional anteroposterior (AP) views may be needed on occasion.
(3) Superselective magnified peripheral views may be needed, especially if prior studies suggest small
peripheral emboli, which can be missed when injections are made centrally (4,5). Of the 76% of Prospective
Investigation of Pulmonary Embolism Diagnosis (PIOPED) I patients
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who had only a single clot on the angiogram, 25% of these clots were located peripherally (1). Moreover,
very high false-positive rate (75%) for subsegmental embolus detection with CTPA in PIOPED II patients
emphasizes the role of superselective magnified peripheral views if a definitive result is required (6).
(4) If a balloon catheter is used for subselective injection, make sure that it is never totally occlusive during
the injections and is rapidly deflated after the injection.
(5) In the event of suspected procedure-related cardiac trauma, stop the procedure immediately. Evaluate
the patient for cardiac tamponade (pressures, ECG, emergency echocardiogram on the table). Proceed
only after the suspicion has been ruled out.
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(6) If a patient with PE on arteriography has a contraindication to anticoagulant or thrombolytic therapy,
percutaneous placement of an IVC filter should be considered before the catheter is removed.
1. Standard postangiographic management
2. Cardiac trauma: Discontinue anticoagulants; admit to cardiac intensive care unit.
3. Arrhythmias: For frequent premature ventricular contractions (PVCs): bolus lidocaine 50 mg IV via catheter into
right atrium (RA) (total up to 100 mg).
Results
Sensitivity
If done promptly and carefully, the sensitivity of pulmonary arteriography is extremely high. A negative
angiogram of high quality essentially rules out a clinically significant PE (1). The false-negative rate of
angiography (determined by follow-up surveillance) was 0.6% in the PIOPED I study (1).
Results of PIOPED II study showed a need for additional testing when multidetector computed tomographic
angiography (CTA)-computed tomographic venography (CTV) results were negative in the setting of high
clinical index of suspicion, given the 18% false-negative rate of CTPA-CTV in such cases (up to 40% false
negatives for CTPA only). However, the additional testing is not necessarily limited to pulmonary DSA but
could include lower extremity venous ultrasound and [V with dot above]/[Q with dot above] scanning (6). A
normal lower extremity imaging study (either by CTV or ultrasound) is needed before anticoagulation is
withheld in patients with suspected PE, but normal pulmonary CTA.
Specificity
Using the rigid criteria of unequivocal intraluminal filling defect or abrupt arterial cutoff, the specificity of
pulmonary arteriography is almost 100% (1).
Image Interpretation
1. A pulmonary angiogram performed 24 hours after the acute episode may be falsely normal because
fragmentation and partial lysis can occur within this period.
2. The only definitive angiographic sign of PE is unequivocal evidence of an intraluminal filling defect or
abrupt arterial cutoff, or both.
3. Careful interpretation of pulmonary angiograms in the setting of chronic pulmonary thromboembolic
disease is essential for determining operability. The angiographic findings of chronic PE can be subtle; they
include pouching defects, webs, mural irregularities, luminal narrowing, and occlusion.
4. The [V with dot above]/[Q with dot above] scan still has diagnostic value particularly in patients with renal
insufficiency or other contraindications to iodinated contrast agents, even in patients with chronic
obstructive pulmonary disease (COPD). Although most scans show
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intermediate probability, high- or low-probability and normal scans are able to diagnose or exclude PE to the
degree that further evaluation is not necessary.
5. Since the publication of the PIOPED I study in 1990, many advances including the introduction of serum
D-dimer level measurements (a byproduct of fibrinolysis that is sensitive for venous thromboembolic
disease), pretest clinical scoring models (e.g., the Wells model*) (3), and high-resolution ultrasound
scanners almost obviated the need to use x-ray for diagnosis of PE in some settings; for instance, the
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diagnosis of massive PE required only two positives out of three assessments (high clinical probability,
echocardiography, ultrasound) (7). Similarly, PE can now be only excluded by a negative serum D-dimer
test in patients with clinically low or moderate scores (4). However, a negative D-dimer level is not helpful
for avoiding further diagnostic imaging tests in the setting of high clinical probability score because more
than 15% of those were shown to have PE (5).
6. Peripheral (subsegmental) PE cases missed by DSA or CTPA may be clinically unimportant, given
existing clinical outcome data (8).
7. The remaining and unchallenged significant advantage of DSA over the other modalities is the ability to
simultaneously diagnose and treat PE in the setting of massive PE and right ventricular dysfunction (9).
8. In patients with severe contrast allergy or renal dysfunction with suspected PE, D-dimer testing, venous
ultrasound, and [V with dot above]/[Q with dot above] scan are recommended instead of pulmonary
arteriography or CTPA/CTV (7).
9. In pregnant patients, preference varies between CTPA and [V with dot above]/[Q with dot above]
scanning (and rarely magnetic resonance imaging [MRI]), but in many centers, dedicated low-dose CTPA
protocols are preferred due to the fact that they result in lower fetal-absorbed radiation doses than
dedicated [V with dot above]/[Q with dot above] scan protocols (10).
Complications
1. Life-threatening complications are very rare and typically secondary to acute cor pulmonale in patients
with preexisting severe pulmonary hypertension and failing right ventricle (RV). Specific reported
complications include RV perforation, endocardial stain, significant symptomatic arrhythmia,
cardiopulmonary arrest, contrast reactions, and renal dysfunction.
2. Among 209 DSA procedures performed in the PIOPED II study, the minor complication rate was 0.5%,
whereas no major complications were observed, indicating the relatively safe nature of pulmonary
arteriography using modern equipment, contrast agents, and techniques.
Pulmonary Thrombolysis and Thrombectomy

The standard treatment for patients diagnosed with acute PE is anticoagulation in hemodynamically stable
patients (11). Systemic thrombolytic treatment (TT) of patients with PE has been available for more than 30
years, and its risks and benefits have been assessed in several (randomized and nonrandomized) trials. The
information regarding catheter-directed thrombolysis and/or catheter thrombectomy is more limited consisting
mainly of uncontrolled case series, case reports, and nonrandomized comparisons between patients receiving a
new treatment and historical controls. The American College of Chest Physicians recommends catheter-directed
pulmonary thrombolysis especially in patients who are not
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candidates for IV thrombolysis or high-risk patients (12). Endovascular techniques discussed in this chapter are
mostly off-label applications of approved devices due to rapid change in technology. Interventional radiologists
and clinicians should be familiar with such minimally invasive, possibly lifesaving, procedures.
Thrombolysis
Systemic Venous Thrombolysis
A review of the literature shows that systemic (IV) thrombolysis for PE reduces the clot burden rapidly and
improves the hemodynamic parameters in patients with shock or systemic hypoperfusion (11). One randomized
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trial showed a survival advantage and one demonstrated a significant favorable change in RV systolic pressure
and improved exercise tolerance in patients receiving heparin plus fibrinolysis versus heparin alone (13).
However, with the possible exception of those with right ventricular dysfunction (13), thrombolysis has not been
proven to reduce mortality or risk of recurrent PE in patients who are hemodynamically stable (11). The risk of
systemic thrombolysis increases with age and body mass index. Risk stratification for early and aggressive
intervention should be performed with the following clinical findings increasing a PE patient’s risk: arterial
hypotension (<90 mm Hg systolic or drop of >40 mm Hg); echocardiographic findings of right ventricular
afterload, right heart strain, and/or pulmonary hypertension; diagnosis of precapillary pulmonary hypertension
(mean pulmonary arterial pressure [PAP] >20 mm Hg, in the presence of normal PAP occlusion pressures);
widened arterial-alveolar O2 gradient >50 mm Hg; and clinically severe PE with a contraindication to
anticoagulation or thrombolytic therapy.
Indications
1. Patients presenting with shock, hypotension, or other signs of systemic hypoperfusion caused by acute
massive PE
2. Patients with submassive PE with right ventricular dysfunction but otherwise stable (controversial)
(11,13)
Contraindications
1. Active internal bleeding and/or disseminated intravascular coagulation
2. History of cerebrovascular accident (within 3 months)
3. Recent (within 3 months) intracranial or intraspinal surgery or trauma
4. Intracranial neoplasm, arteriovenous malformation, or aneurysm
5. Known bleeding diathesis and/or absolute contraindication to anticoagulation
6. Severe, uncontrolled hypertension (relative contraindication)
Procedure
The thrombolytic agents are given through a peripheral IV line. The currently approved protocols are shown
in Table 34.1. During the TT, no heparin is given and vascular access procedures and blood draws should
be avoided. Because all protocols are short and the doses are weight related, the testing for fibrinogen,
fibrin split products, and thrombin time is not mandatory. Peripheral IV application was found to be as
effective as direct application into the main PA (11). A 14-day window for its effective administration has
been demonstrated. Streptokinase, urokinase (UK), and tissue plasminogen activator (TPA) (Alteplase) are
approved by the U.S. Food and Drug Administration (FDA) for treatment of massive PE.
Dosing Protocols
The protocols for systemic thrombolytic agents are shown in Table 34.1.
Results
1. Faster thrombus resolution than the treatment with heparin alone
2. Significantly reduces pulmonary hypertension within 2 hours of treatment
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Table 34.1 Thrombolytic Agents Approved for Systemic IV Treatment of PE
Drug Regimena Approval Date
Streptokinase 250,000 U over 30 min followed by 100,000 U/h for 24 h 1977
UK 4,400 U/kg over 10 min followed by 4,400 U/kg/h for 12-24 h 1978
rt-PA 100 mg over 2 h 1990
UK, urokinase; rt-PA, recombinant tissue plasminogen activator.
aAll agents are administered as a continuous peripheral IV infusion.
3. Significantly improves pulmonary perfusion (scans) within 24 hours

4. Appears to reduce mortality in patients from shock because of massive PE (11)
5. For patients with acute PE and right ventricular dysfunction on echocardiography, but normal systemic
arterial pressure, it may reduce mortality and incidence of recurrent PR (controversial) (11).
6. Does not reduce mortality or recurrent PE in hemodynamically stable patients
7. Possibly improves hemodynamic response to exercise (11,13)
Complications
The major risks of thrombolytic therapy are hemorrhage and stroke. A review of the literature reported a
major hemorrhage rate of 11.9% and a risk of intracranial hemorrhage of 1.2% to 1.9% (11).
Catheter-Directed Thrombolysis
Treating PE with intrathrombus delivery of the thrombolytic drug attempts to maximize the thrombolytic effects
and minimize the required dose of the drug and its complications. This assumption is based on the experience
with catheter-directed thrombolysis of peripheral arterial bypass grafts and dialysis fistulas, supported by results
from animal models of PE showing superiority of the direct intrathrombus delivery (11). Thus, most of the
procedural management principles of peripheral arterial thrombolytic therapy apply here. The required dose of
the thrombolytic agent is approximately 10% to 20% of that required for systemic thrombolysis. In the setting of
hemodynamic shock from massive PE, catheter-directed intervention is a potentially lifesaving treatment for
patients who have not responded to or cannot tolerate systemic thrombolysis or when emergency surgical
embolectomy is unavailable or contraindicated (11,13).
Dosing Protocols, Results, and Complications

Several smaller series have been published to date. A study involving 13 postoperative patients using UK
and heparin (loading dose of 2,200 IU UK per kg body weight, followed by continuous infusion of 2,200 IU
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UK/kg/hour for up to 24 hours, with the concomitant use of heparin at a rate of 500 units per hour) reported
98% clot lysis with no deaths or bleeding complications. Other studies reported similar results with regard to
clot lysis and clinical improvement (11). A series of eight patients treated with rt-PA (10 mg bolus, followed
by continuous infusion at 10 mg per hour for 4 to 9 hours up to a maximum dose of 100 mg) had a higher
incidence of bleeding complications (minor bleeding in all eight, major hemorrhage requiring transfusion in
three of eight, no hemorrhagic stroke). This dose was rather high, and currently, most centers use a bolus
dose of 2 to 5 mg TPA followed by a continuous infusion of 0.5 to 2.0 mg per hour per catheter for less than
24 hours (bolus dose of 2 to 5 mg per catheter). A new drug, Monteplase (Cleactor, Eisai Medical
Research, Tokyo, Japan), a modified rt-PA, was approved in
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2005 in Japan. Postmarketing studies completed in 2008 showed promising results at the approved dose
(13,750 to 27,500 IU per kg) in patients with acute PE and hemodynamic instability (14).
Thrombectomy
Surgical Embolectomy
Surgical embolectomy is the last therapeutic resort for patients with fulminant PE who are too unstable, have
failed, or have contraindications to thrombolytic therapy. Surgical embolectomy has a high morbidity and mortality
in these severely ill patients. A meta-analysis of 597 patients undergoing pulmonary embolectomy with heart-lung
bypass showed an overall mortality of 29%, which increased to 58% in patients requiring cardiopulmonary
resuscitation (11). These numbers are lower in dedicated centers; however, surgical embolectomy is not widely
available, and only a few centers have extensive experience with this procedure (11). This was the impetus for
the development of percutaneous devices for the treatment of massive PE.
Percutaneous Embolectomy/Clot Fragmentation

Catheter-based systems can be divided into devices that remove thrombus and those that fragment existing
thrombus into smaller pieces. Fragmentation decreases pulmonary vascular resistance and improves pulmonary
perfusion. The explanation is that a central occlusive thrombus prevents perfusion of a larger portion of the distal
bed than do the smaller fragments dispersed peripherally. Such dispersion by mechanical clot fragmentation also
increases the efficacy of subsequent catheter-directed thrombolysis by increasing the thrombus surface area for
enzymatic action (11).
Indications—Mechanical Clot Fragmentation

Patients presenting with shock, hypotension, or other signs of systemic hypoperfusion caused by PE who are not
candidates for either pharmacologic thrombolysis or open surgical embolectomy are candidates for mechanical
clot fragmentation.
Devices and Results—Mechanical Embolectomy and Clot Fragmentation

None of the following devices are FDA-approved for the treatment of pulmonary emboli, with the exception of the
Greenfield pulmonary embolectomy catheter.
1. Fragmentation thrombectomy: These devices fragment emboli but do not remove them.
a. Arrow-Trerotola PTD (percutaneous thrombolytic device) (Arrow International, Reading, PA): This 5 Fr.
catheter or 7 Fr. over the wire systems, with a 9-mm rotating basket, are used with an external drive unit. It has
been shown to effectively fragment unilateral massive PE in dogs with moderate intimal injury but without arterial
disruption. Clinically successful use has been reported in massive PE.
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b. Pigtail fragmentation device (William Cook Europe, Bjaeverskov, Denmark): This is a manually rotatable
special 5 Fr. pigtail catheter. It was used in 10 patients with acute massive PE; in 8 cases, additional
pharmacologic thrombolysis was performed. Fragmentation was reported to be successful in 7 of the 10 cases,
resulting in a significant decrease of the shock index and mean PAP and without procedure-related
complications. Overall mortality was 20% (11).
c. Rotational bidirectional thrombectomy (ROBOT): A standard 5 Fr. pigtail catheter for angiography is used as
a fragmentation device and is bidirectionally rotated manually. In one study, systolic PAP following ROBOT
normalized earlier than it did following thrombolysis alone and without associated mortality.
2. Rheolytic thrombectomy: These devices fragment and remove emboli but produce hemolysis. A meta-analysis
showed that the use of these devices in
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conjunction with thrombolytic agents in 49 patients was clinically successful in 45 (92%) without an instance of
ventricular or PA perforation (15).
a. Helix Clot Buster thrombectomy device (Microvena, White Bear Lake, MN): an 8 Fr. catheter with enclosed
impeller, driven at 150,000 rpm by an air turbine, and is introduced through a 10 Fr. guiding catheter. Its use has
been reported in several patients. Associated hemolysis and hemoptysis have been observed.
b. AngioJet Rapid thrombectomy system (Possis Medical, Minneapolis, MN): a high-velocity saline solution jet
from a dedicated drive unit creates a strong Venturi effect at the tip of a 5 Fr. or 6 Fr. catheter. This results in the
fragmentation of the thrombus into microparticles that are aspirated through the catheter. Successful use of this
device has been reported (16). However, the AngioJet device has also been associated with bradyarrhythmias
and deaths when used in the pulmonary arteries and carries an FDA black box warning for that use.
c. Cordis Hydrolyser hydrodynamic thrombectomy catheter (Cordis, Miami Lakes, FL): This 7 Fr. device
employs a standard contrast medium-power injector to create a saline solution jet at its tip. This over-the-wire
system also works on the Venturi principle. Its successful use has been described in number of patients.
d. Oasis Thrombectomy System (Boston Scientific, Natick, MA): an over-the-wire system that uses a standard
angiographic power injector to create a saline solution jet and Venturi effect. Its use has not been described in
PE.
e. The EndoWave System (EKOS, Bothell, WA) uses a low-intensity, highfrequency ultrasound that has no lytic
effect on its own; however, when delivered concomitantly with thrombolytic infusion, it separates fibrin strands
without fragmentation of thrombus. Safe and successful use in massive PE without associated major
complications and a mean infusion time around 24 hours time has been described.
3. Aspiration thrombectomy: removal of thrombi through mechanical aspiration, with suction, requires multiple
catheter passes
a. Greenfield pulmonary embolectomy catheter (Boston Scientific, Natick, MA): Approved by the FDA for
removal of PE, this 10 Fr. catheter has 5-mm or 7-mm suction cups and is steerable with a large control handle.
A large sheath (16 Fr. for 5-mm suction cup) or venotomy is required. Greenfield et al. used the device in 46
patients over 22 years. Emboli were extracted in 76% of the patients, with a 30-day survival of 70% (11).
b. Guiding catheter technique: An 8 Fr. or 9 Fr. coronary guiding catheter (without side holes) is placed through
a 10 Fr. sheath (tip left in PA). Aspiration is performed with a 60-mL syringe, removing small amounts of clot
during each pass. It remains a simple and cost-effective means for thrombus removal .
c. Suction catheter technique: A 14 Fr. custom-made suction catheter is introduced through a 16 Fr. sheath, with
suction performed using a 30-mL syringe (three cases reported; all were technically successful).
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d. ASPIREX (Straub Medical, Wangs, Switzerland): This is an 8 Fr. mechanical thrombus aspiration device
specifically designed for the treatment of PE. The catheter is introduced over a 0.018-in. guidewire to the site of
proximal occlusion of the PA or with the greatest thrombus content, where it is activated. A motor rotates a spiral
located in the body of the catheter at 40,000 rpm, creating negative pressure—thrombus is macerated and
removed through an L-shape aspiration system. The device has been successfully used in PE.
e. AngioVac (AngioDynamics, Albany, NY) is a large-bore (22 Fr.) cannula approved by the FDA for venous
drainage during extracorporeal bypass for up to 6 hours to include removal of fresh, soft thrombi, or emboli. This
device requires a clinical perfusionist and general anesthesia in addition to an interventional radiology team. Its
successful use in massive PE has been reported (17).
4. Clot fragmentation with shaped-diagnostic catheters and percutaneous transluminal angioplasty balloon
catheters: Many techniques have been described.
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Fragmentation has been performed using guidewires, catheters (pigtail, multipurpose, guiding), and
percutaneous transluminal angioplasty (PTA) angioplasty balloon catheters (8- to 20-mm diameter) (11). In most
series, mechanical fragmentation was combined with catheter-directed or systemic pharmacologic thrombolysis.
Flow studies have shown that thrombolytic agents administered via a catheter positioned near the embolus are
rapidly washed out into adjacent patent branches. However, after embolus fragmentation, the agents were
carried completely into the formerly occluded artery. Most published series describe successful outcomes for the
catheter techniques, with improved hemodynamics and blood oxygenation, and decreased PAPs and morbidity
(11).
5. Stent-recanalization of pulmonary arteries: Use of stents after failed percutaneous catheter fragmentation with
Dotter retrieval baskets (Cook Medical, Bloomington, IN) and catheter-directed thrombolysis with UK has been
described. Because of progressive right ventricular decompensation, two 10 × 42-mm Wallstents (Boston
Scientific, Natick, MA) were deployed in the left and right interlobar arteries. The patient recovered fully at 8
months followup (11).
Conclusions
1. The decision to proceed with percutaneous treatment of PE should be made by a multidisciplinary team
consisting of interventional radiologists, internists, cardiologists, and cardiothoracic surgeons who are
familiar with all available treatment options for PE.
2. Physicians performing these procedures should be familiar with the possible complications and their
treatment.
a. Refractory or recurrent cardiopulmonary arrest
b. Hemoptysis and pulmonary edema as a result of reperfusion
c. Hemolysis (with rheolytic devices)
d. Hemorrhage (with lytic enzymes and anticoagulants)
3. If possible, cardiac surgical backup should be arranged prior to intervention.
4. Currently, there is no single technique that is clearly established as superior, and therefore, the choice of
techniques depends on the individual physician’s and institutional experience. A combination of mechanical
clot fragmentation/thrombectomy and catheter-directed thrombolysis is usually the most successful strategy.
5. The placement of an IVC filter prior to or after percutaneous treatment of massive PE should be
considered.
6. An analysis of 2,392 patients, with acute PE and hemodynamic compromise, from the International
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Cooperative Pulmonary Embolism Registry (ICOPER) showed that certain comorbidities were associated
with massive rather than nonmassive PE, including congestive heart failure, reduced left ventricular systolic
ejection fraction, and renal dysfunction. One-third of the massive PE patients had no echocardiographic
right ventricular hypokinesis; at least in some of these patients, cardiopulmonary comorbidities may have
been the main cause of hemodynamic instability (18). Massive PE was associated more often with right
heart thrombi (10%) than nonmassive PE (4%). This finding is important because echocardiographic
evidence of right heart thrombi, in the setting of massive PE, may change the treatment plan from
thrombolysis to surgical embolectomy (19).
References
1. Bozlar U, Kandarpa K, Hagspiel KD. Pulmonary angiography. In: Kandarpa K, Machan L, eds. Handbook
of Interventional Radiologic Procedures. 4th ed. Baltimore, MD: Lippincott Williams & Wilkins, 2011:109-117.
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2. Klok FA, Mos IC, van Kralingen KW, et al. Chronic pulmonary embolism and pulmonary hypertension.
Semin Respir Crit Care Med. 2012;33(2):199-204.
3. Wells PS, Anderson DR, Rodger M, et al. Excluding pulmonary embolism at the bedside without diagnostic
imaging: management of patients with suspected pulmonary embolism presenting to the emergency
department by using a simple clinical model and d-dimer. Ann Intern Med. 2001;135:98-107.
4. van Belle A, Büller HR, Huisman MV, et al. Effectiveness of managing suspected pulmonary embolism
using an algorithm combining clinical probability, D-dimer testing, and computed tomography. JAMA.
2006;11;295(2):172-179.
5. Stein PD, Hull RD, Patel KC, et al. D-dimer for the exclusion of acute venous thrombosis and pulmonary
embolism: a systematic review. Ann Intern Med. 2004;140:589-602.
6. Stein PD, Woodard PK, Weg JG, et al. Diagnostic pathways in acute pulmonary embolism:
recommendations of the PIOPED II Investigators. Radiology. 2007;242:15-21.
7. Wells PS, Rodger M. Diagnosis of pulmonary embolism: when is imaging needed? Clin Chest Med.
2003;24:13-28.
8. Goodman LR, Lipchik RJ, Kuzo RS, et al. Subsequent pulmonary embolism: risk after a negative helical
CT pulmonary angiogram—prospective comparison with scintigraphy. Radiology. 2000;215:535-542.
9. Murphy JM, Mulvihill N, Mulcahy D, et al. Percutaneous catheter and guidewire fragmentation with local
administration of recombinant tissue plasminogen activator as a treatment for massive pulmonary embolism.
Eur Radiol . 1999;9:959-964.
10. Winer-Muram HT, Boone JM, Brown HL, et al. Pulmonary embolism in pregnant patients: fetal radiation
dose with helical CT. Radiology. 2002;224:487-492.
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11. Turba UC, Hagspiel KD. The treatment of pulmonary arterial thrombectomy and thrombolysis. In:
Kandarpa K, Machan L, eds. Handbook of Interventional Radiologic Procedures. 4th ed. Baltimore, MD:
Lippincott, Williams & Wilkins; 2011:338-345.
12. Guyatt GH, Eikelboom JW, Gould MK, et al. Approach to outcome measurement in the prevention of
thrombosis in surgical and medical patients: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed:
American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2
suppl):e185S-e194S.
13. Jaff MR, McMurtry MS, Archer SL, et al. Management of massive and submassive pulmonary embolism,
iliofemoral deep vein thrombosis, and chronic thromboembolic pulmonary hypertension: a scientific statement
from the American Heart Association. Circulation. 2011;123(16):1788-1830.
14. Yamamoto T, Murai K, Tokita Y, et al. Thrombolysis with a novel modified tissue-type plasminogen
activator, monteplase, combined with catheter-based treatment for major pulmonary embolism. Circ J.
2009;73(1):106-110.
15. Skaf E, Beemath A, Siddiqui T, et al. Catheter-tip embolectomy in the management of acute massive
pulmonary embolism. Am J Cardiol . 2007;99(3):415-420.
16. Kuo WT, van den Bosch MA, Hofmann LV, et al. Catheter-directed embolectomy, fragmentation, and
thrombolysis for the treatment of massive pulmonary embolism after failure of systemic thrombolysis. Chest.
2008;134(2):250-254.
17. Pasha AK, Elder MD, Khurram D, et al. Successful management of acute massive pulmonary embolism
using Angiovac suction catheter technique in a hemodynamically unstable patient. Cardiovasc Revasc Med.
2014;15(4):240-243.
18. Goldhaber SZ, Visani L, De Rosa M. Acute pulmonary embolism: clinical outcomes in the International
Cooperative Pulmonary Embolism Registry (ICOPER). Lancet. 1999;353(9162):1386-1389.
19. Kucher N, Rossi E, De Rosa M, et al. Massive pulmonary embolism. Circulation. 2006;113:577-582.
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35
Vena Caval Filters
Jennifer P. Montgomery
John A. Kaufman
Vena caval filters are intravascular devices designed to prevent pulmonary embolus (PE) by trapping venous
emboli. Filters do not prevent formation of new thrombus or promote lysis of a preexisting thrombus or embolus.
The primary means of therapy and prophylaxis for deep vein thrombosis (DVT) and PE are pharmacologic.
There are three basic classes of filters.
1. Permanent filters (1): Permanent vena caval filters are devices that are not intended to be repositioned or
retrieved in any manner. These are the oldest class of filters, for which the greatest experience is available.
2. Optional filters (2): Permanent filters designed to provide the option of percutaneous removal or conversion to
a nonfiltration state. The two basic types are retrievable and convertible filters.
a. Retrievable filters can be retrieved or repositioned percutaneously during a device-specific time window, after
which they become incorporated into the wall of the vena cava and function as permanent devices.
Manufacturers suggest ranges of retrievability on the basis of clinical trials and experience. In practice, filter
retrievability over time may vary. Retrieval of these devices is not required.
b. Convertible filters can be altered structurally after implantation so that they no longer function as filters. After
conversion, some or all of the filter remains in the patient's vena cava without providing protection from PE.
When conversion is by mechanical means and requires a percutaneous procedure, conversion of these devices
is not required, and the filter can provide permanent protection. When conversion is built into the filter so that it
occurs without intervention, then the duration of protection from PE is limited.
3. Temporary filters: Temporary filters are not designed for permanent placement. They frequently have no
means for fixation to the wall of the vena cava but are supported in place by tethers or catheters that either exit
the skin at the insertion site or are buried subcutaneously. Removal of these devices is required, and permanent
filtration requires removal of the temporary filter and placement of a different device. The indications for
placement of temporary filters are the same as those for retrievable filters.
Filter Placement
Indications
There remains significant controversy over the appropriate indications for vena cava filter placement among
professional medical societies (3).
All Filter Types (4,5)
1. Accepted: documented venous thromboembolism (VTE) with one or more of the following:
a. A contraindication to anticoagulation, such as active gastrointestinal bleeding (not fecal occult blood),
recent intracranial hemorrhage or surgery, or vascular brain metastases
b. Documented progression or recurrence of VTE while anticoagulated. The definition of adequate
anticoagulation is vague but is generally accepted to be 7 days of continuous anticoagulation at therapeutic
levels.
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c. A complication of anticoagulation, such as massive retroperitoneal hemorrhage, that requires interruption
or termination of anticoagulation
d. Inability to achieve or maintain therapeutic anticoagulation
2. Relative (evaluated on a case-by-case basis): documented VTE with one or more of the following:
a. Limited cardiac or pulmonary reserve
b. Massive, life-threatening PE that requires thrombolysis or surgical thrombectomy
c. Chronic PE treated with thromboendarterectomy
d. Poor patient compliance with medications, risk of falling, or inability to monitor patient during treatment
e. Large residual burden of thrombus (iliocaval DVT), or “widow-maker” thrombus in the inferior vena cava
(IVC)
f. Recurrent PE in spite of the presence of an existing vena caval filter (failure to trap embolus or
propagation of thrombus above filter) and continued contraindication to anticoagulation
g. Difficulty establishing therapeutic anticoagulation
h. Thrombolysis for iliocaval DVT
3. Prophylactic (evaluated on a case-by-case basis): no documented current VTE and
a. Severe trauma patient with high risk of VTE
b. Closed head injury
c. Spinal cord injury
d. Multiple long bone or pelvic fractures
e. High-risk patients with prolonged immobilization
Optional and Temporary Filters
1. The same as earlier, when the anticipated need for the filter will end within the time limitations during
which the filter can be retrieved or converted
Contraindications
1. There are rare circumstances in which filters may be contraindicated, including
a. Total thrombosis of the vena cava
b. Inability to gain access to the vena cava
c. Inability to image during filter placement
d. Vena cava too small or too big to safely accommodate the filter
e. Confirmed allergy to a component of the filter
2. The following are not contraindications to filter placement:
a. Ongoing sepsis (this includes septic thrombophlebitis, as the alternative to trapping infected thrombus in
a filter is septic pulmonary emboli)
b. Inability to document residual peripheral thrombus in a patient with PE and an indication for a vena caval
filter. Current imaging techniques cannot fully evaluate all possible sources of emboli, and more thrombus
may form and embolize after imaging.
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1. The consent for the placement of a vena caval filter should include all of the usual risks associated with
percutaneous venous procedures as well as the following (6):
a. A 5% risk of recurrent PE
b. A 1% to 5% risk of symptomatic caval thrombosis (remember, the intended purpose of the filter is to trap
emboli)
c. A 1% risk of filter embolization, fracture, or malposition
d. A less than 1% risk of symptomatic perforation by a filter element
e. A 2% risk of pericardial tamponade for superior vena cava (SVC) filter placement (7)
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2. Laboratory values (suggested guidelines—actual practice may vary)
a. International normalized ratio (INR) less than 3.0
b. Platelets greater than 30,000 per μL
3. Patient evaluation
a. Review available cross-sectional imaging of the abdomen for anomalous caval anatomy and presence of
thrombus.
b. Assess for availability of venous access (trauma patients with neck braces, pelvic fixation, existing lines, etc.).
Procedure
1. Obtain access: Depending on the device, vena caval filters can be placed from the femoral veins, jugular
veins (internal or external), subclavian veins, upper extremity veins, or directly into the IVC via translumbar
approach. The preferred approach for filters that are not delivered over a guidewire, or filters of a relatively
rigid design, is either the right femoral or internal jugular vein.
2. Imaging: High-quality imaging during filter placement maximizes the likelihood of a satisfactory outcome.
Poor imaging increases the chance of filter misplacement and other operator errors (8,9).
a. Goals of preplacement imaging
(1) Define vena caval and renal vein anatomy.
(a) Duplicated IVC occurs in less than 1% and usually joins at the left renal vein but may also join lower.
(b) Left-sided IVC is found in less than 1%.
(c) Circumaortic left renal vein is found in 3% to 4%. The lower component of the venous ring lies behind
the aorta and drains into the IVC lower than a normal left renal vein.
(d) Retroaortic left renal vein occurs in 2% to 3% and usually drains into the IVC below the right renal vein
or rarely at the confluence of the iliac veins.
(e) Duplicated SVC occurs in less than 1%.
(f) Persistent left SVC drains into the coronary sinus.
(g) Left-sided SVC is extremely rare.
(2) Determine vena cava size.
(a) “Mega cava” (IVC diameter >28 mm) is found in less than 1%.
(b) IVC is typically oval in cross-section, so measurements in a single plane may not be accurate.
(3) Confirm patency of vena cava.
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b. Cavography
(1) For IVC, position pigtail catheter (4 Fr. or greater) at the confluence of the iliac veins.
(2) For SVC, inject from a brachiocephalic vein.
(3) Use the same positioning and field of view that you will employ during filter deployment.
(4) Injection rate for iodinated contrast of 15 to 20 mL per second for 2 seconds.
(5) CO2 cavography can be performed by hand injection of 30 to 40 mL CO2.
(6) Digital subtraction angiography (DSA) filming at four to six frames per second during suspended
respiration in anterior-posterior projection. Additional projections can be obtained as needed. Contralateral
iliac vein and renal veins are identified as inflow of unopacified blood or by reflux of contrast into orifices of
veins.
(7) If veins cannot be localized, try the following: Reposition pigtail catheter closer to the expected location
of tributaries, increase rate and volume of contrast injection, use oblique projection, selectively catheterize
veins, and use intravascular ultrasound (IVUS).
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c. IVUS: Alone or combined with fluoroscopy, IVUS has been used to guide filter placement in patients with
contraindications to all contrast agents and for bedside filter placement (10,11).
(1) Femoral venous access is easiest when using IVUS alone (avoids negotiating right atrium).
(a) Tandem ipsilateral access, bilateral access, or single puncture technique
(2) Determine IVC dimensions and patency.
(3) Localize renal vein orifices and iliac confluence.
(a) Note locations with fluoroscopy or measure distance from venous access site.
(4) Deploy filter using fluoroscopic guidance if available.
(5) Obtain plain radiograph of the abdomen to document filter position and configuration.
d. Ultrasound: Transabdominal ultrasound (US) guidance for filter placement, usually at the bedside, has
been described (12). This approach has the following limitations:
(1) The IVC is not always easy to image in large patients or those with significant bowel gas.
(2) Variant renal vein and IVC anatomy may not be detected.
3. Filter placement
a. General principles
(1) After performing initial imaging, note the level of renal vein inflow and confluence of iliac veins relative to
a fixed reference point, such as the spine, a radiopaque ruler, or other measuring device.
(2) Without moving the patient or image intensifier, exchange the pigtail catheter over a guidewire for a filter
delivery sheath.
(3) Watch under fluoroscopy when reinserting the guidewire into the pigtail catheter to avoid malpositioning
the guidewire (e.g., into an ascending lumbar vein).
(4) Serial dilation may be required for large delivery systems. A stiff or exchange-length guidewire may be
needed for difficult or remote access.
(5) Position the delivery sheath central to the desired final location of the filter when placing from the
femoral approach; position the sheath peripheral to the renal veins when access is from above.
(6) Leave guidewire in place for over-the-wire delivery system (make sure to use a straight guidewire to
avoid guidewire entanglement in the filter post deployment).
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(7) Before advancing filter into delivery sheath, inspect to be sure that the orientation of the filter is correct
for the chosen access route (i.e., femoral or jugular).
(8) Advance filter to the end of the delivery sheath. Reposition the entire system so that the constrained
filter is in the desired location.
(9) Deploy the filter per manufacturer's instructions.
(10) Withdraw the delivery sheath several centimeters below the filter when access is from the groin; leave
the sheath at the top of the filter when deployed from above.
(11) Repeat cavogram through the delivery sheath using the same injection and filming rate as described
earlier.
b. Filter location (Fig. 35.1)
(1) Normal IVC
(a) The top of a single-level cone-shaped filter should be just at or slightly above the lower edge of the
orifice of the lowest renal vein. This minimizes potential “dead space” above the filter should filter occlusion
occur.
(b) The top of a bi-level cone-shaped filter (a device with upper arms and lower legs) should be below the
orifice of the lowest renal vein to prevent prolapse of one of the arms into a renal vein.
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FIGURE 35.1 • Suggested VC filter placement locations for (A) a normal infrarenal IVC with no intraluminal
thrombus; (B) infrarenal IVC thrombus, not quite approaching renal veins and with adequate room for filter
legs to attach; (C) infrarenal and renal vein thrombus; (D) duplicated IVC—either two infrarenal filters (A) or
a single filter (B) in suprarenal segment; (E) retroaortic (low insertion) of a left renal vein ( A or B); (F)
circumaortic left renal vein; (G) left renal vein insertion at confluence of left iliac vein and IVC ( A or B); (H)
SVC placement to confine upper extremity emboli.
(c) Filters that are not cone-shaped should be placed below the renal vein orifices.
(d) All filters should be placed so that there is adequate wall contact between the stabilizing filter elements
and the IVC.
(e) When a filter is already present and does not contain thrombus and the indication is recurrent PE, a
second filter can be placed below the first if sufficient room is present. Otherwise, place a second filter
above the first (including suprarenal if necessary).
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(2) Thrombus in IVC
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(a) Thrombus does not extend to the renal veins: Place the filter as low as possible in the infrarenal IVC but
above thrombus, even if the body of the filter lies entirely within the intrarenal IVC. If there is little room for
infrarenal attachment of the filter, consider a cone-shaped device or a suprarenal placement.
(b) Thrombus extends to or originates from the renal veins: Place the filter in the suprarenal segment, either
just above the renal veins or in the intrahepatic IVC. Use a short filter (i.e., not Bird's Nest, as wires may
prolapse into the right atrium and cause arrhythmia).
(c) Thrombus extends above the existing filter: Place a second filter above thrombus, usually in the
suprarenal IVC.
(3) Duplicated IVC
(a) Place one filter in each IVC, just below the renal veins.
(b) Place a single suprarenal filter (13).
(c) If the second IVC is an accessory cava, in that it is small and communicates with the main IVC at the
levels of both the common iliac and renal veins, consider occluding the accessory cava with coils or a plug
and place one filter in the normal location in the main IVC (14).
(4) Circumaortic left renal vein
(a) Theoretical concern is embolization via the venous ring if the filter is placed between the two vein
orifices. If a large retroaortic ring is present, place the filter feet below the orifice of the retrocaval
component of the ring.
(b) Place the filter in a suprarenal location.
(5) Retroaortic left renal vein
(a) Place the filter below the orifice of the left renal vein if sufficient room exists.
(b) In case of a very low left renal vein orifice, place the filter with its apex at the level of the right renal vein.
(c) Place one filter in each common iliac vein.
(6) Mega cava
(a) The VenaTech LP (B. Braun Medical, Bethlehem, PA) is approved in Europe for IVC diameters up to 35
mm.
(b) Bird's Nest filter (Cook Medical Inc, Bloomington, IN) is approved for IVC diameters up to 40 mm.
(c) If neither (a) nor (b) are possible, place filters in each common iliac vein.
(7) Woman with current pregnancy: Suprarenal location minimizes fetal radiation exposure.
(8) Woman with upcoming planned pregnancy: Fetal wastage due to IVC filter or trauma to mother due to
compression of the filter by the uterus is theoretical but unsubstantiated concern. Theoretically, suprarenal
placement may minimize risks, but there are no data to support this.
(9) SVC (7)
(a) Use a short filter, ideally single-level cone-shaped without arms.
(b) The feet of the filter should be superior to the azygos vein if possible but still in the SVC.
(c) Avoid placing the filter apex in the right atrium.
(d) Placed too low in the SVC, filter elements can perforate into the pericardial space and possibly cause
hemopericardium and tamponade.
c. Problem solving during deployment
(1) Kinked sheath: This occurs most often with left-sided access, tortuous vessels, and filters not delivered
over a guidewire (15). Pushing the filter against a kink can result in perforation of the sheath and extrusion
of the filter.
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(a) Gently advance the filter and sheath as a unit 1 to 2 cm. This moves the kink central to the acute angle
in the vessel. Attempt to resume delivery.
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(b) If this fails, withdraw the filter and sheath as a unit just peripheral to the acute angulation. This may
allow the kink to straighten but frequently results in formation of a new kink.
(c) If this fails, withdraw the filter and sheath to the skin access site as a unit, leaving as much empty sheath
in the vessel as possible. Cut the sheath and insert a guidewire. Options at this point include
i. Inserting a new sheath that is large enough to accommodate the filter delivery sheath and long enough to
cross the point of kinking. Coaxially advance the filter and delivery sheath through the larger sheath, which
should provide the support necessary to prevent kinking.
ii. Changing to a more flexible filter design
(d) If this fails, abandon the access site and select a more direct alternate access if possible.
(2) Incompletely opened filter: manifests in different ways depending on the filter designs. For example,
with cone-shaped filters, as clustered or crossed legs (16,17).
(a) Usually of little clinical consequence, unless there is incomplete coverage of the IVC, the filter will not
function properly or the filter has been misplaced into a small branch.
(b) If any question, perform cavogram or other imaging.
i. Confirm location and stability of filter.
ii. Evaluate for thrombus.
(c) When intervention is warranted,
i. Ask patient to cough several times (this rarely works but is quick).
ii. Gently manipulate the filter with an angled catheter.
iii. For retrievable and temporary filters, remove andinsert fresh device.
iv. If permanent or convertible filter fails to open completely and migration is a concern, place a second filter
central to the first or consider reposition or removal of the unopened filter using a snare.
(3) Guidewire entrapment: A guidewire can become wedged between two filter elements during over-the-
wire filter placement or with J-tipped guidewires during central line placement. Some filter designs are more
prone than others (18).
(a) Do not pull hard on guidewire. This will only make entrapment more difficult to disengage or may
dislodge the filter.
(b) Advance a catheter over the guidewire to the point of entrapment. Push the guidewire and catheter as a
unit to disengage the guidewire.
(c) From opposite access, engage the caught guidewire with a pigtail or recurved catheter. Slide the
catheter to the point of entrapment and then pull gently. Use a tip deflecting wire to reinforce the curved
portion of the catheter.
(d) These maneuvers may result in caudal migration of the filter.
1. Permanent filters
a. Routine monitoring in immediate postprocedure period for venous access procedures
b. Alert patient and other caregivers to observe for limb edema, which may indicate caval thrombosis or DVT.
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c. Primary pharmacologic treatment or prophylaxis for VTE should commence at the first safe opportunity.
d. Regular abdominal films (every 3 to 5 years) to monitor filter position and integrity. Multiple projections are
helpful for identifying tilt, fracture, or limb migration.
2. Retrievable filters
a. The same as items a. through c. for permanent filters.
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b. These patients require tracking and routine follow-up evaluation to assess anticoagulation status and
continuing need for filter.
(1) Initial follow-up should occur at 1 month to assess appropriate conditions for retrieval (see following text) and
allow filter retrieval during the temporal window of retrievability.
(2) Primary physicians may require guidance regarding the timing of filter retrieval.
(3) The physician who placed the filter should perform the follow-up.
Results (6,19,20)
1. Successful deployment: 99%
2. Post-filter recurrent PE: 0.5% to 6%
Complications (6,19,20)
Concerns have been raised that retrievable filters may have a higher incidence of adverse events than
permanent filters (21).
1. Major procedural: less than 1%
2. Access site thrombosis (symptomatic): 2%
3. Caval thrombosis: 0.6% to 8%
4. Filter fracture: 2% to 10%
5. Filter migration (major): 1%
6. Filter infection: greatly less than 1%
7. IVC penetration/perforation (most asymptomatic): 0% to 86%
8. Thirty-day mortality due to filter: less than 1% (Note: Overall 30-day mortality rate of 17% is primarily due to
concurrent diseases.)
1. Suspected recurrent PE
a. Document PE with objective testing.
(1) No PE, stop.
b. If PE is found
(1) Image filter
(a) Contrast-enhanced CT for filter location, position in IVC, and patency
(b) Abdominal plain film with US or magnetic resonance imaging (MRI) (nonferromagnetic filters) is
alternative for patients who should avoid iodinated contrast agents.
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c. If patient can be anticoagulated
(1) Initiate anticoagulation.
d. If patient cannot be anticoagulated
(1) If the filter is obviously damaged, incompletely opened, malpositioned, or migrated, place a second filter.
(a) For retrievable filters, also consider removal of original filter.
(2) Determine source of PE, including new lower extremity DVT, thrombus extending through the filter, renal
vein thrombus, ovarian vein thrombus, or upper extremity DVT.
(3) When the source is the lower extremities or due to propagation of thrombus through the filter, place a
second filter. If the first filter is free of thrombus, a second filter can be placed above or below. If the first
filter contains trapped thrombus, place a second filter above (in suprarenal IVC if necessary).
(4) If the source is upper extremity thrombus, consider an SVC filter.
(5) If no source can be found, assume that the most likely source is lower extremity DVT and place a
second filter.
2. Suspected occlusion of filter or caval thrombosis
a. Document with objective testing.
(1) If filter and IVC are patent, no further evaluation is needed.
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b. Filter or IVC occlusion is found.
(1) Treatment beyond anticoagulation is not indicated if the patient is asymptomatic.
c. If the patient is symptomatic, document acuity and the level of occlusion.
(1) Evaluate for DVT with imaging modality of choice.
(2) If no lower extremity thrombus is identified, image the IVC and filter with computed tomography (CT),
MRI, or cavogram.
(3) If the patient no longer has contraindication to anticoagulation, consider thrombolysis and/or long-term
anticoagulation.
(4) If the patient has a contraindication to anticoagulation, consider mechanical thrombectomy. Be sure to
use a device that cannot become entangled in the filter. The goal is not to clean up the filter completely but
to restore flow.
(5) If thrombus extends above the filter, place a second filter central to the first if indicated.
(6) Chronic IVC occlusion with filter in place can be recanalized with angioplasty and stents.
(a) Stent through the filter or push filter aside with stents.
(b) Patient will not be protected against PE and may require long-term anticoagulation.
3. Suspected filter migration
a. Confirm that the filter has moved by comparison to old imaging studies.
(1) If the filter remains in a position that protects the patient from PE, then perform no intervention but
continue follow-up.
(a) Reimage in 1 to 3 months.
(b) If filter continues to move, consider second device central to the first.
i. If first filter is a retrievable device, consider removal.
(2) If the filter has migrated into the common iliac vein and continued protection is required, place a second
filter central to the first.
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(a) If first filter is retrievable device, consider removal.
(3) If the filter has migrated to the heart or pulmonary circulation, migration may have been caused by
massive embolus.
(a) Patient is no longer protected from PE, and new filter may be indicated.
(b) Intracardiac filters should be removed. Percutaneous repositioning or retrieval may be feasible, but great
care must be exercised to avoid cardiac trauma. Surgical removal may be necessary (22).
(c) Limited experience with pulmonary arterial filters suggests that removal is not necessary in
asymptomatic patients.
4. Fracture of filter element
a. If fracture results in compromise of filter function, place a second filter.
(1) Consider removal if retrievable filter.
b. Expectant management is exercised for asymptomatic patients.
c. If filter fragment migrates into adjacent tissues, no therapy is necessary unless the patient is
symptomatic.
(1) If the patient is symptomatic, confirm the precise location of the fragment with CT.
(2) Consider surgical removal if the patient is symptomatic and surgery is feasible.
d. If filter fragment has embolized to the heart
(1) Assess patient for arrhythmia, perforation, or chest pain. Urgent intervention is required for symptomatic
patients.
(a) Some fragments may be retrieved percutaneously.
(b) Surgical removal is required if percutaneous retrieval is not possible or there is a perforation.
(2) If asymptomatic
(a) Cross-sectional imaging to localize fragment
(b) Consultation with cardiology and cardiac surgery
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e. If filter fragment has embolized to the pulmonary artery
(1) Complications are rare.
(2) Expectant management
(3) Surgical repair may be required if peripheral fragment causes perforation.
5. Penetration of IVC by filter element
a. Majority of patients are asymptomatic and can be followed expectantly.
b. If the patient is symptomatic
(1) Confirm the location of penetrated elements by CT, endoscopy, and angiography as necessary.
(2) Exclude other etiologies of symptoms, such as lumbar spine disease or gastrointestinal processes.
(3) Treat symptoms with nonaddictive analgesics.
(4) If retrievable filter, consider removal.
(5) Consider surgical exploration and removal of extracaval filter element, if necessary.
(6) For all of the above, assess patient's VTE status and need for protection from PE.
Optional Filter Retrieval or Mechanical Conversion (2)

Radiology Books
Vena caval filtration may be discontinued when the risk of clinically significant PE is reduced to an acceptable
level and is estimated to be less than the risk of leaving the filter in place. There are no adequate published data
to allow the quantification of these relative risks, so the decision to discontinue filtration remains a matter of
physician's judgment. Remember: All optional filters are approved as permanent implants.
Indications
1. Absolute
a. The filter is a documented source of major morbidity that will be relieved by retrieval (e.g., unmanageable
pain secondary to limb perforation).
2. Relative
a. Adequate primary therapy of VTE or prophylaxis is achieved, and filtration is no longer deemed
necessary.
b. The patient is no longer deemed at risk for VTE; thus, filtration is no longer deemed necessary.
c. The filter is no longer protective as a result of a change in position or loss of structural integrity.
Contraindications
1. The patient continues to have an indication for vena caval filtration.
2. Significant retained thrombus within the filter. Small filling defects adherent to the filter elements are not a
contraindication to retrieval. Visual aids to estimating the size of retained thrombus are available (23).
3. The patient is unable to achieve adequate anticoagulation or primary prophylaxis (occasionally, this is a
patient compliance issue).
4. The patient is anticipated to return to a high-risk state for PE in the future.
5. Life expectancy of the patient is less than 6 months (unlikely that the patient will realize the presumed
benefits of filter removal).
6. Lack of vascular access for retrieval
7. The patient wants the filter to remain in place.
1. Recommended conditions prior to filter retrieval or conversion
a. An indication for permanent filtration is not present.
b. The risk of clinically significant PE is acceptably low as a result of a change in clinical status or achievement
of sustained appropriate anticoagulation or prophylaxis.
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c. The patient is not anticipated to return to a condition at high risk for PE.
d. The patient's life expectancy is long enough so that the presumed benefits of filter removal can be realized.
e. The filter can be safely retrieved or converted.
2. A focused history and physical should be performed to assess signs and symptoms of new, recurrent, or
progressive VTE.
3. The performing physician should discuss with the patient the rationale for discontinuing filtration and the
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voluntary nature of filter retrieval or conversion.
4. Laboratory studies
a. Coagulation studies and blood counts for patients on therapeutic anticoagulation. Patients on warfarin should
have stable laboratory values, with no evidence of bleeding for at least 7 days.
b. For patients taking warfarin, measure INR on the day of the procedure to ensure it is within the appropriate
range.
c. Serum creatinine in patients with impaired renal function
5. Imaging
a. In patients suspected of having new, recurrent, or progressive VTE, diagnostic imaging for DVT or PE should
be performed prior to filter retrieval.
b. Conversely, if a patient is therapeutically anticoagulated and has no signs or symptoms of new, recurrent, or
progressive VTE, no additional imaging is required.
c. The vena cava and entire filter should be imaged within the preceding 24 hours of filter retrieval (CT, magnetic
resonance venogram [MRV], US), or at the time of the procedure (DSA with contrast, IVUS).
d. Patients with filters placed for VTE prophylaxis should undergo imaging of the lower extremity veins (duplex
venous US) prior to filter retrieval.
6. Review prior imaging to assess filter type, location, presence of trapped thrombus, filter integrity, caval
penetration, and filter migration.
7. Anticoagulation status
a. The recommended duration of anticoagulation for VTE prior to filter retrieval is 2 to 3 weeks (2).
b. Patients taking warfarin should have a stable INR and no evidence of bleeding for at least 7 days.
c. Do not interrupt anticoagulation for filter retrieval or conversion (24).
d. Do not attempt to remove or convert filter if the patient is not therapeutically anticoagulated.
e. Retrieval may be postponed for INR >3.5 or platelets <50,000 per μL.
8. The consent for retrieval or conversion of a vena caval filter includes all of the usual risks associated with
percutaneous venous procedures as well as the following:
a. Failure to retrieve the filter 5% to 50%
(1) Failure rate increases with the duration of dwell time and specific filter.
b. Filter migration <1%
c. Filter fracture <1%
d. Symptomatic laceration or perforation of the vena cava <1%
e. Vena caval thrombosis <1%
f. Hemodynamically significant arrhythmia <1%
Risks are higher with advanced retrieval techniques (25).
Procedure
1. Access
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a. Dependent on filter design; usually jugular or femoral vein
2. Imaging: High-quality imaging during filter retrieval maximizes the chance of successful filter retrieval and
minimizes the chances of complication or a prolonged or difficult retrieval.
a. Goals of preretrieval imaging
(1) Evaluate the presence of trapped thrombus in the filter.
(2) Define the position of the filter in the vena cava.
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(3) Assess for complicating factors such as an embedded retrieval tip/hook or limb penetration.
(4) If other imaging methods (CT, MRI, US) have accomplished these goals within 24 hours of the
procedure, catheter-based cavography is optional but strongly recommended.
b. Cavography
(1) For IVC, position pigtail catheter (5 to 7 Fr.) below the filter. Take care not to dislodge the filter or entrap
catheters or guidewires in the filter.
(2) For SVC, inject from a brachiocephalic vein.
(3) Injection rate for iodinated contrast of 15 to 20 mL per second for 2 seconds
(4) DSA filming at four to six frames per second during suspended respiration in anterior-posterior
projection. Additional projections can be obtained as needed to evaluate the status of the filter.
c. IVUS: In patients with contraindications to all contrast agents, IVUS can be utilized, in conjunction with
fluoroscopy, to evaluate the filter prior to retrieval.
(1) Evaluate presence of thrombus.
(2) Assess for tip/hook embedment in the caval wall.
(3) Identify limb penetration.
3. Retrieval
a. General technique
(1) Filter elements in contact with the wall of the IVC may be covered with a layer of fibrocellular matrix,
neointima, or pseudointima. Elements that perforate the wall of the IVC are encapsulated (unless they enter
another lumen) with tissue that is in continuity with the IVC adventitia.
(2) Adequate sheath size positioned close to the intended site of engagement with the filter apex. Refer to
manufacturer's documentation regarding appropriate sheath size—it is often larger than delivery sheath
size.
(a) When difficult retrievals are anticipated because of the incorporation of filter elements into the wall of the
IVC, consider coaxial sheaths of similar length.
(3) Introduce a snare and catheter or other recommended retrieval device through the sheath and grasp the
filter.
(4) The technique used to remove filters varies by device. Always refer to the manufacturer's instructions.
There are two basic approaches.
(a) Peeling the filter away from the IVC
i. Maintain the filter in stable position and push the retrieval sheath over the filter until the filter is entirely
captured within the sheath.
(b) Extracting the filter from the IVC
i. Maintain the sheath in stable position and pull the filter into the retrieval sheath.
(5) Once the filter is entirely within the sheath, retrieve the filter through it, taking care to avoid sheath
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damage from sharp filter edges. Inspect the filter for integrity, making sure all pieces were removed.
(6) Postretrieval cavography is recommended when the patient reports pain during or after the procedure or
after a prolonged or difficult retrieval.
b. Retrieval devices
(1) Endovascular snares or snare variants
(2) Proprietary grasping devices
(3) Biopsy forceps
(4) Excimer laser sheath
4. Troubleshooting difficult retrieval (see Chapter e-82, Retrieval of Intravascular Foreign Bodies)
a. Difficulty grasping hook or other locus for engaging the filter—this is often related to filter tilt or tortuosity
of the vena cava (e.g., a patient with scoliosis).
(1) A curved catheter can be advanced to engage the filter and then manipulated to move the filter more
centrally within the vein.
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(2) A directional guide catheter can be used to advance the snare to the appropriate location on the filter.
(3) Use a second wire (buddy wire) to direct the retrieval device to the filter. Thread a 5 Fr. catheter through
the filter adjacent to the hook or engagement site and remove the catheter over a stiff guidewire. Advance a
snare over (track the loop over the wire) or adjacent to the stiff guidewire to capture the filter.
(4) Advance a reverse curve catheter through the filter, taking care to stay above any secondary struts.
Advance a hydrophilic guidewire through this catheter, snare the guidewire from the same venous access
site, and pull the distal end of the wire through the sheath to form a loop snare. Capture the filter using an
appropriately sized sheath and the loop snare or track a snare over both limbs of the loop snare to capture
the filter (26). See Figure e-82.3.
(5) Gently inflate a balloon within the filter to attempt to straighten the filter within the vein.
b. Filter tip adherent to the caval wall. The key imaging feature is an unopacified tissue cap around the filter
tip or projection of the filter tip outside the opacified venous lumen.
(1) Form a loop snare around the filter apex, running the wire between the filter elements and the caval wall
but not through the filter elements. Apply traction on the loop snare to separate the filter apex from the wall
of the cava.
(2) Gently inflate a balloon within the filter to attempt to free the filter apex from the caval wall and straighten
the filter within the vein.
(3) Very cautiously use rigid endobronchial forceps to dissect the embedded filter apex free (27).
(a) Following detailed venography, advance the endobronchial forceps (model 4162; Bryan Corp, Woburn,
MA) through a 12 Fr. or 14 Fr. sheath.
(b) If needed, forceps can be very gently bent to direct them to the filter tip.
(c) Grasp and remove the tissue surrounding the filter tip.
(d) Once the encapsulating tissue is removed, grasp the filter tip and remove the filter through the sheath.
c. Filter is firmly adhered to the wall of the cava. This is usually diagnosed after capturing the filter while
attempting to sheath the filter.
(1) When using a coaxial sheath system, the outer and inner sheaths can be sequentially advanced over
the filter.
(2) Advance a balloon catheter from a separate access and attempt to pry the filter struts off the caval wall
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by gentle balloon inflation.
(3) Advance excimer laser sheath over filter to disrupt adherent tissue (28).
(a) Connect the laser-tipped sheath to the CVX-300 Excimer XeCl Laser System (Spectranetics Corp,
Colorado Springs, CO) and calibrate per protocol to 60 mJ per mm2.
(b) Insert the 12 Fr. laser-tipped sheath over a wire coaxially through a 14 Fr. sheath until resistance is
encountered.
(c) While maintaining gentle traction on the filter with a snare, activate the laser and advance the sheath.
(d) Laser-assisted retrieval utilizes photothermal tissue ablation while tension is applied to the filter, often
with significantly lower force required than other techniques (29).
d. Retrieval attempt is abandoned.
(1) Perform cavogram to assess the status of filter and IVC.
(a) Consider short course of anticoagulation if IVC injury or thrombus is seen.
(b) If filter is no longer protective against PE, communicate this information to the patient and the primary
physician.
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(2) If filter remains collapsed and causes IVC stenosis, perform angioplasty on the filter, with balloon sized
to the IVC, to push filter against the wall.
e. Conversion
(1) General technique
(a) Determine the mechanism of conversion for the patient's device.
i. For example, snare removal of a constraining apical cap
(b) Perform assessment and imaging of the patient as described for retrieval procedures earlier.
(c) Utilize appropriate sheaths and endovascular devices for triggering conversion of the filter.
(d) Confirm removal of all extractable components from the patient.
(e) Perform cavogram to document status of IVC and converted device.
1. Routine monitoring in immediate postprocedure period for venous access procedures
2. Primary treatment or prophylaxis for VTE should continue until no longer clinically indicated.
References
1. Grassi CJ, Swan TL, Cardella JF, et al. Quality improvement guidelines for percutaneous permanent
inferior vena cava filter placement for the prevention of pulmonary embolism. J Vasc Interv Radiol .
2003;14:S271-S275.
2. Kaufman JA, Kinney TB, Streiff MB, et al. Guidelines for the use of retrievable and convertible vena cava
filters: report from the Society of Interventional Radiology multidisciplinary consensus conference. J Vasc
Interv Radiol . 2006;17:449-459.
3. Weinberg I, Kaufman J, Jaff MR. Inferior vena cava filters. JACC Cardiovasc Interv. 2013;6:539-547.
Radiology Books
4. Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease: Antithrombotic Therapy and
Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice
Guidelines. Chest. 2012;141:e419S-e494S.
5. Caplin DM, Nikolic B, Kalva SP, et al. Quality improvement guidelines for the performance of inferior vena
cava filter placement for the prevention of pulmonary embolism. J Vasc Interv Radiol . 2011;22:1499-1506.
6. Angel LF, Tapson V, Galgon RE, et al. Systematic review of the use of retrievable inferior vena cava
filters. J Vasc Interv Radiol . 2011;22:1522.e3-1530.e3.
7. Usoh F, Hingorani A, Ascher E, et al. Long-term follow-up for superior vena cava filter placement. Ann
Vasc Surg. 2009;23:350-354.
8. Hicks ME, Malden ES, Vesely TM, et al. Prospective anatomic study of the inferior vena cava and renal
veins: comparison of selective renal venography with cavography and relevance in filter placement. J Vasc
Interv Radiol . 1995;6:721-729.
9. Kaufman JA, Geller SC, Rivitz SM, et al. Operator errors during percutaneous placement of vena cava
filters. AJR Am J Roentgenol . 1995;165:1281-1287.
10. Jacobs DL, Motaganahalli RL, Peterson BG. Bedside vena cava filter placement with intravascular
ultrasound: a simple, accurate, single venous access method. J Vasc Surg. 2007;46:1284-1286.
11. Gunn AJ, Iqbal SI, Kalva SP, et al. Intravascular ultrasound-guided inferior vena cava filter placement
using a single-puncture technique in 99 patients. Vasc Endovascular Surg. 2013;47:97-101.
12. Amankwah KS, Seymour K, Costanza M, et al. Transabdominal duplex ultrasonography for bedside
inferior vena cava filter placement: examples, technique, and review. Vasc Endovascular Surg. 2009;43:379-
384.
13. Kalva SP, Chlapoutaki C, Wicky S, et al. Suprarenal inferior vena cava filters: a 20-year single-center
experience. J Vasc Interv Radiol . 2008;19:1041-1047.
14. Smith DC, Kohne RE, Taylor FC. Steel coil embolization supplementing filter placement in a patient with
a duplicated inferior vena cava. J Vasc Interv Radiol . 1992;3:577-580.
15. Vesely T, Darcy M, Picus D, et al. Technical problems associated with placement of the Bird's Nest
inferior vena cava filter. AJR Am J Roentgenol . 1992;158:875-880.
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16. Goertzen TC, McCowan TC, Garvin KL, et al. An unopened titanium Greenfield IVC filter: intravascular
ultrasound to reveal associated thrombus and aid in filter opening. Cardiovasc Intervent Radiol .
1993;16:251-253.
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17. Salamipour H, Rivitz SM, Kaufman JA. Percutaneous transfemoral retrieval of a partially deployed Simon-
Nitinol filter misplaced into the ascending lumbar vein. J Vasc Interv Radiol. 1996;7:917-919.
18. Kaufman JA, Thomas JW, Geller SC, et al. Guide-wire entrapment by inferior vena caval filters: in vitro
evaluation. Radiology. 1996;198:71-76.
19. Hammond CJ, Bakshi DR, Currie RJ, et al. Audit of the use of IVC filters in the UK: experience from three
centres over 12 years. Clin Radiol . 2009;64:502-510.
20. Wang SL, Lloyd AJ. Clinical review: inferior vena cava filters in the age of patientcentered outcomes. Ann
Med. 2013;45:474-481.
21. Andreoli JM, Lewandowski RJ, Vogelzang RL, et al. Comparison of complication rates associated with
permanent and retrievable inferior vena cava filters: a review of the MAUDE database. J Vasc Interv Radiol .
2014;25:1181-1185.
22. Owens CA, Bui JT, Knuttinen MG, et al. Intracardiac migration of inferior vena cava filters: review of
published data. Chest. 2009;136:877-887.
23. Wang SL, Timmermans HA, Kaufman JA. Estimation of trapped thrombus volumes in retrievable inferior
vena cava filters: a visual scale. J Vasc Interv Radiol . 2007;18:273-276.
24. Hoppe H, Kaufman JA, Barton RE, et al. Safety of inferior vena cava filter retrieval in anticoagulated
patients. Chest. 2007;132:31-36.
25. Al-Hakim R, Kee ST, Olinger K, et al. Inferior vena cava filter retrieval: effectiveness and complications of
routine and advanced techniques. J Vasc Interv Radiol . 2014;25: 933-939.
26. Rubenstein L, Chun AK, Chew M, et al. Loop-snare technique for difficult inferior vena cava filter
retrievals. J Vasc Interv Radiol . 2007;18:1315-1318.
27. Stavropoulos SW, Dixon RG, Burke CT, et al. Embedded inferior vena cava filter removal: use of
endobronchial forceps. J Vasc Interv Radiol . 2008;19:1297-1301.
28. Kuo WT, Cupp JS. The excimer laser sheath technique for embedded inferior vena cava filter removal. J
Vasc Interv Radiol . 2010;21:1896-1899.
29. Kuo WT, Odegaard JI, Rosenberg JK, et al. Excimer laser-assisted removal of embedded inferior vena
cava filters: a single-center prospective study. Circ Cardiovasc Interv. 2013;6:560-566.
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36
Acute Extremity DVT: Thrombectomy and Thrombolysis
Suresh Vedantham
Acute deep vein thrombosis (DVT) occurs in approximately 300,000 persons per year in the United States alone
(1). Because pulmonary embolism (PE) can be fatal, its prevention using anticoagulant therapy has been the
mainstay of DVT therapy for nearly 50 years (2). However, anticoagulant drugs do not actively eliminate venous
thrombus, so in many cases, their use is not sufficient to prevent serious DVT complications. Early thrombus
progression occurs in a minority of anticoagulated DVT patients and can threaten life, limb, or organ function;
prolong hospitalization; and exacerbate DVT symptoms such as limb pain, swelling, and ambulatory difficulties.
Despite use of anticoagulant therapy, 25% to 50% of proximal DVT patients will develop significant quality of life
(QOL) impairment from the postthrombotic syndrome (PTS), a debilitating late DVT complication characterized by
chronic leg fatigue or heaviness, swelling, pain, paresthesias, venous claudication, stasis dermatitis, and/or skin
ulceration (3,4). PTS can also affect the upper extremity, particularly when the subclavian vein from the dominant
arm is involved with
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the initial DVT episode. The development of PTS is directly related to the continued presence of thrombus within
the deep venous system during the initial weeks and months after DVT via at least two pathways: (a) residual
thrombus physically blocks blood flow (“obstruction”) and (b) thrombosis stimulates inflammation, which directly
damages the venous valves, causing valvular incompetence (“reflux”). When reflux and/or obstruction is present,
ambulatory venous hypertension develops and ultimately leads to the edema, tissue hypoxia and injury,
progressive calf pump dysfunction, subcutaneous fibrosis, and skin ulceration of PTS (5). It is therefore logical
that rapid thrombus elimination and restoration of unobstructed deep venous flow using catheter-directed
thrombolysis (CDT) should rapidly improve initial DVT symptoms and prevent late valvular reflux, venous
obstruction, and PTS.
Indications
1. Urgent first-line CDT is performed as an adjunct to anticoagulant therapy to prevent life-, limb-, or
organ-threatening complications of acute DVT.
a. In patients with acute limb-threatening circulatory compromise (i.e., phlegmasia cerulea dolens)
b. In patients with extensive inferior vena cava (IVC) thrombosis deemed to be at high risk for fatal PE
c. In patients with acute renal failure from thrombus extension into the suprarenal IVC and/or renal veins (6)
2. Nonurgent second-line CDT is performed for patients with symptomatic proximal DVT who exhibit
clinical and/or anatomic progression of DVT on anticoagulant therapy.
a. Rapid iliocaval or subclavian/brachiocephalic thrombus extension
b. Exacerbation or persistence of major lower or upper extremity symptoms
c. Failure to experience sufficient symptom improvement to permit ambulation or normal arm function
3. Nonurgent first-line CDT may be performed as an adjunct to anticoagulant therapy to enable faster
symptom relief and/or long-term prevention of PTS in patients with symptomatic, acute proximal DVT.
a. Patients with acute iliofemoral DVT (defined as DVT that involves the iliac vein and/or common femoral
vein) are likely to be the best candidates for first-line CDT.
b. Patients with acute axillosubclavian DVT related to Paget-Schroetter syndrome also appear to be
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excellent candidates for a combined surgicalinterventional approach in which CDT-mediated thrombus
removal is the first step.
Contraindications
1. Active internal bleeding
2. Recent (<3 months) gastrointestinal bleeding
3. Recent stroke (<6 months)
4. Intracranial or intraspinal bleeding, tumor, vascular malformation, or aneurysm
5. Severe liver dysfunction
6. Severe thrombocytopenia or other bleeding diathesis
7. Pregnancy
8. Severe uncontrolled hypertension
9. Recent (<10 days) major surgery, trauma, cardiopulmonary resuscitation, obstetric delivery, lithotripsy, or
other major invasive procedure
10. Recent (<3 months) eye operation or hemorrhagic retinopathy
11. Bacterial endocarditis or acute bacterial septic thrombophlebitis
12. Moderate-to-severe renal dysfunction
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13. Severe acute illness that precludes adequate sedation or proper positioning on the table.
14. Patients >70 years of age may be at higher risk of bleeding complications.
1. Obtain clinical history and perform physical examination to confirm the presence of a symptom and/or clinical
manifestation that merits aggressive therapy. Know the patient's risk factors for bleeding complications, his or her
baseline ambulatory status, and his or her life expectancy. Patients who are chronically nonambulatory or who
have very short life expectancy may not experience meaningful benefits from CDT.
2. Review duplex venous ultrasound to confirm the diagnosis of DVT, evaluate the extent of thrombus, and plan
the therapeutic approach. If needed, evaluation of central veins may be performed with computed tomography
(CT) scan, magnetic resonance (MR) venography, or injection venography.
3. Laboratory evaluation: serum creatinine, hemoglobin (Hgb)/hematocrit (Hct), platelet count, international
normalized ratio (INR), partial thromboplastin time (PTT). Pregnancy test should be performed in women of
childbearing potential.
4. Provide a balanced discussion of the risks, benefits, alternatives to, and uncertainties surrounding CDT and
obtain informed consent. Discuss the use of adjunctive measures such as angioplasty and stent placement to
treat stenotic lesions that are uncovered.
5. For most patients, ensure that the INR is below 2.0 (preferably 1.5) before starting CDT and stop any
irreversible anticoagulants at least 24 hours before CDT. These parameters can be modified for patients with
severe clinical manifestations or for patients with renal dysfunction (the latter may require longer periods of oral
anticoagulation cessation). If the patient has mild-to-moderate contrast allergy, premedicate with steroids and
histamine antagonists (see Chapter 64).
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6. In selected patients with lower extremity DVT, a retrievable IVC filter may be placed prior to starting CDT.
Because PE rates are known to be low when infusion-first CDT (see “Complications” section) is used, IVC filter
placement is probably unnecessary when this method is used (7,8). However, the need for IVC filter placement
prior to single-session pharmacomechanical catheter-directed thrombolysis (PCDT) therapy is unclear at
present.
Procedure
1. Select a venous access site, ideally peripheral to the extent of the thrombus.
a. Usual sites for lower extremity DVT treatment are the popliteal vein or posterior tibial vein. Other veins
that can be used include the internal jugular vein, small saphenous vein, and other ipsilateral tibial veins.
Use of the contralateral common femoral vein is not recommended (to avoid causing contralateral DVT).
b. For upper extremity DVT, usual sites are the brachial or basilic veins.
c. In choosing an access site, it is important to consider the sheath size needed to accommodate the
planned infusion catheter/device. For example, it may not be wise to select a distal posterior tibial vein
access site if an 8 Fr. sheath will be needed. In some situations when the thrombus extends through the
popliteal vein and into the calf, additional access sites may be used (e.g., popliteal vein and posterior tibial
vein).
2. Administer conscious sedation with appropriate monitoring, perform sterile preparation, and inject local
anesthetic (e.g., 1% lidocaine) into the skin over the selected vein(s).
3. Perform an ultrasound-guided puncture to obtain catheter access into the selected vein(s). A 5- to 7.5-
MHz linear array transducer is routinely used. A 21-gauge micropuncture needle is ultrasound visible, and
its use may help
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to minimize bleeding. Pass a 0.018-in. guidewire and exchange for a transition dilator and then advance a
diagnostic catheter (4 Fr. or 5 Fr.) into the venous system over a 0.035-in. hydrophilic guidewire. Real-time
fluoroscopic monitoring should be used throughout the procedure.
4. Perform a venogram through the diagnostic catheter to define the thrombus extent. This should be done
with serial hand injections of 5- to 10-mL iodinated contrast, diluted as needed with 0.9% normal saline, and
digital subtraction imaging.
5. Exchange the diagnostic catheter for a 7 to 8 Fr. vascular sheath.
6. Decide whether to perform “infusion-first” or “single-session pharmacomechanical” CDT and select an
infusion catheter accordingly. If single-session PCDT will be used, skip to step 8.
7. Patients undergoing infusion-first CDT
a. Select a multi-side-hole infusion catheter with an infusion segment that matches the length of the
thrombosed venous segment. For infusion-first CDT, either a traditional multi-side-hole infusion catheter or
an ultrasoundemitting infusion catheter (EkoWave, EKOS Corporation, Bothell, WA) may be used.
Ultrasound-assisted CDT is hypothesized by some to loosen fibrin strands, facilitate drug dispersion, and
enable faster therapy with a reduced thrombolytic dose.
b. Advance catheter into position over the guidewire and start infusing the thrombolytic drug. Note: None of
these drugs is approved by the U.S. Food and Drug Administration (FDA) for DVT therapy—all are
approved for other indications but are used off-label for DVT (6). By far, the largest published experience,
which includes one rigorous multicenter randomized controlled trial (RCT) (8), has used tissue plasminogen
activator.
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(1) Recombinant tissue plasminogen activator (rt-PA) at 0.01/mg/kg, not to exceed 1.0 mg per hour (8,9)
(2) Urokinase (UK) at 120 000 to 180 000 U per hour
(3) Reteplase at 0.50 to 0.75 U per hour
(4) Tenecteplase (TNK) at 0.25 to 0.50 mg per hour
c. If ultrasound-assisted CDT is being performed, press the Start button on the machine to administer low-
power ultrasound energy during drug delivery.
d. Simultaneously administer concomitant anticoagulant therapy by either (a) infusing subtherapeutic
unfractionated heparin (UFH) through the vascular sheath at an hourly dose that is sufficiently low to
prevent the PTT from becoming supratherapeutic—either one can target the PTT to 1.2— 1.7 times control
or to less than 60 seconds, or simply use a dose in the range of 6 to 12 units/kg/h (8,9), or (b) administering
low-molecular-weight heparin (LMWH) such as enoxaparin at 1 mg per kg subcutaneous injections every 12
hours (9). The use of fondaparinux, rivaroxaban, dabigatran, apixaban, and edoxaban during thrombolytic
therapy is discouraged because these agents are not readily reversible should bleeding occur and there are
no prospective studies of concomitant use with thrombolytic drugs.
e. If treating lower extremity DVT, elevate the symptomatic leg during the infusion.
f. Monitor the patient in a stepdown unit or intensive care unit (ICU) during the infusion and obtain
peripheral blood laboratory studies at least every 8 to 12 hours (Hct/Hgb, PTT). Follow these levels closely
because elevated PTT levels during thrombolysis have been associated with bleeding complications, and a
rapid drop in hematocrit may be a sign of occult bleeding (e.g., retroperitoneal bleeding).
g. The nurse and/or the treating physician should clinically evaluate the patient frequently to assess for
sentinel bleeding (e.g., epistaxis, ear bleeding, profuse access site bleeding) that may indicate a systemic
thrombolytic state of greater intensity than desired.
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h. The fibrinogen level may also be monitored, although there are little data to support its usefulness for
preventing complications of DVT thrombolysis procedures.
i. After 6 to 18 hours of infusion, bring the patient back to the angiographic suite and repeat the venogram.
Skip to step 9.
8. Patients undergoing single-session pharmacomechanical CDT: Patients in whom the goal is to
complete DVT treatment in a single-procedure session may have the thrombolytic drug administered via one
of several catheter/devices. A detailed description of the exact method of use of each of these very different
devices is beyond the scope of this handbook. However, here are key differences between single-session
PCDT and infusion-first CDT:
a. The single-session PCDT techniques involve the delivery and rapid dispersion of a significant dose of
the thrombolytic drug as the first step in thrombus removal. Typically, 5 to 25 mg of rt-PA (or the equivalent)
is administered during this procedure session. Different devices rely on different methods to achieve rapid
drug dispersion within the thrombus. Two commonly used techniques are described in b and c below.
b. Isolated thrombolysis using the Trellis Peripheral Infusion System (Bacchus Vascular/Covidien/Medtronic,
Santa Clara, CA): A Trellis catheter is advanced over a guidewire to the central extent of the thrombus. Two
balloons mounted on the Trellis catheter are first inflated to “isolate” the thrombosed venous segment. The
thrombolytic drug, diluted to 10 mL, is injected via a syringe into the catheter and enters the thrombus
through several side holes. A sinusoidal wire oscillates within the catheter to mechanically macerate the
thrombus and disperse the drug. The liquefied thrombus and drug may then be aspirated through a sideport
in the catheter, and the catheter is repositioned within the remaining thrombus.
c. Power-pulse thrombolysis using the AngioJet Rheolytic Thrombectomy System (Boston Scientific Corp,
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Minneapolis, MN): An AngioJet Solent Proxi catheter is advanced to and from within the thrombus with the
device in power pulse mode (i.e., the outflow port is occluded). This results in powerful pulse-spray delivery
of the thrombolytic drug into the clot. After a dwell period of 30 minutes, the AngioJet is used in aspiration
mode to remove the softened residual clot.
d. Because single-session PCDT may be more mechanically aggressive than infusion-first CDT, most
physicians anticoagulate the patient to therapeutic levels during PCDT.
9. Clean-up of residual thrombus: After the initial thrombolytic drug infusion (infusion-first CDT) or
injection/dispersion (single-session PCDT), repeat venogram is performed. If near-complete (>90%) lysis
and good anterograde flow are observed (by visual estimation) with no venous stenosis or obstruction,
treatment may be stopped. If residual thrombus is present, the physician may use one or more of the
following adjunctive measures to remove it.
a. Balloon maceration of the thrombus: Advance a standard angioplasty balloon catheter (6 to 10 mm for
the femoral vein, 10 to 12 mm for the common femoral vein or iliac vein) over the guidewire into the
thrombus. Inflate the balloon within the thrombus. Deflate the balloon. Repeat these steps as needed with
the balloon positioned in different parts of the thrombus. Remove the angioplasty balloon catheter over the
guidewire.
b. Aspiration thrombectomy: Advance a standard 7 to 8 Fr. catheter over the guidewire to the
cephaladaspect of the thrombus. Attach alarge (30 to 60 mL) syringe to the catheter. Vigorously aspirate
with the syringe during withdrawal of the catheter through the thrombus. Repeat these steps as needed and
then remove the catheter.
c. Rheolytic thrombectomy may be performed using the AngioJet in aspiration mode.
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10. Infusion end point: After each of the preceding measures is used, perform a repeat venogram to assess
progress. If significant residual obstructing thrombus is still present, position a multi-side-hole infusion
catheter within the thrombus and perform infusion CDT in the same manner as stated earlier. The drug may
be infused until near-complete (>90%) thrombolysis is observed, clinically overt bleeding becomes evident,
or until minimal progress is seen on two subsequent venograms. It is probably best to keep the thrombolytic
infusion as short as possible to avoid bleeding issues—less than 24 hours to treat unilateral DVT and less
than 36 hours for bilateral DVT are suggested, although these guidelines have not been prospectively
validated.
11. Treatment of obstructive lesions: After all thrombus removal steps are completed, perform a repeat
venogram.
a. Balloon angioplasty and stent placement may be performed to correct areas of venous stenosis or
obstruction that persist since these lesions, when not treated, have been associated with high rates of
immediate rethrombosis.
b. Self-expanding stents with radial flexibility may be used in the iliac vein and extended into the common
femoral vein if needed.
c. Stents in the femoral or popliteal vein are not likely to remain patent, so balloon angioplasty is a better
choice for femoropopliteal stenotic lesions.
d. Stent placement is contraindicated in the subclavian vein; patients with Paget-Schroetter syndrome
should have their thoracic outlet decompressed surgically at some point soon after CDT.
e. At present, no stent is approved by the FDA for iliac vein use.
12. Perform a final venogram, remove the sheath, and achieve hemostasis by direct compression.
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1. Therapeutic-level anticoagulation should be resumed immediately after hemostasis is obtained using either
UFH or LMWH. For most patients, transition to an oral agent may begin either the same evening (warfarin, target
INR 2 to 3) or the next day (rivaroxaban, dabigatran, apixaban, or edoxaban). If the patient is felt to be at
particularly high risk for rethrombosis, then LMWH may be continued and the transition to oral therapy delayed.
2. Patients with a lower extremity access site should remain at bed rest with the treated leg immobile for at least
4 hours. After that, early ambulation is desirable.
3. For patients who will receive warfarin, continue heparin (UFH or LMWH) until the INR exceeds 2.0 for two
consecutive days. Exception: In patients with cancerrelated DVT, LMWH monotherapy (not warfarin) is the
treatment of choice.
4. For subjects in whom a retrievable IVC filter was placed, the filter may be removed at any time after PCDT is
completed. There is no need to stop anticoagulation for filter retrieval unless it is supratherapeutic. In general,
the patient should be therapeutically anticoagulated and should not have significant (≥25% of the filter's volume)
thrombus within the filter.
5. If the patient has significant lower extremity swelling, offer the patient the option of wearing graduated
compression stockings (either 20 to 30 mm Hg or 30 to 40 mm Hg) on a daily basis. Although their use does not
appear to prevent PTS or to reduce lower extremity pain, they may help to reduce extremity swelling (10).
6. The patient should be seen in follow-up within 1 month of the procedure. In the meantime, careful monitoring
of INR levels with dose adjustment is essential to avoid rethrombosis for patients who are receiving warfarin.
Results
1. Stand-alone infusion-first CDT—early results: Stand-alone infusion-first CDT has been shown to dissolve
acute thrombus in over 80% of patients with
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acute (defined as symptom duration ≤14 days) proximal DVT in a 473-patient prospective multicenter
registry, a multicenter RCT, and in a pooled analysis of observational studies (6,7,8). Disadvantages
compared with other methods include the need for prolonged drug infusions (i.e., around 48 hours) and 1 to
3 days of ICU care, with repeated laboratory and venographic monitoring.
2. Infusion-first CDT—late results: Quality long-term efficacy outcomes data is only available from one
rigorously conducted multicenter randomized trial (the Catheter-directed Venous Thrombolysis in acute
iliofemoral vein thrombosis— [CaVenT] study). In that study, the use of infusion-only CDT with
anticoagulant therapy in patients with DVT involving the iliac and/or upper femoral venous system was
associated with a 26% relative reduction in the risk of PTS over 2-year follow-up (41.1% vs. 55.6%, P =
.04) compared with anticoagulant therapy alone (8). However, factors which limit the generalizability of
CaVenT include its modest sample size (outcomes reported in 189 patients, of whom 92 patients received
CDT) and geographical limitation (southern Norway).
3. PCDT refers to thrombus dissolution via the combined use of CDT and devicebased percutaneous
mechanical thrombectomy (PMT).
a. First-generation PCDT methods typically involved the sequential use of PMT either before or after slow
infusion of a thrombolytic drug (a traditional CDT infusion). Retrospective studies which compared first-
generation PCDT with stand-alone CDT observed that use of PCDT enabled reductions in the thrombolytic
drug dose (by about 50%) and treatment time (by about 40%) as well as reductions in hospital costs and
length of ICU stay. These findings suggest that first-generation PCDT may be more efficient and safer than
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stand-alone CDT.
b. Although retrospective series suggest that Isolated Thrombolysis and Power-Pulse may enable DVT to
be treated in a single session in over 50% of patients, there are no published prospective studies that
directly compare meaningful clinical DVT outcomes with use of single-session PCDT techniques versus
infusion CDT.
4. Because of the aforementioned methodologic limitations, there is significant uncertainty among
physicians as to the actual risk-benefit ratio of endovascular DVT therapy. The ATTRACT (Acute Venous
Thrombosis: Thrombus Removal with Adjunctive Catheter-Directed Thrombolysis) trial, a National Institutes
of Health (NIH)-funded multicenter randomized clinical trial evaluating the ability of PCDT to prevent PTS, is
expected to address these questions with a much higher degree of scientific rigor (9).
Complications
1. Major bleeding occurred in 3.2% (3 of 92) of patients receiving CDT in the CaVenT trial. One bleed
required surgery and one required a blood transfusion. In that study, there were no intracranial bleeding,
suggesting that in the clinical trial setting with careful patient selection and a defined technique, CDT may
be reasonably safe. However, real-world use of CDT as illustrated by registry data suggests that around
11% of patients undergoing CDT may suffer a major bleeding, with 0.4% to 0.9% suffering an intracranial
bleeding. These findings certainly argue for careful patient selection and diligent monitoring.
2. Symptomatic PE occurred in 1.3% of patients in the multicenter urokinase CDT registry. Fatal PE
occurred in 0.2% of patients in the registry. Because most patients had acute iliofemoral DVT in this
registry, these rates do not appear to exceed what would be expected for a similar cohort of patients treated
with anticoagulant therapy alone. To date, serious PE has been reported in at least one patient treated with
single-session PCDT (26), but the rates of symptomatic PE and fatal PE for these techniques have not yet
been established.
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3. Prevention of complications
a. During CDT or PCDT, the physician should reduce the drug dose or stop it entirely at his or her
discretion if there are safety concerns.
b. If serious bleeding occurs at the venous access site (uncontrolled by sheath upsizing or compression),
the drug administration should be stopped. If sheath upsizing and/or compression are effective in stopping
the bleeding, the drug may be restarted at a lower dose with careful repeat evaluations of the access site to
ensure no recurrence.
c. If serious bleeding occurs in a distant location, or if a severe or lifethreatening reaction occurs,
administration of the thrombolytic drug should be permanently stopped.
d. If serious bleeding occurs, infusion of heparin should also be stopped and, at physician discretion,
protamine and/or cryoprecipitate may be given.
References
1. Heit JA, Cohen AT, Anderson FA, et al. On the behalf of the VTE impact assessment group. Estimated
annual number of incident and recurrent, non-fatal and fatal venous thromboembolism (VTE) events in the
US [abstract]. Blood. 2005;106:267a.
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2. Kearon C, Akl EA, Comerota AJ, et al. Antithrombotic therapy for VTE disease: antithrombotic therapy and
prevention of thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice
Guidelines. Chest. 2012;141(2): e419S-e494S.
3. Kahn SR, Shrier I, Julian JA, et al. Determinants and time course of the postthrombotic syndrome after
acute deep venous thrombosis. Ann Intern Med. 2008;149:698-707.
4. Kahn SR, Shbaklo H, Lamping DL, et al. Determinants of health-related quality of life during the 2 years
following deep vein thrombosis. J Thromb Haemost. 2008;6: 1105-1112.
5. Nicolaides AN, Hussein MK, Szendro G, et al. The relation of venous ulceration with ambulatory venous
pressure measurements. J Vasc Surg. 1993;17:414-419.
6. Vedantham S, Sista AK, Klein SJ, et al; Society of Interventional Radiology and Cardiovascular and
Interventional Radiological Society of Europe Standards of Practice Committees. Quality improvement
guidelines for the treatment of lower-extremity deep vein thrombosis with use of endovascular thrombus
removal. J Vasc Interv Radiol . 2014;25: 1317-1325.
7. Mewissen MW, Seabrook GR, Meissner MH, et al. Catheter-directed thrombolysis for lower extremity deep
venous thrombosis: report of a national multicenter registry. Radiology. 1999;211:39-49.
8. Enden T, Haig Y, Kløw NE, et al. Long-term outcomes after additional catheterdirected thrombolysis
versus standard treatment for acute iliofemoral deep vein thrombosis (the CaVenT study): a randomised
controlled trial. Lancet. 2012;379(9810): 31-38.
9. Vedantham S, Goldhaber SZ, Kahn SR, et al. Rationale and design of the ATTRACT study: a multicenter
randomized trial to evaluate pharmacomechanical catheter-directed thrombolysis for the prevention of
postthrombotic syndrome in patients with proximal deep vein thrombosis. Am Heart J. 2013;165(4):523-530.
10. Kahn SR, Shapiro S, Wells PS, et al; for the SOX trial investigators. Compression stockings to prevent
post-thrombotic syndrome: a randomised placebo-controlled trial. Lancet. 2014; 383(9920):880-888.
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37
Angioplasty and Stenting for Chronic Venous Disease
Raj P. Shah
Michael J. Hallisey
Primary balloon angioplasty of the venous system has high technical failure and short-term reocclusion rates.
The use of venous stents improves long-term patency by preventing elastic recoil. The one exception to this high
failure rate of primary venous percutaneous transluminal (balloon) angioplasty (PTA) may be in patients with
previous central venous catheters who are not on chronic hemodialysis; in these patients, balloon angioplasty
alone may provide significant improvement. A technique that is useful and feasible in treating venous stenoses is
ultrahigh-pressure balloon PTA. Ultrahigh-pressure PTA may provide prolongation after venous angioplasty,
especially in the outflow of hemodialysis grafts. Percutaneous cutting balloon (PCB) angioplasty is a technique
that is useful for certain types of highly scarred or resistant stenoses. However, PCB angioplasty should be used
as a backup to suboptimal primary balloon PTA due to higher complication rates and the fact that it may be more
painful than conventional balloon PTA.
Indications
Patient with symptoms resulting from
1. Superior vena cava (SVC) obstruction from malignant and benign causes (1,2). SVC syndrome is most
common with thoracic malignancy (80% to 90%), usually secondary to bronchogenic carcinoma.
2. Subclavian and brachiocephalic vein stenoses secondary to prior indwelling central venous catheters
3. Recurrent subclavian vein stenoses in patients with Paget-Schroetter or thoracic outlet syndrome after
the patient have undergone resection of the first rib and/or head of the clavicle (3).
4. Iliofemoral vein/inferior vena cava (IVC) obstructions: May-Thurner or Cockett syndrome (Fig. 37.1) (4).
Stents should be used when there is residual obstruction after balloon PTA and extrinsic compression of
IVC (e.g., by enlarged caudate lobe of liver or nodular compression).
5. Hemodialysis access-related venous stenoses: see Chapters 31, 32, and 33
6. Budd-Chiari syndrome. Endovascular treatment has become the treatment of choice due to minimal
trauma and fast recovery.
7. Portal vein stenoses or occlusions
8. Chronic venous occlusion: Chronic, occlusive deep venous thrombosis (DVT) and postthrombotic
syndrome (PTS); consider endovascular intervention after maximizing medical management.
9. Pulmonary vein stenosis: There are published reports of venous angioplasty successfully treating
pulmonary vein stenosis following lung transplant. However, further studies are required to validate safety
and long-term efficacy.
10. Multiple sclerosis (MS): Various reports in the peer-reviewed published literature describe a potential
relationship between the abnormal venous circulation termed chronic cerebrospinal venous insufficiency
(CCSVI) and MS. Current evidence on the efficacy of percutaneous venoplasty for CCSVI for MS is
inadequate in quality and quantity. Therefore, this procedure should only be used in the context of
research.
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FIGURE 37.1 • May-Thurner syndrome. The overlying right iliac artery compresses the adjacent left iliac
vein.
Contraindications
1. Paget-Schroetter syndrome (effort thrombosis): Transient, intermittent traumatic extrinsic compression of
the subclavian vein between the subclavius muscle and the costocoracoid ligament, causing local
inflammation and occlusive thrombosis.
2. Thoracic outlet syndrome: Entrapment of the subclavian vein at its exit from the thorax between the first
rib and clavicle. This disorder is not due to an endoluminal abnormality.
Note: Primary stent placement and balloon PTA is contraindicated in these patients. The underlying
pathology is not endoluminal; therefore, angioplasty and/or stenting may complicate the treatment which
requires thrombolysis followed by surgery. Moreover, stenting of these segments leads to repetitive
compressive trauma to the stent and reocclusion. Surgical resection of the compressive lever (first rib or
head of the clavicle) should be initially performed (Fig. 37.2). Stenting should be reserved for those patients
who have previously undergone first rib resection for Paget-Schroetter or benign vein obstruction and have
resistant or repeated failures with balloon PTA.
1. Review of patient history for:
a. Previous central line insertion
b. Weightlifting or heavy arm exercise
c. Previous intrathoracic surgery
d. Malignancy
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2. Review thoracic computed tomography (CT) scan to assess if there is a mass causing compression of the
SVC.
3. For patients with a venous stenosis near other vascular or enteral structures, it is important to do a
preprocedure CT scan before cutting balloon can be used to ensure that the adjacent structures are not
damaged.
4. Stop all oral intake overnight.
5. Obtain laboratory parameters: creatinine, international normalized ratio (INR), prothrombin time (PT), partial
thromboplastin time (PTT), platelets, and hematocrit.
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FIGURE 37.2 • Thoracic outlet syndrome. A: The subclavian vein can be pinched as it exits between the clavicle
and the first rib. B: The typical venogram appearance of an underlying stenosis is due to external and
inflammatory reaction.
6. If the stenosis is in the upper extremity of a patient who is not on hemodialysis, bilateral upper arm intravenous
access is obtained prior to patient arrival in the interventional suite.
7. For patients with laryngeal edema or shortness of breath, who are unable to lie flat for the procedure,
intubation and general anesthesia may be required.
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Procedure
Upper Extremity and Central Venous Stenoses
1. The intravenous line on the affected side is utilized to perform an upper arm venogram. An uninterrupted
segment of vein (preferably at the antecubital fossa) is chosen.
2. Venous road-mapping is performed to identify the length of the occlusion or stenosis. The diameter of the
normal vein is determined.
3. A 7 Fr. access sheath is introduced using sterile Seldinger technique. If the delivery sheath of the chosen
stent requires greater than a 7 Fr. sheath, a femoral or jugular vein approach should be considered.
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4. A 5 Fr. angled catheter (e.g., Berenstein)/hydrophilic-guidewire combination is used to cross the lesion,
with the final exchange-length guidewire tip position preferably in the SVC or down into the IVC but not in
the right atrium (RA) or right ventricle (RV).
5. Because the stenoses are highly elastic, it is preferable to use
a. A balloon and/or stent at least 1 cm longer than the stenosis at each end (Usually, at least a 4-cm balloon
or stent length is necessary to avoid slipping across a focal stenosis.)
b. The diameter chosen is based on the largest diameter of adjacent normal vessel. It is helpful to oversize
the balloon or stent by 2 mm.
c. When needed, a self-expanding stent is preferable in the subclavian or brachiocephalic veins. A large
balloon-expandable stent may be used in the SVC.
6. Digital road-mapping is used to position the center of the balloon or stent at the longitudinal center of the
stenosis.
7. An insufflation device is recommended to achieve at least 10 ATM of pressure. Initial balloon dilation with
a smaller (5-mm-diameter) balloon may be required for patients with severe stenoses.
8. After deployment, dilate the stent to its nominal diameter as necessary. In patients with SVC obstruction,
studies demonstrate improved patency when inserting a stent from the SVC into one innominate vein only,
in comparison to extending stents from the SVC into both innominate veins. Occlusions tend to recur more
frequently with increased complications including mutual obstruction of stents with bilateral insertion
procedures.
9. Angioplasty may be performed following successful thrombolysis of the axillosubclavian venous system.
However, one should resist stent placement until surgical repair of the extrinsic mechanical obstruction is
first performed.
Iliac Vein and IVC Obstructions
1. Intravascular ultrasound can provide important diagnostic and therapeutic information in the
endovascular treatment of May-Thurner syndrome. This procedure is usually performed in conjunction with
thrombolysis of underlying clot.
2. A popliteal vein access using ultrasound guidance and a micropuncture set are recommended. A 5 Fr.
sheath is placed, and diagnostic venography is performed. Thrombolysis may be performed with the
appropriate catheters introduced through this sheath.
3. A 7 Fr. sheath may be necessary for stenting following successful thrombolytic therapy because larger
diameter (10- to 16-mm) angioplasty balloons and stents are frequently necessary. Alternatively, a jugular
vein approach may be considered.
4. Underlying culprit lesions are usually due to extrinsic compression (crossing vessels or retroperitoneal
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fibrosis) or fibrotic webs/synechiae. Hydrophilic-coated wires and catheters are helpful in crossing occluded
segments. On occasion, the back end of the wire may be necessary to initiate crossing of the occlusion.
5. Self-expandable or balloon expandable stents can be used in the vena cava. Self-expanding stents are
preferable in the iliac vein. Iliac vein stents should extend <1 cm into the IVC to minimize the effects on
contralateral blood flow. Optimally, both the proximal and distal end of the stent should be as close to
nominal diameter as possible because this is important in maintaining stent patency. Obstruction of blood
flow within the stent causes low and turbulent flow, which can result in thrombus formation.
Budd-Chiari Syndrome
1. Budd-Chiari syndrome results from webs or focal stenoses of the IVC or hepatic veins. Some of the
hepatic veins can remain occluded, but symptoms will still resolve if a single hepatic vein is opened and
stented.
2. Diagnostic venography may be performed through a right internal jugular or femoral vein access, but a
transhepatic approach may be necessary on rare occasion.
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In the latter case, the skin in the right anterior axillary line should be prepared and draped similarly to a
biliary drainage procedure. Ultrasound guidance is used to access an intrahepatic vein with a small sheath
(6 Fr.). A wire can be manipulated into the IVC from the transhepatic access and the occlusion can be
stented.
3. The venogram may demonstrate patent hepatic veins with webs located at the IVC.
4. An isolated IVC stenosis is best treated from a right internal jugular (or even a femoral vein) approach. If
no suitable hepatic vein is available for catheterization and placement of the access system, left internal
jugular vein access is recommended because this approach offers a more favorable angle in patients
lacking patent right and middle hepatic veins.
5. When required, a wire can be manipulated into the IVC from a transhepatic access and the occlusion can
be stented.
6. For patients presenting weeks to months after hepatic vein thrombosis, the thrombus is no longer
amenable to angioplasty and thrombolysis. In these patients, transjugular intrahepatic portosystemic shunt
(TIPS) is recommended as the next step in management. In the acute setting, TIPS may be considered in
symptomatic patients in whom hepatic vein patency cannot be restored (5,6).
Portal Vein Stenosis
The technique is identical to that used for TIPS placement. Isolated portal vein stenoses causing
symptomatic prehepatic portal hypertension due to pancreatitis, radiation therapy, or surgery may respond
to endovascular stent placement.
Chronic Lower Limb Deep Venous Occlusion
1. Consider CT venography or magnetic resonance (MR) venography for initial assessment.
2. Low-molecular-weight heparin (LMWH) can be used to improve early patency, initiate prior to
endovascular treatment, and continue throughout the procedure.
3. Perform ultrasound-guided micropuncture access-popliteal vein if femoralpopliteal DVT is present and
femoral vein if no infrainguinal DVT. Consider internal jugular (IJ) if unable to cross DVT from lower
extremity access.
4. Traversing the chronic occlusive clot is often challenging. Consider use of a stiff hydrophilic wire, sharp
recanalization, or chronic total occlusion (CTO) catheters/wires; serial dilatation may be required.
Mechanical devices to physically macerate the clot with or without the added use of catheter-directed
thrombolysis might also be considered.
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5. Once the occlusion is successfully crossed, perform balloon maceration of occlusive thrombus with 8-mm
or 10-mm balloons. Overnight EKOS ultrasoundaccelerated thrombolysis can be considered. Infuse 0.5 mg
tissue plasminogen activator (tPA) per hour; increase rate to 1 mg per hour for a more extensive clot. The
typical concentration is 10 mg tPA per 500 mL of normal saline solution (NS).
6. Follow up with venography with venous angioplasty of residual stenoses.
7. Perform venous stenting of chronically narrowed segments in iliac and IVC segments. Perform stenting of
common or upper femoral segments only if no flow from superficial femoral to common femoral veins.
Although there is no U.S. Food and Drug Administration (FDA)-approved venous stent currently available,
self-expanding, bare-metal stents are most commonly used in the venous system (7). In countries where
they are available, dedicated venous selfexpanding stents, which have a higher radial force, are frequently
used.
1. Patients can be discharged home the same day after venous balloon angioplasty or stenting.
2. These patients should receive lifelong aspirin (325 mg) daily. For patients with May-Thurner syndrome and
underlying DVT, treatment with 3 to 6 months
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of warfarin should be considered. There continues to be a debate regarding anticoagulation after venous
stenting in patients with malignant SVC syndrome; long-term anticoagulation after endovascular treatment may
not be mandatory, because risk of rethrombosis is low and risk of bleeding is high; prescribe aspirin for a short
duration (1 month) and no anticoagulation for patients with risk of bleeding. If patient presents with cruoric
thrombosis or paraneoplastic thrombophilic syndrome, prescribe LMWH for 2 to 4 weeks (8).
3. Follow-up is warranted in 6 months with duplex Doppler ultrasound to assess patency.
4. A 1-month venogram and possible maintenance angioplasty may be needed. If a stent is already in place, if
needed, repeat angioplasty of the stent alone is usually sufficient.
Results
1. Malignant SVC obstruction: Endovascular stent technical success >95%, with relief of symptoms noted
in 24 to 72 hours. Failure is secondary to inability to cross the obstructed segment. Primary patency is
reported at 85% to 100% at 3 months; secondary patency is 93% to 100% (1).
2. Benign SVC obstruction: Angioplasty and stenting in these patients result in a primary patency of 77%
to 91% at 1 year, with an 85% secondary patency at 17 months. Endovascular treatment is effective for a
duration of up to 3 years with frequent requirement for repeat intervention. There are still scarce data in
assessing long-term effectiveness of endovascular treatment in benign cases of SVC obstruction (9,10).
3. Subclavian vein and brachiocephalic vein stenoses: For lesions caused by previous central venous
catheters, primary angioplasty followed by >50% recoil suggests a predisposition to recurrence and
thrombosis. Unless there is a preexisting arteriovenous fistula in the ipsilateral arm, sustaining good flow,
stents tend to thrombose as well. Stents should be utilized only when there is significant elastic recoil and
only after repeated failure of angioplasty. For patients with thoracic outlet syndrome, angioplasty and stent
placement should only be used after surgical resection of the first rib (3).
4. Iliofemoral and IVC obstructions (May-Thurner syndrome/Cockett syndrome): Primary patency
rates in iliofemoral venous angioplasty and stenting at 6, 12, and 24 months were 88%, 78.3%, and 78.3%,
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respectively. Secondary patency rates for the same time durations are 100%, 95%, and 95%. Better
outcomes are seen in stenting for May-Thurner syndrome and idiopathic causes, whereas external
compression and thrombophilia portend less favorable outcomes (11). Balloon angioplasty alone is not
indicated, self-expanding stents should be utilized, and late reocclusions of the stents are rare. For IVC
obstructions, the initial technical success rate is 88%. The primary patency rate at 19 months is 80%, with a
primary-assisted patency of 87% (12).
5. Budd-Chiari syndrome: The cumulative 1-, 5-, and 10-year primary patency rates were 95%, 77%, and
58%, respectively. Independent predictors of reocclusion included increased white blood cell count and use
of PTA alone. The cumulative 1-, 5-, and 10-year secondary patency rates were 97%, 90%, and 86%,
respectively. The cumulative 1-, 5-, and 10-year survival rates were 96%, 83%, and 73%, respectively.
Independent risk factors against survival included variceal bleeding, increased alkaline phosphatase and
blood urea nitrogen levels, and reocclusion (13,14).
Complications
1. Bleeding from the puncture site is the most common complication. Local pressure is usually sufficient
treatment.
2. Thrombosis at the angioplasty site: Thrombolysis can be instituted immediately, followed by repeat
angioplasty or stenting.
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3. Vein rupture: Gentle prolonged balloon inflation frequently seals the site of rupture. Small mesh stent
placement may be considered. Stent-graft placement may be indicated for prolonged or profound
extravasation.
4. SVC stent occlusion: This can be treated with thrombolysis, balloon dilation, or further stent insertion with
good secondary patency rates.
References
1. Lanciego C, Pangua C, Chacón JI, et al. Endovascular stenting as the first step in the overall management
of malignant superior vena cava syndrome. AJR Am J Roentgenol . 2009;193:549-558.
2. Kee ST, Kinoshita L, Razavi MK, et al. Superior vena cava syndrome: treatment with catheter-directed
thrombolysis and endovascular stent placement. Radiology. 1998; 206:187-193.
3. Sheeran SR, Hallisey MJ, Murphy TP, et al. Local thrombolytic therapy as part of a multidisciplinary
approach to acute axillosubclavian vein thrombosis (Paget-Schroetter syndrome). J Vasc Interv Radiol .
1997;8:253-260.
4. Mickley V, Schwagierek R, Rilinger N, et al. Left iliac venous thrombosis caused by venous spur: treatment
with thrombectomy and stent implantation. J Vasc Surg. 1998;28:492-497.
5. Tripathi D, MacNicholas R, Kothari C, et al. Good clinical outcomes following transjugular intrahepatic
portosystemic stent-shunts in Budd-Chiari syndrome. Aliment Pharmacol Ther. 2014;39:864-872.
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6. Abujudeh H, Contractor D, Delatorre A, et al. Rescue TIPS in acute Budd-Chiari syndrome. AJR Am J
Roentgenol . 2005;185:89-91.
7. Garcia M. Endovascular options for chronic DVT. Endovascular Today. 2012;54-58.
8. Thony F, Fagedet D, Michoud M, et al. Anticoagulation is not mandatory after stenting for malignant
superior vena cava syndrome. Cardiovasc Intervent Radiol . 2014;37:1403-1404.
9. Sheikh MA, Fernandez BB Jr, Gray BH, et al. Endovascular stenting of nonmalignant superior vena cava
syndrome. Catheter Cardiovasc Interv. 2005;65(3):405-411.
10. Kalra M, Gloviczki P, Andrews JC, et al. Open surgical and endovascular treatment of superior vena cava
syndrome caused by nonmalignant disease. J Vasc Surg. 2003;38(2):215-223.
11. Titus JM, Moise MA, Bena J, et al. Iliofemoral stenting for venous occlusive disease. J Vasc Surg.
2011;53:706-712.
12. Hansch EC, Razavi MK, Semba CP, et al. Endovascular strategies for inferior vena cava obstruction.
13. Meng QY, Sun NF, Wang JX, et al. Endovascular treatment of Budd-Chiari syndrome. Chin Med J
(Engl). 2011;124(20):3289-3292.
14. Han G, Qi X, Zhang W, et al. Percutaneous recanalization for Budd-Chiari syndrome: an 11-year
retrospective study on patency and survival in 177 Chinese patients from a single center. Radiology.
2013;266(2):657-667.
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38
Transvenous Biopsy
Matthew G. Gipson
Rajan K. Gupta
Histopathologic analysis of the liver and kidney remain the gold standard for the diagnosis and evaluation of
acute and chronic liver disease and most renal parenchymal diseases. Percutaneous liver and kidney biopsies
were initially described in 1883 and 1951, respectively, and developments in technique have improved efficacy
and safety of the procedure (1,2). In patients with contraindications to transabdominal biopsy, a transvenous
approach is a well-established method to obtain diagnostic tissue safely (3,4).
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Indications
1. Transvenous liver biopsy (5)
a. Patients with diffuse liver disease who have contraindication to percutaneous biopsy including those with
a coagulation disorder, ascites, peliosis hepatis, or morbid obesity
b. Patients who require hemodynamic assessment as part of their diagnostic workup
2. Transvenous kidney biopsy
a. Patients with suspected renal disease who are at high risk for percutaneous biopsy including those with a
coagulation disorder or morbid obesity
b. After failed percutaneous renal biopsy
Contraindications
Relative
1. Lack of suitable venous access (superior vena cava obstruction)
2. Diagnosis of focal lesions
3. Uncorrectable coagulation parameters
1. Indication for procedure, medical/surgical history, and pertinent imaging is reviewed. Transplantation anatomy
is particularly pertinent.
2. Focused physical exam is performed.
3. Informed consent obtained detailing risks specific for the procedure with discussion regarding need for
possible blood transfusion if periprocedural bleeding occurs. Consent for possible percutaneous biopsy for
all cases; anatomy may preclude safe biopsy in a minority of patients.
4. Prothrombin time (PT)/international normalized ratio (INR), partial thromboplastin time (PTT), platelet count,
and serum creatinine level are obtained. Each institution should establish acceptable coagulation parameters; as
a general guideline, INR <2.0 and platelets >50,000 per μL of blood are acceptable. If the clinical situation
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dictates biopsy, these parameters may be exceeded, for example, in patients with fulminant liver failure where
correction may be impossible.
5. All patients receive peripheral intravenous (IV) access to facilitate sedation.
6. Patients are nil per os (NPO) following institutional guidelines for sedation: clear liquids 8 hours and NPO 4
hours prior to the procedure.
Procedure
1. Transvenous access
a. Patient is positioned supine on the fluoroscopic table.
b. Minimizing sedation initially is helpful for obtaining accurate and reproducible hepatic venous pressures.
Additional sedation may be given prior to biopsy.
c. Right internal jugular access is preferred, given direct anatomic alignment with superior vena
cava/inferior vena cava (IVC).
d. After local anesthesia with 1% lidocaine, internal jugular venous access is achieved using direct
ultrasound guidance. A 5 Fr. introducer catheter is replaced for a 9 Fr. vascular sheath.
2. Liver biopsy
a. Two U.S. Food and Drug Administration (FDA)-approved transjugular liver biopsy sets are available for
use and include (a) TLAB-Patel Set (Argon Medical, Plano, TX)—available with an 18- or 19-gauge
Flexcore biopsy needle and (b) LABS-100/200 set (Cook Medical, Bloomington, IN)—available with an 18-
or 19-gauge Quick-Core biopsy needle.
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b. Using an angled 5 Fr. multipurpose catheter (MPA) (Cook Medical, Bloomington, IN) and hydrophilic
guidewire, cannulate the right hepatic vein (RHV). If the hepatic venous angle is acute, a reverse curve
catheter such as an SOS Omni selective catheter (AngioDynamics, Latham, NY) can be helpful to obtain
access into the hepatic veins. The RHV is preferred because it is posterior in the liver and biopsy will be
directed anteriorly. Selection of the RHV can be confirmed by rotating the fluoroscopic tube into an oblique
orientation to confirm that the wire is directed posteriorly.
c. Perform hepatic venography through the 5 Fr. catheter to assess patency of selected vein. Transvenous
hepatic pressures can be obtained if indicated.
d. Over a 0.035-in., 145-cm Amplatz wire (Cook Medical, Bloomington, IN), advance the stiff-angled guide
cannula supplied in the transjugular biopsy kit distally into the RHV.
e. Advance biopsy needle through guide cannula and before advancing the needle into the hepatic
parenchyma, rotate angled guide cannula (positioned in RHV) anteriorly directed into the right hepatic lobe.
f. Obtain samples from central portion of the liver, avoiding transcapsular punctures. Mild forward pressure
on the cannula during needle exchanges will prevent retraction into the IVC.
g. Deploy biopsy needle after advancing needle into parenchyma. Remove needle from guide cannula and
place specimen in formalin container; care should be taken to reduce sample fragmentation.
h. Repeat biopsy until sample deemed adequate for diagnosis.
i. Stiff-angled guide cannula and vascular sheath are now removed; manual pressure is applied at
venotomy site until hemostasis achieved.
j. Specimen is delivered to appropriate lab.
3. Kidney biopsy
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a. Equipment: renal access and biopsy set (RABS-100, Cook Medical, Bloomington, IN)
b. Using an angled 5 Fr. MPA and hydrophilic guidewire, cannulate the right renal vein. Advance the
catheter into the posterior lower pole branch of the right renal vein.
c. Exchange hydrophilic wire for a 0.035-in., 145-cm Amplatz wire (Cook Medical, Bloomington, IN) and
gently advance the 7 Fr. sheath and inner stiffening cannula distally as possible into a peripheral cortical
vein of the lower pole. Venography is performed through the sheath; when cortical staining occurs, the
sheath is appropriately positioned.
d. With gentle forward pressure on the 7 Fr. sheath, advance the 19-gauge, 20-mm Quick-Core side cut
biopsy needle (70 cm) into the renal parenchyma. Deploy the needle cutting cannula. Four passes are
usually adequate for histologic evaluation (2).
e. After obtaining specimen, inject contrast medium through the 7 Fr. sheath to identify any capsular
perforation. If present, prophylactic embolization can be performed with Gelfoam or coils.
f. Specimen can be evaluated by the pathology department for glomerular adequacy during procedure or
delivered to appropriate lab in formalin.
4. Transvenous hepatic pressure measurement
a. General: The hepatic venous pressure gradient (HVPG) is an indirect, minimally invasive method to
measure portal perfusion pressure. It is obtained by subtracting the free hepatic venous pressure (FHVP),
reflective of intraabdominal pressure, from the wedged hepatic venous pressure (WHVP), reflective of
sinusoidal pressure. In cirrhosis caused by alcoholic liver disease, hepatitis B, and hepatitis C, however,
intersinusoidal communications are lost due to fibrosis and WHVP accurately reflects portal pressure (6).
This makes HVPG reflective of portal perfusion pressure. HVPG is normally ≤5 mm Hg. HVPG ≥10 mm Hg
is considered clinically significant portal
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hypertension because it is predictive of the presence and development of varices, clinical decompensation
in patients without varices, development of hepatocellular carcinoma (HCC), and decompensation at
surgery for HCC (6). Strict technique is required in order to obtain accurate and reproducible results. Sweep
speed of pressures should be set at 5 mm per second or slower so that changes in pressures over time are
visually perceptible. A mean pressure line should also be recorded to help in interpretation (Fig. 38.1).
b. Sedation: Moderate sedation with fentanyl and Versed induces substantial changes in respiration, which
in turn makes measurement of HVPG unreliable and poorly reproducible. Oversedation is the most common
error resulting in poorly obtained pressures. Ideally, only mild anxiolysis is provided with minimal Versed
(0.02 mg per kg).
c. A pressure transducer should be affixed to the angiographic table with a zero level set at the midaxillary
line.
d. FHVPs are typically obtained with the catheter 2 to 4 cm into the hepatic vein. Fifteen to 20 seconds
should be allowed for the pressure to equilibrate.
e. WHVP is measured by arresting hepatic venous outflow to create a static column of blood between the
catheter and the hepatic sinusoids. Although this can be performed with a 5 Fr. end-hole diagnostic catheter
advanced and subsequently wedged into a small hepatic vein, the use of a balloon catheter is
recommended to improve the reliability and reproducibility of measurements (6). Use of a balloon catheter
effectively samples a larger area of liver because there are often regional differences in fibrosis. At the
authors' institution, this is performed with an 11.5-mm occlusion balloon (Boston Scientific,
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Marlborough, MA). WHVP may take 1 to 2 minutes to equilibrate. After the measurement has been
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recorded, a gentle wedged venogram is performed to ensure that the balloon has been occlusive (Fig.
38.2). Wedged venography should not be performed prior to measurement because the different viscosity of
contrast as compared to blood may affect pressure measurements. Hepatic vein to hepatic vein collaterals
should be identified because these will falsely lower the HVPG.
FIGURE 38.1 • This tracing represents excellent, stable wedged (top), and free (bottom) hepatic venous
pressures. Note how the oscillations in the tracing, which are due to respiration, are very regular due to
very little anxiolysis with minimal Versed only. The mean tracing helps to visualize an average and the
compressed waveform (5 mm per second sweep speed) is easy to read. For clinical studies, documentation
of an accurate zero is also recorded.
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FIGURE 38.2 • Wedged hepatic venography. An occlusion balloon is relatively central, and gentle
venography is performed until distal branches are visualized. Notice how large of an area is sampled by
using the balloon; this improves reproducibility and reliability. These images document appropriate wedging
of the balloon, ensuring that the wedged pressure was accurate.
f. Two sets of FHVP and WHVP should be obtained. Each subsequent measurement should be within 1 mm
Hg of the previous or they should be repeated.
g. Select the infrahepatic IVC and obtain an IVC pressure. This pressure should be within 2 mm Hg of the
free hepatic pressure. If it is not, this may be reflective of inaccurate measurement or hepatic venous
outflow stenosis.
h. Right atrial pressure and infrahepatic IVC pressure are normally similar. Ascites can elevate intra-
abdominal pressure compared to right atrial pressure. For this reason, the infrahepatic IVC pressure rather
than the right atrial pressure is used to reference the FHVP.
i. Documentation of right atrial pressure is important in the evaluation of patients following liver
transplantation and patients being evaluated for Budd-Chiari syndrome to exclude hemodynamic IVC
stenosis.
j. Proceed with additional conscious sedation and biopsy if indicated.
a. These procedures are typically well tolerated, and patients can resume normal activity in 24 hours.
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b. Clear liquid diet for first hour; regular diet thereafter if tolerated
c. Monitor vital signs every 15 minutes for 1 hour, then every 30 minutes for 2 hours, and then every hour
postprocedure until discharged.
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d. If vital signs are stable and pain is controlled, the patient may be discharged after bed rest period (2 hours for
transvenous liver biopsies and 4 hours after transvenous kidney biopsies).
e. Patients receive written instructions regarding follow-up for potential late complications.
Results
1. Transvenous liver biopsy
a. Reported technical success is excellent (97%) with the most common cause of failure due to the inability
to catheterize a suitable hepatic vein, seen more often in patients after liver transplantation (3). Lack of
transvenous access is another reason for technical failure; however, the use of the left internal jugular,
external jugular, subclavian, or femoral veins may be utilized to complete the exam (7).
b. Four complete portal tracts (CPTs) are usually considered the minimum for defining a liver transplant
biopsy to rule out rejection, and six complete portal tracts are considered minimum for assessing the
histological diagnosis of diffuse liver disease (i.e., recurrence of viral liver disease). Frequently, one or two
needle passes are adequate for histopathologic diagnosis; however, liver specimens of 20-mm in length
containing 11 complete portal tracts are needed for grading and staging chronic hepatitis (8,9).
c. Sample fragmentation is most often seen with liver cirrhosis and has been reported in 14% to 25% of
transvenous liver biopsy samples. Fragmentation may interfere with diagnostic quality of the specimen (7).
d. Adequate tissue is obtained in up to 96% of the time by reported experiences (10). A larger gauge needle
(18-gauge) may provide better samples for staging liver fibrosis. Four cores are routinely submitted.
2. Transvenous kidney biopsy
a. Technical success is 92% to 96% with most failures resulting from inability cannulating the renal veins
(2,4).
b. Tissue adequacy is 98% and comparable to percutaneous renal biopsy (4).
3. Hepatic venous pressure measurements
a. Technical success is >95% and is only limited by lack of ability to catheterize the hepatic veins (11).
Complications
1. Transvenous liver biopsy (3): Overall complications (7.1%) are either related to liver puncture (3.5%) or
other mechanism (3.3%). Most are minor complications and include fever, neck hematoma, abdominal pain,
or minor bleeding around the liver capsule. Major complications including pneumothorax, intraperitoneal
hemorrhage, and arrhythmias are seen in 0.6% of patients. Mortality is rare (0.1%) resulting from
intraperitoneal hemorrhage or ventricular arrhythmia.
2. Transvenous kidney biopsy (4): Major complications (1%) requiring blood transfusion or intervention are
rare. Transient microscopic hematuria is more common.
3. Hepatic venous pressure measurement: Access site hemorrhage, vagal reactions, and arrhythmias may
be encountered in a similar frequency to transjugular biopsy. Most other more serious complications are
related to concurrent transvenous liver biopsy. No deaths have been reported to date from HVPG
measurement (12).
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1. Complications are mostly minor and can usually be treated with supportive measures including IV fluids
and oral medications.
2. If pain is out of proportion to the examination, parenchymal/subcapsular hemorrhage or bile peritonitis
should be suspected. Intermittent, severe pain suggesting biliary colic may be seen with hemobilia. Cross-
sectional imaging with computed tomography (CT) (+/× intravascular iodinated contrast) is a fast and
reliable way to assess for clinically significant bleeding or other complication. If postprocedure pain is
severe and unable to be controlled adequately, overnight admission to the hospital maybe necessary.
References
1. Bravo AA, Sheth SG, Chopra S. Liver biopsy. N Engl J Med. 2001;344(7):495-500.
2. Thompson BC, Kingdon E, Johnston M, et al. Transjugular kidney biopsy. Am J Kidney Dis.
2004;43(4):651-662.
3. Kalambokis G, Manousou P, Vibhakorn S, et al. Transjugular liver biopsy—indications, adequacy, quality

of specimens, and complications—a systematic review. J Hepatol . 2007;47(2):284-294.
4. Cluzel P, Martinez F, Bellin MF, et al. Transjugular versus percutaneous renal biopsy for the diagnosis of
parenchymal disease: comparison of sampling effectiveness and complications. Radiology. 2000;215(3):689-
693.
5. Strassburg CP, Manns MP. Approaches to liver biopsy techniques—revisited. Semin Liver Dis.
2006;26(4):318-327.
6. Berzigotti A, Seijo S, Reverter E, Bosch J. Assessing portal hypertension in liver diseases. Exper Rev
Gastroenterol Hepatol . 2013;7(2):141-155.
7. Behrens G, Ferral H. Transjugular liver biopsy. Semin Intervent Radiol . 2012;29:111-117.
8. Miraglia R, Maruzzelli L, Minervini M, et al. Transjugular liver biopsy in liver transplant patients using an
18-gauge automated core biopsy needle. Eur J Radiol . 2011;80(3):e269-e272.
9. Cholongitas E, Senzolo M, Standish R, et al. A systematic review of the quality of liver biopsy specimens.
Am J Clin Pathol . 2006;125:710-721.
10. Behrens G, Ferral H, Giusto D, et al. Transjugular liver biopsy: comparison of sample adequacy with the
use of two automated needle systems. J Vasc Interv Radiol . 2011;22(3):341-345.
11. Kumar A, Sharma P, Sarin SK. Hepatic venous pressure gradient measurement: time to learn! Indian J
Gastroenterol . 2008;27(2):74-80.
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12. Suk KT. Hepatic venous pressure gradient: clinical use in chronic liver disease. Clin Mol Hepatol .
2014;20(1):6-14.
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39
Preoperative Portal Vein Embolization
David C. Madoff
David Li
Surgical resection offers the best chances for long-term survival of patients with primary and metastatic diseases
confined to the liver (1,2). Major hepatic resection (i.e., greater than three Couinaud segments) places patients
at risk for developing complications related to liver insufficiency in the perioperative period. The anticipated
volume of liver which remains after surgery, termed the future liver remnant (FLR), has been shown to be a
strong, independent predictor of postoperative complications (3,4). Portal vein embolization (PVE) is an important
tool in the preoperative management of select patients with “marginal”
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anticipated FLR volumes prior to major hepatectomy (5,6). Embolization of the portal vein branches supplying the
liver segments to be resected redirects blood flow to the nondiseased liver. This redistribution induces
hypertrophy of the FLR, thereby making it possible for these patients, not previously considered as candidates to
safely undergo major hepatectomy. PVE continues to demonstrate an essential adjunctive role to major
hepatectomy, even as advances in hepatobiliary surgical techniques evolve and indications for curative
hepatectomy expand, given its high safety profile and proven efficacy at promoting liver remnant hypertrophy.
Indications
1. Patients with primary or metastatic liver disease who are otherwise hepatic resection candidates, other
than:
a. Normal underlying liver and a standardized future liver remnant (sFLR; see definition in the following text)
less than 20% (3,7,8)
b. Cirrhosis and/or advanced fibrosis and an sFLR less than 40% (9,10)
c. Extensive chemotherapy and an sFLR less than 30% (11)
2. Patients with diabetes mellitus without underlying liver disease may benefit from PVE, as the magnitude
of postresection liver hypertrophy is usually less in these patients (12).
3. Patients undergoing complex hepatectomy with concomitant extrahepatic surgery, particularly
pancreatectomy. In this latter group, studies have demonstrated that hepatic regeneration is inversely
proportional to the extent of pancreatectomy (7).
Contraindications
Absolute
1. Overt clinical portal hypertension
2. Extensive invasion of the portal vein precluding safe catheter manipulation and optimal delivery of
embolic material
3. Complete lobar portal vein occlusion (right or left), as portal blood flow will already have been diverted (5)
Relative
1. Extrahepatic metastatic disease, including portal lymphadenopathy
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2. Two-stage hepatectomy has expanded the number of patients with bilobar hepatic disease burden
eligible for PVE and potential curative resection; however, diffuse hepatic disease burden remains a
contraindication to PVE.
3. Tumor precluding safe access into the portal venous system (approach may vary on the basis of location
of tumor—see discussion of ipsilateral and contralateral approaches in the following text)
4. Biliary dilatation within the FLR (biliary decompression prior to PVE is required)
5. Mild portal hypertension
1. Future liver remnant determination
a. Liver volume is directly correlated with a patient's size; hence, normalizing the anticipated liver volume to a
patient's size results in a more accurate assessment of the FLR. This principle led to the proposal and clinical
validation of an sFLR (13).
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b. sFLR is the ratio of the FLR over the total estimated functioning liver volume (TELV):
sFLR = FLR / TELV
c. The total estimated liver volume (TELV) is calculated as follows (14):
TELV = - 794.41 + 1267.28 × BSA
where BSA is the body surface area.
d. Computed tomography (CT) is used to directly measure the FLR. Volumetric three-dimensional contrast-
enhanced computed tomography (3D-CT) is essential for planning hepatic resection. Calculate the 3D-CT
volumes by outlining the hepatic segmental contour area on each slice and summing individual slice volumes
(contour area × slice thickness) (13).
(1) Check for portal vein patency and variant anatomy.
e. Most protocols acquire CT images immediately before PVE and approximately 3 to 4 weeks after the
procedure to assess the degree of FLR hypertrophy. In addition to sFLR, the degree of hypertrophy (DH) and
kinetic growth rate (KGR) are also used as predictors of postoperative course (15). DH = FLR / TELV (post-PVE)
- FLR / TELV (pre-PVE). KGR = DH / no. of weeks elapsed after PVE. Patients whose DH is <5% or KGR <2.0%
per week have higher postoperative complication rates. DH and KGR serve as additional measures for
determining whether or not the involved liver is ultimately resected.
f. If the sFLR is considered inadequate to allow for safe hepatic resection on the initial follow-up CT scan,
additional “waiting time” may be useful as regeneration may still occur albeit as a slower rate dependent on DH
and KGR.
2. Patients are usually admitted the night before the procedure and kept nil per os (NPO). Informed consent is
obtained.
3. Intravenous (IV) antibiotic prophylaxis is usually not required. However, patients with biliary obstruction
involving the liver to be resected and/or a biliary drainage catheter within the FLR should be given prophylactic
antibiotics (ceftriaxone 1 g IV).
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4. PVE can be performed under moderate IV sedation using a combination of fentanyl and midazolam. However,
general anesthesia is recommended for patients with multiple comorbidities or for those who cannot cooperate.
5. Ultrasound examination is performed to verify patency of the intended access branch to the portal vein
immediately before the procedure.
Procedure
1. Although PVE can promote hypertrophy of either lobe, left PVE is not commonly performed because left
hepatectomy results in a remnant liver volume that is sufficient enough that post-hepatectomy liver failure
will be unlikely (16). Furthermore, patients who require an extended left hepatectomy (resection of all but
the right posterior liver—segments 6 and 7) for cure have an FLR approximately 33% of the total liver
volume (TLV; 20% is all that is required). For these reasons, the ensuing discussion will focus on right-
sided PVE approaches.
2. Embolization of the entire tumor-bearing liver. In the appropriate clinical setting (e.g., cirrhosis), right
PVE is performed prior to right hepatectomy. For patients undergoing extended right hepatectomy (i.e.,
resection of the right liver and segment 4), the embolization of the right liver and the segment 4 portal veins
should be performed (not right PVE alone). The reasons are as follows:
a. FLR (segments 2 + 3 ± 1) hypertrophy is increased more with segment 4 embolization than without (17).
b. In the setting of right PVE alone, segment 4 will hypertrophy, thereby increasing the length of the
transection plane and potentially complicating the surgery.
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c. Right PVE alone is associated with an increased risk of tumor growth in segment 4 (i.e., tumors within
segment 4 have been found to grow faster than the regenerating underlying liver parenchyma) (18).
3. Percutaneous PVE can be performed using either the ipsilateral or contralateral transhepatic approach
(19,20,21,22). The choice of approach is based mainly on the tumor burden within the liver, the need for
segment 4 embolization, and the operator preference. The ipsilateral approach does not require puncturing
the FLR but may be technically more challenging. The contralateral approach allows for easy access into
the portal vein and is generally faster but in rare cases may cause damage to the FLR, thereby precluding
curative resection. Furthermore, catheterization of segment 4 portal veins can be difficult using the
contralateral approach (i.e., left portal vein access for right PVE), and this may lead to prolonged catheter
placement within the left portal system that could lead to thrombosis.
Ipsilateral Approach (19,20,21,23)
For transhepatic right portal vein puncture, see Figure 39.1.
1. A 22-gauge Chiba needle (Neff Percutaneous Access Set, Cook, Bloomington, IN) is advanced into a
peripheral portal venous branch within the non-FLR under real-time ultrasound guidance. A 0.18-in.
guidewire is inserted through the needle, which is then exchanged for an appropriately sized dilator using
fluoroscopy.
2. A 5 Fr. or 6 Fr. vascular sheath is placed into the right portal vein branch.
3. Portography is performed with a 5 Fr. angiographic flush catheter positioned within the main portal vein.
Digital subtraction images are acquired in the anteroposterior and craniocaudal projections.
4. Selective right and left portograms are obtained to best delineate variant anatomy and segment 4 portal
venous anatomy.
5. When segment 4 embolization is required, this portion of the procedure is ideally performed first. This
avoids the difficulty of catheter manipulation and the risk of dislodgment of embolic material when
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attempting to embolize segment 4 after ipsilateral right-sided PVE.
6. Segment 4 is embolized using a 3 Fr. microcatheter in a coaxial fashion through a 5 Fr. selective
catheter.
7. Spherical embolic agents, such as tris-acryl microspheres (EmboGold Microspheres, Biospheres
Medical, Rockland, MA) are the embolic agents of choice. The microspheres ranging in size from 100 to 700
μm are delivered in an incremental fashion under fluoroscopy.
8. After embolization with particulate material is complete, fibered microcoils or plugs are deposited in the
more proximal segments to further reduce portal inflow, further promoting hypertrophy and decreasing
recanalization rates (24).
9. Many other embolic materials have been used for PVE, with no remarkable differences reported in the
degree or rate of hypertrophy. These other agents include, but are not limited to, fibrin glue, n-butyl
cyanoacrylate (NBCA) mixed with iodized oil, sodium tetradecyl sulfate (STS) foam, gelatin sponge,
thrombin, metallic coils, other microparticles (e.g., PVA particles), and absolute alcohol (20,25,26,27). The
decision to use a particular agent is at the discretion of the operator and is based primarily on the extent of
the embolization and surgery, the operator's preference for a particular catheter and approach, and the
operator's familiarity with a specific agent.
10. After completion of the segment 4 embolization, the microcatheter is removed and the working catheter
exchanged for a 5 Fr. reverse curve. This shape allows easier catheter manipulation into the right portal
venous branches, given their obtuse angulation with the direction of the sheath.
11. The “normal” portal venous branching anatomy is found in only 65% of cases (28). The most common
variation is a right posterior portal vein arising
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as the first branch of the main portal vein (13% of cases). Portal trifurcation with the left, right anterior, and
posterior branches originating from the main portal vein is also common (9% of cases). Intraprocedural C-
arm cone-beam CT can be used to better delineate portal anatomy.
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FIGURE 39.1 • Diagrams illustrate the technique of transhepatic ipsilateral right PVE extended to segment 4
using particulate embolic agent and coils. A: Vascular sheath provides access into a right portal vein
branch with a selective catheter in the left portal vein. In a coaxial fashion, through the selective catheter, a
microcatheter is positioned in a segment 4 branch just prior to embolization. B: After completion of segment
4 embolization, a reverse-curve selective catheter is used to deliver the embolic material to the right portal
vein branches. C: After completion of the right PVE extended to segment 4, redistribution of blood flow into
the nonembolized liver (FLR) is noted.
12. Embolization of the right portal vein branches is performed in a similar fashion, using smaller particles
first to occlude the distal, smaller branches, and the larger particles used subsequently to occlude the more
proximal, larger branches. After near-stasis embolization is achieved, coils and/or plugs are placed within
the secondary portal branches to further reduce the venous inflow (24).
13. Final portography is obtained with the flush catheter positioned within the main portal vein.
14. After completion of the embolization, the working catheter and vascular sheath are removed and the
access tract is occluded with coils.
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Contralateral Approach (21,29)
For transhepatic left portal vein puncture, see Figure 39.2.
1. The portal venous system is accessed using similar technique. This approach has the advantage of
antegrade catheterization of the main right portal vein and its branches without the sharp angles
encountered during PVE using the ipsilateral approach.
2. The portal vein branch to be punctured in the FLR must be upstream to any branches targeted for
embolization.
3. A peripheral portal branch, preferably belonging to segment 3, is accessed via the subxiphoid route.
4. Extreme care must be taken during the puncture because any substantial injury to the FLR will preclude
further surgical therapy.
5. Catheter and vascular sheath are introduced. The tip of the vascular sheath may be positioned in the
main portal vein, which facilitates the acquisition of repeat portograms.
FIGURE 39.2 • Diagram illustrates the technique of transhepatic contralateral right PVE. Vascular sheath
provides access into a left lateral liver portal vein branch in the FLR with a balloonocclusion catheter
positioned in the right portal vein. The balloon is inflated and liquid embolic agent is delivered into the right
portal vein. The balloon prevents reflux of embolic material into the main and left portal vein branches.
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6. A short selective catheter is preferred because it provides a smaller “dead space.”
7. Because the embolization is performed with the working catheter positioned along the direction of the
portal venous flow, embolization is technically easier. This may be particularly advantageous when liquid
embolic agents are employed.
8. Selection and delivery of other embolic agents follow the same principles used for the ipsilateral
approach.
9. Multiple portograms may be obtained throughout the procedure without additional catheter manipulation,
which decreases the risk of dislodgment of embolic material.
10. When segment 4 embolization is required, the contralateral approach makes this portion of the
procedure more challenging because of the proximity of the segment 4 branches to be embolized and the
puncture site. These branches are the last ones to be embolized, usually only performed after the
embolization of the right portal venous branches is complete.
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Combining Transarterial Embolization and PVE
1. PVE can be combined with other interventional radiology techniques such as transarterial embolization (TAE).
2. TAE followed by PVE has also been advocated in the setting of cirrhosis complicated by hepatocellular
carcinoma (HCC). This dual preparation with either bland embolization or chemoembolization performed 2 to 3
weeks before PVE is used to prevent tumor progression during the waiting period and to occlude arterioportal
shunts commonly observed in cirrhosis and HCC, thereby strengthening the effects of the PVE (30,31).
3. In select settings, TAE can also be performed when FLR hypertrophy is inadequate after PVE. The
mechanism of TAE is complementary as a component of inflammation and necrosis is added to the apoptosis-
mediated cell death induced by PVE to stimulate liver hypertrophy (32).
4. With combination therapies, both arterial and portal venous hepatic supplies are embolized, placing patients at
greater risk for liver necrosis. To reduce this risk, PVE should be staged at least 2 to 3 weeks after TAE. In
addition, chemoembolization protocols should be modified. Chemoembolization should not be carried out to
complete stasis, and use of particulate embolic agents should be avoided or limited.
5. Following chemoembolization, the interventional radiologist should confirm patency of the hepatic artery
supplying the targeted liver segment in order to avoid occlusion of arterial and portal hepatopetal flow and the
potential of parenchymal necrosis.
1. PVE is well tolerated, and unless patients have significant comorbidities, they are discharged the day after the
procedure. The mechanism of action for PVE is predominantly apoptosis-mediated, and patients typically do not
develop postembolization syndrome seen with hepatic transcatheter arterial embolization (necrosis-mediated)
(23).
2. Vigorous hydration until oral intake is adequate
3. If needed, narcotics, antiemetics, and antipyretics are supplied for control of pain, nausea, and fever.
4. Patient is discharged as soon as oral intake is adequate and parenteral narcotics are not required for pain
control (although pain is atypical after PVE).
5. CT of the abdomen is repeated after 3 to 4 weeks to verify the DH.
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Results
1. PVE is indicated with normal underlying liver and sFLR less than 20%. A series of 112 patients found that
both sFLR less than 20% and degree of sFLR hypertrophy after PVE less than 5% predicted poor outcome
after resection (3).
2. In a series of 301 consecutive patients who underwent extended right hepatectomy, patients with a
preoperative sFLR less than 20% had significantly higher rates of postoperative liver insufficiency and
death from liver failure compared with patients with sFLR greater than 20% ( P <.05). In addition, patients
who underwent PVE before surgery to increase their sFLR from less than 20% to greater than 20% had
statistically equivalent rates of liver insufficiency as patients with greater than 20% at baseline. This study
confirmed the beneficial role of PVE in reducing perioperative complication rates in those patients who
hypertrophy their normal liver to an sFLR greater than 20% (8).
3. Liver regeneration occurs at a reduced rate and capacity in diseased livers, an observation directly
correlated to clinical outcomes.
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4. PVE is indicated in cirrhosis and/or advanced fibrosis and an sFLR less than 40%. A prospective
alternative allocation trial in which patients with chronic liver disease were allocated to PVE or no PVE
before resection validated the higher minimum sFLR cutoff of less than 40%; the PVE group had a mean
sFLR size of 35% and demonstrated significantly lower incidence of complications including liver failure (9).
5. PVE is indicated after chemotherapy greater than 12 weeks and an sFLR less than 30%. A retrospective
analysis of 194 patients with colorectal liver metastasis who underwent extended right hepatectomy found
that both long duration of chemotherapy (defined as greater than 12 weeks) and sFLR less than or equal to
30% were predictors of hepatic insufficiency. No cases of postoperative mortality and only two cases of
postoperative hepatic insufficiency were reported if the sFLR is greater than 30% (11).
6. PVE does not preclude chemotherapy. A series of 64 consecutive patients who underwent PVE were
stratified into two groups: those who received chemotherapy (n = 25) and those who did not (n = 39), in
anticipation of extended right hepatic resection. The chemotherapy group demonstrated a clear survival
benefit as compared to the no chemotherapy group (49% vs. 24% 5 year survival; P = .006) in both the
surgical resection and nonsurgical cohorts (33).
7. In addition to sFLR, DH and KGR are correlated with postoperative hepatic dysfunction. Of the three
measures, a KGR cutoff value of less than 2.0% per week demonstrated the highest accuracy (81%), with
sensitivity of 100% and specificity of 71% in predicting postoperative hepatic insufficiency in a series of 107
patients who underwent PVE and subsequent hemi or extended right hepatectomy (15).
Complications
1. Quality improvement guidelines from the Society of Interventional Radiology suggest thresholds for PVE-
related major complications of 6% and morbidity of 11%. Most published complication rates fall well below
this range (34,35).
2. Complications of PVE are similar to other image-guided transhepatic procedures and include subscapular
hematoma, hemoperitoneum, hemobilia, abscess formation, cholangitis and sepsis, arterioportal shunts,
arterioportal fistula, and pneumothorax (5,23).
3. Although rare, complications more specific to percutaneous PVE include nontarget embolization,
recanalization of embolized segments, and extension of portal vein thrombosis to involve the left or main
branches. Portal thrombosis may respond well to chemical and/or mechanical thrombolysis.
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References
1. Imamura H, Seyama Y, Kokudo N, et al. Single and multiple resections of multiple hepatic metastases of
colorectal origin. Surgery. 2004;135(5):508-517.
2. Benson AB III, Bekaii-Saab T, Chan E, et al. Metastatic colon cancer, version 3.2013: featured updates to
the NCCN guidelines. J Natl Compr Canc Netw. 2013;11(2):141-152.
3. Ribero D, Abdalla EK, Madoff DC, et al. Portal vein embolization before major hepatectomy and its effects
on regeneration, resectability and outcome. Br J Surg. 2007;94(11):1386-1394.
4. Shoup M, Gonen M, D'Angelica M, et al. Volumetric analysis predicts hepatic dysfunction in patients
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undergoing major liver resection. J Gastrointest Surg. 2003;7(3):325-330.
5. Madoff DC, Abdalla EK, Vauthey JN. Portal vein embolization in preparation for major hepatic resection:
evolution of a new standard of care. J Vasc Interv Radiol . 2005;16(6):779-790.
6. May BJ, Talenfeld AD, Madoff DC. Update on portal vein embolization: evidence-based outcomes,
controversies, and novel strategies. J Vasc Interv Radiol . 2013;24(2):241-254.
7. Abdalla EK, Barnett CC, Doherty D, et al. Extended hepatectomy in patients with hepatobiliary
malignancies with and without preoperative portal vein embolization. Arch Surg. 2002;137(6):675-680.
8. Kishi Y, Abdalla EK, Chun YS, et al. Three hundred and one consecutive extended right hepatectomies:
evaluation of outcome based on systematic liver volumetry. Ann Surg. 2009;250(4):540-548.
9. Farges O, Belghiti J, Kianmanesh R, et al. Portal vein embolization before right hepatectomy: prospective
clinical trial. Ann Surg. 2003;237(2):208-217.
10. Shirabe K, Shimada M, Gion T, et al. Postoperative liver failure after major hepatic resection for
hepatocellular carcinoma in the modern era with special reference to remnant liver volume. J Am Coll Surg.
1999;188(3):304-309.
11. Shindoh J, Tzeng CW, Aloia TA, et al. Optimal future liver remnant in patients treated with extensive
preoperative chemotherapy for colorectal liver metastases. Ann Surg Oncol . 2013;20(8):2493-2500.
12. Nagino M, Nimura Y, Kamiya J, et al. Changes in hepatic lobe volume in biliary tract cancer patients after
right portal vein embolization. Hepatology. 1995;21(2):434-439.
13. Vauthey JN, Chaoui A, Do KA, et al. Standardized measurement of the future liver remnant prior to
extended liver resection: methodology and clinical associations. Surgery. 2000;127(5):512-519.
14. Vauthey JN, Abdalla EK, Doherty DA, et al. Body surface area and body weight predict total liver volume
in Western adults. Liver Transpl . 2002;8(3):233-240.
15. Shindoh J, Truty MJ, Aloia TA, et al. Kinetic growth rate after portal vein embolization predicts
posthepatectomy outcomes: toward zero liver-related mortality in patients with colorectal liver metastases
and small future liver remnant. J Am Coll Surg. 2013;216(2):201-209.
16. Leelaudomlipi S, Sugawara Y, Kaneko J, et al. Volumetric analysis of liver segments in 155 living donors.
Liver Transpl . 2002;8(7):612-614.
17. Kishi Y, Madoff DC, Abdalla EK, et al. Is embolization of segment 4 portal veins before extended right
hepatectomy justified? Surgery. 2008;144(5):744-751.
18. Kokudo N, Tada K, Seki M, et al. Proliferative activity of intrahepatic colorectal metastases after
preoperative hemihepatic portal vein embolization. Hepatology. 2001;34(2):267-272.
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19. Madoff DC, Abdalla EK, Gupta S, et al. Transhepatic ipsilateral right portal vein embolization extended to
segment IV: improving hypertrophy and resection outcomes with spherical particles and coils. J Vasc Interv
Radiol . 2005;16(2 pt 1):215-225.
20. Madoff DC, Hicks ME, Abdalla EK, et al. Portal vein embolization with polyvinyl alcohol particles and coils
in preparation for major liver resection for hepatobiliary malignancy: safety and effectiveness—study in 26
patients. Radiology. 2003;227(1):251-260.
21. Avritscher R, Duke E, Madoff DC. Portal vein embolization: rationale, outcomes, controversies and future
directions. Expert Rev Gastroenterol Hepatol . 2010;4(4):489-501.
22. de Baere T, Roche A, Elias D, et al. Preoperative portal vein embolization for extension of hepatectomy
indications. Hepatology. 1996;24(6):1386-1391.
23. Madoff DC, Hicks ME, Vauthey JN, et al. Transhepatic portal vein embolization: anatomy, indications,
and technical considerations. Radiographics. 2002;22(5):1063-1076.
24. Malinowski M, Geisel D, Stary V, et al. Portal vein embolization with plug/coils improves hepatectomy
outcome. J Surg Res. 2015;194:202-211.
25. Fischman AM, Ward TJ, Horn JC, et al. Portal vein embolization before right hepatectomy or extended
right hepatectomy using sodium tetradecyl sulfate foam: technique and initial results. J Vasc Interv Radiol .
2014;25(7):1045-1053.
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26. Guiu B, Bize P, Gunthern D, et al. Portal vein embolization before right hepatectomy: improved results
using n-butyl-cyanoacrylate compared to microparticles plus coils. Cardiovasc Intervent Radiol .
2013;36(5):1306-1312.
27. Bent CL, Low D, Matson MB, et al. Portal vein embolization using a nitinol plug (Amplatzer vascular plug)
in combination with histoacryl glue and iodinized oil: adequate hypertrophy with a reduced risk of nontarget
embolization. Cardiovasc Intervent Radiol . 2009;32(3):471-477.
28. Covey AM, Brody LA, Getrajdman GI, et al. Incidence, patterns, and clinical relevance of variant portal
vein anatomy. AJR Am J Roentgenol . 2004;183(4):1055-1064.
29. de Baere T, Roche A, Vavasseur D, et al. Portal vein embolization: utility for inducing left hepatic lobe
hypertrophy before surgery. Radiology. 1993;188(1):73-77.
30. Aoki T, Imamura H, Hasegawa K, et al. Sequential preoperative arterial and portal venous embolizations
in patients with hepatocellular carcinoma. Arch Surg. 2004;139(7):766-774.
31. Ogata S, Belghiti J, Farges O, et al. Sequential arterial and portal vein embolizations before right
hepatectomy in patients with cirrhosis and hepatocellular carcinoma. Br J Surg. 2006;93(9):1091-1098.
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32. Denecke T, Seehofer D, Steffen IG, et al. Arterial versus portal venous embolization for induction of
hepatic hypertrophy before extended right hemihepatectomy in hilar cholangiocarcinomas: a prospective
randomized study. J Vasc Interv Radiol . 2011;22(9):1254-1262.
33. Fischer C, Melstrom LG, Arnaoutakis D, et al. Chemotherapy after portal vein embolization to protect
against tumor growth during liver hypertrophy before hepatectomy. JAMA Surg. 2013;148(12):1103-1108.
34. Angle JF, Siddiqi NH, Wallace MJ, et al. Quality improvement guidelines for percutaneous transcatheter
embolization: society of interventional radiology standards of practice committee. J Vasc Interv Radiol .
2010;21(10):1479-1486.
35. Denys A, Bize P, Demartines N, et al. Quality improvement for portal vein embolization. Cardiovasc
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40
Transjugular Intrahepatic Portosystemic Shunts
Ziv J. Haskal
A transjugular intrahepatic portosystemic shunt (TIPS) is a percutaneous method of reducing portal vein
pressure for treatment of complications of portal hypertension. A decompressive channel is created between a
hepatic vein and an intrahepatic branch of the portal vein. Creating a TIPS involves several steps:
1. Catheterization of the hepatic veins and hepatic venography
2. Passage of a long, curved transjugular needle from the chosen hepatic vein through the liver parenchyma into
an intrahepatic branch of the portal vein
3. Direct measurement of the systemic and portal vein pressures through the transjugular access
4. Balloon dilatation of the tract between the hepatic and portal veins
5. Deployment of an expanded polytetrafluorethylene-lined stent graft or metallic stent within the tract to maintain
it against the recoil of the surrounding liver parenchyma and tissue ingrowth
6. Angiographic and hemodynamic assessment of resultant pressure changes
7. Serial dilatation of the stent until satisfactory pressure levels have been reached
8. Variceal embolization, when indicated
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Indications (1,2,3,4,5,6,7,8,9,10)
1. Efficacy determined by controlled trials:
a. Secondary prevention of variceal bleeding
b. Refractory cirrhotic ascites
2. Efficacy assessed in uncontrolled series:
a. Refractory acutely bleeding varices
b. Portal hypertensive gastropathy
c. Bleeding gastric varices
d. Refractory hepatic hydrothorax
e. Hepatorenal syndrome (type 1 or 2)
f. Budd-Chiari syndrome
3. Unclear, variable efficacy described in small series or case reports
a. Veno-occlusive disease (VOD)
b. Hepatopulmonary syndrome
c. Prophylactic preoperative decompression
d. Restoration of portal vein patency prior to transplantation or during catheter directed therapy of
splenomesenteric thromboses
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Contraindications
Absolute
1. Severe or rapidly progressive liver failure
2. Severe or uncontrolled encephalopathy
3. Heart failure
4. Severe pulmonary hypertension
These contraindications hold for most surgical portosystemic diversion procedures. Patients with very
advanced stages of liver disease will not tolerate deprivation of nutrient portal flow that occurs after total or
partially decompressive shunts. In these cases, shunts may accelerate liver failure and should be
considered only as last measures, ideally as bridges to imminent transplantation.
Relative
1. Contraindications to angiographic procedures
a. Recent myocardial infarction, serious arrhythmia, or substantial electrolyte imbalance
b. Past serious documented contrast reaction—prophylaxis is required, or TIPS creation using carbon
dioxide
c. Uncorrectable coagulopathies
d. Inability to lie flat on angiographic table due to congestive heart failure or compromised respiratory status
—intubation may be required
e. Pregnancy because of risk of exposure of fetus to ionizing radiation
2. Conditions that may increase the technical difficulty of creating a TIPS:
a. Biliary obstruction
b. Hepatic or pancreatic malignancy
c. Polycystic liver disease
d. Inferior vena caval or hepatic vein thrombosis
e. Portal system thromboses (portal, splenic, or mesenteric)
f. In cases of caval, hepatic vein, or portal system thromboses, modified procedures using transcaval,
transhepatic, or transplenic approaches have been described. Targeting can be further aided by use of
intravascular ultrasound (IVUS) for creation of TIPS in routine approaches, direct intrahepatic portosystemic
shunt (DIPS), or complex anatomy.
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1. Obtain informed consent. Table 40.1 lists procedural complications that can be discussed with the patient (7).
2. Preprocedure sonography, computed tomography (CT), or magnetic resonance (MR) imaging to assess portal
vein patency and hepatic parenchyma because the incidence of hepatocellular carcinoma is increased in
patients with cirrhosis.
3. Provide standard hemodynamic monitoring, including electrocardiogram (ECG), oxygen saturation, blood
pressure, and possibly capnography, as appropriate for administration of sedation per hospital protocols.
4. In acutely bleeding patients, ensure that satisfactory resuscitation efforts are being undertaken prior to
starting. These may include blood or plasma transfusions, pressor support, and placement of balloon tamponade
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catheters. Generally, platelet counts are corrected to >50,000/μL and international normalized ratio to ≤1.5.
5. Intravenous antibiotic prophylaxis should be provided. Many medications may provide satisfactory coverage,
including ceftriaxone, ampicillin/sulbactam, or, in penicillin-allergic patients, levofloxacin, ciprofloxacin,
clindamycin, or vancomycin.
6. TIPS can be created under conscious sedation with intravenous fentanyl and midazolam. When anesthesia
support is available, many centers use general anesthesia, especially for pediatric patients, or monitored
anesthesia care (MAC) with propofol administration.
7. Assemble required components:
a. TIPS set. Several kits exist, including the Haskal, Rösch-Uchida, and Ring sets (Cook Medical, Bloomington,
IN). The factor most governing kit choice is operator preference. The Haskal and Rösch-Uchida sets are suitable
for VIATORR delivery (W. L. Gore & Associates, Flagstaff, AZ), by virtue of the inclusion of a 10 Fr. vascular
sheath. The Ring set contains a 9 Fr. vascular sheath, suitable for delivering bare metal stents, not U.S. Food
and Drug Administration (FDA)-approved TIPS endografts.
b. Metallic stents. Nearly every available metal stent has been used to support the parenchymal tract of a TIPS,
including balloon expandable, selfexpanding braided and laser-cut nitinol stents, and polytetrafluoroethylene
(PTFE) stent grafts. However, only two devices are FDA-approved specifically for use in TIPS creation: the
WALLSTENT (bare stent) and the VIATORR (expanded polytetrafluoroethylene [ePTFE]-lined stent graft)
(8,9,10,11,12,13,14).
Table 40.1 Procedural Complications of Transjugular Intrahepatic Portosystemic Shunts
Reported Rate (%)
Major complications 3.00
Hemoperitoneum 0.50
Stent malposition 5.00
Hemobilia 2.00
Radiation skin burn 0.10
Hepatic Infarction 0.50
Renal failure requiring dialysis 0.25
Death —
Minor complications 4.00
Transient contrast-induced renal failure 2.00
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Hepatic artery puncture causing clinically apparent injury 1.00
Fever 2.00
Entry site hematoma 2.00
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c. Guidewires for portal entry are a matter of operator preference. If using the Haskal or Ring TIPS set, a long-
taper stiff shaft hydrophilic wire is useful, for example, Roadrunner (Cook Medical, Bloomington, IN) or Glidewire
(Terumo Corporation, Tokyo, Japan).
d. Balloon angioplasty catheters, 8 to 10 mm diameter
e. Pressure transducer
8. Preprocedure echocardiography, in elective cases, is obtained at the discretion of the operator, especially if
elevated right-sided heart pressures and pulmonary hypertension are suspected.
Procedure
1. The preferred access is through the right internal jugular vein; however, shunts can be easily created
using a left jugular approach. External jugular, femoral, transhepatic, and transcaval approaches have all
been used. Sonographicguided puncture of the internal jugular vein is performed. Once a guidewire is
advanced toward the right atrium (RA), alert personnel to pay particular attention to the ECG. Arrhythmias
may be induced during attempts to cross the Eustachian valve into the inferior vena cava (IVC). The author
ensures that the ECG signal is audible to provide prompt indication of possible arrhythmias.
2. The vascular sheath is advanced into RA. Initial atrial pressures are recorded. If the mean RA pressure
exceeds 10 mm Hg, consider reducing all unnecessary fluids. If the pressure is exceedingly high, consider
whether unrecognized pulmonary hypertension or cardiac or valvular insufficiency may be present. As a
general rule, TIPS patients should be “dry” with respect to intravenous fluids. TIPS increases cardiac
preload by diverting higher pressure portal blood to the right atrium. Purposefully minimize intravenous
fluids during TIPS.
3. A curved multipurpose (MPA/B) catheter is used to catheterize a suitable hepatic vein. The right hepatic
vein ostium is typically one interspace higher than “expected” by fluoroscopy. The vascular sheath is
advanced into the vein. Hand-injected free and wedged hepatic venography are performed. Wedged
catheter or balloon occlusion carbon dioxide (due to the low viscosity of the gas) venography may be useful
in opacifying the portal system. Alternatively, carbon dioxide portography can be performed by gas injection
directly through the TIPS needle into the hepatic parenchyma. Caveat: Excessively forceful injection of
iodinated contrast or carbon dioxide during wedged venography has led to serious or lethal hepatic
lacerations and bleeding.
4. An Amplatz guidewire is placed through the catheter into the selected hepatic vein, the diagnostic
catheter removed, and the transjugular puncture needle, and its surrounding sheaths are advanced into the
hepatic vein. Advancing the needle system over a “reversed” wire, that is, back-end of the Amplatz wire in
the hepatic vein, can be helpful. The guidewire is removed, and gentle forward pressure is applied to the
needle to prevent its retraction due to patient respiration. A partly filled syringe with contrast is attached to
the needle hub.
5. In difficult cases (e.g., transcaval TIPS, Budd-Chiari, portal vein thromboses), a 60-cm coaxial fine needle
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can be used through the Colapinto needle. If using a coaxial fine needle, a 180-cm long, 0.018-in. nitinol
wire is used when a suitable portal branch is entered.
6. When using the right hepatic vein approach, the needle is rotated anteriorly and moved centrally within
the vein to approximately 2 cm of the hepatic vein ostium. It is advanced parallel to the spine to the
anticipated location of the intrahepatic portal vein (Fig. 40.1). The length of the needle pass is variable; it
depends on the size of the actual liver and the relative positions of the portal and hepatic veins. Operators
can modify the curve of the needle by bending it prior to insertion. This can be useful in cases of shrunken
cirrhotic livers. These
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can often be estimated by fluoroscopic assessment of the liver or with wedged portographic images. Employ
caution to avoid capsular transgression.
FIGURE 40.1 • A Colapinto puncture needle exits the right hepatic vein, passes through the liver
parenchyma, and enters the right portal vein.
7. Aspirate the contrast syringe during slow needle and sheath withdrawal. When fluid is aspirated, inject
contrast to identify the structure entered (portal vein, hepatic vein, hepatic artery, bile duct, lymphatic).
8. If a suitable portal branch has been punctured, the portal entry wire is manipulated through the main
portal vein into the splenic or mesenteric veins. This is a critical step in TIPS creation—converting nearly
any portal vein entry into one through which subsequently a stiff guidewire, sheath, angioplasty balloon and
stent can be advanced. Due to respiratory motion, the liver is moving in a cephalocaudal direction (with
needle in place), so it is important to maintain the rotatory orientation of the needle within the portal vein
branch and advance the guidewire into the needle as quickly as possible to prevent loss of access to the
portal vein. In cases performed under general anesthesia, some operators ask for brief respiratory
cessation during these maneuvers.
9. Prior to needle removal, the needle guide and outer vascular sheaths are advanced forward into the
parenchyma to the portal vein entry site, and occasionally into the portal vein. This step eases subsequent
catheter and balloon passage across fibrotic periportal tissue. The needle is removed, and a 5 Fr.
diagnostic catheter is advanced into the parent vessel supplying the varices (splenic vein for esophageal
and gastric varices, superior mesenteric vein [SMV] for intestinal varices). For patients with ascites and
hydrothorax, imaging of varices is not relevant because no embolization should be undertaken.
10. Portography is performed, and portal pressures are recorded.
11. The parenchymal tract is dilated with an 8-mm balloon (Fig. 40.2). Thereafter, a marker catheter (often a
marker pigtail used previously for portography) is positioned within the parenchymal tract. Contrast
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venography is performed through the side arm of the vascular sheath (“tractogram”), positioned within the
tract or cephalic portion of the main portal vein. Stent length measurements are obtained from these
images.
12. The entirety of the TIPS tract is paved with VIATORR TIPS endografts, WALLSTENTS, or other bare
stents, extending from the portal entry site to several millimeters into the IVC (Fig. 40.3). The bare leading
end of the VIATORR should just reach the main portal vein, as should the WALLSTENT. For adults,
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as a general rule, 10-mm diameter WALLSTENTS or VIATTORS should be used. The specific technical
aspects of VIATORR measurement (using a radioopaque marker catheter) and deployment should be
encompassed in specific device training.
FIGURE 40.2 • The liver tract is dilated with an angioplasty balloon.
13. End points

a. Primary objective: Create the smallest diameter shunt that achieves the desired clinical end point.
b. Esophageal variceal bleeding—reduction of the portosystemic (porto-right atrial) gradient to ≤12 mm Hg.
If there are large spontaneous splenorenal shunts in a patient with gastric varices, a lower gradient may be
needed to divert flow from the varices into the TIPS, followed or preceded by ablative variceal embolization
using coils, sclerosants, or other liquid embolics.
c. Refractory ascites (or hepatic hydrothorax)—pressure gradient end points are less clear. Some argue
that the gradient needs to be lower than for esophageal varices; this must be offset against the often
greater baseline
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encephalopathy seen in patients with longstanding refractory ascites. Because TIPS is palliative, the
ascites effect should be balanced against causing excessive portosystemic encephalopathy (or worsened
liver function). For ascites patients, the shunt can always be enlarged at a second outpatient setting, once
the clinical effect is measured after 2 to 3 weeks. For Budd-Chiari patients, there is evidence that higher
initial gradient end points may be sufficient for treatment of acute or subacute Budd-Chiari syndrome. In
these patients, the gradients often rapidly drop as autodiuresis ensues.
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FIGURE 40.3 • The liver tract is lined with a stent.
14. The VIATORR was designed with a higher radial expansile force than the WALLSTENT or other bare
metal stents. It is often advantageous to purposefully not postdilate this stent graft after deployment,
allowing it to, at early stages, remain somewhat smaller that its 10-mm nominal diameter.
15. If the patient is actively bleeding at the time of TIPS and a balloon tamponade catheter is present,
deflate all balloons and repeat splenic venography and pressure measurements after shunt creation. If
notable variceal flow remains, further expand the shunt and/or supplement with variceal embolization.
Overdilatation of WALLSTENTS with balloons 1 to 2 mm larger than their nominal diameters will offset their
relatively low radial expansile force and aid in achieving full stent expansion. Overdilation is not performed
with nitinol bare stents, VIATORRs, or other ePTFE endografts.
16. Remove all access catheters. It is preferred to not leave access site catheters in place, given prior
reports of higher risks of site-related infection and fever.
1. Postprocedure instructions and observation are governed by the patient's clinical status, that is, intensive care
or floor recovery.
2. The right atrial pressure is routinely increased by TIPS formation. When the mean RA pressure is >10 mm Hg
after TIPS, the author prescribes overnight diuresis of >1 L. The cardiac output, cardiac index, and right atrial
pressure may remain elevated for more than 1 month after TIPS. Excessively high final right atrial pressures,
particularly in acutely bleeding patients receiving fluid resuscitation, may both limit the decompressive effects of
the shunt and lead to preventable secondary pulmonary edema (which may be confused with adult respiratory
distress syndrome).
3. The majority of shunts are lined with ePTFE endografts. If the TIPS was created with bare metal stents,
postprocedure baseline TIPS sonography should be performed prior to discharge. This will serve as a baseline
for comparison during outpatient shunt follow-up and detect any acute shunt thromboses or stenoses, such as
those due to biliary-TIPS fistulae or hypercoagulability (e.g., in Budd-Chiari patients). If a VIATORR was used,
avoid the immediate in-hospital post-TIPS sonogram; in the acute phase, the airspaces within the graft material
will reflect sound, mimicking shunt occlusion. Within 1 to 2 weeks, the graft typically “wets out” by capillary
action, becoming sonographically transparent. Perform the baseline post-VIATORR TIPS sonogram at the time of
the first outpatient TIPS clinic visit.
4. If bare metal stents are used, sonography should be performed at 3, 6, and 12 months in the first year and
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every 3 to 6 months after that depending on clinical status. Given the predilection for bare metal shunts to
develop stenoses, plans to line them with ePTFE endografts should be considered at each point. Sonographic
follow-up may be less frequent in patients with VIATORR devices given expectations for long term patency.
Results
1. Technical success: creation of a TIPS between the hepatic vein and intrahepatic branch of the portal
vein: 95% (7)
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2. Hemodynamic success: successful post-TIPS reduction of the portosystemic gradient below a threshold
chosen for that indication: 95% (7)
3. Clinical success: Many randomized trials have compared TIPS to endoscopic treatment of esophageal
variceal bleeding. The mean rates of rebleeding following TIPS and endoscopic treatment were 19% (range
9.8% to 24%) and 47% (range 24% to 57%), respectively (1,4,5,7,8,10).
Complications
1. Procedural complications are listed in Table 40.1.
2. Hepatic encephalopathy: Spontaneous or worsened hepatic encephalopathy can occur after all forms of
portosystemic diversion. The strongest prognostic factor is preexisting encephalopathy. Generally, the risk
is greater in patients with refractory ascites because of more severe underlying liver disease.
3. TIPS created with uncovered stents are prone to shunt stenoses resulting in portal hypertension in 25%
to 50% of cases within 6 to 12 months postprocedure. This emphasizes the mandatory need for routine
TIPS follow-up and prophylactic revision. TIPS stenosis is vastly reduced with ePTFE-lined endografts
(11,12,13,14). Establishing routine clinical follow-up of TIPS patients is a required aspect of interventional
radiology care. Coordination with hepatologists, gastroenterologists, and when appropriate, liver transplant
physicians is important.
4. Recurrent bleeding is almost always associated with recurrent portal hypertension due to shunt stenosis
or thrombosis. In the setting of recurrent bleeding or fluid accumulation, “negative” TIPS sonograms should
not dissuade operators from direct shunt catheterization and hemodynamic assessment.
1. Hepatic encephalopathy: First-line therapies include oral rifaximin, 550 mg twice a day or oral lactulose.
Lactulose is often started at 30 mL two or three times a day. Instruct capable patients to self-titrate their
doses to an average of two to three bowel movements per day. If these measures prove inadequate (or liver
function notably deteriorates after TIPS), shunt size reduction may be needed. This can be accomplished
by deployment of a stenotic stent within the original TIPS. In cases of uncontrolled encephalopathy and
progressive liver failure, intentional shunt occlusion can be performed using a balloon occlusion catheter.
This should be reserved for extreme cases because it may precipitate recurrent variceal bleeding or
hepatorenal failure (15).
2. Shunt stenosis or thrombosis. Stent thrombosis usually is secondary to an underlying stenosis or
occlusion. Shunt thrombus can be cleared by balloon dilation; chemical thrombolysis is rarely ever required.
Stenoses occurring at the junction of the portal vein may be treated by angioplasty, although stents have a
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lower recurrence rate and may prevent restenosis in the future. The most common site of shunt stenosis is
an unstented segment of native hepatic vein, emphasizing the need for extending endografts to the caval
ostium. Stenosis within the intrahepatic portion of the bare stent-TIPS tracts may indicate a communication
with bile ducts. If the occluded TIPS tract cannot be recanalized, a new TIPS can be created, usually from
another hepatic vein.
3. Hyperbilirubinemia after TIPS. A partial differential diagnosis is provided: excessive (over)shunting,
ischemic hepatopathy (due to hypotension related to acute bleeding or resuscitation—marked
transaminitis), bile duct compression by the TIPS stents (elevated alkaline phosphatase without
transaminase elevations), hemolysis (change in reticulocyte count, haptoglobin, low hemoglobin), ischemic
liver due to hepatic artery injury (transaminitis), hemobilia (lower gastrointestinal bleeding or melena).
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References
1. Burroughs AK, Vangeli M. Transjugular intrahepatic portosystemic shunt versus endoscopic therapy:
randomized trials for secondary prophylaxis of variceal bleeding: an updated meta-analysis. Scand J
Gastroenterol . 2002;37:249-252.
2. Salerno F, Cammà C, Enea M, et al. Transjugular intrahepatic portosystemic shunt for refractory ascites: a
meta-analysis of individual patient data. Gastroenterology. 2007;133:825-834.
3. Garcia-Tsao G. The transjugular intrahepatic portosystemic shunt for the management of cirrhotic
refractory ascites. Nat Clin Pract Gastroenterol Hepatol . 2006;3:380-389.
4. Henderson JM, Boyer TD, Kutner MH, et al. Distal splenorenal shunt versus transjugular intrahepatic
portal systematic shunt for variceal bleeding: a randomized trial. Gastroenterology. 2006;130:1643-1651.
5. Khan S, Tudur Smith C, Williamson P, et al. Portosystemic shunts versus endoscopic therapy for variceal
rebleeding in patients with cirrhosis. Cochrane Database Syst Rev. 2006;(4):CD000553.
6. Qi X, Yang M, Fan D, et al. Transjugular intrahepatic portosystemic shunt in the treatment of Budd-Chiari
syndrome: a critical review of literatures. Scand J Gastroenterol . 2013;48:771-784.
7. Haskal ZJ, Martin L, Cardella JF, et al; for the Society of Cardiovascular & Interventional Radiology,
Standards of Practice Committee. Quality improvement guidelines for transjugular intrahepatic portosystemic
shunts. J Vasc Interv Radiol . 2001;12:131-136.
8. García-Pagán JC, Caca K, Bureau C, et al. Early use of TIPS in patients with cirrhosis and variceal
bleeding. N Engl J Med. 2010;362:2370-2379.
9. Salerno F, Cammà C, Enea M, et al. Transjugular intrahepatic portosystemic shunt for refractory ascites: a
meta-analysis of individual patient data. Gastroenterology. 2007;133:825-834.
10. Boyer TD, Haskal ZJ. American Association for the Study of Liver Diseases Practice Guidelines: the role
of transjugular intrahepatic portosystemic shunt creation in the management of portal hypertension: update
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2009. Hepatology. 2009;51:306.
11. Echenagusia M, Rodriguez-Rosales G, Simo G, et al. Expanded PTFE-covered stentgrafts in the

treatment of transjugular intrahepatic portosystemic shunt (TIPS) stenoses and occlusions. Abdom Imaging.
2005;30:750-754.
12. Jung HS, Kalva SP, Greenfield AJ, et al. TIPS: comparison of shunt patency and clinical outcomes
between bare stents and expanded polytetrafluoroethylene stent-grafts. J Vasc Interv Radiol . 2009;20:180-
185.
13. Perarnau JM, Le Gouge A, Nicolas C, et al. Covered vs. uncovered stents for transjugular intrahepatic
portosystemic shunt: a randomized controlled trial. J Hepatol . 2014;60:962-968.
14. Hausegger KA, Karnel F, Georgieva B, et al. Transjugular intrahepatic portosystemic shunt creation with
the Viatorr expanded polytetrafluoroethylene-covered stent-graft. J Vasc Interv Radiol . 2004;15:239-248.
15. Madoff DC, Wallace MJ, Ahrar K, et al. TIPS-related hepatic encephalopathy: management options with
novel endovascular techniques. Radiographics. 2004;24:21-36.
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41
Balloon-Occluded Retrograde Transvenous Obliteration
Nicholas J. Hendricks
Ziv J. Haskal
Gastric variceal bleeding is a life-threatening complication of portal hypertension. Balloon-occluded retrograde

transvenous obliteration (BRTO) is a procedure by which upstream occlusion of a pathologic portosystemic
shunt is achieved using sclerosants and/or embolic solutions. Retrograde transvenous obliteration of gastric
varices using sclerosants such as ethanolamine has been used in Asia for over
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20 years (1). In recent years, it has become widely propagated in the West, and technique, device, and agents
used have evolved. Variations of this procedure include plug- and coil-assisted techniques using gelfoam instead
of sclerosant agents, which have shown to be quite effective (2).
Indications
1. Secondary prevention of recurrent gastric variceal hemorrhage. In most cases, BRTO (and variants) are
not performed during acute variceal hemorrhage, although procedural evolution may allow its increasing
use in this setting.
2. Primary prophylaxis of gastric variceal hemorrhage. In contrast to Western hemisphere, this is a common
indication in Asia. Comparing published results of respective series must take this into account.
3. Treatment of excess portosystemic encephalopathy (shunting-type) aggravated portal hypertension or
secondary development of ascites or increased esophageal varices. Improved liver function can occur after
such shunt obliteration (3).
4. Bleeding ectopic varices (e.g., duodenal). Anatomically, all target varices (be they gastric or ectopic) must
have a catheter-accessible efferent drainage (e.g., gastrorenal or gastrocaval shunt).
Contraindications
Absolute
1. Uncorrected coagulopathy
2. Patient is too unstable to tolerate time required for procedure. These patients may be more suitable for
transjugular intrahepatic portosystemic shunt (TIPS).
Relative
1. Refractory ascites
2. Severe liver dysfunction
3. Associated high-risk esophageal varices
1. Informed consent
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2. Preprocedure imaging with either triple phase contrast computed tomography (CT) or magnetic resonance
angiography (MRA)/magnetic resonance venography (MRV) to evaluate the portal vein and the extent of
portosystemic shunts. CT may be advantageous due to its accessibility because it still allows multiplanar
reconstructions. It is important to evaluate the size of the gastrorenal shunt for suitability of the procedure and
device selection. It is also important to understand the portal inflow to the shunt. This can be difficult because
some of these shunts can have multiple small inflow veins. Imaging can also be used to identify collateral veins
that may require embolization prior to instillation of sclerosants (e.g., phrenic or pericardiophrenic veins).
3. Laboratory evaluation to include basic metabolic and electrolyte panels, complete blood counts, coagulation
parameters, and liver function tests. Platelet counts above 50,000 are adequate to perform this procedure.
4. Hemodynamic monitoring with electrocardiography, blood pressure, and oxygen saturation
5. Aggressive resuscitation should be implemented in acutely bleeding patients with hemodynamic instability.
This may require packed red blood cells, fresh frozen plasma, platelets, cryoglobulin, pressor support, and
intravenous (IV) fluids.
6. Conscious sedation using IV fentanyl and midazolam is suitable for most patients.
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7. Accumulate the required components:
a. Embolic versus sclerosant agent
(1) Sodium tetradecyl sulfate (Sotradecol, AngioDynamics, Queensbury, NY)
(2) Ethanolamine oleate (Oldamin, Grelan Pharmaceutical, Tokyo, Japan) Haptoglobin is often required as part
of its use.
(3) Polidocanol foam (Polidocasklerol, ZERIA Pharmaceutical, Tokyo, Japan)
(4) n-Butyl cyanoacrylate
(5) Gelfoam (Pharmacia & Upjohn, New York, NY) is used during plugassisted retrograde transvenous
obliteration (PARTO) procedures.
b. Balloon-occlusion catheters (others may be equally suitable)
(1) Coda (Cook Medical, Bloomington, IN)
(2) Python occlusion balloon (Applied Medical, Rancho Santa Margarita, CA)
(3) Equalizer (Boston Scientific Corporation, Natick, MA)
c. Plugs (needed for PARTO technique)
(1) Amplatzer plug (St. Jude Medical, St. Paul, MN)
d. Coils (for coil-assisted techniques)
(1) Pushable versus detachable, metallic, or polymer embolization coils
Procedure
Balloon-Occluded Retrograde Transvenous Obliteration
1. Access is usually through the femoral or internal jugular veins. An appropriate sheath is then placed
based on estimated size of the shunt ostium and the occlusion balloon needed. Typically, 7 to 9 Fr., 50- to
70-cm long vascular sheaths are suitable.
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2. Catheterization of gastrorenal shunt arising from the left renal vein
a. A 4 Fr. or 5 Fr. catheter (Cobra, reverse curve, Simmons 1, or Headhunter) is used to select the left renal
vein. It is advanced toward the renal hilum and then gently rotated while being drawn back, directed at the
cephalic wall of the left renal vein. The gastrorenal vein empties into the left renal vein through the enlarged
adrenal vein along its central cephalic aspect.
b. A soft Teflon-coated metallic or hydrophilic guidewire is advanced into the gastrorenal shunt after which
the long sheath advanced over the diagnostic catheter and guidewire beyond the junction of the shunt and
renal vein. A parallel, “buddy wire” or catheter may be placed alongside the original guidewire. After shunt
venography, the catheter is exchanged for an appropriately sized occlusion balloon. The balloon is
positioned in a secure caudal location within the shunt, gently inflated and retrograde contrast venography
performed, to begin to map the shunt. Iodinated contrast and carbon dioxide can be used as well as cone-
beam CT.
c. Reverse curve single and double balloon BRTO occlusion catheters are available in Asia; these can
potentially reduce the number of steps in gastrorenal vein catheterization.
3. Balloon occlusion venography evaluation of shunt anatomy can reveal collateral veins, for example,
paravertebral, pericardial, pericardiophrenic, or inferior phrenic veins, that may warrant coil embolization
before instillation of the sclerosant. When using liquid sclerosants, these large veins may otherwise thwart
contrast filling the entirety of varix, hence the need to skeletonize the shunt. The “inflow” of the shunt
should be identified (i.e., its path toward the splenic vein) so that the proper amount of embolic solution is
instilled, both sufficient to occlude the majority of the varix but not spill into the splenic vein.
4. Advance a microcatheter through the balloon lumen into the varix as far as feasible. The intent is to
expose the majority of the varix to the occlusive agent or sclerosant, without reflux into the splenic vein.
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5. The sclerosant agent of choice is mixed with gas and contrast agent. The following preparation of
Sotradecol can be used: 2 mL of sodium tetradecyl sulfate (STS) 3%, 1 mL of Lipiodol, and 3 mL of air (4).
Carbon dioxide can be used and may be preferable.
6. The sclerosant is injected under fluoroscopic guidance, and the occlusion balloon is left inflated.
7. The balloon is typically deflated ×4 hours later, although shorter protocols have been reported. Should
flow persist, reinflation and re-sclerosis can be performed.
Plug/Coil-Assisted Retrograde Transvenous Obliteration (Fig. 41.1)
1. Access into the shunt as described earlier. Use a long vascular sheath of sufficient caliber to allow
delivery of a suitable plug (or coil mass) and parallel (paraaxial) catheter for delivering the embolic solution.
2. Perform shunt venography.
3. Advance a microcatheter or diagnostic catheter deep into the shunt.
4. For plug-assisted retrograde occlusion, an oversized AMPLATZER Vascular Plug II (AVP-II) (available in
sizes up to 22 mm diameter) is extruded into the shunt but not detached from its delivery mandril . If coils
are used, these are deployed alongside the microcatheter.
5. A thick slurry of Gelfoam and iodinated contrast is injected into the varix via the catheter within the shunt.
The occlusive plug prevents egress of this solution. Relatively large volumes of this solution may be
required. The static column can be readily visualized as the varix is progressively filled. Some operators
have chosen to mix sclerosant agents into the gelfoam solution. Once a sufficient extent of varix stasis has
been achieved, the plug is released at the distal “base” of the varix and the procedure is concluded.
6. The advantages of this approach include single-session only, lesser need for collateral embolization, and
lesser risk of sclerosis of nontarget vessels.
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1. Elective BRTO patients should be admitted for overnight observation.
2. Laboratory evaluation in the first 48 hours may demonstrate a mild increase in total bilirubin and liver function
tests, usually self-limited, perhaps related to increase portal flow and pressure. Persistent deterioration in liver
function should prompt a liver Doppler ultrasound to exclude portal vein thrombosis.
3. The patient's fluid status and renal function should be monitored.
a. Ascites, hepatic hydrothorax, and lower extremity edema may develop or increase after varix obliteration.
b. Renal function can be affected by hemoglobinuria, contrast, renal vein thrombosis, or the development of
hepatorenal syndrome.
4. Upper endoscopy in combination with endoscopic ultrasound can be used in the postoperative period to verify
obliteration of the gastric varices.
5. Cross-sectional imaging (computed tomography venography [CTV] or magnetic resonance venography [MRV])
should be performed at least once during outpatient clinic follow-up at 3 to 6 months and then as clinically
indicated.
Results (1,2,4,5,6,7,8,9,10,11)
1. Technical success reported between 80% and 100%.
2. Complete gastric varix thrombosis 75% to 100%. The majority of reports suggest greater than 95% complete
thrombosis.
3. Recurrent GV bleeding between 0% and 9%
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Radiology Books
FIGURE 41.1 • Fifty-eight-year-old man with recurrent gastric variceal bleeding undergoing elective BRTO. A:
CT demonstrates large gastric varices (GV) (arrow) draining through a gastrorenal shunt (arrowhead) into the left
renal vein. B: The shunt has been catheterized. A 1.5-mm J “buddy” wire is present within the caudal shunt. A
microcatheter has been advanced into a prominent left phrenic vein (arrows). This collateral vessel was
embolized using coils. C: An AVP-II (black arrow) was deployed alongside the infusion catheter but not detached.
Plug-occluded venogram demonstrates contrast stasis within the shunt (white arrows). Embolization coils are
seen within the phrenic vein (arrowhead). D: Gelfoam slurry was then injected via the 5 Fr. catheter. After
venography affirmed that the embolic had filled most of the varix (white arrows), the catheter was removed and
the plug detached. The image demonstrates stasis of the Gelfoam and contrast slurry in the varix. Endoscopy
and endoscopic ultrasound confirmed varix thrombosis 24 hours later. This was reaffirmed with CT imaging 4
weeks later.
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Complications
1. Increased ascites and hepatic hydrothorax (12)
2. Hemoglobinuria when using ethanolamine oleate-iopamidol sclerosing agent, which causes hemolysis.
Haptoglobin 2,000 to 4,000 units can be given to prevent onset of renal failure (13).
3. Balloon rupture with leak of sclerosant or embolic agent can cause pulmonary embolus or renal vein
thrombosis.
4. Worsening esophageal varices (2,9,10)
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5. Portal vein thrombosis rate of 1% (11)
6. Abdominal pain
7. Fever
References
1. Kanagawa H, Mima S, Kouyama H, et al. Treatment of gastric fundal varices by balloonoccluded
retrograde transvenous obliteration. J Gastroenterol Hepatol . 1996;11:51-58.
2. Gwon DI, Ko GY, Yoon HK, et al. Gastric varices and hepatic encephalopathy: treatment with vascular
plug and gelatin sponge-assisted retrograde transvenous obliteration— a primary report. Radiology.
2013;268:281-287.
3. Kumamoto M, Toyonaga A, Inoue H, et al. Long-term results of balloon-occluded retrograde transvenous

obliteration for gastric fundal varices: hepatic deterioration links to portosystemic shunt syndrome. J
Gastroenterol Hepatol . 2010;25:1129-1135.
4. Sabri SS, Swee W, Turba UC, et al. Bleeding gastric varices obliteration with balloonoccluded retrograde
transvenous obliteration using sodium tetradecyl sulfate foam. J Vasc Interv Radiol . 2011;22:309-316.
5. Fukuda T, Hirota S, Sugimura K. Long-term results of balloon-occluded retrograde transvenous

obliteration for the treatment of gastric varices and hepatic encephalopathy. J Vasc Interv Radiol .
2001;12:327-336.
6. Ninoi T, Nishida N, Kaminou T, et al. Balloon-occluded retrograde transvenous obliteration of gastric

varices with gastrorenal shunt: long-term follow-up in 78 patients. AJR Am J Roentgenol . 2005;184:1340-
1346.
7. Kitamoto M, Imamura M, Kamada K, et al. Balloon-occluded retrograde transvenous obliteration of gastric

fundal varices with hemorrhage. AJR Am J Roentgenol . 2002;178:1167-1174.
8. Hirota S, Matsumoto S, Tomita M, et al. Retrograde transvenous obliteration of gastric varices. Radiology.
1999;211:349-356.
9. Akahoshi T, Hashizume M, Tomikawa M, et al. Long-term results of balloon-occluded retrograde

transvenous obliteration for gastric variceal bleeding and risky gastric varices: a 10-year experience. J
Gastroenterol Hepatol . 2008;23:1702-1709.
10. Cho SK, Shin SW, Lee IH, et al. Balloon-occluded retrograde transvenous obliteration of gastric varices:
outcomes and complications in 49 patients. AJR Am J Roentgenol . 2007;189:W365-W372.
11. Park JK, Saab S, Kee ST, et al. Balloon-occluded retrograde transvenous obliteration (BRTO) for
treatment of gastric varices: review and meta-analysis. Dig Dis Sci . 2015;60:1543-1553.
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12. Sonomura T, Sato M, Kishi K, et al. Balloon-occluded retrograde transvenous obliteration for gastric
varices: a feasibility study. Cardiovasc Intervent Radiol . 1998;21:27-30.
13. Miyoshi H, Ohshiba S, Matsumoto A, et al. Haptoglobin prevents renal dysfunction associated with
intravariceal infusion of ethanolamine oleate. Am J Gastroenterol . 1991;86:1638-1641.
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42
Varicocele Embolization
Eric H. Reiner
Lindsay Machan
Jeffrey S. Pollak
A varicocele is a collection of varicose veins within the pampiniform (spermatic venous) plexus secondary to
reflux in the internal spermatic vein (ISV). The condition affects 10% to 15% of the general population; however,
they are detected in as many as 30% to 40% of men undergoing infertility workup. Depending on the method
used for diagnosis, they are reported as being bilateral in 17% to 77% of men (1,2). Isolated right varicoceles are
rare and should initiate cross-sectional imaging to exclude renal or retroperitoneal tumor, or situs inversus.
Diagnosis was traditionally made by clinical examination; however, as for other venous reflux disorders,
ultrasound has become the mainstay of diagnosis (3).
The proof that varicocele repair improves infertility remains elusive; however, there is general acceptance that
treatment does improve abnormalities of semen production: by the traditional measures of decreased sperm
motility, abnormal morphology, and decreased sperm count and by newer means of assessment including
seminal reactive oxygen species, DNA fragmentation index, and abnormal sperm chromatin condensation (4,5).
Although the connection between varicoceles and infertility remains controversial, associations with chronic groin
pain and testicular atrophy in adolescent varicoceles are not.
Indications (6,7,8)
1. Chronic groin pain (other etiologies excluded)
2. Infertility and appropriate semen abnormalities
3. Recurrent varicocele after surgical repair
4. Testicular atrophy in a pediatric patient
Contraindications
1. Severe coagulopathy
2. Demonstrated severe prior contrast reaction
1. These are outpatient procedures.
2. Standard preangiography workup and preparation
3. Scrotal ultrasound. Universally accepted diagnostic criteria have not been established. Abnormal reflux with
Valsalva maneuver rather than rigid size criteria are increasingly used as venous diameter varies significantly
with hydration, anxiety, and inspiratory effort.
4. Laboratory workup (may be omitted in young patients with no pertinent medical history): hemoglobin
(Hgb)/hematocrit (Hct), platelet count, prothrombin time (PT)/partial thromboplastin time (PTT), creatinine (Cr)
(estimated glomerular filtration rate [eGFR])
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Procedure
1. Direct x-ray/fluoroscopic imaging of the scrotum should be avoided. Almost the entire procedure is
performed using spot films and “fluoro capture.” Pulsed fluoroscopy should be used to further minimize
radiation exposure. Testicular shielding is seldom used.
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2. Right common femoral vein, right internal jugular vein, or antecubital vein access can be used. The
internal jugular vein allows the most direct route to the right spermatic vein.
3. Catheters
a. Femoral approach
(1) Left varicocele: A 7 Fr. gonadal catheter (Cordis Corporation, Miami Lakes, FL) is used to coaxially
introduce a 4 Fr. or 5 Fr. glide Berenstein catheter. If needed, a 3 Fr. microcatheter may be used to
manipulate across difficult valves and/or tortuous collateral vessels.
(2) Right varicocele: A reverse curve catheter such as a Simmons 1 (“Sidewinder”—shepherd's crook)
catheter is helpful for selecting the right ISV.
b. Right internal jugular or axillary vein: Multipurpose catheters can be used to select the right and the left
spermatic veins, usually without the need for coaxial catheters or catheter exchange.
4. The catheter is passed into the left renal vein to select the ostium of the left ISV (Fig. 42.1). A gentle
injection of contrast may be needed, while the patient performs a Valsalva maneuver, to ensure seating of
the catheter tip in the ISV and for identifying reflux through incompetent valves. If access is from the femoral
route, a 4 Fr. or 5 Fr. glide Berenstein catheter can be coaxially advanced down the ISV, gently injecting
contrast. If there are incompetent valves, contrast should fill in a retrograde fashion, down the ISV, toward
the testis, especially during a Valsalva maneuver. Collaterals that originate from the renal hilum or
paralumbar region may be noted. A tilt table may be of additional benefit, if the patient is unable to perform
an adequate, sustained Valsalva maneuver. When using a right jugular vein approach, the ostium is
accessed, and with the assistance of an angle-tipped glidewire, the catheter is directed into the proximal left
ISV.
5. Measure the size of the vein and note the position of all collateral channels, including parallel, colic, hilar,
and capsular pathways.
6. Particular care should be taken to avoid vessel spasm, which hinders the ability to proceed with the
procedure and obscures collaterals—predisposing to a false impression of successful occlusion.
7. Methods of embolization. Several have been described, each with its own merits. Current literature
remains nonstandardized; the use of liquid embolics with or without metallic coils has become the most
common practice (6,9).
a. Metallic coils and sodium tetradecyl sulfate (STS): The 0.035-in. or 0.038-in. metallic coils are
deployed within the lower ISV, usually at the level of the inguinal canal (Fig. 42.2).
(1) A 14-cm platinum Nester coil (Cook Medical, Bloomington, IN), approximately 20% larger than the
estimated diameter of the ISV, is deployed using the anchor technique or following deployment of a high
radial force stainless steel or MReye coil (Cook Medical Inc., Bloomington, IN). Near total occlusion of the
lumen can usually be achieved with two or three coils.
(2) A venogram during Valsalva maneuver should again be performed. Sluggish flow or nonfilling of the
pampiniform plexus will be seen.
(a) Collateral veins: Contrast injection after distal spermatic vein occlusion will often reveal new collaterals
that have become visible with the higher pressure now present in the occluded spermatic vein. Each of
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these collaterals may cause failure of the procedure and, therefore, must be occluded either directly or at its
opening into the spermatic vein. If the collaterals are large enough, they can be entered directly and
embolized with an appropriately sized coil placed as distally as possible. Alternatively, they can be occluded
with sclerosant or glue, as in the following text.
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FIGURE 42.1 • Anatomy of the left ISV, testicular varicocele, and collateral drainage pathways.
(3) STS
(a) STS foam
i. Can be injected to displace the visualized contrast, while the patient maintains a Valsalva maneuver for 1
to 2 minutes, if possible. This maneuver should then be repeated as needed.
ii. The STS foam is mixed in the following manner. A 2:1 mixture of 3% STS to sterile saline is aggressively
mixed with an equal volume of air, thereby resulting in a 2% STS foam. This foam is injected into the
catheter to displace the contrast. One milliliter of saline flush is used to clear the catheter. When a
microcatheter is used, a similar technique may be used after 0.018-in. coils are deployed.
iii. The catheter should be retracted from the mid to upper ISV, and a repeat venogram is performed, paying
particular attention to
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the presence of any previously unidentified collateral channels. Although a second nest of coils can be
placed, displacement of the contrast with a couple of additional injections of the foam can be performed,
taking care not to reflux proximally into the renal vein. If coils should be used, additional foam is still injected.
FIGURE 42.2 • STS and coil technique. A first nest of coils is placed at the level of the internal inguinal ring.
After placing the first nest of coils, 2 to 3 mL of STS foam is injected above the site of occlusion. If additional
parallel collaterals are identified, a second injection is done at the level of the second nest of coils. The rest
of the ISV is generally left patent as long as no other parallel collaterals are identified, in case the patient
needs to be retreated.
iv. Some interventionists use STS foam alone, without coils (10). In this instance, the vein is occluded at
the inguinal ring by applying external pressure with a compression device or the patient's hand.
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(b) STS liquid
i. Can be opacified by mixing 2 mL of 3% STS with 1 mL of contrast
ii. The vein is occluded by external pressure as earlier. Static contrast in the ISV is aspirated or displaced
by saline injection.
iii. While the patient is performing a Valsalva maneuver, the STS is injected along the course of the vein
from immediately above the coils at the inguinal ring to above the iliac crest (colic collateral) if a proximal
Radiology Books
coil is to be used. Otherwise, STS is injected to within 1 cm of the ISV origin. A solution of 2.5 to 5 mL is
typically adequate.
(4) Metallic coils: The 0.035-in. or 0.038-in. coils may be delivered through a 4 Fr. or 5 Fr. catheter with a
hydrophilic coating. If distal access is difficult, then 0.025-in. or 0.018-in. coils are delivered via any of the
standard appropriately sized coaxial microcatheters currently available. The coils are appropriately sized to
the diameter of the spermatic vein at the desired level of occlusion. Typically, the coils are placed to
maximize the occlusion of collaterals and ideally reduce the recurrence rate. Place the last coil with care so
as to occlude the most cephalad portion of the spermatic vein without protruding into the left renal vein.
Poorly deployed coils may migrate into the central venous circulation, eventually lodging in the pulmonary
circulation. Occlusive plugs have been utilized; however, in most cases, the extra cost is not justified.
b. Glue: Cyanoacrylate, particularly in countries where it is inexpensive, is increasingly used for varicocele
occlusion with equal efficacy to coil/sclerosant embolization (8,11).
(1) Glue:lipiodol ratios (reported ratios range from 1:1 to 1:6), type of cyanoacrylate, or balloon occlusion
versus injection from standard angiographic catheter are matters of individual choice.
(2) Essential points
(a) The bolus of glue is introduced into the catheter after it has been flushed with 5% dextrose solution
(D5W) and is pushed out of the catheter by another bolus of D5W.
(b) Optimally, glue will fill the vein and collaterals from immediately deep to the inguinal ring (immediately
above the roof of the acetabulum) to 1 to 2 cm from the ISV origin (Fig. 42.3). Some practitioners place coils
in the distal ISV before injecting glue. Coils in the proximal ISV are not necessary.
(c) Avoiding injection of glue into the scrotum is essential, either by previously placed distal coils or external
compression.
(d) Over-injection of glue will result in extension into the renal vein or embolization into the pulmonary
artery.
(3) There are two modes of injection:
(a) When the catheter can be advanced into the distal ISV, the easiest method is to dribble a trail of glue as
the catheter is withdrawn, with the patient performing a Valsalva maneuver.
(b) If the catheter cannot be advanced distally, glue can be refluxed from a secure proximal position. This is
done with the patient performing a Valsalva maneuver and may be improved by a tilt table. Having an
assistant poised to apply compression as the glue flows into the distal ISV and considerable dexterity with
glue injection are required.
c. Metallic coils or plugs (without sclerosant): This method has fallen from favor due to high recurrence
rates, even when there is apparent single-vein reflux.
8. The right renal vein is cannulated in the same manner as the left using a multipurpose catheter from the
jugular approach or through a Simmons 1 catheter
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(or similar) from the femoral approach. Renal venography is performed. Although the right ISV drains into
the IVC the majority of the time in 1% to 6% of patients, it drains into the right renal vein. If the ISV does not
fill from the renal vein, it is usually located immediately anterior and inferior to the right renal vein ostium. If
using femoral access, a 3 Fr. microcatheter should be used to navigate the ISV ostium, advancing into the
upper right ISV. If using the jugular approach, an angled glidewire and multipurpose catheter will suffice in
most cases. Right spermatic venography, and if positive, embolization are performed as on the left.
Radiology Books
FIGURE 42.3 • Left varicocele embolization using glue. A: Venogram after coils placed in lower vein, during
Valsalva maneuver with external compression. Multiple collateral channels are demonstrated, which were
not apparent on initial venogram. B: Filling of collateral channels with glue/lipiodol injected under similar
conditions as catheter was withdrawn.
1. Remove all catheters and the sheath; attain hemostasis at the puncture site.
2. Monitor patient in the recovery room for 1 to 2 hours prior to discharge (outpatient discharge evaluation criteria
must be met).
3. Ten percent of patients will have some back pain that lasts for 24 to 48 hours. Non-narcotic analgesic and
nonsteroidal anti-inflammatory drugs (NSAIDs) and avoidance of vigorous activity for 3 days will usually suffice.
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4. With the lower vein coil and STS foam method, up to 10% of patients may have mild scrotal swelling and
discomfort, relieved easily with NSAIDs and a heating pad for 24 to 48 hours.
5. Follow-up scrotal ultrasound in 3 months
Results
1. Results of surgical or endovascular techniques are almost identical (4).
2. Technical success of embolization for previously untreated varicoceles and postsurgical recurrences is
93% to 100% (6,8).
Radiology Books
3. Thirty percent to 35% of infertile couples will have a normal pregnancy if there are no female infertility
factors. In the literature, pregnancy rates from 11% to 60% have been reported (12).
4. Patients usually return to work the next day, compared with an average of 6 days following microsurgical
techniques (13,14). Patients who have surgery initially and then embolization for recurrence express a
strong preference for embolization (15).
Complications
1. Coils
a. Misplacement of coil or migration into the central venous circulation
b. Venous perforation, usually self-limiting, may occur when venospasm is present, and one perseveres
with catheter manipulation. The best option is to stop the procedure and wait about 5 to 10 minutes for the
spasm to abate spontaneously.
2. Sclerosant and glue
a. Phlebitis, by means of reflux of STS foam into the pampiniform plexus. Usually self-limiting. It can be
treated with ibuprofen or Toradol and limitation of activity to nothing more strenuous than walking until
symptoms subside for severe cases.
References
1. Masson P, Brannigan RE. The varicocele. Urol Clin North Am. 2014;41:129-144.
2. Kadyrov ZA, Teodorovich OV, Zokirov OO, et al. Bilateral varicocele: epidemiology, clinical presentation
and diagnosis [in Russian]. Urologiia. 2007;(3):64-68.
3. Cantoro U, Polito M, Muzzonigro G. Reassessing the role of subclinical varicocele in infertile men with
impaired semen quality: a prospective study. Urology. 2015;85:826-830.
4. Kroese AC, de Lange NM, Collins J, et al. Surgery or embolization for varicoceles in subfertile men:
summary of a Cochrane review. Fertil Steril . 2014;102:1553-1555.
5. Wang YJ, Zhang RQ, Lin YJ, et al. Relationship between varicocele and sperm DNA damage and the
effect of varicocele repair: a meta-analysis. Reprod Biomed Online. 2012;25:307-314.
6. Iaccarino V, Venetucci P. Interventional radiology of male varicocele: current status. Cardiovasc Intervent
Radiol . 2012;35:1263-1280.
7. Nork JJ, Berger JH, Crain DS, et al. Youth varicocele and varicocele treatment: a metaanalysis of semen
outcomes. Fertil Steril . 2014;102:381.e6-387.e6.
8. Sze DY, Kao JS, Frisoli JK, et al. Persistent and recurrent postsurgical varicoceles: venographic anatomy
and treatment with N-butyl cyanoacrylate embolization. J Vasc Interv Radiol . 2008;19(4):539-545.
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9. Reiner E, Pollak JS, White RI, et al. Initial experience with 3% sodium tetradecyl sulfate foam and fibered
coils for management of adolescent varicocele. J Vasc Interv Radiol . 2008;19:207-210.
10. Gandini R, Konda D, Reale CA, et al. Male varicocele: transcatheter foam sclerotherapy with sodium
tetradecyl sulfate—outcome in 244 patients. Radiology. 2008;246:612-618.
11. Vanlangenhove P, Everaert K, Van Maele G, et al. Tolerance of glue embolization under local anesthesia
in varicoceles: a comparative study of two different cyanoacrylates. Eur J Radiol . 2014;83:559-563.
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12. Baazeem A, Belzile E, Ciampi A, et al. Varicocele and male factor infertility treatment: a new meta-
analysis and review of the role of varicocele repair. Eur Urol . 2011;60: 796-808.
13. Sayfan J, Soffer Y, Orda R. Varicocele treatment: prospective randomized trial of 3 methods. J Urol .
1992;148:1447-1449.
14. Enquist E, Stein BS, Sieman M. Laparoscopic versus subinguinal varicocelectomy: a comparative study.
Fertil Steril . 1994;61(6):1092-1096.
15. Feneley MR, Pal MK, Nockler IB, et al. Retrograde embolization and causes of failure in the primary
treatment of varicocele. Br J Urol . 1997;80:642-646.
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43
Ovarian and Pelvic Vein Embolization
Lindsay Machan
Indications
1. Unexplained chronic pelvic pain
2. Pelvic varicosities seen at laparoscopy, ultrasound, or open operation in a patient with appropriate
symptoms
3. Lower extremity varicose veins recurrent immediately after adequate surgical treatment or of an atypical
distribution
4. Symptomatic labial/perineal varicosities
Contraindications
a. Severe anaphylactoid reactions to radiographic contrast media
c. Severe renal insufficiency
2. Phobia to medical implants
3. Another cause of pelvic pain not adequately treated coexists (relative).
1. If the patient suffers from pelvic pain
a. Detailed clinical assessment by gynecologist or pelvic pain specialist
b. Diagnostic laparoscopy
c. Pelvic ultrasound or magnetic resonance imaging (MRI) (1)
d. Patient education: Even before diagnostic venography, the patient should be informed that pelvic congestion
syndrome is controversial and is not accepted as a cause of pelvic pain by many physicians (2,3). Gynecologists
will frequently see dilated pelvic veins in parous women who don't have symptoms and may not see dilated veins
in patients who do. Pelvic venous ectasia can be a normal consequence of pregnancy but flow is antegrade,
whereas in pelvic congestion syndrome, the patients have retrograde flow in the ovarian vein. Chronic pelvic
pain does not respond to embolization in all patients and as with other chronic pain syndromes may take up to 6
months to respond.
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2. If the patient suffers from lower extremity varicosities
a. Detailed clinical assessment by physician expert in venous disease
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b. Lower extremity duplex ultrasound assessment of venous reflux
Patient Preparation
1. Timing of the procedure in relation to menstrual or pain cycle is unimportant.
2. Clear fluids after midnight for morning appointment, clear fluids after breakfast for afternoon appointment
3. Admit the patient to a day care bed. Obtain informed consent. Make sure someone can drive the patient home.
4. Establish a peripheral intravenous (IV) line.
5. Sedate with midazolam (Versed) 2 mg and fentanyl 100 μg IV. These patients may be anxious and require a lot
of sedation.
Procedure (4,5)
1. Transjugular route
a. Position the patient supine on the table with her head turned to the left.
b. Sterile skin preparation and draping
c. Puncture the jugular vein. Ultrasound guidance is recommended.
d. Using Seldinger technique, introduce a 5 to 7 Fr. sheath into the jugular vein.
e. Advance multipurpose shape (MPA) catheter through sheath into the peripheral left renal vein.
f. Perform a left renal venogram by forceful injection of 20 mL of contrast with the patient performing a Valsalva
maneuver to identify all collateral channels.
g. If there is no reflux into the ovarian vein, and it clearly arises from the renal vein, this is considered a negative
study. Selective ovarian venography to detect reflux in nondilated veins is usually not necessary.
h. If there is ovarian vein reflux and varicosities, direct the catheter into the main trunk of the ovarian vein and
repeat injection of 20 mL of contrast with the patient performing a Valsalva maneuver to identify all varicosities
and collateral channels. Include bottom of pubic bones at inferior aspect of image and obtain delayed images
because varicosities may fill and drain slowly.
i. Advance the catheter into each of the major branches of the ovarian vein and embolize each branch, the main
ovarian vein, and all visible collateral channels with glue, sclerosant (liquid or foam), or coils, extending back to
within 2 cm of the ovarian vein origin. The author's preferred method is infusing 3% tetradecyl sulfate, each 2 mL
mixed with 0.5 mL of contrast into the lower ovarian vein while the patient does a Valsalva until there is stasis at
the end of the catheter and then occluding the main ovarian vein with 1 or 2 long (e.g., 38-8-10) coils.
j. Perform a left renal venogram with the catheter in the peripheral renal vein to confirm left ovarian vein
occlusion.
k. Direct the MPA catheter into the right renal vein and perform a right renal venogram to ensure that the right
ovarian vein does not arise from it (4%).
l. If not, direct the catheter immediately anterior and inferior to the right renal vein orifice. If the right ovarian vein
is not there, gentle probing along inferior vena cava wall in an up-and-down motion extending from the right renal
vein orifice to the iliac confluence is performed, beginning laterally, and rotating anteriorly slightly between each
sweep. It may arise to the left of the midline.
m. A right ovarian venogram and, if needed, embolization are performed in the same fashion as described for the
left.
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n. Select each internal iliac vein sequentially and inject 20 mL of contrast with the patient performing a Valsalva
maneuver. Some physicians perform internal iliac venography and embolization using a balloon occlusion
catheter. The author uses the same MPA catheter in the fashion described earlier for selective embolization if
there is reflux and varicosities.
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2. Transfemoral route
a. Sterile skin preparation as for femoral angiography
b. Insert a 5 to 7 Fr. sheath into the right femoral vein and direct a Cobra catheter into the peripheral left renal
vein and each internal iliac vein. Selective venography and embolization are performed using the same
diagnostic criteria and methods as described for the transjugular route.
c. The catheter is exchanged for a Simmons II catheter or equivalent and directed into the right ovarian vein.
3. Labial varicosities
a. Very difficult to eradicate; multiple sessions often needed
b. Exclude and treat ovarian, pelvic, and greater saphenous vein reflux first.
c. Direct puncture with 27-gauge butterfly needle under direct vision or ultrasound. Tilt table may help.
Venography is not necessary in most cases.
d. Inject sclerosant of choice (e.g., 0.5% tetradecyl sulfate).
e. Patient to wear compression shorts or similar for at least 2 days after
1. Observe the patient on bed rest for 60 minutes, and if stable and alert, discharge to a responsible adult who
can drive her home.
2. Analgesic requirements vary greatly. Nonsteroidal anti-inflammatory drugs (NSAIDs) or
acetaminophen/codeine for 3 days are usually adequate.
Complications
Eighty percent to 90% of patients suffer a postembolization syndrome, characterized by pain, fever, and
nausea. The severity varies tremendously from minor ache to agony and can last from a few hours to
several days. Treatment is analgesia and avoidance of strenuous activity. Other significant toxicities are
rare.
Results (6,7,8)
1. Technical success ranges from 96.7% to 100%.
2. Reported improvement in pain occurs in 73.7% to 100%, most commonly approximately 75%. Pain resolution
is complete in 0% to 57.9%.
3. This compares to bilateral oophorectomy and hysterectomy with subsequent hormone replacement (symptom
improvement in 66% of women) and surgical ligation of the left ovarian vein (improvement in 73%).
References
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1. Knuttinen MG, Xie K, Jani A, et al. Pelvic venous insufficiency: imaging diagnosis, treatment approaches,
and therapeutic issues. AJR Am J Roentgenol . 2015;204:448-458.
2. Ball E, Khan KS, Meads C. Does pelvic venous congestion syndrome exist and can it be treated? Acta
Obstet Gynecol Scand. 2012;91:525-528.
3. Phillips D, Deipolyi AR, Hesketh RL, et al. Pelvic congestion syndrome: etiology of pain, diagnosis, and
clinical management. J Vasc Interv Radiol . 2014;25:725-733.
4. Durham JD, Machan L. Pelvic congestion syndrome. Semin Intervent Radiol . 2013;30: 372-380.
5. Koo S, Fan CM. Pelvic congestion syndrome and pelvic varicosities. Tech Vasc Interv Radiol . 2014;17:90-
95.
6. Ganeshan A, Upponi S, Hon LQ, et al. Chronic pelvic pain due to pelvic congestion syndrome: the role of
diagnostic and interventional radiology. Cardiovasc Intervent Radiol . 2007;30:1105-1111.
7. Nasser F, Cavalcante RN, Affonso BB, et al. Safety, efficacy, and prognostic factors in endovascular
treatment of pelvic congestion syndrome. Int J Gynaecol Obstet. 2014;125:65-68.
8. Chung MH, Huh CY. Comparison of treatments for pelvic congestion syndrome. Tohoku J Exp Med.
2003;201:131-138.
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44
Thermal and Nonthermal Saphenous Vein Ablation
Ronald S. Winokur
Neil M. Khilnani
Robert J. Min
Introduction
Chronic venous disease (CVD) of the lower extremity results from venous hypertension most commonly caused
by incompetent valves in the saphenous veins and their primary tributaries and less frequently by chronic deep
venous obstruction and reflux after prior deep vein thrombosis (DVT). In patients with saphenous vein reflux,
treatment often begins with ablation of these veins.
Thermal versus Nonthermal Ablation

Thermal ablation is the induction of nonthrombotic vein occlusion by delivery of thermal energy directly to the
vein walls. Thermal ablation procedures require tumescent anesthesia (TA) for compressing and insulating the
treated veins as well as pain control. Endovenous laser ablation (ELA) (also called endovenous ablation [EVA] or
endovenous laser treatment [EVLT]) and radiofrequency ablation (RFA) are the most commonly used
techniques. Nonthermal, nontumescent requiring techniques developed for closure of the saphenous vein
include cyanoacrylate glue (CA) (VenaSeal, Sapheon/Covidien/Medtronic, Morrisville, NC), mechanochemical
ablation (MOCA) (ClariVein, Vascular Insights, Quincy, MA), and polidocanol endovenous microfoam (Varithena,
BTG International, West Conshoshocken, PA).
The underlying mechanism of thermal and nonthermal ablative procedures is to produce irreversible occlusion
and fibrosis of the vein by thermal injury, mechanical injury for MOCA, vein wall coaptation, and a giant cell
inflammatory response for VenaSeal or protein theft denaturation for Varithena (1,2).
Thermal ablative modalities have a proven track record of safe, effective, and durable elimination of varicose
veins, whereas newer nonthermal techniques are being studied and show promise to produce effective closure
with possibly improved patient acceptability and decreased risk of adjacent thermal nerve injury.
Anatomy of Superficial Veins of the Leg

Successful outcomes require a thorough understanding of the disease process and the anatomy of the
superficial venous system and a thorough exam utilizing duplex ultrasound. The superficial venous system of the
lower extremity is composed of innumerable subcutaneous collecting veins and the saphenous trunks and their
tributaries. The most recognized components of the superficial venous system are the great and small
saphenous veins. The saphenous veins are between the superficial and muscular fascia in a compartment
known as the saphenous space.
The great saphenous vein (GSV) begins on the dorsum of the foot and ascends the medial calf and thigh to join
the common femoral vein at the fossa ovale (Fig. 44.1). Important tributaries include the anterior and posterior
circumflex veins of the thigh and calf, the anterior accessory great saphenous vein (AA-GSV), the posterior
accessory GSV, and the superficial accessory great saphenous vein (SA-GSV). These common veins are often
found segmentally in the calf and/or thigh but may serve to be the primary flow channel when the true GSV is
either congenitally very small or absent in segments.
The small saphenous vein (SSV) begins on the lateral aspect of the foot, passes posterior to the lateral
malleolus, and then ascends up the midline of the calf (Fig. 44.2). The cephalad termination of the SSV is
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variable. The classic anatomy is for the SSV to drain into the popliteal vein just above the level at which the two
heads of the gastrocnemius diverge. However, a dominant popliteal termination
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is present in at most 60% of cases. In the remainder of cases, the SSV will extend more cephalad in a space
between the deep muscular and superficial fascia. These cephalad terminations of this vein are variable and
include termination into a perforating vein in the posterior thigh as well as a vein that communicates with the GSV
(also known as Giacomini or intersaphenous vein). Practically, combinations of the described SSV termination
patterns are common in many patients.
FIGURE 44.1 • Diagram of the GSV and its named tributaries.
Thermal ablation has been successfully performed in the GSV and SSV, the AA-GSV, the anterior and posterior
circumflex veins of the thigh as well as the thigh extension of the SSV.
Indications
1. Clinical
a. Symptoms of venous insufficiency affecting quality of life including aching, throbbing, heaviness, fatigue,
restlessness, night cramps, edema, and pruritus
b. Skin changes associated with chronic venous hypertension such as lipodermatosclerosis, atrophie
blanche, healed or active ulceration, recurrent superficial venous thrombophlebitis (SVT) in varicose veins,
and spontaneous bleeding
c. Cosmetic (restorative) concerns
2. Anatomic
a. Significant reflux documented on Duplex ultrasound (DUS) examination (reflux >0.5 second)
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FIGURE 44.2 • Diagram of the veins of the posterior calf and thigh. The SSV begins posterior to the lateral
malleolus and ascends the midline of the calf. In about two-thirds of cases, its primary termination is into the
popliteal vein about 2 cm about the knee crease. In the remainder of cases, its primary termination extends
more cephalad.
b. Straight vein segment

c. Reflux responsible for venous hypertension leading to the clinical abnormalities
Contraindications
Absolute
1. Patients in whom the saphenous vein to be ablated is responsible for a significant portion of the
antegrade collateral flow around a deep vein occlusion
Relative
1. Related to the clinical condition of the patient
a. Pregnancy or nursing female patients (concerns related to anesthetic use, heated blood effluent which may
pass through the placenta to the fetus or exposure to drugs associated with sclerosis or adhesives). “Pump and
dump” of breast milk would mitigate this contraindication in the postpartum period.
b. Liver dysfunction or allergy making it impossible to use a local anesthetic (cold saline may be useful as an
alternative)
c. Severe uncorrectable coagulopathy. Ablation can be performed on patients receiving warfarin or antiplatelet
agents (3). The procedures have not been studied in patients on newer oral agents.
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d. Severe hypercoagulability syndromes (where risk of treatment outweighs potential benefits despite
prophylactic anticoagulants)
e. Inability to wear compression stockings secondary to inadequate arterial circulation, hypersensitivity to the
compressive materials, or musculoskeletal or neurologic limitations to donning the stocking itself
f. Inability to adequately ambulate postprocedure
2. Related to anatomy
a. Vein segments like some SA-GSV that cannot be displaced from the skin despite TA
b. Sciatic vein reflux because of proximity to sciatic and common peroneal nerves
Preprocedural Evaluation
1. Complete medical history including symptoms of venous insufficiency, family history, pregnancy history, prior
treatment for varicose veins, and personal or family history of DVT, SVT, and/or hypercoagulable states.
2. Directed physical exam of the lower extremity including the lower abdomen.
3. Use of the physician-reported Venous Clinical Severity Score (VCSS) and the Clinical, Etiologic, Anatomic,
Pathophysiologic (CEAP) classifications establish the baseline condition of the patient. Assessment of quality of
life affecting symptoms before and then again after any treatment should also be performed. Several validated
instruments exist including, but not limited to, the Venous Insufficiency Epidemiological and Economic Study
(VEINES)-Quality of Life (QOL), Aberdeen Varicose Vein Questionnaire (AVVQ), Chronic Venous Insufficiency
Questionnaire (CIVIQ), Specific Quality of Life and Outcome Response-Venous (SQOR-V) (4).
4. Complete DUS examination of the entire deep and superficial venous system should be performed. The
superficial venous exam should be performed while the patient is upright or in a steep reverse Trendelenburg
position to avoid both false negative and false positive evaluations for the presence of significant reflux. This
exam should identify all incompetent venous segments and should explain all abnormal visible veins (5).
1. No dietary restrictions. Procedure usually is performed with only local anesthetics.
3. Use a procedure table that allows a supine patient to be tilted into both Trendelenburg position as well as
elevation of the patient's head and torso.
4. Perform DUS (patient upright) to mark the location and extent of the vein or veins to be ablated and the
locations of important anatomic landmarks including the deep vein junctions; aneurysmal, tortuous, hypoplastic,
and aplastic segments; and large vein tributaries or communication with incompetent perforating veins. The
ultrasound (US) unit should have a linear 7.5- to 13-MHz probe.
5. If performing thermal ablation, prepare TA fluid. This is performed at our institution by mixing 440 mL 0.9%
normal saline, 50 mL 1% lidocaine, and 10 mL 8.4% sodium bicarbonate.
Procedure
Thermal Ablation
1. The patient is placed on the procedure table in the reverse Trendelenburg position and prepared in
standard sterile fashion. The GSV and its tributaries are treated in a supine position with the knee turned
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outward. The SSV and the thigh extension are treated in the prone position.
2. Using US guidance, access at the most peripheral point of the incompetent vein segment to be treated.
Occasionally, more than one access point may be
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necessary to allow treatment of the entire incompetent segment for aplastic, hypoplastic, tortuous vein
segments; previously treated veins, webs, or vein spasm preventing advancement of the ablation device; or
sheath. It is recommended that when venous access for ablation is required directly into a tributary vein or
into the accessory GSV that these veins are accessed first and efficiently because they are most likely to
undergo spasm or empty first.
3. Insert a vascular sheath (if needed) and position the thermal ablation device typically just peripheral to
the superficial epigastric vein (SEV) confluence (or 2 cm peripheral to the saphenofemoral junction [SFJ])
for the GSV. For the SSV, the catheter tip/ablation tool is positioned peripheral to the thigh extension of the
SSV or just below the point that the vein angles deep to join the popliteal vein. Some laser and
radiofrequency (RF) tools can be inserted without the need for a guidewire and positioned as above.
4. Place the patient in 10 to 15 degrees of Trendelenburg position.
5. Using US guidance, inject TA solution around the veins to be treated, from the entry point to the most
central location to be ablated.
a. The purpose of the tumescent fluid is to empty the vein by extrinsic compression to improve heat transfer
to the vein wall, to separate the vein from surrounding structures, and provide a protective halo of fluid to
prevent extravenous thermal injury to them (Fig. 44.3A,B) as well as for its anesthetic effect.
b. Tumescent delivery can be accomplished using a syringe and needles, a syringe connected to a
reservoir with a one-way valve, or a needle connected to a mechanically driven foot-accentuated TA pump.
A standard 25-gauge, 1.5-in.-long needle is well tolerated by nonsedated patients. Others use 21- to 23-
gauge needles such as micropuncture or spinal needles.
6. The thermal energy is then delivered.
a. For ELA, the laser fiber is withdrawn at a rate allowing for adequate heat transfer to the vein wall and
varies depending on the wavelength and power settings of each system. Data suggest that for 810 to 980
nm laser ablation, at least 80 J per cm is needed to accomplish successful ablation judged by occlusion and
resorption at 12 months (6). Larger vein segment diameters and the proximal part of the vein may require
larger amounts of energy.
b. For RFA with the ClosureFAST system (Covidien/Medtronic), withdrawal is performed in 6.5-cm
segments after each 7-cm section has been treated with a standard “cycle.” A double cycle of the first 7 cm
is recommended in the instructions for use (IFU).
7. Aspirating the sheath or external compression of the skin over the tip of the ablation catheter is used by
some in an attempt to empty the vein and to contain any heated blood from entering the deep vein beyond
the junction.
8. Upon completion of ablation and sheath removal, manual compression is applied to the vein puncture site
to gain hemostasis and a sterile dressing is applied.
9. After the procedure, the treated leg is placed in a graduated compression stocking (30 to 40 mm Hg,
usually thigh high) for 2 weeks (an additional compressive dressing is often used for the first 48 hours if
microphlebectomy is performed concurrently). There is no evidence to support the need for compression
after thermal ablation.
VenaSeal Cyanoacrylate Closure
1. Patient preparation, positioning, and target vein access is the same as for thermal ablation.
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2. After venous access at the lowest level of GSV reflux, an 80-cm long 7 Fr. introducer sheath provided by
the manufacturer in the kit is then advanced to near the SFJ over a 0.035-in. guidewire.
3. A syringe with a proprietary cyanoacrylate (CA) is connected to a dispensing gun, connected to a
specially designed delivery catheter that is highly visible on DUS and designed not to induce polymerization
of the adhesive and primed
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by advancing the glue to within 3 cm of the catheter tip. It is very important to avoid injecting saline into this
catheter as the saline will initiate polymerization.
FIGURE 44.3 • A: Axial US image of the GSV prior to insertion of the laser sheath. B: Axial US image at the
same level as A with the ELA fiber and sheath in place and surrounding TA fluid.
4. The hydrophobic delivery catheter is placed into the sheath and positioned approximately 5 cm below the
SFJ. Compression with the US probe about 2 to 3 cm above this point of injection is initiated to cause vein
coaptation.
5. The initial delivery of CA is performed in two injections of 0.09 mL (one 3-second trigger pull at 5 cm and
then immediately afterward, a second 3-second trigger pull at 6 cm below the SFJ). The catheter is then
withdrawn another 3 cm while maintaining external compression, both with the US probe as above as well,
as with a hand over the injection site, to coapt the vein segment containing CA for 3 minutes. Additional CA
is subsequently repetitively delivered at 3-cm intervals followed by 30 seconds of US probe and hand
compression to cause coaptation. The last injection site is 2 to 4 cm from the access site. The catheter is
removed with a quick tug to separate any CA that might connect the catheter
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to the intravenous (IV) CA. If any is left extending to the skin, it is trimmed with a scissor.
6. Graduated compression stockings are not recommended in the IFU following VenaSeal.
Mechanicochemical Ablation
1. Patient preparation, positioning, and target vein access is the same as for thermal ablation.
2. The ClariVein (MOCA) catheter with its dispersion wire protected within it is inserted into a short sheath
at the puncture site. The dispersion wire is unsheathed from the catheter and is positioned 1 cm from the
SFJ under US guidance.
3. The patient position is changed from reverse Trendelenburg to flat.
4. The catheter wire rotation is activated at approximately 3,500 rpm for 2 to 10 seconds to induce
venospasm and prevent central flow of sclerosant.
5. The catheter is withdrawn at a maximum rate of 1.5 mm per second (7 seconds per cm) with
simultaneous instillation of 1.5% sodium tetradecyl sulfate. The delivery of the drug is titrated to spread it
out over the full length of the vein, generally 6 to 10 mL in the GSV and 2 to 4 mL in the SSV. The device is
then removed and manual compression applied to the puncture site (7).
6. The patient is placed in a graduated compression stocking postprocedure, which is worn during the day
for 10 to 14 days.
Polidocanol Injectable Foam (Varithena)
1. Varithena is approved for use for the GSV, accessory saphenous veins, and their varicose tributaries. In
addition to marking the course of the incompetent GSV, the SFJ, any mid-thigh perforating vein, and high
calf paratibial perforating veins should be marked. The skin 5 cm below the SFJ is also marked for ease of
identification. Finally, the varicose tributaries that are to be treated at the same time are also marked
including the re-entry perforating veins.
2. The patient is prepped in a similar fashion to thermal ablation.
3. The target vein is accessed with an angiocatheter or micropuncture set. The optimal initial place is in the
mid-thigh, unless a mid-thigh perforating vein is found in which case the access needs to be at a higher
level. Take care not to access too close to the SFJ. The catheter is then connected to a saline-filled
connecting tube and confirmed intraluminal by aspiration of blood flushed with saline and secured to the
skin with tape.
4. The Varithena canister is charged according to the IFU and allowed to sit for 1 minute.
5. A specifically designed syringe is connected to the canister and 3 mL of Varithena is purged to eliminate
air in the syringe and canister top. Then 5 mL of Varithena is withdrawn into the syringe and left on the
canister for an additional 3 seconds.
6. The leg is then elevated to at least 45 degrees. The syringe is then removed and an initial aliquot of the
drug is injected into the connecting tube under US guidance and while manually compressing the vein
below the IV access. When the injection reaches approximately 3 to 5 cm below the SFJ, the injection is
stopped temporarily and pressure is placed on the GSV just above this level (to prevent foam progression to
the common femoral vein) until venous spasm occurs, which generally takes a few seconds to 3 minutes.
Additional drug is then injected distally after releasing pressure in that location to fill the distal GSV and
visible varicose vein tributaries (2). Additional needle or IV access for injections into the tributary varices can
then be performed with pressure placed over important perforating veins to minimize filling of the deep
venous system. A maximum of 5 mL per injection, for a total of 15 mL per session, are the maximum
amounts recommended in the IFU.
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7. A 30 to 40 mm Hg, thigh high graduated compression stocking is placed, with or without additional
compression rolls, over the treated veins. The patient's leg is lowered and the patient allowed to ambulate.
8. The patient may need a second treatment in up to 25% of cases. The Varithena canister lasts for 1 week,
so having the patient return for a DUS and possible second treatment 5 to 7 days after the first treatment is
recommended.
1. Ambulation is initiated immediately and encouraged following all of the aforementioned procedures. We
recommend 2 hours of walking a day for 2 weeks and a 1-hour walk immediately, although no scientific data exist
for this recommendation.
2. Vigorous exercise is generally discouraged for the first 2 weeks following treatment. Long periods of immobility
such as those that occur with long air flights or car rides soon after endovenous ablation should likely be
discouraged to minimize venous stasis that could increase the risk of DVT. These practices are not based on
data.
3. Patients should return for clinical and DUS evaluation to confirm vein closure and exclude complications.
a. If a physician is attempting to identify thrombus extension across the saphenopopliteal junction (SPJ) or SFJ, a
DUS in the first 72 hours postprocedure seems to be necessary (8). However, given the transient and benign
clinical course of endothermal heat-induced thrombus (EHIT) extension in the deep veins at the junctions as well
as the seemingly low rate of thrombosis in the deep veins of the calf, the necessity of evaluating all patients at 72
hours for thrombus cannot be substantiated.
b. Clinical evaluation and DUS at 1-month postablation allow one to assess the early outcome of the ablation
and plan further treatment as needed.
4. The value of periodic DUS is controversial. However, follow-up DUS of a treated vein is not needed once it is
no longer visible. Periodic follow-up DUS may be needed to evaluate the etiology of any new tributary
varicosities.
a. The natural history of a successfully thermally treated truncal vein includes acute vein wall thickening without
significant intraluminal thrombus in the first few weeks after treatment. This is followed over the next few months
by progressive vein shrinkage and eventual disappearance on US examination (8,9,10).
b. The disappearance of the treated vein apparently occurs more slowly after ClariVein and Varithena, with skip
segments and in the case of Varithena, recanalization is more common. After VenaSeal ablation, the vein lumen
appears more echogenic immediately after the ablation and will remain echogenic and not completely shrink
when followed over the first year, with few recanalizations beyond 6 months.
Results
1. Thermal ablation
a. ELA and RFA result in durable obliteration of the great saphenous vein in 97% (11).
b. Endovenous ablation of the SSV has a technical success rate approaching 100% and at least a 90%
closure of the vein at 3 to 6 months (12,13).
c. Successfully treated veins occlude and shrink with time and become difficult to detect. The average
period for a treated GSV to shrink to a fibrous cord of <2.5 mm diameter is 6 months (10). At 1 year
following ELA of the GSV, 95% of the treated segments were not visualized, 2% were occluded but visible,
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and 2% were still patent (14).
d. There is no clear difference in outcomes between RFA and ELA; however, four trials have suggested
decreased immediate postprocedure pain with RFA and
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higher long-term venous closure rates with ELA although this difference is very small (15).
2. VenaSeal
a. Two studies have shown a 94% to 99% total occlusion rate at 3 months following treatment with no
serious adverse events (16).
3. MOCA
a. In a clinical trial of 30 veins treated with MOCA, the primary closure rate at 260 days was 96.7% with no
adverse events up to 6 months following treatment (17).
b. This study also noted no complaints of pain during the procedure, which only required 1 mL of local
anesthesia at the cannulation site and no postprocedure bruising (17).
4. Varithena
a. The VANISH-2 trial reported the outcomes of 232 patients randomized to receive ablation with
polidocanol endovenous foam or placebo with 8-week follow-up. Treatment with Varithena showed a
statistically significant improvement in patient-reported outcomes Varicose Vein Symptom Questionnaire
(VVSymQ), appearance from the patient perspective and by a blinded physician, and DUS response (83%
and 86% closure rates with 0.5% and 1% polidocanol foam, respectively) at 3 months (2).
b. Preliminary data presented as an abstract suggest a closure rate of 78% at 1 year.
Complications
1. Thermal Ablation
a. Most adverse events (AE) following endovenous ablation are minor (18).
(1) Soreness, bruising, tenderness, and induration over the treated segment frequently occurs and normally
resolves by 7 to 14 days. Following GSV ablation, patients may develop a feeling of tightness similar to that
after a strained muscle in the medial thigh, which is self-limited and usually improves with stretching, the
use of nonsteroidal anti-inflammatory drugs and graduated compression stockings.
(2) Superficial phlebitis of the varicose tributaries is reported in about 5% of cases and can occasionally be
avoided with the concurrent use of ambulatory phlebectomy if ablation isolates the inflow and outflow from a
varicose vein tributary (18).
b. Significant AE include nerve injuries, skin burns, and DVT. The overall rate of these complications is
higher at low case-volume centers. Dysesthesia and skin burns have been reported in a small number of
cases, and DVT in less than 1% of patients after ELA and RFA (19).
2. VenaSeal
a. Reddening and tenderness to palpation over the treated vein was seen in 11.4% in a multicenter trial of
70 patients (1).
b. In the initial feasibility trial in 38 patients, there were 8 (21.1%) incidences of threadlike thrombus
extension across the SFJ; however, in the follow-up multicenter trial using a greater starting point distance
from the SFJ, there was only 1 case (1.4%) of thrombus extension across the SFJ (1).
3. MOCA
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a. In the initial clinical trial using MOCA, there were 3 cases of minor ecchymosis but no incidence of DVT,
skin injury, or nerve injury in 30 cases (17).
4. Varithena
a. Polidocanol endovenous microfoam (PEM) has a low risk of AE with 95% of them classified as mild or
moderate and no cerebrovascular events or migraines.
b. At the approved formulation (1% PEM), the most commonly reported AE was retained coagulum (27.6%),
which can be expected with chemical sclerosis.
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c. The incidences of DVT, common femoral vein thrombus extension, and superficial thrombophlebitis were
8.6%, 6.9%, and 3.4%, respectively. None of the cases of common femoral vein (CFV) thrombus extension
were occlusive. There was no difference in the outcome of the patients who received anticoagulation to
treat a thrombotic complication, which was used in about half of the patients with such complications.
References
1. Proebstle TM, Alm J, Dimitri S, et al. The European multicenter cohort study on cyanoacrylate
embolization of refluxing great saphenous veins. J Vasc Surg. 2015;3(1):2-7.
2. Todd KL III, Wright DI; and the VANISH-2 Inverstigator Group. The VANISH-2 study: a randomized,
blinded, multicenter study to evaluate the efficacy and safety of polidocanol endovenous microfoam 0.5%
and 1.0% compared with placebo for the treatment of saphenofemoral junction incompetence. Phlebology.
2014;29(9):608-618.
3. Sharifi M, Mehdipour M, Bay C, et al. Effect of anticoagulation on endothermal ablation of the great
saphenous vein. J Vasc Surg. 2011;53(1):147-149.
4. Vasquez MA, Munschauer CE. Venous Clinical Severity Score and quality-of-life assessment tools:
application to vein practice. Phlebology. 2008;23(6):259-275.
5. Min RJ, Khilnani N, Zimmet SE. Endovenous laser treatment of saphenous vein reflux: long-term results. J
Vasc Intervent Radiol . 2003;14:991-996.
6. Niedzwiecki G. Endovenous thermal ablation of the saphenous vein. Semin Intervent Radiol .
2005;22:204-208.
7. Elias S, Lam YL, Wittens CH. Mechanochemical ablation: status and results. Phlebology. 2013;28(suppl
1):10-14.
8. Kundu S, Lurie F, Millward SF, et al. Recommended reporting standards for endovenous ablation for the
treatment of venous insufficiency: joint statement of the American Venous Forum and the Society of
Interventional Radiology. J Vasc Interv Radiol . 2007;18(9):1073-1080.
9. Pichot O, Kabnick LS, Creton D, et al. Duplex ultrasound scan findings two years after great saphenous
vein radiofrequency endovenous obliteration. J Vasc Surg. 2004;39(1):189-195.
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10. Yang CH, Chou HS, Lo YF. Incompetent great saphenous veins treated with endovenous 1,320-nm
laser: results for 71 legs and morphologic evolvement study. Dermatol Surg. 2006;32(12):1453-1457.
11. Pan Y, Zhao J, Mei J, et al. Comparison of endovenous laser ablation and high ligation and stripping for
varicose vein treatment: a meta-analysis. Phlebology. 2014;29(2):109-119.
12. Huisman LC, Bruins RM, van den Berg M, et al. Endovenous laser ablation of the small saphenous vein:
prospective analysis of 150 patients, a cohort study. Eur J Vasc Endovasc Surg. 2009;38(2):199-202.
13. Proebstle TM, Vago B, Alm J, et al. Treatment of the incompetent great saphenous vein by endovenous
radiofrequency powered segmental thermal ablation: first clinical experience. J Vasc Surg. 2008;47(1):151-
156.
14. Theivacumar NS, Beale RJ, Mavor AI, et al. Initial experience in endovenous laser ablation (EVLA) of
varicose veins due to small saphenous vein reflux. Eur J Vasc Endovasc Surg. 2007;33(5):614-618.
15. Gloviczki P, Comerota AJ, Dalsing MC, et al. The care of patients with varicose veins and associated
chronic venous diseases: clinical practice guidelines of the Society for Vascular Surgery and the American
Venous Forum. J Vasc Surg. 2011;53:2S-48S.
16. Lawson J, Gauw S, van Vlijmen C, et al. Sapheon: the solution? Phlebology. 2013;28 (suppl 1):2-9.
17. Elias S, Raines JK. Mechanochemical tumescentless endovenous ablation: final results of the initial
clinical trial. Phlebology. 2012;27(2):67-72.
18. Khilnani NM, Grassi CJ, Kundu S, et al. Multi-society consensus quality improvement guidelines for the
treatment of lower-extremity superficial venous insufficiency with endovenous thermal ablation from the
Society of Interventional Radiology, Cardiovascular Interventional Radiological Society of Europe, American
College of Phlebology and Canadian Interventional Radiology Association. J Vasc Interv Radiol .
2010;21(1):14-31.
19. van den Bos R, Arends L, Kockaert M, Neumann M, Nijsten T. Endovenous therapies of lower extremity
varicosities: a meta-analysis. J Vasc Surg. 2009;49:230-239.
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45
Varicose, Perforator, and Spider Veins: Liquid Ablation
Lindsay Machan
Introduction (1,2)
Distension and dysfunction of the small veins which ultimately feed into the superficial venous system can occur
alone or in association with truncal vein reflux. Abnormal small veins include telangiectasias (“spider veins”), flat
red vessels smaller than 1 mm in diameter, and reticular veins which have a cyanotic hue and are 2 to 4 mm in
diameter. Telangiectasias are present in up to 28.9% of men and 40.9% of women. Risk factors include heredity,
pregnancy, female hormones, weight gain, and prolonged sitting or standing.
Perforator veins, when competent, shunt blood from the superficial to the deep system. Except when directly
related to active venous ulceration, there continues to be controversy regarding the need to treat incompetent
perforators.
Sclerotherapy is the ablation of a vascular structure by injection of a chemical irritant. In the legs, it is the primary
treatment for small-vessel venous disease. Sclerotherapy for large vein ablation, usually performed under
ultrasound guidance, is primarily used when the techniques discussed in the prior chapter are not applicable,
such as large tortuous varicosities. Particularly for patients presenting for cosmetic treatment, excellent
sclerotherapy is essential to achieving patient satisfaction and clinical success.
Indications (1,3)
1. Small and large vein sclerotherapy
a. Cosmesis
b. Symptom relief
(1) Pain
(2) Burning
c. Remnant disease after surgical or endovenous treatment of truncal reflux
2. Perforator incompetence
a. All treatments of coexisting superficial reflux have been exhausted.
b. Diameter >3.5 mm
c. Reflux >0.5 seconds
d. Close proximity to active ulceration
Contraindications (4)
Absolute
1. Allergy to sclerosing agent
2. Acute thrombophlebitis/deep vein thrombosis (DVT)
3. Hypercoagulable state
Relative
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1. Pregnancy/breastfeeding
2. Needle phobia
3. Inability to tolerate compression
4. Peripheral vascular disease
5. Systemic or infectious skin disease
6. Uncontrolled asthma or migraine
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7. Known patent foramen ovale
8. Inability to ambulate/impending immobilization (e.g., surgery or prolonged travel)
1. History and physical exam as for saphenous venous reflux. The patient's expectations should be clearly
defined and, if necessary, realistically modified.
2. Duplex ultrasound. If reflux is demonstrated in the saphenous or other superficial truncal veins, this must be
treated first. Some practitioners will perform sclerotherapy in the same session after truncal vein obliteration,
others prefer to wait up to 12 weeks.
3. Consider taking pretreatment photographs for documentation and comparison with the postoperative results.
4. Informed consent should include discussion that multiple treatment sessions are typically necessary and that
new vessels are likely to develop over time.
Procedure (5,6)
A list of injectable agents used for sclerotherapy is shown in Table 45.1. Only the detergents sodium tetradecyl
sulfate and polidocanol are U.S. Food and Drug Administration (FDA)-approved for intravenous injection. The
most commonly used sclerosants are tetradecyl sulfate and hypertonic saline (the 23.4% concentration is FDA-
approved, but its use in sclerotherapy is off-label).
Small Vein Sclerotherapy

1. The guiding principle is to ablate the desired vessels while avoiding damage to normal collaterals and
surrounding tissue by using the lowest effective volume and concentration of sclerosant. Suggested
concentrations of commonly used sclerosing agents are listed in Table 45.2.
2. Larger veins are treated before smaller vessels. Treatment of the pretibial area and ankle may have poorer
outcomes, so injection in these locations should not be first and should be limited in each session.
3. Clean the skin with sterile solution. No sedation or anesthesia is generally required.
4. Puncture a straight segment of the spider or reticular vein with a 30-gauge needle, bevel up.
5. Ensure there is blood return with aspiration.
6. Slowly and gently inject 0.1 to 0.4 mL of sclerosant. The injected area will change color. Remove needle and
compress. Massaging may enhance sclerosant distribution.
Table 45.1 Common Agents Used for Sclerotherapy
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Detergents—disrupt endothelial cell membrane
Sodium tetradecyl sulfate (Sotradecol)

Polidocanol (Aethoxysclerol)
Sodium morrhuate (Scleromate)
Ethanolamine oleate (Ethamolin)
Osmotic agents—endothelial cell dehydration and cell membrane denaturation
Hypertonic saline
Saline solution with dextrose (Sclerodex)
Chemical irritants—caustic endothelial destruction
Chromated glycerin (Sclermo)

Polyiodinated iodine
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Table 45.2 Suggested Concentrations for Small Vessel Sclerotherapy
Reticular Veins and Venulectasias Telangiectasias (Spider Veins)
Hypertonic saline 23.4% 11.7%
Sodium tetradecyl sulfate 0.25%-0.4% 0.1%-0.2%
Polidocanol 0.5%-1.0% 0.25%-0.75%
7. Repeat the injection procedure at 2 to 3 cm intervals until the entire vessel has been treated.
Large Vein Sclerotherapy

1. Using sterile technique, cannulate the vessel with a 25-gauge or larger butterfly needle (if using foam, a
smaller needle disrupts the bubbles).
2. Ultrasound guidance can be used to guide the puncture and to monitor dissemination of the sclerosant during
injection.
3. If using a liquid sclerosant, inject 0.5% to 3 % sodium tetradecyl sulfate or equivalent until thrombus is seen
throughout the desired distribution by ultrasound or direct vision.
4. Foam sclerotherapy (injection of a detergent sclerosing agent mixed with air) requires a smaller volume of
sclerosing agent, results in a lesser dilution with blood, achieves a homogeneous effect in the injected veins, and
is more visible on ultrasound (6). One percent to 1.5% sodium tetradecyl sulfate or 2% to 3% polidocanol are
mixed 1:4 with room using two syringes connected by a three-way stopcock, alternatively moving the syringe
pistons up and down. The syringe containing foam is then connected to the butterfly needle in the vein and
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depending on the vein size, total volumes of 3 to 5 mL are typically injected (until foam is distributed throughout
the desired vein), although some authors report using volumes up to 20 mL.
Perforator Veins (7)

1. Sclerotherapy is typically performed with foam under ultrasound guidance.
a. With patient supine cannulate the perforator, or preferably a tributary, with a 21-gauge or 22-gauge needle.
b. Foam is injected until just before it extends into the deep vein, usually a volume of 0.5 to 1 mL. Ask the patient
to contract the calf as soon as the injection is completed to prevent extension of foam into the deep system.
2. Other treatment methods include surgery, thermal ablation with laser or radiofrequency, and occlusion with
cyanoacrylate. These techniques are beyond the scope of this chapter.
1. Compression after sclerotherapy improves clinical outcomes, but there is no consensus on duration (8).
Although 3 days of compression results in greater improvement than no compression, 3 weeks of continuous
compression with 20 to 30 mm Hg or 30 to 40 mm Hg graded compression stockings yields the best results.
a. Patient compliance can be an issue; if a patient does not tolerate compression well, graded compression
stockings should at the least be worn the first night and then daily for 1 week.
2. The patient should begin walking immediately but avoid aggressive exercise for 1 week.
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3. Nonsteroidal anti-inflammatory drugs (NSAIDs) should be taken as needed for small vessel sclerotherapy;
maximal daily dose is prescribed for 1 week following ultrasound-guided sclerotherapy of larger veins.
4. Arrange further small vessel treatment sessions at 2- to 8-week intervals.
Results
1. Small vein sclerotherapy—there are no publications of evidence-based treatment results. Published
reports indicate 60% to 80% patient satisfaction and statistically significant reduction of detectable
telangiectasias compared with untreated regions (9).
2. Nontruncal varicosities—limited published data are available (3,5).
a. Veins >5 mm diameter—81% technical success (occlusion seen by duplex ultrasound)
b. Veins <5 mm diameter—92% technical success
c. Persistence of occlusion at 2-year follow-up
(1) 53% after foam injection
(2) 12% after liquid sclerotherapy
3. Perforator sclerotherapy—with perforator incompetence alone, sclerotherapy can result in rapid ulcer
healing in 86.5% of patients with a mean time of healing of 36 days (10).
Complications (11,12)
1. Allergic reactions—0.3% including anaphylaxis. The highest incidence is with ethanolamine oleate.
2. Bruising—common and self-limited
3. Extravasation
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4. Hyperpigmentation—10% to 30%
5. Telangiectatic matting (development of fine red telangiectasias in the area of treatment)—15% to 20%. This
can occur spontaneously but may be due to too rapid injection or too high concentration of sclerosant.
6. Superficial thrombophlebitis
7. Tissue necrosis—most common with hypertonic saline. The cause may be extravasation or injection into an
arterial branch.
8. DVT—extremely rare
9. Foam sclerotherapy-specific adverse effects—especially in patients with a patent foramen ovale (12)
a. Visual (scotoma or amaurosis)
b. Neurologic (transient ischemic attack [TIA], stroke, migraine)
c. Pulmonary symptoms (cough, pain)
Management of Complications (13)

1. Extravasation—if there is extravasation of a large volume or high concentration of sclerosant, immediate
dilution by regional injection of hyaluronidase (75 units in 3 mL), normal saline, lidocaine, or a mixture of the latter
two should be performed immediately.
2. Hyperpigmentation—reassurance is usually adequate as spontaneous resolution occurs in 70% of patients at
6 months and 99% at 1 year.
3. Telangiectatic matting
a. May resolve spontaneously in 3 to 12 months
b. Gentle sclerotherapy and search for and treatment of feeding veins can provide resolution
c. Can be permanent
4. Superficial thrombophlebitis—treatment is with compression stockings and NSAIDs. If there is a distended
tender vein, evacuation of the liquefied thrombus
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by nicking the vein with a 0.018 needle and manually expressing the thrombus will provide immediate relief.
5. Tissue necrosis—the cause may be extravasation or injection into an arterial branch. If blanching of the skin is
encountered while injecting sclerosant, massage, topical 2% nitroglycerin ointment, or both may lessen or
prevent necrosis. If the patient develops skin necrosis after sclerotherapy, cosmetic surgery consultation is
recommended.
References
1. Winokur RS, Khilnani NM. Superficial veins: treatment options and techniques for saphenous veins,
perforators, and tributary veins. Tech Vasc Interv Radiol . 2014;17:82-89.
2. Meissner MH, Gloviczki P, Bergan J, et al. Primary chronic venous disorders. J Vasc Surg. 2007;46(suppl
S):54S-67S.
3. Leopardi D, Hoggan BL, Fitridge RA, et al. Systematic review of treatments for varicose veins. Ann Vasc
Surg. 2009;23:264-276.
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4. Brown KR, Rossi PJ. Superficial venous disease. Surg Clin North Am. 2013;93:963-982.
5. Coleridge Smith P. Foam and liquid sclerotherapy for varicose veins. Phlebology. 2009;24:62-72.
6. Sadick N. Sclerotherapy and alternatives. In: Sadick N, Khilnani N, Morrison N, eds. Practical Approach to
the Management and Treatment of Venous Disorders. London, United Kingdom: Springer-Verlag; 2013:61-
82.
7. Gloviczki P, Comerota A, Dalsing MC, et al. The care of patients with varicose veins and associated
chronic venous diseases: clinical practice guidelines of the Society for Vascular Surgery and the American
Venous Forum. J Vasc Surg. 2011;53:2S-48S.
8. El-Sheikha J, Carradice D, Nandhra S, et al. Systematic review of compression following treatment for
varicose veins. Br J Surg. 2015;102:719-725.
9. Hamel-Desnos C, Allaert FA. Liquid versus foam sclerotherapy. Phlebology. 2009;24: 240-246.
10. Masuda EM, Kessler DM, Lurie F, et al. The effect of ultrasound-guided sclerotherapy of incompetent
perforator veins on venous clinical severity and disability scores. J Vasc Surg. 2006;43:551-556.
11. Guex JJ, Allaert FA, Gillet JL, et al. Immediate and midterm complications of sclerotherapy: report of a
prospective multicenter registry of 12,173 sclerotherapy sessions. Dermatol Surg. 2005;31:123-128.
12. Ceulen RP, Sommer A, Vernooy K. Microembolism during foam sclerotherapy of varicose veins. N Engl J
Med. 2008;358:1525-1526
13. Weiss MA, Hsu JT, Neuhaus I, et al. Consensus for sclerotherapy. Dermatol Surg. 2014;40:1309-1318.
Radiology Books
46
Biopsy Procedures of the Lung, Mediastinum, and Chest Wall
Matthew D. Cham
Claudia I. Henschke
David F. Yankelevitz
Indications
1. Evaluation of a solitary pulmonary nodule (solid, part-solid, and nonsolid nodules) with features
suspicious for primary lung cancer and lacking benign features such as fat composition or calcification in a
benign pattern (1,2)
2. Evaluation of pulmonary nodules with documented growth at a malignant rate
3. Evaluation of positron emission tomography (PET)-positive pulmonary lesions that are suspicious for
malignancy
4. Evaluation of pulmonary nodules as part of a staging strategy in patients with known malignancies (lung
cancer and extrathoracic malignancies)
5. Obtaining tissue for molecular characterization to guide therapy
6. Evaluation of focal pulmonary infections that are refractory to standard therapy
7. Evaluation of pleural masses, pleural thickening, or pleural fluid collections
8. Evaluation of mediastinal masses, hilar masses, and lymphadenopathy
9. Evaluation of chest wall masses and lytic rib lesions
Contraindications
1. An uncooperative patient (considered by some as the sole absolute contraindication)
2. Bleeding diathesis (international normalized ratio [INR] >1.3, platelet count <50,000 per μL)
3. Medications associated with increased risk of bleeding (relative risk, some or all can be discontinued
prior to procedure; consideration also as to location of the lesion)
4. Severe bullous emphysema
5. Contralateral pneumonectomy or severely limited function in the contralateral lung
6. Intractable cough
7. Suspected hydatid cyst (due to risk of an anaphylactic reaction)
8. Possible pulmonary arteriovenous malformation (AVM), vascular aneurysm, or pulmonary sequestration
(intralobar or extralobar)
9. Pulmonary hypertension (especially when biopsy of a central lesion is considered) (3)
10. Patients on positive pressure ventilation
1. Explain the procedure and its possible complications to the patient 1 week prior to the biopsy if performed in
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the outpatient setting. Referring clinicians can also provide suitable information about the procedure at that time
which can be reviewed prior to the procedure when obtaining consent.
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2. Discontinue aspirin 5 days before biopsy. Discontinue other nonsteroidal antiinflammatory drugs (NSAIDs) 2
days prior to the procedure. Patients on oral anticoagulants should be switched to heparin for 2 to 3 days, which
in turn should be discontinued several hours before the procedure.
3. Obtain INR, prothrombin time, partial thromboplastin time, and platelet count 1 day prior to biopsy.
4. Correct any bleeding disorders with fresh frozen plasma, platelets, or vitamin K.
5. Patient instructed to not eat or drink 8 hours prior to the biopsy.
6. Choose the appropriate image guidance for the procedure.
a. Computed tomography (CT) guidance is used for most transthoracic needle biopsies (TNB) (4). CT may
allow planning of a trajectory that avoids traversing aerated lung. If this is impossible, CT can help plan a needle
path that bypasses potential obstacles such as interlobar fissures, bullae, large vascular structures, and bone. In
addition, CT may help to differentiate necrotic from viable areas within tumor.
b. CT fluoroscopy offers the advantages of CT combined with real-time imaging but is not as widely available
as CT. There is also the potential risk of increased radiation exposure for radiologists performing this procedure
frequently.
c. Fluoroscopic guidance offers real-time imaging for lesions visualized in two projections. Although previously
the standard of care, currently this modality is less useful for smaller pulmonary nodules and has been largely
replaced by CT guidance.
d. Ultrasound guidance is useful for biopsy of chest wall, pleural, anterior mediastinal, and peripheral lung
lesions (5).
7. Choose the appropriate needle for the procedure (Table 46.1).
a. There are two main types of biopsy needles: aspiratingneedles, which provide a cellular aspirate for
cytologic examination, and cutting needles, by which a core of tissue for histologic examination is obtained.
Some needles, such as Turner needles and Westcott needles, yield small fragments as well as a cellular
aspirate. Most biopsy needles are available in diameters ranging from 16 to 22 gauge; 25-gauge needles have
also been developed.
b. When a single-needle technique is used, multiple pleural punctures are required to obtain multiple samples.
Alternatively, a coaxial needle system can be used to obtain multiple samples using a single pleural puncture.
In this type of needle system, a thinner inner needle is inserted through a larger outer needle called an
introducer. Therefore, the pleura will be punctured by a needle that is larger than the one used to obtain the
sample. Tru-Cut-type cutting needles powered by spring-activated handles can be used to obtain a large core of
tissue, which is of particular value in the diagnosis of benign lesions (e.g., hamartomas, granulomas) and
lymphoma (6).
Table 46.1 Needles Used for Transthoracic Needle Biopsy
Type of Needle Brand and Manufacturer Commonly Used

Gauge
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Aspiration needle Chiba (Cook Catheter, Bloomington, IN) 20-25
Aspiration needle that also yields Westcott (BD Medical, Franklin Lakes, 20-22
tissue fragments NJ) 18-22
Turner (Cook Catheter)
Coaxial needle system Greene (Cook Catheter) Outer needle: 19

Inner needle: 22
Cutting needle with springactivated Biopty (USCI Bard, Billerica, MA) 18-20
handle Temno (BD Medical)
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c. No single type of needle design has been shown to be consistently superior to other types in terms of higher
diagnostic yield and lower complication rate. Choice is often a matter of preference (7).
8. Review the procedure, possible complications, and alternatives with the patient. Obtain signed informed
consent minutes prior to the biopsy.
Procedure
1. Position the patient on the biopsy table so that the skin entry site is placed upright. When ease of
performance and risk of complications are not substantially affected by the patient's position, prone position
is preferred to minimize chest wall motion and to minimize patient anxiety from seeing the needle. Biopsy
side down post procedure is also facilitated.
2. Perform preliminary examination.
a. For CT-guided biopsies, a scout view is obtained followed by localizing transaxial images through the
lesion. Upper lobe lesions generally do not require any special breathing instructions. When nodule motion
is observed near the diaphragm, breath-holding instructions are given. A small inspiration is requested so
that there will be minimal amount of motion once the needle has passed through the pleura and less chance
of a pneumothorax, as with deeper breath holds there will be greater motion and more chance of tearing the
pleural surface. The patient is requested to maintain the same degree of inspiration each time he or she is
asked to breath-hold (whenever the lesion is scanned or the biopsy needle is advanced). It is often useful to
practice breath-holding with the patient before beginning the procedure.
b. When ultrasound guidance is used, a preliminary examination is performed to confirm visibility of the
lesion.
3. When CT is used for guidance. The dose should be reduced to the minimal amount necessary for
monitoring of the procedure as it is not being performed for diagnostic purposes. Typically, this can be less
than the range of exposure factors used in lung cancer screening CT. Both kVp and mAs should be lowered
to achieve an estimated dose of less than 1.0 mSv for the entire procedure.
4. Plan the desirable needle path and mark the skin entry site.
a. Whenever possible, a needle path that avoids aerated lung should be chosen to reduce the likelihood of
developing a pneumothorax. A technique that can be used in selected cases to avoid puncture of aerated
lung is expansion of the extrapleural space by injecting a lidocaine-saline mixture (8). If aerated lung must
be traversed, structures such as interlobar fissures, bullae, cysts, and large vascular structures should be
avoided. Lesions that lie directly underneath an obstructing rib can be accessed using an oblique approach,
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with or without angling of the gantry (9).
b. A convenient way to localize the skin entry site is to place a row of metallic objects (e.g., injection
needles) on the skin at the desired level and scan them. Commercial skin markers are also widely available
for this purpose. The skin directly underneath or in between these objects can be marked with a felttipped
pen. It is useful to trace the anticipated biopsy-needle path on the CT console so it can be followed at a
later stage.
5. Cleanse the skin entry site using a povidone-iodine or chlorhexidine disinfectant. Cover the skin with
sterile drapes. Anesthetize the skin and subcutaneous tissue by infiltrating 5 to 10 mL of 1% lidocaine down
to, but not crossing, the pleura. The pleural surface can be very sensitive, and adequate anesthesia is
needed to minimize discomfort and motion. The patient should also be informed of the normal pressure
sensations during needle manipulation because patients who do not anticipate such pressure sensations
may become anxious with the false notion that the local anesthesia was insufficient. Patient reassurance
and cooperation are paramount to a successful lung biopsy.
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6. Use the anesthetic needle as a guide for placement of the biopsy needle. Advance the biopsy needle
along the planned trajectory until the needle tip is within the target lesion. When the procedure is performed
with CT guidance, at least one image superior and inferior to the needle tip must be obtained to document
that the needle tip is actually within the lesion and to avoid sampling error due to a partial volume-averaging
effect (10).
7. Sample the lesion. The actual sampling process varies depending on the needle design and biopsy
technique used (core biopsy or fine-needle aspiration). Generally, the needle's central stylet is removed and
a syringe is attached to the needle's hub. The plunger is then pulled back to generate suction, and the
needle is carefully shaken up and down to cut away cells from the lesion and draw them into the syringe.
The suction is then relieved as the needle and the attached syringe are withdrawn.
8. Ideally, the needle and attached syringe are then given to an on-site cytopathologist for immediate
processing, often referred to as immediate cytologic evaluation or ROSE (rapid on site evaluation). As the
evaluation of small samples of material has become far more sophisticated in recent years, the need to
have a well-developed protocol with the cytologist is increasingly important. The specimens may need to be
divided and allocated to the various necessary tests (11). In the absence of an on-site pathologist, the
aspirate is smeared on slides and fixed in 95% alcohol for cytologic evaluation, while larger fragments are
placed in a formalin solution for histopathologic evaluation. Additional analyses for molecular markers such
as epidermal growth factor receptor (EGFR) and Kirsten Rat Sarcoma Viral Oncogene Homolog (K-RAS)
are also performed for newly diagnosed lung cancers to determine their susceptibility to targeted drug
therapies. If an infectious cause is suspected, part of the obtained sample should be placed in a sterile test
tube for further microbiologic evaluation.
9. If a coaxial needle system is used, the blood patch technique can be used to reduce the likelihood of
developing a pneumothorax. The blood patch technique involves the injection of 4 mL of autologous blood
into the most peripheral 2 cm of the needle tract (12). This requires the use of a coaxial needle, with the
inner needle used to perform the biopsy and the outer needle used to inject the autologous blood. The
blood patch technique has been shown to significantly reduce the rate of pneumothoraces (13). The
success of the blood patch technique depends on the injection of autologous blood into
nonemphysematous lung parenchyma. Injection of autologous blood into an area of bullous emphysema
may result in an inadequate seal of the pleural puncture. Materials other than autologous blood have also
been used.
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1. If the biopsy was performed using CT guidance, obtain an immediate postbiopsy scan at approximately the
level of the biopsy site to detect a possible pneumothorax. Alternatively, an expiratory anteroposterior (AP) chest
radiograph can be obtained with the patient sitting upright (Fig. 46.1).
2. If no significant pneumothorax is noted and the patient is asymptomatic, transport the patient on a gurney to
the recovery area for observation.
3. Observe the patient for 2 hours following the procedure. The patient should remain recumbent throughout the
observation period. Vital signs should be monitored at least twice an hour. Measures that can prevent the
occurrence of pneumothorax and can facilitate the resorption of an existing small pneumothorax include placing
the patient in a “puncture site down” position and administration of supplemental nasal oxygen (14,15). Stable
inpatients can be monitored from their patient rooms.
4. If you suspect a significant pneumothorax has occurred during the observation period, obtain images of the
chest immediately, either by an expiratory upright sitting chest radiograph (CXR) or by several CT slices of the
chest. Otherwise, obtain additional images of the chest following the observation period.
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FIGURE 46.1 • Patient management after CT-guided lung biopsy. bx, biopsy; pcxr, portable chest x-ray; ptx,
pneumothorax; s/p, status post.
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5. If there is no significant pneumothorax and there are no symptoms attributable to pneumothorax, the patient
can be discharged after 2 hours of observation. The vast majority of all pneumothoraces requiring chest tube
placement occur within 1 hour of biopsy. Instruct patients to abstain from strenuous activities for 3 days and to
visit the nearest emergency room promptly if dyspnea or pleuritic chest pain develops. A contact number for the
physician who performed the procedure should also be provided.
6. Pneumothoraces that are small, asymptomatic, and stable do not require treatment. A postbiopsy
pneumothorax must be treated if:
a. The patient is dyspneic or has an acute onset of chest pain that may be attributable to pneumothorax.
b. The size of the pneumothorax exceeds 30%.
c. The pneumothorax continues to increase in size.
7. Two general approaches can be undertaken in the treatment of a postbiopsy pneumothorax:
a. Aspiration of the pneumothorax by insertion of an 18-gauge Angiocath or 6 Fr. drainage catheter into the
pleural space. This is connected to a
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three-way stopcock and air is withdrawn using a 60-mL syringe. The catheter is removed upon re-expansion of
the lung. The patient is placed in the “biopsy side down” position and serial CXRs are obtained to observe for
recurrence of pneumothorax (9). An alternative is to position the patient in the biopsy side down position and
then chose a new position to aspirate from on the nondependent side.
b. Placing a small (11 Fr.) thoracic catheter at the second or third intercostal space at the midclavicular line. The
thoracic catheter may be connected to a one-way Heimlich valve. Commercial thoracic vents are widely available
for this purpose. Patients in whom a small thoracic catheter has been inserted may be admitted to the hospital for
observation although successful outpatient management has been reported (16). If the air leak has ceased, the
catheter can be removed several hours following placement, and the patient can be discharged (17).
Results
1. TNB is highly accurate for diagnosing intrathoracic malignancy, including malignancies of the lung, hila,
mediastinum, and pleura. In general, the sensitivity for malignant nodules is reported to be as high as 95%
(18), whereas the sensitivity reported for benign nodules is more highly variable depending on the
technique used to perform the procedure, either core biopsy or fine needle aspiration. This is further
complicated by whether specific or nonspecific diagnosis is considered as benign. Under those
circumstances where a nonspecific benign diagnosis is made based on multiple samples and
documentation of the needle tip within the lesion, sensitivity of 90% has been reported (19). However,
because there is a possibility of missing a malignant lesion, a plan for further follow-up must be made. As
the procedure has matured along with advances in CT technology, biopsy of smaller subcentimeter lesions
is now far more commonplace. However, the diagnostic accuracy may decrease substantially as improving
techniques now allow attempts to biopsy smaller lesions (20,21).
2. A false-positive diagnosis is exceedingly rare and is estimated at less than 2% (22).
3. Although TNB is accurate for the diagnosis of malignancy, the rate of specific benign diagnoses is low,
ranging from 16% to 68% in series where such data are available (8). A negative cytologic or
histopathologic diagnosis should be interpreted with caution, as it may not represent a truly benign
diagnosis but merely failure to reach a malignant one.
4. Factors that improve the diagnostic yield of TNB (6,8,18,23)
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a. Careful positioning of the patient and documentation of the needle tip in the lesion
b. When necessary, sampling different areas within the lesion. Guidance by analysis of PET images, when
available, to areas of increased activity may be helpful.
c. Larger size and favorable site of the lesion
d. Experience of the performing radiologist and of the cytopathologist
e. Use of a cutting needle. This has been shown to be particularly beneficial in improving the likelihood of
obtaining a specific diagnosis in noninfectious benign lesions.
5. The presence of an on-site cytopathologist is ideal. Several prospective studies have shown that
immediate cytologic evaluation can significantly improve the diagnostic accuracy of CT guided TNB
(11,24,25,26).
Complications
Common
1. Pneumothorax: The reported incidence of pneumothorax related to TNB ranges from 5% to 60%. The
typically reported frequency of developing a postbiopsy pneumothorax is 20% to 25%, whereas the reported
frequency of pneumothoraces
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requiring thoracic vent or chest drain placement is 2% to 15% (12,27). Risk factors that increase the
occurrence of pneumothorax include (23,28):
a. Underlying emphysema or chronic obstructive lung disease
b. The use of cutting needles or biopsy guns (vs. aspirating needles)
c. Large-gauge needles (especially 18-gauge needles or introducers)
d. Traversing more than one visceral pleural surface (e.g., crossing an interlobar fissure)
e. Decreased needle-to-skin angle
f. Inability to place the patient with biopsy site in the dependent position following the procedure
g. Increased length of needle path (controversial)
2. Hemorrhage
a. The occurrence of hemorrhagic complications depends on the presence of a bleeding diathesis,
vascularity of the lesion, and use of medications that induce a bleeding tendency. Pulmonary hemorrhage,
manifesting as hemoptysis, occurs in 5% to 10% of biopsies and is usually self-limited (12). Patients should
be alerted about the possibility of hemoptysis as part of the informed consent.
b. If hemoptysis occurs, the patient should be reassured and placed biopsy site down to prevent
transbronchial aspiration of blood. Although massive pulmonary hemorrhage is rare, hemorrhage is the most
frequent cause of death following needle biopsy of the lung (4). Death results from massive
tracheobronchial aspiration and asphyxia.
c. To decrease the risk of serious hemorrhage, a small-caliber aspiration needle can be used (23).
Infrequent
1. Hemothorax and chest wall hematoma
2. Vasovagal reaction
Rare
1. Air embolism (29)
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2. Massive hemoptysis
3. Cardiac tamponade
4. Malignant seeding of the needle tract
5. Lung torsion
6. Fatal hemorrhage
References
1. MacMahon H, Austin JH, Gamsu G, et al. Guidelines for management of small pulmonary nodules
detected on CT scans: a statement from the Fleischner Society. Radiology. 2005;237:395-400.
2. Henschke CI, Yankelevitz DF, Naidich DP, et al. CT screening for lung cancer: suspiciousness of nodules
according to size on baseline scans. Radiology. 2004;231:164-168.
3. Moore EH. Needle-aspiration lung biopsy: a comprehensive approach to complication reduction. J Thorac
Imaging. 1997;12:259-270.
4. Protopapas Z, White CS, Miller BH, et al. Transthoracic needle biopsy practices: results of a nationwide
survey. Radiology. 1996;201:270-271.
5. White CS, Meyer CA, Templeton PA. CT fluoroscopy for thoracic interventional procedures. Radiol Clin
North Am. 2000;38:303-322.
6. Klein JS, Salomon G, Stewart EA. Transthoracic needle biopsy with coaxially placed 20-gauge automated
cutting needle: result in 122 patients. Radiology. 1996;198:715-720.
7. Aviram G, Schwartz DS, Meirsdorf S, et al. Transthoracic needle biopsy of lung masses: a survey of
techniques. Clin Radiol . 2005;60:370-374.
8. Klein JS, Zarka MA. Transthoracic needle biopsy. Radiol Clin North Am. 2000;38:235-266.
9. Yankelevitz DF, Vasquez M, Henschke CI. Special techniques in transthoracic needle biopsy of pulmonary
nodules. Radiol Clin North Am. 2000;38:267-279.
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10. Yankelevitz DF, Henschke CI, Davis SD. Percutaneous CT biopsy of chest lesions: an in vitro analysis of
the effect of partial volume averaging on needle positioning. AJR Am J Roentgenol . 1993;161:273-278.
11. Crapanzano JP, Saqi A. Adequacy and tissue preservation of small biopsy and cytology specimen. In:
Moreira AL, Saqi A, eds. Diagnosing Non-small Cell Carcinoma in Small Biopsy and Cytology. New York,
NY: Springer; 2015:39-59.
12. Moore EH. Technical aspects of needle aspiration lung biopsy: a personal perspective. Radiology.
1998;208:303-318.
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13. Lang EK, Ghavami R, Schreiner VC, et al. Autologous blood clot seal to prevent pneumothorax at CT-
guided lung biopsy. Radiology. 2000;216:93-96.
14. Moore EH, LeBlanc J, Montesi SA, et al. Effect of patient positioning after needle aspiration lung biopsy.
Radiology. 1991;181:385-387.
15. Moore EH. Percutaneous lung biopsy: an ordering clinician's guide to current practice. Semin Respir Crit
Care Med. 2008;29:323-334.
16. Gupta S, Hicks ME, Wallace MJ, et al. Outpatient management of postbiopsy pneumothorax with small-
caliber chest tubes: factors affecting the need for prolonged drainage and additional interventions.
Cardiovasc Intervent Radiol . 2008;31:342-348.
17. Brown KT, Brody LA, Getrajdman GI, et al. Outpatient treatment of iatrogenic pneumothorax after needle
biopsy. Radiology. 1997;205:249-252.
18. Yankelevitz DF, Bulman W. Advances in nonsurgical sampling techniques for the diagnosis and staging
of lung cancer. In: Moreira AL, Saqi A, eds. Diagnosing Non-small Cell Carcinoma in Small Biopsy and
Cytology. New York, NY: Springer; 2015:15-38.
19. Gelbman BD, Cham MD, Kim W, et al. Radiographic and clinical characterization of false negative results
from CT-guided needle biopsies of lung nodules. J Thorac Oncol . 2012;7(5):815-820.
20. Li H, Boiselle PM, Shepard JO, et al. Diagnostic accuracy and safety of CT-guided percutaneous needle
aspiration biopsy of the lung: comparison of small and large pulmonary nodules. AJR Am J Roentgenol .
1996;167:105-109.
21. Wallace MJ, Krishnamurthy S, Broemeling LD, et al. CT-guided percutaneous fineneedle aspiration
biopsy of small (< or = 1-cm) pulmonary lesions. Radiology. 2002;225: 823-828.
22. Charig MJ, Stutley JE, Padley SP, et al. The value of negative needle biopsy in suspected operable lung
cancer. Clin Radiol . 1991;44:147-149.
23. Shaham D. Semi-invasive and invasive procedures for the diagnosis and staging of lung cancer. I.
Percutaneous transthoracic needle biopsy. Radiol Clin North Am. 2000;38: 525-534.
24. Kücük CU, Yilmaz A, Yilmaz A, et al. Computed tomography-guided transthoracic fineneedle aspiration in
diagnosis of lung cancer: a comparison of single-pass needle and multiple-pass coaxial needle systems and
the value of immediate cytological assessment. Respirology. 2004;9:392-396.
25. Santambrogio L, Nosotti M, Bellaviti N, et al. CT-guided fine-needle aspiration cytology of solitary
pulmonary nodules: a prospective, randomized study of immediate cytologic evaluation. Chest.
1997;112:423-425.
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26. Tsou MH, Tsai SF, Chan KY, et al. CT-guided needle biopsy: value of on-site cytopathologic evaluation
of core specimen touch preparations. J Vasc Interv Radiol . 2009;20:71-67.
27. Yankelevitz DF, Henschke CI, Koizumi JH, et al. CT-guided transthoracic needle biopsy of small solitary
pulmonary nodules. Clin Imaging. 1997;21:107-110.
28. Cham MD, Lane ME, Henschke CI, et al. Lung biopsy: special techniques. Semin Respir Crit Care Med.
2008;29:335-349.
29. Tomiyama N, Yasuhara Y, Nakajima Y, et al. CT-guided needle biopsy of lung lesions: a survey of
severe complication based on 9783 biopsies in Japan. Eur J Radiol . 2006;59:60-64.
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47
Catheter Drainage of Intrathoracic Collections
Jared D. Christensen
Jeremy J. Erasmus
Edward F. Patz Jr.
Indications
1. Malignant pleural effusion (1,2,3,4)
a. Tumor invasion into the pleural space may lead to lymphatic obstruction resulting in pleural fluid
accumulation.
b. Indications for treatment
(1) Patients with dyspnea, cough, and/or chest pain
(2) Large effusions prior to chemotherapy to prevent accumulation of therapeutic agents in the pleural
space
(3) Symptomatic refractory/recurrent effusions
(4) Predictors of need for definitive therapy (indwelling catheter and/or pleurodesis) at diagnosis are low pH
(< 7.2), large size, and increasing patient age.
c. Staging
(1) Cytologic evaluation of pleural fluid may provide important clinical staging information. The presence of
a malignant effusion indicates stage IV disease for most cancers.
(2) The cellular yield for genetic diagnostic and prognostic tumor markers from pleural fluid is often
insufficient for analysis; however, small studies have reported potential applications for lung cancer and
malignant pleural mesothelioma (5,6). Further investigation is required for validation.
2. Parapneumonic effusion/empyema (3,7,8,9,10)
a. Sequential stages in the evolution of a parapneumonic effusion and development of an empyema with
associated treatment recommendations
(1) Exudative —Interstitial parenchymal fluid accumulates adjacent to a site of infection and flows across
the visceral pleura into the pleural space (high protein, sterile fluid, normal pH, and glucose). Antibiotic
therapy is generally effective in treating both the underlying pneumonia and effusion.
(2) Fibropurulent—Bacteria, polymorphonuclear leukocytes, and cellular debris within the pleural space. In
addition, fibrin barriers can create loculated pockets. Percutaneous drainage is recommended when the
fluid analysis shows a pleural glucose <60 mg per dL or a pH <7.2.
(3) Organizing—Fibroblasts produce an extensive fibrotic response (pleural peel), creating significant
resistance to respiratory motion and rendering percutaneous drainage of limited value.
b. Parapneumonic effusions occur in 20% to 57% of patients with pneumonia and 10% require drainage.
Categorization of the effusion determines management. The American College of Chest Physicians
classifies effusions on the basis of size, chemistry, and bacteriology.
(1) Category 1: Free-flowing pleural effusion <1 cm in thickness on decubitus radiograph does not require
treatment.
(2) Category 2: Small to moderate (>1 cm, <50% of hemithorax) free-flowing effusions with pleural pH >7.2,
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glucose >60 mg per dL, lactate dehydrogenase (LDH) less than three times the upper limit of serum, and
Gram stain and culture negative do not usually require drainage as most patients respond to antibiotic
therapy.
(3) Category 3: Large (>50% of hemithorax) free-flowing effusions, loculated effusions, or effusions with
thickened parietal pleura and/or pleural pH
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<7.2, and/or pleural glucose <60 mg/dL, and/or Gram stain and culture positive require drainage.
(4) Category 4: Frank pus in the pleural space requires drainage.
3. Lung abscess (8)
a. A total of 10% to 20% of patients with a pyogenic abscess will fail to respond to medical therapy
(systemic antibiotics, postural drainage), and drainage is recommended when
(1) There is persistent sepsis 5 to 7 days after initiation of antibiotic therapy.
(2) The abscess is >4 cm with an air fluid level.
(3) The abscess increases in size while the patient is on medical therapy.
(4) In children <7 years of age as these abscesses often do not drain spontaneously and are less likely to
respond to medical management
Contraindications
1. Relative
a. Clotting deficiency
(1) International normalized ratio (INR) >1.5
(2) Thrombocytopenia (<50,000 platelets per μL)
(3) Anticoagulation therapy
b. Extensive fibrothorax: prevents lung reexpansion and limits the value of percutaneous drainage
2. Absolute: There are no absolute contraindications to tube thoracostomy.
Choice of Drainage Catheter (1,2,3,4,7,8,9)

1. Malignant pleural effusion
a. Inpatient drainage: 14 Fr. all-purpose drainage (APD) catheter (Flexima APD, Boston Scientific Inc, Natick,
MA)
b. Outpatient (ambulatory) drainage: 10 Fr. APD catheter
c. Treatment of refractory/recurrent malignant effusions and symptomatic malignant pleural effusion with
underlying trapped lung: indwelling 15.5 Fr. drainage catheter (PleurX catheter, Denver Biomaterials Inc, Golden,
CO)
2. Parapneumonic effusion/empyema
a. Inpatient drainage: 12 to 14 Fr. APD catheter or 10 to 14 Fr. Malecot catheter
b. Outpatient (ambulatory) drainage: A 10 Fr. APD catheter is usually sufficient.
3. Lung abscess
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a. Tube selection often depends on the size of the cavity, although an 8 to 14 Fr. APD catheter is usually
sufficient. In children, tube size may also depend on the age of the patient.
1. Stop oral intake, preferably 8 hours prior to procedure.
3. Lab work: Clotting indices (prothrombin time [PT]/INR) and platelets. If the patient is on anticoagulation
therapy, the procedure should be timed to coincide after the cessation of therapy per manufacturer
pharmacologic recommendations to minimize bleeding risk.
4. Establish IV access.
5. Monitor vital signs: electrocardiogram (ECG), blood pressure, and pulse oximetry
6. Imaging/guidance selection: fluoroscopy, ultrasound (US), or computed tomography (CT). Most malignant
effusions can be drained with fluoroscopic or US guidance, although complicated fluid collections in the pleural
space (parapneumonic effusion, empyema) and lung abscesses may require CT guidance.
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7. Administer sedation/analgesia. Although a local anesthetic may be sufficient in some circumstances, pleural
drain placement is well tolerated with minimal (light) conscious sedation; commonly achieved by midazolam and
fentanyl administered in combination.
8. Choose a drainage system based on the underlying pathology and clinical considerations as detailed earlier.
9. Prepare and drape skin entry site.
Procedure
Malignant Pleural Effusions (1,2,3,4,11,12,13)
1. Common in cancer patients (15%) with more than 75% being due to lung malignancy, breast malignancy,
and lymphoma
2. Are a preterminal event with median survival usually between 4 and 6 months
3. Aim of treatment is palliation (relief of symptoms, prevention of recurrence).
Contraindications
1. Thick pleural peel of malignant tissue encasing the visceral pleura prevents complete lung
reexpansion after drainage of effusion (trapped lung syndrome); pleurodesis is rarely successful.
2. Central mass obstructing the airway that prevents reexpansion of the lung
3. Multiple loculated, complex fluid collections
4. Karnofsky index <40
Procedure
1. Patient position
a. Usually performed using US or fluoroscopy with patient in supine position
2. Percutaneous drainage approach
a. Typically sixth or seventh intercostal space in the midaxillary line. Enter at mid-two-thirds of
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intercostal space to avoid subcostal neurovascular structures and irritation of the periosteum.
3. Placement of APD catheters
a. Small-bore APD catheters (12 to 14 Fr.) are the treatment of choice as they are easy to insert, well
tolerated, and have response rates similar to large-bore catheters.
b. Inject local anesthesia, usually 1% to 2% lidocaine, into the soft tissues to the level of the pleura.
Always aspirate after advancing the needle tip prior to injection to avoid intravascular injection of
lidocaine.
c. Cut skin with a small blade to facilitate needle and catheter entry. Make sure incision is larger in size
than the catheter.
d. Insert an 18-gauge trocar needle into the pleural space; entry into the pleural space is indicated by
an abrupt decrease in resistance to forward movement of the needle. Accurate placement is facilitated
by image guidance.
e. Remove the inner stylet. Confirm needle position by aspirating a small quantity of pleural fluid. If the
tip is in the pleural space, fluid will usually flow back freely.
f. Introduce a 0.038-in. 100-cm floppy-tip guidewire (Cook Medical Inc, Bloomington, IN) through the
trocar into the pleural space. Remove the trocar, leaving the wire in place.
g. Serially dilate the track up to the required catheter French size.
h. Set up previously selected catheter assembly with the metal stiffener and introduce over the
guidewire. The metal stiffener is used to facilitate passage of the APD catheter through the
subcutaneous tissues. As soon as the catheter tip enters the pleural space, the stiffener is
disconnected from the catheter and held fixed as the catheter is advanced into the pleural space.
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i. The metal stiffener is slowly removed when the catheter is in satisfactory position, followed by
guidewire removal, leaving the catheter in place.
j. The pigtail catheter is locked and anchored externally with a suture or an adhesive skin disc (Molnar
external retention disc, Cook Medical Inc, Bloomington, IN or Hollister, Inc, Libertyville, IL).
k. Up to 1 L of fluid is aspirated. If the patient begins to cough before 1 L is removed, active aspiration
is discontinued.
1. A postprocedure radiograph is obtained to ensure proper tube placement and establish a baseline for
follow-up.
2. Bed rest for 2 to 4 hours
3. Check vital signs every 15 minutes for 1 hour, every 30 minutes for 1 hour, and then every 60 minutes for
2 hours.
4. Inpatient tubes are connected to a Pleur-Evac system (DeKnatel Division, Pfizer Hospital Products
Group, Fall River, MA) with continuous suction at 20-cm H2O.
5. Outpatient tubes are connected to a Tru-Close 600-mL bag (UreSil, Skokie, IL) or Dover urine leg bag
(Sherwood Medical, St. Louis, MO) for gravity drainage.
6. Tubes are flushed with 5 to 15 mL bacteriostatic saline every 8 hours.
7. Daily fluid output is recorded, and while drainage remains high, daily chest radiographs are not required.
When drainage decreases to approximately 100 to 200 mL over a 24-hour period, a chest radiograph is
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obtained to exclude loculated fluid and ensure complete lung re-expansion. If pleural fluid and air have been
completely evacuated (usually 2 to 5 days), pleurodesis with a sclerosing agent is undertaken.
8. Several sclerosing agents have been used to treat malignant pleural effusions. Talc is currently the agent
of choice for pleurodesis (poudrage, slurry 5 g talc, 50 mL saline, 10 mL 1% Xylocaine). Doxycycline (500
mg, 30 mL saline, 30 mL 1% Xylocaine), bleomycin (60 units in 50 mL saline), and silver nitrate (20 mL
0.5%) (14,15,16) can be used as alternatives to talc for pleurodesis, but effectiveness is lower and pain on
instillation is common.
a. Sclerosing agent is introduced into the pleural space through the drainage catheter.
b. Patient changes position every 15 minutes for 2 hours in an effort to distribute the sclerosing agent
completely throughout the pleural space.
c. The APD catheter is then reopened to suction for 24 hours.
d. The APD catheter is removed if drainage remains less than 200 mL over 24 hours over the same period.
A second dose of the sclerosing agent can be administered if the fluid drainage level is higher than 200 mL.
9. APD catheter removal is performed by cutting across the distal aspect of the catheter. This allows the
locking suture to be freed, and the pigtail loop to uncoil as the catheter is withdrawn. The skin site is
covered with a Vaseline gauze dressing.
10. In patients with long-term drainage catheters, fluid is drained periodically into 600-mL vacuum bottles by
placing the preconnected tube with a firm dilator into the valve at the distal end of the PleurX catheter.
Results
1. Response, as noted by improvement of symptoms and prevention of fluid reaccumulation, depends
on complete drainage of fluid and lung reexpansion.
2. A total of 70% to 90% of patients will respond (notably, without sclerosis, drainage will fail in more
than 90% of patients, and reaccumulation of fluid can occur as early as 3 days after APD catheter
removal).
3. In patients with long-term/indwelling catheters, the degree of symptomatic improvement in dyspnea
is comparable to pleurodesis. Late recurrence of
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effusions is uncommon (<15%), and about 50% of patients will have spontaneous pleurodesis usually
within a month.
4. Most patients with trapped lung have symptomatic improvement following drainage (decreased
dyspnea, improved exercise tolerance).
Complications
1. Tube malfunction (e.g., clotting, kinking, malposition). In patients with longterm catheters, tube
malfunction is uncommon, and the catheters usually remain in place until the patient's demise (mean,
115 days).
2. Infection
3. Hemorrhage
4. Pneumothorax: Up to 30% of patients following chest tube placement will have air in the pleural
space. This is most likely due to an ex vacuo phenomenon, as the lung is relatively stiff and cannot
rapidly reexpand. In most cases, the air resolves completely over a few days.
5. Loculation: This is an unusual complication, and multiple drainage catheters may be required.
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Fibrinolytic agents such as streptokinase and urokinase can be used to successfully drain
complex/loculated malignant pleural effusions with a low complication rate (see “Parapneumonic
Effusions and Empyema”).
6. Reexpansion pulmonary edema: uncommon; the incidence can be decreased by judicious removal
of fluid (i.e., <500 mL per hour).
Parapneumonic Effusions and Empyema (3,7,8,9,10)

1. Parapneumonic effusions occur in up to 57% of patients with pneumonia.
2. Early diagnosis and intervention is important to decrease morbidity associated with complicated pleural
effusions and empyemas.
Contraindications
Thick pleural rind/fibrothorax, which prevents lung reexpansion and limits the value of percutaneous
drainage
Procedure
Placement of APD catheters (see earlier)
follow-up.
3. Check vital signs every 15 minutes for 1 hour, every 30 minutes for 1 hour, and every 60 minutes for 2
hours.
4. Record daily drainage.
5. If the pleural fluid is loculated, multiple drainage catheters may be required, although fibrinolytic agents
can be useful in the drainage of complex collections.
6. Tubes are typically left in place until the patient demonstrates clinical improvement, drainage is minimal
(<50 mL per 24 hours), and antibiotics are changed from intravenous (IV) to by mouth (PO).
Results
Catheter drainage is usually successful or complete within 5 to 10 days of insertion, and resolution of
fluid collection is reported in 70% to 90% of cases.
Complications
1. Tube malfunction (e.g., clotting, kinking, malposition)
2. Hemorrhage
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3. Pneumothorax
4. Loculation: not uncommon due to fibrin content within the pleural exudate. Multiple drainage
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catheters may be required, although fibrinolytic agents can be used to facilitate drainage of
complex/loculated pleural collections. Fibrinolytic agents decrease fluid drainage time and
hospitalization. Contraindication to use is a bronchopleural fistula.
a. Recombinant-tissue plasminogen activator (r-tPA) (2 to 6 mg in a volume of between 50 mL and 250
mL depending on the size of the effusion, infused daily for 1 to 3 days), streptokinase (250,000 units in
100 mL normal saline daily for 1 to 3 days), or urokinase (80,000 units every 8 hours for 1 to 3 days)
instilled into the pleural space may be used to mobilize viscous purulent fluid.
b. r-tPA and urokinase have the advantage of being non-antigenic and are not associated with fever
that occurs in approximately 25% of patients after streptokinase instillation.
c. After instillation, the APD catheter is closed for 2 hours to allow the fibrinolytic agent to distribute
through the pleural space and is then reopened to continuous suction.
d. Although fibrinolytics may be useful in patients with parapneumonic effusions, they should not be
used in patients with an empyema.
Lung Abscess (3,8,9,17)

1. Usually caused by anaerobic bacteria and typically occurs after aspiration
2. Medical therapy (systemic antibiotics, postural drainage) is the initial treatment of choice and is curative
in most patients.
3. Percutaneous drainage may be considered when medical therapy fails or complications develop (see
“Indications” section).
Contraindications
1. None
2. It is important in children to differentiate a lung abscess from necrotizing pneumonia as
percutaneous aspiration of necrotizing pneumonia is associated with a high complication rate (i.e.,
bronchopleural fistula and persistent pneumothoraces).
Procedure
1. Patient position
a. This is important for safe and successful drainage. Although percutaneous drainage can be
performed with the patient supine, prone, or in decubitus position, the abscess should be in a gravity-
dependent position to avoid aspiration of pus into the normal lung.
2. Percutaneous drainage approach
a. Optimal approach ensures that the needle catheter traverses contiguous abnormal pleura and lung
en route to the abscess.
b. Avoidance of normal lung can prevent development of a bronchopleural fistula or pyopneumothorax.
3. Placement of drainage catheter
a. Drainage can be performed either using a trocar or Seldinger technique. Although direct puncture of
the abscess cavity with a single-puncture trocar drainage system saves time, Seldinger technique with
placement of the drainage catheter over a guidewire allows more control and may decrease the
complication rate.
b. With Seldinger technique, an 18-gauge trocar needle is placed through the chest wall into the
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abscess. Transthoracic needle aspiration of pus is performed and may completely drain the abscess.
Aspiration of pus can be used as both a diagnostic and therapeutic measure and may be all that is
required for effective treatment. If drainage is incomplete, a catheter is placed.
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c. First, a 0.038-in. guidewire with a floppy distal segment (Cook Medical Inc, Bloomington, IN) is
inserted through the needle into the collection, followed by sequential dilators until the diameter of the
drainage catheter is reached.
d. A 12 to 14 Fr. APD catheter (Flexima APD, Boston Scientific, Natick, MA) is inserted into the
collection. Pus is aspirated and the locking loop (pigtail) is locked in place.
e. The catheter is maintained in place by an adhesive skin disc (Hollister Inc, Libertyville, IL) or Molnar
external retention disc (Cook Medical Inc, Bloomington, IN).
f. Repeat CT scan is performed to confirm correct catheter placement and determine drainage. If the
abscess is loculated, additional catheters can be inserted.
g. Catheters are connected to an underwater drainage system such as a Pleur-Evac system (DeKnatel
Division, Pfizer Hospital Products Group, Fall River, MA) with continuous suction at 20- to 30-cm
water. Periodic irrigation of the catheter with 5 to 15 mL of saline is performed to facilitate the drainage
of viscous purulent fluid.
follow-up.
3. Check vital signs every 15 minutes for 1 hour, every 30 minutes for 1 hour, and every 60 minutes for 2
hours.
4. Record daily drainage.
5. When clinical parameters (e.g., temperature, white cell count) and chest radiographs indicate resolution
of the abscess, the catheter can be removed.
Results
1. Placement of a drainage catheter is usually curative, and in most cases, surgery is avoided. Clinical
and radiologic improvement usually occurs rapidly after catheter drainage (mean time to resolution is
10 to 15 days although marked improvement of sepsis [i.e., fever, leukocytosis] usually occurs within
48 hours).
2. Failure of drainage occurs when the abscess
a. Contains viscous, organized material
b. Is multiloculated
c. Has a thick, noncollapsible wall
Complications
1. Potential complications include bleeding, bronchopleural fistula, and empyema.
2. Mortality rate is <5%. The morbidity and mortality of patients treated with percutaneous catheter
drainage is, however, lower than surgical resection even though these patients are typically more ill
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than those undergoing surgery.
References
1. Tan C, Sedrakyan A, Browne J, et al. The evidence on the effectiveness of management for malignant
pleural effusion: a systematic review. Eur J Cardiothorac Surg. 2006;29:829-838.
2. Al-Tariq QZ. Percutaneous strategies for the management of pulmonary parenchymal, chest wall, and
pleural metastases. AJR Am J Roentgenol . 2014;203:709-716.
3. Haas AR, Sterman DH. Advances in pleural disease management including updated procedural coding.
Chest. 2014;146:508-513.
4. Davies HE, Mishra EK, Kahan BC, et al. Effect of an indwelling pleural catheter vs chest tube and talc
pleurodesis for relieving dyspnea in patients with malignant pleural effusion: the TIME2 randomized
controlled trial. JAMA. 2012;307:2383-2389.
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5. Porcel JM, Vives M, Esquerda A, et al. Use of a panel of tumor markers (carcinoembryonic antigen, cancer
antigen 125, carbohydrate antigen 15-3, and cytokeratin 19 fragments) in pleural fluid for the differential
diagnosis of benign and malignant effusions. Chest. 2004;126:1757-1763.
6. Creaney J, Dick IM, Meniawy TM, et al. Comparison of fibulin-3 and mesothelin as markers in malignant
mesothelioma. Thorax. 2014;69:895-902.
7. Rahman NM, Maskell NA, West A, et al. Intrapleural use of tissue plasminogen activator and DNase in
pleural infection. N Engl J Med. 2011;365:518-526.
8. Colice GL, Curtis A, Deslauriers J, et al. Medical and surgical treatment of parapneumonic effusions: an
evidence-based guideline. Chest. 2000;118:1158-1171.
9. Maskell N. British Thoracic Society Pleural Disease Guidelines—2010 update. Thorax. 2010;65(8):667-
669.
10. Janda S, Swiston J. Intrapleural fibrinolytic therapy for treatment of adult parapneumonic effusions and
empyemas: a systematic review and meta-analysis. Chest. 2012;142:401-411.
11. Parulekar W, Di Primio G, Matzinger F, et al. Use of small-bore vs large-bore chest tubes for treatment of
malignant pleural effusions. Chest. 2001;120:19-25.
12. Pien GW, Gant MJ, Washam CL, et al. Use of an implantable pleural catheter for trapped lung syndrome
in patients with malignant pleural effusion. Chest. 2001;119:1641-1646.
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13. Saffran L, Ost DE, Fein AM, et al. Outpatient pleurodesis of malignant pleural effusions using a small-
bore pigtail catheter. Chest. 2000;118:417-421.
14. Paschoalini Mda S, Vargas FS, Marchi E, et al. Prospective randomized trial of silver nitrate vs talc slurry
in pleurodesis for symptomatic malignant pleural effusions. Chest. 2005;128:684-689.
15. Stefani A, Natali P, Casali C, et al. Talc poudrage versus talc slurry in the treatment of malignant pleural
effusions. A prospective comparative study. Eur J Cardiothorac Surg. 2006;30:827-832.
16. Goodman A, Davies CW. Efficacy of short-term versus long-term chest tube drainage following talc slurry
pleurodesis in patients with malignant pleural effusions: a randomised trial. Lung Cancer. 2006;54:51-55.
17. Erasmus JJ, McAdams HP, Rossi S, et al. Percutaneous management of intrapulmonary air and fluid
collections. Radiol Clin North Am. 2000;38:385-393.
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48
Thoracic Duct Embolization for Chylothorax
Mikhail C.S.S. Higgins
Maxim Itkin
Chylous leaks are the leakage of intestinal lymph (chyle) from the lymphatic system. They may occur at any point
along the course of chyle transit, beginning in the intestinal lymphatic ducts, through the cisterna chyli (CC) and
finally within the thoracic duct (TD) (Fig. 48.1). Primary thoracic manifestations include chylothorax and
chylopericardium. Injury of the branches of the TD during neck surgery can result in chylous leak from the
surgical wound.
Chylous leaks may be traumatic or, less commonly, nontraumatic in etiology. Traumatic causes include
iatrogenic injury of the TD or its branches during thoracic, cardiac, or neck surgery and secondary to blunt or
penetrating chest trauma.
Nontraumatic causes include idiopathic, malignancy (e.g., lymphoma), congenital, lymphatic vessel disease (e.g.,
Gorham disease, lymphangiomyomatosis), systemic diseases (e.g., sarcoidosis, systemic lupus erythematosus,
and Behçet disease), and infection (e.g., tuberculosis) (1). In cases of nontraumatic chylothorax, the anatomic
cause of the chylous leaks can be occlusion of the TD, presence of lymphatic malformations, and chylous
ascites. In chylous ascites, chylothorax is a result of migration of the lymphatic fluid through diaphragmatic
fenestrations due to negative pressure in the chest cavity.
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FIGURE 48.1 • Schematic representation of the chyle path (arrows). Chylous fluid originates in the intestinal
lymphatics and then it passes through intestinal lymphatic vessels into the CC and then in the TD. Interruption of
this flow can result in chylous effusions (chylous ascites, chylothorax, chylopericardium, etc.). In rare cases, this
path can be altered (lymphatic malformations) and the chyle can be redirected outside the usual path, for
example, into the perineum or lower extremities.
Thoracic duct embolization (TDE) is a percutaneous, image-guided, minimally invasive alternative to surgical
interventions for treating chylous leaks above the diaphragm. This technique comprises two steps: first, the
lymphangiogram followed by transabdominal access and embolization of the TD. A lymphangiogram is performed
in order to visualize the access point into the lymphatic system and the location of the chylous leak. Compared to
the “blind” surgical method, visualization of the leak and lymphatic anatomy significantly improves the outcome
(2).
Indications
In the setting of failed initial conservative management
1. Lifestyle-altering chylothorax
2. Chylopericardium
3. Chyle leak post neck surgery
Initial conservative management includes treatment of the underlying disease (e.g., lymphoma), repeated
thoracentesis, and dietary modification.
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Contraindications
Absolute
Relative
1. Pregnancy
2. Prior severe anaphylactic reaction to iodinated contrast media
1. History and physical exam should be conducted with an emphasis on the lymphatic system and assessment
for prior thoracic trauma or intervention.
a. An assessment of American Society of Anesthesiologists' (ASA) classification for conscious sedation should be
performed.
b. Contrast allergy and reaction should be carefully documented with appropriate preprocedural treatment
prescribed.
2. Laboratory analysis of the fluid is performed.
a. Chylothorax is assessed for a significantly elevated triglycerides level in patients on a regular diet. In patients
on a fat-free diet or nil per os (NPO), the triglycerides level can be low (3).
b. In addition, the lymphatic fluid is assessed for a significant level of lymphocytes in the cell differential (more
than 60%) (4).
c. Presence of chylomicrons is diagnostic for chyle unless the fluid contains blood.
3. Obtain informed consent with comprehensive discussion of possible complications.
4. Imaging
a. In cases of nontraumatic chylothorax, heavily T2-weighted magnetic resonance imaging (MRI) of the chest and
abdomen is initially performed (5). The goal is to exclude ascites and lymphatic malformations as well as to
define the anatomy of the TD.
(1) If noninvasive imaging demonstrates free fluid in the abdomen, chylous ascites with chyle transmigration into
the chest through diaphragmatic fenestrations should be suspected. Abdominal fluid sampling and analysis for
chyle is advised.
(2) If lymphatic malformation is identified on the MRI, and TD is found to be patent on conventional
lymphangiogram, TDE should not be attempted. Instead, sclerotherapy or direct injection of the lymphatic
malformation with embolization performed.
5. Coagulation profile should be within acceptable limits—international normalized ratio (INR) <1.5. In case of
coagulopathy, blood products are administered to correct coagulopathy.
6. Conscious sedation is managed by nursing staff with incremental administration of midazolam and fentanyl.
a. Oral intake should be appropriately restricted for at least 6 hours preprocedure with the exception of normal
medications taken with a sip of water.
b. For insulin-dependent diabetics fasting preprocedure, morning insulin doses should be halved.
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7. Prophylactic periprocedure antibiotics (e.g., Cefazolin 1 g intravenously [IV]) are administered.
Procedure
1. Intranodal lymphangiogram is an alternative to the technically challenging and laborious traditional pedal
lymphangiographic technique (6).
a. Ultrasound guidance is used to directly access bilateral inguinal lymph nodes using a 25-gauge spinal
needle (BD Medical, Franklin Lakes, New Jersey, NJ).
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b. After accessing the hilum of the lymph node, the position of the needle is confirmed by injecting an oil-
based contrast agent (Lipiodol, Guerbert, Villepinte, France) using fluoroscopic guidance. The contrast is
injected by hand using either a 3-mL polycarbonate syringe or a balloon inflator at a rate of approximately 1
to 2 mL per 5 minutes.
2. Up to 6 mL of contrast should be injected into each lymph node to achieve appropriate opacification of
abdominal and pelvic lymphatics in an average-sized adult patient.
a. In case the opacification of the target vessels is not achieved at the completion of the contrast injection,
20 mL of saline is injected through the same needles (“saline push”). Less viscous saline propels the
contrast further into the lymphatic system. Saline push results in faster and better opacification of the TD
and CC which significantly reduces the procedure and fluoroscopy time, and improves the success of
embolization.
3. Once the contrast has advanced to the level of the pelvic and retroperitoneal lymphatic network (L1-L2),
there is an expected decrease of opacification of the lymphatic ducts at this level. This usually reflects the
inflow of unopacified lymph from intestinal and hepatic lymphatics.
4. When the target duct is confirmed, a 21- or 22-gauge, 15- to 20-cm Chiba needle (Cook Inc,
Bloomington, IN) is used for access of the lymphatic system.
a. Access is performed transabdominally regardless of the abdominal structures which could be in the
needle trajectory. A gentle 5- to 10-degree bend of the distal, 2 cm of the needle is made manually to
augment directionality. Under fluoroscopic guidance, swift staccato-like thrusts with the Chiba needle are
made. This latter technique helps minimize needle deflection by bowel and other intervening structures.
b. The safest access to the lymphatic system below the CC through one of the lumbar feeders. Although
technically more challenging due to the smaller size of these feeders, this approach prevents one of the
potential complications from TDE-leak from the CC.
5. As double wall penetration of the duct is achieved, a stiff 0.018-in. guidewire (V18 Control, Boston
Scientific, Natick, MA) is engaged to probe for the duct.
a. Successful access of the TD is confirmed by easy advancement of the wire into the upper thorax.
6. A 3 Fr. 65-cm microcatheter (Rapidtransit, Cordis, Hialeah, Florida, FL) is advanced over the wire in the
TD. Upon reliable catheterization of the TD, the guidewire may be safely removed.
7. Using a 1-mL syringe, water-soluble iodinated contrast is injected to assess for the source of the chylous
leak and TD anatomy. This may be characterized by ductal obstruction or contrast extravasation.
8. The TD or its branches are embolized proximal (upstream) to the leak or lymphatic abnormality with a
combination of embolization coils and n-butyl cyanoacrylate (NBCA) (Truefill Cordis, Hialeah, Florida, FL).
a. Coils are placed proximal (upstream) to the leak/abnormality which may be identified in the TD or within
one of its lymphatic branches. The coils provide a scaffold for polymerization of the glue. Optimal coil
deployment is promoted by controlled gentle to-and-fro maneuvers of the catheter. Of note, if visualized leak
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is suspected to arise from multiple diminutive collaterals, embolization with glue alone can be performed.
b. Prior to glue injection, 0.2 mL of 5% dextrose solution (D5W) is used to flush the catheter to avoid
intracatheter polymerization of the glue. The use of greater volumes of D5W tends to result in retarding of
the glue polymerization in the TD, which often results in recanalization of the glue cast.
(1) NBCA diluted 1:1 in lipiodol is prepared for embolization. The rate at which the NBCA polymerizes is
determined by the speed at which the
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glue is exposed to the ionic compounds. Experience suggests that 1:1 glue/lipiodol dilution provides
sufficient time for injection.
(2) The glue mixture is injected immediately proximal (upstream) to the site of leak or occlusion.
(3) In cases of access to the TD via lumbar lymphatics, it is possible to administer a small amount of glue at
the site of lymphatic ductal access.
(4) The microcatheter is removed immediately following glue embolization.
9. When TD catheterization fails, TD needle disruption may be performed. A “twiddling” motion with the
needle is used to disrupt the retroperitoneal lymphatics. This controlled trauma to the lymphatic vessels
produces local venous thrombosis and an inflammatory cascade which seals the leak.
a. Patients need not be routinely admitted overnight; however, a decision to admit a patient for postprocedural
monitoring may be made on clinical grounds.
b. Postembolization pain is usually minimal. Adequate pain management should align with the care of the
patient's underlying disease state in conjunction with referring clinicians.
2. Chylous output management
a. Monitor output from pleural drainage tubes following embolization.
(1) If output has decreased significantly shortly after the procedure, a food challenge test consisting of
administration of ice cream or cream is prescribed.
(2) If food challenge test is negative (no increase in chest tube output), the patient's diet may be advanced and
chest drains removed.
b. In patients without a chest tube, serial follow-up chest radiographs may be used to monitor the success of the
treatment.
c. In cases of technically successful catheterization and embolization of the TD but a failed clinical response
marked by persistent chylous effusions, repeat embolization should be considered. The causes of the failed first
embolization attempt include second parallel duct and leakage from the CC access point.
Results
1. Traumatic chylothorax: Overall intent-to-treat success rate of largest series of 109 patients was 71% (2).
Success rate directly relates to technical ability to catheterize the cisterna chyli and/or the TD. If TDE was
technically successful, the clinical success was 90%.
a. TDE with coil embolization alone demonstrates a lower clinical success rate than embolization with the
combination of coils and glue (84% vs. 91%) (2). Coils not only serve as a matrix for glue polymerization but
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also provide a dual source of embolization when the liquid embolic fails.
2. Nontraumatic chylothorax: Overall intent-to-treat clinical success rate of largest series of 34 patients was
53%, which is favorable to the 27% success rate reported by Maldonado et al. (7) who employed combined
conservative and surgical management for nontraumatic chylothoraces.
a. In the study of Nadolski et al. (8), four lymphangiographic patterns were observed with varying clinical
success rates:
(1) Normal TD (17.6%): 16% clinical success rate
(2) Occlusion of TD (58.8%): 75% clinical success rate; 88% when technically successful
(3) Failure to opacify TD (17.6%): 16% clinical success, on basis of lymphangiogram alone. No attempt to
access or embolize the TD made.
(4) Extravasation of chyle from TD or ductal tributaries (5.9%): 50% clinical success rate
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FIGURE 48.2 • Treatment algorithm of the nontraumatic chylothorax. LM, lymphatic malformation.
b. Recently, we developed a treatment algorithm for treatment for nontraumatic chylothorax (Fig. 48.2).
(1) Exclude chylous ascites. In case of presence of fluid in abdomen, we assume that the source of the leak
is in the abdomen, and in this case Denver shunt is preferable treatment.
(2) Next, perform contrast- and noncontrast-enhanced MRI to exclude lymphatic malformation, define
anatomy, and detect the leak. MRI is followed by conventional intranodal lymphangiogram. If TD is occluded
or leak is identified, the embolization of the TD is indicated.
(a) In case of patent TD with no abnormal collaterals and presence of the retroperitoneal lymphatic masses,
attempt to embolized the masses with lipiodol is performed.
Complications
1. Immediate complication
a. Misembolization: Two reported cases of embolization of the pulmonary artery from isolated embolization
with TRUFILL glue.
(1) First case (asymptomatic) involved retrograde spilling of glue into the inferior vena cava and then into
the pulmonary circulation.
(2) Second case (symptomatic) likely involved over injection of glue into the TD, with antegrade spillage of
glue through the TD into the subclavian vein and into the pulmonary circulation (1,2).
2. Long-term complications
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a. Protein-losing enteropathy, lymphedema, and chylous ascites manifesting as chronic diarrhea (12%),
lower extremity edema (7%), bilateral breast swelling (2%), and abdominal swelling (5%) (9).
1. Misembolization: Given that 1 to 4 mL of glue is used for TDE, escape of a fraction of this volume into the
pulmonary arterial circulation is not deemed enough to cause symptoms in patients with adequate lung
reserve. To preempt this complication, embolize the TD with coils just proximal (upstream) to the leak to
construct a scaffold on which the glue may polymerize.
2. Chronic sequelae: Treatment is expectant and often conservative.
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References
1. Nadolski GJ, Itkin M. Thoracic duct embolization (TDE) for non-traumatic chylous effusion: experience in
34 patients. Chest. 2013;143:158-163.
2. Itkin M, Kucharczuk JC, Kwak A, et al. Nonoperative thoracic duct embolization for traumatic thoracic duct
leak: experience in 109 patients. J Thorac Cardiovasc Surg. 2010;139(3):584-590.
3. Skouras V, Kalomenidis I. Chylothorax: diagnostic approach. Curr Opin Pulm Med. 2010;16(4):387-393.
4. Agrawal V, Doelken P, Sahn SA. Pleural fluid analysis in chylous pleural effusion. Chest.
2007;133(6):1436-1441.
5. Yu DX, Ma XX, Wang Q, et al. Morphological changes of the thoracic duct and accessory lymphatic
channels in patients with chylothorax: detection with unenhanced magnetic resonance imaging. Eur Radiol .
2013;23:702-711.
6. Nadolski GJ, Itkin M. Feasibility of ultrasound-guided intranodal lymphangiogram for thoracic duct
embolization. J Vasc Interv Radiol . 2012;23(5):613-616.
7. Maldonado F, Cartin-Ceba R, Hawkins FJ, et al. Medical and surgical management of chylothorax and
associated outcomes. Am J Med Sci . 2010;339(4):314-318.
8. Nadolski G, Itkin M. Thoracic duct embolization for the management of chylothoraces. Curr Opin Pulm
Med. 2013;19(4):380-386.
9. Laslett D, Trerotola SO, Itkin M. Delayed complications following technically successful thoracic duct
embolization. J Vasc Interv Radiol . 2012;23(1):76-79.
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49
Percutaneous Abdominal Biopsy
Nisha I. Sainani
Stuart G. Silverman
Image-guided percutaneous abdominal biopsy, the most common radiologic intervention, has been widely
accepted for its clinical effectiveness and safety and has largely replaced costly exploratory laparotomy and the
ensuing hospitalization. This chapter describes established and emerging indications and techniques for
common biopsy procedures performed in the abdomen (1).
Indications
Including, but not limited to (2)
1. Diagnosis of primary malignancy
2. Confirmation of suspected metastasis
3. Determination of malignancy stage
4. Diagnosis of benign process (tumor, cyst, infection, inflammation)
5. Molecular analysis for treatment planning
6. Monitoring treatment
Contraindications
2. Lesion inaccessible (e.g., surrounded by bone, no safe path)
3. Uncooperative or unwilling patient
Preprocedure Assessment and Preparation

1. Consultation—Is a percutaneous biopsy indicated? Are special preparation steps needed? Evaluate medical
record; review pertinent imaging examinations
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to establish indication and determine feasibility. Establish consentability, determine need for anesthesiology;
assess need for preprocedure laboratory tests.
a. Consider inpatient biopsies when
(1) Patient is in hospital for other reasons.
(2) Risk of biopsy is increased (e.g., medical comorbidities, lesion type, and location).
(3) Patient lives alone or far away.
2. Preprocedure patient preparation: Deliver preparation instructions to patient. Withhold solid food (except
medications) for 6 hours and clear liquids for 3 hours when minimal or moderate sedation (formerly known as
conscious sedation) is planned. Withhold solid food for 8 hours when deep sedation or general anaesthesia is
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planned; both require presence of an anesthesiologist.
a. Instruct patient to arrive 1 hour prior to procedure.
b. Ask patient to arrange for a responsible adult companion to provide transport to home, and, if possible,
someone to accompany overnight.
c. Advise patient of possible signs and symptoms of complications and provide contact information.
d. Discontinue medications that affect hemostasis (3,4,5) (e.g., heparin, warfarin, aspirin, clopidogrel). Discuss
risks of discontinuing medications (e.g., prior cerebrovascular event, myocardial infarction, or prior coronary stent
placement) with care providers (e.g., a cardiology consult) before considering for biopsy.
e. Warfarin should be discontinued (typically 5 days); low-molecular-weight heparin (LMWH) bridge can be
considered if high risk, for example, heart valve surgery, recent pulmonary embolism, and deep vein thrombosis.
f. Discontinue aspirin or clopidogrel for at least 5 days especially with high risk for bleeding. Other nonsteroidal
anti-inflammatory drugs (NSAIDs) could be stopped for 48 hours. Restart aspirin, clopidogrel, or NSAIDs >12
hours after the procedure when low risk for bleeding and >24 hours when high risk for bleeding.
g. Heparin (unfractionated, intravenous [IV] or subcutaneous [SQ]): If prophylactic dose, discontinue for 4 to 6
hours, no need to recheck partial thromboplastin time (PTT); restart >12 hours when low risk for bleeding and
>24 hours when high risk for bleeding. If therapeutic dose, discontinue for 4 to 6 hours, recheck PTT; restart >12
hours when low risk for bleeding and >24 hours when high risk for bleeding. For patients on LMWH, prophylactic
dose (5,000 IU once per day) stop 12 hours before and therapeutic dose (≥5,000 IU once per day) stop 24 hours
before the procedure. Restart prophylactic and therapeutic dose >12 hours after the procedure when low risk of
bleeding >24 hours when high risk for bleeding.
3. Day of procedure: Obtain written informed consent. Detail indications as they relate to the patient's medical
problem, the benefits, risks (including specific potential complications, their probability of occurrence, and steps
to minimize their risk), alternative procedures, and other relevant aspects of the procedure (e.g., the planned
approach and how long the procedure will take). Give patient specific instructions on how to cooperate during
the biopsy (e.g., breath holding).
4. Laboratory tests
a. Obtain serum prothrombin time (PT) (international normalized ratio [INR]) and complete blood count (CBC) if
normal values have not been documented in the medical record in the prior 30 days. If normal values have been
documented, these tests do not need to be repeated unless there are risk factors for bleeding such as
medications that could alter coagulation, diseases known to alter hemostasis (e.g., liver disease), or other
reasons to suspect a bleeding diathesis. Obtain serum PTT only if a normal documented value has not been
documented in the past. PTT does not need to be remeasured unless there are new risk factors such as
medications, diseases, or other reasons to suspect an alteration in PTT.
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General guidelines for hemostatic parameters include PT <15 seconds, INR <1.5, PTT <1.5 × control, and
platelet count >50,000 per μL; however, deviation from these guidelines can be considered if clinically indicated.
b. Adrenal mass biopsy: If pheochromocytoma (6) is a consideration, measure plasma-free fractionated
metanephrines (high sensitivity especially in patients with hereditary predisposition to pheochromocytoma, but
false positives possible especially in sporadic cases), and if positive, the specificity can be increased by 24-hour
measurement of urine-fractionated metanephrines and catecholamines.
c. Liver cyst aspiration: Consider echinococcal serology in suspected cases.
5. Arrange for “on-site” cytopathologist for preliminary reading of cytology; this has several advantages (7).
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a. Offers immediate assessment of adequacy of specimen and improves yield
b. Allows for altering approach or technique if preliminary tissue specimen is insufficient
c. Allows selective processing of specimen for special studies (e.g., culture if material suggests infection, marker
studies for lymphoma, electron microscopy, cytogenetics for some tumors, and measurement of tumor-specific
markers).
d. Limits the number of passes to no more than what is necessary, particularly in high-risk procedures.
6. Choose an image-guidance system (1,8).
a. Fluoroscopy—utilization for image-guided biopsy is largely obsolete except for transjugular liver parenchymal
biopsy.
b. Ultrasound (US)
(1) Advantages: rapid localization, real-time and multiplanar, flexible patient positioning, no ionizing radiation,
Doppler can reveal vascularity
(2) Disadvantages: Deeply located lesions, especially those that are small, may not be visible due to intervening
structures such as bowel.
c. Computed tomography (CT)
(1) Advantages: helps visualize deep small lesions, depicts tissue components, vascularity, precise anatomic
relationships (e.g., bowel and pleural space), precise needle localization possible, multiplanar guidance possible
with reconstructions. CT fluoroscopy with either intermittent “quick check” scans or continuous, near real-time
scans can shorten needle placement time.
(2) Disadvantages: ionizing radiation, more expensive, and time-consuming compared to US
d. Magnetic resonance imaging (MRI)
(1) Advantages: useful for lesions seen on MRI alone, multiplanar, no ionizing radiation
(2) Disadvantages: expensive, limited availability, MRI-compatible equipment required
Procedure
Intraprocedure Preparation (8)
a. Establish IV access.
b. Sedation and analgesia: Minimal or moderate sedation using parenteral narcotics and benzodiazepines
are typically satisfactory. Deep sedation and general anesthesia are rarely needed.
c. Position the patient comfortably without compromising access to needle entry site.
d. Sterilize the overlying skin (field) with iodinated scrub and alcohol, or chlorhexidine.
e. Place sterile drapes and towels surrounding the field of intervention.
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2. Physician preparation
a. Thorough hand washing
b. Wear impermeable gowns, caps, masks, and facial shields. Double gloving has been showing to reduce
hand contact with patient's blood and/or body fluids.
c. Protective equipment, such as needle receptacles, and specially designed biopsy trays can be used.
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Never recap needles.
Procedure (9,10,11)
1. Anesthetize the skin and subcutaneous tissues with local 1% or 2% lidocaine. Make a 3- to 5-mm
superficial skin incision with scalpel blade.
2. Biopsy needle selection
a. Needle size
(1) Fine needles (20 to 25 gauge): ideal for cytology, can transgress bowel to access solid structure,
minimal hemorrhagic potential
(2) Large needles (14 to 19 gauge): Samples can be analyzed for cytology or histology, increases yield,
helps subtype tissue particularly in lymphoma, may have increased hemorrhagic potential, but may be
needed in some patients.
b. Cutting edge
(1) End-cutting needle types
(a) Acute bevel
(b) 90-degree bevel
(2) Side-cutting needle types
(a) Cannula gap
(b) Stylet gap
c. Spring-loaded/automated (side cutting)
d. Choose a biopsy needle based on the following:
(1) Lesion size and depth: Small, deep lesions may require a 20-gauge needle (or larger) that is stiff enough
to be directed accurately, as 22-gauge and 25-gauge needles tend to “bow” out of intended track.
(2) Access route: If bowel or pleural space needs to be traversed, a fine needle (20 to 25 gauge) is
preferred.
(3) Suspected diagnosis
(a) Known primary diagnosis: Requires less tissue, fine needle is often sufficient.
(b) Unknown primary diagnosis: Larger needles (14 to 19 gauge) may be needed particularly if prior fine
needle biopsy is not diagnostic.
(c) Suspected lymphoma: Fine needles (20 to 25 gauge) often adequate alone, but larger needles (14 to 19
gauge) may be needed for subtyping lymphomas.
(d) Increased hemorrhagic potential (bleeding diathesis, hypervascular lesion): Fine needles (20 to 25
gauge) probably have less hemorrhagic potential. Larger needles (14 to 19 gauge) may have increased
hemorrhagic potential but may be needed in some cases.
(4) Cytopathologist preference: A preliminary “cell-layer thick” specimen for slide preparation is often
preferred; hence, the first pass should be with a fine needle, but large samples may be subsequently
needed.
(5) General principle: Use the thinnest needle that can be used successfully to target the lesion and obtain
sufficient material. Needles as thin as 25 gauge have been shown to be diagnostic.
3. Image-guidance technique (1)
a. US-guided biopsy
(1) Perform full US examination of lesion and surrounding region to confirm lesion and plan biopsy. This
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should be done by the radiologist who will be performing the biopsy.
(2) Localize the lesion, assess path, distance, and angle.
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(3) Free-hand technique: Prepare transducer by placing sterile cover. Monitor needle placement with real-
time US using a sterile, covered transducer.
(4) Biopsy transducer guide: Consider use of biopsy transducer guide with built-in needle slots to direct the
needle at a predetermined angle within the plane of view of the transducer.
(5) Demonstrate needle tip in target lesion, preferably on two views. Some prefer scanning with the
transducer perpendicular to the target, whereas others prefer scanning close proximity to the entry site.
Regardless of where the transducer is placed, the US beam should parallel the needle shaft. Needle
“jiggling” or “bobbing” (in and out motion) may help. Biopsy needles with echogenic tip which ensure a
strong echo reflection resulting in clearly visible needle tip during scanning can be used.
b. CT-guided biopsy
(1) Review prior imaging exams to determine the skin entry site. Commercially available grids may be used
to mark the skin entry site.
(2) Perform preprocedure CT scan of lesion and surrounding region with patient in the biopsy position to
confirm lesion and plan approach. Consider IV contrast material to assess lesion vascularity and
surrounding vessels.
(3) The angle, distance, and structures in the path of the needle are learned by drawing a line connecting
the skin entry site determined by the grid marker and the lesion.
(4) Plan and then place needle. Maintaining trajectory in axial plane allows subsequent scans to visualize
entire needle length. Angled approach (out of the axial plane) may be necessary and may require multiple
scans to visualize needle path and tip.
(5) CT fluoroscopy can be used to directly monitor needle placement either in real time or intermittently after
partial insertions or to quickly scan the position of an already placed needle.
4. Biopsy technique
a. General principles
(1) When biopsying masses that move with respiration, a breath hold is generally desired for all needle
placements and CT scans. Breath holds at end expiration, half-breaths, or simply stopping breathing can be
used. Regardless of which is used, it is helpful to have the patient practice before the procedure (e.g.,
during the consent process), and with an explanation to the patient that the goal is consistency. Rarely, the
procedure can be performed in between shallow breaths, particularly in heavily sedated patients. A bellows
device has been used to help achieve consistent breath holds.
(2) Choose shortest path possible.
(3) In general, initial placement with fine needle, the safest instrument to target a structure is advised,
particularly if several passes may be needed. However, with the increasing need for large (typically 18
gauge) needle specimens and increased use of the coaxial technique, targeting with a large gauge
introducer is required. However, targeting can still be performed with a fine needle followed by the tandem
placement of the introducer.
(4) Use the least number of needle placements to obtain diagnostic tissue.
(5) Structures to avoid during needle placement
(a) Lung: Be sure that the position of the lung is known in the biopsy position, and at the breath hold used
at the time of the needle insertion.
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(b) Gallbladder
(c) Pancreas
(d) Dilated duct (biliary, pancreatic)
(e) Small and large bowel: The colon and small intestines should not be transgressed if a fluid-containing
structure is targeted so as not to contaminate the patient or the specimen with flora; however, the colon
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and small intestines can be transgressed with a fine needle, if absolutely necessary, to biopsy a solid
lesion.
b. Needle placement techniques: This requires precise placement of one needle, which serves as a
reference (tandem technique) or a conduit (coaxial technique) guide for all subsequent needle placements.
(1) Tandem technique
(a) Mandatory short (3 to 5 mm) superficial incision
(b) Place initial 20-gauge or 22-gauge reference needle.
(c) Image and confirm needle-tip in lesion.
(d) Tandem place a second, 20- to 25-gauge needle alongside reference needle via same incision site
(e) Biopsy with the second needle for cytology smear
(f) Obtain additional (typically two or three) tandem passes, using larger gauge needles if necessary.
(g) Complete procedure using reference needle as the final specimen.
(2) Coaxial technique is most helpful with small and deep lesions requiring greater precision.
(a) The initial placement of a reference needle can be an introducer or a biopsy needle.
(b) Image needle tip within lesion to confirm optimal location for biopsy.
(c) A 17-gauge introducer is needed for 18-gauge side-cutting needle specimen, 19-gauge introducer is
needed for 20-gauge side-cutting needle specimen, 22-gauge end-cutting needles can be placed coaxially
through 19-gauge (or larger introducers or needles), 25-gauge end-cutting needles can be placed coaxially
through a 20-gauge needle, and multiple biopsy specimens can be acquired.
(d) Complete biopsy with reference needle in selected cases (may not be possible if introducers used).
c. Technical maneuvers that may be helpful (1,12,13,14,15)
(1) The patient may be placed in a different position, such as oblique or lateral decubitus, to remove bowel
loops from the planned needle path.
(2) Hydrodissection: Sterile saline, contrast material, or dextrose water injection may help displace
intervening bowel loops and pleura.
(3) Use of a manually curved 22-gauge needle advanced coaxially through a larger gauge reference needle
may help target a mass that is not in direct line with the reference needle.
(4) Isodense lesions not visible on preprocedure unenhanced CT can be targeted using adjacent fixed
anatomic structures or other landmarks; after initial needle is placed, contrast material can be administered
to help refine targeting further.
(5) Dual-modality image fusion can be used to guide the biopsy of lesions which are inconspicuous on one
modality, for example, fusing positron emission tomography (PET) images to unenhanced CT for lesions
visible only on PET and fusing contrast-enhanced CT or MR images to US for lesions visible only with CT
or MRI.
(6) Electromagnetic tracking using skin fiducials and needles with internal sensors allows spatial tracking of
the needle tip and can facilitate US- or CT-guided needle placement. Multiplanar image displays and
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multimodality image coregistration can be used with real-time feedback.
(7) Triangulation method may be used to determine optimal angle and calculate distance to lesion.
(8) Gantry tilt technique (maintains needle in imaging plane)
5. Sampling technique
a. Use rotatory corkscrew drilling motion, maintaining continuous suction on a small volume syringe.
Transgress the most optimal portion of the lesion with each insertion and retraction. Release suction before
withdrawing needle.
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b. Automatic spring-loaded devices may be used to obtain a core of tissue.
c. Cytology smears are obtained dry.
d. Specimen processing can be aided by the presence of a cytologist.
(1) Needle with biopsy specimen can be handed to cytotechnologist for smears and cell block. Alternatively,
smears can be prepared using sterile slides; the remaining material in the needle and syringe can be
submitted in sterile solution for cell block, and the needle reused.
(2) Tissue cores and larger fragments should be submitted in formalin for histology examination. If
lymphoma is suspected, specimen should be submitted in saline.
(3) Gram stains and cultures are obtained as necessary.
6. Fine needle specimens are generally sufficient for diagnosis of epithelial malignancies. Large needle
specimens may be needed for nonepithelial malignancies such as lymphoma and sarcoma, for rebiopsy of
lesion, and for genetic and molecular testing. Choice of needle gauge is often made on individual basis.
7. Organ-specific approaches to focal masses (1,12,16,17,18,19)
a. Liver (under US, CT, or MRI guidance): Use a transparenchymal route by interposing normal “cuff” of
liver tissue to decrease the risk of hemorrhage into the peritoneal space, particularly when sampling a
hypervascular lesion.
b. Adrenal gland: CT and MRI approaches are given (consider using US for large lesions).
(1) Right (lateral) transhepatic
(2) Left (anterior) transhepatic
(3) Transrenal (only if necessary)
(4) Alternative approaches (all designed to avoid or minimize pleural space transgression)
(a) Prone position, skin entry site caudal to the posterior sulcus with needle angled superiorly
(b) Lateral decubitus (affected side down) offers a posterior approach with a path that is caudal to posterior
sulcus and avoids transgressing the lung and compresses/pushes the ipsilateral lung out of the posterior
sulcus.
(c) Triangulation method and gantry tilt techniques
c. Kidney (under US, CT, or MRI guidance)
(1) Lateral or prone posterior approach
(2) Fine needles are often sufficient; large (18-gauge) needles may increase diagnostic yield (oncocytoma)
and determine renal cell carcinoma (RCC) subtype and grade.
(3) Historical indications include the following:
(a) Patients with a renal mass and known extrarenal primary malignancy
(b) Patients with a renal mass and imaging findings that suggest unresectable renal cancer
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(c) Patients with a renal mass and surgical comorbidity
(d) Patients with a renal mass that may have been caused by an infection
(4) Recently established indications include the following:
(a) Patients with a small (≤3 cm), hyperattenuating, homogeneously enhancing renal mass
(b) Patients with a renal mass considered for percutaneous ablation
(c) Patients with an indeterminate cystic renal mass
(d) Patients with multiple, solid renal masses
d. Retroperitoneum (under CT or MRI guidance; US rarely used): Although anterior and posterior
approaches can be used, the latter is generally preferred employing needles 19 gauge or larger (e.g.,
suspected lymphoma). Also, an anterior approach may necessitate transgressing the bowel (see (e) under
“Structures to avoid during needle placement” section).
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e. Presacral/pelvic mass (under CT or MRI guidance; US rarely used)
(1) Transgluteal: posterior half of greater sciatic notch, close to sacrum posteriorly, to avoid the sciatic
nerve anteriorly, and below the level of piriformis muscle, to avoid the gluteal vessels anterior to piriformis
(2) Alternative approaches include transvaginal and transrectal biopsy (only using US guidance) if no other
safe access route is possible.
f. Spleen (under US, CT, or MRI guidance)
(1) Traversing the least amount of parenchyma en route to the lesion may help reduce bleeding risk.
g. Pancreas: Because of the close anatomic relationship of the pancreas to the stomach and duodenum,
many pancreatic lesions are biopsied with endoscopic ultrasound (EUS). However, tissue sampling is
generally limited to fine needles. When tissue is needed for histologic evaluation, a percutaneous approach
may be needed.
(1) Anterior approach can be attempted. If a transgastric or transduodenal route is necessary, cystic masses
could be contaminated if gastric pH is not normal.
(2) When an anterior approach is not feasible, posterior approach may be possible in some cases for
lesions in body and tail of pancreas.
(3) The risk of pancreatitis can be reduced by not traversing normal pancreas and not including pancreatic
tissue in the sample.
8. Organ parenchymal biopsy (20,21)
a. Liver
(1) US is adequate in most cases. CT may be required in large patients.
(2) Left lobe approach: Epigastric subxiphoid approach to the left hepatic lobe avoids pleural space
transgression. This technique is performed near the midline away from major vessels, in the region of the
linea alba.
(3) Right lobe approach: Subcostal or low intercostal approach should be attempted.
(4) Two or three, 18-gauge specimens are often sufficient.
(5) The patient typically recovers for 6 hours after the procedure.
b. Kidney
(1) Obtain blood for type and screen.
(2) US may be used for guidance. CT may be required in large patients.
(3) Target the lower pole cortex. Sample should be obtained from the most peripheral portion of the kidney
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as possible.
(4) Two or three, 18-gauge specimens are often sufficient.
(5) Admit patient for a short (typically <24 hours) observation.
(6) Follow hematocrit closely.
9. Reduction of bleeding risk: optional intraprocedural steps (22,23)
a. Pressure on skin entry site
b. Tamponade by positioning ipsilateral side down
c. Plugging the track with autologous clot or foam: When postprocedure bleeding is suspected or risk is
high and a coaxial technique is used, the stylet can be inserted half way and left for 1 to 2 minutes to allow
the subsequent clot to be injected by advancing the stylet before removing the stylet-introducer assembly.
Alternatively, absorbable compressed gelatin sponge (Gelfoam, Pfizer Inc, New York, NY) or polyvinyl
alcohol foam (Ivalon, Unipoint Lab, High Point, NC) can be injected along the track as the introducer is
withdrawn.
1. Consider chest x-ray or expiratory chest CT scan to rule out pneumothorax if pleural space transgression is
suspected.
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2. Monitor vital signs in recovery area every 15 minutes for 1 hour, every 30 minutes for 2 hours, and then every
hour.
3. Bed rest for 1 to 2 hours; bathroom use with assistance; lounge chair thereafter as tolerated
4. Clear liquid diet for the first hour; regular diet thereafter as tolerated
5. If vital signs are stable and no complications are noted, the patient may be discharged, usually after 2 to 4
hours.
6. Advise patient of possible signs and symptoms of complications and provide contact information. Give
instructions to outpatients regarding follow-up.
Results
1. Diagnostic tissue should be recovered in at least 80% to 95% of cases.
2. False negatives are most often due to inaccurate targeting of small lesions or sampling necrotic portions
of large lesions. Diagnostic yield is improved by assuring that the needle tip is within the lesion at the time
of the procedure (2).
3. Biopsy of the periphery of a large lesion may avoid a necrotic center.
Complications
1. Overall, variable, and estimated (2,24): <2%
2. Hemorrhage: Most common complication but clinically significant hemorrhage occurs in less than 2% of
biopsies (excluding parenchymal renal biopsy in which there is a slightly greater risk); death due to
hemorrhage is extremely rare.
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3. Infection: extremely rare
4. Organ injury needing surgery or other intervention (primary organ or adjacent organ [e.g., viscous or duct
perforation], often depends on route): <2%
5. Pneumothorax: variable, depends on access route, probably <1%
6. Pancreatitis (depends on access route): 2% to 3% if normal pancreas is biopsied; less if normal pancreas
not transgressed
7. Needle-tract tumor seeding. Reported with most tumors but overall extremely rare; approximate
frequency: 0.003% to 0.009%
8. Mortality rate: 0.006% to 0.031%
Genomics
In the era of personalized medicine and targeted therapy (25), a molecular pathology test (e.g.,
immunohistochemistry, polymerase chain reaction, fluorescence in situ hybridization, sequencing, messenger
RNA arrays, methylation) may be often performed on the biopsy specimen to identify.
1. Molecular biomarkers that predict the natural course of disease and prognosis
2. Expressed receptors (e.g., vascular endothelial growth factor [VEGF]) and genetic variability that has been
linked to differing therapeutic response and toxicity
3. Hallmarks of cancer outline pathways and targets for specific drug interventions
4. Heterogeneity that is inherent to many cancers and affects success of therapies
References
1. Sainani NI, Arellano RS, Shyn PB, et al. The challenging image-guided abdominal mass biopsy:
established and emerging techniques ‘if you can see it, you can biopsy it’. Abdom Imaging. 2013;38:672-
696.
2. Gupta S, Wallace MJ, Cardella JF, et al. Quality improvement guidelines for percutaneous needle biopsy.
2009;193:1656-1664.
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2012;23:727-736.
5. Patel IJ, Davidson JC, Nikolic B, et al. Addendum of newer anticoagulants to the SIR consensus guideline.
6. Lenders JW, Pacak K, Walther MM, et al. Biochemical diagnosis of pheochromocytoma: which test is
best? JAMA. 2002;287:1427-1434.
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7. Tsou MH, Tsai SF, Chan KY, et al. CT-guided needle biopsy: value of on-site cytopathologic evaluation of
core specimen touch preparations. J Vasc Interv Radiol . 2009;20: 71-76.
8. Chan D, Downing D, Keough CE, et al. Joint Practice Guideline for Sterile Technique during Vascular and
Interventional Radiology Procedures: from the Society of Interventional Radiology, Association of
Perioperative Registered Nurses, and Association for Radiologic and Imaging Nursing, for the Society of
Interventional Radiology [corrected] Standards of Practice Committee, and Endorsed by the Cardiovascular
Interventional Radiological Society of Europe and the Canadian Interventional Radiology Association. J Vasc
Interv Radiol . 2012;23:1603-1612.
9. Gazelle GS, Haaga JR. Guided percutaneous biopsy of intraabdominal lesions. AJR Am J Roentgenol .
1989;153:929-935.
10. Gazelle GS, Haaga JR. Biopsy needle characteristics. Cardiovasc Intervent Radiol . 1991;14:13-16.
11. Erturk SM, Silverman S, Mortele K, et al. Percutaneous biopsy of abdominal masses using 25-gauge
needles. Abdom Imaging. 2010;35:70-74.
12. Gupta S, Nguyen HL, Morello FA Jr, et al. Various approaches for CT-guided percutaneous biopsy of
deep pelvic lesions: anatomic and technical considerations. Radiographics. 2004;24:175-189.
13. Sainani NI, Schlett CL, Hahn PF, et al. Computed tomography-guided percutaneous biopsy of
isoattenuating focal liver lesions. Abdom Imaging. 2014;39:633-644.
14. Tatli S, Gerbaudo VH, Feeley CM, et al. PET/CT-guided percutaneous biopsy of abdominal masses:
initial experience. J Vasc Interv Radiol . 2011;22:507-514.
15. Krücker J, Xu S, Glossop N, et al. Electromagnetic tracking for thermal ablation and biopsy guidance:
clinical evaluation of spatial accuracy. J Vasc Interv Radiol . 2007;18: 1141-1150.
16. Silverman SG, Gan YU, Mortele KJ, et al. Renal masses in the adult patient: the role of percutaneous
17. Maturen KE, Nghiem HV, Caoili EM, et al. Renal mass core biopsy: accuracy and impact on clinical
management. AJR Am J Roentgenol . 2007;188:563-570.
18. Tam A, Krishnamurthy S, Pillsbury EP, et al. Percutaneous image-guided splenic biopsy in the oncology
patient: an audit of 156 consecutive cases. J Vasc Interv Radiol . 2008;19:80-87.
19. Li L, Liu LZ, Wu QL, et al. CT-guided core needle biopsy in the diagnosis of pancreatic diseases with an
automated biopsy gun. J Vasc Interv Radiol . 2008;19:89-94.
20. Song JH, Cronan JJ. Percutaneous biopsy in diffuse renal disease: comparison of 18- and 14-gauge
automated biopsy devices. J Vasc Interv Radiol . 1998;9:651-655.
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21. Vijayaraghavan GR, David S, Bermudez-Allende M, et al. Imaging-guided parenchymal liver biopsy: how
we do it. J Clin Imaging Sci . 2011;1:30.
22. Tsang WK, Luk WH, Lo A. Ultrasound-guided plugged percutaneous biopsy of solid organs in patients
with bleeding tendencies. Hong Kong Med J. 2014;20:107-112.
23. Paulson EK, Stephenson GR, Neal MC, et al. Use of fibrin sealant as a hemostatic agent after liver
biopsy in swine. J Vasc Interv Radiol . 2000;11:905-911.
24. Smith EH. Complications of percutaneous abdominal fine-needle biopsy. Review. Radiology.
1991;178:253-258.
25. Abi-Jaoudeh N, Duffy AG, Greten TF, et al. Personalized oncology in interventional radiology. J Vasc
Interv Radiol . 2013;24:1083-1092.
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50
Drainage of Abdominal Abscesses and Fluid Collections
Ashraf Thabet
Ronald S. Arellano
Percutaneous drainage of abdominal and pelvic fluid collections is one of the most commonly performed
interventional procedures and is a well-established management option in patients who do not have another
indication for immediate surgery (1).
Indications
1. Fluid characterization
a. Distinguish purulent fluid, blood, bile, urine, lymph, and pancreatic secretions.
b. Determine if collection is infected or sterile.
2. Treatment of sepsis
a. Curative in patients with simple abscesses
b. Curative or temporizing in patients with complex or pancreatic abscesses
3. Relief of symptoms
a. Alleviate pressure and pain due to size or location of collection (e.g., pancreatic pseudocyst)
b. Obliterate recurring cysts or collections with sclerosing agents (2)
Contraindications
Absolute
1. Lack of a safe pathway to the collection due to interposed vessels or viscera
2. Uncooperative patient. General anesthesia could be considered.
Relative
1. Coagulopathy: requires correction with appropriate blood products before proceeding
2. Sterile collections (e.g., hematoma): Prolonged catheter drainage may increase the risk of secondary
infection.
3. Procedure requires transgression of pleura: risk of pneumothorax, pleural effusion, and empyema.
4. Echinococcal cyst: Leakage of contents may elicit anaphylactic reaction. Prior medical treatment may
reduce this risk.
5. Tumor abscess: may require lifelong catheter drainage
6. Hemodynamic instability or cardiopulmonary compromise
1. Nil per os (NPO) for 8 hours before procedure. ( Note: If oral contrast use is anticipated for computed
tomography [CT] guidance, time for NPO requirement is altered appropriately.)
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2. Written informed consent
3. Intravenous access: 20-gauge or larger
4. Recent coagulation studies. Laboratory studies: prothrombin time (PT) <15 seconds, international normalized
ratio (INR) <1.5, platelets >50,000 per μL
5. Stop anticoagulation and antiplatelet medications such as warfarin (Coumadin) and aspirin when clinically
appropriate.
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6. Prophylactic antibiotics required when draining abscess or potentially infected collection; preprocedure
antibiotics generally do not affect cultures.
7. Conscious sedation with monitoring of physiologic parameters, including blood pressure, pulse, and oxygen
saturation.
8. General anesthesia in young children, uncooperative patients, or patients with significant medical
comorbidities
Imaging Guidance
1. Ultrasound (US)
a. Enables real-time visualization of anatomy and needle/catheter during the procedure
b. Produces no radiation
c. May be used to guide primary needle access into the collection; for drainages performed using Seldinger
technique, can then transition guidance to fluoroscopy for wire manipulation and tract dilation
d. Provides ability to perform portable procedures
e. Visualization is degraded by body habitus, bowel gas, and bone. This may make drainage of retroperitoneal
and pelvic collections more difficult, particularly in obese patients.
2. Computerized tomography
a. Provides excellent tomographic visualization of anatomy and fluid collections irrespective of the overlying
structures
b. Lack of real-time imaging guidance; this is mitigated with the use of CT fluoroscopy, although radiation dose to
patient and operator is increased.
3. Fluoroscopy
a. Used in combination with other modalities, most often US, particularly when using Seldinger technique
b. Used to guide catheter exchanges and upsizing
Procedure
1. Preliminary imaging
a. Review prior imaging to (a) visualize the abnormality, (b) decide on the appropriate guidance method to
be used, and (c) select route for drainage.
b. Immediately prior to the procedure, confirm that the collection is clearly seen with the imaging-guidance
method selected and verify safe route to the collection.
c. Preliminary CT
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(1) Place the patient in the optimal position for drainage (supine, prone, lateral decubitus) and attach a
radiopaque grid over the area of collection.
(a) The lateral decubitus position may help reduce the risk of pleural transgression because it splints the
ipsilateral hemithorax.
(b) If possible, both of the patient's arms are placed above the head to optimize image quality for drainage
of upper quadrant collections.
(2) The 5- to 10-mm thick contiguous slices are obtained through the region of interest. If there is concern,
bowel (oral, rectal) and/or intravenous (IV) contrast medium may be given and imaging repeated to
distinguish collection from surrounding normal structures.
(3) From these preliminary images and with the aid of grid markings, a safe route for drainage is identified
and the site of skin puncture, angle of needle entry, and distance to the collection are determined.
Occasionally, when there is no safe route for puncture, angling the gantry or changing patient position may
reveal a safe path for drainage.
2. Determination of catheter route
a. The optimal path for catheter drainage should consider the size and shape of the abscess and the safest
route from skin to collection that does not
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transgress vital structures. If possible, an extraperitoneal approach is preferable because this reduces the
risk of peritoneal contamination.
(1) When performing fine-needle aspiration alone, it is safe to traverse certain viscera such as liver, kidney,
stomach, and small bowel. However, these structures should be avoided as much as possible when using
catheter drainage.
(2) Traversing colon and normal pancreas should be avoided because this may risk superinfection of
collections or pancreatitis, respectively.
(3) Interloop abscesses in inflammatory bowel disease may not be drainable due to surrounding small bowel
loops, although fine needle aspiration may be performed.
b. The usual anterior approach may not be possible in the pelvis due to overlying structures. In such cases,
alternative routes such as the transgluteal, transvaginal, or transrectal approaches may be considered.
c. Organ displacement techniques may help displace nonvascular vital structures or create a window for
percutaneous needle aspiration or drainage.
3. Diagnostic needle aspiration
a. Prior to drainage, preliminary fine needle aspiration (22-to 20-gauge) of the collection is helpful to
determine the nature of the collection. No more than 5 mL of fluid should be aspirated to prevent the cavity
from collapsing should catheter drainage become necessary. If fluid is not obtained on initial aspiration and
needle tip is optimally placed, then aspiration using a larger needle (18-gauge) may be attempted, with
subsequent needles placed parallel and in tandem to the first needle. If no fluid is obtained on reaspiration,
then, depending on the clinical suspicion, either a biopsy of the area or a trial with catheter drainage may be
performed.
b. When fluid is aspirated, it can be inspected macroscopically, assessing for color, viscosity, turbidity, and
smell. Fluid may be sent for laboratory testing to determine its origin. If the question of infection is important,
as in the case of a sterile hematoma where catheter insertion may not be desirable, a rapid Gram stain
analysis of the aspirate will determine the presence of bacteria and neutrophils. Thus, information from the
preliminary needle aspiration can determine if no further action is to be taken, complete needle aspiration
alone is sufficient, or catheter drainage is required.
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c. If after aspiration the needle is found to be in a good position, it can be left in place and used as a parallel
guide to place a catheter into the collection when using the trocar technique (i.e., tandem trocar technique),
or it can be used for introduction of an 0.018-in. guidewire as the first step in drainage using the Seldinger
technique.
4. Seldinger versus trocar technique
a. Percutaneous catheters are placed using the modified Seldinger or trocar techniques. The particular
technique used is determined by the size of the collection, its location, operator preference/experience, and
imaging guidance employed.
(1) Generally, large superficial collections are drained using the trocar technique because it is a one-stick
procedure that is quick, simple, and safe to perform.
(2) The Seldinger technique is preferred in potentially difficult drainages where the collection is small, is
remotely situated, or has limited access.
With this technique, multiple passes can be made using a thin needle such as a 20-gauge Chiba needle or
a Ring needle. Once safe access is obtained, the tract can be serially dilated using coaxial exchanges of
guidewires and dilators until insertion of a large catheter is possible. However, in inexperienced hands,
particularly when not using real-time guidance, several complications including guidewire kinking, loss of
access, and catheter malposition can occur.
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b. The catheters used commonly range in size from 7 to 14 Fr. and can be either single-lumen or double-
lumen (sump).
(1) Larger catheters are traditionally used in the bigger and more complex collections. The 12 to 14 Fr.
double-lumen sump catheters should theoretically allow better drainage; however, smaller bore catheters
may be just as effective.
(2) The use of a multi-side-hole catheter, such as a Cope-type loop biliary catheter, placed over the length
of the collection may provide better drainage of spread-out collections, such as a subphrenic collection.
c. CT-guided drainages performed using the trocar technique
(1) The optimal path for drainage between the abscess and skin is determined from the preliminary CT. The
skin puncture site is marked on the patient using combined information from CT slice position and
radiopaque markers. The skin is cleaned and draped using sterile technique.
(2) Approximately 10 to 20 mL of 1% lidocaine is given as local anesthesia. A small skin incision is made
and the subcutaneous tissue stretched using clamps or hemostats.
(3) The angle of needle entry and distance to the collection are calculated from the preliminary CT images.
Using these measurements, a 20-gauge needle is advanced into the collection. Repeat imaging is
performed to confirm needle position. If the position is not optimal, the same needle is repositioned correctly
or a second needle advanced in tandem.
(4) Once the needle is optimally positioned, up to 5 mL of fluid is aspirated. The catheter is then loaded on
a trocar delivery system (stiffening cannula and sharp inner stylet) and its tip placed in the skin wound while
holding the shaft parallel to the diagnostic needle. The catheter is then advanced in tandem to the needle to
the predetermined depth to enter the cavity.
(5) As the catheter pierces the proximal wall of the abscess, there is usually a palpable “give” suggesting
cavity puncture. This is confirmed by removal of the inner stylet and aspiration of fluid through the metal stiff
ener. Once fluid is aspirated, the catheter is unlocked from the stiffening cannula and slid forward to coil
within the collection while holding the cannula steady. The cannula is removed and, if applicable, pigtail
locked.
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5. Aspiration and irrigation
a. The catheter is attached to a drainage bag through a three-way stopcock. The use of a three-way
stopcock provides a convenient, clean, and closed system through which the contents of the cavity can be
aspirated and subsequently irrigated.
b. The cavity should be aspirated until there is no more return. The cavity should then be irrigated with
small volumes of saline (5 to 20 mL) no larger in volume than the total volume of fluid initially aspirated from
the cavity because overdistention may elicit bacteremia. Irrigation should be continued until the aspirate
becomes clear or is merely blood-tinged.
c. Following this, a completion CT is performed through the drainage area to (a) ensure that the cavity is
completely emptied, (b) detect any undrained separate collections, (c) form a baseline for future evaluation,
and (d) screen for complications such as bleeding. If the cavity is incompletely drained due to loculation or
there are additional separate collections, then additional needle aspiration or catheter drainage may be
required.
6. Catheter fixation: Most catheters have some form of intrinsic locking device such as a string that can be
tightened to coil and fix the catheter tip within the cavity. Additional security can be obtained by externally
fixing the catheter to the skin. This can be achieved by attaching a tape around the catheter near the skin
and suturing this tape to a skin adhesive (disk-type) device.
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7. Visceral collections
a. Liver
(1) When draining hepatic collections, avoid transgression of large vessels, dilated bile ducts, and the
gallbladder.
(2) Care should be exercised to avoid transgression of the pleura, although this is not always possible.
Employ a subcostal and as anterior an approach when possible; such access may be more obtainable
when using a combination of US and fluoroscopy rather than CT because the needle can be angled and
advanced cranially.
(3) Pyogenic abscesses are the most common hepatic collections amenable to percutaneous drainage.
(4) Medical therapy is considered first-line therapy for echinococcal (hydatid) cysts. Drainage can be
performed in refractory disease in patients who have undergone at least 2 weeks of medical therapy (3).
Small aspirates can be replaced with hypertonic saline prior to placing catheter to help reduce the risk of
intraperitoneal spillage.
(5) Medical therapy is also considered first-line therapy for amebic disease, although drainage can be
performed for refractory disease or peripheral hepatic collections that may be more prone to rupture.
(6) Bilomas, particularly if superinfected, are also amenable to percutaneous drainage.
b. Spleen: Abscesses may also be aspirated or drained as long as coagulation parameters are normalized
(4). Traverse as little splenic parenchyma as possible.
c. Pancreas: Symptomatic pseudocysts and abscesses are amenable to drainage. Persistent output from
catheters suggests pancreatic fistula, which may be confirmed by contrast injection of the catheter;
adjunctive octreotide therapy may be helpful to close the fistula.
d. Urinomas: can be treated with catheter drainage but may need an adjunctive nephroureteral catheter or
percutaneous nephrostomy catheter with ureteral stent if there is persistent output
8. Subphrenic collections (5)
a. Given their location, there is a risk of pleural transgression that may lead to pleural effusion, empyema, or
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pneumothorax.
b. Combination of US and fluoroscopy may allow a subcostal approach to be used, where cranially located
collections can be accessed by angling the needle superiorly.
c. CT guidance may also be utilized and pleura traversed if no other access available; however, lung
parenchyma generally should not be transgressed. Assess for pneumothorax and hemothorax on
postprocedure images.
9. Transgluteal drainage (6): Catheter insertion should be as close to the sacrococcygeal margin as
possible and below the piriformis muscle, generally at the level of the sacrospinous ligament. This helps
avoid neurovascular structures that are located more laterally and superiorly; inadvertent traversal of the
sacral plexus or inferior gluteal vessels may lead to transient buttock pain or bleeding, respectively. Angling
the gantry may help achieve optimal access. The transgluteal approach is suitable in children as well.
10. Transrectal and transvaginal drainage (5,7)
a. Transrectal: suitable for collections anterior or posterior to rectum as well as prostatic abscess. For this
approach, the patient is placed in the left lateral decubitus position.
b. Transvaginal: Given the concern for seeding in certain pelvic malignancies, the transvaginal approach is
used in specific circumstances, including recurrent endometriotic cysts, symptomatic hemorrhagic cysts,
postoperative collections, poor surgical candidates, and pregnant patients. But it is not suitable for
presacral collections. For the transvaginal approach, the
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patient is placed in the dorsal lithotomy position, a speculum inserted, and vaginal vault sterilized with
povidone-iodine solution.
FIGURE 50.1 • Probe-guide assembly. The modified guide (fashioned from catheter protector tubing from
packaging) is securely attached to the probe along the guide-groove with two sterile rubber bands (straight
arrows). It should not project past the transducer head (curved arrow). The guide needs to be cut to the
right length to allow at least 5 cm of catheter advancement through the vaginal vault. This stiff plastic tube is
large enough to accept up to a 14 Fr. trocar catheter. It needs to be preslit along its length so that it can be
removed from the catheter after deployment. (From O'Neill MJ, Rafferty EA, Lee SI, et al. Transvaginal
interventional procedures: aspiration, biopsy, and catheter drainage. Radiographics. 2001;21:657-672.)
c. A Foley catheter is helpful to decompress the bladder.

d. Seldinger technique may be used. Once the wire is placed into the collection under US, further
exchanges are performed using fluoroscopy. However, the Seldinger technique may be difficult due to wire
kinking and distance of hand to point of wire entry. In transvaginal approaches, the muscular wall of the
vagina is tough and may make wire exchanges challenging.
e. Generally, trocar technique is preferred because it is quicker to perform and can be done using only US.
A peel-away sheath may be attached to the biopsy guide of the US probe. However, this occasionally may
not be adequately stiff to maintain catheter position during manipulations. Alternatively, the plastic
connector that comes with the catheter can be used as a guide (Fig. 50.1).
(1) A longitudinal slit is cut along the length of the protector catheter. The protector is then shortened such
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that approximately 5 cm of catheter protrudes from its distal tip.
(2) A sterile condom is placed over the probe and secured with rubber bands. The protector is then
attached to the guide and secured with a distal and proximal rubber band. A second sterile condom is
placed over the assembly.
(3) A needle may be placed initially through the protector for diagnostic aspiration.
(4) Subsequently, the catheter with stiffening cannula and sharp inner stylet are advanced into the protector
(Fig. 50.2A).
(5) The catheter is advanced at least 2.5 cm into the collection to allow the pigtail to form. Doppler US may
be helpful to avoid vessels. The stylet is removed, distal rubber band cut, and outer condom peeled away.
The probe is carefully removed, the proximal rubber band cut, and protector guide removed (Fig. 50.2B).
(6) The inner stiffener is removed from the catheter and catheter secured to the medial thigh.
11. Percutaneous abscess drainage in children (8)
a. The most common indication for percutaneous drainage in children is periappendiceal abscess.
b. Technique and success rates are similar to adults.
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FIGURE 50.2 • Catheter delivery and probe-guide removal. A: Photograph shows the trocar catheter
advanced through the guide and projecting approximately 5 cm past the end of the probe (arrow). B:
Photograph shows that the catheter has been advanced and the pigtail has been formed (straight white
arrow). The inner needle of the trocar has been removed for safety, but the outer metal cannula stiffener
(curved arrow) is left in the straight portion of the catheter to stiffen it and ease the peeling away of the
guide (attached to hemostat) from the catheter (black arrow). (From O'Neill MJ, Rafferty EA, Lee SI, et al.
Transvaginal interventional procedures: aspiration, biopsy, and catheter drainage. Radiographics.
2001;21:657-672.)
c. As with other interventional procedures, consideration should be made of potential body heat losses in
children. Special attention is given to the use of blankets, heat lamps, and warm US gel.
d. Radiation dose should be minimized in all patients but especially in children. This can be achieved by the
use of pulsed fluoroscopy, low CT dose, use of gonadal shields, minimizing the distance between the
patient and the image intensifier, acquiring fluoro stores rather than spot images, judicious use of
magnification, and collimation.
e. The transrectal approach may be used for periappendiceal abscesses.
However, if the patient is too young that an endorectal probe is not suitable, a transrectal catheter can be
placed with sonography performed from an anterior transabdominal view; the bladder should be distended
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to provide an acoustic window.
1. Catheter care
a. Catheter care is best undertaken by the radiologists who have intimate knowledge of the procedure and
catheter complications. This is best achieved by daily inpatient rounds where a member of the interventional
team sees the patient and deals with any problems related to the procedure.
b. The catheter should be inspected to make sure that the stopcock is open to the drainage bag, the catheter
has not been externally retracted, there is no pericatheter leak, and there are no local skin complications such as
cellulitis.
c. Orders should be written to flush the catheter with 10 mL of saline every 8 hours, 5 mL toward the collection,
and 5 mL toward the bag, for catheter
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occlusion prophylaxis. It is not necessary to attach catheters to suction because gravity drainage to a bag is just
as effective.
d. This visit also provides an opportunity to review recordings of the patient's catheter outputs and vital signs,
assess clinical progress, and make progress note report.
2. Catheter removal
a. Catheter drainage is required until the patient's vital signs return to normal and the body can promote
complete healing of the abscess cavity. Early removal will result in recurrence of the collection, while prolonged
drainage will increase morbidity.
b. Usually, the catheter is removed when there is drainage of less than 20 mL per day from the catheter coupled
with return of vital signs to normal. Repeat imaging is only required if (a) the patient's condition is not improving,
(b) there is less than expected drainage, or (c) there is sudden reduction in drainage from the catheter.
c. If there is high output from the catheter (>50 mL per day) after the fourth day of catheter insertion, the
possibility of a fistula to the bowel, pancreatic duct, or biliary system should be considered and a catheter
injection performed to identify any communication. If a fistula is found, prolonged (4 to 6 weeks) percutaneous
catheter drainage or primary treatment of the fistula is required before the catheter can be removed. Adjunctive
treatment of pancreatic fistulas with octreotide may be helpful.
d. If there is a persistent collection and poor outputs from the catheter, adjunctive use of tissue plasminogen
activator (tPA) can be very helpful (9).
Generally, 4 to 6 mg of tPA is diluted in 50 mL normal saline. Up to 50 mL is injected into the catheter twice daily
for 3 days (care should be taken not to inject a volume larger than the collection size), with the catheter clamped
for 30 minutes after injection. This can be successful up to nearly 90% of the time, with failure more likely in
patients with pancreatic collections, fungal infection, or enteric fistula.
Results
1. The success of percutaneous drainage of uncomplicated collections can exceed
90% (1,10). However, this decreases significantly with complex collections such as those with loculation or
inflammation (e.g., pancreatic abscess).
2. The recurrence rate of a collection after drainage is between 8% and 20% and is commonly due to early
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removal of catheter, undetected fistula, or drainage of tumor abscess.
Complications
Overall, complication rates are reported to be less than 15% (2) and 30-day mortality approximately 1% to
6%. Complications may be categorized as major or minor (3).
Major
1. Major complications include hemorrhage, septic shock, enteric fistula, peritonitis, and
hemopneumothorax.
2. Puncture of a blood vessel can cause brisk and severe bleeding that may require blood transfusion,
angiography with embolization, or even laparotomy for treatment. Therefore, all patients require close
monitoring of their vital signs after a drainage procedure to detect occult bleeding.
3. Underlying viscera such as bowel can be punctured during catheter insertion. If there are signs of
peritonitis, bowel obstruction, or enteric fluid draining from the catheter, catheter injection should be
performed to check for catheter position, detect any fistula, and identify free peritoneal spill. If bowel
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communication, with or without free peritoneal leak, is found, immediate surgical consultation is required.
This allows a combined decision to be made as to whether to remove the catheter immediately, remove it
during laparotomy if peritonitis is present, or leave it in position for 3 to 4 weeks for a mature tract to
develop.
Minor
1. Minor complications include pain, bleeding, infection, and pericatheter leak.
2. The reasons for catheter nonfunction and pericatheter leak include kinking, blockage, or dislodgment. If
simple bedside measures such as aspiration or flushing are not effective, then catheter injection and
manipulation or replacement under fluoroscopy may be required. If the catheter falls out inadvertently, then,
depending on the duration and volume of drainage, nature of drainage, imaging findings, and patient clinical
condition, a trial without catheter may be undertaken or a new catheter inserted using a new tract.
3. If infection is suspected at the catheter insertion site, swabs may be sent for culture and appropriate
antibiotics started.
4. Bleeding from the catheter insertion site is usually self-limiting but occasionally may require angiographic
investigation.
References
1. Wallace MJ, Chin KW, Fletcher TB, et al. Quality improvement guidelines for percutaneous
drainage/aspiration of abscess and fluid collections. J Vasc Interv Radiol . 2010;21:431-435.
2. Akinci D, Akhan O, Ozmen M, et al. Long-term results of single-session percutaneous drainage and
ethanol sclerotherapy in simple renal cysts. Eur J Radiol . 2005;54:298-302.
3. D'Agostino HB, Hurvitz D, Nall L, et al. Transcatheter fluid drainage. In: Valji K, ed. Vascular and
Interventional Radiology. 2nd ed. Philadelphia, PA: Saunders/Elsevier; 2006:516-531.
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4. Lucey BC, Boland GW, Maher MM, et al. Percutaneous nonvascular splenic intervention: a 10-year
review. AJR Am J Roentgenol . 2002;179:1591-1596.
5. Maher MM, Gervais DA, Kalra MK, et al. The inaccessible or undrainable abscess: how to drain it.
Radiographics. 2004;24:717-735.
6. Harisinghani MG, Gervais DA, Maher MM, et al. Transgluteal approach for percutaneous drainage of deep
pelvic abscesses: 154 cases. Radiology. 2003;228:701-705.
7. O'Neill MJ, Rafferty EA, Lee SI, et al. Transvaginal interventional procedures: aspiration, biopsy, and
catheter drainage. Radiographics. 2001;21:657-672.
8. Gervais DA, Brown SD, Connolly SA, et al. Percutaneous imaging-guided abdominal and pelvic abscess
drainage in children. Radiographics. 2004;24:737-754.
9. Beland MD, Gervais DA, Levis DA, et al. Complex abdominal and pelvic abscesses: efficacy of adjunctive
tissue-type plasminogen activator for drainage. Radiology. 2008;247:567-573.
10. Gervais DA, Ho CH, O'Neill MJ, et al. Recurrent abdominal and pelvic abscesses: incidence, results of
repeated percutaneous drainage, and underlying causes in 956 drainages. AJR Am J Roentgenol .
2004;182:463-466.
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51
Percutaneous Gastrostomy, Percutaneous Gastrojejunostomy,
Jejunostomy, and Cecostomy
Ji Hoon Shin
Andrew J. Lipnik
Ho-Young Song
Daniel B. Brown
Percutaneous Enteral Tubes

Although temporary enteral tubes (e.g., nasogastric [NG] and nasojejunal) may be placed through natural
orifices, percutaneously placed feeding tubes offer the best options for patients who require long-term nutrition.
Percutaneous radiologic gastrostomy (PRG) is associated with low morbidity and mortality rates. These
minimally invasive procedures are generally simpler, associated with higher technical success rates, and have
lower complication rates than percutaneous endoscopic gastrostomy (PEG) or surgical placement techniques.
Types of Tubes
1. Dedicated single function (feeding or decompression alone)
a. Gastrostomy (G-tube)
(1) Simplest technically, requiring the least manipulation
(2) Shortest tube, providing for less clogging over time
(3) Preserves gastric function, allowing for high diet variety and simplicity in maintenance
(4) Can be converted into gastrojejunostomy tube after percutaneous tract matures (10 to 21 days)
b. Jejunostomy (J-tube)
(1) Bypasses stomach, requires elemental diet and slow pump infusion to prevent dumping syndrome
(2) A higher level of tube care is required.
(3) Single lumen gastrojejunostomy (GJ)
(a) Catheter placed via the stomach with tip at or beyond the ligament of Treitz
(b) Simpler to place under fluoroscopy than direct J-tube
(c) Longer catheter than direct J-tube, making it more prone to clogging
2. Split function: Double lumen gastrojejunostomy (DLGJ)
a. Requires elemental diet and slow jejunal infusion using a pump
b. Gastric lumen required for either of the following:
(1) Decompression in patients with gastroparesis or gastric outlet obstruction
(2) Medications that are only absorbed by the stomach
Percutaneous Gastrostomy
Indications (1,2,3,4,5,6)
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1. Nutritional support for patients with inadequate oral intake due to dysphagia, risk of aspiration, or obstruction
secondary to
a. Stroke and neuromuscular disorders
b. Esophageal mass/neoplasm
c. Lesions of the head, neck, and mediastinum (including recent surgery or radiation)
2. Diversion of feedings from esophageal leaks caused by recent surgery or trauma
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3. Decompression of gastroenteric contents and/or need for jejunal feeding
a. Gastric outlet or proximal small bowel obstruction
b. Patients with gastroparesis (e.g., diabetic gastropathy, scleroderma)
4. Intestinal access for biliary procedures (e.g., patients with Roux-en-Y anastomosis)
Contraindications (1,2,3,4,5,6)
Absolute
1. Unsatisfactory anatomy (e.g., no safe percutaneous access to stomach secondary to interposed colon or liver)
Relative
1. Prior gastric surgery with anatomic distortion (e.g., subtotal gastrectomy or gastric bypass). Access to the
stomach may be extremely difficult and require advanced techniques and/or CT guidance.
2. Massive ascites. Preprocedural paracentesis and gastropexy can help reduce the incidence of peritoneal
leakage.
3. Gastric or abdominal wall varices due to portal hypertension
4. Inflammatory, neoplastic, or infectious involvement of the gastric wall (may result in poor wound healing and
tract formation)
5. Severe gastroesophageal reflux. Feedings should be delivered into the jejunum via PGJ or percutaneous
jejunostomy (PJ) tube.
6. Ventriculoperitoneal shunt
1. Review surgical history and prior imaging for evidence of altered gastric anatomy, safe percutaneous access
route, and ascites.
2. Review and correct as necessary any coagulopathy.
3. Approximately 200 mL of dilute barium suspension is given 12 hours before the procedure to outline the colon.
Alternatively, colonic gas is typically sufficient to outline the colon, or when not present, a small amount of air or
contrast can be instilled retrograde per rectum at the time of the procedure.
4. Maintain nil per os (NPO) status for 8 hours prior to procedure.
5. An NG tube (preferably placed bedside the evening before the procedure) is necessary for insufflating air to
bring the stomach into apposition with the anterior abdominal wall, displacing adjacent viscera, and facilitating
safe gastrostomy tube placement. If there is difficulty placing the NG tube at bedside, an angiographic catheter
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placed under fluoroscopic guidance immediately prior to the procedure may be used for insufflation.
6. Conscious sedation should be given judiciously in patients with head and neck malignancies or respiratory
compromise in neuromuscular disorders such as amyotrophic lateral sclerosis (ALS). In fact, the ability to safely
and comfortably place radiologic gastrostomy tubes with minimal sedation is a particular advantage in this patient
population.
Procedure
1. Prepare the left subcostal area and epigastrium in a sterile manner.
2. Glucagon (0.5 to 1.0 mg) or Butylscopolamine (20 mg) intravenously (IV) may be administered to diminish
gastric peristalsis.
3. Insufflate air into the stomach via NG tube until adequate gastric distention is achieved fluoroscopically.
4. Although the need for routine gastropexy remains debated, clinical scenarios suggesting an impaired
ability to form a mature tract (e.g., patients on chronic steroids) or at high risk for peritoneal leakage
(patients with ascites) mandate secure gastropexy (1,2,7,8).
5. If gastropexy is not employed, it may be necessary to continue air insufflation during the procedure to
keep the stomach distended—so it is wise to limit
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the volume of air used initially. In patients with partial gastrectomy or other surgeries involving a vagotomy,
it will be more challenging to maintain gastric distension during tube placement. Conversely, the presence
of adhesions often simulates a gastropexy.
6. After air insufflation, frontal and oblique views of the upper abdomen are helpful to determine the depth to
the anterior gastric wall and location of the transverse colon. Rarely, lateral imaging may be needed.
7. Choose the puncture site—distal body of the stomach, equidistant from the lesser and greater curvatures
to minimize the risk of arterial injury (Fig. 51.1). Avoid punctures that transgress the colon or left lobe of the
liver. The risk of hemorrhage is minimized by avoiding the inferior epigastric artery as it courses the junction
of the medial two-thirds and lateral one-third of the rectus muscle (Fig. 51.1).
8. Infiltrate local anesthesia (1% lidocaine) down to the peritoneal surface; a small skin incision is made.
9. Many operators routinely use gastropexy devices (Saf-T-Pexy T-Fasteners [Halyard Health, Alpharetta,
GA], or 18-gauge slotted needle preloaded with a T-fastener [Boston Scientific, Natick, MA]). Two to four T-
fasteners are deployed to fix the anterior gastric wall to the abdominal wall (1,2). Gastric puncture is
performed with the kit needle preloaded with an anchor system. An intragastric position is confirmed both by
aspiration of air into a syringe and injection of contrast with visualization of gastric rugae. A stylet is
introduced through the needle, advancing the anchor into the stomach. The stylet and needle are
subsequently removed and the stomach is gently approximated to the anterior abdominal wall by gentle
traction on the anchor suture. Alternatively, the needle is removed over a safety guidewire (GW) to retain
original access. If gastropexy is not employed, a Seldinger needle is used for a new gastric puncture.
10. Whatever the choice, the puncture should be made with a brief, deliberate thrust so as not to push the
anterior gastric wall away from the anterior abdominal wall. Usually, the puncture needle is directed slightly
toward the pylorus, to facilitate future conversion to a PGJ if needed (Fig. 51.2). When placing a pulltype
gastrostomy tube under fluoroscopy, access can be directed slightly toward the gastroesophageal junction
to facilitate cannulation of the esophagus.
11. Once the gastric lumen is entered, the needle position is confirmed by injection of contrast, outlining
gastric rugal folds. With the Seldinger needle tip within the stomach, a stiff 0.035-in. GW is inserted and
looped in the stomach.
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12. Fascial dilators, of adequate diameter to accommodate the feeding tube, are introduced over the 0.035-
in. GW to make a tract (Fig. 51.2). Because of the thick muscular wall of the stomach, the dilator can easily
push the stomach wall forward rather than dilating the puncture hole within the wall. If this happens, the GW
may prolapse outside the stomach into the peritoneum. A GW with the proper stiffness and fluoroscopic
visualization during manipulation helps avoid this problem.
13. Place the selected gastrostomy tube over the wire, through an appropriately sized peel-away sheath if
placing a balloon retention gastrostomy tube (typically 2 to 4 Fr. larger than the gastrostomy tube to
accommodate the balloon). A 12-Fr. or larger pigtail-retained gastrostomy catheter (Wills-Oglesby
percutaneous gastrostomy catheter, Cook, Bloomington, IN) can also be used (Fig. 51.2).
14. Following tube placement, contrast is injected and fluoroscopic images of the upper abdomen are
obtained to confirm proper position.
15. The feeding tube is secured to the skin with sutures or commercially available retaining devices.
1. Vital signs and serial abdominal examination must be closely followed, looking for signs of peritonitis that may
indicate leakage of gastric contents.
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Pneumoperitoneum on routine imaging is not unexpected and slowly resolves over 24 to 72 hours.
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FIGURE 51.1 • A: Axial cross-section of abdomen at the level of the body of the stomach with patient supine. No
liver or colon noted anteriorly. B: Frontal cutaway view shows window to body of the stomach (X), avoiding the
inferior epigastric artery, left lobe of the liver, and transverse colon. (continued)
FIGURE 51.1 • (Continued) C: Sagittal view demonstrating superficial location of the anterior wall of a distended
stomach. Liver is cephalad to, and lumen of transverse colon is caudal to, the stomach.
2. The PG tube should remain connected to a gravity drainage bag or to low, intermittent suction for the first 24
hours following placement, before attempting feedings. If documented overnight output is not excessive, and if
the abdominal exam is benign, feedings may begin the next morning.
3. For a PG tube, the initial infusion rate is usually 10 mL per hour, increased as tolerated by 10 mL per shift to
goal rate as determined by the nutritional support team. J-tubes require a slower infusion rate. Although gastric
residuals are commonly checked and recorded by the nursing staff, what more accurately predicts a well-
functioning feeding tube is the absence of symptoms such as reflux, aspiration, nausea, and bloating.
4. If these symptoms persist over several days after initiating feeding, the patient should be assessed for
presence of ileus; if absent, agents to increase gastric motility may be initiated. If motility agents are not
successful in decreasing tube residuals, the G-tube may be converted to a G-J tube to allow more distal feeding
while providing the option for proximal decompression.
5. If the PG tube is placed for decompression of small bowel obstruction, low, intermittent suction should begin
early and continued as needed.
6. Long-term management: Routine G-tube changes are not usually performed; commonly, the clinical team,
patient, or outside caretaker calls if there are problems—this usually results in a tube change in 4 to 6 months.
However, a proactive involvement by the interventional radiology (IR) service with patients is preferable. Most
problems are resolved by asking the right questions of the person (caregiver or the patient) accessing the tube
most frequently. Common scenarios and their management are as follows:
a. The retention device failed, causing the tube to partially back out.
(1) If the catheter is functioning normally, it should be refixed in place.
(2) If malfunction of the catheter is suspected, it is appropriate to check under fluoroscopy and possibly replace
the catheter.
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FIGURE 51.2 • Alternative method for placement of a percutaneous gastrostomy tube. A: The stomach is inflated
with air through the nasogastric tube to bring the gastric wall close to the abdominal wall. B: The puncture is
made with a 16-gauge needle/catheter pointing vertically down, and a 0.035-in. J-tipped guidewire is advanced
through it. C,D: Before inserting the peel-away introducer sheath, fascial dilators are advanced over the
guidewire until an adequate diameter is reached. E: The catheter is advanced over the guidewire through the
peel-away sheath. F: After the catheter is in place, the guidewire is removed and the sheath is peeled away.
(From Maynar M, et al. Gastrointestinal tract intervention. In: Castaneda-Zuniga WR, Tadavarthy SM, eds.
Interventional Radiology. 2nd ed. Baltimore, MD: Lippincott Williams & Wilkins; 1992: 1218-1219, with
permission.)
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b. The tube fell out/was pulled out completely: In the setting of a mature tract, the tube can be replaced at the
bedside. If the tract has constricted, there is difficulty with bedside replacement, or concern about tube
malposition, fluoroscopy can be used to recannulate the existing tract with an angled catheter and wire,
facilitating placement of a new tube.
c. The tube is leaking around the skin insertion site.
(1) If the patient has a balloon retention catheter, the balloon is likely ruptured. Instruct the patient to fix the
catheter to the skin until arriving in IR for tube replacement.
(2) If the patient has a multi-side-hole catheter, either the side holes have backed into the tract or the patient is
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developing gastric outlet obstruction. Rarely, this occurs from the catheter loop migrating to, and obstructing, the
pylorus.
d. The tube is clogged.
(1) This is typically from inadequately crushed pills or suboptimal flushing after use. The catheter should be
vigorously flushed with a 3-mL syringe.
(2) If the above is unsuccessful, the catheter should be exchanged. In the setting of a mature tract, if the tube is
too obstructed to allow GW passage, it may be removed completely and the tract recanalized. Alternatively, the
external hub is cut and a properly sized peel-away sheath is coaxially introduced over the old tube to retain
original access.
e. The patient is not tolerating feeds or has diarrhea: This history is classic for a gastrostomy tube that has
migrated to the duodenum. Bolus feeds no longer slowly drain through the pylorus and the patient develops
dumping syndrome. The tube should be repositioned into the stomach with fluoroscopy.
f. The patient has abdominal pain: Physical examination is important to determine the cause: skin infection, tube
migration, gastric outlet obstruction, or other causes.
g. The patient is complaining of skin irritation/breakdown at the insertion site.
(1) A liquid antacid may be applied topically to the area.
(2) Evaluate for infection and treat with antibiotics as appropriate.
Modifications of PG Placement
1. One-anchor technique
a. Controversy exists as to the number of anchors that is sufficient—one placed through the gastrostomy tract
(i.e., one-anchor technique) to four placed in the form of a square around the tract (2).
b. With this technique, a single anchor is inserted through the preloaded 17-gauge puncture needle (Cope
gastrointestinal suture anchor sets, Cook, Bloomington, IN) (Fig. 51.3). After confirming its location within the
stomach, the anchor is released by pushing with the GW. The anchor is pulled firmly toward the anterior
abdominal wall; serial dilators are introduced over the GW through the same tract. Finally, a gastrostomy tube
(10 to 16 Fr.) is introduced over the GW into the stomach (Fig. 51.3).
c. Although the one-anchor technique is a simple procedure, there is an increased risk of anchor dislodgment
and related peritonitis.
2. Pull-type gastrostomy tube placement: The problem associated with the retention of radiologically inserted
gastrostomy tubes led to the development of peroral endoscopic placement of pull-type gastrostomy tubes (9).
However, these tubes may also be placed percutaneously using fluoroscopic guidance:
a. The pull-type gastrostomy tube is pulled down through the oropharynx. Because this may transport oral
bacteria to the gastrostomy site, prophylactic antibiotics are advised (generally penicillin-based prophylaxis) (10).
b. Percutaneous gastric access is similar to that of PG tube placement, but the use of gastropexy is debated.
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FIGURE 51.3 • One-anchor technique. A: The puncture is made with a 17-gauge needle preloaded with a single
anchor. B: After confirming its location within the stomach, the anchor is released by pushing with a guidewire.
C: After removing the 17-gauge needle, the anchor is pulled firmly toward the anterior abdominal wall. D: Fascial
dilators are advanced over the guidewire until an adequate diameter is reached. E,F: A gastrostomy tube (10 to
16 Fr.) is introduced over the guidewire into the stomach. Note: A similar technique is employed for percutaneous
jejunostomy tube placement.
c. Following successful access, a 5 to 7 Fr. angiographic catheter and GW are used to cross the
gastroesophageal junction from the stomach to the esophagus. The catheter and GW are advanced in a
retrograde direction and pulled out of the patient's mouth.
d. After exchanging the GW for a “traction wire” or preferably an exchangelength GW, a pull-type gastrostomy
tube is introduced coaxially, passing in an antegrade direction down the mouth into the esophagus and out the
anterior abdominal wall. The tapered tip of the gastrostomy tube is then cut to the desired length. A 20 Fr.
mushroom-retained catheter (removable pull-PEG, Medical Innovations, Draper, UT) is commonly used.
e. The tube is affixed externally at the skin.
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Results
Technical success of PRG and PGJ placement approaches 100% (1,2,3,4,5,6).
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Complications
1. 30-day mortality from all causes ranges from around 4% (1) to 8% (3) depending on the severity of the
underlying illness, according to one meta-analysis of the literature (3). Procedure-related 30-day mortality is
under 0.5%.
2. Major complications (hemorrhage, peritonitis, wound infection, gastrointestinal perforation, aspiration,
displacement of the tube requiring a repeat procedure, and sepsis) are under 8% (3). Surgical and
endoscopic gastrostomies carry higher mortality and complication rates (3); PRG is often the preferred
approach.
3. Peritonitis associated with PRG is a rare but most serious major complication (8). This devastating
complication is caused by extravasation of gastric contents into the peritoneum, either from intraperitoneal
leakage around an enteral puncture site or from tube migration and erosion causing frank perforation of the
stomach (or small bowel in the case of direct jejunostomy). Tube feeding should be held; clinical evaluation
should dictate surgical consultation and exploratory laparotomy, if necessary.
4. Aspiration pneumonia occurs less frequently with PRG (0.8% to 5%) than with PEG (6% to 20%, related
to profound sedation and the technique used in during the endoscopic procedure).
5. Minor complications (superficial wound infection, minor peritubal leakage, tube dislodgment) are reported
in 5% to 10% of cases (3).
6. Gastrointestinal complications such as hemorrhage and perforation following PRG or PGJ tube
placement occur in less than 2% of cases (3). Transarterial embolotherapy is useful for controlling massive
hemorrhage (2,11).
7. Other potential complications—laceration of the liver, pancreas, or spleen, and gastroenteric fistula—are
very rare.
Percutaneous Gastrojejunostomy
In patients with a history or risk of gastroesophageal reflux or aspiration, percutaneous gastrojejunostomy (PGJ)
is considered. PGJ can be performed as an initial feeding tube placement (primary PGJ) or by converting a prior
gastrostomy tube to a gastrojejunostomy (conversion PGJ) tube (12). Conversion may be performed any time
after successful placement of a PG if gastropexy is used, or if not, after the tract matures (usually in 1 to 3
weeks). A successfully placed or converted PGJ tube may be used within hours of insertion. Three types of
gastrojejunostomy tubes are usually used: a 10.2 Fr. 100-cm single lumen GJ tube (Carey-Alzate-Coons
Gastrojejunostomy Set, Cook), a 14.0 Fr. 63-cm single lumen GJ (Shetty Gastrojejunostomy Set, Cook), and a
16.5 Fr. 80-cm double lumen gastrojejunostomy tube (Carey-Alzate-Coons Gastrojejunostomy Set, Cook).
Conversion of a Mature PG Tube to PGJ Tube

1. Conversion PGJ can be difficult if the initial angle of entry of the PG tube is directed toward the fundus. An
angled 5 Fr. vascular catheter (usually C-1), 7 Fr. seeking catheter, and a rigid sheath or vascular dilator have all
been described to facilitate the redirection of the tract (12). Redirection can avoid proximal migration and recoil of
a PGJ tube after it has been successfully placed.
2. If the original tract is unfavorable for redirection, a new puncture directed toward the pylorus is needed.
3. Regardless of the type of tube deployed (coaxial configuration or a single tube with dual ports), the tip of PGJ
tubes should be placed well beyond the ligament of Treitz and the gastric port should be located within the
stomach lumen.
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Primary Placement of a PGJ Tube
1. For primary PGJ tube placement, follow all steps as described for PG placement but direct the initial needle
puncture toward the pylorus.
2. Using an angled catheter-guidewire combination, maneuver the catheter into the jejunum.
3. Replace the initial GW for a stiffer exchange GW, with the tip well into the jejunum.
4. Dilate the entry site and place a peel-away sheath.
5. Introduce the PGJ tube with jejunal and gastric ports optimally positioned as described above.
6. Inject a small amount of contrast through each port to confirm satisfactory position.
7. Secure the catheter at the skin.
8. The jejunal port (not the gastric, if a fresh introduction) may be used immediately for feeding.
9. Irrigate copiously with fresh tap water after each use to prevent clogging.
Percutaneous Jejunostomy
Primary PJ tube placement is indicated for patients with a history of chronic aspiration, gastric surgery (i.e.,
gastrectomy), or abnormal gastric position. Percutaneous puncture of the jejunum is more difficult than that of
stomach because of the high mobility and easy collapsibility of the jejunum. The technical success of the PJ
placement ranges between 85% and 95% (13,14). A 12 Fr. or larger pigtail-retained gastrostomy catheter (Wills-
Oglesby percutaneous gastrostomy catheter, Cook) is usually used.
1. A 5 Fr. angled catheter (cobra or head-hunter) and a 0.035-in. GW (hydrophilic, if needed—these wires may
be stiffer than necessary) are introduced through the nostril and directed through the esophagus into the jejunum
under fluoroscopic guidance.
2. Dilatation of jejunal loops is achieved by slow saline injection. Upon frontal and lateral fluoroscopy, the
catheter tip is located in an air-filled proximal jejunal loop, as a target, in a portion that is sufficiently close to the
anterior abdominal wall.
3. Puncture of the distended jejunum is performed under fluoroscopic and/or ultrasound guidance (13). A 17-
gauge needle preloaded with a Cope suture anchor is commonly used (13)— Note: The technique is similar to
that illustrated in Figure 51.3 for gastrostomy tube placement. A 21-gauge Chiba needle (Cook) can alternatively
be used for puncture (14). After confirming the intraluminal positioning of the needle, a 0.018-in. GW is advanced
as far as possible into the jejunum to allow insertion of 6-Fr. Neff catheter (Cook). A single Cope suture anchor is
then deployed into the jejunum through the Neff catheter. Following serial dilation of the entry site, the tube is
inserted.
4. Postprocedure feeding and tube management are similar to PGJ tubes.
Percutaneous Cecostomy
Cecostomy is indicated for decompression and/or diversion in the setting of fecal incontinence, colonic pseudo-
obstruction (Ogilvie syndrome), or cecal volvulus (15,16). Cecostomy tubes can also be used to deliver laxatives
for antegrade irrigation for patients who have chronic constipation caused by a neurogenic colon, avoiding the
need for multiple retrograde enemas (15,16). The posterolateral extension of the peritoneum around the cecum
along with the overlying posterolateral iliac bone is the rationale for using an anterior intraperitoneal approach
rather than a retroperitoneal approach.
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1. When needed, the cecum is distended using air introduced through a Foley catheter placed through the
rectum.
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2. A single-wall puncture is made under fluoroscopic guidance with a Majestic 18-gauge, 7-cm, single-wall
needle with a Seldinger shield (Merit Medical, South Jordan, UT) (15). The needle is preloaded with two metallic
retention sutures (Cook). After confirming intraluminal location of the needle tip with contrast injection, a 0.035-in.
Amplatz guidewire is used to deploy the retention sutures, and the needle is removed leaving the GW in place.
3. Although the retention sutures are pulled tight for the cecum to be drawn close to the abdominal wall, the tract
is dilated (using a Coons Dilator, Cook) over the GW so that an 8.5 to 10 Fr. cecostomy tube (Dawson-Mueller
Catheter, Cook) can be accommodated. Conversions to a cecostomy button (Trapdoor Catheter, Cook) with a
coil-shaped distal tip may be needed for long-term use.
4. The tube is attached to external drainage for decompression or used for antegrade irrigation/enemas as
needed.
5. Technical success is high in patients with fecal incontinence (˜100%); 89% of them have improvement of fecal
incontinence (15).
6. Complications are rare. Granulation tissue formation around the tube insertion site or tube dislodgment can
occur.
References
1. Brown AS, Mueller PR, Ferrucci JT Jr. Controlled percutaneous gastrostomy: nylon T-fastener for fixation
of the anterior gastric wall. Radiology. 1986;158:543-545.
2. Kim JW, Song HY, Kim KR, et al. The one-anchor technique of gastropexy for percutaneous radiologic
gastrostomy: results of 248 consecutive procedures. J Vasc Interv Radiol . 2008;19:1048-1053.
3. Wollman B, D'Agostino HB, Walus-Wigle JR, et al. Radiologic, endoscopic, and surgical gastrostomy: an
institutional evaluation and meta-analysis of the literature. Radiology. 1995;197:699-704.
4. Kuo YC, Shlansky-Goldberg RD, Mondschein JI, et al. Large or small bore, push or pull: a comparison of
three classes of percutaneous fluoroscopic gastrostomy catheters. J Vasc Interv Radiol . 2008;19:557-563.
5. Park JH, Shin JH, Ko HK, et al. Percutaneous radiologic gastrostomy using the oneanchor technique in
patients after partial gastrectomy. Korean J Radiol. 2014;15: 488-493.
6. Shin JH, Park AW. Updates on percutaneous radiologic gastrostomy/gastrojejunostomy and jejunostomy.
Gut Liver. 2010;(4)(suppl 1):S25-S31.
7. Thornton FJ, Fotheringham T, Haslam PJ, et al. Percutaneous radiologic gastrostomy with and without T-
fastener gastropexy: a randomized comparison study. Cardiovasc Intervent Radiol . 2002;25:467-471.
8. Dewald CL, Hiette PO, Sewall LE, et al. Percutaneous gastrostomy and gastrojejunostomy with
gastropexy: experience in 701 procedures. Radiology. 1999;211:651-656.
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9. Clark JA, Pugash RA, Pantalone RR. Radiologic peroral gastrostomy. J Vasc Interv Radiol . 1999;10:927-
932.
10. Ahmad I, Mouncher A, Abdoolah A, et al. Antibiotic prophylaxis for percutaneous endoscopic gastrostomy
—a prospective, randomised, double-blind trial. Aliment Pharmacol Ther. 2003;18:209-215.
11. Seo N, Shin JH, Ko GY, et al. Incidence and management of bleeding complications following
percutaneous radiologic gastrostomy. Korean J Radiol . 2012;13:174-181.
12. Shin KH, Shin JH, Song HY, et al. Primary and conversion percutaneous gastrojejunostomy under
fluoroscopic guidance: 10 years of experience. Clin Imaging. 2008;32: 274-279.
13. van Overhagen H, Ludviksson MA, Laméris JS, et al. US and fluoroscopic-guided percutaneous
jejunostomy: experience in 49 patients. J Vasc Interv Radiol . 2000;11: 101-106.
14. Yang ZQ, Shin JH, Song HY, et al. Fluoroscopically guided percutaneous jejunostomy: outcomes in 25
consecutive patients. Clin Radiol . 2007;62:1060-1068.
15. Chait PG, Shlomovitz E, Connolly BL, et al. Percutaneous cecostomy: updates in technique and patient
care. Radiology. 2003;227:246-250.
16. Sierre S, Lipsich J, Questa H, et al. Percutaneous cecostomy for management of fecal incontinence in
pediatric patients. J Vasc Interv Radiol . 2007;18:982-985.
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52
Percutaneous Biliary Interventions
David W. Hunter
Endoscopic techniques are improving particularly as a result of the incorporation of ultrasound guidance (1).
Access to the intra- or extrahepatic biliary tree can be achieved not only via the usual transampullary route but
also from the stomach or duodenum. With the ultrasound probe within a few centimeters of the target, the
punctures rarely fail. Through the puncture needle, a wire is passed through the ducts to the duodenum. A
through-and-through, “rendezvous technique” wire is used to complete the procedure through the usual
transampullary approach. Because the puncture, in most cases, involves only a needle and a wire, the tract is
small. Bleeding problems are relatively minor and infrequent.
Percutaneous biliary intervention remains useful when endoscopy fails or is unlikely to succeed and in a recent
meta-analysis, percutaneous techniques showed a greater therapeutic success rate than endoscopic retrograde
cholangiopancreatography (ERCP) for malignant occlusions (2). However, as a result of the new “selection”
process, most percutaneous cases are technically and medically challenging. They require careful planning,
meticulous technique, long-term clinical follow-up, and close cooperation with liver surgeons and endoscopists.
Indeed, many of the most rewarding and remarkable successes result from combined efforts with an endoscopist
or surgeon to surmount an obstacle that would have stymied either working independently.
Indications
Percutaneous transhepatic cholangiography (PTC)
1. Prior to percutaneous biliary intervention when the cause is apparent
2. In pediatric, uncooperative, or very ill patients in whom an extra diagnostic test especially magnetic
resonance imaging (MRI) would require an additional sedation event or might result in a delay in needed
therapy
3. When there is clinical and laboratory evidence of obstruction, in patients with choledochojejunostomy
who do not appear obstructed on noninvasive imaging as a result of decreased ductal compliance and
minimally dilated or nondilated ducts (e.g., liver transplant or post-pancreatectomy/duodenectomy surgical
patients)
Percutaneous biliary drainage (PBD)
1. Palliation or treatment of biliary obstruction resulting from benign (e.g., postoperative or posttransplant) or
malignant strictures following failed ERCP drainage
a. Preoperative decompression prior to surgery is no longer felt to be routinely indicated; several recent
evaluations of this practice and one meta-analysis have shown that it is actually associated with increased
morbidity and should be avoided unless there is another compelling reason, such as cholangitis, that must
be corrected before surgery (3).
2. Cholangitis or infected bile
3. Bile duct injury or bile leak resulting from traumatic or iatrogenic causes
4. Complex strictures involving both left and right ducts (e.g., Billroth IV cholangiocarcinoma, sclerosing
cholangitis, and ischemic cholangitis)
5. To facilitate intraductal procedures
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a. Stricture biopsy
b. Brachytherapy for cholangiocarcinoma
Percutaneous stricture dilation and self-expanding metallic stents are inserted for
1. Stricture dilation
a. Benign strictures
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b. Anastomotic strictures in both transplant and nontransplant patients who have undergone
choledochoenterostomy (duct to bowel) or choledochocholedochostomy (duct to duct) anastomoses
c. Intraductal strictures (e.g., postoperative, inflammatory, ischemic, particularly posttransplant, or drug-
induced)
2. Metallic stent placement
a. Palliation of malignant biliary obstruction to both improve quality of life as well as to improve candidacy
for alternative therapies such transarterial chemoembolization (TACE) or systemic chemotherapy
b. Palliation of bowel obstruction, at or distal to, ductal entry
Contraindications
Absolute
2. Obligatory use of Plavix
Relative
1. Uncorrectable moderate coagulopathy or use of aspirin
a. Consider infusion of fresh frozen plasma (FFP), cryoprecipitate, or platelets during the procedure.
2. Large volume ascites
a. Consider paracentesis before and during the procedure.
b. Use a left-sided approach because ascites is frequently absent anteriorly.
3. Hemodynamic instability
a. Consider that it may be due to an infected bile leak that may be corrected by drainage.
Self-expanding metallic stent insertion specifically:
Absolute
1. Active hemobilia
2. Infected bile
Relative
1. Coagulopathy, including antiplatelet agents (e.g., Plavix)
2. Worsening liver function in the face of adequate external drainage
3. Less than 30-day life expectancy and patient is stable with an external catheter
4. Visible infection involving the percutaneous tract or entry site
5. Visible intraductal debris or stones
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1. Directed history and physical examination
2. Review imaging studies, clarify the indication, and develop a plan.
a. Consider whether magnetic resonance cholangiopancreatography (MRCP), ultrasound, or computed
tomography (CT) will provide the needed information without a more invasive procedure.
b. MRCP has become so accurate that even when intervention is likely, MRCP is performed to verify the problem
and get an accurate picture of the ductal anatomy.
3. Review blood tests including at a minimum of the following:
a. Complete blood count (CBC) and platelet count
(1) Correct platelet count to >50,000 per dL.
(2) Evaluate falling hemoglobin (Hgb) or Hgb less than 8 g per dL.
(3) Evaluate rising white blood cell (WBC) or a WBC greater than 12 billion cells per L.
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b. International normalized ratio (INR) and activated partial thromboplastin time (APTT) or anti-10A activity
(1) Correct INR to <1.7.
c. If bleeding is a real concern, consider either a simple test like bleeding time or activated clotting time (ACT), or
one of the more sophisticated modern tests that measure global clotting function such as thromboelastography,
thrombodynamics, or thrombin generation.
d. Liver function tests particularly conjugated and unconjugated bilirubin levels to establish baseline.
e. Renal function. Renal dysfunction before, during, and after biliary drainage can be a significant cause of
morbidity and can potentially be avoided by nasogastric or intravenous (IV) infusion of normal saline or Ringer's
lactate along with a systemic dopamine infusion.
4. Obtain informed consent after discussing expected complications and outcomes. Use this opportunity to
educate and establish a positive relationship.
5. Establish IV access for medications and hydration.
6. Administer preprocedural antibiotics within 1 hour of the start of the procedure; antibiotics given before that
time or after the procedure is completed have decreased effectiveness. This is particularly important if there is
clinical evidence of infection or suspicion of any degree of obstruction. Cultures from obstructed biliary systems
are positive in approximately 50% of cases. The most common organism continues to be Escherichia coli
especially extended-spectrum betalactamase (ESBL)-producing E. coli (4). Recommendations for antibiotic
coverage include
a. A carbapenem (e.g., ertapenem 1 g IV) because they cover many of the organisms found in biliary cultures
b. A fluoroquinolone: ciprofloxacin 500 mg IV, levofloxacin 1 g IV, or moxifloxacin 400 mg IV
c. Unasyn (ampicillin plus sulbactam) 3 g IV
7. Follow institution's guidelines for food and clear liquid consumption prior to sedation or anesthesia. General
anesthesia is recommended for PBD. There have been studies suggesting that IV sedation is adequate for PBD;
however, given our anecdotally poor experience with sedation, especially when the case gets long and difficult,
we prefer general anesthesia unless there is a compelling reason to avoid it. The most common guidelines are
no food or non-clear liquids for 6 hours and clear liquids up to 2 hours before the procedure.
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Procedure
Percutaneous Transhepatic Cholangiography
1. Position the patient supine.
a. Abduct the right arm onto an arm board. To avoid brachial plexus injury, do not abduct it more than 90
degrees if the patient is under general anesthesia.
b. Ensure that the C-arm rotates freely around the patient at the level of the liver from at least 40 degrees
right anterior oblique (RAO) to 40 degrees left anterior oblique (LAO).
2. Perform a quick ultrasound survey of the upper abdomen and right lower chest.
a. Confirm that liver anatomy and pathology are as expected.
b. Outline the area for skin preparation. Be generous. Include the entire epigastrium to the navel, the right
upper quadrant above and below the costal margin, and the entire right lateral chest wall from the
diaphragm to the tip of segment 5. Think not only about where your needle is expected to enter the skin but
also of other potential puncture and ultrasound probe placement sites.
3. Clean and drape the skin in sterile fashion.
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4. Perform a “Time Out” to make sure that the patient, procedure, and location are correct; that any desired
antibiotics have been administered; and that sedation is appropriate.
5. Ductal puncture
a. Locate the target with ultrasound.
b. Administer local anesthetic (1% lidocaine) at the puncture site. Generously inject from the skin through
the subcutaneous (SC) tissues, muscles, and peritoneum and then into the very sensitive liver capsule.
c. The duct is adjacent to the portal vein and artery. If the duct is not dilated, use the portal vein as your
target. The relationship of the duct to the vein is unpredictable, so multiple passes may be necessary.
d. Left duct puncture
(1) The epigastric approach avoids problems that can occur when crossing the pleural space. Entry into a
peripheral portion of the duct reduces the chance of crossing a large central vessel and allows easier
placement of drainage catheters.
(2) The safest target is the segment 3 duct, which is inferior and anterior to the segment 2 duct. In addition,
the duct is often just slightly anterior and superior to the portal vein, which makes it a safe target (Fig. 52.1).
(3) Start scanning transversely and then rotate the transducer until it is parallel to the segment 2 and 3
ducts (see Fig. 52.1).
(4) The needle can then be placed into the liver in the plane of the transducer and monitored for its entire
passage through the epigastric tissues and liver to the duct (Fig. 52.2). Make absolutely sure, before your
needle enters the liver, that the trajectory is in the plane of the duct you wish to enter. If you are close
enough, even if the needle fails to enter the duct, you will only need to pull back 1 to 2 cm to redirect the
needle. The goal is to cross the liver capsule once.
(5) The needle is usually passed a few millimeters deep to the duct, and a slow, high magnification pullback
injection of contrast is performed. A mixture of 7 mL contrast to 3 mL saline is easily seen yet not so dense
to obscure repeat attempts if there is parenchymal staining.
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FIGURE 52.1 • The transverse scan in the epigastrium shows the segment 3 duct (arrow) with-out color
flow immediately anterior to the red portal vein.
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FIGURE 52.2 • The needle (arrow) is entering parallel to the transducer and is well seen passing from the
skin (upper right side of image) down to the tip, which is just anterior to the segment 3 duct.
(6) During the pullback injection, use rapid, small intermittent “puff” injections to produce a continuous tract
barely wider than the needle tip. Contrast in the portal vein or hepatic artery will clear toward the periphery
of the liver, clear rapidly and completely, and result in a parenchymal stain in the peripheral distribution of
the vessel. Contrast in a bile duct will clear centrally, clear slowly, and not cause staining (Fig. 52.3).
Contrast in a hepatic vein will clear in a cephalad and central direction, clear rapidly, and not cause
staining.
(7) Overinjection of infected biliary ducts is the most common cause of sepsis during a PTC and must be
avoided. If you begin to see tiny peripheral ducts and slight sinusoidal staining when injecting into a duct,
stop immediately and reassess what you are doing and what you need to see or accomplish.
(8) If there is an obstruction, take a specimen for culture and then advance a catheter to the obstruction
(Fig. 52.4) to make small injections and decide on therapy.
(9) If there is no obstruction, obtain images in multiple projections. Ensure that contrast clears from the
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ducts and the bowel.
(10) When the cholangiographic findings are indeterminate, a pressureflow study, a variation of the urinary
Whitaker test, can be done (Chapter e-88). We often follow a simplified protocol of 10 mL per minute for 20
minutes taking pressures at baseline then every 2 minutes. Obstruction is present if there is ductal dilatation
associated with a pressure rise above 15 mm Hg (20 cm saline if using a manometer).
e. Right duct puncture
(1) Whenever possible, aim for segment 5. One great benefit of puncturing into a segment 5 duct is that
gentle contrast injections plus gravity will show you all of the other ducts in the right lobe except for the most
anterior ducts in segment 8. That is often very helpful in accurately defining the extent and severity of any
obstructing process. In addition,
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a segment 5 approach often allows an approach from below the right anterolateral costal margin. In
addition, if an intercostal approach is required, it can usually be made anterior to the midaxillary line. If at all
possible, it is advisable to stay below the 10th rib and anterior to the midaxillary line in order to minimize the
chance of traversing the pleural space. If you go through the pleural space, the negative intrapleural
pressure of each inspiration can suck in blood, bile, air, and even carefully secured catheters.
FIGURE 52.3 • On the second pass, as the needle was being withdrawn, the duct was entered as seen by
contrast clearing centrally, very slowly. The contrast reached an obstruction and then went peripherally into
a second duct. This was adequate to define the anatomy and further injection was not warranted.
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FIGURE 52.4 • A 5 Fr. sheath was placed in the duct. A 4 Fr. catheter was advanced part-way through the
obstruction and an injection done until all of the ducts were seen but no staining had occurred. There are
multiple strictures, likely ischemic, at the junction of the segment 2 (long arrow) and 3 (short arrow) ducts,
several segment 4 (curved arrow) branch duct origin stenoses, and a patent duct-to-duct anastomosis (fat
arrow) that bends 180 degrees to flow back through the common bile duct (CBD) to the duodenum.
(2) If you are making an intercostal puncture, rotation of the transducer is limited to a few degrees in the
plane of the intercostal space, but it is important to keep the transducer in that space so you don't lose the
needle tip behind a rib. Before puncturing, select the best target. Look for a duct bifurcation in segment 5 to
find a three-dimensional chance of a duct with one pass.
(3) If you go through the intercostal space, stay as close as possible to the superior aspect of a rib to avoid
blood vessels, and, as you go through the intercostal space, consider injecting extra local anesthetic,
especially 0.25% or 0.5% bupivacaine, which can cut down remarkably on postprocedure discomfort.
(4) The left-sided ducts often do not fill after right duct contrast injection in supine patients, particularly if
there is no obstruction. The left ducts can be seen by injecting air or CO2 in the supine patient or by
injecting more contrast and carefully rotating the patient left side down.
Percutaneous Biliary Drainage
1. After ultrasound-guided fine needle (usually 21-gauge or 22-gauge) puncture of a duct, perform a careful
preliminary contrast injection with at least two oblique views to define the needle position and the angle of
entry into the duct. If necessary, use the first needle for contrast injections to visualize a better entry point,
which can be punctured under fluoroscopic guidance.
2. Advance a 0.018-in. wire into the bile duct. Use a short (35 to 60 cm) 0.018-in. nitinol wire with a gently
curved soft platinum tip. If you can get this wire into the ducts, its stiffness will make the following steps
much easier.
a. If it does not advance, stop, think, and be patient, which is an undervalued step and is often the key to a
successful procedure. The angle between the needle and the duct may be too obtuse (close to or greater
than 90 degrees), the wire may be travelling parallel to the duct but not actually be inside the duct but
instead in the portal triad tissue, there may be severe scarring in the duct, or the wire may be travelling
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through or around the duct in the needle tract. Take time to get oblique views and then, if necessary, repeat
the puncture in a position and/or alignment that gives you improved access to the ducts.
(1) Consider increasing the fluoroscopic magnification, pulse rate, and dose.
(2) Use multiple angles, especially use cephalad and caudad angles, which are an accurate and quick way
to use parallax to help you figure out if you are short of the duct, or through it, with your needle and wire.
b. Anytime you get a needle into the ductal system and can opacify the ducts, do not move it. If you cannot
advance a wire and are getting frustrated, resist the temptation to just pull the needle back a little and
redirect it. Instead, leave the needle where it is, use it to opacify the ducts, and repuncture with a second
needle.
c. “Dance” the wire out of the needle with gentle twirling movements. If it buckles or hits resistance, stop,
pull back, and try again.
d. In sclerosing or ischemic cholangitis, or any case in which the nitinol wire will not advance, switch to a
0.018-in., 0.016-in., or 0.014-in. hydrophilic wire.
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3. Advance a triaxial set into the ducts by spinning more than pushing, and making sure not to push the
metallic stiffener past the straight part of the tract.
4. Place a floppy or Rosen wire (Cook Inc, Bloomington, IN) into the ducts. Leave the 0.018-in. guidewire in
place until the entire procedure is completed. A safety wire is a must for all biliary procedures.
5. Insert a 5 Fr. or 6 Fr. sheath into the ducts. Decompress the ducts by allowing bile to flow out of the
sheath sidearm, and take a bile sample for culture. It is very helpful to leave the sheath sidearm open
throughout the procedure to help keep intraductal pressures down, which will help prevent postprocedure
sepsis.
6. Navigate a 4 Fr. or 5 Fr. glide catheter to the point of obstruction or leak. Do careful limited contrast
injections (see Fig. 52.4) at the obstruction site in at least two projections. If the patient is unstable or the
obstruction cannot be easily crossed, consider placing a locking pigtail catheter above the obstruction.
a. A 6 Fr. pigtail for pediatric patients or when you wish to limit the size of the tract
b. An 8 to 10 Fr. pigtail for most adult patients
c. A 12 to 14 Fr. pigtail in patients in whom future percutaneous transhepatic interventions are planned
(e.g., biopsy or stone removal) and especially any conjoint procedures in which an endoscope may be used
7. Alternatively, cross the obstruction or leak point and place an internal-external catheter.
a. You can perform balloon dilation or metallic stent placement during the first procedure, but only if the
patient and the bile are not visually or clinically suspicious for infection.
8. Tips for complex or multilevel strictures
a. Do a rotational, digital, nonsubtracted ductogram to define precisely the course of the lumen through the
stricture.
b. Insert a 6 Fr., 25 cm long sheath 2 to 5 cm above the obstruction to allow more forward force on a coaxial
catheter.
c. Try different guidewires. Workhorse wires are a straight, floppy tip wire and the 0.035-in. curved tip
hydrophilic wire. If they fail, then consider a 0.035-in. straight hydrophilic wire or a coaxial microcatheter
with a 0.014-in. or 0.016-in. steerable wire.
d. Try different catheters including unformed reverse curve catheters, and reverse curve catheters (Sos
Omni Selective Catheter, Angiodynamics, Latham, NY) with the entire reversed tip part cut off so that you
have a catheter that looks like a “C” curve at the tip with the “C” cut the way you want it so that it points the
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direction you want to go.
e. Inflate a balloon occlusion catheter near the stenosis allowing contrast to be forced through the lumen of
the stenosis. While injecting through a “Y”-adapter, maneuver or “float” a 0.014-in. or 0.016-in. steerable
wire through the stenosis.
f. Puncture the duct on the other side of an uncrossable stenosis and cross the stenosis in a retrograde
direction, then snare the wire, create a through-andthrough wire, and finish off the procedure antegrade
(Fig. 52.5A-C).
9. If all attempts to diagnostically or therapeutically enter the biliary system have failed, consider a puncture
of the gallbladder. Obviously, this access will not work for most problems, especially intrahepatic ones, but
for common duct or ampullary problems, it can be a very helpful solution.
10. Secure the catheter to the skin.
a. Get a large bite of skin and subcutaneous tissue to decrease the chance of the suture “pulling out” of the
skin.
b. Put the metal stiffener into the catheter, then tie around the catheter with a slip knot to get a good “bite”
on the catheter, followed by square knots to lock it in place. Do not tie the knots so tight that the stiffener
cannot be pulled out or so that the lumen flow is compromised.
c. Put on the dressing so that there is no tension on the suture.
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Biliary Stricture Dilation and Self-expanding Metallic Stent Insertion
In this section, the term stent will be used to refer to a self-expanding metal stents. Stents will be classified
as “bare” or “covered.” If a catheter is the only device used to “stent” open a duct, it will be referred to as a
“catheter” and not a “stent.” Consistent with the wording in the current literature, plastic tubes placed into
the biliary ducts by ERCP will be called “plastic stents.”
Techniques for treating strictures include percutaneous techniques (e.g., dilation and internal-external
catheter), endoscopic techniques (e.g., sphincterotomy, removable stents, multiple plastic stents), or
surgical revision. There are no accepted indications for percutaneous placement of internalized plastic
stents. Stricture dilation and catheter placement are the only accepted percutaneous technique for treating
benign strictures. Multiple attempts to develop a reliable, percutaneously deployed, removable, or
biodegradable stent have not been successful to date. Malignant strictures are generally treated with
stents; and benign strictures are currently treated without stents due to their limited duration of patency.
Bare stents are often adequate for compressive tumors and suffer less frequent problems with intra-stent
obstruction by debris. Covered stents are used for invasive tumors.
1. Stricture dilation
a. Place a sheath large enough for the expected balloon.
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FIGURE 52.5 • In this patient with severe sclerosing cholangitis, ERCP and initial antegrade PTD failed. An
internal “rendezvous procedure” was performed. A: Cholangiogram demonstrates five areas of occlusion.
1) The junction from the left central duct to the common hepatic duct
2) The distal common bile duct leading to the duodenum (A-C)
3) The junction between the left duct and the right duct
4) The junction between the anterior and posterior right ducts
5) The junction between an isolated right duct and the common right duct
B: With the injected contrast as a guide, the slightly dilated portion of the common duct just above the
ampulla was punctured under fluoroscopic guidance with a cephalad angled 21-gauge needle. (continued)
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FIGURE 52.5 • (Continued) C: A 0.014-in. wire would not advance through the complex stricture, so it was
replaced with a microcatheter over a stiff 0.014 wire and the catheter advanced until the wire tip could be
grabbed by a snare placed through an antegrade approach in the right duct. Similar intervention to cross
the remaining occlusions was performed and four retrograde ERCP stents kept in place for 9 months.
Patency was demonstrated on a MRCP 8 years later.
b. Dilation of ductal strictures

(1) Choose a high-pressure balloon with a maximum of 20% oversizing to avoid rupture, which can cause
bleeding or a bile leak.
(2) If balloon dilation fails, use a non-oversized cutting balloon then another high-pressure oversized
balloon, shooting for the 20% oversize limit.
c. Dilation of anastomotic strictures
(1) The tissue at a surgical anastomosis is fibrotic and may have fibrous tissue encasing it. Therefore,
leaks, if they do occur, usually remain contained.
(2) Utilize high-pressure balloons, which can safely be oversized by 20% to 30%.
(3) Cutting balloons sized to the adjacent duct may be helpful in refractory stenoses.
(4) If the stenosis is truly refractory, it may be due to an overly exuberant tissue response to the dilation
injury that results in some hyperplasia. There is currently no good solution. Drug-eluting or drug-coated
balloons may be useful in such situations, and the best answer in the near future may be absorbable, drug-
eluting stents.
(5) If you dilate an anastomosis and the stenosis seems to recur immediately or within 48 to 72 hours,
consider the following:
(a) Elastic recoil, which may not be dynamically important, which a pressure-flow (Whitaker) study may
prove; or it may be a dynamic flowlimiting problem and may respond to either very prolonged dilation for 20
to 30 minutes, or to placement of a removable metallic stent for 4 to 6 months, which may need a conjoined
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procedure with endoscopy to remove it. Prior to placement of a removable stent, ensure an endoscopist is
available to facilitate removal from below or through your transhepatic tract when appropriate.
(b) Two techniques to evaluate the anastomosis
i. Leave the balloon almost fully inflated in the anastomosis but with “zero” pressure in the gauge. Using a
digital nonsubracted angiographic technique, start injecting contrast through the sheath
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until ducts fill. Suddenly push the inflate balloon forward over a super stiff wire into the bowel, which pulls a
flush of contrast through the anastomotic opening showing it true size.
ii. With the balloon above the anastomosis, gently inflate the balloon, remove the wire, and do a rapid-flow,
balloon-occluded injection from the duct.
(6) To keep a fibrotic, narrowed duct or anastomosis open with a catheter after dilation would require a
larger diameter catheter than is typically used. Capping a smaller catheter and using the flow of bile around
the catheter to keep dilated strictures open is a priority.
d. After dilation, insert an internal-external catheter. To keep a fibrotically narrowed duct or anastomosis
open with a catheter after dilation would require a bigger diameter catheter than we would typically use, so,
because we do not have good options for a removable or biodegradable stent, capping the catheter and
using the flow of bile around the catheter to keep dilated structures open should be a high priority.
e. Biliary stone removal is often performed at the same time as dilation. Methods include
(1) Over dilation of the ampulla to allow stones to be pushed or flushed into the bowel
(2) Dilation of the tract to accommodate a large sheath and a percutaneous basket, with which the stones
can be “crushed” and removed through the sheath.
(3) Combined endoscopic procedures where the transhepatic tract is dilated to accommodate a flexible
endoscope, with which the stones and debris are pushed or flushed under direct vision into the bowel or
pulled out in a basket.
(4) If there is a well-developed percutaneous or T-tube tract (at least 6 weeks), stones can be removed
through the tract using a basket or can be fragmented with a basket, laser, or intracorporeal lithotripsy and
either flushed internally or removed via the tract.
f. Stricture biopsy can also be done through the same percutaneous access using a long sheath and a
standard cardiac biopsy forceps. Newly available “steerable” sheaths may be an important advance for this
technique.
2. Self-expanding metallic stent insertion
a. Define the length of the stenosis, the ductal diameter above the stenosis, and the proximal and distal
landing sites.
b. Choose the stent length so that there is at least 1 cm of stent expanded above and below the stenosis.
For rapidly growing tumors, use a longer stent to delay overgrowth.
c. Stents of 7- to 10-mm diameter are usually appropriate for intrahepatic ducts and 10- to 12-mm stents for
the common duct.
d. If possible, the upper landing zone should be below the first ductal bifurcation. The lower end of the stent
may be kept above the ampulla to decrease reflux and secondary cholangitis. However, the ampulla can be
easily obstructed by stent-induced debris or bleeding, tumor growth, or by mechanical distortion due to the
stent; so, if the lower end of the stent or the tumor is close to the ampulla, or the tumor is invasive or rapidly
growing, stenting across the ampulla would be prudent.
(1) If the stent extends into the duodenum, it is important to prevent it from protruding into the opposite
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duodenal wall. If the duodenal lumen is narrowed or the opposite wall is hard to avoid, extending the stent 2
to 3 cm into the lumen of the duodenum is recommended.
e. Somewhat surprisingly, it seems that bare metal and even covered stents can be placed across the
cystic duct, pancreatic duct, and biliary duct origins with acceptable complication rates.
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f. Predilate rigid strictures with a balloon 2 to 3 mm smaller than the stent to avoid stent migration. Also, a
smaller balloon will cause less bleeding, which can result in stent occlusion. Deploy the stent then check
position and flow with gentle injections through the sheath in at least two projections.
g. Intrahepatic bifurcation tumors
(1) Through a unilateral approach, stents can be placed so that they drain one side only, or placed to drain
both sides using a “T” configuration.
(2) Using a bilateral approach, stents can be placed from both sides in a “Y” configuration.
(a) Use kissing balloons prior to bilateral “Y” stent placement.
(b) “Y” stents are best deployed simultaneously rather than sequentially.
(c) As technically challenging as these “T” and “Y” stents are, with careful attention to detail, excellent
outcomes can be obtained (5).
h. Place a drainage catheter above the stent(s) and cap it unless there is bleeding.
1. Following cholangiography, bed rest for 2 hours. After stricture dilation, most patients can be managed as
outpatients with discharge after 4 to 6 hours of observation once the risk of postprocedure sepsis is reduced.
a. Follow your hospital's guidelines for discharge after sedation. The patient should be driven home by a
responsible adult.
b. The patient should be instructed to seek medical attention for new or worsening chest or right upper quadrant
pain, dyspnea particularly with deep breathing, shortness of breath, symptoms of infection, or red or tarry stool.
These typically occur 1 to 72 hours after the procedure.
2. After drainage
a. Monitor vital signs every 30 minutes for 1 hour, then every hour for 4 hours, then every 6 hours for 24 hours,
and then as needed, usually every shift. If there is a concern for sepsis, more frequent vital signs may be needed
and the patient may need to be in an intensive care unit (ICU).
b. Check CBC and cultures (blood and bile) as needed.
c. Check liver function tests daily for 2 to 3 days then every 2 to 3 days until a clear trend emerges. This is
especially important if they were markedly elevated because the speed with which laboratory values normalize
can be an indicator of the adequacy of drainage; and a slow or minimal correction or worsening of the laboratory
values can indicate inadequate drainage, which should be immediately evaluated and corrected; or it may
indicate severe hepatocyte damage, which may not be correctable.
d. Order appropriate follow-up tests including cholangiograms, dilations, or other procedures.
3. Catheter care
a. There are no guidelines or “best practice” clinical processes available for catheter management. You will need
to develop institutional guidelines.
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b. Take the time to write detailed orders about catheter care, skin care, and dressing changes. Communicate
with the treatment team including physician who will be taking care of the patient in the hospital and the patient's
hospital nurse.
c. Site cleaning with a bactericidal or antiseptic solution such a Betadine (povidone-iodine), carefully drying the
site with sterile gauze, and a dressing change daily, or more frequently if needed, all play an important part in
preventing skin infections and potentially even cholangitis.
d. Record the output every 8 hours in the hospital and daily at home.
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e. If the catheter is capped, flush it gently with 10 mL of normal saline over 10 to 15 seconds at least every other
day. Do not aspirate.
f. If the catheter is to gravity drainage, it only needs to be flushed gently with 5 to 10 mL of normal saline if
drainage stops. If drainage does not start again immediately, an IR study of the catheter is recommended.
g. Leakage around the catheter, leakage or pain with flushing, or a significant change in output or position of the
catheter require an IR evaluation.
h. If a catheter remains in place chronically, it should be changed at least every 3 months.
4. Education
a. Teach the patient and any caregivers how to monitor for fever, right upper quadrant pain, abdominal or chest
pain, respiratory status change, or pain or erythema around the catheter site.
b. Provide the patient or caregivers with the appropriate contact information so that if they are worried about any
of the signs mentioned previously, they can communicate directly with IR so that timely corrective measures can
be taken.
c. Providing printed information, such as that available from the Society of Interventional Radiology (SIR), is
especially valuable for complex patients such as these.
5. Follow-up studies
a. After stricture dilation, perform a cholangiogram after the acute swelling has resolved, usually 3 weeks after
stricture dilation. A recent study of benign postoperative strictures showed that simply placing a percutaneous
drain across the stricture and waiting for 4 to 6 weeks, will often allow the edema or mechanical problems to
spontaneously relax (6). In their study, they saw that a somewhat surprising 72% of such cases resolved without
further treatment.
(1) Do a pressure-flow study if there is a question of persistent obstruction.
(2) If the result is adequate, place a capped drainage catheter above the stenosis. Schedule lab studies and a
cholangiogram follow-up in 2 weeks.
(3) If a repeat dilation is needed, use a cutting balloon or larger high-pressure balloon, or both.
b. After stent placement
(1) Do a follow-up cholangiogram and possible catheter removal in 2 to 4 weeks.
(2) In immunocompromised or very sick patients in whom the ability to repair the tract may be impaired, it is best
to wait 6 weeks, and even then to do a tract study before removing the final wire.
(3) Liver function tests (LFTs) and clinical evaluation should be obtained in all patients between 3 months and 6
months after external catheter removal.
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Results
1. The technical success for performing a cholangiogram, which means getting a needle into a duct and
injecting contrast into the duct adequate to make a diagnosis, should be greater than 95% in patients with
dilated ducts and by published standards be greater than 65% in patients with nondilated ducts (7). Using
careful ultrasound-guided techniques, using the portal triad as a target, being patient, and filling the needle
with contrast as much as possible before injecting to minimize the injection of air, the technical success rate
in patients with nondilated ducts should actually be much higher, closer to 90%. This is the reported
technical success rate in modern reports of patients with nondilated ducts and will hopefully improve even
more with the fused guidance techniques that are emerging.
2. Drainage should be established in greater than 90% of bile ducts that have been successfully cannulated
and opacified (7).
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3. In patients with a bile leak due to surgery, particularly laparoscopic cholecystectomy injury, percutaneous
drainage transhepatically through the ducts and percutaneously into the biloma if needed can successfully
resolve the acute problem in 90% or more. However, most of these injuries are severe enough that surgery
is required for final correction. Having the percutaneous catheter as a marker of the duct location is,
however, critical to the surgical success.
4. Dilation
a. Data are limited for the usual potpourri of benign strictures in nontransplant patients, but a recent report
suggested that a clinical success rate of 76.5% can be achieved with current percutaneous techniques (8).
(1) Reported technical success—100%
(2) Restenosis rates at anastomotic and nonanastomotic sites are similar— except in transplant
anastomosis where results depend on site and method of treatment.
(3) Overall secondary patency rates range from 45% to 80% (8).
(4) Ischemic ductal or perianastomotic strictures secondary to transplant arterial compromise fare much
more poorly with a secondary patency at 12 months of 0% (9).
5. Stent placement
a. Recent reports have partially clarified the respective roles and success rates for bare stents, covered
stents, and ERCP plastic stents for malignant disease. Almost all investigators of covered stents mention
specifically that the complication rates, especially cholecystitis and pancreatitis, are not worse for covered
stents. However, this assertion must be received with caution because the number of patients in all these
studies is small, and if a case of cholecystitis or pancreatitis is reported, it is almost always in the covered
stent group. For this reason, when placing covered stents, these complications should be reviewed during
informed consent. In addition, if you evaluate the biliary stent studies in both the percutaneous (metal
stents) and ERCP (plastic stents and bare and covered metal stents) literature, you need to be careful
about comparing the median stent patency data because it is clear if you look at the patency and survival
data for each study that they are dealing with very disparate patient populations in which the survival times
often differ markedly.
b. ERCP results from several studies including a recent prospective randomized trial have shown that either
bare or covered metal stents are superior to plastic stents with significant improvement in median patency
rates (385 days vs. 153 days) and a concomitant reduction in cholangitis (4.9% vs. 24.5%) and additional
procedures (10).
c. In much of the ERCP literature, including a recent prospective, randomized, double-blind study, there
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does not appear to be any significant differences between covered and bare stents in the median patency
rate (153 days vs. 127 days), median patient survival (154 days vs. 157 days), or complications of which
there were only two, sepsis and pancreatitis, both of which occurred with covered stents (11).
d. Fortunately, there have been larger and better studies done of percutaneous stents in recent years, and
the clinical and technical results are impressive. Technical success rates are almost always 100%, and with
the new biliaryspecific coatings, the complications and problems have decreased substantially. Unlike the
ERCP literature, a recent prospective trial of percutaneously placed covered or bare stents suggests that
the mean patency of bare stents (413.3 days) was significantly longer than covered stents (207.5 days)
(12). Overall survival was similar for bare (359.9 days) and covered (350.5 days) stents. Although minor
complications of tumor overgrowth and obstruction by debris occurred in both groups, only bare stents also
suffered from tumor ingrowth, whereas only covered stents suffered from stent migration
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and the one case of cholecystitis. It must always be kept in mind that stents in the bile ducts, especially if
they extend into the duodenum are subject to many biologic and mechanical problems that can result in
obstruction. Even with modern technology, if patients live long enough, stents will inevitably become
obstructed.
e. The fear of placing a metal stent into infected bile has prevented most operators from placing the stent
on the first procedure. However, if it were possible, the benefits could be many including fewer procedures,
fewer sedation or anesthesia events, fewer or no days with an external catheter, lower cost, decreased
hospital resource utilization, and fewer nonproductive days for the patient. In a recent retrospective study,
not only did stent placement on the first procedure fare better than a staged approach but also actually
seemed safer as well (13). Such a result warrants follow-up with a prospective randomized trial.
6. Stone removal. Overall success rates have been around 90% or greater historically and are similar in a
more recent studies using techniques and instrumentation that have not changed substantially.
Complications
Percutaneous Transhepatic Cholangiography
Major complications (2%). A complication rate of 4% should prompt a review of technique (7).
1. Bleeding
a. Subcapsular or peritoneal
b. Pleural (only with right-sided punctures)
c. Biliary
2. Infection
a. Cholangitis
b. Sepsis
3. Bile leak
a. Peritoneal
b. Pleural (only with right-sided punctures)
Percutaneous Biliary Drainage
Major complications (8%) with rates for individual complications ranging from 0.5% for pleural complications
to 2.5% for both sepsis and bleeding (7). In addition to the complications listed for PTC, the following
complications are more specific to PBD:
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1. Ductal perforation with secondary bile leak, extravasation, or bleeding
2. Catheter complications
a. Obstruction
(1) Debris, blood, or mucus
(2) Kinking and suture problems
b. Dislodgment
3. Delayed infection
a. Delayed recurrent cholangitis
4. Delayed bleeding
a. This is often due to a growing pseudoaneurysm, which can bleed into an adjacent duct and present as a
gastrointestinal (GI) bleed.
b. Bleeding from the drainage catheter
Percutaneous Stricture Dilation and Self-expanding Metallic Stents
1. Early (<30 days) complication rates range from 7% to 35%.
a. Balloon-induced duct rupture or bleeding
b. Stent misplacement
c. Pancreatitis, cholecystitis, or cholangitis
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2. Late (>30 days) complication rates range from 18% to 60%.
a. Stent occlusion
(1) Tumor ingrowth or overgrowth
(2) Debris, blood, or stones
b. Stent migration
c. Infection or cholangitis: usually due to stent obstruction
d. Jaundice: usually due to stent obstruction
1. Pleural fluid. Chest tube placement is usually required.
2. Bleeding. Most bleeding is self-limited; however, if there is increasing discomfort, signs of blood loss
(e.g., tachycardia, hypotension), or the patient becomes restless, initiate standard measures for active
internal bleeding:
a. Make the patient nil per os (NPO) except for necessary medications. Obtain blood tests (CBC, platelets,
INR, renal, and liver function tests). If bleeding is symptomatic, persistent or severe, crossmatch the patient
for at least two units of packed red blood cells.
b. Ensure there is good IV access and give normal saline at 500 mL per hour.
c. Correct coagulation problems.
d. Consider ICU admission.
e. Begin continuous monitoring with at least blood pressure (BP) and pulse oximetry. Add an
electrocardiogram (ECG) if there is any cardiac history.
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f. Manage moderate or severe pain and anxiety with IV medications such as midazolam (Versed) and
fentanyl.
g. Imaging
(1) If the renal function allows, a contrast enhanced three-phase CT scan should be performed.
(2) A limited right upper quadrant ultrasound is useful to monitor the subcapsular or perihepatic space.
h. Bleeding into or around the catheter may be due to a side hole in the tract where a blood vessel was
crossed. A gentle contrast injection will often show filling of a vascular structure. Advancing the catheter will
stop most bleeding of this type because it is usually from a small vein and will often heal completely just by
tamponading the site with the catheter for several days.
(1) If tract tamponade is unsuccessful, the bleeding may be from an artery or larger portal vein branch.
i. If there is continuous major bleeding or an episode that stops then recurs within 24 to 48 hours, do an
arteriogram concentrating on the area where the punctures were done.
(1) The most common finding when a vessel has been lacerated is a sudden cutoff. Coil embolization, distal
and proximal to the bleeding site, is the most effective way to get control. If the site is difficult to reach, coil
embolization proximal to the site, or Gelfoam or large particle embolization of the general area may be
effective.
(2) If there is no definite leak or abnormality, remove the drainage catheter over a wire and repeat the
arterial injection. Quickly reinsert the catheter to tamponade the site and perform embolization in the manner
described earlier.
(3) If embolization fails or the patient is unstable, remove the catheter and at the same time embolize the
tract. A combination of coils and Gelfoam plugs can be used. An elongated, slightly oversized Amplatz Plug
or similar vascular occlusion device would also be a good substitute. If there is time, use the existing
catheter to opacify the ducts and establish new percutaneous access before you sacrifice the old.
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j. Balloon-induced bleeding
(1) Gentle (low pressure of 2 to 5 atm) intraductal balloon inflation for 15 minutes.
(2) Repeat for 30 minutes if needed.
(3) If balloon tamponade fails, consider a covered stent insertion, which has been a life-saving maneuver for
us on two occasions when ballooninduced rupture of pericholedochal varices caused massive bleeding into
the common duct.
(4) Balloon-induced duct rupture without bleeding will usually heal with adequate external drainage. Internal
drainage does not work as well.
3. Infection
a. Cholangitis is usually adequately treated with a 7- to 10-day course of antibiotics.
b. Sepsis mandates an ICU admission.
c. If bile is cultured in an asymptomatic patient with a chronic catheter, it will usually yield a positive result
often polymicrobial. In general, because these catheters often communicate with the bowel as well as the
skin along the pericatheter tract, “positive cultures” are not treated unless it is a “large” growth or the
patient is symptomatic. Symptoms of cholangitis can be very subtle, and even minor changes in appetite,
energy, or mood; or pain in other body areas, particularly joints, can be indicators of a smoldering infection.
4. Cellulitis or infection at the catheter site
a. Check the catheter for misplaced side holes. What may look like “pus” around the catheter may be
infected or cloudy bile.
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b. Replace sutures if erythema seems to arise from them or replace them with some type of sutureless
retention device.
c. Treat skin problems with twice daily antibiotic or antiseptic scrubs and dressing changes.
d. Catheter-related
(1) Obstruction of the catheter, or even sluggish drainage, requires a cholangiogram and, frequently,
replacement.
(2) Dislodgment requires rapid evaluation. If the catheter has come out of the liver entirely, the tract will
close within hours unless it is chronic.
5. Stent occlusion
a. Perform a new PBD.
b. Recanalize or replace the stent.
c. Given the terminal status of many of these patients, a simple internal-external catheter often suffices.
Percutaneous Cholecystostomy
Although not commonly performed, when cholecystostomy is requested, the situation is always emergent and
complex. The benefits are typically immediate and pronounced. However, these patients are usually very sick,
and their eventual course, whether to surgery or to a nonsurgical outcome, is fraught with problems and
setbacks. Once you place a catheter in their gallbladder, these patients deserve and need your continued
involvement.
Indications
1. Cholecystitis in a patient who is temporarily or permanently a poor surgical candidate.
2. Unexplained sepsis in an ICU patient when other sources have been excluded
3. Access to the biliary tree is required for intervention and other methods to obtain that access, including
PBD have failed (14).
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Contraindications
Absolute
Most patients requiring percutaneous cholecystostomy are so ill; there are no absolute contraindications.
Relative
1. Coagulopathy or antiplatelet or anticoagulant medication
2. Ascites
1. As described for PBD
2. Define the gallbladder anatomy by ultrasound or CT.
Procedure
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1. The procedure can be performed entirely under ultrasound guidance, even portably.
2. Repeat the ultrasound imaging to confirm the anatomy and plan the approach.
3. Do a sterile skin preparation and drape the patient and ultrasound transducer.
4. Inject lidocaine into the skin and along the entire proposed tract to the liver or gallbladder.
a. Choose an approach that is easiest based on the patient and the gallbladder anatomy.
b. There is debate as to whether a transhepatic or a subhepatic, transperitoneal approach is safer or more
stable. There is little data to suggest that one approach is better than the other and there are advantages
and disadvantages with both. If you use a transhepatic approach, use a blunt needle for the portion of the
tract that goes through the liver to reduce post-cholecystostomy bleeds.
5. Puncture the gallbladder under ultrasound guidance.
a. If you use the Seldinger technique, perform tract dilation and catheter placement under fluoroscopic
control to minimize chances of losing access to the gallbladder, which is unfortunately common when doing
“blind” maneuvers in CT or ultrasound-only procedures.
b. If the tract is going directly through the peritoneal cavity into a distended gallbladder, consider using a 6
Fr. or 8 Fr. trocar catheter so that there is no need to do exchanges of dilators and catheters over a wire.
This will eliminate the problem of bile spill into the peritoneum, which can cause excruciating pain.
c. Direct gallbladder entry can also be made with a “single exchange” technique by puncturing with a 5 Fr.
sheathed needle through which a guidewire is placed followed immediately by catheter placement.
d. If you are using a technique that requires separate placement of dilators and catheters, consider
removing 10 to 20 mL of bile after your original puncture to decrease the intracholecystic pressure and
minimize bile leak.
6. If performing the procedure with fluoroscopy, inject 3 to 5 mL of contrast through the first needle to enter
the gallbladder. This will provide a rough outline of the gallbladder, which is enough to give you confidence
that you are in the gallbladder lumen throughout the catheter placement and that the wall is not so necrotic
that it is leaking even at low pressure. Perform diagnostic injections later when the patient's condition has
improved. Avoid doing things that will cause leaks and sepsis.
7. Curl the soft, floppy wire three or four times in the gallbladder. A floppy wire does not exert undue force
on the wall. Alternatively, a stiff wire advanced only until the stiff portion is in the gallbladder can be used.
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8. If necessary, dilate carefully. Be careful not to push the gallbladder away.
9. Insert an 8 Fr. locking pigtail catheter over the wire with equal care. Keep the metal stiffener unmoving
inside the gallbladder lumen as you slowly “push the catheter off” the wire. Try very hard to advance the
catheter in a full loop so that the pigtail is eventually located back at the lateral end of the fundus. This
gives you the extra length you need to avoid inadvertent dislodgment due to respiratory motion.
10. Secure the catheter to the skin.
11. Take a sample for Gram stain and culture if you haven't already. Although the incidence of and
implications of a positive culture seem very unclear, a positive culture result and sensitivity determination
can be of great value in the management of the patient.
12. Do a limited (5 mL) contrast injection to confirm tube position. If the procedure has been done at the
bedside, a portable radiograph is recommended.
13. Leave the catheter to gravity drainage, not bulb suction. That gooey stuff will plug up the side holes of a
drain catheter very quickly if suction is used.
14. If you are placing a sheath into the gallbladder for a biliary intervention, choose a sheath that is long
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enough so that the tip extends into the neck and the first 1 to 2 cm of the duct. Otherwise, manipulation
through the spiral folds (valves) of Heister can prove to be extremely difficult.
As described for PBD with the following additions:
1. Flush the catheter slowly with 10 to 15 mL normal saline every 6 to 8 hours.
2. If at any time the patient's condition worsens, image the upper abdomen immediately, preferably with CT,
although ultrasound may be adequate.
3. Once the patient has stabilized, perform a cholecystogram with approximately 50% diluted contrast. Assess
the gallbladder, the catheter position, and cystic and common duct patency with particular attention to the
presence or absence of stones and debris.
4. As soon as practical, develop a definitive plan regarding the fate of the gallbladder.
5. If the ducts are patent, the patient is doing well and the decision is made to remove the catheter, consider first
capping the tube for 72 hours to ensure that the patient remains asymptomatic.
a. The tract must be mature before catheter removal. Usually this takes 3 weeks, although 4 to 6 weeks may be
needed for purely transperitoneal tracts.
b. Remove the catheter over a guidewire and insert a 4 Fr. or 5 Fr. sheath. Do a gentle contrast injection as the
sheath is pulled out of the tract. If contrast spills into the peritoneal cavity, the tube should be reinserted and the
procedure repeated in 1 to 2 weeks.
6. If the catheter is left in place, it should be changed every 1 to 3 months.
Results
1. Technical success—95% (15)
2. Most patients improve within 72 hours and the improvement can be dramatic.
3. Patients with gallbladder calculi respond better than those without.
4. Interestingly, the endoscopic ultrasound interventionists have also recently begun to perform direct
transmural gallbladder drainage (16) and have reported results that are comparable to percutaneous
techniques.
5. If the gallbladder is used for a central duct procedure, the results vary widely based on the type of
procedure and the ability to obtain access to the common duct, which can be extremely difficult or even
impossible depending on the anatomy and pathology involving the cystic duct (14).
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Complications
Major complication rates vary from 0% to approximately 10%.
1. Bile leak with peritonitis
2. Bleeding
a. Within the gallbladder
b. From the transhepatic tract
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3. Vasovagal reaction during the procedure due to gallbladder manipulation.
4. Catheter dislodgment. This is a very important issue and a high-frequency, highmorbidity complication.
Anecdotal data suggests that a tract through the liver and bare area may be more stable, but unfortunately,
even under the best of circumstances, it is difficult to achieve a puncture through the bare area due to the
wide anatomic variation in the size and shape of the bare area. However, regardless of the tract that the
catheter follows, a more important issue seems to be respiratory movement of the liver and gallbladder that
slowly tugs the catheter out of the gallbladder. If you notice fairly pronounced respiratory movement of the
gallbladder when you are inserting a drain, put as long a segment of catheter curled in the gallbladder as
possible, and check the position after 3, 7, and 14 days to make sure that you are not losing purchase.
Even wellformed pigtails have been known to “pull out” of the gallbladder, which usually results in a large
leak that may require emergency surgery to correct.
5. Sepsis
1. As for PBD
2. Bile leak
a. If this occurs during the insertion procedure, establish catheter drainage as quickly as possible. Give
extra medication for sedation and pain control. Consider continuing antibiotics for at least 5 to 7 days until
bile cultures are completely analyzed.
b. If due to catheter dislodgment or occlusion, emergent treatment is necessary.
(1) Drain any fluid collections outside the gallbladder.
(2) If gallbladder access has been lost, it must be reestablished.
3. Bleeding
a. Bleeding from the gallbladder wall is usually due to rapid decompression. This can be prevented by
allowing the gallbladder to drain slowly by gravity. If bleeding occurs, it is usually a slow ooze from vessels
in the gallbladder wall, and if enough blood collects in the gallbladder, the resulting low-pressure
tamponade will usually stop the bleeding. The tissue plasminogen activator levels in bile will eventually lyse
the clot and restore normal drainage.
b. Arterial injury in the liver—management as described for CBD
4. Vasovagal reaction
a. Rapid infusion of IV fluids
b. Atropine 0.5 to 1.0 mg IV, if needed
References
1. Iwashita T, Doi S, Yasuda I. Endoscopic ultrasound-guided biliary drainage: a review. Clin J
Gastroenterol . 2014;7(2):94-102.
2. Zhao XQ, Dong JH, Jiang K, et al. Comparison of percutaneous transhepatic biliary drainage and
endoscopic biliary drainage in the management of malignant biliary tract obstruction: a meta-analysis. Dig
Endosc. 2015;27(1):137-145.
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3. Fang Y, Gurusamy KS, Wang Q, et al. Meta-analysis of randomized clinical trials on safety and efficacy of
biliary drainage before surgery for obstructive jaundice. Br J Surg. 2013;100(12):1589-1596.
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4. Kwon JS, Han J, Kim TW, et al. Changes in causative pathogens of acute cholangitis and their
antimicrobial susceptibility over a period of 6 years. Korean J Gastroenterol . 2014;63(5):299-307.
5. Karnabatidis D, Spiliopoulos S, Katsakiori P, et al. Percutaneous trans-hepatic bilateral biliary stenting in

Bismuth IV malignant obstruction. World J Hepatol . 2013;5(3):114-119.
6. Rajab MA, Go J, Silverman WB. Clinical outcome of single plastic stent treatment of benign iatrogenic
biliary strictures: is the outcome predetermined? Surg Laparosc Endosc Percutan Tech. 2014;24(6):e221-
e223.
7. Saad WE, Wallace MJ, Wojak JC, et al. Quality improvement guidelines for percutaneous transhepatic
cholangiography, biliary drainage, and percutaneous cholecystostomy. J Vasc Interv Radiol . 2010;21:789-
795.
8. Janssen JJ, van Delden OM, van Lienden KP, et al. Percutaneous balloon dilatation and long-term
drainage as treatment of anastomotic and nonanastomotic benign biliary strictures. Cardiovasc Intervent
Radiol . 2014;37(6):1559-1567.
9. Saad WE, Saad NE, Davies MG, et al. Transhepatic balloon dilation of anastomotic biliary strictures in
liver transplant recipients: the significance of a patent hepatic artery. J Vasc Interv Radiol . 2005;16(9):1221-
1228.
10. Moses PL, Alnaamani KM, Barkun AN, et al. Randomized trial in malignant biliary obstruction: plastic vs
partially covered metal stents. World J Gastroenterol . 2013;19(46):8638-8646.
11. Ung KA, Stotzer PO, Nilsson A, et al. Covered and uncovered self-expandable metallic Hanarostents are
equally efficacious in the drainage of extrahepatic malignant strictures. Results of a double-blind randomized
study. Scand J Gastroenterol . 2013;48(4):459-465.
12. Lee SJ, Kim MD, Lee MS, et al. Comparison of the efficacy of covered versus uncovered metallic stents
in treating inoperable malignant common bile duct obstruction: a randomized trial. J Vasc Interv Radiol .
2014;25(12):1912-1920.
13. Chatzis N, Pfiffner R, Glenck M, et al. Comparing percutaneous primary and secondary biliary stenting for
malignant biliary obstruction: a retrospective clinical analysis. Indian J Radiol Imaging. 2013;23(1):38-45.
14. Hatzidakis A, Venetucci P, Krokidis M, et al. Percutaneous biliary interventions through the gallbladder
and the cystic duct: what radiologists need to know. Clin Radiol . 2014;69(12):1304-1311.
15. Sosna J, Kruskal JB, Copel L, et al. US-guided percutaneous cholecystostomy: features predicting
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culture-positive bile and clinical outcome. Radiology. 2004; 230(3):785-791.
16. Jang JW, Lee SS, Song TJ, et al. Endoscopic ultrasound-guided transmural and percutaneous
transhepatic gallbladder drainage are comparable for acute cholecystitis. Gastroenterology.
2012;142(4):805-811.
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53
Percutaneous Nephrostomy and Antegrade Ureteral Stenting
Anne M. Covey
Krishna Kandarpa
Introduction
There are four types of percutaneous urinary drainage catheters:
1. Percutaneous nephrostomy (PCN) refers to an external drainage catheter, placed via a flank approach,
positioned in the renal pelvis (Fig. 53.1A).
2. A nephroureteral stent/nephroureterostomy enters the collecting system via a flank approach (like a PCN) with
a locking loop in the renal pelvis, and extends down the ureter terminating in the bladder, allowing both internal
and external drainage (Fig. 53.1B). These catheters are less prone to dislodgment than a PCN, especially in
large patients.
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FIGURE 53.1 • Types of renal drainage: (A) Percutaneous nephrostomy is an obligate external drainage
catheter; (B) nephroureteral catheter can drain both internally and externally; (C) ureteral stent is an internal
device draining into the native bladder; and (D) retrograde nephrostomy, placed via an ileal conduit, drains the
renal pelvis to the urostomy device on the anterior abdominal wall.
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3. A ureteral or “double-J” stent is an internal catheter that extends from the renal pelvis to the bladder and can
be placed in patients who are able to fill and empty their bladder normally (Fig. 53.1C). Stents relieve patients of
the lifestyle limitations associated with an exteriorized device.
4. Retrograde percutaneous nephrostomy catheters are placed through a urinary stoma (i.e., ileal conduit). The
locking loop of the catheter is positioned in the renal pelvis and the hub exits the stoma draining directly into the
ostomy bag (Fig. 53.1D).
Indications (1,2,3,4)
1. Obstructive uropathy including ureteral obstruction from iatrogenic, neoplastic, or inflammatory causes
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2. Urinary diversion
a. Urine leak
b. Vesicovaginal or vesicocolic fistula
3. Access for percutaneous intervention
a. Percutaneous nephrolithotomy
b. Tumor biopsy and/or ablation
c. Stricture dilation
4. Preoperative localization of the ureter
5. Before and after extracorporeal shock wave lithotripsy (ESWL)
6. Following a surgical procedure involving the ureter to maintain patency during healing
Contraindications
1. Uncorrectable coagulopathy—the risk of not performing drainage is weighed against the risk of bleeding
and kidney loss. Specific to antegrade ureteral stents
1. Untreated bladder outlet obstruction
2. Untreated urinary tract infection
3. Spastic or noncompliant bladder
4. Bladder fistula
5. Nonnative bladder
1. Prior to renal drainage, cross-sectional imaging is important to evaluate the presence of hydronephrosis,
anatomic variants (duplication, malposition, horseshoe kidney), cysts, tumors, stones, and/or perinephric
urinoma. On occasion, radionuclide renography can be useful in measuring differential renal function.
2. Patient education should include a description of the procedure, risks and complications, alternative therapies,
catheter maintenance, and long-term plan.
3. Relevant labs include hematocrit (Hct), white blood cell (WBC), platelet count, international normalized ratio
(INR), and creatinine (Cr).
4. Coagulopathy should be corrected to local guidelines. Typical goals include an INR of <2.0 and a platelet
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count >50,000 per μL. Oral anticoagulation should be withheld, utilizing a bridging strategy if anticoagulation
cannot be stopped entirely.
5. Obtain urinalysis and urine culture and sensitivity, if relevant to the case.
6. Nil per os (NPO) according to hospital guidelines to allow safe sedation. Patients can have up to 8 oz of clear
liquids 2 to 6 hours prior to the procedure and are strict NPO for the 2 hours prior.
a. Anesthesia consultation may be considered for patients who have difficulty with prone positioning or with
respiratory compromise that may be exacerbated by prone position.
7. Establish intravenous (IV) access for sedation and preprocedure antibiotic prophylaxis, if needed:
a. Risk stratified appropriate prophylactic antibiotics reduce the rate of infectious complications (5,6).
(1) Patients at low risk are given 1 g of cefazolin IV prior to tube placement.
(2) High-risk patients (including patients with stones) receive ceftriaxone 1 g IV every 24 hours or ampicillin 1 to
2 g IV every 6 hours plus gentamicin at 5 mg per kg IV every 24 hours.
b. Antibiotics are not routinely given after the procedure but may be warranted based on signs of infection.
c. The American Heart Association no longer recommends antibiotics for the purpose of preventing bacterial
endocarditis in patients who are to undergo urinary tract procedures (7).
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FIGURE 53.2 • The two basic shapes of self-retaining drainage tubes. A: Malecot or tulip type. B: Cope self-
retaining loop.
8. Catheter selection
a. Options to consider when choosing catheters for urinary drainage include catheter material, locking
mechanism, size, and shape. The most common materials include hydrophilic- or nonhydrophilic-coated silicone
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or polyurethane. Hydrophilic coating facilitates placement by reducing friction but may promote encrustation
because it is permeable to inorganic salts. Silicone is softer and generally more comfortable for patients, but it is
less strong, requiring a thicker wall to have the same tensile strength as polyurethane (8).
b. A Malecot- or tulip-type locking mechanism is designed so the distal sides of the catheter flare outward (Fig.
53.2A). This occupies less space than a loop catheter and is useful when there is a very small renal pelvis or
when a staghorn calculus fills the renal pelvis. The most common locking mechanism is the Cope or “locking
loop” that is formed by pulling on a monofilament suture that runs through the body of the catheter (Fig. 53.2B).
c. In most cases, an 8 Fr. catheter is sufficient for drainage. In cases of pyonephrosis or hematuria with clots, 10-
Fr. or 12-Fr. catheters may decrease the incidence of catheter occlusion.
Procedure
Percutaneous Nephrostomy
1. Patient position: Prone or prone-oblique when possible. During pregnancy, the patient may only be
comfortable lying on her side.
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2. Fluoroscopy and/or ultrasound are used to determine an appropriate access site which is then prepped
and draped.
3. The skin entry site is along the ipsilateral posterior axillary line, preferably below the 11th rib to avoid
entering the thorax. A subcostal approach is most comfortable for patients.
a. To avoid bleeding complications, the needle path to the kidney should be along “Brodel bloodless line”
(Fig. 53.3). This path, typically 30 to 45 degrees with respect to the table, surface should also avoid other
interpositioned structures such as the liver and colon. Ideally, a posterior lower zone calyx should be
targeted.
b. If the PCN is being placed for treating stones, the choice of the calyx for entry is critical and should be
selected for optimal access to the stone.
c. A direct posterior entry is only useful for opacifying the collecting system; this approach should not be
used to place a catheter as it is uncomfortable for the patient and leads to catheter kinking and poor
function.
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FIGURE 53.3 • Cross-section of kidney showing needle pathway through Brodel avascular line and the
relationship of the anterior and posterior divisions of the renal artery to the renal pelvis and infundibula.
Plane of arterial division is the least vascular area of the kidney and is usually the place where nephrostomy
punctures are performed to avoid damage to large vascular structures. (Redrawn from Hunter DW, et al.
Percutaneous urologic techniques, ch 15, part 1. In: Castaneda-Zuniga WR, Tadavarthy SM, eds.
Interventional Radiology. 2nd ed. Baltimore: Williams & Wilkins; 1992:787.)
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d. Direct puncture into the renal pelvis for the purpose of catheter placement should be avoided due to the
risk of bleeding.
4. Administer local anesthesia (1% lidocaine) at the chosen skin entry site.
5. Make a small skin incision through the dermis to facilitate catheter passage.
6. Commonly used introduction systems include the Cope, Jeff, or Neff (Cook, Bloomington, IN) and
AccuStick (Boston Scientific, Marlborough, MA) sets that allow initial access with a skinny (21-gauge or 22-
gauge) needle and subsequent placement of 0.035-in. or 0.038-in. guidewire through a coaxial 6 Fr.
introducer.
a. During gentle respiration, advance the skinny needle toward the intended calyx using either fluoroscopic
or ultrasound guidance (Fig. 53.4A).
(1) Ultrasound guidance is preferred when there is hydronephrosis.
(2) Fluoroscopic guidance is more appropriate when radiopaque landmarks (e.g., calcified stones, surgical
clips, indwelling ureteral stent) are present.
(3) For nondilated collecting systems in patients with normal or nearnormal Cr, 50 to 100 mL IV contrast can
be injected to opacify the target.
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b. When the needle enters the renal parenchyma, the tip will move synchronously with the kidney. When
the collecting system is entered, there is an abrupt decrease in resistance to forward movement of the
needle.
c. Remove the stylet from the needle. In cases of hydronephrosis, urine will drain freely. Otherwise, slowly
retract the needle while aspirating with a plastic syringe half filled with contrast on a connecting tube until
urine emerges.
d. Inject a small amount of dilute contrast to confirm needle position and, only if there is no suspicion of
infection, to opacify the collecting system. In cases of suspected infection, the system should be partially
decompressed prior to contrast injection to minimize bacterial translocation due to further distension of the
collecting system (9). Complete decompression should be avoided as it will make subsequent entry difficult
if access is inadvertently lost.
e. If a central puncture is made, the collecting system may be gently opacified to visualize an appropriate
peripheral calyx for puncture with a second needle.
f. Once access into the target calyx is achieved, the needle is exchanged over a 0.018-in. wire for the
coaxial introducer (Fig. 53.4B,C). ( Note: Internal metallic stiffeners should be advanced only to the entry
point of the collecting system in order to avoid inadvertent perforation of the renal pelvis.)
g. Urine is aspirated through the 6 Fr. introducer for culture and/or cytology. Patients at high risk for positive
urine culture include those with urinary diversion, cystectomy, recent catheter or stent placement, or clinical
signs of infection (9).
h. Widen the skin nick with a hemostat to a depth of about 0.5 cm prior to introducing the catheter.
7. The coaxial introducer is exchanged over a 0.035-in. or 0.038-in. guidewire for a PCN catheter (typically
8 Fr.) (Fig. 53.4D-G).
a. Introduction of an 8 Fr. or larger PCN catheter may be facilitated by the passage of Teflon dilators.
b. The metal stiffener of the PCN is used only to facilitate passage through the extrarenal soft tissues and
should not be advanced beyond the renal parenchyma. If it is difficult to pass the catheter through the soft
tissues, a peel-away sheath may be used.
c. Once the catheter tip is well within the renal pelvis or proximal ureter, reform the pigtail tip within the renal
pelvis. To do this, remove the metal stiffener, partially retract the guidewire, and lock the tip by applying
slight tension on the external string (Fig. 53.4).
8. Remove the guidewire completely and inject contrast to confirm catheter position.
9. Open the catheter to external drainage and obtain an image to document decompression of the collecting
system, confirming good function of the catheter.
10. Anchor the catheter to the skin with a retention disk and/or suture.
11. Attach a drainage bag to the external hub.
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FIGURE 53.4 • Percutaneous nephrostomy using Cope introduction system. A: Skinny 22-guage, 15-cm
long puncture needle tip in pelvis through a posterior midpole calyx. B: An 0.018-in. wire is introduced
through the puncture needle after the stylet is removed. (continued)
Nephroureterostomy (Nephroureteral Stent) Placement

1. After accessing the renal collecting system as discussed earlier, advance a straight or angled 5 Fr.
catheter, such as a multipurpose or Berenstein catheter, into the ureter over the guidewire. Advance the
catheter over the wire to just above the level of obstruction. Use a small amount of dilute contrast to opacify
the ureter and optimize the angle of approach to the obstruction using the optimal oblique angulation of the
image intensifier.
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FIGURE 53.4 • (Continued) C: A 6 Fr. dilator with tip tapered for a 0.018-in. wire is introduced over the
wire. The metal cannula is removed. D: The 0.018-in. wire is removed, and a 0.038-in. standard J-tipped
guidewire is introduced through the dilator and exits through the distal side hole. (continued)
2. Use an angled 0.035-in. hydrophilic-coated guidewire to probe for the narrowed orifice. A stiff hydrophilic-
coated guidewire may be necessary to cross fibrotic obstructions. Use care, as these low-surface-friction
wires may perforate the ureter.
3. If the guidewire cannot be passed across a redundant or S-shaped ureter, advance an angled catheter
such as a Berenstein catheter to a level approximately 5 mm above the first bend and advance a floppy-
tipped or angled-tipped
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hydrophilic-coated guidewire across the bend. Deep expiration may also partially straighten the redundant
segment.
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FIGURE 53.4 • (Continued) E: Optional tract dilation with fascial dilator over wire is performed. F: The
nephrostomy catheter is introduced over wire with stiffening cannula providing support while crossing
subcutaneous soft tissue. (continued)
4. Once a guidewire is passed into the bladder, advance the nephroureterostomy catheter over the wire
until several centimeters are in the bladder. Once the wire is retracted the distal pigtail will form in the
bladder. The wire is then pulled back to the kidney and the proximal pigtail is formed in the renal pelvis by
slight tension applied to the external string.
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FIGURE 53.4 • (Continued) G: Cope PCN catheter with pigtail formed in renal pelvis.
Antegrade Ureteral Stent Placement

Antegrade ureteral stents are reserved for patients with functioning native bladders. It is common to wait at
least 1 week following placement of a nephrostomy tube before stent placement to decrease the risk of clot
or debris occluding the lumen of the stent. However, clinical judgment should be used, and stents may be
placed sooner. If the patient has a nephroureterostomy in place, a capping trial can be performed to assess
whether the patient will tolerate internalization with a ureteral stent. If the Cr remains stable and there is no
pericatheter leakage or fever with the catheter capped for several days, there is a high likelihood that a
ureteral stent will provide adequate drainage.
1. If there is a nephroureterostomy in place, pass a guidewire through the catheter into the bladder.
Otherwise, obtain access to the bladder as described for nephroureterostomy placement.
2. The length of the ureter can be measured by passing a Teflon-coated guidewire through the catheter into
the bladder. When the tip of the guidewire is at the intended position of the distal J of the stent, place a
clamp on the guidewire at the skin. Withdraw the guidewire tip to the intended position of the proximal loop
of the stent and place a second clamp on the guidewire at the skin surface. The distance between clamps is
the desired stent length. Stents are sized in centimeters (22 to 28 cm) by the distance between the pigtail or
J curves (Fig. 53.5).
3. Coil an Amplatz Super Stiff (Boston Scientific/Medi-Tech) 0.035-in. guidewire in the bladder.
4. Mount the stent on the guidewire and advance over the wire down the ureter into the bladder. Depending
on the type of stent being deployed, it may be premounted on a long delivery system or may need to be
advanced by using a stiff “pusher” mounted on the guidewire behind the stent (Fig. 53.6A).
5. When the tip of the stent is beyond the ureteral orifice of the bladder (UVJ), retract the guidewire and the
flexible stiffener, if one is used. The distal loop of the stent will then coil if free in the bladder. If the stent has
been measured properly, the proximal loop will form within the renal pelvis when the guidewire and stiffener
are removed (Fig. 53.6B,C).
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FIGURE 53.5 • Measuring the ureter to determine stent catheter length. A: The guidewire and catheter
extend past the ureterovesical junction (UVJ). When the guidewire is positioned in the bladder 2 to 3 cm
from the UVJ, the guidewire that extends from the flank is bent at the catheter hub. B: The guidewire is
retracted until the tip is located in the renal pelvis approximately 1 cm above the ureteropelvic junction. A
second kink is now made in the guidewire at the catheter hub. C: The distance between the two guidewire
bends will determine the length of the catheter between the pigtail curves. (Reprinted from Fritzsche P,
Lang EK. Stenting of the ureter—antegrade and retrograde techniques. In: Pollack HM, ed. Clinical
Urography: An Atlas and Textbook of Urological Imaging, vol. 3. Philadelphia, PA: WB Saunders;
1990:2771.)
6. It may be desirable to leave a nephrostomy until stent patency is confirmed (Fig. 53.6D). In this situation,
a nephrostomy catheter can be used as the “pusher” to advance the ureteral stent into place. The loop of
the nephrostomy is formed adjacent to the proximal loop of the ureteral stent. The nephrostomy tube can be
capped for a physiologic trial so that drainage is internal through the stent. The tube is fixed to the patient's
skin in the usual manner and is left in place for at least 24 hours. After a successful capping trial, the
nephrostomy should be removed over a wire to straighten the pigtail and prevent inadvertent dislodgement
of the ureteral stent.
7. Very tight or hard strictures will not allow soft ureteral stents to pass easily. The stricture may be widened
by passage of a Van Andel Teflon dilator (Cook, Inc) over the wire, 0.5 to 1.0 Fr. diameter larger than the
stent to be placed (usually 8 Fr. or 10 Fr.) into the ureter. Balloon ureteroplasty can also be performed to
dilate the stricture prior to stent placement. Another option is to pass a guidewire into the bladder, snare
through the bladder, and externalize it through the urethra. With control of both ends of the guidewire, a
stent may be passed in an antegrade manner. These maneuvers may be painful; adequate sedation and
analgesia are necessary.
8. If a stent still cannot be passed, a nephrostomy may be placed. A second attempt to convert to ureteral
stent may be successful after a period of external drainage.
9. If the indication is to treat a ureteral leak, a stent with holes only in the renal pelvis and bladder (rather
than along the entire course of the catheter) should be used.
10. After stent placement, when the patient passes the physiologic trial of a capped nephrostomy (i.e., the
Cr is stable, the patient is able to void, and remains
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asymptomatic without pain or fever), the nephrostomy can be removed. An antegrade contrast study may
first be performed to document stent patency. Because flow of urine through the stent is gravity-dependent,
using a tilting fluoroscopy table facilitates quick assessment of the stent:
FIGURE 53.6 • Silastic double-J stent. A: Advancement of double-J stent over guidewire passed beyond
site of obstruction. B: Close-up view of proximal end of a Silastic double-J stent with suture passed through
a side hole for repositioning purposes. C: With the proximal end of the stent held in place with the pusher,
the suture is removed, thus releasing the proximal loop. D: Stent has doubled back into the lower pole
infundibulum, and the pusher has been replaced by a pigtail catheter for temporary external drainage.
(Redrawn from Hunter DW, et al. Percutaneous urologic techniques, ch 15, part 1. In: Castaneda-Zuniga
WR, Tadavarthy SM, eds. Interventional Radiology. 2nd ed. Baltimore: Williams & Wilkins; 1992:881.)
a. If contrast is seen to traverse the stent and collect within the bladder, remove the nephrostomy tube over
a guidewire under fluoroscopy to ensure
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that the proximal loop of the ureteral stent is not dislodged by removal of the PCN tube.
b. If contrast does not pass into the bladder, ask the patient to void completely, or, if this is not possible,
place a Foley catheter and repeat the antegrade injection through the PCN tube. One cause of stent
malfunction is elevated pressure in a bladder that cannot be emptied completely.
Retrograde Nephrostomy
When an ileal conduit is present following cystectomy, a retrograde nephrostomy is the preferred urinary
drainage system (10) (Fig. 53.1D).
1. Antegrade access to the kidney is achieved as for PCN placement.
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2. An angled catheter and hydrophilic wire are advanced past the obstruction into the conduit.
3. With the patient semiprone, the urostomy site is prepped. The catheter and wire are directed out of the
ostomy (this requires a second operator).
4. A stiff wire is then advanced retrograde from the end of the catheter (exiting the stoma) to the hub (at the
flank) and the angled catheter is removed.
5. A retrograde nephrostomy catheter (40 to 50 cm in length) is advanced over the wire through the stoma
until the locking loop is in the renal pelvis.
6. An antegrade “safety” catheter may be advanced over the floppy end of the wire (via the flank) into the
kidney before the wire is removed to maintain antegrade access.
7. The wire is removed and the locking mechanisms of the catheter(s) are deployed.
8. Contrast is injected into either catheter to confirm adequate drainage through the retrograde catheter into
the urostomy.
9. If an antegrade catheter has been left in place, it can be capped and removed at the first successful
exchange of the retrograde catheter in 1 to 3 months. Because the conduits are of variable length and
tortuosity, exchange of the retrograde catheter can be difficult and it may be necessary to revert to
antegrade access.
Removal or Exchange of PCN or Nephroureterostomy
1. The hub and locking mechanism are cut from the tube with a scissors. This allows the locking suture to
be free when the loop is uncoiled.
2. A guidewire (with a firm distal body) is used to uncoil the fixation loop and to retain access to the renal
pelvis or bladder, if a replacement is to be made. The replacement catheter can then be advanced over the
wire into the renal pelvis or bladder.
3. Remove the nephrostomy tube over a guidewire:
a. It is more comfortable for the patient.
b. It helps prevent the PCN tube from catching and dragging a ureteral stent with it, if one is in place.
c. It maintains access to the collecting system in situations where bleeding into the tract is suspected.
Exchange of Ureteral Stents
1. Routine exchange is usually performed cystoscopically, especially in men because access to the ureter
may be lost when the stent is pulled through the penile urethra.
2. In women, a short sheath can be placed into the urethra and a snare (e.g., Gooseneck) advanced
through the sheath and used to snare the distal pigtail of the ureteral stent.
a. The stent is pulled through the sheath, taking care to make sure access to that access the ureter is
maintained by the proximal portion of the stent.
b. A stiff wire (e.g., Amplatz) is advanced through the stent into the renal collecting system.
c. The stent is removed and exchanged for a 5 Fr. catheter. Dilute contrast is injected into the catheter to
evaluate for hydronephrosis (which would suggest stent malfunction).
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d. The catheter is exchanged over a stiff wire for a stent which is advanced to the renal pelvis. The wire is
pulled back to allow the pigtail to form in the renal pelvis.
e. A “pusher” is used to advance the end of the stent through the urethra while the wire is pulled back,
allowing the distal pigtail to form in the bladder. The sheath in the urethra can then be removed.
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1. For new catheter placement or catheter exchanges with sedation, bed rest and every 15- to 30-minute vital
sign monitoring for 2 to 4 hours.
2. If drainage was performed to relieve obstruction, there may be a profuse postobstructive diuresis. Monitoring
urine output permits IV replacement of volume.
3. If PCN is for decompression, continue external drainage until antegrade flow is restored. If PCN is to provide a
tract for later stone removal and there is no obstruction, the catheter may be capped until the stone removal
procedure.
4. Resume preprocedure diet.
5. Continue antibiotics only if signs of infection are present.
6. Treat pain and fever symptomatically.
7. If blood clot(s) obstruct the catheter and prevent good drainage, forward-flush 5 to 10 mL of bacteriostatic
normal saline every 4 to 8 hours.
8. Blood-tinged urine may be seen for up to 48 hours:
a. If gross hematuria persists, a tract study may be performed.
b. If Hct falls without gross hematuria, check for retroperitoneal hemorrhage.
9. After nephroureterostomy or antegrade stent placement, patients may experience bladder irritation and urinary
frequency for a few days. It resolves in the majority.
10. PCN catheters and nephroureterostomy catheters are routinely changed every 3 months (or more commonly
as needed) to prevent occlusion from encrustation and debris (8). Routine exchange generally requires little or
no IV sedation. Antegrade ureteral stents are routinely changed every 3 to 6 months.
11. Patients with frequent catheter occlusions may benefit from routine forward flushing with normal saline (10
mL twice daily).
12. The use of antibiotic prophylaxis for routine catheter exchange is debatable.
Results
1. Placement of a PCN tube, especially into dilated collecting systems, is highly successful (95% to 100%).
2. Overall ureteral stent patency is 80%, with most failures occurring within 2 months of placement.
a. Stent life can be optimized by
(1) Increasing urine flow by encouraging patients to keep well-hydrated
(2) Administering prophylactic antibiotics at the time of stent placement
(3) Avoiding placement of stents into bloody or infected collecting systems
Complications and Management (1,4,5,6,7,9)

Major: 4.0%
1. Massive hemorrhage requiring surgery or transcatheter embolization: 1% to 3.6%
a. Angiography and embolization may, on rare occasion, be necessary.
b. If a culprit vessel is not seen, the PCN should be retracted over a wire and repeat renal arteriogram performed
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to allow visualization of any bleeding or abnormal vessels that are obscured or tamponaded by the catheter.
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Immediately after the angiogram, the PCN is quickly reinserted to tamponade the bleed.
2. Sepsis: 1% to 2%
3. Pneumothorax: <1%
4. Death due to hemorrhage: <0.2%
5. Peritonitis: rare
Minor: 15%, Usually Without Sequelae

1. Macroscopic hematuria: very common, clears within 12 to 24 hours
2. Pain: common; usually treated with acetaminophen but occasionally requires short-term opioids
3. Urine extravasation: <2.0%
4. Perirenal bleeding: rare
5. Urinary infection: 1.4% to 21% (45% of patients with struvite stones) will develop signs of infection following
PCN tube placement.
a. Postprocedure rigors may respond to meperidine (Demerol): 25 to 50 mg IV.
6. Catheter-related problems
a. Dislodgment: 1% in early postprocedural period; 2% by end of the first month; and as high as 11% to 30% with
longer follow-up
(1) If the catheter has been in for at least several weeks, the existing tract can usually be recatheterized after it is
opacified using a 5 Fr. dilator inserted into the skin entry site. Then, a 0.035-in. angled Glidewire (Terumo Corp,
Tokyo, Japan) may be manipulated through the dilator and into the renal collecting system.
(2) When there is dislodgment before a tract can form, a new puncture may be required.
b. Catheter occlusion occurs in 1% of patients; these tubes require replacement. PCN tubes placed to relieve
hydronephrosis during pregnancy seem particularly susceptible to blockage by gritty material.
c. Encrustation of the tube with the inability to uncoil the loop during attempted removal
(1) If the tube becomes encrusted from being bathed in infected urine or has been in situ for too long, the loop
may not open when a guidewire is advanced within the lumen (Fig. 53.7).
(2) The hub and locking mechanism are cut off from the end of the tube and a 2-0 silk suture is sewn through the
cut end of the indwelling tube and secured.
(3) The suture material is brought through the lumen of the outer portion of a peel-away sheath that is the same
size or 1 Fr. larger than the failed nephrostomy tube.
(4) A 0.035-in. guidewire is advanced through the indwelling nephrostomy tube and coiled in the renal collecting
system. With traction placed on the suture material, the sheath is advanced over the indwelling tube until it is in
the renal collecting system. The loop can then be straightened against the Teflon peel-away sheath and
removed.
(5) A new tube can be placed through the lumen of the peel-away sheath that has its tip within the renal
collecting system. If the peel-away sheath should become dislodged in the removal process, the guidewire
should remain in place to provide access for placement of a replacement nephrostomy tube.
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Complications Specific to Antegrade Ureteral Stent Placement
1. Stent migration due to improper positioning or size
2. Stent occlusion, most commonly from an obstructing blood clot, but transient ureteral obstruction from severe
mucosal edema has been described.
3. Bladder irritation and urinary frequency that usually resolves within days. Agents that decrease bladder
muscle spasm may provide relieve; however,
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occasionally severe irritation and discomfort persist, and stent removal and PCN placement is necessary.
FIGURE 53.7 • Diagram illustrating removal of stuck Cope loop. A: Severe incrustation of urinary salts has
produced binding of loop drawstring in Cope loop. Hub of catheter has been cut and a silk suture has been
passed through the blunt end of catheter. B: The silk suture has been passed into the lumen of the peel-away
sheath, which has then been advanced over the shaft of the Cope loop, forcing the leading edge of the
introducer to release the drawstring and straighten the loop. C: Once the loop has been straightened, a 0.035-in.
guidewire is passed through the lumen of the loop into the collecting system. D: While the guidewire is kept in
position, the Cope loop is pulled back through the peel-away sheath. (Redrawn from Hunter DW, et al.
Percutaneous urologic techniques, ch 15, part 1. In: Castaneda-Zuniga WR, Tadavarthy SM, eds. Interventional
Radiology. 2nd ed. Baltimore: Williams & Wilkins; 1992:838.)
References
1. Adamo R, Saad WE, Brown DB. Management of nephrostomy drains and ureteral stents. Tech Vasc Interv
Radiology Books
Radiol . 2009;12(3):193-204.
2. Marcovich R, Smith AD. Percutaneous renal access: tips and tricks. BJU Int. 2005;95 (suppl 2):78-84.
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3. Dyer RB, Regan JD, Kavanagh PV, et al. Percutaneous nephrostomy with extensions of the technique:
step by step. Radiographics. 2002;22:503-525.
4. Hausegger KA, Portugaller HR. Percutaneous nephrostomy and antegrade ureteral stenting: technique-
indications-complications. Eur Radiol . 2006;16:2016-2030.
5. Farrell TA, Hicks ME. A review of radiologically guided percutaneous nephrostomies in 303 patients. J
6. Venkatesan AM, Kundu S, Sacks D, et al; for the Society of Interventional Radiology Standards of Practice
Committee. Practice guidelines for adult antibiotic prophylaxis during vascular and interventional radiology
procedures. Written by the Standards of Practice Committee for the Society of Interventional Radiology and
endorsed by the Cardiovascular Interventional Radiological Society of Europe and Canadian Interventional
Radiology Association [corrected]. J Vasc Interv Radiol . 2010;21(11):1611-1630.
7. Wilson W, Taubert KA, Gewitz M, et al. Prevention of infective endocarditis: guidelines from the American
Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and
Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical
Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes
Research Interdisciplinary Working Group. Circulation. 2007;116:1736-1754.
8. Vanderbrink BA, Rastinehad AR, Ost MC, et al. Encrusted urinary stents: evaluation and endourologic
management. J Endourol . 2008;22(5):905-912.
9. Brody LA, Brown KT, Covey AM, et al. Routine urine culture at the time of percutaneous urinary drainage:
does every patient need one? Cardiovasc Intervent Radiol . 2006;29(4):595-598.
10. Alago W Jr, Sofocleous CT, Covey AM, et al. Placement of transileal conduit retrograde nephroureteral
stents in patients with ureteral obstruction after cystectomy: technique and outcome. AJR Am J Roentgenol .
2008;191(5):1536-1539.
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54
Lymphocele and Cyst Drainage and Sclerosis
Danny Cheng
Parag Amin
Thuong G. Van Ha
Cystic lesions are commonly encountered on cross-sectional imaging and are usually an incidental finding
without associated symptoms. They can be classified as either congenital or acquired. Cysts can occur in
virtually any solid organ. When congenital, they are most common in the liver, pancreas, kidney, and ovary.
Acquired cystic lesions such as lymphoceles, hematomas, seromas, urinomas, and bilomas can occur after
surgery, trauma, or infection. Histologically, there are two broad categories: (a) true cysts, which are lined by
epithelium, or (b) pseudocysts lined by fibrous or granulation tissue without epithelium. Symptoms may arise if
they are large, complicated by hemorrhage or infection, or have undergone torsion. Excepting torsion (which
should be treated surgically), single-session or multisession percutaneous aspiration and catheter drainage with
or without sclerotherapy is a viable management strategy (1,2).
Percutaneous aspiration allows diagnostic analysis and can be therapeutic. When a cyst is large, catheter
drainage is more efficient because a liter or more of fluid may be present (1). The catheter can be left in place for
persistent drainage in the case of fluid reaccumulation. Cyst obliteration can occasionally be achieved via
chronic drainage alone. If a cyst recurs after aspiration or drainage, sclerotherapy is a safe and effective option
(3,4).
Sclerosants include povidone-iodine, tetracycline/doxycycline, bleomycin, cyanoacrylate, sodium tetradecyl
sulfate, hypertonic saline, and acetic acid.
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Although no consensus exists on sclerosant of choice, ethanol is readily available, inexpensive, and well-
tolerated (2). More recently, sclerosis of lymphoceles has been performed with a fibrin-based tissue sealant
(TISSEEL).
Indications
1. Pain/discomfort: referred or localized (5)
2. Secondary infection
3. Functional sequelae of mass effect
a. Renal cysts—hematuria, collecting system compression, hypertension (2)
b. Lymphoceles—leg swelling, thrombophlebitis, renal transplant dysfunction (6)
c. Hepatic, renal, splenic cysts—biliary (jaundice/cholestasis) or bowel obstruction (constipation/early
satiety)
Contraindications
Absolute
1. Communication with vital structures such as blood vessels, biliary system, pancreatic duct, or renal
Radiology Books
collecting system
2. Communication with the peritoneal cavity/retroperitoneum (particularly in cases of prior surgery)
3. Lack of a safe window for percutaneous access
Relative
1. Coagulopathy
2. Noncompliant patient (particularly if a drain is to be left in place for multisession therapy)
1. Symptom/laboratory evaluation with imaging correlation
a. Do patient symptoms (early satiety, urinary frequency, pain, etc.) correlate to site of known cystic lesion?
b. Do laboratory abnormalities (hyperbilirubinemia, elevated serum creatinine, etc.) correlate to site of known
cystic lesion?
2. Imaging
a. Ultrasound, computed tomography (CT), and/or magnetic resonance (MR) imaging to characterize the lesion
(simple vs. complex, soft tissue nodularity to suggest malignancy, vascularity). If lesion is large and/or poorly
seen on ultrasound, obtain CT or MR imaging to fully characterize its extent and internal structure.
b. Evaluate safety/possibility of percutaneous access, adjacent vital structures, and choose mode of imaging
guidance. Because most symptomatic cystic lesions are large and fluid-filled, the majority are easily accessed
under sonographic guidance.
c. If cystic/necrotic neoplasm is suspected, reconsider drainage procedure and do not perform sclerosis.
Drainage of cystic collections from tumor is occasionally performed for palliative purposes but sclerosis should
not be considered given risk to, and likely communication with, adjacent vital structures.
3. Defining clinical expectations
a. Clarify and communicate management plan to referring physician(s) as well as the patient. Multiple sessions
are often required and the need for patient cooperation (e.g., postprocedural body position changes after
sclerosant injection) should be emphasized.
b. The patient should be informed that he or she may have a drainage catheter during the course of treatment for
which daily outputs should be recorded.
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4. Routine interventional radiology (IR) preparation
a. Baseline laboratory values: coagulation status (partial thromboplastin time [PTT], prothrombin time
[PT]/international normalized ratio [INR], platelet count), white blood cell (WBC) count (Is patient currently
infected?). Correct coagulopathy/thrombocytopenia prior to drainage
b. Except for aspirin therapy, stop anticoagulation prior to the procedure. Most cyst drainage procedures are low
(superficial lesions) to moderate risk for bleeding.
c. If TISSEEL is to be used, the exceedingly rare risks of minor and serious allergic reactions and theoretical risk
of viral transmission (7) should be discussed with the patient before the procedure.
Procedure
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Diagnosis
1. Initial aspiration/drainage can be done upon needle insertion without catheter placement (if easy
access) or with catheter placement (if difficult access) to send fluid for laboratory evaluation (complete
blood count [CBC], fluid creatinine/blood urea nitrogen [BUN], triglycerides, lymphocytes, cytology, and
Gram stain/culture).
2. Urinomas may require aspiration/drainage for symptom management or to prevent superimposed
infection. They should not contain lymphocytes or triglycerides but do exhibit creatinine concentrations
greater than serum and equal to urine. Urinomas are not sclerosed; the underlying leak should be
targeted for recalcitrant collections.
3. Seromas and lymphoceles are seen postoperatively and can require not only aspiration/drainage
but recurrent collections may require sclerosis. Seromas should not contain lymphocytes or
triglycerides while lymphoceles contain lymphocytes and possibly triglycerides (and chylomicrons).
4. Collections suspected of infection should be aspirated/drained in the setting of antimicrobial therapy.
Sclerosis has been performed in certain circumstances, for example, hydatid cyst disease (8).
Aspiration and Drainage

1. Cyst drainage and/or sclerotherapy can be performed in an outpatient setting, either single-session or
multi-session treatment. Treatment of infected collections (such as in echinococcal disease) should be
performed on inpatients only for prolonged monitoring.
2. It is worth attempting initial aspiration/drainage of a symptomatic cystic lesion without sclerosis until
coincident cyst and symptom/sign recurrence has been established.
3. Either Seldinger or direct trocar technique may be used depending on operator comfort, and lesion size
and location.
4. Ultrasound guidance is usually preferred (especially for clearly visualized superficial lesions). CT is
useful for lesions difficult to visualize with ultrasound.
5. Upon establishing a safe percutaneous window to the lesion, initial access may be obtained with a
coaxial micropuncture system or with an 18-gauge trocar needle.
6. If a drainage catheter is deemed necessary, for example, for larger collections or if long-term suction
drainage is attempted, an 8- to 12-Fr. all-purpose drainage catheter may be placed.
7. Persistent drainage (or recurrence of cyst and symptoms after drain removal) warrants consideration for
sclerotherapy. Cross-sectional imaging with CT or ultrasound is recommended prior to therapy to
reevaluate cyst characteristics/accessibility.
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Sclerotherapy
1. Prior to sclerotherapy, a cystogram is performed to ensure the cyst is selfcontained.
a. Once confirmed, sclerotherapy can proceed. Multiple sclerotherapy sessions are generally required.
2. Procedural details
a. Povidone-iodine: volume of 10% povidone-iodine (Betadine; Purdue Pharma, Stamford, CT) instilled
equals half of the volume of fluid aspirated, not exceeding 100 mL. The catheter is then capped for 2 hours
and the patient rotated 360 degrees, spending 15 minutes in each position (i.e., supine, right lateral
decubitus, prone, left lateral decubitus). The catheter is then connected to gravity drainage (6).
b. Dehydrated ethanol (95% to 99%): Procedural details are similar to povidoneiodine. Amount instilled is
equal to half of the volume of fluid aspirated with a maximum of 100 mL in order to avoid ethanol toxicity.
Radiology Books
The catheter is capped and the patient rotated 360 degrees, spending approximately 5 to 10 minutes in
each position. The ethanol should be completely aspirated before catheter removal. If pain is encountered
during injection, 10 to 15 mL of 1% lidocaine can be instilled into the cyst cavity (2,6).
c. Doxycycline: Five vials of doxycycline powder (100 mg each, total 500 mg; American Pharmaceutical
Partners, Los Angeles, CA) are reconstituted in 20 mL of normal saline and 5 mL of 1% lidocaine. The
mixture is injected into the cyst cavity and the tube capped for 1 to 2 hours. The patient should be
maneuvered to allow contact with the entire cyst wall. The sclerosant should then be aspirated (6,9).
d. Fibrin sealant (TISSEEL VH; 5 mL, two-component kit; Baxter Healthcare, Westlake Village, CA): The
cyst should be entirely aspirated to maximize wall contact. A 7 Fr., three-lumen central venous catheter
(AK15703; Arrow, Reading, PA) can be used to deliver the fibrin sealant. A dual-lumen catheter will suffice
but a single-lumen catheter is not compatible because the agents will polymerize in the catheter during
delivery. The fibrin sealant is prepared per manufacturer's recommendations. The two syringes are warmed
to a temperature of 37°C and the solutions are simultaneously injected through separate lumens of the
catheter for a total of 10 mL. The 80 mg of gentamicin can be added to one of the syringes, but there is no
evidence that this decreases the rate of postprocedural infection. The catheter is removed and the site
massaged to limit leakage and maximize surface contact. Treatment with TISSEEL can be performed in one
session followed by catheter removal. Repeat treatments in separate sessions can be performed if
necessary (7).
1. The patient should be monitored immediately postprocedurally for 1 to 2 hours in an observation/holding area
for hemodynamic stability and pain control (2 hours is advised if a drain is left in place).
2. Drain intolerance and/or marked pain should warrant inpatient management or drain removal. Typically,
therapy is well-tolerated without need for excessive pain control.
3. If a catheter is placed, the patient is instructed to record daily drain output for review upon a follow-up visit.
Catheter dwell times can range from several days to weeks for sclerotherapy or even up to several months in
some cases.
4. Catheter removal or cessation of sclerotherapy is considered when drain output is less than 10 to 20 mL per
24 hours. Drain evaluation is advocated prior to removal, either with CT or with contrast injection under
fluoroscopy, to confirm cyst collapse and exclude drain malposition as a cause of decreased drainage.
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Results
1. Drainage and sclerotherapy has proven efficacy in the management of symptomatic cystic lesions
(1,2,3,4,6). Expected success rates:
a. Simple renal cysts—93% to 98% volume reduction for single session alcohol sclerosis
b. Simple hepatic cysts—95% volume reduction (range 40% to 100%)
c. Lymphoceles—percutaneous drainage success rate as high as 94% and sclerosis as high as 100% (2)
2. The size of the cyst likely affects success rates with larger cysts often proving more difficult to treat
successfully (6).
3. Surgical treatment options exist, such as cyst marsupialization/deroofing; however, comparative studies
generally show sclerotherapy to be as effective (1,2,3,4,6). Surgery may be considered in lesions difficult to
Radiology Books
access or lesions unsuccessfully treated with drainage/sclerotherapy.
4. Drainage and sclerotherapy is also an option when initial surgical management fails (10).
Complications
Major
1. Rare and can be minimized with appropriate planning of access route and careful evaluation prior to
sclerosant instillation
2. Absorption or unintentional intravascular injection of ethanol into the bloodstream stream can result in
prolonged hypotension, increased pulmonary vascular resistance, or decreased level of
consciousness/central nervous system (CNS) depression.
Minor
1. Catheter-related infections
2. Localized pain and/or tissue injury (e.g., renal: acute tubular necrosis; hepatic: tissue infarction, biliary
strictures; peritoneal spillage: intense pain).
3. Cyst recurrence
References
1. Lucey BC, Kuligowska E. Radiologic management of cysts in the abdomen and pelvis. AJR Am J
Roentgenol . 2006;186(2):562-573.
2. Cheng D, Amin P, Van Ha T. Percutaneous sclerotherapy of cystic lesions. Semin Intervent Radiol .
2012;29(4):295-300.
3. Agarwal M, Agrawal MS, Mittal R, et al. A randomized study of aspiration and sclerotherapy versus
laparoscopic deroofing in management of symptomatic simple renal cysts. J Endourol . 2012;26(5):561-565.
4. Moorthy K, Mihssin N, Houghton PW. The management of simple hepatic cysts: sclerotherapy or
laparoscopic fenestration. Ann R Coll Surg Engl . 2001;83(6):409-414.
5. Bajwa ZH, Gupta S, Warfield CA, et al. Pain management in polycystic kidney disease. Kidney Int.
2001;60:1631-1644.
6. Mahrer A, Ramchandani P, Trerotola SO, et al. Sclerotherapy in the management of postoperative

lymphocele. J Vasc Interv Radiol . 2010;21:1050-1053.
7. Silas AM, Forauer AR, Perrich KD, et al. Sclerosis of postoperative lymphoceles: avoidance of prolonged
catheter drainage with use of a fibrin sealant. J Vasc Interv Radiol. 2006;17:1791-1795.
8. Smego RA Jr, Bhatti S, Khaliq AA, et al. Percutaneous aspiration-injection-reaspiration drainage plus
albendazole or mebendazole for hepatic cystic echinococcosis: a metaanalysis. Clin Infect Dis.
2003;37(8):1073-1083.
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9. Caliendo MV, Lee DE, Queiroz R, et al. Sclerotherapy with use of doxycycline after percutaneous drainage
of postoperative lymphoceles. J Vasc Interv Radiol. 2001;12:73-77.
10. Karam AR, Connolly C, Fulwadhva, et al. Alcohol sclerosis of a giant liver cyst following failed deroofings.
J Radiol Case Rep. 2011;5(2):19-22.
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55
Pulmonary Tumors
Bradley B. Pua
Stephen B. Solomon
Thermal ablation of pulmonary tumors is an option for local tumor control for unresectable tumors.
Radiofrequency ablation (RFA), first described in the lungs in 2000, has since been proven to be both feasible
and efficacious in the treatment of lung cancers (1). Ablative techniques have been used to treat primary lung
cancers, metastatic disease to the lungs, and in palliation for painful chest wall masses. Thermal ablative
techniques include heat-based modalities such as RFA and microwave ablation (MWA) in addition to cold-based
techniques such as cryoablation.
RFA utilizes frictional energy imparted by oscillating ions within tissue to heat and treat tumors. Cells undergo
coagulation necrosis when heated to more than 54°C for more than 1 second. Therapeutic RFA strives to bring
tissue temperatures to the range of 60°C to 100°C. Because this technology relies on tissue and electrical
conduction, RFA can be difficult to apply in lung where air is a poor conductor.
The mechanism of cell death caused by MWA is similar to RFA. With microwave, a continuously oscillating
microwave field targets polar molecules (predominately water), which align with this field resulting in increased
kinetic energy and tissue temperatures. This does not require electrical conduction and therefore allows
microwave energy to penetrate more effectively allowing for generation of a larger volume of heat surrounding
each applicator.
Cryoablation causes cell death through cell membrane disruption from both intra- and extracellular ice crystal
formation and subsequent release of intracellular material. Although cellular necrosis is related to tissue type,
temperatures of — 35°C to —20°C are usually required. Current cryoablation systems utilize the Joule-Thomson
effect to induce these extreme temperatures. Gases (typically argon) are delivered at high pressures through an
internal feed line into an expansion chamber in the cryoprobe; as the gas expands, a heat sink is created cooling
the probe and surrounding tissues. As thermal conductivity is secondary to passive conduction, the probes'
cooling capacity is related to the size of the cryoprobe.
Lung Cancer
Primary lung cancer is the leading cause of cancer death in the United States. Non-small cell lung cancer
(NSCLC) represents 85% of these cancers, whereas small cell represents approximately 15%. Small cell lung
cancers are generally more aggressive, and patients with this subtype generally present with extensive lymph
node involvement and metastatic disease. Currently, this characteristic limits ablation of this tumor subtype to
salvage therapy, with the mainstay of therapy being systemic chemotherapy and radiotherapy. Patients with
NSCLC, on the other hand, present much earlier, allowing these patients to be treated with local therapies such
as surgery, stereotactic body radiotherapy, and ablation. Currently, surgical therapy (lobar resection) is
considered as first line for treatment of early-stage lung cancer with ablation reserved for patients who are not
surgical candidates. Additional indications for treatment of NSCLC may include (a) salvage (poor or no response
to chemotherapy, radiation, or surgery) or (b) a single growing focus of tumor in a patient with otherwise stable
metastatic disease.
Treatment of metastasis in the lungs is still a much-debated topic. Treatment of limited metastatic disease with
surgical metastasectomy has been validated retrospectively with improved actuarial survival seen if complete
surgical excision (R0 resection) is achieved (2). Thermal ablation is an option for this subset of patients as well,
Radiology Books
and offers this patient population, who often may face additional future metastases, a lung function preserving
treatment.
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Indications
Biopsy-Proven Malignancy
1. Early-stage primary lung cancer
a. Medically inoperable/refusing surgery
(1) Limited pulmonary reserve (see “Preprocedure Preparation” section)
b. Recurrence: after surgery, radiation, or chemotherapy
2. Limited metastatic disease Widely metastatic disease responding to systemic chemotherapy with a single
focus that is not responding
3. Salvage therapy
a. Prior radiation: local recurrence in postradiation bed
b. Prior surgery: local recurrence in postsurgical bed
c. Symptom palliation: usually pain
Contraindications
Absolute
a. Uncorrected laboratory abnormality
(1) INR >1.5
(2) Platelets less than 50,000 per μL
b. Uncorrected bleeding diathesis
2. Bacteremia or active infection
a. Post-ablated tissue can serve as a nidus for infection, which may result in abscess formation.
Relative
1. Tumors adjacent to vital organs
a. Mediastinum, large blood vessels (aorta, main pulmonary artery), esophagus, and chest wall
b. This is considered a relative contraindication; separation techniques (as described later) can be used to
help create a buffer zone between tumor and neighboring vital structures.
2. Proximity to vessels larger than 3 mm
a. Although not a true contraindication, studies have suggested that proximity to vessels of this size may
cause a significant enough “heat sink” effect resulting in higher rate of local tumor progression (3).
1. History and physical examination with attention to
a. History of bleeding diathesis
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b. Concurrent cardiopulmonary compromise, which may affect choice of sedation.
(1) Compromised pulmonary function may contraindicate surgical resection.
(a) Pulmonary function tests may be transiently affected after ablation.
(2) Ablation can be performed in the contralateral lung in a patient with prior pneumonectomy (4).
c. Pacemakers and metallic implants
(1) Although RFA and MWA in patients with pacemakers/defibrillators has been reported, it is still
recommended that these devices be deactivated during ablation of pulmonary tumors (5). Deactivation with a
magnet over the pacemaker or defibrillator will remove sensing activity temporarily until the magnet is removed.
Cryoablation may be utilized in these instances.
(2) Metal implants, when small, can heat up due to the circuit created from the RFA probe to the grounding pad.
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2. Team approach
a. Treatment of patients with primary and metastatic tumors should ideally be performed after discussion with the
patient's multidisciplinary team.
(1) Ideally, patients should be presented and discussed in a multidisciplinary setting, such as tumor board.
3. Preprocedure biopsy
a. Lesions to be treated should generally be biopsy-proven malignancy.
(1) Some prefer biopsies be performed on a separate occasion because
(a) Biopsy findings may alter management.
(b) Potential of hemorrhage during biopsy may obscure lesion to be treated, thus decreasing effectiveness. A
short interval between biopsy (˜1 week) and ablation will allow these postbiopsy changes to resolve.
4. Preprocedure imaging and choice of guidance
a. Preprocedure computed tomography (CT) and/or positron emission tomography (PET)/CT should be
performed to assess stage, trajectory planning, and serve as baseline for follow-up.
b. Guidance
(1) CT: Vast majority of lung ablations will be performed under CT guidance.
(2) Ultrasound (US): helpful in treatment of peripheral lung lesions or chest wall masses
(3) CT fluoroscopy: has the advantage of real-time imaging during applicator placement
5. Factors affecting ablation effectiveness
a. Tumors larger than 3 cm
(1) Primary cancer: Treatment of tumors less than 3 cm found to be associated with higher rate of complete
tumor necrosis and local progression-free survival (6).
(2) Metastatic cancer: Treatment of tumors less than 3 cm is associated with improved overall survival (7).
b. Proximity to large vessels may act as a heat sink limiting effectiveness.
Procedure
1. Anesthesia
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a. Moderate sedation or general anesthesia with local anesthesia can be used.
(1) General anesthesia advantages
(a) Airway control
(b) Ventilation control (rate and tidal volume) can aid lesion targeting.
(c) Limited patient motion
2. Patient positioning
a. Grounding pads (RFA)
(1) Dispersive grounding pads should be placed in a well-prepared area, without hair/shaved, equidistant
from target. Attention to proper placement before and during ablation will decrease potential risk of skin
burns.
b. Padding
(1) It is important to place padding in areas with important neurovascular bundles.
(a) Brachial plexus injuries have been reported in poorly positioned patients.
3. Antibiotics
a. May be given within 1 hour before procedure to cover skin flora
(1) No studies demonstrate the need for antibiotics. However, devitalized tissue may serve as a nidus for
infection.
4. Positioning and access sites (similar to lung biopsies)
a. Trajectory should
(1) Limit number of interlobular fissures traversed
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(2) Avoid bullae and cysts
(3) Avoid mediastinal structures and large vessels
b. Ablation settings vary by manufacturer: Probe selection varies by size of lesion to be ablated,
location, and familiarity with system. Advantages of certain systems over others are controversial.
c. Synergistic effects can be seen when multiple probes are combined allowing for more optimal ablation
coverage. Consult manufacturer thermal maps.
5. Probe positioning
a. Ideal probe positioning allows for post-ablative zone to cover tumo (Fig. 55.1).
(1) Similar to surgery, the effective ablation zone should ideally cover 0.5 to 1 cm beyond the boundaries of
the tumor.
(2) Immediate postprocedure imaging shows ground-glass opacity in the ablated area. This region of
ground-glass opacity has been associated with completeness of ablation.
(a) One study suggests that post-ablation ground-glass opacity four times the original size of the tumor is
predictive of complete ablation (8).
(b) Another study suggests that a minimum of 5-mm ground-glass opacity surrounding the tumor is needed
for complete ablation (9).
6. Ablating lung tissue
a. Lung parenchyma is less thermally and electrically conductive as compared to liver.
b. Power settings for RFA usually start at a lower wattage (˜20 W) and gradually increase.
c. Conductivity and therefore ablation times may be longer in lung tissue as compared to liver.
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FIGURE 55.1 • Radiofrequency ablation multitined applicator with tines deployed covering entire tumor. It is
important to ensure that there is adequate coverage in multiple planes.
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7. Additional techniques
a. Overlapping probes
(1) Can use more than one probe or ablate at multiple locations using a single probe when treating tumors
larger than 3 cm
(a) May increase risk of pneumothorax
b. Separation techniques
(1) For treatment of juxtapleural and paramediastinal lesions, an artificial pneumothorax can be created to
separate the lesion from the aforementioned structures.
c. Thermocouples
(1) Thermocouples placed on the edge of the tumor or near sensitive structures can guide ablation device
parameter choices.
8. Take advantage of imaging
a. Routine use of three-dimensional (3D) reconstructions can help optimize probe placement.
9. Choice of ablation energy (RFA, microwave, or cryoablation)
a. Microwave should be avoided with lesions <1 to 2 cm from the pleural surface. Microwave ablation zones
abutting pleural surfaces are prone to bronchopleural fistula.
b. A pretreatment short cycle of freeze and thaw (3-minute freeze, 3-minute thaw) may allow better ice ball
formation when cryoablation is used secondary to enhanced conductivity of hemorrhage versus air.
c. Cryoablation is often better tolerated in the patient who is undergoing the procedure under conscious
sedation versus general anesthesia.
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1. Immediate postprocedure patient management
a. Postprocedure CT to evaluate ablation zone, potential collateral damage, and assess for pulmonary
hemorrhage or pneumothorax. If significant pneumothorax exists, a trial of aspiration of the air prior to removal of
the ablation applicator can be performed.
b. Procedure may be done on a same-day discharge basis, although overnight observation may be prudent in
patients with multiple medical comorbidities.
c. Postprocedure chest x-ray should be performed immediately after the procedure and 2 hours afterward. If
patient is symptomatic, imaging should be performed earlier.
d. Overnight stay
(1) Pain control: Pain is usually well controlled with Percocet, with significant improvement by next day. Most
patients are pain-free or with mild pain controlled with over-the-counter analgesics prior to discharge.
(2) Chest x-ray should be performed prior to discharge to assess for late pneumothorax needing treatment or
other complications.
e. Chest tube: Chest tubes are placed in enlarging pneumothoraces and recurrent pneumothorax (if it recurs
after initial aspiration).
(1) Most symptomatic patients should receive chest tube.
(2) Many chest tubes can be removed the day after the procedure.
2. Imaging follow-up
a. Computed tomography
(1) A new baseline contrast-enhanced CT is usually obtained in 1 to 3 months and a repeat CT obtained every 3
months to assess for local tumor recurrence.
(2) Normal findings: ground-glass opacity surrounding the treated tumor that consolidates in 2 to 3 months
(3) Abnormal findings: enhancement
(a) New or irregular contrast enhancement in previously ablated areas in comparison to baseline study
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FIGURE 55.2 • PET and CT follow-up imaging after RFA. Preprocedure imaging demonstrates an
fluorodeoxyglucose (FDG)-avid lesion (white arrow) within the lung parenchyma (black arrow). Four and a half
months after treatment, the lesion appears larger (black arrow) secondary to surrounding inflammatory changes
with PET demonstrating a smooth, surrounding circular rim of FDG avidity (white arrow), which is an expected
finding. Forty months after RFA, the treated lesion is smaller than the pretreatment lesion (black arrow) with no
significant FDG activity within the tumor site (white arrow). Continued routine follow-up is needed to assess for
an enlarging lesion or changes/increases in FDG activity.
(b) One animal study suggests a 10-Hounsfield unit (HU) increase in enhancement between pre- and post-CT
images represents residual unablated tumor (10).
b. Magnetic resonance imaging (MRI): not usually used for follow-up secondary to poor lung visualization
c. PET (Fig. 55.2)
(1) Normal findings: Uniform rim of FDG low activity can be seen in the postablative region secondary to
surrounding inflammatory tissue, which can remain for several months after therapy (11).
(2) Abnormal findings
(a) Maximum standardized uptake value (SUVmax) of 3.0 or greater is suspicious (our clinical practice).
(b) One study demonstrated that a cutoff value of SUVmax of 1.5 at 3 to 9 months after RFA showed 77.8%
sensitivity and 85.7% to 90.5% specificity for recurrence (12).
(c) Increasing SUV on serial imaging
Results
1. Treatment of primary lung tumors
a. RFA
(1) Radiofrequency Ablation of Pulmonary Tumors Response Evaluation (RAPTURE) trial: prospective,
multicenter, intention-to-treat clinical trial (13)—cancer-specific survival with NSCLC 92% at 1 year, 73% at
2 years (tumors less than 3.5 cm)
(2) Simon et al. (6): with 5-year follow-up, overall survival (treated NSCLC) 78% at 1 year, 27% at 5 years
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(tumors less than 3.0 cm)
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(3) de Baère et al. (8): with 18-month follow-up, overall survival 76%; tumors less than 4.0 cm, patients with
five tumors or less were treated.
b. Cryoablation
(1) Yamauchi et al. (14): with 29-month mean follow-up, overall survival 88% at 2 years, 88% at 3 years.
Tumors treated—stage I NSCLC.
c. Microwave
(1) Wolf et al. (15): with mean 10-month follow-up, cancer-specific survival 83% at 1 year, 73% at 2 years,
61% at 3 years. Tumors treated included primary and metastatic cancers.
2. Treatment of metastasis (RFA)
a. RAPTURE (13): for colorectal metastasis, cancer-specific survival 93% at 1 year, 67% at 2 years
b. Simon et al. (6): for colorectal metastasis, overall survival 87% at 1 year, 57% at 5 years.
c. de Baère et al. (8): with 18-month follow-up, overall survival 71%; tumors less than 4.0 cm, patients with
five tumors or less
d. Petre et al. (16): for colorectal metastasis, 3-year progression free survival 77%; median survival from
time of RFA 46 months

1. Pneumothorax
a. Risk of pneumothorax ranges, with newer studies suggesting rates as low as 9% to 13% (17), pneumothorax
requiring chest tube 3.5% (18).
b. Rates of pneumothorax reported by larger studies
(1) RAPTURE (13): 19.7%
(2) Simon et al. (6): 28.4%
(3) de Baère et al. (8): 54%
2. Hemoptysis
a. Moderate hemoptysis in 3% of cases
b. Transient blood in sputum after ablation can occur; patients are counseled that this is self-limiting.
3. Neuropathy
a. Paresthesias or pleuritic pain from treatment of juxtapleural tumors can occur.
(1) Although usually self-limiting with time, antiseizure medications such as pregabalin (Lyrica) or gabapentin
(Neurontin) can be helpful.
b. Phrenic nerve injury from treatment of paramediastinal masses has been reported.
(1) Usually self-limiting, however, avoidance is preferred.
c. Brachial plexus injury: usually due to poor patient positioning
4. Pain
a. Patient-controlled analgesias (PCAs) or narcotics can be used the night of the procedure with the vast majority
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of pain either resolving or becoming significantly improved by the days after the procedure.
5. Others
a. Fever
b. Infection/abscess, Aspergillus in cavity
c. Bronchopleural fistula
References
1. Dupuy DE, Zagoria RJ, Akerley W, et al. Percutaneous radiofrequency ablation of malignancies in the
lung. AJR Am J Roentgenol . 2000;174:57-59.
2. Pastorino U, Buyse M, Friedel G, et al. Long-term results of lung metastasectomy: prognostic analyses
based on 5206 cases. J Thorac Cardiovasc Surg. 1997;113:37-49.
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3. Steinke K, Haghighi KS, Wulf S, et al. Effect of vessel diameter on the creation of ovine lung
radiofrequency lesions in vivo: preliminary results. J Surg Res. 2005;124:85-91.
4. Ambrogi MC, Fanucchi O, Lencioni R, et al. Pulmonary radiofrequency ablation in a single lung patient.
Thorax. 2006;61:828-829.
5. Donohoo JH, Anderson MT, Mayo-Smith WW. Pacemaker reprogramming after radiofrequency ablation of
a lung neoplasm. AJR Am J Roentgenol. 2007;189:890-892.
6. Simon CJ, Dupuy DE, DiPetrillo TA, et al. Pulmonary radiofrequency ablation: long-term safety and
efficacy in 153 patients. Radiology. 2007;243:268-275.
7. Yan TD, King J, Sjarif A, et al. Percutaneous radiofrequency ablation of pulmonary metastases from
colorectal carcinoma: prognostic determinants for survival. Ann Surg Oncol . 2006;13:1529-1537.
8. de Baère T, Palussière J, Aupérin A, et al. Midterm local efficacy and survival after radiofrequency ablation
of lung tumors with minimum follow-up of 1 year: prospective evaluation. Radiology. 2006;240:587-596.
9. Anderson EM, Lees WR, Gillams AR. Early indicators of treatment success after percutaneous
radiofrequency of pulmonary tumors. Cardiovasc Intervent Radiol . 2009;32:478-483.
10. Goldberg SN, Gazelle GS, Compton CC, et al. Radio-frequency tissue ablation of VX2 tumor nodules in
the rabbit lung. Acad Radiol . 1996;3:929-935.
11. Kang S, Luo R, Liao W, et al. Single group study to evaluate the feasibility and complications of
radiofrequency ablation and usefulness of post treatment positron emission tomography in lung tumours.
World J Surg Oncol . 2004;2:30-35.
12. Higaki F, Okumura Y, Sato S, et al. Preliminary retrospective investigation of FDG-PET/CT timing in
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follow-up of ablated lung tumor. Ann Nucl Med. 2008;22:157-163.
13. Lencioni R, Crocetti, Cioni R, et al. Response to radiofrequency ablation of pulmonary tumours: a
prospective, intention-to-treat, multicentre clinical trial (the RAPTURE study). Lancet Oncol . 2008;9:621-628.
14. Yamauchi Y, Izumi Y, Hashimoto K, et al. Percutaneous cryoablation for the treatment of medically
inoperable stage I non-small cell lung cancer. PLoS One. 2012;7:e33223.
15. Wolf FJ, Grand DJ, Machan JT, et al. Microwave ablation of lung malignancies: effectiveness, CT
findings, and safety in 50 patients. Radiology. 2008;247:871-879.
16. Petre EN, Jia X, Thornton RH, et al. Treatment of pulmonary colorectal metastases by radiofrequency
ablation. Clin Colorectal Cancer. 2013;12:37-44.
17. Belfiore G, Moggio G, Tedeschi E, et al. CT-guided radiofrequency ablation: a potential complementary
therapy for patients with unresectable primary lung cancer—a preliminary report of 33 patients. AJR Am J
Roentgenol . 2004;183:1003-1011.
18. Okuma T, Matsuoka T, Yamamoto A, et al. Frequency and risk factors of various complications after
computed tomography-guided radiofrequency ablation of lung tumors. Cardiovasc Intervent Radiol .
2008;31:122-130.
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56
Hepatic Tumors
Laura Crocetti
Riccardo Lencioni
The development of image-guided percutaneous techniques for local tumor ablation has been one of the major
advances in the treatment of liver malignancies. Among these methods, radiofrequency (RF) ablation is currently
established as the primary ablative modality at most institutions. RF ablation is accepted as the best therapeutic
choice for patients with very early and early stage hepatocellular carcinoma (HCC) when liver transplantation or
surgical resection is not a suitable option (1,2,3). In addition, RF ablation is considered as a viable alternative to
surgery for inoperable patients with limited hepatic metastatic disease, especially from colorectal cancer (CRC),
in patients deemed ineligible for surgical resection because of extent and location of the disease or concurrent
medical conditions (3).
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Table 56.1 BCLC Classification in Patients Diagnosed with Hepatocellular Carcinoma
Very early stage PS 0, Child-Pugh A, single HCC <2 cm
Early stage PS 0, Child-Pugh A-B, single HCC <5 cm or 3 nodules <3 cm each
Intermediate PS 0, Child-Pugh A-B, multinodular HCC

stage
Advanced stage PS 1-2, Child-Pugh A-B, portal neoplastic invasion, nodal metastases, and distant
metastases
Terminal stage PS >2, Child-Pugh C
PS, performance status.
Indications
1. Very early and early stage HCC according to the Barcelona Clinic Liver Cancer (BCLC) classification
(Table 56.1) when patients are not candidates for either liver resection or transplantation. Patients are
required to have a single tumor smaller than 5 cm or as many as three nodules smaller than 3 cm each, no
evidence of vascular invasion or extrahepatic spread, performance status test of 0, and if liver cirrhosis,
Child-Pugh class A or B.
2. Nonsurgical patients with CRC oligometastases isolated to the liver. Selected patients with limited
hepatic and pulmonary CRC metastatic disease may qualify provided that extrahepatic disease is deemed
curable.
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3. Hepatic metastases from other primary cancers. Promising initial results have been reported in the
treatment of breast and endocrine tumors (3).
Contraindications
Absolute
1. Tumor located <1 cm from a major biliary duct due to risk of delayed stenosis
2. Intrahepatic bile duct dilation
3. Anterior exophytic location of the tumor, due to the risk of tumor seeding
4. Untreatable/unmanageable coagulopathy
Relative
1. Anatomic considerations
a. Greater than five lesions. The number of lesions should not be considered an absolute contraindication
to RF ablation if successful treatment of all metastatic deposits can be accomplished. Nevertheless, most
centers preferentially treat patients with five or fewer lesions (3).
b. Tumor size should not exceed 3 cm in longest axis to achieve best rates of complete ablation with most of
the currently available devices (3).
2. Bilioenteric anastomosis, because of the risk of hepatic abscesses
3. Superficial lesions, because of a higher risk of complications
4. Superficial lesions that are adjacent to any part of the gastrointestinal tract, because of the risk of thermal
injury of the gastric or bowel wall (consider hydro/gas dissection)
5. Tumors located in the vicinity of the gallbladder, due to the risk of iatrogenic cholecystitis
6. Ferromagnetic prostheses that may act as heat sinks and cause skin burns
7. Pacemaker/defibrillators. If necessary, deactivate device and reprogram.
1. Evaluate patient records, history, physical examination, and prior imaging studies to determine the indication
and the feasibility of ablation.
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2. Preprocedural imaging—the tumor staging protocol must be tailored to the type of malignancy.
a. In patients with HCC, the detection of a nodule by ultrasound (US) is usually followed by multidetector spiral
computed tomography (CT) or dynamic magnetic resonance (MR), following the recommendations of the
American Association for the Study of Liver Diseases (AASLD) and of the European Association for the Study of
the Liver (EASL) (1,2).
b. Patients with liver metastases should undergo abdominal US and CT or MR of the abdomen. Chest CT and
positron emission tomography (PET) or PET-CT may be required to exclude or confirm extrahepatic metastatic
disease.
c. Pretreatment imaging must carefully define the location of each lesion with respect to surrounding structures.
(1) Lesions located on the surface of the liver can be considered for RF ablation, although their treatment
requires adequate expertise and may be associated with a higher risk of complications. Thermal ablation of
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superficial lesions that are adjacent to any part of the gastrointestinal tract must be avoided because of the risk
of thermal injury of the gastric or bowel wall. The use of special techniques—such as intraperitoneal injection of
dextrose to displace the bowel—can be considered in such instances.
(2) Treatment of lesions adjacent to the hepatic hilum increases the risk of thermal injury of the biliary tract.
Thermal ablation of tumors located in the vicinity of the gallbladder has been shown to be feasible, although
associated in most cases with self-limited iatrogenic cholecystitis.
(3) Thermal ablation of lesions adjacent to hepatic vessels is possible because flowing blood usually protects the
vascular wall from thermal injury; in these cases, however, the risk of incomplete treatment of the neoplastic
tissue close to the vessel may increase because of heat loss by convection (3).
3. Preprocedural laboratory testing
a. Measurement of serum tumor markers, such as alpha-fetoprotein for HCC and carcinoembryonic antigen for
colorectal metastases
b. Evaluation of the patient's coagulation status including measurement of the complete blood count and
international normalized ratio (INR). An INR <1.5 and a platelet count higher than 50,000 per μL is required to
keep the risk of bleeding at an acceptable low level.
4. Antiplatelet medications (e.g., aspirin, ticlopidine, clopidogrel, IIb/IIIa receptor antagonists) and nonsteroidal
anti-inflammatory medications should be discontinued 7 to 10 days before thermal ablation. Antiplatelet therapy
may be restarted 48 to 72 hours after thermal ablation.
5. Anticoagulants should be discontinued before liver ablation.
a. Warfarin should be discontinued at least 5 days before liver ablation and may be restarted the following day.
b. Heparin and related products should be discontinued 12 to 24 hours before ablation and may be restarted
after 24 hours.
Procedure
1. Thermal ablation can be performed under intravenous sedation or general anesthesia with standard
cardiac, pressure, and oxygen monitoring. In some centers, general anesthesia with tracheal intubation is
used. The American Society of Anesthesiologists (ASA) score can be used to assess the patient's physical
status prior to RF ablation; patients with scores up to ASA III can be treated (3).
2. Technical considerations
a. RF ablation
(1) The goal of RF ablation is to induce thermal injury to tissue through electromagnetic energy deposition.
With RF ablation, the patient is part of a closed-loop circuit that includes an RF generator, an electrode
needle,
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and a large dispersive electrode (grounding pad). An alternating electric field is created within the tissue of
the patient. Because of the relatively high electrical resistance of tissue in comparison with the metal
electrodes, there is marked agitation of the ions present in the target tissue that surrounds the electrode, as
the tissue ions attempt to follow the changes in direction of alternating electric current. The agitation results
in frictional heat around the electrode. The discrepancy between the small surface area of the needle
electrode and the large area of the grounding pads causes the generated heat to be focused and
concentrated around the needle electrode.
(2) To achieve low rates of local tumor recurrence with RF ablation, which are comparable to those
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obtained with hepatic resection, physicians should produce a 360-degree, 0.5- to 1-cm-thick tumor free
margin around each tumor. This cuff will assure that all microscopic invasions around the periphery of a
tumor have been eradicated. Thus, the target diameter of an ablation must be ideally 1 to 2 cm larger than
the diameter of the tumor that undergoes treatment (3) (Fig. 56.1).
FIGURE 56.1 • RF ablation of HCC. Pretreatment CT shows the lesion as a small hypervascular nodule ( A,
arrow) in the arterial phase, with slightly hypodense appearance in the delayed phase (B, arrow). On CT
images obtained in the arterial (C) and the portal venous phase (D) 1 month after treatment, the tumor is
replaced by a nonenhancing ablation zone that exceeds in size the diameter of the naive tumor. The
findings are consistent with complete response.
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(3) The thermal damage caused by RF heating is dependent on both the tissue temperature achieved and
the duration of heating. Heating of tissue at 50°C to 55°C for 4 to 6 minutes produces irreversible cellular
damage. At temperatures between 60°C and 100°C, near immediate coagulation of tissue is induced, with
irreversible damage to mitochondrial and cytosolic enzymes of the cells. At more than 100°C to 110°C,
tissue vaporizes and carbonizes. For adequate destruction of tumor tissue, the entire target volume must be
subjected to cytotoxic temperatures. Thus, an essential objective of ablative therapy is the achievement and
maintenance of 50°C to 100°C temperature throughout the entire target volume for at least 4 to 6 minutes.
However, the relatively slow thermal conduction from the electrode surface through the tissues increases
the duration of application to 10 to 20 minutes. To accomplish the increase in energy deposition into
tissues, the RF output of all commercially available generators has been increased to 150 to 250 W.
(4) On the other hand, the tissue temperature should not be greater than 100°C to 110°C, so as to avoid
carbonization with significant gas production that both serves as an insulator and diminishes the ability to
effectively establish an RF field. After activation, the generators are run by automated programs, designed
to modulate the released power relying on direct temperature measurement or on electrical measurement of
tissue impedance, to avoid overheating and carbonization.
(5) At the end of the procedure, coagulation of the needle track is performed to prevent tumor seeding.
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(6) Another important factor that affects the success of RF thermal ablation is the heat loss through
convection by means of blood circulation, the so-called heat sink effect. This may limit target volume and
therefore the ability to ablate all viable tumors and produce an adequate tumor-free margin. To minimize
heat loss by heat sink effect, several strategies for reducing blood flow during ablation therapy have been
proposed. Total portal inflow occlusion (Pringle maneuver) has been used at open laparotomy and at
laparoscopy. Angiographic balloon catheter occlusion of the hepatic artery or embolization of the tumor-
feeding artery has also been shown to be useful in hypervascularized tumors.
(7) One or multiple electrodes have to be inserted directly into the tumor to deliver RF energy current.
Electrodes are coupled with RF generators and can be monopolar or bipolar, and they can have different
designs (multitined expandable, internally cooled, perfused) (3). There is no current evidence that one
device is superior to the others. Similar results in term of technical success can be obtained by adjusting the
time at target temperature and the number of overlapping ablations according to different device designs.
(a) Monopolar electrode: There is a single active electrode, with current dissipated at one or several return
grounding pads.
(b) Bipolar electrode: There are two active electrode applicators, which have to be placed in proximity.
(c) Multitined expandable electrode: Multiple electrode tines that expand from a larger needle cannula. They
permit the deposition of this energy over a larger volume and ensure more uniform heating that relies less
on heat conduction over a large distance.
(d) Internally cooled electrode: The electrode has an internal lumen, which is perfused by saline without
coming into direct contact with patient tissues. They have been designed to minimize carbonization and gas
formation around the needle tip by eliminating excess heat near the electrode.
(e) Perfused electrode: The tip of the electrode has small apertures that allow the fluid (usually saline) to
come in contact with the tissue.
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Administration of saline solution during the application of RF current increases tissue conductivity and
thereby allows greater deposition of RF current and increased tissue heating and coagulation.
b. Microwave ablation (MWA)
(1) MWA is emerging as a valuable alternative to RF ablation for thermal ablation of HCC. Electromagnetic
microwaves heat matter by inducing an ultra-high-speed (between 900 MHz and 2,450 MHz) alternating
electric field, causing the rotation of water molecules. The main features of MW technology, when
compared with existing thermoablative technologies, include consistently higher intratumoral temperatures,
larger tumor ablation volumes, faster ablation times, and an improved convection profile. As a result, the
advantage of MWA over RF ablation is that treatment outcome is less affected by vessels located in the
proximity of the tumor (4).
(2) In addition, because MWA does not rely on an electrical circuit as does RF ablation, multiple applicators
can be applied simultaneously.
c. Irreversible electroporation (IRE)
(1) A new, nonchemical, nonthermal image-guided ablation technique that is currently undergoing clinical
investigation is IRE (4). IRE is a method to induce irreversible disruption of cell membrane integrity, by
changing the transmembrane potential, resulting in cell death without the need for additional pharmacologic
injury (4). IRE creates a sharp boundary between the treated and untreated area in vivo. This would
suggest that IRE has the ability to sharply delineate the treatment area from the nontreated, and that
treatment planning can be precisely performed according to mathematical predictions. Moreover, because
IRE is a nonthermal technique, there appears to be complete ablation to the margin of blood vessels without
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compromising the functionality of the blood vessels. Therefore, issues associated with perfusion-mediated
tissue cooling or heating (a significant challenge with thermal methods) are not relevant. IRE may be a
treatment option for centrally located liver tumors with margins adjacent to major bile ducts where thermal
ablation techniques are contraindicated.
3. Imaging guidance/monitoring. Targeting of the lesion can be performed with US, CT, or MR imaging (5).
The guidance system is chosen largely on the basis of operator preference and local availability of
dedicated equipment such as fluoro-CT or open MR systems.
a. During the procedure, important aspects to be monitored include adequate tumor coverage and whether
any adjacent normal structures are being affected.
b. Although the transient hyperechoic zone that is seen with US within and surrounding a tumor during and
immediately after RF ablation can be used as a rough guide to the extent of tumor destruction, MR is
currently the only imaging modality with validated techniques for real-time temperature monitoring.
c. Contrast-enhanced US performed after the procedure may allow an initial evaluation of treatment effects.
However, contrast-enhanced CT and MR imaging are recognized as the standard modalities to assess
treatment outcome (1,2,5,6) (Fig. 56.2 ).
1. After ablation, bed rest for 1 to 2 hours is advised.
2. Vital sign monitoring is performed in the recovery room. If vital signs are stable, blood count and liver function
tests are not significantly changed, and no complications are noted; the patient can be discharged the day after
the procedure.
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FIGURE 56.2 • Immediate preliminary evaluation of RF ablation efficacy by contrast-enhanced ultrasound.

Pretreatment CT obtained in the arterial (A) and the delayed phase (B) shows the lesion as a small
hypervascular nodule. Preprocedural contrast ultrasound examination confirms arterial-phase enhancing tumor (
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arrows, C). B-mode low-mechanical index image is shown on the left side of the image; the contrast-specific
mode during the arterial phase is shown on the right side. After treatment with RF ablation under US guidance, a
large hyperechoic cloud covering the tumor as well as a cuff of surrounding liver parenchyma is seen on US (D).
(continued)
3. Tumor response evaluation

a. CT and MR images obtained 4 to 8 weeks after treatment show successful ablation as a nonenhancing area
with or without a peripheral enhancing rim (5,6).
b. The enhancing rim that may be observed along the periphery of the ablation zone appears as a relatively
concentric, symmetric, and uniform process in an area with smooth inner margins. This is a transient finding that
represents a benign physiologic response to thermal injury (initially, reactive hyperemia; subsequently, fibrosis
and giant cell reaction). Benign periablational enhancement needs to be differentiated from irregular peripheral
enhancement due to residual tumor that occurs at the treatment margin. In contrast to benign periablational
enhancement, residual unablated tumor often grows in scattered, nodular, or eccentric patterns (6).
c. Later follow-up imaging studies should be aimed at detecting the recurrence of the treated lesion (i.e., local
tumor progression), the development of new hepatic lesions, or the emergence of extrahepatic disease.
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FIGURE 56.2 • (Continued) Contrastenhanced ultrasound study performed at the end of the procedure shows
the ablation zone as unenhancing area completely covering the tumor. Periablation enhancement is also seen,
representing reactive hyperemia (E). On CT images obtained in the arterial (F) and the portal venous phase (G)
1 month after treatment, the tumor is replaced by a nonenhancing ablation zone and complete response is
confirmed.
d. Evaluation of tumor response should be performed following modified Response Evaluation Criteria in Solid
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Tumors (mRECIST) adopting the concept of viable tumor—tumoral tissue showing uptake in arterial phase of
contrast enhanced radiologic imaging techniques—to formally amending RECIST (7).
Results
1. Hepatocellular carcinoma
a. Very early stage HCC
(1) Nodules less than 2 cm, that are not subcapsular or perivascular, are the ideal target for percutaneous
RF ablation. Histologic data from explanted liver specimens in patients who underwent RF ablation showed
that tumor size and the presence of large (>3 cm) lesions abutting vessels significantly affect local treatment
effect. The complete response rate approaches 97%, with 5-year survival rates of 68% (8).
(2) In these small centrally located tumors, RF ablation seems to challenge the role of surgical resection,
allowing long-term survival rates similar to those of resection, with the preservation of liver parenchyma.
Recently, confirmatory information about the respective role of resection and RF ablation in the clinical
management of very early stage HCC has been provided by a decision analysis study by Cho et al. (9) who
concluded that
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RF ablation and hepatic resection are to be considered equally eff ective for the treatment of very early
stage HCC.
(3) Individual characteristics belonging to each patient—whether the tumor is central or peripheral, close or
distant form bile ducts, occurring in a patient who is lean or overweight, who presents with or without portal
hypertension, influence the results of each treatment making it better or worse than average. Because
clinical experience suggests that treatment in a subcapsular location or adjacent to the gallbladder is
associated with an increased risk of major complications and incomplete ablation, such tumor locations are
considered favorable for hepatic resection (3). Th erefore, in patients with very early stage HCC, RF
ablation can be off ered as a first-line treatment, considering a surgical approach when individual variables,
including tumor location, would make RF ablation not feasible or not safe.
b. Early stage HCC
(1) Patients with early stage HCC (single tumor ≤5 cm, or fewer than three tumors each ≤3 cm) can be
effectively treated by resection, liver transplantation, or percutaneous ablation with the possibility of long-
term cure and 5-year survival estimates ranging from 50% to 75% (4).
(2) Among different ablative techniques, RF ablation is currently considered the best treatment option.
Recent reports on long-term outcomes of RF ablation-treated patients have shown that in patients with
Child-Pugh class A and early stage HCC, 5-year survival rates are as high as 51% to 64% and may reach
76% in patients who meet the BCLC criteria for surgical resection (4). Therefore, an open question is
whether RF ablation can compete with surgical resection as first-line treatment not only for patients with
very early stage HCC but also for the subcategory of early stage patients with small, solitary HCC >2 cm.
Published results on this topic remain controversial.
(3) Solitary HCC >3 cm and <5 cm
(a) In patients with solitary HCC >3 cm and <5 cm in size, the success rate of RF ablation alone is
decreased; combination with intra-arterial treatment could be considered (4). A combination of TACE
followed by RF ablation has been used to minimize heat loss due to perfusionmediated tissue cooling and to
increase the therapeutic effect of RF ablation.
(b) Recently, the results of a randomized controlled trial (RCT) aimed at evaluating the therapeutic efficacy
of combining RF ablation with transarterial chemoembolization (TACE) for treating intermediatesized (3.1 to
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5 cm) HCCs have been published. Local tumor progression rates were significantly lower in the TACE-RF
ablation treated group compared to the RF only group (6% vs. 39%, P = .012) (10).
(c) TACE with drug-eluting beads has also been performed after an RF ablation procedure to increase
tumor necrosis in the peripheral part of the tumor by exposure to high drug concentration, where only
sublethal temperatures may be achieved in a standard RF ablation treatment (4) (Fig. 56.3). Further
research to determine optimal methods of combining chemotherapeutic regimens (both agent and route of
administration) with RF ablation is needed.
2. Colorectal hepatic metastases
a. Many studies have investigated the use of RF ablation in the treatment of limited CRC hepatic metastatic
disease in patients who were excluded from surgery. In a large number of leading centers, the use of
thermal ablation is limited to patients with fewer than five tumors that measure less than 3 cm each. In
studies in which percutaneous RF ablation for colorectal liver metastases was evaluated, median survival
varied between 28 and
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52 months, with a 5-year overall survival of 22% to 30% after the first RF ablation (11,12,13). These figures
are substantially higher than those obtained with any chemotherapy regimens and provide indirect evidence
that RF ablation therapy improves survival in patients with limited hepatic metastatic disease (14).
FIGURE 56.3 • HCC treated with a combination of RF ablation and drug-eluting bead chemoembolization.
Pretreatment CT shows hypervascular HCC in segment 7 (A). RF ablation is carried out under US guidance
by using a multitined expandable electrode (RITA Medical System, AngioDynamics) (B). Treatment is
completed with intra-arterial injection of 2 mL of 100 to 300 μm drug-eluting bead uploaded with 50 mg of
doxorubicin (DC Bead, Biocompatibles). CT obtained immediately after the procedure confirms
accumulation of the injected material along the periphery of the ablation zone (C). Follow-up CT scans
show complete response (D).
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b. An important issue to be considered is that the interval between resection of the primary CRC and the
occurrence of liver metastases has been reported to impact the results of liver surgery. Patients with CRC
liver metastases within 1 or 2 years after primary bowel resection have a worse prognosis compared with
patients with a longer disease-free interval. Although new liver metastases may eventually prompt repeated
hepatic surgery, extrahepatic disease may reduce the benefit of preceding liver resection. To avoid futile
surgery in early occurring hepatic metastases, percutaneous RF ablation has been used as the method of
first choice even where the lesions were amenable to surgery. The authors compared the group of patients
initially submitted to RF
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ablation to that of patients submitted to surgery. Local recurrence at the site of ablation or resection
occurred in 32% and 4% ( P <.001), new metastases apart from the site of previous treatment in 50% and
34% ( P = .179), and systemic recurrence in 32% and 37% ( P = .820) of the patients after RF ablation and
surgery, respectively. Time to progression was significantly shorter in patients primarily treated with RF
ablation (203 vs. 416 days; P = .017). After primary treatment, an identical 3-year overall survival was
demonstrated in both treatment groups: 67% and 60%, respectively; P = .93. The authors concluded that in
this specific subset of patients, despite striking differences in local tumor recurrence and shorter time to
progression, survival in patients with early CRC liver metastases does not depend on the mode of primary
hepatic treatment (15).
Complications (3,6)
1. Major complications (2.2% to 3.1%)
a. Intraperitoneal bleeding (1%)
b. Liver abscess (0.3%)
c. Intestinal perforation (0.3%)
d. Pneumothorax/hemothorax (0.1%)
e. Bile duct stenosis (0.1%)
f. Tumor seeding along the needle tract (0.5%)
g. Skin burns (0.1%)
2. Minor complications (5% to 8.9%)
a. Pain
b. Fever
c. Asymptomatic pleural effusion
d. Asymptomatic self-limiting intraperitoneal bleeding
3. Mortality (0.1% to 0.5%). The most common causes of death are sepsis, hepatic failure, colon perforation,
and portal vein thrombosis.
References
1. Bruix J, Sherman M. Management of hepatocellular carcinoma. Hepatology. 2005;42: 1208-1236.
2. European Association For The Study Of The Liver; European Organisation For Research And Treatment
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Of Cancer. EASL-EORTC clinical practice guidelines: management of hepatocellular carcinoma. J Hepatol .
2012;56:908-943.
3. Crocetti L, de Baere T, Lencioni R. Quality improvement guidelines for radiofrequency ablation of liver
tumours. Cardiovasc Intervent Radiol . 2010;33:11-17.
4. Lencioni R, Crocetti L. Local-regional treatment of hepatocellular carcinoma. Radiology. 2012;262:43-58.
5. Crocetti L, Della Pina C, Cioni D, et al. Peri-intraprocedural imaging: US, CT, and MRI. Abdom Imaging.
2011;36:648-660.
6. Ahmed M, Solbiati L, Brace CL, et al; for International Working Group on Image-Guided Tumor Ablation;
Interventional Oncology Sans Frontières Expert Panel; Technology Assessment Committee of the Society of
Interventional Radiology; Standard of Practice Committee of the Cardiovascular and Interventional
Radiological Society of Europe. Image-guided tumor ablation: standardization of terminology and reporting
criteria— a 10-year update. J Vasc Interv Radiol . 2014;25:1691-1705.
7. Lencioni R, Llovet JM. Modified RECIST (mRECIST) assessment for hepatocellular carcinoma. Semin
Liver Dis. 2010;30:52-60.
8. Livraghi T, Meloni F, Di Stasi M, et al. Sustained complete response and complications rates after
radiofrequency ablation of very early hepatocellular carcinoma in cirrhosis: is resection still the treatment of
choice? Hepatology. 2008;47:82-89.
9. Cho YK, Kim JK, Kim WT, et al. Hepatic resection versus radiofrequency ablation for very early stage
hepatocellular carcinoma: a Markov model analysis. Hepatology. 2010;51:1284-1290.
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10. Morimoto M, Numata K, Kondou M, et al. Midterm outcomes in patients with intermediate-sized
hepatocellular carcinoma: a randomized controlled trial for determining the efficacy of radiofrequency ablation
combined with transcatheter arterial chemoembolization. Cancer. 2010;116:5452-5460.
11. Machi J, Oishi AJ, Sumida K, et al. Long-term outcome of radiofrequency ablation for unresectable liver
metastases from colorectal cancer: evaluation of prognostic factors and effectiveness in first- and second-
line management. Cancer J. 2006;12: 318-326.
12. Sørensen SM, Mortensen FV, Nielsen DT. Radiofrequency ablation of colorectal liver metastases: long-
term survival. Acta Radiol . 2007;48:253-258.
13. Veltri A, Sacchetto P, Tosetti I, et al. Radiofrequency ablation of colorectal liver metastases: small size
favorably predicts technique effectiveness and survival. Cardiovasc Intervent Radiol . 2008;31:948-956.
14. Gillams A, Goldberg N, Ahmed M, et al. Thermal ablation of colorectal liver metastases: a position paper
by an international panel of ablation experts, the interventional oncology sans frontières meeting 2013
[published online ahead of print May 22, 2015]. Eur Radiol . doi:10.1007/s00330-015-3779-z.
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15. Otto G, Düber C, Hoppe-Lotichius M, et al. Radiofrequency ablation as first-line treatment in patients with
early colorectal liver metastases amenable to surgery. Ann Surg. 2010;251:796-803.
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57
Renal Tumors
Joseph P. Erinjeri
Timothy W.I. Clark
Cancer of the kidney accounts for approximately 4% of all malignancies in the United States. The American
Cancer Society estimates that 63,920 cases of kidney and renal pelvis cancer will be discovered in 2014, with
14,594 deaths attributable to the disease (1). Although surgical extirpation remains the standard of care for small
renal tumors, trends toward nephron-sparing techniques in the treatment of kidney cancer have made thermal
ablation of renal tumors a viable alternative to both open and laparoscopic partial nephrectomy.
Indications
T1 renal masses (<7 cm) in patients who:
1. Have comorbidities that preclude surgery
2. Have comorbidities that preclude general endotracheal anesthesia
3. Require conservation of renal parenchyma (solitary kidney, renal insufficiency)
4. Have multiple tumors in the same kidney (Von Hippel-Lindau or Birt-Hogg-Dubé) where surgical
extirpation would make renal reconstruction difficult
5. Have complex tumors where surgical resection would require an extended ischemia time
6. Prefer minimally invasive techniques over open or laparoscopic surgery
Contraindications
Absolute
1. Uncorrectable coagulopathy (when international normalized ratio [INR] >1.5, platelet count <50,000 per
μL).
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Relative
1. Anatomic considerations
a. Anteromedial masses, without a safe percutaneous route to the lesion
2. Contraindications to radiofrequency ablation (RFA)
a. Hip prosthesis, which may act as an electrical conduit, increasing risk of skin burn.
b. Pacemaker/defibrillator. Radiofrequency energy can interfere with pacer/defibrillator function. To
minimize risk, consider cryoablation in these patients; alternatively, patients can wear a magnet to
deactivate the device and have it calibrated and reprogrammed after the procedure.
1. Clinical consultation
a. Complete history and physical
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b. Laboratory studies with attention to coagulation parameters (INR, platelet count) and renal function
(creatinine, glomerular filtration rate [GFR]). A baseline hematocrit/hemoglobin should be obtained.
c. Review of medications. For most patients, aspirin and other antiplatelet medication should be stopped 5 days
before the procedure. However, in patients with prior coronary artery or vascular stents, it may be prudent to
continue these medications to reduce the risk of possible stent thrombosis. Warfarin should be adjusted to an
INR < 1.5. Enoxaparin should be withheld for at least 12 hours before the procedure.
2. Preprocedure imaging
a. Contrast-enhanced computed tomography (CT) urogram provides optimal preprocedure imaging, allowing for
staging, characterization of the renal mass, and evaluation of the proximity of the mass to the collecting system
and other vital structures (bowel, ureter, organs, nerves). Dynamic contrastenhanced magnetic resonance
imaging (MRI) is an alternative. Patients with GFR 30 to 60 mL/min/1.73 m2 should undergo intravenous (IV)
hydration (before contrast CT) or receive a decreased contrast dose (before MRI). Patients with GFR <30
mL/min/1.73 m2 should not receive iodinated or gadolinium contrast. Although ultrasound imaging can clearly
define the tumor and its relation to the collecting system and renal hilum, cross-sectional imaging provides a
comprehensive survey of surrounding tissues, which can be helpful for treatment planning.
b. Comparison with prior imaging should be performed to evaluate the growth rate of the lesion. Tumor size and
growth rate of renal lesions are correlated with their malignant potential. More than 40% of renal masses <1 cm
are benign, 25% of renal masses <3 cm are benign (2).
c. Typically, exophytic tumors can be treated more effectively, as perirenal fat acts as a thermal insulator that
helps to maintain target temperature during ablation. Conversely, central lesions which are in close proximity to
the collecting system or hilar vessels suffer from heat sink effects, which can limit the ability to reach target
temperature throughout the lesion.
3. Biopsy. For biopsy of small renal masses, sensitivity of biopsy for the diagnosis of malignancy is 80% to 92%,
whereas specificity is 83% to 100% (3). Up to 5% of biopsies of small renal masses result in diagnosis of benign
tumors. Several special cases exist when biopsy should be performed before proceeding with ablation to avoid
unnecessary or ineffective procedures:
a. Extrarenal malignancy (where the renal mass could represent metastatic disease rather than a primary renal
malignancy)
b. Suspected lymphoma
c. Renal “mass” found in association with a urinary tract infection (where the mass could represent an abscess
or inflammatory mass)
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4. Overnight fast, nil per os (NPO) for procedure
5. Informed consent
6. Device selection
a. Radiofrequency ablation. Both linear and multitined array (umbrella) applicators are available. Array
applicators come in different geometries and can be deployed to different sizes, which allows the operator to
tailor the ablation zone to the tumor size and shape. It is important to note whether an array “burns forward” (from
the tip to the undeployed applicator distally after deployment of the tines) or “burns backward” (from the tip to the
undeployed applicator proximally after deployment of the tines). Linear probes are somewhat simpler to use,
since they do not require deployment of the tines, which can be difficult to deploy after the initial ablation due to
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change in the consistency of the coagulated renal tissue. Targeting tumors with linear applicator is done in a
manner analogous to needle biopsy. With most radiofrequency devices, only one applicator can be used at a
time. If the tumor is large, multiple serial ablations must be performed to ensure adequate coverage of the lesion.
b. Cryoablation. The major technical advantage of cryoablation over RFA is that ablation zones can be monitored
in real-time with CT, MRI, or ultrasound. Two parameters can be varied in the selection of cryotherapy
applicators to shape the ablation zone: (a) length of the active area of applicator, which affects the length of the
cryoablated region or “ice ball,” and (b) diameter of the shaft, which affects the axial diameter of the ice ball. A
larger applicator shaft diameter yields a larger axial diameter ice ball. Because multiple applicators can be placed
simultaneously and the ablation zones coalesce, complex-shaped tumors can be targeted using a combination of
different lengths and shaft diameter applicators.
c. Emerging technologies. Preclinical and early phase trials are being conducted in new image-guided renal
ablation modalities.
(1) Microwave ablation. A needle antenna emits microwave energy to surrounding tissue, which results in
cytotoxic tissue heating.
(2) High-intensity focused ultrasound (HIFU). Ultrasonic energy is focused to produce high acoustic intensities in
tissue, which results in cytotoxic heat generation due to absorption of the acoustic energy.
(3) Irreversible electroporation (IRE). This nonthermal technique uses pulsed electrical fields to create permanent
nanoscale defects or pores in the plasma membrane of cells resulting in cell death.
(4) Laser ablation. Laser light applied directly to tissue results in cytotoxic tissue heating.
7. Antibiotics. Cefazolin 1 g IV
Procedure
1. Monitoring of vital signs for conscious sedation/anesthesia (electrocardiogram [ECG], blood pressure,
pulse oximetry, and respiration)
2. Sedation/anesthesia. Thermal injury due to cold is associated with minimal pain, whereas thermal injury
with heat can be considerably painful. Patients undergoing cryoablation generally tolerate the procedure
with moderate sedation (fentanyl and midazolam), whereas patients undergoing RFA may require deep
sedation or general anesthesia.
3. Patient positioning and approach. Patients are typically positioned prone. Prone positioning facilitates
probe placement for lower pole, posterior lesions. For upper pole lesions, ipsilateral decubitus positioning
deflates the ipsilateral lung, minimizing the risk of pneumothorax. Oblique supine positioning (ipsilateral up
to 30 degrees) can be helpful for lateral lesions and can aid in displacing bowel medially away from the
kidney. Supine transhepatic approaches have been described. For upper pole lesions, especially on the
left, proximity to the lung and
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pleura can limit access options. An iatrogenic pneumothorax or pleural effusion can be created by insertion
of a 22-gauge needle into the pleural space, with infusion of air or 5% dextrose solution (D5W),
respectively. A transpleural intercostal approach can then be performed. Following the procedure, a small-
bore chest tube should be inserted and placed to water seal. The chest tube can be removed the morning
after the procedure after clamping trial and serial chest x-rays.
4. Ablation technique
a. Scout imaging is obtained to localize the target. If necessary, contrast can be given to increase
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conspicuity of the target. The CT gantry can be angled on scout imaging to maintain longitudinal needle
visualization during subcostal needle placement. The point of skin entry is determined based on the
planned needle trajectory.
b. The skin entry site is prepped and draped. The site is anesthetized with lidocaine. A small dermatotomy
is made to facilitate needle placement.
c. Biopsy (fine needle aspiration or core) can be performed, if tissue diagnosis of the lesion has not been
performed previously.
d. Under imaging guidance, the ablation probe(s) are placed. With cryoablation, multiple applicators may be
placed simultaneously to ensure that the ice ball will encompass the lesion. With RFA, the electrode is first
placed at one margin of the lesion, allowing subsequent electrode placements to create an overlapping
ablation zone.
e. Ablation
(1) Cryoablation. After confirming needle placement(s), ablation is usually conducted with two freeze-thaw
cycles (e.g., a 10-minute freeze, 8-minute thaw, and 10-minute refreeze). The diameter of the ice ball
initially increases rapidly; cross-sectional imaging during the procedure may be performed at 3- to 5-minute
intervals to minimize nontarget ablation. Ice ball temperature readings are usually in the - 80°C to - 150°C
range. Cytotoxic intracellular ice formation in renal cells occurs best with rapid cooling below - 20°C (4). Ice
ball formation can be monitored in real time via CT (hypoattenuating ice ball), MRI (hypointense ice ball),
and ultrasound (shadowing ice ball). It should be noted that the edge of the ice ball marks the 0°C isotherm,
and the - 20°C isotherm is deep to the ice ball margin. Therefore, to ensure cytotoxic target temperature
within the lesion, an ice ball margin should exceed the margin of the lesion by at least 5 to 10 mm. Some
operators utilize a thermocouple at the tumor margin to ensure that the target temperature at the margin of
the lesion reaches - 20°C. Following the freeze-thaw-freeze cycle, active thawing to 15°C should be
performed before attempting to remove the applicator; the applicator should not be removed forcefully if it
remains frozen to the lesion as renal fracture can occur.
(2) Radiofrequency ablation. After confirming needle placement (which may include deploying the multitined
array prior to ablation), ablation is begun according to device protocol. Protocols usually involve at least 10
minutes of ablation, with temperature measurements during or immediately after ablation depending on the
device. Devices with impedance-based end points utilize protocols with stepwise increases in power until
maximal impedance, a surrogate marker for cytotoxic cellular change, is reached. During the ablation, the
tines of the cluster are advanced periodically (according to device protocol) to allow for a larger volume of
ablation. Care should be taken when advancing the tines with slight forward pressure on the shaft of the
needle, as the increased firmness of the ablated tissue can lead to “backing out” of the needle and failure of
the tines to advance through the previously ablated tissue. Cytotoxic coagulation necrosis occurs rapidly at
temperatures of 60°C to 100°C (5). The area of the ablation zone cannot be directly monitored during RFA;
however, ablated
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tissue becomes slightly lower in attenuation on CT due to tissue edema. The needle can be repositioned,
and this process repeated with overlapping ablations until the lesion is adequately covered. In the event
that the electrode is to be removed from the kidney for repositioning or following the last ablation, track
ablation of intervening normal renal parenchyma should be performed according to the device instructions.
In general, the needle should be withdrawn to ensure a temperature within the tract of 80°C. Track ablation
should be halted at least 1 cm from the skin surface to avoid skin burn.
f. Immediate postprocedure imaging should be performed following removal of the ablation probe to assess
for immediate complications.
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g. A sterile dressing is applied.
5. Special techniques to limit nontarget ablation
a. Ureteral stent placement. To protect the ureter and collecting system from thermal injury, retrograde
ureteral stent placement can be performed cystoscopically for infusion of D5W through the renal collecting
system, dissipating heat and minimizing injury. Dextrose is used rather than saline to minimize conduction
effects during RFA.
b. Hydrodissection and pneumodissection. Adjacent or intervening tissues (bowel, pancreas, adrenal, and
spleen) can be displaced by infusion of D5W or air. A 22-gauge needle or sheath can be placed between
the kidney and intervening structure, and D5W or air injected as needed to create a buffer of 1 to 2 cm. The
choice of D5W or air is based on whether structures should be moved in a dependent or nondependent
manner. If necessary, a large occlusion balloon (14 mm) can be inflated between the kidney and the
adjacent structure to create a buffer between the lesion and tissue.
1. Bed rest for 4 hours or until hematuria begins to clear
2. Check vital signs every 15 minutes for 1 hour, every 30 minutes for 2 hours, every hour for 4 hours, and then
every 8 hours.
3. Monitoring fluid input and output. Blood-tinged urine may be seen up to 48 hours after procedure. “Pink
lemonade” appearance is typical.
4. Resume preprocedure diet.
5. Continue antibiotics for 8 hours after procedure.
6. Patients can be discharged the same day, but given the age and performance status of many patients, an
overnight stay is often prudent.
7. Imaging
a. CT or MRI at 1 to 3 months should be obtained to identify residual tumor from an incomplete ablation. Subtle
enhancement can be seen in the periphery of the ablation zone on early imaging (which may represent
inflammation) but is usually resolved by 6 months. Follow-up imaging every 3 to 6 months for the first year should
be continued as surveillance for recurrent disease.
b. If the patient shows no residual enhancement over a 1-year period, longer imaging intervals (1 to 2 years) can
be employed.
Results
1. No randomized controlled trials have been performed to compare thermal ablation (RFA or cryoablation)
to partial nephrectomy—the reference standard for treatment of T1 renal cancer.
2. Local recurrence is seen in 2.6% of patients following nephron-sparing surgery, 4.6% following
cryoablation, and 11.7% following RFA (as determined by a
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meta-analysis of 99 studies of 6,471 tumors treated with partial nephrectomy, cryoablation, RFA, or active
surveillance) (6). Local recurrence was higher in patients with larger tumors.
3. The 5- and 10-year survival rates are 98% and 94% in those undergoing nephronsparing surgery, and
96% and 82% in those undergoing ablation in a population study of 8,818 Surveillance, Epidemiology, and
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End Results (SEER) database patients (7).
4. Percutaneous ablation has a significantly lower major complication rate than surgical ablation (3% vs.
7%, respectively, P < .05) and a significantly lower length of hospital stay (1.4 vs. 3.0 days, respectively, P
< .05), as determined by a meta-analysis of 46 studies of percutaneous and surgical ablations of 1,180
renal tumors in 1,055 patients) (8).
5. Cryoablation has significantly lower rates of local tumor progression than RFA (5.2% vs. 12.9%), in a
meta-analysis of 47 studies representing 1,375 kidney lesions (9).
Complications
1. Bleeding: 20% to 40%, usually self-limited
a. Gross hematuria: Passage of clots is rare.
b. Hematoma (subcapsular, extracapsular): Drainage is rarely helpful as bleeding will be tamponaded by
the capsule. If severe, worsened renal function or hypertension can be seen (Page kidney).
2. Urine leak: 1%; capsular disruption with urine leak can range from a small amount of urine seen outside
the kidney on follow-up imaging to frank urinoma. Animal studies and human case series suggest that the
risk of collecting system injury may be less with cryoablation than with RFA (10).
3. Nerve injury: <1%; thermal damage to the intercostal nerve can result in trunk numbness. The
ilioinguinal, iliohypogastric, or genitofemoral nerves run along the anterior aspect of the psoas muscle and
can be injured during ablation of posteromedial renal lesion, resulting in groin/leg numbness and/or hip
flexion weakness. These effects can be transient or permanent depending on the degree of nerve injury.
Treatment options are limited.
4. Track seeding: 0.6% to 2.5%, rare, but track ablation may minimize risk.
5. Skin burns: <1%; grounding pad burns with RFA can be minimized by shaving the skin under the pad (to
ensure uniform conduction through the skin), placing the long axis of the grounding pad perpendicular to the
long axis of leg, and minimizing pressure on the grounding pad. Most important, frequent physical checks of
the grounding pad should be performed to identify overheating.
6. Infection: rare; prophylactic antibiotics may minimize risk.
7. Nontarget ablation: rare if a 1-cm margin from vital organs, nerves, or bowel is maintained. It is important
to note that the location of critical structures may change when comparing procedural and preprocedural
imaging as well as intraprocedurally.
1. Bleeding
a. Hematuria. Gross hematuria can indicate damage to the renal collecting system. Even with passage of
clots, hematuria usually resolves in 24 to 48 hours. Life-threatening bleeding may require arterial
embolization. If a large amount of clot is seen, the urology service can be consulted, as the patient may
benefit from bladder irrigation.
b. Hematoma. Small subcapsular or extracapsular hematoma can be managed with serial hemoglobin
measurement. Attention to follow-up creatinine levels and blood pressure is indicated. Follow-up imaging to
document resolution
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of the hematoma is typically not necessary. Life-threatening retroperitoneal hemorrhage may require arterial
embolization.
2. Urine leak. Small amounts of perirenal contrast on delayed follow-up imaging likely represents a small
urine leak, which can resolve spontaneously via urothelial healing. Frank urinoma may require
percutaneous drainage, as well as diversion, preferably with double-J ureteral stents. If the patient has an
ileal conduit, a course of broad-spectrum antibiotics should be given, as the urinary tract is likely colonized
and may lead to superinfection of the urinoma.
3. Infection. May require broadening of antibiotic coverage. Drainage may be required if perirenal abscess
formation occurs.
4. Nerve injury. Numbness, paresthesias, or weakness can be self-limited. However, in some cases,
sensory and motor deficits can persist.
5. Track seeding. If nodular, enhancing, or enlarging tissue is seen along the ablation track on follow-up
imaging, a surgical consult is warranted. Biopsy and excision may be necessary.
6. Skin burns. First-degree burns require simple dressing. However, a plastic surgery consult should be
obtained for second- and third-degree burns. Skin grafting is rarely necessary.
7. Nontarget ablation. Ablation of the pancreas can result in pancreatitis while thermal ablation of the bowel
can lead to bowel necrosis or perforation. NPO status and supportive care should be initiated. Surgical
consultation should be considered because bowel repair or resection may be necessary on rare occasions.
References
1. Siegel R, Ma J, Zou Z, et al. Cancer statistics, 2014. CA Cancer J Clin. 2014;64:9-29.
2. Frank I, Blute ML, Cheville JC, et al. Solid renal tumors: an analysis of pathological features related to
tumor size. J Urol . 2003;170:2217-2220.
3. Silverman SG, Gan YU, Mortele KJ, et al. Renal masses in the adult patient: the role of percutaneous
4. Chosy SG, Nakada SY, Lee FT Jr, et al. Monitoring renal cryosurgery: predictors of tissue necrosis in
swine. J Urol . 1998;159:1370-1374.
5. Rehman J, Landman J, Lee D, et al. Needle-based ablation of renal parenchyma using microwave,
cryoablation, impedance- and temperature-based monopolar and bipolar radiofrequency, and liquid and gel
chemoablation: laboratory studies and review of the literature. J Endourol . 2004;18:83-104.
6. Kunkle DA, Egleston BL, Uzzo RG. Excise, ablate or observe: the small renal mass dilemma—a meta-
analysis and review. J Urol . 2008;179:1227-1234.
7. Whitson JM, Harris CR, Meng MV. Population-based comparative eff ectiveness of nephron-sparing
surgery vs ablation for small renal masses. BJU Int. 2012;110: 1438-1443.
8. Hui GC, Tuncali K, Tatli S, et al. Comparison of percutaneous and surgical approaches to renal tumor
ablation: metaanalysis of effectiveness and complication rates. J Vasc Interv Radiol . 2008;19:1311-1320.
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9. Kunkle DA, Uzzo RG. Cryoablation or radiofrequency ablation of the small renal mass: a meta-analysis.
Cancer. 2008;113:2671-2680.
10. Warlick CA, Lima GC, Allaf ME, et al. Clinical sequelae of radiographic iceball involvement of collecting
system during computed tomography-guided percutaneous renal tumor cryoablation. Urology. 2006;67:918-
922.
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58
Musculoskeletal Biopsies and Ablations
Peter L. Munk
Musculoskeletal Biopsy
Introduction
Responsibility for musculoskeletal biopsy varies considerably from one department to the next. In many
institutions, this has fallen into the hands of the interventional radiologist because biopsy of bone is quite
different than traditional soft tissue biopsy of the type typically practiced in abdominal or pelvic imaging (1,2). The
instruments and technique utilized are different, and analgesia with or without sedation is almost always
required. The way in which a biopsy is performed also has profound implications on the surgery performed by
the orthopedic oncologist if a sarcoma is diagnosed. Because of this, the importance of proper planning of the
biopsy (the route that the biopsy is performed through, and the area of the tumor sampled) cannot be
overemphasized. This latter point will be repeatedly made. Biopsy of soft tissue masses of the musculoskeletal
system is very similar to that of soft tissue biopsy elsewhere with the proviso, once again, that biopsy requires
careful planning so that the definitive surgery is not compromised (1).
Indications
1. Diagnosis of a tumor of bone, muscle, or connective tissue. A sarcoma must be suspected until proven
otherwise (1).
2. Confirmation of suspected metastases
3. Exclusion of malignancy in a lesion that may be benign
Contraindications
Absolute
1. Incomplete imaging and staging of the lesion prior to biopsy (1)
2. International normalized ratio (INR) greater than 1.5
3. Uncooperative or unwilling patient or inability to obtain informed consent from the patient or responsible
caregiver
4. Uncertainty about planned definitive surgical excision route. The biopsy path must follow the same path
that the surgeon plans to use to definitively excise the tumor as sarcomas have a high propensity to seeding
the biopsy tract. Because of this, the biopsy tract must be removed at the time of definitive surgery, and an
ill-conceived or incorrectly planned route can significantly compromise surgery performed—it may convert a
limb-sparing procedure into an amputation, or a curative procedure into one for which cure cannot be
achieved. If any uncertainty whatsoever exists about the biopsy path, consultation with the surgeon who will
perform the definitive surgery is mandatory (1,2).
Relative
1. Platelet count below 50,000 per μL or recent use of platelet inhibitors. The risk of hematoma is increased
in these situations, and tracking of a hematoma can spread sarcoma.
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1. Definitive locoregional imaging must have been completed. In most instances, this consists of cross-sectional
imaging, preferably magnetic resonance imaging (MRI).
2. The type of image guidance for the procedure should be decided, and the equipment booked.
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3. Surgical consultation, including full clinical assessment and tentative planning of definitive surgery in order to
permit assessment of the required biopsy route
4. Informed consent must be obtained for the biopsy either from the patient or a responsible caregiver.
5. Arrangement of day care bed and availability of nursing staff to monitor the patient and to provide analgesia +
/ - sedation (which is often required for bone biopsies).
6. The patient should be on nil per os (NPO) except for medications from midnight the day before the procedure.
7. Arrangements should be made for the patient to be escorted home after the procedure if medications have
been administered. Under rare circumstances, where this is not possible, it may be necessary for a longer day
care admission or possibly even an overnight stay.
Procedure
a. Intravenous access is required. Patients are closely monitored by a nurse who can administer sedation
(midazolam) and/or analgesia (fentanyl) during the procedure. Electrocardiogram (ECG) and oxygen
saturation monitoring are recommended.
b. The patient must be placed in a comfortable position that can be maintained throughout the course of the
procedure.
c. Bone tumors with mineralization present are usually done in the author's institution with computed
tomography (CT) guidance in order to accurately document the position of the needle. In this way, the
portion of the tumor being sampled is known. Very large destructive tumors can on occasion be biopsied
under fluoroscopic guidance, although this is exceptional. Soft tissue masses are usually biopsied with
sonographic guidance. Bone tumors with soft tissue components associated with the osseous lesion can
often be successfully biopsied using sonographic guidance as well (1).
d. Patient positioning must allow optimal access to the biopsy site via the route decided upon at the time of
surgical planning and consultation with the orthopedic oncologist.
e. The area to be accessed is then sterilized and draped.
a. Thorough hand washing and gloving are mandatory, and the use of facial shield or goggles is
recommended.
b. Use of needle receptacle and devices that avoid the necessity of recapping needles is strongly
recommended.
3. Biopsy procedural details
a. Typically, the patient receives a small amount of midazolam (Versed) prior to initiating the procedure.
b. The skin is anesthetized with 2% lidocaine and a 25-gauge needle.
c. A skin incision is made longitudinally (never transversely) approximately 1 cm in length. This not only
allows easier access for instruments but also allows the surgeon to clearly see the puncture site utilized for
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the biopsy and ensure that it should be excised at the time of surgery. (If preferred, a suture can be placed
afterward to aid in identification of the biopsy site.)
d. Infiltration of biopsy tract with local anesthesia (2% lidocaine using a 20- or 22-gauge spinal needle): The
tract is first carefully planned (which with CT may require placement of a localization grid), and calculation
of the distance from the puncture site to the target area within the tumor is made so an appropriate-length
needle can be selected. The target area in the tumor is chosen based on the route to be used by the
surgeon and the location of viable (non-necrotic or mucinous) tissue. The route to be selected should not
violate an uncontaminated compartment and must avoid neurovascular structures
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(which would have to be resected at the time of surgery if contaminated with sarcoma). These issues will
have been discussed ahead of time with the referring surgeon (1,2).
e. The needle is then introduced along the preplanned route.
(1) All biopsies of both bone and soft tissue should be core biopsies; fine needle aspiration is of no value in
this situation.
(2) A large variety of different devices suitable for core biopsy exist on the market. Most will provide cores
between 20 gauge and 12 gauge in diameter; in the author's institution, a 14-gauge device is used. Devices
for bone biopsy are typically variants of the Jamshedi-type needle. This needle has small teeth at the end
and is capable of cutting through bone.
(3) It is recommended that biopsies be done coaxially, the Jamshedi needle going through an outer sheath
allowing for multiple core biopsies to be obtained through the same access site. The tip of the needle where
the sample is being obtained from should be recorded in order to document the tissue site being sampled.
(4) Soft tissue samples can be obtained using spring-loaded cutting needles as with biopsies performed in
the abdomen and pelvis (1).
f. A minimum of three cores should be obtained whenever possible. Different departments will have
different protocols for evaluation of musculoskeletal tumors, so consultation ahead of time with the reading
pathologist will be helpful in ensuring that the number and type of samples required are obtained (i.e., fresh
vs. formalin, etc.). The type of samples and pathologic examination required should be decided ahead of
time and the appropriate tubes, receptacles, and requisitions prepared in advance.
g. At the conclusion of the procedure, the needle is removed, and pressure is placed over the puncture site
in order to ensure that homeostasis is achieved. This is particularly important in patients who may have
borderline laboratory values or be on platelet inhibitors.
1. The patient is monitored from 2 to 4 hours, depending on the amount of analgesia and sedation administered.
In most cases, at the conclusion of this time, the patient is ready to go home.
2. The puncture site is checked every 15 minutes for the first hour and hourly thereafter.
Results
1. Core needle musculoskeletal biopsy is a highly successful technique producing diagnostic results in 90%
to 93% of patients. Diagnostic yields tend to be slightly higher with patients with malignant disease and
slightly lower in patients with benign disease.
2. Typically, in patients with extensive myxoid or necrotic material, there is a higher risk of obtaining
nondiagnostic biopsy material; therefore, every effort must be made to sample solid, viable portions of
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tumor.
3. Patients having definitive surgical procedures after poorly planned biopsies require a different or more
complex procedure in up to 19% of cases, with conversion to amputation from limb-sparing procedure in
approximately 5% of this subset.
Complications
1. Tumor seeding along the tract of the biopsy. This may occur in 5% to 10% of cases; however, because
the tract is usually excised at the time of definitive surgery, this does not pose a problem in most patients
(1).
2. Bleeding and hematoma
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3. Contamination of the neurovascular bundle or an uncontaminated compartment. This is usually the result
of a poorly planned biopsy route.
4. Infection—very rare
5. Inadequate tissue: This is due to either obtaining an inadequate number of samples or sampling a
necrotic or myxoid tumor. It is always preferable to obtain additional core biopsies if any doubt exists as to
whether sufficient tissue is available.
1. If a poorly planned biopsy/attempted excision has been performed (a “whoops” procedure), consultation
with the surgeon with complete disclosure of procedural details is essential. This may allow construction of
a suitable alternate surgical plan that may still permit a satisfactory clinical outcome. This is often highly
challenging or may not be possible. Use of radiotherapy and/or chemotherapy prior to or following the
surgical excision may be of benefit (1).
2. Hematomas can be minimized by careful compression and monitoring of the biopsy site, particularly in
patients with coagulopathy or platelet dysfunction.
3. Infection may require treatment with antibiotics.
Radiofrequency and Cryoablation of Musculoskeletal Lesions

Introduction
Radiofrequency (RF) ablation is a technique that involves the use of electrodes to heat target tissue to a
sufficiently high temperature to induce coagulation and necrosis. This technique has been widely utilized in
ablation of liver and abdominal tumors but has also found an important role in management of selected osseous
lesions, particularly osteoid osteoma (3). More recently, additional target sites in the musculoskeletal system
have become the subject of treatment with this technique, particularly metastatic lesions in bone and soft tissue
(4,5,6,7).
At the present time, treatment of osteoid osteoma remains the most widely accepted application for this
technique in the musculoskeletal system, and indeed RF ablation has become the standard of care for treatment
of this condition. A variety of different generator types and probes exist that are suitable for treatment of both
benign lesions such as osteoid osteoma as well as metastatic deposits. Careful adherence to the specifications
of the manufacturer is important in order to ensure successful clinical outcomes and avoidance of complications.
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Cryoablation uses generation of an ice ball to freeze lesions rather than destroying them with elevated
temperatures as in RF ablation. With advances in this technology, it has increasingly displaced the use of other
more well-established techniques, such as RF ablation. Use of cryoablation in the musculoskeletal system is, at
present, relatively limited, but it appears to be an effective and promising technique that is increasingly being
applied to treatment of both malignant and benign lesions (8,9,10).
Indications
1. Treatment of osteoid osteoma and selected other benign tumors, such as osteoblastoma and
fibromatosis (9)
2. Palliative treatment of metastatic deposits in bone and muscle. In bone, this may be done in combination
with injection of methylmethacrylate cement (cementoplasty) in order to provide additional structural support
(11,12,13,14).
3. Palliative rhizotomy for intractable pain when other more conservative techniques have failed
Contraindications
Absolute
1. RF ablation in general should not be performed if a nerve is likely to be in the ablation zone. Rarely, in
select patients who require palliation for unremitting
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pain, this may be an acceptable trade-off. Ablation of other organs, such as bowel, may also constitute an
unacceptable risk.
2. Coagulopathy (INR >1.5, platelet count <50,000 per μL)
Relative
1. Platelet inhibitors: Procedures can be performed allowing that an increased risk for developing hematoma
exists.
2. Presence of nearby overlying articular cartilage/normal joint surface: The ablation of subjacent bone may
result in cartilage/bone necrosis and possible collapse/arthritis. This may be acceptable if life expectancy is
limited, or no other readily satisfactory solution to achieving pain control is felt to be available. Patients must
be fully informed of this potential risk.
3. Close proximity to an epiphyseal growth plate may result in necrosis or fusion of the plate. This may be
an acceptable risk if the growth plate is near closure.
1. Imaging for procedural planning
a. Osteoid osteoma: The diagnosis of osteoid osteoma is usually established by a characteristic clinical picture
of nighttime pain relieved by nonsteroidal anti-inflammatory drugs.
(1) Imaging features are generally sufficient to establish the diagnosis (particularly cross-sectional imaging
findings of a soft tissue nidus surrounded by sclerosis).
(2) The access route is planned avoiding important normal structures such as the neurovascular bundle. This will
also permit anesthesia to be planned (i.e., prone or supine positioning).
b. Metastatic disease: Patients with metastatic disease require cross-sectional imaging (CT and/or MRI) to fully
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define the extent of the lesion and the adjacent structures involved.
(1) It is important to determine whether intact cortical bone remains between the lesion and any critical
structures. Cortical bone is an important thermal insulator providing an additional degree of safety for normal
structures during RF ablation but NOT cryoablation.
(2) Evaluation of the degree of necrosis and/or sclerosis of the lesion will help in planning the portions of the
lesion that require ablation as well as what type of probe will likely be deployed (umbrella-type probes in large
nonsclerotic lesions vs. straight probes in more mineralized lesions or smaller lesions).
(3) The access route is planned avoiding important normal structures such as a neurovascular bundle.
2. INR and platelet count are obtained.
3. Informed consent must be obtained outlining possible risks of ablation, in particular possible destruction of
nearby normal structures. This in particular should emphasize possible damage to nerve roots, spinal cord, and
joints.
4. Many of these procedures require general anesthesia, osteoid osteoma almost inevitably so if the bone must
be drilled into for treatment. This requires assessment by anesthesiologist well before the time of admission.
Procedures on lesions other than osteoid osteomas can often be performed under spinal anesthesia, regional
nerve block, or even conscious sedation (3).
a. General anesthesia may not be required for superficial lesions treated with cryoablation as the tip of the probe
can be brought alongside the cortex rather than transgressing it.
5. Most ablations of osteoid osteomas are day care procedures, and suitable arrangements must be made ahead
of time to keep the patient 4 hours postprocedure. In patients undergoing ablation for metastatic disease (+ / -
cemento plasty), overnight admission is far more frequently required as a larger interface of tumor, and normal
bone is often ablated. This is particularly
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painful if pelvic lesions are being treated. Patients undergoing spinal ablation can usually be done as day care
procedures (1,13,14).
6. Use of prophylactic antibiotics is used by many practitioners, but there is little objective data to support this
practice.
Procedure
1. An intravenous line is established. As a general rule, patients are given prophylactic antibiotics prior to
commencement of the procedure unless there is a specific contraindication to do so. A small amount of
sedative is then administered.
2. General anesthesia or spinal or regional nerve block is performed. It is important to determine the route of
access of the lesion prior to induction of anesthesia so that the patient can be properly positioned for
optimal imaging and anesthesia access. Ablation is usually performed under CT or cone-beam CT guidance
for osteoid osteoma ablations and by CT, cone-beam CT, or fluoroscopic guidance for metastatic lesions.
3. Preliminary imaging is performed in order to select a route that will target the lesion without transgressing
any important neurovascular structures. If treating a bone lesion with an intact cortical surface, whenever
possible, a route that allows the lesion to be entered perpendicular to the osseous surface should be
favored because this makes needle access easier.
4. The skin is sterilized and draped.
5. Local anesthesia (2% lidocaine is injected using a 25-gauge needle, and the length of the needle tract is
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infiltrated, which may require use of a 20-gauge or 22-gauge spinal needle)
6. A coaxial system is needed to access the lesion if intact cortex is to be traversed. Many ablation systems
come as a coaxial set whereby the probe passes through a larger outer cannula or needle. The cannula is
placed under imaging guidance, either CT, cone-beam CT, or fluoroscopy, and the probe is then placed
coaxially through it. Prior to placement of the probe, it may be necessary to create a pilot channel if the
tissue is firm and/or mineralized, using a bone biopsy needle that passes through the cannula and into the
targeted lesion. The probe can then be placed down the pilot channel. It should be confirmed that the probe
is in the expected target area and not adjacent to any important normal structures prior to beginning
ablation.
a. If a soft tissue lesion is being treated, a coaxial system does not have to be utilized. Multiple probes may
be introduced in order to cover the lesion to be treated thereby allowing a larger volume of tumor to be
treated in a shorter period of time.
7. Ablation is performed. If a coaxial system is used, it is important with both RF and cryoablation to ensure
that the active tip of the probe does not overlap with the outer needle as either heat or ice ball formation will
be propagated along the whole length of the outer needle. a. Radiofrequency ablation. Careful
adherence to the protocols used by the manufacturer is essential. Most generators come with
recommended protocols for ablation of different organ systems, and these provide a very helpful starting
point for ablation. Generally, ablation of musculoskeletal lesions requires much lower energies than those in
soft tissues such as liver or kidney. The greater the degree of sclerosis and mineralization, the less the
required amount of energy application, as bone and mineralized tissue function as thermal insulators (14).
(1) For RF ablation in most cases, placement of appropriately located grounding pads is required, and it
must be verified that these are in position and properly hooked up to the generator prior to beginning the RF
protocol in order to prevent nontarget area patient burns.
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b. Cryoablation. Two freeze-thaw cycles are recommended for complete tissue necrosis. It should be
remembered that, unlike with RF ablation, cortical bone does not function as an insulator and the ice ball
will propagate through mineralized tissue with ease. If available, MR monitoring is helpful as the ice ball can
be readily visualized as a low signal region. CT will show a low attenuation area when soft tissue ablation is
performed, but this is not the case in the presence of mineralized tissue.
8. The probe is retracted through the guide cannula, and if necessary, the needle can then be readvanced
further into the lesion and cement injected (13,14).
9. Pressure should be placed over the puncture site in order to minimize hematoma development. A small
amount of lidocaine is injected in the tract as the needle cannula is removed in order to minimize patient
discomfort.
1. If the patient has been under the care of an anesthesiologist during the course of the procedure, the patient
may be transferred for further monitoring to the postanesthetic recovery area.
2. Patients who are not sent to the postanesthetic recovery area should have their vital signs monitored every 15
minutes for 30 minutes and then hourly thereafter. Most patients can be discharged after 4 hours. Patients with
procedures close to major nerve routes such as those in the spine and pelvis should also have motor and
sensory function of the lower extremity monitored hourly to rule out neural damage.
3. Most patients require only symptomatic management for minor pain at the puncture site for a few days, which
usually can be managed with nonsteroidal anti-inflammatory drugs or acetaminophen with codeine. Many of
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these patients already have these drugs on hand because they have been taking them for the pain associated
with osteoid osteomas.
4. Patients who have undergone RF ablation as part of their palliative procedure may experience a pain flare,
particularly those in the pelvis. These pain flares may last from 6 to 48 hours and then typically rapidly improve.
For this reason, patients who undergo RF ablation of pelvic lesions may benefit from overnight admission
following the procedure. Pain flares from cryoablation can often be avoided/minimized with a single dose of IV
ketorolac 30 mg on completing the procedure.
Results
1. Osteoid osteoma
a. More than 90% of patients who undergo RF ablation for treatment of osteoid osteomas experience
complete relief of pain (3). Of the remaining less than 10%, approximately 90% will have relief of pain if
retreated. For this reason, RF ablation has become the standard of care in any center where it is available.
2. Palliative treatment of metastatic tumors
a. Pain relief depends on the location of the lesion, size, and the patient's underlying medical condition. In
several series, pain relief has been reported as being complete or markedly improved from 60% to 80% of
cases (3,4,5,6,7,10).
b. Anecdotal evidence suggests that in selected cases, combination with cementoplasty may be of
additional benefit and can provide structural support in load-bearing areas such as the acetabulum.
c. RF ablation is becoming increasingly utilized but is not yet considered the standard of care. It is
recognized as an important and valuable adjunct.
Complications
1. Damage to adjacent neural structures resulting in motor and/or sensory dysfunction in the target
distribution of the nerve. Damage to other immediately adjacent organs such as bowel, skin surface, or
other structures is possible
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with either RF ablation or cryoablation. In selected instances, it is possible to displace adjacent structures
from the ablation area by injection of either saline or gas.
2. Skin burns may result with RF ablation if grounding pads are not properly applied or if the target lesion is
near the skin surface.
3. Hemorrhage along the tract or in tissues adjacent to the ablation zone if penetrated by the probe
4. Infection
5. Necrosis of overlying cartilage and bone in an adjacent joint which may result in joint pain/avascular
necrosis and/or accelerated degenerative changes. This is more likely to occur with cryoablation.
1. Management of complications is typically symptomatic and depends on the tissue that has been
damaged.
2. Damage to skin may require grafting.
3. Injury to tendons may require tendon repair or grafting.
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4. Damage to a nerve trunk may resolve spontaneously if the thermal neurapraxia is not severe.
a. If neural damage is suspected (i.e., compromised motor function, pain, or anesthesia in a nerve
distribution), an oral nonsteroidal anti-inflammatory drug may be administered (e.g., ibuprofen 200 to 600
mg every 4 hours).
b. Percutaneous injection of steroid (e.g., triamcinolone 80 mg) adjacent to the site of the affected nerve
may be of benefit, although no objective data exist to validate this.
c. If expected survival is sufficiently long, the patient may be a candidate for a nerve grafting. However, in
the case of patients undergoing palliative RF ablation, survivorship may not make this a practical
consideration.
5. Infection may require treatment with antibiotics.
References
1. Gogna A, Peh WC, Munk PL. Image-guided musculoskeletal biopsy. Radiol Clin North Am. 2008;46:455-
473.
2. Liu PT, Valadez SD, Chivers FS, et al. Anatomically based guidelines for core needle biopsy of bone
tumors: implications for limb-sparing surgery. Radiographics. 2007; 27:189-205.
3. Ward E, Munk PL, Rashid F, et al. Musculoskeletal interventional radiology: radiofrequency ablation.
Radiol Clin North Am. 2008;46:599-610.
4. Posteraro AF, Dupuy DE, Mayo-Smith WW. Radiofrequency ablation of bony metastatic disease. Clin
Radiol . 2004;59:803-811.
5. Goetz MP, Callstrom MR, Charboneau JW, et al. Percutaneous imaging-guided radiofrequency ablation of
painful metastases involving bone: a multicenter study. J Clin Oncol . 2004;22:300-306.
6. Kojima H, Tanigawa N, Kariya S, et al. Clinical assessment of percutaneous radiofrequency ablation for
painful metastatic bone tumors. Cardiovasc Intervent Radiol . 2006; 29:1022-1026.
7. Thanos L, Mylona S, Galani P, et al. Radiofrequency ablation of osseous metastases for the palliation of
pain. Skeletal Radiol . 2008;37:189-194.
8. Filippiadis DK, Tutton S, Mazioti A, et al. Percutaneous image-guided ablation of bone and soft tissue
tumours: a review of available techniques and protective measures. Insights Imaging. 2014;5:339-346.
9. Coupal TM, Mallinson PI, Munk PL, et al. CT-guided percutaneous cryoablation for osteoid osteoma: initial
experience in adults. AJR Am J Roentgenol. 2014;202: 1136-1139.
10. McMenomy BP, Kurup AN, Johnson GB, et al. Percutaneous cryoablation of musculoskeletal
oligometastatic disease for complete remission. J Vasc Interv Radiol. 2013;24:207-213.
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11. van der Linden E, Kroft LJ, Dijkstra PD. Treatment of vertebral tumor with posterior wall defect using
image-guided radiofrequency ablation combined with vertebroplasty. J Vasc Interv Radiol . 2007;18:741-747.
12. Hoffman RT, Jakobs TF, Trumm C, et al. Radiofrequency ablation in combination with osteoplasty in the
treatment of painful metastatic bone disease. J Vasc Interv Radiol . 2008;19:419-425.
13. Lane MD, Le HB, Lee S, et al. Combination radiofrequency ablation and cementoplasty for palliative
treatment of painful neoplastic bone metastasis: experience with 53 treated lesions in 36 patients. Skeletal
Radiol . 2011;40:25-32.
14. Munk PL, Murphy KJ, Gangi A, et al. Fire and ice: percutaneous ablative therapies and cement injection
in management of metastatic disease of the spine. Semin Musculoskelet Radiol . 2011;15:125-134.
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59
Vertebroplasty and Kyphoplasty
Martin G. Radvany
Kieran Murphy
Percutaneous vertebroplasty (PV) and kyphoplasty (KP) are safe and effective, minimally invasive techniques for
treatment of patients suffering from back pain due to osteoporotic and tumor-related vertebral body (VB)
compression fractures (1,2) as well as hemangiomas (3).
With PV, a needle is advanced into the VB under image guidance. Th rough this needle, the bone cement is
injected into the vertebral body under real-time image guidance. KP is a more involved procedure as compared
to PV. With KP, a needle/pin is advanced into the VB under image guidance. A stylet and cannula are advanced
over the pin into the pedicle. The cannula serves as a working channel for the remainder of the procedure. A drill
is inserted through the cannula to create a larger channel in the bone. An inflatable bone tamp (balloon) is
inserted into the channel and inflated within the VB; this compacts the bone and creates a cavity. Bone cement is
injected into the cavity under real-time image guidance.
Indications
Compression fracture secondary to (1,2)
1. Osteoporosis
2. Malignancy
3. Hemangioma
Contraindications
Absolute (1,2)
1. Asymptomatic VB compression fractures
2. Patient improving on medical therapy
3. Ongoing local or systemic infection
4. Retropulsed bone fragment resulting in myelopathy or neurologic symptoms
5. Spinal canal compromise secondary to tumor resulting in myelopathy
6. Uncorrectable coagulopathy; prothrombin time (PT) (international normalized ratio [INR]) greater than 1.3
× control, partial thromboplastin time (PTT) greater than 1.3 × normal, platelets less than 70,000 per μL
7. Allergy to bone cement or opacification agent
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Relative (1,2)
1. Radiculopathy in excess of vertebral pain caused by a compressive syndrome unrelated to vertebral
collapse. Occasionally, preoperative PV or KP can be performed before a spinal decompressive procedure.
2. Asymptomatic retropulsion of a fracture fragment causing significant spinal canal compromise, and thus
increasing the possibility that if any cement gets in the epidural space, the patient will be acutely
symptomatic.
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3. Asymptomatic tumor extension into the epidural space
1. Patient evaluation: Evaluate patient records, history, physical examination, and prior imaging studies to
determine need for and the feasibility of PV or KP. Order additional studies as needed to evaluate levels to be
treated. The cross-sectional imaging will also help determine the size of needle to be used for PV or KP.
a. At a minimum, plain films should be reviewed to evaluate level and degree of VB compression.
b. Magnetic resonance imaging (MRI) has the advantage of documenting additional spine conditions which may
contribute to the pain syndrome, in particular spinal degenerative disease.
c. Some patients may have contraindications to MRI such as a pacemaker or spinal instrumentation that
compromises image quality. In these patients, nuclear medicine bone scans can help localize symptomatic levels
amenable to treatment (4).
d. Computed tomography (CT) is essential to identify fractures that are potential routes of cement extravasation.
Furthermore, pedicle fractures are best seen on CT, and this can determine which pedicle will be available for
access.
2. Preprocedure visit: The risks, benefits, alternatives, and objectives should be discussed with the patient.
Written informed consent should be obtained. Specific instructions should be given to the patient on how to
prepare for the procedure and what to expect during and after the procedure. This should include discussion of
the possibility of adjacent level fracture particularly in people with severe osteoporosis and Kummell disease,
which is essentially a VB bone infarct resulting in large cleavage planes in the VB that are like vacuum clefts.
a. Perform a physical exam to include heart, lungs, and airway, as required for sedation. Document neurologic
status to include lower extremity strength, sensation (i.e., light touch and/or pinprick), and proprioception.
b. Dietary adjustment as per institutional protocol, for example, nothing by mouth except medications for 8 to 12
hours before the procedure
c. Most PV procedures are performed on an outpatient basis; KP can be performed on an inpatient or outpatient
basis, depending on medical need.
(1) Instruct patients on arrival time and expected starting time for the procedure.
(2) The patient must have an adult companion to escort and drive them.
(3) Instruct patients on signs or symptoms of complications of the procedure and provide a contact telephone
number.
d. For patients who are unable to lie prone, intubation and general anesthesia may be required.
3. Laboratory tests: Obtain routine laboratory tests.
a. PT (INR): INR should be <1.3
b. Platelet count should be >70,000 per μL; however, adequate platelet function is important as well.
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Procedure
a. An intravenous (IV) line should be placed.
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b. The patient should receive preprocedure antibiotics to cover skin flora. Ancef, 1 g IV, 30 minutes before
the procedure may be used. If patients are allergic to Ancef, vancomycin 500 mg or clindamycin 600 mg
may be substituted.
c. The patient is placed prone on the angiography table and the levels to be treated are localized.
d. Sterilize the skin (field) with iodinated scrub and place drapes.
a. Hand washing is mandatory. This is a permanent orthopedic implant.
b. Double gloving is recommended as the solvent for the cement is a lipid solvent and may dissolve gloves
causing tissue damage. Therefore, the cement should not contact the gloved hand until it is the consistency
of dough (5). Some operators develop a contact dermatitis to the cement after repeated use.
Vertebroplasty
Using fluoroscopy, localize the vertebral body at the level to be treated. The anteroposterior (AP) image
intensifier should be aligned so that it is perpendicular to the pedicle at the level to be treated.
Superior/inferior as well as ipsilateral angulations are usually required. It is critical that the medial wall of the
pedicle can be well seen so that the needle does not transgress the spinal canal during insertion. In the
lateral plane, the image intensifier should be angled so that the posterior wall is clearly seen along with the
tissue tract.
1. Anesthetize the skin and subcutaneous tissues liberally with 1% lidocaine. Advance a 21-gauge spinal
needle along the planned soft tissue tract to the periosteum. Anesthetize the periosteum and soft tissue
tract. Good local anesthesia at the periosteum will decrease the need for sedation.
2. Needle selection
a. Needle size: In the lumbar region, an 11-gauge needle is usually adequate. In the thoracic region, the
pedicles are smaller and often a 13-gauge needle, and sometimes 15-gauge needle, may be needed due to
the smaller size of the pedicles in this region.
b. Needle tip: A 45-degree bevel tip allows the needle to be steered as it is advanced. The 45-degree bevel
may slip off the pedicle, and for beginners, a diamond point stylet may be preferable, as it is less likely to
slip off the pedicle. However, the bevel needle allows one to get closer to the midline, as the flat face can
be used to slide along the inner cortex of the pedicle, a trick that can't be performed with a diamond stylet.
3. Advance the needle down to the VB. Position it at the upper, outer edge of the pedicle. Advance the
needle and monitor with fluoroscopy to make sure it does not cross the medial wall of the pedicle until the
needle is past the posterior wall of the VB in the lateral projection. Advance it to the anterior one-third of the
VB (6). Take a baseline image in the AP and lateral plane.
4. Mix the polymethylmethacrylate (PMMA) cement per manufacturer's instructions. When the PMMA is the
consistency of toothpaste, begin injecting under constant fluoroscopic monitoring. If the PMMA begins to
leak out a vein or into the disc space, stop injecting for 30 seconds. Turn or pull back the needle and inject
some more. Stop when the PMMA reaches the posterior one-third of the VB. If there is adequate filling of
the VB from a single needle placement, this is considered a single pedicle technique (Fig. 59.1); otherwise,
a bipedicular approach (Fig. 59.2) is needed. The key is to distribute the cement to be structurally
supportive, in the anterior two-thirds of the VB. It is not about volume; filling the VB like a container from
front to back simply makes it stiff and shifts the load to the adjacent VB, increasing its risk of fracture.
Excessive filling also increases the risk of extravasation.
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FIGURE 59.1 • Vertebroplasty—single pedicle technique. (Courtesy of Lydia Gregg.)
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FIGURE 59.2 • Vertebroplasty—bipedicular technique. (Courtesy of Lydia Gregg.)
5. Keep a small amount of “reference” cement off to the side, in a container such as a 20-mL syringe or
sterile urine cup to monitor its consistency at room temperature. When it has solidified, in about 20 minutes,
the patient can be moved from the procedure table.
Kyphoplasty
1. Using fluoroscopy, localize the VB at the level to be treated. The AP image intensifier should be aligned
so that it is perpendicular to the pedicle at the level to be treated. Superior/inferior as well as ipsilateral
angulations are usually required. It is critical that the medial wall of the pedicle can be well seen so that the
needle does not transgress the spinal canal during insertion. In the lateral plane, the image intensifier
should be angled so that the posterior wall is clearly seen along with the tissue tract.
2. Anesthetize the skin and subcutaneous tissues liberally with 1% lidocaine. Advance a 21-gauge spinal
needle along the planned soft tissue tract to the periosteum. Anesthetize the periosteum and soft tissue
tract. Good local anesthesia at the periosteum will decrease the need for sedation.
3. Advance the guide pin down to the VB. Position it in the middle of the pedicle. Advance the pin and
monitor with fluoroscopy to make sure it does not cross the
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medial wall of the pedicle. When the pin is within the VB, advance the obturator over the guide pin, into the
posterior VB. A working cannula is then advanced over the obturator, until it is in the posterior of the VB.
4. Using the hand drill, ream a channel for the inflatable bone tamp, making sure it stays within the VB.
Inflate the bone tamp while monitoring the inflation pressure. The inflation should be terminated when the
recommended pressure limit is reached, the balloon abuts any of the cortical margins, or the maximum
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volume of the balloon is reached.
5. Mix the PMMA cement per manufacturer's instructions. When the PMMA is the consistency of toothpaste,
begin injecting under constant fluoroscopic monitoring. If the PMMA begins to leak out of the VB, stop
injecting for 30 seconds. Pull back the needle and inject some more. Cement injection is stopped when the
cement mantle reaches two-thirds of the way back to the posterior VB cortex on the lateral fluoroscopic
images.
6. Keep a small amount of “reference” cement off to the side, in a container such as a 20-mL syringe or
sterile urine cup, to monitor its consistency at room temperature. When it has solidified, in about 20 minutes,
the patient can be moved from the procedure table.
1. Postprocedure observation typically involves monitoring of the patient until discharge criteria for the type of
sedation or anesthesia administered are met.
2. If the patient has new radicular or spinal cord signs, a CT scan should be obtained to evaluate deposition of
the cement.
Results
Success is defined as achievement of significant pain relief and/or improved mobility as measured by
validated measurement tools (1).
1. Vertebroplasty. As there are different etiologies for vertebral compression fractures, there are differences
in the outcomes and success rates.
a. In the setting of osteoporosis, success rates of 90% have been reported by several authors (7,8,9,10).
b. With neoplastic involvement, reported success rates are as high as 97% (11); however, most series
report rates of success of 70% to 80% (8,12).
2. Kyphoplasty. There is not as much literature regarding KP as there is for PV.
a. In osteoporosis, success rates of up to 96% have been reported (13,14,15).
b. With neoplastic involvement, success rates as high as 100% have been reported (16,17,18), although
the number of patients in these studies is very small.
Complications
1. Vertebroplasty
a. Clinically significant complications occur in patients with spinal metastatic disease at a rate of 10%
versus a rate of 3% in patients with osteoporotic fractures (19).
b. Most complications are transient and minor. These include
(1) Hemorrhage
(2) Rib or vertebral posterior element fracture
(3) Cement embolization to the lungs via the paravertebral venous plexus
(4) Nerve root irritation
(5) Pneumothorax in thoracic lesions
(6) Infection
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c. Permanent complications requiring decompressive surgery to remove extruded cement occur in less than
1% of cases (20). Nearly all complications happen because of the use of poor imaging equipment. Portable
C-arms are not adequate for this procedure.
2. Kyphoplasty
a. The most common reported complication is cement extravasation, which is encountered in approximately
10% of cases (21).
b. Clinically significant complications are rare; however, the following have been reported:
(1) Delivery of cement into the spinal canal resulting in partial motor loss
(2) Anterior cord syndrome associated with an extrapedicular approach
(3) Cement pulmonary embolus
References
1. McGraw JK, Cardella J, Barr JD, et al. Society of Interventional Radiology quality improvement guidelines
for percutaneous vertebroplasty. J Vasc Interv Radiol. 2003; 14:827-831.
2. Maynard AS, Jensen ME, Schweickert PA, et al. Value of bone scan imaging in predicting pain relief from
percutaneous vertebroplasty in osteoporotic vertebral fractures. AJNR Am J Neuroradiol . 2000;21:1807-
1812.
3. U.S. Food and Drug Administration. Class II special controls guidance document: polymethylmethacrylate
(PMMA) bone cement; guidance for industry and FDA. http://www.fda.gov/cdrh/ode/guidance/668.pdf.
Published July 17, 2002. Accessed November 8, 2008.
4. Kallmes DF, Jensen ME. Percutaneous vertebroplasty. Radiology. 2003;229:27-36.
5. Jensen ME, Evans AJ, Mathis JM, et al. Percutaneous polymethylmethacrylate vertebroplasty in the
treatment of osteoporotic vertebral body compression fractures: technical aspects. AJNR Am J Neuroradiol .
1997;18:1897-1904.
6. Deramond H, Depriester C, Galibert P, et al. Percutaneous vertebroplasty with polymethylmethacrylate.

Technique, indications, and results. Radiol Clin North Am. 1998; 36:533-546.
7. McGraw JK, Lippert JA, Minkus KD, et al. Prospective evaluation of pain relief in 100 patients undergoing
percutaneous vertebroplasty: results and follow-up. J Vasc Interv Radiol . 2002;13:883-886.
8. Cotten A, Dewatre F, Cortet B, et al. Percutaneous vertebroplasty for osteolytic metastases and myeloma:
effects of the percentage of lesion filling and the leakage of methyl methacrylate at clinical follow-up.
Radiology. 1996;200:525-530.
9. Weill A, Chiras J, Simon JM, et al. Spinal metastases: indications for and results of percutaneous injection
of acrylic surgical cement. Radiology. 1996;199:241-247.
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10. Klazen C, Lohle P, de Vries J, et al. Vertebroplasty versus conservative treatment in acute osteoporotic
vertebral compression fractures (Vertos II): an open label randomized trial. Lancet. 2010;376:1085-1092.
11. Murphy K, Deramond H. Percutaneous vertebroplasty in benign and malignant disease. Neuroimaging
Clin N Am. 2000;10:535-545.
12. Cotten A, Boutry N, Cortet B, et al. Percutaneous vertebroplasty: state of the art. Radiographics.
1998;18:311-320.
13. Wardlaw D, Cummings SR, Van Meirhaeghe J, et al. Efficacy and safety of balloon kyphoplasty
compared with non-surgical care for vertebral compression fracture (FREE): a randomised controlled trial.
Lancet. 2009;373:1016-1024.
14. Hadjipavlou A, Tosounidis T, Gaitanis I, et al. Balloon kyphoplasty as a single or as an adjunct procedure
for the management of symptomatic vertebral haemangiomas. J Bone Joint Surg Br. 2007;89:495-502.
15. Garfin SR, Yuan HA, Reiley MA. New technologies in spine: kyphoplasty and vertebroplasty for the
treatment of painful osteoporotic compression fractures. Spine. 2001;26:1511-1515.
16. Phillips FM, Ho E, Campbell-Hupp M, et al. Early radiographic and clinical results of balloon kyphoplasty
for the treatment of osteoporotic vertebral compression fractures. Spine. 2003;28:2260-2265.
17. Wong WH, Olan WJ, Belkoff SM. Balloon kyphoplasty. In: Mathis JM, Deramond H, Belkoff SM, eds.
Percutaneous Vertebroplasty. New York, NY: Springer-Verlag; 2002:109-124.
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18. Fourney DR, Schomer DF, Nader R, et al. Percutaneous vertebroplasty and kyphoplasty for painful
vertebral fractures in cancer patients. J Neurosurg. 2003;98:21-30.
19. Gaitanis I, Hadjipavlou AG, Katonis PG, et al. Balloon kyphoplasty for the treatment of pathological
vertebral compressive fractures. Eur Spine J. 2005;14:250-260.
20. Dudeney S, Lieberman IH, Reinhardt MK, et al. Kyphoplasty in the treatment of osteolytic vertebral
compression fractures as a result of multiple myeloma. J Clin Oncol . 2002;20:2382-2387.
21. Garfin SR, Buckley RA, Ledlie J. Balloon kyphoplasty for symptomatic vertebral body compression
fractures results in rapid, significant, and sustained improvements in back pain, function, and quality of life for
elderly patients. Spine. 2006;31:2213-2220.
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60
Spinal Injections for Pain Control
Manraj K.S. Heran
Mohammed T. Alshammari
Selective Lumbar Nerve Root and Epidural Steroid Injections

Introduction
Lumbar radiculopathy is defined as the objective loss of sensory and/or motor function as a result of a
connection block in the axons of a spinal nerve or its roots (1). Selective nerve root block (SNRB) was first
described by Macnab (2) in 1971 as a diagnostic test for the examination of patients with positive clinical findings
of nerve root irritation but negative imaging. SNRB is more commonly now used for temporizing pain related to
lumbar radicular syndrome. Although an epidural steroid injection (ESI) may produce the same effect, an SNRB
is a more focused injection that has a greater therapeutic and diagnostic value. Patients who have a positive
response to an SNRB are likely to have a positive surgical outcome (3).
Indications
1. Selective nerve root block
a. Diagnostic workup for back pain
(1) Imaging findings not definitive
(2) Define a specific pain source presurgery when there are multilevel imaging abnormalities.
(3) Postoperative unexplained pain
(4) Equivocal neurologic examination
b. Temporary pain relief of radiculopathy in those with
(1) Disc herniation
(2) Recurrent radiculopathy after discectomy
2. Epidural steroid injection
a. Temporary relief of radiculopathy
(1) Pathology located centrally in spinal canal (e.g., central disk protrusion, spinal stenosis)
(2) When individual nerves cannot be identified as the most likely source of the symptoms
(3) Recurrent radiculopathy after laminectomy
b. As a diagnostic tool to determine type and level of surgical treatment
c. Symptoms related to a nerve root but no definite radiologic diagnosis explaining the symptoms
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Contraindications
Absolute
1. Coagulopathy (platelet count ≤50,000 per μL; international normalized ratio [INR] ≥1.5)
2. Systemic or local infection
3. Pregnancy
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4. Technical inability to target the nerve root
5. Maximal dose of corticosteroid reached due to other pain procedures
Relative
1. Severe medication allergy
2. Confounding clinical exam, suspicious for other etiology
1. Performed as an outpatient procedure without premedication
2. Careful review of the indication(s) and goals of the procedure, and pertinent laboratory and imaging results
3. Record pain distribution and severity (e.g., Visual Analog Scale).
a. Using a model of the spine to demonstrate the procedure can facilitate the patient's understanding of the
technique, goals, and expectations.
Procedure
1. Imaging
a. Traditionally has been performed using rotating single plane fluoroscopy
b. Biplane fluoroscopy can reduce procedure time.
c. In some centers, computed tomography (CT) scan or CT fluoroscopy is used, especially where
fluoroscopic guidance is considered challenging or has failed.
2. Medications and injectables. There is great variability in type, volume, and amount of local anesthetic
and corticosteroid used.
a. In general, diagnostic SNRB and ESI can be performed with 1 to 2 mL of either 2% lidocaine or 0.25% to
0.5% bupivacaine.
b. For therapeutic injections, the total volume of corticosteroid is typically 1 mL.
c. The total injection volume of local anesthetic and corticosteroid should not exceed 3 mL. In situations
where multiple injections are performed on the same visit, consideration should be given to reducing the
corticosteroid dose injected at each site, so as to minimize the cumulative dose.
d. There is no clear benefit of one corticosteroid preparation versus another (1). A list of corticosteroids
commonly used is provided in Table 60.1.
e. Note: The U.S. Food and Drug Administration (FDA) has convened a panel on the safety of epidural
steroid injections (http://www.fda.gov/Drugs/DrugSafety/ucm394280.htm). This has caused considerable
controversy; however, many practitioners have not altered their practice.
f. Commonly used is a solution of 40 mg triamcinolone and 2 mL 0.5% bupivacaine (total volume of 3 mL).
3. The patient is placed prone on the fluoroscopy table.
4. The lower back is cleansed and draped using sterile precautions.
5. Needle insertion
a. L1-L4 SNRB
(1) Angle fluoroscopy tube cranial/caudal to place the disc space of the target level as parallel to the x-ray
beam as possible, with the spinous process positioned in the midline between the two pedicles, so as to
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achieve a true anteroposterior (AP) projection.
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Table 60.1 Commonly Used Corticosteroid Preparations
Corticosteroid Brand Name Typical Dosage (mg)a
Methylprednisolone acetate Depo-Medrol 20-80
Triamcinolone diacetate Aristocort 40-120
Triamcinolone acetonide Kenalog 20-40
Triamcinolone hexacetonide Aristospan 20-40
Betamethasone acetate/phosphate mixture Celestone Soluspan 3-6
aThe lowest effective dose is recommended to avoid potential for systemic adverse reactions.
(2) Rotate fluoroscopy to an ipsilateral oblique angle until the ventral aspect of the superior articulating
process (ear of the “Scotty dog”) of the vertebra numbered the same as the nerve root to be injected is
midway between the anterior and the posterior aspects of the superior end plate.
(3) After skin anesthesia, approach the neural foramen from a posterolateral direction with a 22-gauge, 3.5-
in. spinal needle (although, in larger patients, a longer 22-gauge needle may sometimes be necessary).
(4) Advance the needle under fluoroscopic guidance toward the inferolateral aspect of the pedicle (in the
so-called safe triangle).
(5) The safe triangle is defined by the pedicle superiorly, the lateral border of the vertebral body laterally,
and the outer margin of the spinal nerve medially (Fig. 60.1A). The nerve root normally passes a few
millimeters inferior to the pedicle.
(6) If the patient's typical pain distribution is stimulated (or the needle is midway along the pedicle on the
lateral projection), 1 to 3 mL of nonionic contrast medium (e.g., Iohexol) is injected to confirm the needle
position adjacent to the nerve root sheath.
b. L5 SNRB
(1) The needle is passed through a triangular window formed by the inferior margin of the transverse
process of L5, the superior articulating process of S1, and the iliac crest (Fig. 60.1B).
(2) Through prior appropriate angulation of the fluoroscopy C-arm, the needle commonly has a craniocaudal
orientation to pass over the iliac wing. The needle is advanced through the center of the triangle until
radicular pain is achieved, or it is inferior to the L5 pedicle in the ventral portion of the intervertebral
foramen.
(3) The vertebral body limits the depth of needle penetration.
(4) If the patient's typical pain distribution is stimulated (or the needle is inferior to the L5 pedicle in the
ventral portion of the intervertebral foramen), contrast is injected as above.
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c. S1 SNRB
(1) The procedure is performed through the dorsal S1 foramen in AP projection or at most 5 to 15 degrees
of ipsilateral angulation.
(2) The S1 sacral foramen is seen as a well-defined round lucency in the upper sacrum, inferior to the
lumbosacral junction (Fig. 60.1C).
(3) Slight caudal angulation of the x-ray facilitates optimal needle placement.
(4) The needle is advanced into the center of the sacral foramen until radicular pain is elicited or the tip of
the needle is 2 to 3 mm inside the anterior cortex of sacral canal, then contrast is injected as above.
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FIGURE 60.1 • Needle position for spinal pain procedures. A: L4 SNRB. Right posterior oblique (RPO)
projection shows “the safe triangle” (arrow). B: Oblique projection showing needle position for L5 SNRB.
(continued)
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FIGURE 60.1 • (Continued) C: S1 SNRB. PA image demonstrates the needle within the left S1 sacral
foramen. D: L3 or L4 epidural contrast injection. Lateral projection.
d. Interlaminar ESI
(1) With the C-arm angled to visualize the target interlaminar space, after local anesthetic, insert a 22-gauge
spinal or Tuohy needle from the posterior midline directed slightly cephalad.
(2) Once the needle tip is at the halfway point of the spinous process, connect a connecting tube with a 10-
mL syringe of sterile saline (or air) attached.
(3) Using lateral fluoroscopy, the needle is advanced slowly.
(4) While advancing the needle, continuous pressure is applied on the plunger of the syringe. Firm
resistance should be felt when doing this.
(5) The needle tip should be kept in the midline. This may require rotating fluoroscopy between lateral and
AP.
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(6) When the needle enters the epidural space, there will be a sudden loss of resistance.
(7) Under lateral fluoroscopy, 1 to 3 mL of nonionic contrast medium is injected to confirm the needle is in
the epidural space (Fig. 60.1D). Confirm in AP projection.
(a) When there are multilevel abnormalities or the desired level can't be targeted, an increased dose of
steroid (e.g., 80 mg vs. 40 mg of triamcinolone) may be injected.
(b) When contrast is limited to one side on AP imaging, the patient should be placed on his or her
nonopacified side for 10 minutes.
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e. Caudal ESI
(1) Locate the sacral hiatus at the top of the buttock cleft by palpation or fluoro. It can be easily
demonstrated by ultrasound.
(2) After local anesthetic, insert a 22- to 25-gauge needle from the posterior midline angled sharply
cephalad. Using the loss-of-resistance technique described earlier, a pop will be felt when the needle
passes through the sacrococcygeal ligament into the epidural space.
(3) Confirm epidural access with contrast as described earlier.
(4) Some practitioners will dilute the injectate up to a total volume of 20 mL with normal saline.
6. Once proper needle position has been established, the anesthetic/steroid solution is slowly injected.
7. The needle is removed, and an adhesive bandage applied.
1. The patient is observed for 15 to 20 minutes, with discharge to the care of a responsible adult.
2. Instructions are given to not drive or operate heavy machinery for the remainder of the day, with return to
normal activities the following day.
3. No tub bath or soaking in water (i.e., Jacuzzi, pool) for the remainder of the day.
4. Taper pain medication as appropriate, given the response to procedure.
5. An intermediate and long-term plan should be discussed, including appropriate timing and physician for follow-
up.
6. A discharge sheet can be provided (optional), outlining
a. Type of procedure performed
b. Expected postprocedural issues (e.g., procedure-related pain)
c. Methods of addressing common concerns
d. Issues requiring urgent reassessment (e.g., symptoms and signs of infection)
e. Contact information for proceduralist or designate
Results (4)
1. Diagnostic blocks with only local anesthetic may be effective within minutes; steroid within several days,
maximal after 7 days.
2. Local anesthesia will wear off within 6 to 24 hours, depending on whether lidocaine or bupivacaine is used.
The patient should be advised of return of the preprocedure symptoms until the steroid takes effect.
3. Therapeutic blocks have a mean duration of 3 to 6 months.
4. Efficacy of SNRB and ESI is dependent on the pathology causing pain.
a. Pain from disc herniation has better pain relief than pain caused by spinal stenosis (1).
b. Patients with severe lateral recess stenosis respond less favorably to SNRB.
Complications (5)
1. General
a. Infection
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b. Bleeding
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c. Transient headache, resolved within 24 hours
d. Transient lower extremity weakness or paresthesias
e. Thecal sac puncture
f. Steroid side effects
(1) Glucose disturbance in patients with diabetes mellitus (DM)
(2) Sleeplessness/insomnia
(3) Aggressive behavior/mood disturbance
(4) Transient decrease in immunity
2. Nerve root blocks
a. Direct nerve root injection may result in severe sustained radicular pain.
b. Intravascular injection of steroid may lead to vascular occlusion or thrombosis. Extremely rarely, this may
result in spinal cord infarction if a radiculomedullary artery is injected.
3. ESIs
a. Dural puncture: 7% incidence. The procedure should be terminated and rescheduled at least 24 hours later.
b. Epidural hematoma—approximately 1:200,000
Spinal Facet Procedures

Introduction
Facet-mediated pain can account for a significant percentage of people with back pain. Facet joint disease
may be aggravated by superimposed spinal degenerative conditions, such as disc height loss, or by
asymmetric spinal loading as seen in scoliosis or spondylolysis. As a consequence, it is relatively
uncommon to see single-level facet degenerative changes. Determining the relative contribution of facet-
mediated pain in the complex spinal pain patient can be extremely challenging as conditions such as
degenerative disc disease, spinal stenosis, and other pathologies of the spinal axis may have variable
importance, as may other factors, such as psychosocial, medicolegal, and systemic medical concerns.
Despite this, there are some clinical features which may suggest spinal pain of a facet origin. These include
the absence of root tension signs or other radicular features, pain eased by flexion but aggravated by
rotation, lateral bending, or hyperextension (as the greatest pressure in the lumbar facet joints occurs when
the spine is in extension), low back stiffness, worst in the mornings and improving through the day,
unilateral low backpain, typically tender on palpation over the offending facet joint or ipsilateral transverse
process.
In facet degenerative change, there is poor correlation between imaging and clinical symptoms. Magnetic
resonance imaging (MRI), CT, and other imaging modalities are best considered as methods to assess for
other contributors of back or neck pain. Through careful clinical evaluation, including assessing the point of
maximal tenderness to palpation, as well as the cutaneous distribution of the pain, determination of the
culprit facet joint(s) can be made.
The two major types of facet procedures are intra-articular injections and medial branch blocks (MBB). As
both are most commonly performed for lumbar facet-mediated pain, details for cervical or thoracic facet
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procedures will not be discussed. Whereas intra-articular injections have both diagnostic and therapeutic
benefit, MBB offer information regarding potential efficacy of future radiofrequency rhizotomy procedures. In
some respects, MBB are more straightforward to perform than intra-articular injections, with better defined
landmarks and consistent targeting accuracy independent of the degree of facet degenerative change.
However, intra-articular injections may have a greater therapeutic efficacy than MBB (6).
Indications
1. Back or neck pain consistent with a facet syndrome
2. Complex spinal axis pain felt to have a facet mediated component
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3. Management for those having failed other spine-directed procedures, such as vertebroplasty, nerve
root block, or epidural steroid injection
Contraindications
As for selective nerve root blocks and epidural steroid injections
1. Facet procedures are performed on an outpatient basis.
a. The patient is instructed to have made alternate arrangements for the commute home.
b. Sedation is rarely required; typically no oral intake restrictions.
c. There is no need to discontinue antiplatelet agents as this procedure is low risk in terms of bleeding.
However, anticoagulants should be discontinued for an appropriate period of time to ensure adequate
clotting profile.
d. The patient is typically told to discontinue his or her pain medications on the day of the procedure to
obtain the best assessment possible.
2. Preprocedural assessment should include a focused review of systems, as well as determining allergy
status, current medications, and obtaining information regarding the location, nature, and severity of the
patient's back pain. Ideally, the assessment is done using accepted tools such as the Visual Analog Scale
or Oswestry Disability Index Score. Review of all relevant imaging studies is also crucial to ensuring
technical and clinical success.
Procedure
1. Imaging. Can be done using either fluoroscopic or CT guidance. Either is appropriate, with most
interventionalists preferring fluoroscopy, reserving CT for difficult facet access, such as in cases of
marked facet hypertrophy and sclerosis, with exuberant osteophyte formation.
2. Medications and injectables (see Table 60.1). There is no clear benefit of using one
corticosteroid preparation versus another (4).
a. A lumbar facet joint will typically accept 1 to 1.5 mL of fluid. The total injection volume of local
anesthetic and corticosteroid should not exceed 2 mL.
b. If contrast confirmation is required for intra-articular needle positioning, any low osmolar contrast
medium (LOCM) (0.25 mL to 0.5 mL) can be used.
c. In general, diagnostic facet joint injections can be performed with 0.5 to 1.5 mL of either 2%
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lidocaine or 0.5% bupivacaine.
d. For therapeutic injections, the total volume of corticosteroid is 0.5 to 1.0 mL.
e. Similar guidelines can be used for MBB.
Intra-articular Lumbar Facet Injection
2. Position patient prone on the fluoroscopy table.
3. The target facet joint is localized, with emphasis on identifying the inferior aspect of the joint (Fig.
60.2). The superior aspect of the joint can also be targeted.
4. Angle the fluoroscopy tube 10 to 45 degrees until appropriate visualization of the posterior portion of
the facet joint is achieved.
a. Increasing the target angle within this range is required with lower lumbar levels (Fig. 60.3).
b. Slight craniocaudal angulation is helpful to “open up” access for lower lumbar levels.
5. Sterile preparation of target area is performed.
6. Infiltrate local anesthesia (1% to 2% lidocaine) as deeply as possible, aspirating prior to injection to
avoid intravascular injection.
7. Advance a 22-gauge, 3.5-in. spinal needle (with inner stylet in place) under fluoroscopic guidance to
the facet capsule. A longer 22-gauge needle may be required in some patients.
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FIGURE 60.2 • Schematic diagram of a right posterior oblique projection of the lumbar spine,
demonstrating the “Scotty dog” appearance. The asterisk denotes the desirable point of entry for
performing a right L3 or L5 intra-articular facet joint injection.
8. Advance the needle further until a release of resistance is noted (feeling of a “clunk”).
a. The patient often expresses pain upon contact of the facet joint capsule, relieved upon entry into the
joint.
b. It is important to note the character and distribution of pain (i.e., how similar is it to preprocedure
pain).
9. It is optional to inject contrast to confirm intra-articular needle position.
10. If the procedure is a diagnostic block, anesthetic is injected; if it is a therapeutic injection,
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corticosteroid is used.
FIGURE 60.3 • Axial diagram highlighting how the posterior aspect of the facet joint is the first to be
visualized as one goes laterally from midline. Increasing lateral angulation will actually demonstrate the
anterior aspect of the facet joint. As such, the least amount of angulation required to visualize the facet
joint under fluoroscopy will allow for optimal targeting when performing an intra-articular injection.
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Lumbar Medial Branch Block
Each facet joint has a dual nerve supply consisting of the medial branches of the dorsal rami from the
levels immediately above and at the facet joint (Fig. 60.4). However, because each medial branch
nerve joins the dorsal primary ramus from the level above in the thoracic and lumbar spine, numbering
of these medial branch nerves is one higher than the transverse processes they course over (i.e., the
L4 medial branch nerve courses over the base of the L5 transverse process).
2. The patient should be positioned prone on the fluoroscopy table.
3. The junction of the superior articular process and the base of the transverse process is localized (at
and above the target facet joint; done sequentially; see Fig. 60.4).
a. Ipsilateral fluoroscopic angulation of 10 to 30 degrees is required.
b. Craniocaudal angulation for correct target profile may also be needed.
4. Sterile preparation of the target area is performed.
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FIGURE 60.4 • Diagram of the lumbar spine in a right posterior oblique projection shows the
orientation and position of the medial branch nerves relative to the bony anatomy. The asterisks
denote points of needle targeting for performing MBB for a right L4 or L5 facet joint. The targeted
nerves actually correspond to the right L3 and L4 medial branches, respectively.
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5. Infiltrate local anesthesia (1% to 2% lidocaine) as deeply as possible, aspirating prior to injection to
avoid intravascular injection.
6. Advance a 22-gauge, 3.5-in. spinal needle (with inner stylet in place) under fluoroscopic guidance
such that it contacts bone at the base of where the transverse process, superior articular process, and
pedicle meet. A longer 22-gauge needle may be required in some patients.
7. After positioning the bevel caudally, advance the needle further such that it just passes over the
transverse process.
a. Prior to drug injection, keep the bevel of the needle directed caudally to maximize contact of
pharmaceutical with the medial branch nerve.
b. Lateral fluoroscopy is extremely helpful to ensure that the needle is not positioned too far anteriorly
(it should not be anterior to the posterior cortex of the superior articular process).
8. If the procedure is a diagnostic block, anesthetic is injected; if it is a therapeutic injection,
corticosteroid is used. See the paragraph on “Medications and injectables” for more details.
9. Injection of the L5 “medial branch nerve” is done similar to the earlier technique with the principle
difference being that the target is just lateral to the superior articular process of S1, along the
superomedial aspect of the ipsilateral sacral ala.
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10. Injection of the S1 medial branch nerve is not commonly required. However, if necessary, the
target is the superolateral margin of the S1 foramen, best accessed with a caudocranial trajectory.
1. The patient is observed for 15 to 20 minutes, with eventual discharge in the care of responsible adult.
2. Limitations on activities are highly dependent on the individual.
3. Instructions are given to not drive or operate heavy machinery for the remainder of the day, with return to
normal activities the following day.
4. No tub bath or soaking in water (i.e., Jacuzzi, pool) for the remainder of the day
5. Taper pain medication as appropriate, given the response to procedure. If the patient is taking opioid
analgesics, plan for tapering medications must be reviewed by the prescribing physician.
6. A discharge sheet can be provided (optional; see previous).
7. An intermediate and long-term plan should be discussed, including appropriate timing and physician for
follow-up.
Results
1. Diagnostic blocks performed with only local anesthetic may be effective within minutes,
corticosteroid effects typically take several days to become noticeable, and are usually maximal after
approximately 7 days.
2. Local anesthesia used as a diagnostic block agent will wear off within 6 to 24 hours, depending on
whether lidocaine or bupivacaine is used.
3. Therapeutic blocks have a mean duration of 3 to 6 months (4,7).
4. Depending on the degree of benefit achieved, patients may be candidates for repeat intra-articular
injections or MBB. However, reassessment with objective pain scores and clinical examination is
extremely important. It should be kept in mind that there continues to be controversy regarding the role
of therapeutic facet blocks in the management of chronic back pain.
Complications
1. Infection
2. Bleeding
3. Lower extremity weakness or paresthesias (transient)
4. Postprocedural pain “flare.” This is uncommon and can usually be relieved with oral analgesics.
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Sacroiliac Joint Injection
Introduction
Discomfort originating from the sacroiliac (SI) joints can be extremely difficult to assess as chronic low back pain
without radicular findings may have many etiologies. Clinically, patients with pain suspected to be originating
from the SI joint(s) complain of unilateral pain (although it may be bilateral), with no evidence of arthropathy.
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They may have sitting intolerance, groin pain, or referred numbness, tingling, or burning in the lower extremity
and buttock region. However, clinical assessment has questionable validity (8), and it has been forwarded that
the only objective method of determining whether a patient's low back pain has a contributing component from
the SI joints is by doing an intra-articular injection. As the inferior one-half to two-thirds of the SI joint is a true
synovial joint, image guidance is imperative to ensure procedural success.
Indications
1. Diagnostic—to assess the role of the SI joint(s) as a source of pain in patients with low back pain
2. Therapeutic—treatment of known painful conditions of the SI joints
a. Inflammatory
b. Degenerative
c. Others
Contraindications
As for selective nerve root blocks and epidural steroid injections
As for facet joint procedures
Procedure
Percutaneous SI joint procedures can be done using either fluoroscopic or CT guidance.
1. Obtain informed consent, with testing of lower extremity motor strength.
2. Consider the use of mild intravenous sedative and analgesics (optional)
a. If given, ensure appropriate patient monitoring.
b. Beware of oversedation.
3. The patient should be positioned prone on the fluoroscopy table.
4. The target SI joint is localized, aiming approximately 1 cm above its most caudal extent, thus avoiding the
fibrous articulation superiorly (Fig. 60.5).
a. The degree of ipsilateral obliquity to optimally visualize the inferior component of the SI joint may range
from 0 degrees to 20 to 30 degrees.
b. The fluoroscope is caudally angulated approximately 20 to 25 degrees.
5. Sterile preparation of the target area is performed.
6. Advance a 22-gauge, 3.5-in. spinal needle into the posteroinferior aspect of the SI joint.
7. Injection of low osmolar contrast for confirmation of intra-articular needle position is optional but
recommended.
8. Injection of local anesthetic (bupivacaine) versus combination bupivacaine/corticosteroid depends on
whether a diagnostic or therapeutic block is being performed.
9. If CT or CT fluoroscopy are used preliminary, CT of the SI joints is performed, typically in 5-mm slices.
The remainder of the procedure is the same as outlined; the injection of nonionic contrast material is
optional but recommended to ensure appropriate needle tip positioning. Usually 0.2 to 0.5 mL of LOCM is
sufficient.
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FIGURE 60.5 • Schematic diagram of the right SI joint (slight right posterior oblique projection). The asterisk
represents the optimal point for needle placement to insure entry into the synovial portion of the joint.
As for facet joint procedures
Results
1. Approximately 90% of patients without history of previous spine surgery can be expected to have pain
relief within 12 hours, with 50% to 80% of patients having immediate pain relief (9,10).
2. Unlike many other percutaneous spinal pain procedures, patients receiving therapeutic SI joint injections
have a longer period of symptomatic relief, averaging approximately 10 months (11).
Complications
1. Infection
2. Bleeding
3. Lower extremity weakness or paresthesias (transient)
4. Difficulty voiding (transient)
References
1. Datta S, Manchikanti L, Falco FJ, et al. Diagnostic utility of selective nerve root blocks in the diagnosis of
lumbosacral radicular pain: systematic review and update of current evidence. Pain Physician.
2013;16:SE97-SE124.
2. Macnab I. Negative disc exploration. An analysis of the causes of nerve-root involvement in sixty-eight
patients. J Bone Joint Surg Am. 1971;53:891-903.
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3. Derby R, Kine G, Saal JA, et al. Response to steroid and duration of radicular pain as predictors of
surgical outcome. Spine. 1992;(17)(6 suppl):S176-S183.
4. Heran MK, Smith AD, Legiehn GM. Spinal injection procedures: a review of concepts, controversies, and
complications. Radiol Clin North Am. 2008;46:487-514.
5. Abram SE, O'Connor TC. Complications associated with epidural steroid injections. Reg Anesth.
1996;21:149-162.
6. Ackerman WE III, Ahmad M. Pain relief with intraarticular or medial branch nerve blocks in patients with
positive lumbar facet joint SPECT imaging: a 12-week outcome study. South Med J. 2008;101(9):931-934.
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7. Gorbach C, Schmid MR, Elfering A, et al. Therapeutic efficacy of facet joint blocks. AJR Am J Roentgenol .
2006;186(5):1228-1233.
8. Dreyfuss P, Michaelsen M, Pauza K, et al. The value of medical history and physical examination in
diagnosing sacroiliac joint pain. Spine. 1996;21(22):2594-2602.
9. Dussault RG, Kaplan PA, Anderson MW. Fluoroscopy-guided sacroiliac joint injections. Radiology.
2000;214(1):273-277.
10. Pulisetti D, Ebraheim NA. CT-guided sacroiliac joint injections. J Spinal Disord. 1999;12(4):310-312.
11. Bollow M, Braun J, Taupitz M, et al. CT-guided intraarticular corticosteroid injection into the sacroiliac
joints in patients with spondyloarthropathy: indication and follow-up with contrast-enhanced MRI. J Comput
Assist Tomogr. 1996;20(4):512-521.
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61
Universal Protocol in Interventional Radiology
Rathachai Kaewlai
Hani H. Abujudeh
Wrong site, wrong procedure, and wrong patient (WSWPWP) interventions result in devastating injuries to the
patient. They are generally rare (1 in 50,000 to 100,000 procedures) but more prevalent in procedures
associated with laterality (1,2) and probably occur equally in nonsurgical interventions and surgical disciplines
(3). Medical errors attract negative media attention, undermine public confidence in the health care system, and
devalue and demoralize physicians. These preventable errors are frequently caused by a failure in
communication and poor operating physician leadership (4). Organizational culture and steep hierarchical
structures in the procedure room also play a role (2,5). To prevent such errors and improve patient safety, The
Joint Commission (JC; effective 2004) requires the establishment of a Universal Protocol at all hospitals,
ambulatory care, and office-based surgery facilities seeking accreditation. In 2008, the Society of Interventional
Radiology (SIR) published supplemental guidelines for fulfilling this requirement (6). The JC's latest revision of
the Universal Protocol was effective January 1, 2010 (7). However, even in the Universal Protocol era,
prevalence of WSWPWP is still significant and unacceptable. Multifaceted strategy (Universal Protocol, WHO
surgical safety checklist, medical team training) is required to eliminate these errors (8).
Universal Protocol
1. The Universal Protocol, a three-step process, includes multiple strategies to prevent WSWPWP errors:
a. Preprocedure verification
b. Site marking
c. Time-out
2. Each step in the Universal Protocol is complementary to the other and is intended to introduce redundancy to
the practice of confirming the correct site, procedure, and patient (5).
3. Any step used alone is unlikely to reduce the incidence of WSWPWP errors (5).
Indications
All surgical and nonsurgical invasive procedures that expose patients to more than minimal risk must have
an indication (9).
1. JC defines “invasive procedures” as those involving “the puncture or incision of the skin, insertion of an
instrument, or insertion of foreign material into the body. Invasive procedures may be performed for
diagnostic or treatment-related purposes.”
2. Common procedures such as peripherally inserted central catheters (PICC) line insertion, as well as all
central line and chest tube insertions, must fulfill the Universal Protocol requirement.
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Exemptions to Universal Protocol
1. Routine “minor” procedures, relevant to interventional radiology (IR) are (9)
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a. Puncture of small peripheral veins
b. Peripheral intravenous line placement
c. Insertion of a nasogastric tube or urinary bladder catheter
d. Lithotripsy
e. Performance of dialysis (does not include insertion of dialysis catheter)
f. Minor procedure, posing minimal patient risk, whose need is discovered during a routine clinic visit, for
example, drainage of a newly discovered seroma/cyst
2. Patient-related
a. Profoundly medically unstable patient
b. Patient in cardiopulmonary arrest
Preprocedure Verification
1. Essentials
a. The purposes of preprocedure verification are to ensure (a) availability of all relevant documents, information,
and equipment prior to the start of the procedure; (b) understanding of the patient about the procedure to be
performed; and (c) correct identification of the patient and procedure to be performed by all members of the
operating or procedure area.
b. Confirmation of correct site, procedure, and patient is made at every stage from the time of decision to
perform the procedure to the time the patient undergoes the procedure. The verification may occur at more than
one time and place before the procedure is performed.
c. Verification should be performed with patient involvement, being awake and aware of the process, as much as
possible.
d. A standardized list can be used in the verification process. The list helps verify that all information, relevant
documents, and necessary equipment are:
(1) Available prior to the start of the procedure
(2) Correctly identified, labeled, and matched to the patient's identifiers
(3) Reviewed and consistent with the patient's expectations and with the team's understanding of the intended
patient, procedure, and site
2. When
a. At the time the procedure is scheduled
b. At the time of preadmission testing and assessment
c. At the time of admission or entry to the facility for the procedure, whether elective or emergent
d. Before the patient leaves the preprocedural area or enters the procedure room
e. At any time, responsibility for care is transferred to any other member of the care team.
3. How
a. Patient identification (hospital wristband), proper labeling of patientrelated items, and cross-confirmation by
checking patient records, including imaging studies. This is done using a standardized list (previously called
“checklist”).
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(1) A standardized list counteracts human failures of omission.
(2) A meaningful standardized list includes simple clearly defined information that physicians need and induces
them to adhere to safety measures in daily practice (10).
(3) Successful safety standardized lists improve communication and consistency of care, decreasing
complications and death rates. In a prospective,
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multinational trial involving 7,688 patients, the rate of any complication dropped from a baseline of 11% to 7%,
and in-hospital mortality decreased from 1.5% to 0.8%, after standardized list implementation (11).
b. Standardized list
(1) Can be in paper, electronic, or other medium (e.g., wall-mounted board)
(2) Reviews and verifies that all items are available and accurately matched to the patient:
(a) Confirmation of correct patient by two identifiers: (a) If no identifying band on the patient, use full name and
date of birth, and (b) if there is an identifying band on the patient, use full name and medical record number.
(b) Confirmation of correct procedure and site by verbal/self-report by the patient or family member
(c) Reverification of correct procedure and site with history and physical examination note, nursing assessment
note, or progress note
(d) Accurately completed and signed procedure consent form
(e) Verification of laboratory and radiology results (are in fact those of the patient; pay special attention to
projections—anterior or posterior— in which images were obtained, so as to not confuse laterality), required
blood products (properly matched and verified), implants, devices, and/or special equipment (sterile and not
expired) needed for the procedure.
c. Consent process
(1) Consent must be obtained while the patient is awake and alert, prior to any sedation, and has the capacity to
understand the details and implications of the procedure.
(2) Consent must be in a language that the patient understands (or employ an interpreter).
(3) Consent form should include a clear statement of the procedure to be performed and the site of the
procedure.
(4) Consent form can be waived in emergency cases with a threat to life or limb.
Site Marking
1. Essentials
a. Site marking is required for any procedure involving an incision, percutaneous puncture, or insertion of an
instrument before the procedure (see exemptions in the following text).
(1) When both right- and left-sided structures are abnormal, the SIR recommends that skin marking be performed
even if intraprocedural imaging is to be employed (6).
(2) Site marking for bilateral procedures (for identical procedure, team, and equipment) is recommended but not
required by the Joint Commission (JC) (9).
b. Site to be marked must be unambiguous, clearly visible, and at or next to the procedure site. Nonprocedural
site should not be marked unless necessary for some other aspect of care.
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c. Site marking takes place with the patient involved awake and aware, if possible.
d. In specific circumstances (i.e., nonspeaking, comatose, or incompetent patients, children), the site-marking
process should be handled similar to the informed consent process.
2. When
a. The procedure site is initially marked before the patient is moved to the location where the procedure will be
performed.
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3. Exemption from site marking
a. Interventional procedures for which there is no predetermined site of insertion (e.g., angiography, central line
placement). This is because
(1) Side is irrelevant for the procedure (6) and
(2) Imaging guidance is an inherent part of the procedure (6).
(3) For angiographic procedures, it is the opinion of SIR that vascular access is simply a means to provide a
route to perform a procedure or to provide access to central veins. Skin marking at the vascular access is not
needed. For angioplasty procedures, SIR recommends that the side (left or right) of intervention be confirmed
with appropriate intraprocedural imaging (6).
b. When technically or anatomically impossible or impractical to mark the site
c. Procedures that have a midline approach intended to treat a single, midline organ/lesion
d. Endoscopy without intended laterality
e. Patient refusal of site marking. The situation should be handled the same way (i.e., gentle explanation and
documentation) as for any other refusal by a patient offered care, treatment, or services. The Universal Protocol
does not require that the procedure be canceled because the patient refuses site marking.
f. Premature infants where there could be permanent tattooing of immature skin
g. For procedures in which site marking is not required, the other requirements of the Universal Protocol still
apply.
4. Two-stage marking
a. Spinal procedures
(1) The general level of the procedure (cervical, thoracic, or lumbar) must be marked preoperatively.
(2) If the procedure involves anterior versus posterior, or right versus left approaches, the mark must indicate
this.
(3) The exact interspace(s) to be treated should be precisely marked using standard intraprocedural radiographic
marking technique (9).
5. Two-site marking
a. When patient is having two procedures performed at diff erent sites (i.e., regional anesthetic block prior to an
interventional procedure), two separate marks are to be made.
6. Who performs site marking?
a. The interventionist, as a licensed hospital-privileged practitioner, who will be performing the procedure should
mark the site.
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b. Site marking can be delegated to another individual in limited situations: A licensed practitioner—such as a
fellow, resident, advanced practice nurse, or physician assistant—can be delegated by an interventionist. This
individual must be familiar with the patient, present, and actively involved during the procedure.
c. Even when the site marking is delegated to another practitioner, the interventionist still remains responsible
and accountable for all aspects of the procedure.
d. Any delegation of responsibility for site marking must be consistent with applicable laws and regulations (6).
7. How
a. Use a permanent marker so that it is not removed during site preparation. Adhesive site markers should not be
used as the sole means of marking the site (6).
b. The mark must be clearly visible after the patient is in final on-table position, with the skin prepped and sterile
draping in place.
c. Types of mark
(1) The Universal Protocol does not specify the type of mark but leaves the choice to the institution. However,
the mark must be unambiguous and consistent throughout the institution.
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(2) The word YES, initials of the interventionist who will perform the procedure (12), or an arrow pointing to the
site (13) is generally used.
(3) The cross (X) should not be used because this could denote a site that should not be operated upon and
introduces ambiguity.
Time-out
1. Essentials
a. Time-out is a brief pause before the procedure starts to CONFIRM—correct site, correct procedure, correct
patient!
b. It is an opportunity to
(1) Identify any wrong site, wrong patient, or wrong procedure
(2) Ensure correct patient positioning
(3) Ensure availability of necessary instruments and equipment
(4) Foster communication among team members
(5) Clarify any inconsistencies or concerns from any team members
c. The design and deployment of the time-out process is up to the individual institution. Documentation of
adherence to Universal Protocol and the “time-out” process is mandatory.
2. When
a. Immediately prior to the start of the procedure, after the patient is appropriately positioned, regardless of the
venue—interventional suite, computed tomography (CT) suite, or at bedside with ultrasound guidance (6)
3. Who
a. The interventionist (person who will perform the procedure) initiates time-out.
b. The time-out must not occur without the individual performing procedure present (9).
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4. How
a. The time-out must be verbal and interactive with all team members involved in the procedure. The
interventionist confirms:
(1) Correct patient identity
(2) Accurate and signed consent form
(3) Agreement on the procedure to be done
(4) Correct patient positioning
(5) Correct side and site are marked
(6) Relevant images and results are properly labeled and displayed
(7) Appropriate antibiotic administration and/or fluids for irrigation
(8) Special safety precautions due to patient's health and medication history
b. During the time-out, all unnecessary activities (those that do not compromise patient safety) within the room
are suspended.
c. All team members must be in agreement before proceeding with incision or skin puncture.
d. Time-out can be improved (14) when the team (a) is aware of an ideal model of a good time-out, (b) has a
culture to reward safety, (c) does not allow deviation from the standard time-out, and (d) constantly voices
concerns and feedbacks.
5. Two time-outs
a. When two or more procedures are to be performed on the same patient by separate teams, a complete time-
out is performed before each procedure begins.
(1) Example: epidural placement by anesthesiologist, followed by cesarean section by obstetrician
(2) The exception is that when the same team is performing multiple components during a single procedure.
b. When hospital policy or law/regulation requires two separate consents
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Documentation
1. Documentation of Universal Protocol must be completed and included in patient's medical record.
a. Adequate documentation includes one checkbox or a brief note regarding the successful completion of the
time-out, located in a consistent location in the patient record. It is not necessary to individually document each
step of timeout if the full content is specified elsewhere (policy, procedure manual, etc.) (9).
2. Any team members directly involved in the procedure can complete the Universal Protocol documentation.
3. An example of Universal Protocol checklist is provided in Figure 61.1.
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FIGURE 61.1 • Sample Universal Protocol checklist. (Adapted from MGH Radiology.)
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References
1. Kwaan MR, Studdert DM, Zinner MJ, et al. Incidence, patterns, and prevention of wrong-site surgery. Arch
Surg. 2006;141:353-358.
2. Seiden SC, Barach P. Wrong-side/wrong-site, wrong-procedure, and wrong-patient adverse events: are
they preventable? Arch Surg. 2006;141:931-939.
3. Stahel PF, Sabel AL, Victoroff MS, et al. Wrong-site and wrong-patient procedures in the universal
protocol era: analysis of a prospective database of physician self-reported occurrences. Arch Surg.
2010;145:978-984.
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4. Sentinel event data: root causes by event type, 2004-2013. The Joint Commission Web site.
http://www.jointcommission.org/assets/1/18/Root_Causes_by_Event_Type_2004-2Q2013.pdf. Accessed
November 15, 2014.
5. World Alliance for Patient Safety. World Health Organization Web site.
http://whqlibdoc.who.int/publications/2009/9789241598552_eng.pdf. Accessed November 15, 2014.
6. Angle JF, Nemcek AA Jr, Cohen AM, et al. Quality improvement guidelines for preventing wrong site,
wrong procedure, and wrong person errors: application of The Joint Commission “Universal Protocol for
Preventing Wrong Site, Wrong Procedure, Wrong Person Surgery” to the practice of interventional radiology.
J Vasc Interv Radiol. 2008;19:1145-1151.
7. Facts about the Universal Protocol. The Joint Commission Web site.
http://www.jointcommission.org/facts_about_the_universal_protocol. Accessed November 15, 2014.
8. Adelman J, Chelcun J. Evidence-based safe surgical practices as adjuncts to the universal protocol. Arch
Surg. 2011;146:489.
9. National patient safety goals. The Joint Commission Web site

http://www.jointcommission.org/assets/1/6/2015_NPSG_HAP.pdf. Accessed November 12, 2015.
10. Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheterrelated bloodstream

infections in the ICU. N Eng J Med. 2006;355:2725-2732.
11. Haynes AB, Weiser TG, Berry WR, et al. A surgical safety checklist to reduce morbidity and mortality in a
global population. N Engl J Med. 2009;360:491-499.
12. Information statement wrong-site surgery. American Academy of Orthopaedic Surgeons Web Site.
http://www.aaos.org/about/papers/advistmt/1015.asp. Accessed November 15, 2014.
13. Masud D, Moore A, Massouh F. Current practice on preoperative correct site surgical marking. J
Perioper Pract. 2010;20:210-214.
14. 4 keys to a better time out, now. Association of periOperative Registered Nurse Web site.
http://www.aorn.org/News.aspx?id=24882. Published May 15, 2013. Accessed November 15, 2014.
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62
Sedation, Analgesia, and Anesthesia
Marcus A. Lehman
Leonard J. Lind
The practice of vascular and interventional radiology often requires the use of medication to relieve anxiety,
provide sedation, and minimize discomfort. Unfortunately, administration of local anesthetics, sedatives, and
opioids can impose an additional element of risk to patients, mandating care in patient preparation, monitoring,
and discharge from the radiology suite (1).
Analgesia and Anesthesia: Options and Indications

1. Local anesthesia. Infiltration of skin and underlying tissues or peripheral nerve block (e.g., intercostal
nerve block). For brief diagnostic procedures where little discomfort is expected beyond the local puncture
site in adult patients who are cooperative and tolerate the initial local anesthetic infiltration at the puncture
site
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2. Local anesthesia with sedation. Provision of care by
a. Local anesthesia with sedation provided by radiology care team
(1) Appropriate for most patients undergoing diagnostic and interventional procedures
(2) May require consultation with an anesthesiologist concerning the choice of medication and appropriate
dosage in certain patient populations, for example, in patients during the first trimester of pregnancy
b. Local anesthesia with sedation provided by anesthesia care team (monitored anesthesia care)
(1) With poor-risk, critically ill, or difficult patients. Often difficult patients have a history of poor tolerance for
invasive procedures, usually resulting from inadequate analgesia and sedation.
(2) When intense analgesia or deep levels of sedation are required
(3) When procedure or positioning may compromise the airway
(4) When procedure may require or be facilitated by rapid raising or lowering of the systemic arterial
pressure (2)
3. Neuraxial or regional anesthesia. Induction of segmental anesthesia and muscle relaxation with local
anesthetics (e.g., spinal or epidural anesthesia)
a. Neuraxial block via spinal or epidural is used when intense analgesia for the procedure and the
postprocedural period is required, without the use of excessive opioid medication.
b. When muscle relaxation is desirable or required 4. General anesthesia. Induction and maintenance of a
controlled state of unconsciousness characterized by a loss of protective airway reflexes, absence of
response to painful stimuli, and inability to recall procedural events
a. Appropriate for the uncooperative patient or the patient who refuses local or regional anesthesia
b. When there is potential for airway obstruction as a result of the procedure or when airway patency or
protection may be compromised by sedative medication
Patient Evaluation
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1. History and physical examination
a. Age. Advanced age alters dose requirements and elimination of many medications. For sedatives and
analgesics, the elderly patient usually requires smaller increments and less frequent dosing intervals compared
with younger adults. A reduction of 30% to 50% is a practical approach to initial dosing administration.
Metabolism and drug elimination are both slowed in the elderly, which can result in excessive postprocedure
sedation and delayed recovery (3). Elderly patients often require more extensive preparation for procedures, and
they are at an increased risk for periprocedural complications because of significant concomitant medical
disease and age-related impairment of cardiovascular, hepatic, and renal function (4).
b. Cardiovascular disease. Coronary artery disease (CAD), congestive heart failure (CHF), cerebrovascular
disease, insulin-dependent diabetes, and serum creatinine >2.0 are important factors associated with increased
risk of perioperative cardiac complications. In addition, self-reported exercise ability remains an effective
screening tool and has been found to be independently linked with the risk for adverse cardiovascular events (5).
Well-controlled hypertension does not present an increased risk (6).
c. Pulmonary disease. Smoking is an important cause of perioperative respiratory morbidity and mortality. Before
a procedure, cessation of smoking should be encouraged. Other important patient-related risk factors include
poor exercise capacity, chronic obstructive pulmonary disease, acute exacerbations of asthma, and morbid
obesity (7).
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d. Obesity. Recognition of associated comorbid issues is essential as the prevalence of obesity continues to rise.
Obese individuals are at an increased risk for CAD, obstructive sleep apnea (OSA), hypertension, diabetes, and
gastroesophageal reflux. In general, the risk will rise with increasing weight, often in a nonlinear fashion.
Assessment of exercise tolerance may be difficult to assess secondary to body habitus. Limited pulmonary
reserve and OSA contribute to the substantial risk of hypoventilation and obstruction caused by oversedation.
Recently published practice guidelines by the American Society of Anesthesiologists may assist in determining
the severity and appropriate perioperative management of patients with OSA (8). Additionally, there are
pharmacokinetic alterations in the obese patient. In general, the loading dose is based on the volume of
distribution and maintenance dose on clearance; however, in the obese population, published dosing information
may not be appropriate (9). It has been suggested that dosing of medications, opioids in particular, should be
based on lean body mass rather than actual weight (9,10). Morbidly obese patients who require deep sedation
should be monitored by an experienced anesthesia provider.
e. Hepatic disease. Reduced hepatic mass is associated with a decreased production of coagulation and drug-
binding proteins (e.g., albumin). Initial doses of sedative and analgesic medications should be reduced because
altered drug-protein binding can allow excessive “free” (i.e., unbound) drug to enter the central nervous system
(CNS). In addition, drug metabolism can be markedly slowed, resulting in prolonged postprocedural sedation (3).
f. Renal disease. Impairment of renal function will slow the ultimate elimination of many drugs, and although initial
and maintenance doses may not require reduction, dosing intervals may need to be lengthened. The glomerular
filtration rate (GFR) is the best laboratory metric available to determine overall measure of kidney function (11).
In patients with renal dysfunction, specific care should be exercised with administration of meperidine (Demerol),
since normeperidine, a primary metabolite, can accumulate and lead to CNS stimulation, excitement, and
seizures (12).
g. Medication history. Assessment of drug usage patterns and adverse reactions to medications are essential to
the provision of safe patient care. Often, a drug effect or side effect (e.g., nausea) is described as an allergy.
True allergic reactions to amide local anesthetics (lidocaine and bupivacaine) or benzodiazepines (diazepam and
midazolam) are rare.
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(1) Maintenance cardiovascular medication should be continued before the procedure. Attention should be given
to the beneficial effects of continuing chronic perioperative β-blocker therapy, although starting this therapy
immediately preoperatively is of uncertain benefit and may increase risk of complications (6). These can be given
with sips of water while maintaining the patient in an otherwise fasted state.
(2) The insulin-dependent diabetic patient requires special consideration. Elective studies in these patients
should be scheduled for early in the day. Often, half the usual morning dose of insulin is given and an infusion of
5% dextrose is begun on the day of the procedure. For lengthy procedures, frequent blood sugar determinations
should be performed and an insulin infusion considered.
(3) In the elderly patient, adverse drug events from prescribed medications are common but often preventable.
Meticulous care must be taken to review the current medication list so that appropriate monitoring of the patient
for adverse events can be performed. Specifically, cardiovascular, diuretic, nonopioid analgesic, oral
hypoglycemic, and anticoagulant drugs are common medication categories associated with preventable adverse
events (13).
2. Laboratory testing
a. Overview. Preprocedural laboratory screening is expensive and often contributes little to patient care. When
tests are ordered by protocol without
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specific indications, few significant abnormalities are found, and many of these determinations could be
eliminated without measurably decreasing patient safety (14).
b. Indications
(1) Risk assessment for pregnancy (e.g., urine or serum beta human chorionic gonadotropin hormone [β hCG])
(2) Risk assessment for cardiovascular morbidity (e.g., electrocardiogram [ECG])
(3) Risk assessment for hemorrhagic complications
(4) Evaluation of hepatic and renal function
(5) Guide for preprocedural medical therapy (e.g., transfusion, electrolyte repletion, additional medical
consultation)
Recommended Monitoring
1. Standards. Meticulous cardiovascular and respiratory monitoring facilitates earlier detection of
anesthesia-related complications and should reduce overall patient morbidity or mortality. In an effort to
improve patient safety during anesthesia, minimum standards for monitoring have been outlined and
implemented in most institutions (15).
2. Designated monitoring personnel. An individual (registered nurse [RN] or medical doctor [MD]) must
be designated to be responsible for monitoring vital signs, administering medication, and record keeping.
This person should be in attendance throughout the procedure and have no other significant responsibilities
during the monitoring period.
3. Temperature. All anesthetic agents, opioids, and sedatives have the ability to lower the vasoconstriction
and shivering thresholds increasing the potential for periprocedural hypothermia. The maintenance of
normothermia leads to improved patient outcomes (16). Additionally, the Surgical Care Improvement Project
(SCIP) requires that active warming be used to maintain temperature ≤96.8°F within 30 minutes
postprocedure (17).
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4. Recommendations. For radiologic procedures, minimum monitoring standards should be adopted
(Table 62.1).
Required Resuscitation Equipment

1. In procedure room
a. Oxygen source
b. Face masks and nasal prongs for oxygen delivery
Table 62.1 Recommended Monitoring Parameters for Various Forms of Anesthesia
Anesthetic Option
Local Local with

Parameter Monitor Only Sedation Regional General
Circulation BP x x x x
Cardiac rhythm ECG x x x x
Oxygenation Pulse x x x x
oximeter
Respiratory Respiration x x x
depression rate
Ventilation ETCO2 x x x
Temperature x x x
Extent of block Sensory level x
ETCO2, end-tidal carbon dioxide.
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c. Oral and nasal airways
d. Suction
e. Functional bag and mask device (e.g., Ambu bag)
f. Supraglottic airway devices (e.g., laryngeal mask airway [LMA])
g. Intravenous (IV) supplies (e.g., catheters, tubing, infusion pumps)
h. Naloxone (Narcan) and flumazenil (Romazicon)
i. Epinephrine
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2. In radiology suite
a. Intubation equipment (e.g., laryngoscopes, endotracheal tubes)
b. Defibrillator
c. Advanced life-support medications (e.g., epinephrine, lidocaine, amiodarone, norepinephrine, and
dopamine)
Medication Prior to Procedure

1. Guidelines. The administration of medication prior to a procedure should never be routine. The choice
of agent, dosage, and route of administration must be individualized. After oral and intramuscular (IM)
administration, sufficient time (30 to 60 minutes) may be required for drug absorption to obtain desired
effects. If continuous patient observation cannot be provided after an IM injection, IV administration of
medication just prior to the procedure (with patient monitoring) is recommended.
2. Summary of frequently used drugs
a. Midazolam (Versed)
(1) Indications: anxiolysis, induction of sedation, and amnesia
(2) Dose/route of administration: 2 to 7 mg IM or 1 to 3 mg IV
(3) Adverse effects: profound sedation in patients over 70 years old. In patients aged 60 to 69 years,
midazolam, 2 to 3 mg IM, is usually quite effective (18).
(4) Contraindication: first trimester of pregnancy, acute narrow-angle glaucoma
b. Droperidol (Inapsine)
(1) Indications: prevention and treatment of nausea and vomiting
(2) Dose/route of administration: 2.5 to 5.0 mg IM or 0.625 to 1.250 mg IV
(3) Adverse effects: prolonged sedation with IM administration, hypotension, extrapyramidal symptoms, and
exacerbation of Parkinson disease
(4) Contraindication: prolongation of corrected QT interval [QTc] c. Hydroxyzine (Vistaril)
(1) Indications: prevention of nausea and vomiting, pruritus, anxiolysis
(2) Dose/route of administration: 25 to 100 mg IM
(3) Adverse effects: excessive sedation, dry mouth
(4) Contraindication: narrow-angle glaucoma
d. Diphenhydramine (Benadryl)
(1) Indications: sedation, prophylaxis against contrast reaction
(2) Dose/route of administration: 25 to 50 mg by mouth (PO), 25 to 50 mg IM, or 12.5 to 25 mg IV
(3) Adverse effects: excessive sedation, dizziness, dry mouth, difficult urination, thickening of bronchial
secretions
(4) Contraindication: acute asthma, narrow-angle glaucoma
e. Morphine sulfate
(1) Indications: analgesia, sedation
(3) Adverse effects: respiratory depression, hypotension, nausea, vomiting, itching, biliary spasm
f. Fentanyl citrate (Sublimaze)
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(1) Indications: analgesia
(2) Dose/route of administration: 25 to 50 μg IV
(3) Adverse effects: respiratory depression, bradycardia, nausea, vomiting, muscle rigidity, biliary spasm
(19)
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g. Nalbuphine hydrochloride (Nubain)
(1) Indication: analgesia, sedation
(3) Adverse effects: excessive sedation, nausea, vomiting, dizziness, limited analgesia, restlessness,
reversal of analgesia produced by other opioids
(4) Biliary tract: less elevation of biliary pressure than fentanyl and butorphanol (19)
h. Ketorolac (Toradol)
(1) Indication: analgesia without respiratory depression; can be used in combination with opioids
(2) Dose/route of administration: 15 to 60 mg IM/IV
(3) Adverse effects: reversible platelet dysfunction (24 to 48 hours after drug discontinuation), gastritis,
peptic ulceration, and inhibition of renal autoregulation Acute renal failure has been reported in patients
following one dose of ketorolac because of its effect on renal autoregulation and therefore must be used
cautiously during procedures in which a high contrast-dye load is being administered (20).
i. Propofol (Diprivan)
(1) Indication: sedation for monitored anesthesia care, sedation with neuraxial anesthesia, induction and
maintenance of general anesthesia, sedation of intubated, mechanically ventilated intensive care unit (ICU)
patients
(2) Dose/route of administration: 1 to 2 mg per kg IV bolus for induction of general anesthesia;
maintenance 25 to 200 μg/kg/min IV infusion depending on depth of sedation desired
(3) Adverse effects: hypotension, cardiovascular depression, apnea. Stinging at injection site.
Anaphylactic reaction to emulsion; caution in egg and soy allergic patients. Propofol infusion syndrome can
occur with long-term use or in short-term, high dose use. Should be used only by providers able to
rescue patients from deeper level of sedation than intended (21,22).
j. Dexmedetomidine (Precedex)
(1) Indication: sedation or supplemental sedation, often in the intensive care setting; maintains spontaneous
respiration
(2) Dose/route of administration: 0.5 to 1.0 μg per kg IV over 10 minutes loading dose, followed by 0.2 to 1.0
μg/kg/h IV for up to 24 hours
(3) Adverse effects: bradycardia, hypotension (23)
k. Prednisone
(1) Indication: prophylaxis against contrast reaction
(2) Dose/route of administration: 50 to 75 mg PO the evening before and 1 to 2 hours prior to the
examination
(3) Adverse effects: hyperglycemia, hypertension, fluid retention
l. Methylprednisolone (Solu-Medrol [IV/IM], Medrol [PO])
(1) Indication: prophylaxis against contrast reaction
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(2) Dose/route of administration: 32 mgPO the evening before and 1 to 2 hours prior to the examination
(3) Adverse effects: hyperglycemia, hypertension, fluid retention
Techniques of Sedation, Analgesia, and Anesthesia during the Procedure

Local Anesthesia
1. Indications: anesthesia at puncture site
2. Drug classification
a. Amides: lidocaine (Xylocaine), mepivacaine (Carbocaine), bupivacaine (Marcaine, Sensorcaine)
b. Esters: chloroprocaine (Nesacaine), procaine (Novocaine)
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3. Choice of drug. Most commonly used agents are amide local anesthetics. These local anesthetics are
preferred over the esters because of increased potency, prolonged duration, and far fewer documented
allergic reactions. For radiologic procedures, lidocaine (1% to 1.5%) is the most frequently used amide local
anesthetic since it has a rapid onset of action and duration of 1 to 1.5 hours. However, both mepivacaine
(1.0% to 1.5%) and bupivacaine (0.5%) provide longer durations of action (1.5 to 4 hours).
4. Alkalinization of local anesthetics. Subcutaneous and intradermal infiltration of local anesthetics can
be painful. However, alkalinization of local anesthetics (with the addition of sodium bicarbonate) can lessen
the discomfort associated with skin and subcutaneous infiltration (24). For lidocaine, 1 mEq of sodium
bicarbonate is added to 10 mL of anesthetic. Alkalinization of bupivacaine is not recommended because
even small amounts of sodium bicarbonate may result in precipitation of the local anesthetic.
5. Injection technique and dosage. Careful needle placement, aspiration prior to injection and after each
3 to 5 mL, and frequent patient observation during infiltration are required to avoid intravascular injections of
local anesthetic. Rapid IV injection of local anesthetics can cause toxic manifestations. The total dose of
lidocaine should not exceed 4 to 5 mg per kg (healthy adult), whereas bupivacaine doses should not exceed
3 mg per kg. A dose reduction of 30% to 50% is recommended in elderly patients and those with hepatic
dysfunction and CHF, whereas maximum doses in the obese population should be based on lean body
weight (10). Excessive local anesthetic doses, resulting in high serum concentrations, can result in
prolonged lethargy following radiologic procedures, especially in the pediatric population (25).
Local Anesthesia with Sedation/Analgesia
1. Indications
a. Anxious patient
b. Procedures that produce discomfort distant from puncture site
2. Anesthesia consultation
a. Extremes of age
b. Hemodynamically unstable patient
c. Severe cardiovascular or pulmonary disease
d. Multiple maintenance medications (especially monoamine oxidase (MAO) inhibitors, chronic opioid use,
heart failure medications, hypoglycemic agents)
e. Pregnancy
3. Anesthesia attendance
a. Critically ill patients
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b. Procedures that require intense analgesia or deep levels of sedation (e.g., difficult percutaneous biliary
drainage or nephrostomy)
c. Procedures or positioning that may comprise the airway
d. Procedures that require or may be facilitated by close monitoring of the blood pressure and the ability to
titrate vasoactive medication
4. Sedatives
a. Midazolam: 0.5 to 2.0 mg IV every 30 to 60 minutes
b. Diphenhydramine: 12.5 to 25.0 mg IV every 1 to 2 hours
5. Opioid analgesics
a. Fentanyl: 25 to 75 μg IV every 15 to 60 minutes
b. Morphine: 1 to 5 mg IV every 30 to 60 minutes
c. Nalbuphine: 1 to 5 mg IV every 30 to 60 minutes
d. Dilaudid: 0.5 to 1 mg IV every 2 to 3 hours
6. Biliary procedures. There may be an advantage to the use of nalbuphine for analgesia without marked
elevations in biliary duct pressures and resistance to bile flow (19). IM or IV ketorolac can provide additional
pain relief when used in combination with the nalbuphine, improving patient comfort during these
procedures.
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Table 62.2 Suggested Drugs and Intravenous Doses for PCA and PCSA (Adult 70 kg)
Intermittent Frequency Usual Basal Infusion

Drug Dose (Lockout) System Rate
Hydromorphone 0.2-0.5 mg 6-10 min PCA 0.2-0.5 mg/h
Meperidine 10-15 mg 6-10 min PCA 15-50 mg/h
Morphine 1-2 mg 6-10 min PCA 0.5-1 mg/h
Fentanyl 10-25 μg 2-5 min PCA 25-50 μg/h
Alfentanil 0.01-0.03 mg 1-3 min PCA Not recommended
Propofol 5-20 mg 1-3 min PCSA Not recommended
7. Coadministration of benzodiazepines and opioids. Extreme care must be exercised when

administering these medications in combination. Hypoxemia and apnea may occur. Supplemental oxygen
must be given to these patients, and personnel skilled in airway management must be available to attend
these procedures (26).
8. Patient-controlled analgesia (PCA) and patient-controlled sedation (PCSA). This method of drug
delivery can enhance patient satisfaction and decrease the total dosage needed to control acute pain. With
PCA, the patient can self-administer small doses of opioid analgesic by means of a computercontrolled
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infusion by IV, subcutaneous (SQ), or epidural route. In comparison to IM opioids given at “as-needed”
intervals, self-administered doses provide more effective, sustained, and satisfactory analgesia (27). The
PCA device is programmable to control dose delivered, time between doses (lockout interval), total dose
limit over an hour or 4-hour period (4-hour maximum) and background continuous infusion. These
parameters are adjusted to provide optimal patient comfort and safety. Nevertheless, side effects can occur
including oversedation and respiratory depression. The PCA pump can also be used to provide sedation
during surgical procedures under local or regional anesthesia (28,29). Drugs used for this technique include
propofol, alfentanil, and fentanyl (Table 62.2). Using patient-controlled methods, midazolam and propofol
have each been shown to provide sedation and amnesia for local anesthetic injection prior to dental surgery
(28,29,30).
9. Nonpharmacologic considerations. Procedures performed while the patient is awake expose the
subject to visual and auditory stimuli that may be anxiety provoking. Headset music may offer a relaxing
distraction and provide a useful adjunct to a comprehensive sedation plan, decreasing sedative and
analgesic requirements (31).
Neuraxial Anesthesia
1. Indications
a. When intense analgesia for the procedure is required without use of excessive opioid medication
b. Regional muscle relaxation
c. Postprocedure pain management
2. Thoracic and lumbar epidural. Epidural anesthesia may be indicated for upper abdominal (hepatobiliary),
renal, lower abdominal, or pelvic procedures (32).
a. Suggested placement sites for radiologic procedures
(1) Upper abdominal procedures at T4-L1
(2) Renal procedures at T6-L1
(3) Lower abdominal, pelvis, and lower extremities at T10-L3
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b. Choice and dosage of agents
(1) The selection of the local anesthetic depends on the duration of the procedure. For long procedures (>2
hours), bupivacaine can be used, whereas lidocaine is best suited for shorter procedures.
(2) The amount and area of anesthesia coverage can be adjusted throughout the procedure by intermittently
dosing the epidural catheter. Postprocedure analgesia without muscle weakness can be provided by epidural
opioid administration.
c. Complications/side effects
(1) Motor blockade
(2) Hypotension
(3) Pruritus
(4) Urinary retention
(5) Postdural puncture headache
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(6) Intravascular injection (epidural vein)
(7) Intrathecal injection (“total” spinal)
General Anesthesia
1. Indications
a. If procedure may compromise the patient's airway
b. Highly anxious patients who refuse local anesthesia with sedation or regional anesthesia
c. Patients who are unable to cooperate and potentially combative due to a mental disability or acute mental
status
2. Disadvantages
a. Risks are inherent to general anesthesia.
b. Need to arrange anesthesia coverage and transport of anesthesia equipment to the radiology suite
c. Increased patient care costs
d. Inhalational anesthetics have vasodilatory effects that reduce renal blood flow and glomerular filtration, which
may increase the susceptibility to radiocontrast-induced nephropathy. Therefore, attention should be taken to
adequately hydrate those patients that are anticipated to receive a significant volume of radiocontrast dye (33).
Other Procedural Considerations

1. SCIP criteria. The SCIP mandates periprocedural consideration of timely antibiotic dosing, glucose
monitoring, and temperature monitoring and control (17). Additional equipment for dosing antibiotics and for
active warming (fluid warmers, warming blankets) should be available and used as needed during procedures.
Consideration for this equipment should be incorporated into the procedural planning, such as using active
warming while in a scanner.
2. Positioning. During procedures involving sedation, a patient will not adjust body and limb position in
response to reduced blood flow from compression for an extended period. Patient's limbs and body parts should
be positioned with this in mind, minimizing extreme flexion and extension of limbs and padding particularly
susceptible areas, such as the ulnar nerve as it passes through ulnar groove behind the medial epicondyle of the
humerus (34).
3. Intensive care unit (ICU) patients. ICU patients, some of whom are already intubated and sedated, will
present for interventional radiologic procedures. In such cases, the line is often blurred between moderate
sedation and general anesthesia in that sedative medications and airway devices are already in place. Many of
these medications have the capability of a deeper level of sedation than desired, including general anesthesia
with its concomitant hemodynamic and
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respiratory consequences. It is recommended that practitioners who are able to handle such consequences, as
well as other complications of these medications and devices be engaged in the patient's management.
1. Monitoring. Patient's vital signs should be monitored in a recovery area and observed for complications
following interventional procedures performed with sedative/opioid medication, regional or general anesthesia.
2. Discharge criteria for outpatients
a. Vital signs returning to preprocedural values and stable for 1 hour. Consider 1- to 2-hour additional time for
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OSA patients (8)
b. Must be sufficiently recovered from sedative/hypnotic medications to allow ambulation with assistance
c. Should be oriented
d. Able to void and to tolerate oral fluids
3. Discharge instructions for outpatients
a. Should be written and given to the responsible companion
b. Expected problems should be listed
c. Should have a telephone or beeper number to call for questions or complications
4. Follow-up
a. Inpatient. All patients should be visited after an interventional procedure. A chart note documenting the
effectiveness of sedation or anesthetic technique employed and any complications of the procedure is
recommended. These comments can be invaluable in planning future interventional radiologic and surgical
procedures.
b. Outpatient. Outpatient follow-up is also important and can be accomplished via a telephone or mailed patient
questionnaire.
References
1. Lind LJ, Mushlin PS. Sedation, analgesia, and anesthesia for radiologic procedures. Cardiovasc Intervent
Radiol . 1987;10:247-253.
2. Arteriovenous Malformation Study Group. Arteriovenous malformations of the brain in adults. N Engl J
Med. 1999;340:1812-1818.
3. Cheng EY, Cheng RM. Impact of aging on preoperative evaluation. J Clin Anesth. 1991;3:324-343.
4. Lind LJ. Anesthetic management in surgical care of the elderly. Oral Maxillofac Surg Clin North Am.
1996;8:(2):235-243.
5. Lee TH, Marcantonio ER, Mangione CM, et al. Derivation and prospective validation of a simple index for
prediction of cardiac risk of major noncardiac surgery. Circulation. 1999;100:1043-1049.
6. Fleisher LA, Fleischmann KE, Auerbach AD, et al. 2014 ACC/AHA Guideline on perioperative
cardiovascular evaluation and management of patients undergoing noncardiac surgery. A Report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines J Am Coll
Cardiol . 2014;64:e77-e137.
7. Smetana GW. Preoperative pulmonary evaluation. N Engl J Med. 1999;340:937-944.
8. Gross JB, Bachenberg KL, Benumof JL, et al. Practice guidelines for the perioperative management of
patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on
Perioperative Management of patients with obstructive sleep apnea. Anesthesiology. 2006;104:1081-1093.
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9. Egan TD, Huizinga B, Gupta SK, et al. Remifentanil pharmacokinetics in obese versus lean patients.
Anesthesiology. 1998;89:562-573.
10. Casati A, Putzu M. Anesthesia in the obese patient: pharmacokinetic considerations. J Clin Anesth.
2005;17:134-145.
11. Stevens LA, Coresh J, Greene T, et al. Assessing kidney function—measured and estimated glomerular
filtration rate. N Engl J Med. 2006;354:2473-2483.
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12. Kaiko RF, Foley KM, Grabinski PY, et al. Central nervous system excitatory effects of meperidine in
cancer patients. Ann Neurol . 1983;13:180-185.
13. Gurwitz JH, Field TS, Harrold LR, et al. Incidence and preventability of adverse drug events among older
persons in the ambulatory setting. JAMA. 2003;289:1107-1116.
14. Schein OD, Katz J, Bass EB, et al. The value of routine preoperative medical testing before cataract
surgery. Study of medical testing for cataract surgery. N England J Med. 2000;342:168-175.
15. Tobin MJ. Respiratory monitoring. JAMA. 1990;264:244-251.
16. Taguchi A, Kurz A. Thermal management of the patient: where does the patient lose and/or gain
temperature? Curr Opin Anaesthesiol . 2005;18:632-639.
17. Specifications Manual for National Hospital Inpatient Quality Measures. Discharges 01-01-14 (1Q14)
through 12-31-14 (4Q14): Section 2.4, SCIP-1-1, INF-10.
http://www.jointcommission.org/assets/1/6/2w_SCIP-Inf-4.pdf. Accessed November 21, 2014.
18. Wong HY, Fragen RJ, Dunn K. Dose-finding study of intramuscular midazolam preanesthetic medication
in the elderly. Anesthesiology. 1991;74:675-679.
19. McCammon RL, Stoelting RK, Madura JA. Effects of butorphanol, nalbuphine, and fentanyl on intrabiliary
tract dynamics. Anesth Analg. 1984;63:139-142.
20. Quan DJ, Kayser SR. Ketorolac induced acute renal failure following a single dose. J Toxicol Clin
Toxicol . 1994;32(3):305-309.
21. Garnier M, Bonnet F. Management of anesthetic emergencies and complications outside the operating
room. Curr Opin Anaesthesiol . 2014;27(4):437-441.
22. ASA Committee on Ambulatory Surgical Care. Statement on Safe Use of Propofol. 2009.
http://www.asahq.org/For-Members/Standards-Guidelines-and-Statements.aspx. Accessed November 21,
2014.
23. Hoy SM, Keating GM. Dexmedetomidine: a review of its use for sedation in mechanically ventilated
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patients in an intensive care setting and for procedural sedation. Drugs. 2011;71(11):1481-1501.
24. Ferrante FM, Steinbrook RA, Hughes N, et al. 1% lidocaine with and without sodium bicarbonate for
attenuation of pain of skin infiltration and intravenous catheterization. Anesthesiology. 1991;75:A736.
25. Palmisano JM, Meliones JN, Crowley DC, et al. Lidocaine toxicity after subcutaneous infiltration in
children undergoing cardiac catheterization. Am J Cardiol . 1991;67: 647-648.
26. Bailey PL, Pace NL, Ashburn MA, et al. Frequent hypoxemia and apnea after sedation with midazolam
and fentanyl. Anesthesiology. 1990;73:826-830.
27. Etches RC. Patient controlled analgesia. Surg Clin North Am. 1999;79:297-312.
28. Rodrigo C, Chow KC. Patient-controlled sedation: a comparison of sedation prior to and until the end of
minor oral surgery. Aust Den J. 1996;41(3):159-163.
29. Zacharias M, Bridgman J, Parkinson R. Two methods of administration of propofol for dental sedation. Br
J Oral Maxillofac Surg. 1998;36:19-23.
30. Torpe SJ, Balakrishnan VR, Cook LB. The safety of patient-controlled sedation. Anaesthesia.
1997;52:1144-1150.
31. Koch ME, Kain ZN, Ayoub C, et al. The sedative and analgesic sparing effect of music. Anesthesiology.
1998;89:300-306.
32. Cousins MJ, Veering BT. Epidural neural blockade. In: Cousins MJ, Bridenbaugh PO, eds. Neural
Blockade in Clinical Anesthesia and Pain Management. 3rd ed. Philadelphia, PA: Lippincott-Raven;
1998:243-322.
33. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of
contrast medium-induced nephropathy in patients undergoing coronary angiography: a randomized trial.
JAMA. 2008;300:1038-1046.
34. Winfree CJ, Kline DG. Intraoperative positioning nerve injuries. Surg Neurol . 2005;63(1):5-18.
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63
Drug Administration
Ellen McKeon-Levine
Petra Clark
Preprocedural Considerations
Premedication orders should never be routine but must be individualized considering patient's age, weight,
medical and physical condition, anxiety level, allergy history, previous drug reactions, tolerance or abuse of
drugs, lab data, and duration and type of procedure.
1. Patients with a history of a contrast reaction need premedication to prevent an adverse reaction or
anaphylaxis to the contrast agent. The Modified Greenberger Protocol recommends the administration of
prednisone 50 mg by mouth (PO) given at 13, 7, and at 1 hour prior to contrast administration—the last dose is
given in combination with cetirizine hydrochloride (Zyrtec) 10 mg PO or diphenhydramine (Benadryl) 50 mg
intravenously (IV). The Modified Laser Protocol is used for patients with diabetes, for those who are steroid
intolerant, and for those who have previously tolerated it. This protocol consists of the administration prednisone
40 mg PO given 12 and 2 hours before contrast administration—the last dose is again given in combination with
cetirizine hydrochloride (Zyrtec) or diphenhydramine (Benadryl) as described with the Modified Greenberger
Protocol.
2. Antimicrobial prophylaxis, for prevention of infections, is recommended to all patients receiving a tunneled
central venous catheter (CVC) or drainage catheter.
3. Antiemetics are recommended for patients who experience postoperative nausea and vomiting.
4. Patients on anticoagulation need to be given a plan by the physician for holding these medications or
instituting bridging therapy until routine anticoagulants can be restarted.
5. Patients with renal insufficiency should be hydrated (as tolerated) and considered for pretreatment with PO
acetylcysteine (Mucomyst).
Procedural Considerations
1. During the preprocedural phase, a nurse will verify the patient's nil per os (NPO) status (American Society of
Anesthesiologists [ASA] recommendations are NPO 6 hours for food and milk and 2 hours for clear liquids) and
obtain and document vital signs and a complete history including oxygenation: ASA status, age, height, weight,
medical problems, current medications, and allergies. All allergies will be discussed with all involved parties.
Comfort, anxiety, level of consciousness, and orientation will be assessed using hospital-based criteria. A
peripheral IV (minimum of a 22 gauge) will be started, or an existing robust functioning access will be confirmed.
2. A licensed independent radiology provider (medical doctor, fellow resident, physician's assistant, nurse
practitioner) evaluates the patient prior to the procedure. A focused history and physical examination are
obtained. Current lab data, electrocardiograms (ECGs), and pertinent imaging studies are reviewed. The
practitioner, trained in procedural sedation and responsible for the patient's care and treatment, will discuss
procedural sedation with the patient. Recredentialing for operators and monitors is required every 2 years.
3. Consultation with an anesthesiologist may be necessary in selected cases, such as when (a) the patient has
not tolerated or has failed sedation in the past, (b) the patient is unlikely to tolerate the procedure with sedation
alone, (c) the patient has a history of difficult airway, or (d) the patient is too critically ill to
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tolerate procedural sedation. In these cases, the anesthesiologist should evaluate the patient and provide direct
care during the procedure.
4. Informed consent for the procedure and required sedation is obtained and documented in the medical record.
Informed consent must include discussion of the risks and benefits of the procedure and sedation and alternative
treatments. The patient's code status must be confirmed and reversal, or the maintenance of a do not resuscitate
(DNR)/do not intubate (DNI) status should be addressed, if required.
5. A qualified nurse (certified in administering procedural sedation) is assigned to him or her for individualized
care and monitoring during the period of time that the patient is in the special procedure area. The procedure
room should have undergone a complete safety check. Emergency resuscitation equipment, supplies, and
medications need to be readily available. All procedure rooms must be equipped with the following:
a. Resuscitation cart
b. Defibrillator with multifunctional pads, paddles, and external pacemaker
c. Full patient monitoring equipment including cardiac monitor, blood pressure monitor with a variety of sized
cuffs, various oxygen delivery systems, pulse oximeter, capnography, flashlight, stethoscope, thermometer,
airways and a self-inflating positive pressure oxygen delivery system, as well as a source of suction
d. Contrast reaction kits including specific pharmacologic antagonists/reversal agents for the type(s) of sedation
to be used
e. All equipment must be inventoried and maintained on a regularly scheduled basis in conjunction with policies
established by the hospital.
6. The operator and/or monitor must be available as soon as the patient enters the procedure room. All patients
will receive supplemental oxygen. Medications will be titrated to desired effect while maintaining adequate
oxygenation and hemodynamic status. Blood pressure, heart rate and rhythm, respiratory rate, oxygenation and
capnography, and sedation levels should be continuously monitored and documented every 5 minutes during the
procedure and for 30 minutes following the last dose of procedural sedation. Arterial hemodynamic monitoring
may be used if indicated during select procedures.
7. Recovery and postprocedure care
a. During the recovery period, and depending on the institution, the procedure and the amount of procedural
sedation and physiologic parameters should be monitored every 10 minutes, for a minimum of 30 minutes, or
until the patient reaches baseline physiologic status (prior to the administration of sedation).
b. Any patient receiving reversal agents requires a minimally extended recovery period of 2 hours following the
last dose of reversal agents or until the patient reaches baseline as stated. Outpatients are given written
discharge orders and on-call contact telephone numbers. A telephone follow-up is recommended at 24 hours in
order to evaluate and correct late sequelae of the procedure or medications.
Table 63.1 Abbreviations and Equivalents for Common Units
Abbreviations Equivalents
Microgram μg 1,000 μg = 1 mg
Milligram mg 1,000 mg = 1 g
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Gram g 1,000 g = 1 kg
Kilogram kg 1 kg = 2.2 lb
Microdrop μgtt 60 μgtt = 1 mL
Milliliter mL 1,000 mL = 1 L
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Dosage Calculations
Units (Table 63.1)
1. Body weight is measured in kilograms (kg).
2. Drug concentration is measured in micrograms per milliliter (μg/mL).
3. Dosage is measured in micrograms per kilogram (of body weight) per minute (μg/kg/min).
Calculating Infusion Doses

1. Dose in microgram per minute: dose (μg/kg/min) × body weight (kg)
2. Dose in milliliters per minute: dose (μg/min)/concentration (μg/mL)
Suggested Readings
Anderson DJ, Podgorny K, Berríos-Torres SI, et al. Strategies to prevent surgical site infections in acute care
hospitals: 2014 update. Infect Control Hosp Epidemiol . 2014;35(6):605-627.
Asif A, Epstein M. Prevention of radiocontrast-induced nephropathy. Am J Kidney Dis. 2004;44(1):12-24.
Blayney MR. Procedural sedation for adult patients: an overview. Contin Educ Anaesth Crit Care Pain.
2012;12(4):176-180.
Clinical practice guidelines for antimicrobial prophylaxis in surgery. In: Best Practices for Hospital & Health-
System Pharmacy. Ipswich, MA: CINAHL Complete; 2014:582-667. Website
http://connection.ebscohost.com/c/articles/99013387/clinical-practice-guidelinesantimicrobial-prophylaxis-
surgery. Accessed 17, 2015.
Douketis JD, Spyropoulos AC, Spencer FA, et al. Perioperative management of antithrombotic therapy:
Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians
Evidence-Based Clinical Practice Guidelines. Chest. 2012;141(2 suppl):e326S-e350S.
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64
Treatment of Contrast Media Reactions
Michael A. Bettmann
General Principles (1)

1. The radiologist should have the expertise, experience, and equipment to treat most (i.e., non-life-threatening)
contrast media reactions without assistance.
2. Access to expertise and equipment for effectively responding to life-threatening reactions should be readily
available: fully trained, advanced cardiac life support (ACLS)-certified personnel as well as code cart and code
team.
3. The medications and equipment to treat all reactions, from minor to acutely lifethreatening, must be readily
available and regularly updated. These include commonly needed medications (diphenhydramine, β-agonist
inhalers, atropine, and epinephrine) and equipment (endotracheal tubes, laryngoscope, monitor, external
pacemaker, and defibrillator). If not in the room, all this equipment must be located so it is accessible within
seconds to the suite in which contrast is administered.
4. The response time to the treatment should be minimized (1). Not all contrast reactions present with a classical
complex of signs and symptoms. Failure to consider and recognize that a patient is actually having an adverse
reaction may delay the appropriate treatment (2). Conversely, the reaction must be accurately diagnosed and
understood—an anxiety reaction may mimic an early anaphylactoid one.
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5. Three basic requirements for all patients
a. Know the patient.
b. Recognize that there is a problem.
c. Be prepared to deliver treatment and call for help quickly. (Know the ABCs of basic life support [BLS]:
airway/assessment, breathing, and circulation.)
d. Know exactly where the code cart, with automatic external cardioverterdefibrillator (AECD), is located; ensure
it is regularly inspected and updated (2,3).
6. Three reactions of greatest concern, as all may mimic cardiovascular collapse
a. Anaphylactoid reaction: life-threatening
b. Vasovagal: more common, must be treated to resolution
c. Anxiety or syncope: diagnosed by exclusion, but do not immediately treat with epinephrine
Know the Patient

1. Before the procedure, inquire about prior exposure to iodinated contrast material, previous adverse reactions,
and relevant history.
a. Does the patient have a history of asthma? If so, is the patient actively wheezing? Contrast media can provoke
bronchospasm and worsen preexisting airway constriction.
b. Does the patient have a strong history of multiple and/or severe allergies? This increases the risk of an
adverse reaction to contrast agents.
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c. Does the patient have a history of coronary artery disease, aortic stenosis, or other significant cardiac
problem? Contrast material can compromise cardiac function (4).
d. Is the patient being treated for congestive heart failure? Contrast material will increase the effective circulating
volume and may cause pulmonary edema in the poorly compensated patient.
e. Are there any reasons why the patient may have compromised renal function? (See Chapter 65.) This
includes known renal dysfunction, bladder outlet obstruction (male or female), long-term diabetes, recurrent
infections, or renal calculi.
f. Does the patient have any other major active medical problems? Is the patient particularly anxious or unable to
cooperate?
2. The radiologist performing the procedure should have knowledge of the patient's routine medications. Some
medications may mask the symptoms of a contrast reaction.
a. β-Blockers slow the heart rate and block the tachycardiac response to physiologic stress. β-Blockade blunts
the effects of epinephrine (an α- and β-agonist), requiring increased doses to achieve similar physiologic effect.
Once the β-blocker effect is overcome, an unopposed α-adrenergic effect of epinephrine predominates, with a
marked increase in peripheral vascular resistance and a subsequent hypertensive response.
Additionally, vasovagal reactions are characterized by hypotension and bradycardia. In patients on β-blocker
therapy, an anaphylactoid reaction may be misjudged as a vagal reaction because of the absence of
tachycardia.
b. Calcium-channel blockers are frequently prescribed for hypertension, coronary insufficiency, and
arrhythmias. They are peripheral vasodilators; correction of hypotension by fluid replacement may be more
difficult due to persistent peripheral vasodilation.
c. Metformin, an oral hypoglycemic agent, can rarely lead to lactic acidosis, which is fatal in a high
percentage of patients. Because of the renal excretion, it has been thought to be contraindicated in patients with
elevated serum creatinine, although this caution is being reconsidered, based on empirical information (5,6,7).
Current U.S. Food and Drug Administration (FDA) recommendations still indicate that metformin should be
stopped for 48 hours at the time of contrast administration (5) (see Chapter 65).
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d. Nonsteroidal anti-inflammatory drugs (NSAIDs) are widely used. Although unproven, it is thought that
high-dose NSAID use may predispose to contrastinduced nephropathy (CIN).
Recognize that There Is a Problem

1. Look for both the classical/expected and the more subtle signs that the patient is having an adverse reaction.
a. First, talk to the patient and assess ABC status. Many “reactions” may simply be manifestations of anxiety,
with resultant tachycardia, tachypnea, and light-headedness.
b. Dermal reactions: urticaria, pruritus, diffuses erythema, skin flushing
c. Angioedema may present with increased production of tears, difficulty in swallowing, nasal congestion, or
laryngeal edema with hoarseness. Facial edema may also, rarely, occur.
d. Bronchospasm occurs almost solely in patients with asthma. It is characterized by dyspnea, sometimes
tachypnea and end-expiratory wheezing. In contrast, laryngospasm, which is less frequent and more concerning,
is characterized by stridor or inspiratory wheezing.
e. Sudden loss of consciousness may be due to central nervous system (CNS), cardiac, or pulmonary reactions,
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or to benign syncope. It is crucial that vital signs be evaluated (and then monitored) to try to distinguish the
cause so that appropriate treatment can be given immediately.
f. Vagal reactions are characterized by light-headedness, feelings of anxiety, diaphoresis, hypotension, and
bradycardia. Full-blown anaphylactoid reactions, which are far less frequent than vagal reactions, are
characterized by hypotension, tachycardia, and, often, loss of consciousness.
g. Other mental status changes, such as confusion, are rare, usually not related to a contrast agent, and most
often due to sedation or other medication or to a cerebral event.
2. All patients in the interventional/angiography suite should have continuous blood pressure (BP) monitoring,
pulse oximetry, and capnography. Patients who receive contrast for computed tomography (CT)-guided
procedures or intravenous (IV) urography may be less closely monitored. The person in attendance (radiologist,
registered nurse [RN], respiratory therapist [RT]) will have to depend on the physical signs and the patient's
symptoms to determine whether the patient is having an adverse reaction.
Be Prepared to Deliver Treatment Quickly and Call for Help Early

Evaluate the situation, categorize the type of adverse reaction and patient status, and determine whether
immediate treatment is necessary and, if so, which specifically, or whether continued monitoring alone is
appropriate. Regardless of whether the patient is monitored or treatment is started, reevaluate the patient
frequently and decide whether the situation is improving, stabilizing, or worsening. Monitoring must be
continued until the reaction resolves. Always document as promptly and thoroughly as you can.
Treatment of Adverse Reactions (Table 64.1)

1. Cutaneous
a. Urticaria: often, but not always, associated with pruritus—essentially always self-limited. Incidence increases if
looked for (i.e., often is asymptomatic, seen if you look under patient garment). Treat if symptomatic, with
diphenhydramine, 25 to 50 mg by mouth (PO) or IV. Caution patients not to drive after this treatment. Urticaria is
not a good predictor of a recurrent reaction, particularly not a more severe one.
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Table 64.1 Treatment of Major Adverse Reactions
Symptoms Treatment (in Order of Increasing Severity)
Symptomatic urticaria (pruritus) 25-50 mg diphenhydramine IM or IV
Bronchospasm 1. Nasal oxygen, IV access, monitor ECG, and oxygen saturation

2. β-Agonist inhaler (metaproterenol, terbutaline, albuterol)
3. Epinephrine 1:1,000; 0.1-1.0 mL SC or
4. Epinephrine 1:10,000; 1.0-3.0 mL IV
Laryngotracheal edema or 1, 3, then 4 (do not use a β-agonist inhaler)

symptomatic facial edema
Pulmonary edema 1. Oxygen, IV access; monitor ECG and oxygen saturation; obtain
cardiac enzymes serially
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2. Elevate head; apply rotating extremity tourniquets
3. Furosemide 40 mg slow IV push—carefully monitor respiratory
status, BP
4. MSO4 1-10 mg slow IV push
Vagal reaction (hypotension and 1. Monitor vital signs; ensure IV access

bradycardia or lack of 2. Elevate legs (more effective than Trendelenburg position)
tachycardia) 3. Push IV fluids
4. Atropine 0.6-1.0 mg IV push (+0.5-mg increments) as needed to
stabilize BP and pulse
5. Crucial consideration to avoid significant complications is
observation and treatment until BP and HR return to baseline
levels
Seizure 1. Diazepam 1-10 mg IV push, in 1-mg increments

2. Monitor vital signs
3. Obtain neurologic consultation
Cardiopulmonary arrest 1. Monitor vital signs and ECG

2. Ensure IV access
3. Ensure functional airway
4. Begin resuscitation
5. Call code team (Do 1-5 simultaneously.)
6. Epinephrine 1:10,000; IV 1-3 mL
MSO4, morphine sulfate.
b. Generalized exanthem: Rare. May be associated with cardiovascular collapse (i.e., a severe, full-blown
anaphylactoid reaction). Treat symptomatically, if associated with hypotension and tachycardia, will require
epinephrine 1:10,000 IV.
c. Delayed: Incidence as high as 9%, but often not recognized, as these may occur 24 hours to 10 days after the
administration of contrast and are often ascribed to other causes, such as clopidogrel, warfarin, use of a new
detergent. Take various forms but most often maculopapular rash. Tend to recur on reexposure to a contrast
agent, particularly the same contrast agent, and they are clearly immune-mediated. Rarely may be severe and
life-threatening. Treat symptomatically, with topical steroids or, as needed, systemic steroids. Consider
dermatology consult.
d. Contrast extravasation: Not usually a cause of major concern or complications, particularly with low-osmolality
contrast agents and limited volume. May be a concern in the pediatric age group, in diabetics with neuropathy or
vasculopathy, or if volume of extravasation is very large. Treatment is
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symptomatic; use cold or hot soaks initially, follow closely if symptomatic, and consider plastic surgery consult, if
severe, for pressure release.
2. Pulmonary
a. Bronchospasm: Generally seen in patients with active asthma, rarely if ever in others. Treat as needed
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symptomatically. β-Agonist inhalers are usually sufficient, with monitoring of pulse oximetry and supplemental
oxygen as needed. Occasionally, may need epinephrine (either 0.1 to 0.3 mL of 1:1,000 given subcutaneously
[SC] or 1 to 3 mL of 1:10,000 given IV, actual dose is the same, IV action is faster and more predictable).
b. Laryngospasm: Rare; may be a component of generalized edema. If symptomatic, treat with nonrebreather O2
mask, IV epinephrine (1:10,000 dilution), and observe until symptoms and signs (i.e., stridor, inspiratory
wheezing) resolve completely.
c. Tachypnea: A not infrequent anxiety reaction. Generally not associated with any further signs or symptoms
and requires only reassurance and occasionally sedation. Nasal O2 may help. Auscultation to rule out wheezing
or stridor.
3. Generalized systemic
All such reactions, including diffuse erythema, should be considered potentially life-threatening. Patients
should be observed and evaluated with the BLS's ABCs. AECD at bedside.
a. Vasovagal: Characterized by anxiety, diaphoresis, hypotension, and bradycardia. Not a true contrast reaction,
usually related to general anxiety. Generally benign in course but must be followed and treated until full
resolution. Treatment: Raise legs (more effective than Trendelenburg position at increasing intravascular
volume), IV fluids, and atropine as needed (0.6 to 1.0 mg IV, repeat as needed).
b. Respiratory: O2 via nonrebreather mask, β-agonist (metaproterenol or similar) inhaler for bronchospasm,
epinephrine SC (1:1,000; 0.1 to 0.3 mL) or IV (1:10,000; 1 to 3 mL) if bronchospasm is unresponsive and for
laryngospasm/laryngeal edema.
c. Cardiovascular
(1) Vasovagal (see earlier): fluids, leg elevation, atropine (minimum initial dose 0.6 to 1.0 mg) IV
(2) Anaphylactoid: characterized by hypotension, tachycardia, often loss of consciousness. Treatment is
symptomatic: fluids, particularly if there is vascular compromise (e.g., severe hypotension), general vascular
support; use epinephrine 1:10,000; 1 to 3 mL IV as needed. Call code team (better to call too early than too late).
(3) Ventricular tachycardia (VT)/ventricular fibrillation: Call code; initiate cardioversion.
(4) Pulmonary edema: Again, may be caused not by the contrast per se but rather by acute cardiac
decompensation with or without acute volume expansion. May be indicative of an acute myocardial infarction.
d. Seizures: diazepam 1 mg IV in increments to effect, with careful monitoring of respiratory status
4. Remember
a. Hypotension + bradycardia = vasovagal reaction
b. Hypotension + tachycardia = anaphylactoid or cardiac reaction. Note: If patient is on a β-blocker, tachycardic
response may be blunted or absent.
c. Respiratory distress with a wet cough and pink frothy sputum = pulmonary edema. Consider: Is this patient
having an acute myocardial infarction? Treat with O2, rotating tourniquets, MSO4, and furosemide; obtain
electrocardiogram (ECG) and cardiac enzymes.
d. Corticosteroids and diphenhydramine have no role in the acute treatment of contrast reactions, due to both
the pathophysiology of the reaction and the delayed action of these medications in an acute setting. The key
medications to consider are IV fluids, epinephrine, and atropine.
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References
1. American Heart Association. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency
Cardiovascular Care. Part 6: advanced cardiovascular life support: section 7: algorithm approach to ACLS
emergencies: section 7A: principles and practice of ACLS. The American Heart Association in collaboration
with the International Liaison Committee on Resuscitation. Circulation. 2000;102(8 suppl):I136-I139.
2. Bush WH Jr. Treatment of acute contrast reactions. In: Bush WH Jr, Krecke KN, King BF Jr, et al. eds.
Radiology Life Support. New York, NY: Oxford University Press; 1999:31-51.
3. Rousek JB, Hallbeck MS. Improving medication management through the redesign of the hospital code
cart medication drawer. Hum Factors. 2011;53(6):626-636.
4. Fleetwood G, Bettmann MA, Gordon JL. The effects of radiographic contrast media on myocardial
contractility and coronary resistance: osmolality, ionic concentration, and viscosity. Invest Radiol .
1990;25:254-260.
5. Bush WH Jr, Bettmann MA. Metformin (Glucophage) therapy and the risk of lactic acidosis. ACR Bulletin.
1997;53:18-19.
6. Khanal A, Peterson GM, Castelino RL, et al. Potentially inappropriate prescribing of renally cleared drugs
in elderly patients in community and aged care settings. Drugs Aging. 2015;32(5):391-400.
7. Inzucchi SE, Lipska KJ, Mayo H, et al. Metformin in patients with type 2 diabetes and kidney disease: a
systematic review. JAMA. 2014;312(24):2668-2675.
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65
Contrast-Induced Nephropathy: Prevention and Management
Michael A. Bettmann
Contrast-induced nephropathy (CIN) may occur after administration of any iodine-based contrast agent. Its
importance is not that it leads to the need for temporary or permanent renal replacement therapy (i.e., dialysis—
on the order of 1% even in those at risk) but rather that it is associated with increased all-cause morbidity and
mortality (1,2,3,4). The incidence depends on risk factors and the definition of CIN. The incidence of CIN
approaches zero in patients with truly normal renal function (glomerular filtration rate [GFR] >90 mL/min/1.73m2).
In patients with stage 4 or 5 chronic kidney disease (CKD) (GFR <30), the incidence may be as high as 20% to
40%, in part as a function of contrast volume and associated risk factors. Arriving at an accurate definition of
incidence is difficult for several reasons, in addition to the factors noted above. For example, particularly among
hospitalized patients, there are many nephrotoxic risk factors other than contrast administration: age (related to
decreased muscle mass), surgery, hypotension, congestive heart failure (CHF), and many medications. It is often
difficult, therefore, to be certain that a specific occurrence of transient worsening of renal function is actually
solely or even primarily related to contrast administration. Currently, criteria for the diagnosis of CIN vary widely.
Until the pathophysiology is completely understood, however, prevention will not be completely effective. Both
the risk for and the occurrence of CIN are best defined and evaluated by using an estimated GFR (eGFR).
Although the overall accuracy of the eGFR may be limited, it remains a better indicator of both baseline risk and
of the course of CIN than serum creatinine alone. The reader is directed to the e-book for an in depth discussion
of this topic.
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Diagnosis
CIN is defined most often as a 25% or 50%, or a 0.5 mg per dL increase in serum creatinine, or a 25% or
greater decrease in eGFR. The best approach to making a clinically relevant diagnosis of CIN is
nonetheless to obtain a baseline serum creatinine and eGFR, followed in those at risk by a serum creatinine
at 24 and/or 48 hours, with repeated measurements for 7 to 14 days if an initial elevation is seen (5,6,7,8).
Although a rise in serum creatinine at 24 hours has been shown to be the single best predictor for CIN
currently, because there are normal day-to-day variations in serum creatinine, a single such measurement
may not be either sufficiently sensitive or sufficiently accurate.
Natural History
In most cases, CIN is characterized by an increase in serum creatinine over 1 to 7 days after contrast
administration, with a return to baseline renal function by 2 to 4 weeks. Development of end-stage renal disease
is rare, even in patients with significantly compromised renal function (CKD grade 3 or worse, that is, GFR <60)
(9).
Risk Factors
1. In patients with truly normal renal function (i.e., not just normal serum creatinine but also normal eGFR of >90
mL/min/1.73m2) the risk is very low, probably even absent. See the caveat later, however, regarding acute
changes in renal function due to changes in renal perfusion.
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2. Patients with preexisting renal dysfunction are at risk. Risk is very limited in patients with stage 1 or 2 CKD
(GFR ˜60-89). Although it is logical to think that the risk increases with increasing dysfunction, it is not clear that
this is true. The reason is that it is likely that numerous other risk factors play a role in the incidence and severity
of CIN (e.g., nephrotoxic medications, poor cardiac output).
3. The risk is increased roughly by a factor of 2 in patients with diabetes mellitus (10). Again, the risk appears to
be confined to those with CKD stage 3 or worse (GFR <60). This risk has been shown almost solely in patients
with type I diabetes; the risk among the increasing population with type II diabetes is not clearly defined. There is
likely to be an increased risk, as a function of the duration and severity of the diabetes.
4. Increasing age also is a risk factor, again only in those with compromised renal function. It is important to
remember that renal function normally decreases with age, as reflected in both true GFR and eGFR but not
necessarily in serum creatinine.
5. Dehydration is thought to be a major risk factor. Many elderly patients are relatively dehydrated at baseline.
Furthermore, it is, unfortunately, a usual practice to keep patients nil per os (NPO) for 12 or more hours prior to
procedures, thereby worsening dehydration. This is in large part done for forgotten reasons (perhaps related to
the fear of nausea, vomiting, and aspiration after contrast administration) and is generally not necessary. Even in
patients who are to receive sedation, there is no need to avoid fluid intake for more than 3 to 4 hours prior to the
procedure.
6. Poor renal perfusion is also a concern, and this may occur in the presence of heart failure, severe trauma with
major blood loss, or other causes of hypotension or hypovolemia (e.g., major surgery). These situations may
lead to an acute decrease in renal function that is not necessarily reflected in serum creatinine.
7. Various medications (e.g., aminoglycosides, angiotensin-converting enzyme inhibitors, β-blockers, diuretics,
nonsteroidal anti-inflammatory [NSAIDs]) have been postulated to predispose to CIN. To date, there is reason for
caution with
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certain known nephrotoxins (aminoglycosides, certain chemotherapy drugs) but not with most drugs. NSAIDs
block prostacyclins that are important in intrarenal vasodilatation. In the presence of vasoconstriction, as in heart
failure, high-dose NSAID use may precipitate renal failure. Vasoconstriction is not thought to be a major factor in
the etiology of CIN, so NSAID use in general is not likely an important factor in the development of CIN.
8. Metformin is a separate consideration (11,12). It is not directly nephrotoxic. It is, however, associated with
lactic acidosis that may be fatal in up to 50%. Due to hepatic metabolism and renal excretion, the effect of
metformin is prolonged in the presence of renal or hepatic failure. Metformin is, therefore, contraindicated in
patients with severe hepatic disease, renal dysfunction, or poor hepatic or renal perfusion (as in CHF). There is
no specific association between contrast agents and metformin-related lactic acidosis. Because it is thought that
contrast agents may lead to acute renal failure, recommendations currently are that metformin be stopped at the
time contrast is given and then be restarted after 48 hours if there is no clinical indication of renal dysfunction. A
follow-up serum creatinine is needed only if there is clinical concern. Again, the crucial consideration is that
metformin and metformin combinations should not be used in patients with an elevated creatinine. Unfortunately,
this may not be well-known or well-understood among health care providers who prescribe metformin.
9. Paraproteinemias such as multiple myeloma are also a separate concern. Renal failure related to these
diseases occurs because of underlying dehydration, with resultant precipitation of protein in the renal tubules
and consequent, often irreversible renal failure. The concern in these patients is not the contrast agents; use of
contrast is safe as long as patients are well-hydrated before, during, and after contrast administration.
Patient Preparation
Radiology Books
Prior to contrast administration, it is important to determine whether or not there are any risk factors present,
primarily underlying renal dysfunction. In generally healthy, younger individuals, this can be accomplished
effectively by obtaining a good history. The crucial questions are:
1. Do you have diabetes?
2. Do you have kidney problems?
3. Do you have a history of kidney stones; kidney, bladder, or other urinary tract infections; or prostate or bladder
problems?
4. What medicines do you take?
It is also important to evaluate patients for dehydration (skin turgor, blood pressure) and to try to achieve and
maintain adequate intravascular volume, through both oral and parenteral hydration before, during, and after the
administration of contrast.
Prophylaxis
There are currently no effective means of treating CIN after it has developed. There have, however, been major
advances in prevention. The most widely accepted approach is hydration, which is universally accepted as being
important. Studies (13,14) have demonstrated that:
1. Intravenous (IV) hydration is more effective than oral (perhaps only because it is more reliable).
2. Normal saline is more effective than half normal saline.
3. Twelve hours of normal saline (NS) is more effective than 4 hours.
The usual protocol, if feasible, is 12-hour prehydration with NS at 1 mL/kg/h, followed by continued hydration at
the same rate during and for 6 to 12 hours after the procedure. This regimen is obviously not practical for most
outpatients.
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In these patients, oral hydration should be strongly encouraged and carefully explained, and IV hydration should
be started as soon as possible. Dehydration should be avoided as much as possible, recognizing that patients
may need to be NPO for 3 to 6 hours prior to sedation (depending on local standards).
Many other approaches to prophylaxis have been tried, essentially all in conjunction with some hydration
protocol. Many of these have been poorly effective or ineffective. Currently, the two most widely investigated and
widely used prophylactic tools are n-acetyl cysteine (nAC; one generic formulation is Mucomyst) and sodium
bicarbonate (NaHCO3) hydration. nAC has previously been most widely used for the treatment of acetaminophen
overdose.
1. nAC: may be effective in preventing CIN, particularly when administered orally. The usual dose of nAC has
been 600 mg by mouth (PO) twice on the day before and twice on the day of contrast administration. More
recently, four doses of 1,200 mg orally have been shown to be more effective (15,16). This double dose is
justified because the medication is inexpensive, safe, generally well-tolerated (but for an unappealing smell), and
may be helpful.
2. NaHCO3: This has been widely used, with mixed results, although less wellstudied (17,18,19). There is
evidence that there is an additive effect to the use of both nAC and NaHCO3 as compared to either alone (19).
The most common protocol for use is three vials of NaHCO3 (approximately 1,000 mEq) in 1,000 mL D5W, given
at 3 mL per kg for 1 hour before the procedure and then 1 mL/kg/hr over 6 hours following the procedure.
3. Many other means of prophylaxis have been investigated and the optimal approach remains unclear.
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Conversely, prehydration is universally accepted as is limiting the volume of contrast injected.
The Role of Specific Contrast Agents

The classical fully substituted, tri-iodinated, high-osmolality contrast agents, widely used from the 1950s through
the 1990s, are now rarely used for radiographic or angiographic studies. Although they are far less expensive
than current lowosmolality agents and have a very similar safety profile, they cause pain with peripheral arterial
injection. They do not increase the risk of CIN in patients with normal renal function, but they do lead to a higher
incidence in patients with underlying renal dysfunction. In one very large study, the incidence of CIN with
highosmolality contrast agents (HOCA) versus low-osmolality contrast agents (LOCA) was equal in patients with
normal serum creatinine, slightly higher in patients with an elevated creatinine without diabetes, and much higher
in patients with both elevated creatinine and diabetes (10,20). There has been an ongoing debate in the
literature as to whether or not there is a difference in the incidence of CIN between most LOCA and the single
available isotonic contrast agent, iodixanol (Visipaque, GE Healthcare, Princeton, NJ). Several studies have
suggested that iodixanol is less nephrotoxic, while others have not shown a benefit. Overall, studies seem to
support the conclusion that confirm that there is some, probably small benefit with the use of iodixanol (21). The
major downside to its use is a relatively minor increase in cost. Consequently, it is reasonable to at least
consider iodixanol in patients with renal dysfunction (eGFR <60), particularly if large volume contrast use (>100
mL) is anticipated.
Other Considerations
1. Patients on acute or chronic renal replacement therapy (hemodialysis, peritoneal dialysis).
These patients do not appear to have an added risk from the nephrotoxicity of contrast agents. As a general rule,
the more residual renal function, the better the prognosis. It is important, therefore, to limit contrast volume.
Prophylaxis,
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other than hydration as possible, is not usually considered in patients on dialysis. However, that increased
intravascular volume is often a concern.
2. Patients with heart failure or poor cardiac output. Such individuals may be at increased risk both from volume
overload and from poor renal perfusion that may lead to decreased renal function. The usual prophylactic
approaches should be undertaken, again with the proviso that fluid volume may be a real concern.
3. As noted, many other causes of nephrotoxicity exist. This has led some to question whether or not CIN is a
real clinical concern, particularly with IV administration. While it is very likely that it is, comorbidities are so hard
to exclude that this remains a real question. Regardless, whenever the administration of contrast is considered, it
is important to determine, first, that it is truly necessary; second, whether or not there are risks that might
predispose to worsening renal dysfunction; and third, whether the use of prophylaxis is worth considering. This
last point clearly depends on the individual patient and clinical setting; in the presence of an acute, life-
threatening trauma, it is usually not appropriate to delay a contrast-enhanced CT to allow for administration of
prophylactic hydration and sodium bicarbonate. Finally, it is important to be aware that factors other than
contrast administration, such as other medications or cholesterol emboli related to an angiographic or surgical
procedure, may be the true cause of worsened renal function (22).
4. Gadolinium contrast agents
The specific concern for nephrogenic systemic fibrosis (NSF) has been welldocumented (23). The risk of any
gadolinium agent overall is very small but the risk of NSF increases with decreasing renal function, particularly
with certain specific chelates. The risk overall appears small even in stage 4 to 5 CKD with certain agents, but
great care should be taken with the use of any Gadoliniumbased agent in any patient with stage 3 or worse
Radiology Books
CKD. The use of such agents was advocated in the past for angiography in patients with severe renal
dysfunction, but this approach is now contraindicated.
References
1. Bettmann MA. Contrast medium-induced nephropathy: critical review of the existing clinical evidence.
Nephrol Dial Transplant. 2005;20(suppl 1):i12-i17.
2. Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after
percutaneous coronary intervention. Circulation. 2002;105:2259-2264.
3. Gundlach PJ, van Beek-Peeters JA, Ruissen J, et al. Contrast-induced nephropathy and mortality after
contrast-based investigation. Ned Tijdschr Geneeskd. 2015;159:A8501.
4. Gruberg L, Mintz GS, Mehran R, et al. The prognostic implications of further renal function deterioration
within 48 hours of interventional coronary procedures in patients with preexistent chronic renal insufficiency.
J Am Coll Cardiol . 2000;36:1542-1548.
5. Stevens LA, Levey AS. Measured GFR as a confirmatory test for estimated GFR. J Soc Nephrol .
2009;20:2305-2313.
6. Herget-Rosenthal S, Bökenkamp A, Hofmann W. How to estimate GFR-serum creatinine, serum cystatin C

or equations? Clin Biochem. 2007;40(3-4):153-161.
7. Endre ZH, Pickering JH. Outcome definitions in non-dialysis intervention and prevention trials in acute
kidney injury (AKI). Nephrol Dial Transplant. 2009;25(1):107-118.
8. Levey AS, Schwartz WD, Inker LA, et al. GFR estimation: from physiology to public health. Am J Kidney
Dis. 2014;63(5):820-834.
9. James MT, Samuel SM, Manning MA, et al. Contrast-induced acute kidney injury and risk of adverse
clinical outcomes after coronary angiography: a systematic review and meta-analysis. Circ Cardiovasc Interv.
2013;6(1):37-43.
10. Rudnick MR, Goldfarb S, Wexler L, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196
patients: a randomized trial. Kidney Int. 1995;47:254-261.
11. Bettmann MA. Use of intravenous contrast agents in patients receiving metformininvited response.
Radiology. 2002;225:312.
12. Inzucchi SE, Lipska KJ, Mayo H, et al. Metformin in patients with type 2 diabetes and kidney disease: a
systematic review. JAMA. 2014;312(24):2668-2675.
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13. Trivedi HS, Moore H, Nasr S, et al. A randomized prospective trial to assess the role of saline hydration
on the development of contrast nephrotoxicity. Nephron Clin Pract. 2003;93:C29-C34.
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14. Bader BD, Berger ED, Heede MB, et al. What is the best hydration regimen to prevent contrast media-
induced nephrotoxicity? Clin Nephrol . 2004;62:1-7.
15. Trivedi H, Daram S, Szabo A, et al. High-dose N- acetylcysteine for the prevention of contrast-induced
nephropathy. Am J Med. 2009;122(9):874.
16. Jo SH, Koo BK, Park JS, et al. N- acetylcysteine versus ascorbic acid for preventing contrast-induced
nephropathy in patients with renal insufficiency undergoing coronary angiography NASPI study—a
prospective randomized controlled trial. Am Heart J. 2009;157(3):576-583.
17. Brar SS, Shen AY, Jorgensen MB, et al. Sodium bicarbonate vs sodium chloride for the prevention of
contrast medium-induced nephropathy in patients undergoing coronary angiography: a randomized trial.
JAMA. 2008;300(9):1038-1046.
18. Zoungas S, Ninomiya T, Huxley R, et al. Systematic review: sodium bicarbonate treatment regimens for
the prevention of contrast-induced nephropathy. Ann Intern Med. 2009;151(9):631-638.
19. Brown JR, Block CA, Malenka DJ, et al. Sodium bicarbonate plus N-acetylcysteine prophylaxis: a meta-
analysis. JACC Cardiovasc Interv. 2009;2(11):1116-1124.
20. Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-risk patients undergoing angiography.
N Engl J Med. 2003;348(6):491-499.
21. Reed M, Meier P, Tamhane UU, et al. The relative renal safety of iodixanol compared with low-osmolar
contrast media: a meta-analysis of randomized controlled trials. JACC Cardiovasc Interv. 2009;2(7):645-654.
22. Olin JW. Atheroembolic renal disease: underdiagnosed and misunderstood. Catheter Cardiovasc Interv.
2007;70(6):789-790.
23. Zhang B, Liang L, Chen W, et al. An updated study to determine association between gadolinium-based
contrast agents and nephrogenic systemic fibrosis. PLoS One. 2015;10(6):e0129720.
Radiology Books
e-66
Noninvasive Evaluation: Lower Extremity Arteries
Joseph F. Polak
James F. Benenati
Segmental Pressure Measurements of the Lower Extremity: Ankle-Brachial

Index and Stress Testing
Indications
1. History of claudication
2. Clinical findings of arterial insufficiency
3. Prognostic indicator for healing of skin lesions of the toes or feet (1,2)
4. Postoperative surveillance of infrainguinal bypass grafts (traditional)
5. Short- and long-term follow-up of endovascular interventions, including thrombolysis, balloon angioplasty,
and endovascular stenting
Contraindications
1. Open wounds
2. Recent surgery
None
Procedure
1. Pressure cuffs are positioned around the upper and lower thigh and the upper and lower calf. The
segments have been designated high thigh (HT), above-knee (AK), below-knee (BK), and ankle (A). Most
commonly, cuffs of 10 to 12 cm in diameter with expandable bladders long enough to encircle the extremity
are used (3).
2. Doppler signals are detected in either the dorsalis pedis or the posterior tibial artery.
3. Each blood pressure (BP) cuff is inflated in turn, and the systolic pressure determines when a Doppler
signal is detected in the dorsalis pedis or posterior tibial branch.
4. A systolic BP measurement is taken from both arms at the brachial artery. By convention, the higher of
the two systolic pressure values is used to calculate the pressure index for both legs. A difference of greater
than 10 mm Hg in the systolic pressures should prompt an investigation of the upper extremities.
5. A ratio is constructed between the peak systolic pressure measured during deflation of the ankle cuffs
and the systolic brachial pressure: the ankle-brachial index (ABI).
6. Stress testing is essential when evaluating claudication because exams at rest may be near normal.
a. Stress testing is performed with the patient walking on a treadmill with a 12-degree incline, moving at 2
miles per hour. BP cuffs are placed on the ankles. Electrocardiogram (ECG) monitoring is performed during
stress.
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b. The patient exercises for 5 minutes or until the symptoms are reproduced. Sequential ankle pressures
are measured at 30-second intervals for the first
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4 minutes and then every minute until the pressure measurement returns to normal or to the pre-exercise
level (3).
None
Results
1. ABI
a. Normal: ABI = 1.0 or slightly greater, but greater than 1.2 indicates disease.
b. Claudication (mild stenosis or occlusion): ABI = 0.8 to 0.9
c. Moderate claudication: 0.5 to 0.8
d. Severe claudication: 0.4 to 0.5
e. Rest pain (severe occlusive disease): ABI <0.4
2. Prognosis for healing skin lesions of toes and feet (1): The probability of healing in diabetic and
nondiabetic patients is listed in Table e-66.1.
3. A drop of 15 to 30 mm Hg or greater in peak systolic pressure between the different segments is
considered abnormal, indicating a significant lesion located between the two cuffs (4).
4. If the segmental BP at a particular level has a discrepancy of at least 20 mm Hg less than the opposite
limb measured at the same level, a “horizontal” pressure gradient is present. This is indicative of a critical
lesion proximal to the cuff of the extremity with the lower pressure (4).
5. An HT pressure less than 20 mm Hg above the brachial pressure is considered abnormal. This is
consistent with:
a. Stenosis or occlusion of the aorta, iliac artery, or common femoral artery
b. Superficial femoral artery disease combined with stenosis or occlusion of the deep (profunda) femoral
artery. The pulse volume recordings (PVRs) should help in the differential diagnosis (see the section on
“Pulse Volume Recording”).
c. Significant stenosis of the brachiocephalic vessels.
6. Normal response to exercise is unchanged or there is slight elevation of the pressure measurement. Any
decline in pressure is a marker for significant arterial disease. The severity of the disease is indicated by
the time it takes for the pressures to return to the pretest level.
a. Single level of disease: 2 to 6 minutes
b. Multiple levels of disease: 6 to 12 minutes
c. Severe occlusive disease: up to 30 minutes or longer
7. Ankle pressures during exercise and rest are used as objective criteria for the clinical categories of
chronic limb ischemia (Table e-66.2) (5).
8. A decrease in the ABI of 0.15 or greater is considered a significant change.
9. An increase in the ABI of greater than 0.15 as a stand-alone criterion is defined as hemodynamic
improvement. An increase of 0.10 if associated with categorical clinical improvement (see Table e-66.2) is
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also defined as hemodynamic improvement (6).
Complications
None
Table e-66.1 Prognosis for Healing Skin Lesions of Toes and Feet
Probability of Healing (%)
Pressure (Ankle) (mm Hg) Nondiabetic Diabetic
Below 55 0 0
55-90 85 45
Above 90 100 85
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Table e-66.2 Clinical Categories of Chronic Limb Ischemia
Grade Category Clinical Description Objective Criteria
0 Asymptomatic, no Normal results of treadmill stress testa

hemodynamically significant
disease
I 1 Mild claudication Treadmill exercise completed,

postexercise AP >50 mm Hg but >25
mm Hg less than normal
2 Moderate claudication Symptoms between those of categories

1 and 3
3 Severe claudication Treadmill exercise cannot be completed;

postexercise AP <50 mm Hg
II 4 Ischemic rest pain Resting AP of ≤40 mm Hg; flat or barely

pulsatile ankle or metatarsal
plethysmographic tracing; toe pressure
<30 mm Hg
III 5 Minor tissue loss: nonhealing Resting AP of <60 mm Hg; ankle or

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ulcer, focal gangrene with metatarsal plethysmographic tracing flat
diffuse pedal ischemia or barely pulsatile; toe pressure <40 mm
Hg
6 Major tissue loss: extending Same as for category 5

above transmetatarsal level,
functional foot no longer
salvageable
aFive minutes at 2 mph on a 12-degree incline.
AP, ankle pressure.
Limitations and Artifacts

1. Diabetic patients typically can have a high ABI despite significant stenoses of their arteries. This occurs
because of the noncompressibility of the vessel. In some cases, the arteries are so rigid that no pressure
measurements can be obtained.
2. Pulsatile venous signals present in patients with congestive heart failure may be mistaken for arterial signals
(3).
3. Extreme obesity may distort pressure measurements.
4. Absence of Doppler signal because of severely diminished flow or complete occlusion may prevent
measurements.
Pulse Volume Recording

Indications
1. To complement pressure measurements in the evaluation of arterial disease
2. In the evaluation of compression syndromes such as the thoracic outlet syndrome and the popliteal
entrapment syndrome
3. In the evaluation of arterial disease when noncompressible calcified arteries do not permit the meaningful
interpretation of pressures
4. To perform anatomical localization of hemodynamically significant peripheral vascular lesions
Contraindications
1. Open wounds
2. Recent surgery
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None
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Procedure
1. Studies may be performed at rest or before and after exercise.
2. PVR cuffs are placed around the thighs, calves, and ankles of both legs.
3. The cuffs are inflated with a measured quantity of air (75 ± 10 mL) until a determined pressure (65 mm
Hg) is achieved.
4. The cuffs are calibrated so that a 1-mm Hg pressure change in the cuff provides a 20-mm chart
deflection.
5. Cuff pressure changes are proportional to cuff volume changes, which are related to instantaneous limb
volume changes.
Results
1. Normal and abnormal pulse volume waves are shown in Figure e-66.1.
2. PVR data have been classified into five categories (2) (Table e-66.3).
FIGURE e-66.1 • Pulse volume recording of a patient with a left common iliac artery stenosis. Right leg with
normal pulse volume wave demonstrating: (1) anacrotic rise, (2) pulse crest, (3) catacrotic decline, and (4)
reflected diastolic wave. The left pulse crest is rounded with absence of the reflected diastolic wave at the
thigh, calf, and ankle. (Study courtesy of the Vascular Laboratory of Virginia Beach General Hospital,
Virginia Beach, VA.)
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Table e-66.3 PVR Categories by Amount of Chart Deflection
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Chart Deflection (mm)
PVR Category Thigh and Ankle Calf
1 >15a >20a
2 >15b > 20b
3 5-15 5-29
4 <5 <5
5 Flat Flat
aWith reflected wave.
bWithout reflected wave.
3. Pulse volume amplitudes have been found to remain highly reproducible in the same patient if constant
cuff volumes and pressures are used (7). Significant changes correlate well with the appearance of
significant occlusive vascular lesions.
4. Pulse volume amplitudes will vary with alterations in ventricular stroke volume, BP, vasomotor tone, and
volume.
5. Exercise: The normal response to exercise is an increase in amplitude. Patients with occlusive arterial
disease uniformly show a decrease in pulse volume at the ankle following exercise (8).
6. Other indications of significant arterial disease as indicated by the PVR contour include:
a. Decrease in the rise of the anacrotic limb
b. Rounding and delay in the pulse crest
c. Decreased rate of fall of the catacrotic limb
d. Absence of the reflected diastolic wave
7. Outcomes of PVR evaluation by PVR category (2) are presented in Table e-66.4.
a. Rest pain can be evaluated to determine the likelihood that the pain is of vascular etiology.
b. Limiting claudication can be evaluated to determine the likelihood that exercise pain is of vascular
etiology.
c. Lesion healing can be predicted according to PVR category.
Complications
None
Table e-66.4 Outcomes by PVR Category for Rest Pain, Postexercise Pain, and Lesion
Healing
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Unlikely Probable Likely
Likelihood that rest pain is due to vascular etiology (diabetic and 1-3 3, 4 4, 5
nondiabetic)
Likelihood that postexercise pain (from limiting claudication) is 2, 3 4 4, 5

due to vascular etiology
Likelihood of lesion healing (diabetic and nondiabetic) 4, 5 3 1-3
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References
1. Sumner DS. Noninvasive assessment of peripheral arterial disease. In: Rutherford RD, ed. Vascular
Surgery. 3rd ed. Philadelphia, PA: WB Saunders; 1989.
2. Raines JK, Darling RC, Buth J, et al. Vascular laboratory criteria for the management of peripheral
vascular disease of the lower extremities. Surgery. 1976;79:21-29.
3. Gerlock AJ Jr, Giyanani VL, Krebs C. Noninvasive vascular examinations of the lower extremity arteries. In:
Applications of Noninvasive Vascular Techniques. Philadelphia, PA: WB Saunders, 1988:299-322.
4. Rose SC. Noninvasive vascular laboratory for evaluation of peripheral arterial occlusive disease: part II—
clinical applications: chronic, usually atherosclerotic, lower extremity ischemia. J Vasc Interv Radiol .
2000;11:1257-1275.
5. Rutherford RB, Becker GJ. Standards for evaluating and reporting the results of surgical and
percutaneous therapy for peripheral arterial disease. J Vasc Interv Radiol . 1993;2:169-174.
6. Ahn SS, Rutherford RB, Becker GJ, et al. Reporting standards for lower extremity arterial endovascular
procedures. Society for Vascular Surgery/International Society for Cardiovascular Surgery. J Vasc Surg.
1993;17:1103-1107.
7. Darling RC, Raines JK, Brener BJ, et al. Quantitative segmental pulse volume recorder: a clinical tool.
Surgery. 1972;72:873.
8. Raines JK. The pulse volume recorder in peripheral arterial disease. In: Bernstein EF, ed. Vascular
Diagnosis. 4th ed. St. Louis, MO: Mosby-Year Book; 1993: chap 42.
Radiology Books
e-67
Color Doppler and Duplex Ultrasound Imaging of Peripheral
Arteries
Joseph F. Polak
Carotid Artery Disease

Indications
1. To detect the presence and degree of carotid artery stenosis in patients with neurologic symptoms
2. To evaluate individuals with carotid bruits
3. To detect recurrent stenosis following carotid endarterectomy and carotid stent placement
4. To monitor patients with known carotid stenosis for disease progression
5. To evaluate patients undergoing extensive cardiac procedures for significant asymptomatic carotid artery
disease
Contraindications
Open wounds
None
Procedure
1. Equipment: a 5 MHz or greater linear array transducer with color Doppler frequency of 3 MHz or more
2. The examination is performed with the patient supine, head rotated away from the side being evaluated.
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3. The transducer is placed in the transverse plane and moved from the low common carotid artery to above
the bifurcation of the internal and external carotid arteries. This is used to survey carotid artery anatomy
and identify key landmarks.
4. The transducer is placed longitudinally, parallel to the artery. The color Doppler window is angled 20
degrees in either direction or vertically depending on the angle between the transducer surface and the
artery. The color Doppler velocity scale is typically set at 20 to 30 cm per second. The transducer is
sequentially moved to evaluate the full length of the common carotid and internal carotid arteries. The
external carotid artery is evaluated in its proximal portion.
5. The examination begins at the common carotid artery and includes Doppler tracings from the low and
upper common carotid artery; the external carotid artery; and the proximal, mid, and distal internal carotid
arteries. Doppler velocity waveforms are obtained at sites of abnormal color signal (increased velocity).
Doppler velocities are measured before, at, and just distal to the site of abnormal blood flow velocity. A
velocity ratio is calculated from the peak systolic velocity (PSV) at the point of increased velocity in the
internal carotid artery peak systolic velocity (ICA PSV) divided by the common carotid artery peak systolic
velocity (CCA PSV) measured 2 to 4 cm proximal to the common carotid bulb.
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6. Apparent absence of blood flow signals is confirmed with power Doppler imaging because it is more
sensitive to low-velocity signals than color Doppler.
7. Following carotid endarterectomy or stent placement, imaging should include the artery segment below
the site of intervention, a thorough sampling of the area of intervention, and the artery segment downstream
from the site.
None
Results
1. The degree of carotid narrowing is estimated using Doppler velocity values calibrated against the degree
of stenosis measured on arteriography according to the North American Symptomatic Carotid
Endarterectomy Trial (NASCET) method (residual lumen at the stenosis compared to the ICA diameter
distal to the stenosis) (1). In the presence of plaque, a 50% to 69% ( diameter) stenosis corresponds to a
PSV of 125 cm per second or greater (2) but less than 230 cm per second, whereas a greater than 70%
stenosis corresponds to a velocity above 230 cm per second (3). An ICA PSV/CCA PSV velocity ratio of 2
to 4 corresponds to a 50% to 69% stenosis and a ratio of more than 4 to a greater than 70% stenosis (4).
2. Very high-grade ICA stenoses can cause a decrease in velocities and a lowresistance pattern (tardus-
parvus waveform) (5) distal to the lesion. Color Doppler and power Doppler imaging are then used to
confirm the presence of a very narrow residual lumen (6) (Fig. e-67.1). Distinguishing between a subtotal
occlusion and a total occlusion can be difficult (7) and may require confirmation by magnetic resonance
angiography (8) or computed tomographic angiography (9).
3. Blood flow velocities can be moderately elevated for up to 1 year following standard carotid
endarterectomy. Following patch endarterectomy, the lumen of the artery can be enlarged to the point that
areas of blood flow stagnation can occur (10).
4. The presence of a carotid stent is often associated with an artificial increase in blood flow velocities.
Grading of stent stenosis can be based on a velocity ratio greater than 2.7 or a PSV greater than 220 cm
per second for a 50% stenosis and higher values such as a PSV of 340 cm per second for reintervention on
a stenosis greater than 80% stenosis (11).
Complications
None
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FIGURE e-67.1 • A: Blood flow proximal to a high-grade stenosis is laminar. At the stenosis proper, all the
red cells tend to travel at the same velocity (blunt flow profile or plug flow). The spectrum is therefore
narrower than that sampled in the artery proximal to the stenosis, and it has a larger amplitude because all
of the red cells must pass through the orifice. Distal to the stenosis, a more distinct jet of increased
velocities develops surrounded by a zone of flow reversal. The jet is often asymmetric, hitting one or the
other of the arterial walls rather than being directed toward the center of the artery. The zone of flow
reversal is seen as a site where eddy currents cause the blood to flow back on itself. The jet will continue to
dissipate energy as its effective radius grows. At the appropriate velocity/effective radius, turbulence will
occur. B: Distal to the stenosis, it is possible to obtain a combination of forward- and backward-moving red
cells. If the sample gate is large enough and placed at the interface between the zone of flow reversal and
the velocity jet, a complex blood flow pattern will be registered. (From Polak JF. Peripheral Vascular
Sonography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004, with permission.)
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Renal Artery Disease
Indications
1. To detect renal artery stenosis in hypertensive patients
Radiology Books
Contraindications
Relative contraindications include obesity, recent meal, and a large amount of intra-abdominal gas.
An overnight fast is preferred. No recent ingestion of medication. No recent smoking or chewing gum.
Procedure
1. Equipment: a 3 to 5 MHz curved or sector array transducer with color Doppler frequency of 3 MHz or
more
2. The examination is performed with the patient supine.
3. The transducer is placed transverse to the abdominal aorta. The color Doppler window is angled
vertically or angled toward the side being imaged.
4. The sample gate is placed in the proximal renal artery for Doppler spectral analysis. As much of the renal
artery length is sampled. A ratio is calculated from the PSV at the point of maximal increased velocity in the
renal artery divided by the PSV measured in the abdominal aorta (12).
5. Partial decubitus positions are also used to sample the renal arteries from a posterolateral or an
anterolateral approach through the kidney tissues (13).
6. Sampling of the Doppler signals is also done in the segmental or interlobar branches to the upper,
middle, and lower segments of the kidney in order to gauge the downstream effects of a proximal stenosis
(14).
7. Sites of prior intervention (atherectomy, angioplasty, or stent placement) should be evaluated. Imaging
should include the artery segment before the site of intervention, a thorough sampling of the area of
intervention, and the artery segment downstream from the site.
8. The overall appearance and size of the kidneys is evaluated with grayscale imaging. Harmonic imaging is
often used.
None
Results
1. Using a renal artery PSV, sensitivity and specificity for the detection of significant stenosis are 85% and
92%, respectively (14). The ratio of the PSV in the renal artery to the PSV in the abdominal aorta (range, 3
to 4.5) is less accurate with a sensitivity of 82% and specificity of 89% (14).
2. Indirect indices of proximal disease as determined by the acceleration time in the intrarenal branches
(greater than 0.10 to 0.12 second) have sensitivity of 80% and specificity of 82% (14).
Complications
None
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Peripheral Arterial Disease
Indications
1. To differentiate a stenosis from occlusion in symptomatic patients
2. To grade the degree of stenotic narrowing and determine the length of a lesion
3. To determine the length of an occlusion
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4. To evaluate iatrogenic arterial injuries
5. To confirm the short-term technical adequacy of endovascular intervention
6. To perform the long-term follow-up of lesions following endovascular intervention
7. To evaluate peripheral aneurysms
8. Evaluate the suitability of radial arteries for arteriovenous fistula placement or harvesting.
Contraindications
Open wounds or ulcerations
None
Procedure
1. Equipment: a 5 MHz or greater linear array transducer with color Doppler and pulsed Doppler
frequencies of 3 MHz or more
2. The examination is performed with the patient supine.
3. The transducer is placed longitudinally, parallel to the artery. The color Doppler window is angled 20
degrees in either direction or vertically depending on the angle between the ultrasound probe and the
artery.
4. Above the knee evaluation: The examination begins at the common femoral artery and ends at the distal
popliteal artery. The transducer is moved along the course of the superficial femoral artery, and all areas of
abnormal color signal (increased velocity) are sampled with Doppler spectral analysis. A ratio is calculated
from the PSV at the point of increased velocity divided by the systolic velocity measured in a segment 2 to 4
cm proximal to the site of blood flow abnormality.
5. Targeted examinations can be performed in the iliac and tibioperoneal arteries depending on the
indication.
6. Sites of prior intervention (atherectomy, angioplasty, or stent placement) should be evaluated. Imaging
should include the artery segment above the site of intervention, a thorough sampling of the area of
intervention, and the artery segment downstream from the site.
7. Aneurysms are evaluated with and without color Doppler imaging. The diameter of the aneurysm and
estimation of the amount of thrombus are made with grayscale images (15). The proximal and distal extent
of the aneurysm is documented, and the diameters of the vessel are recorded with electronic calipers (outer
wall to outer wall). Color Doppler imaging and Doppler spectral analysis are used to confirm flow within the
aneurysm.
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8. Pseudoaneurysms formed from iatrogenic injury are evaluated in a similar fashion. The channel from the
artery to the aneurysm should be evaluated with Doppler waveforms sampled in the communicating neck
typically show bidirectional flow in and out of the pseudoaneurysm sac, the so-called “to-andfro” sign (16)
(Fig. e-67.2).
9. Iatrogenic arteriovenous (AV) fistulas are evaluated with color Doppler to confirm the connection between
the artery and vein and with Doppler waveform analysis to demonstrate the pulsatility in the draining vein
and the low-resistance diastolic flow in the feeding artery. Pseudoaneurysms may be associated with AV
fistulas.
10. A dissection will either have a discrete intimal flap in the vessel lumen or present as a stenosis or
occlusion.
11. Use of a closure device can be associated with a pseudoaneurysm, stenosis, or occlusion at the site of
placement. All can be evaluated with Doppler ultrasound imaging.
12. Radial artery diameter measurements are predictive of dialysis AV fistula failure (17).
None
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FIGURE e-67.2 • The compliant nature of the soft tissues surrounding and containing a pseudoaneurysm
explains the persistent flow pattern that is established within it and at its communication with the native artery.
During systole, blood flows into the collection due to the relatively higher pressure in the artery lumen. Energy is
Radiology Books
stored in the collection as the surrounding soft tissues are compressed. During systole, the stored energy is
released as the pressure within the artery becomes less than that generated by the elastic recoil of the soft
tissues. This promotes flow into the artery. The swirling pattern of blood flow normally persists during the full
cardiac cycle. A longer communicating channel will increase resistance to flow and disrupt the steady state
responsible for setting up this constant motion. (From Polak JF. Peripheral Vascular Sonography. 2nd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2004, with permission.)
Results
1. The criteria for significant focal stenoses of greater than 50% diameter narrowing are increased color
Doppler flow velocities and a corresponding doubling in the PSV (a PSV ratio greater than 2) (18,19). A
PSV ratio above 4 corresponds to a stenosis above 75% lumen diameter narrowing. Accuracy has been
estimated at approximately 90%.
2. Arterial ultrasound can be used to survey for the extent and severity of native atherosclerotic disease or
in a targeted fashion (20).
3. Monitoring of arterial sites following angioplasty and stenting can be accurately done, but Doppler
velocity thresholds need to be modified (21,22).
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4. Popliteal aneurysms are evaluated with grayscale and color Doppler imaging. A relative diameter
increase in the artery segment of 20% or more serves as a functional criterion for early aneurysm formation
(ectasia).
5. The ultrasound Doppler examination is considered the first-line study for the evaluation of iatrogenic
arterial injuries such as pseudoaneurysms, AV fistulas, stenoses, occlusions, dissections, and closure
device malfunctions.
Complications
None
Lower Extremity Bypass Grafts

Indications
1. To detect early stenotic lesions and allow for interventions that preserve graft patency using scheduled
evaluations of saphenous vein bypass grafts in asymptomatic patients. Early stenoses due to fibro-intimal
hyperplasia can be detected with imaging at every 3 months for the first year and then every 6 months
during the second year (23). Additional yearly and biyearly examinations can be performed to evaluate for
progression of atherosclerotic disease.
2. To confirm the source of symptomatic ischemic changes following bypass grafting by detecting area(s) of
intragraft or anastomotic stenosis
3. To detect persistent venous fistulas following in situ vein bypass graft placement
4. Detect anastomotic stenoses in synthetic bypass grafts.
Contraindications
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Open surgical wounds or ulcerations
None
Procedure
1. Equipment: a 5.0 MHz or greater liner array transducer with Doppler frequency of 3 MHz or above. Color
Doppler imaging is the key component of the study.
2. The transducer is held parallel to the graft while the proximal anastomosis is imaged. Presence of blood
flow is confirmed both by color Doppler imaging and by Doppler waveform analysis.
3. The transducer remains oriented parallel to the graft conduit. The transducer is advanced in successive
increments equal to the length of the probe. The color window is kept at a 20-degree angle to the graft
lumen in order to enhance Doppler signals. The color scale is set to a maximal mean velocity between 20
cm and 40 cm per second in order to visualize blood flow patterns within the graft. Aliasing should be
absent. The distal graft anastomosis is identified with color Doppler imaging and the Doppler waveforms
sampled.
4. Doppler waveforms are sampled from any areas with abnormal color Doppler signals. Doppler velocity
measurements are made every 10 cm even if color Doppler signals are normal.
5. Absence of color Doppler signals within the graft is confirmed with power Doppler imaging and Doppler
waveform acquisition to confirm graft thrombosis.
6. Particular note is made of the PSV at the point of the graft with the smallest diameter.
None
Results
1. A complete examination takes 10 to 20 minutes.
2. Doubling of the Doppler PSV at a site of abnormal color Doppler signal is considered indicative of a
greater than 50% lumen narrowing. This method has a
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sensitivity of 95% and a specificity of 100%. Velocity ratios of 4 or above indicate a greater than 75%
stenosis and a lesion likely to need intervention.
3. A PSV of less than 40 to 45 cm per second (24) or a decrease of greater than 30 cm per second
compared to earlier evaluations should prompt further investigation for a stenotic lesion. These grafts
usually fail within 3 to 9 months of the examination. However, this method is limited in large diameter grafts
because they typically have low blood flow velocities.
Complications
None
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References
1. Grant EG, Benson CB, Moneta GL, et al. Carotid artery stenosis: gray-scale and Doppler US diagnosis—
Society of Radiologists in Ultrasound Consensus Conference. Radiology. 2003;229:340-346.
2. Polak JF, Dobkin GR, O'Leary DH, et al. Internal carotid artery stenosis: accuracy and reproducibility of
color-Doppler-assisted duplex imaging. Radiology. 1989;173:793-798.
3. Hunink MG, Polak JF, Barlan MM, et al. Detection and quantification of carotid artery stenosis: efficacy of
various Doppler velocity parameters. AJR Am J Roentgenol . 1993;160:619-625.
4. Moneta GL, Edwards JM, Chitwood RW, et al. Correlation of North American Symptomatic Carotid
Endarterectomy Trial (NASCET) angiographic definition of 70% to 99% internal carotid artery stenosis with
duplex scanning. J Vasc Surg. 1993;17:152-157.
5. Kotval PS. Doppler waveform parvus and tardus. A sign of proximal flow obstruction. J Ultrasound Med.
1989;8:435-440.
6. Schmidt P, Sliwka U, Simon SG, et al. High-grade stenosis of the internal carotid artery assessed by color
and power Doppler imaging. J Clin Ultrasound. 1998;26:85-89.
7. AbuRahma AF, Pollack JA, Robinson PA, et al. The reliability of color duplex ultrasound in diagnosing total
carotid artery occlusion. Am J Surg. 1997;174:185-187.
8. Back MR, Rogers GA, Wilson JS, et al. Magnetic resonance angiography minimizes need for arteriography
after inadequate carotid duplex ultrasound scanning. J Vasc Surg. 2003;38:422-430.
9. Koelemay MJ, Nederkoorn PJ, Reitsma JB, et al. Systematic review of computed tomographic
angiography for assessment of carotid artery disease. Stroke. 2004;35:2306-2312.
10. Hayes PD, Allroggen H, Steel S, et al. Randomized trial of vein versus Dacron patching during carotid
endarterectomy: influence of patch type on postoperative embolization. J Vasc Surg. 2001;33:994-1000.
11. Lal BK, Hobson RW II, Tofighi B, et al. Duplex ultrasound velocity criteria for the stented carotid artery. J
Vasc Surg. 2008;47:63-73.
12. Miralles M, Cairols M, Cotillas J, et al. Value of Doppler parameters in the diagnosis of renal artery
stenosis. J Vasc Surg. 1996;23:428-435.
13. Isikoff MB, Hill MC. Sonography of the renal arteries: left lateral decubitus position. AJR Am J
Roentgenol . 1980;134:1177-1179.
14. Williams GJ, Macaskill P, Chan SF, et al. Comparative accuracy of renal duplex sonographic parameters
in the diagnosis of renal artery stenosis: paired and unpaired analysis. AJR Am J Roentgenol . 2007;188:798-
811.
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15. Hall HA, Minc S, Babrowski T. Peripheral artery aneurysm. Surg Clin North Am. 2013;93:911-923.
16. Abu-Yousef MM, Wiese JA, Shamma AR. The “to-and-fro” sign: duplex Doppler evidence of femoral
artery pseudoaneurysm. AJR Am J Roengenol . 1988;150:632-634.
17. Parmar J, Aslam M, Standfield N. Pre-operative radial arterial diameter predicts early failure of
arteriovenous fistula (AVF) for haemodialysis. Eur J Vasc Endovasc Surg. 2007;33:113-115.
18. Polak JF, Karmel MI, Meyerovitz MF. Accuracy of color Doppler flow mapping for evaluation of the
severity of femoropopliteal arterial disease: a prospective study. J Vasc Interv Radiol . 1991;2:471-479.
19. Ramaswami G, Al-Kutoubi A, Nicolaides AN, et al. The role of duplex scanning in the diagnosis of lower
limb arterial disease. Ann Vasc Surg. 1999;13:494-500.
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20. London NJ, Nydahl S, Hartshorne T, et al. Use of colour duplex imaging to diagnose and guide
angioplasty of lower limb arterial lesions. Br J Surg. 1999;86:911-915.
21. Baril DT, Marone LK. Duplex evaluation following femoropopliteal angioplasty and stenting: criteria and
utility of surveillance. Vasc Endovascular Surg. 2012;46:353-357.
22. Shrikhande GV, Graham AR, Aparajita R, et al. Determining criteria for predicting stenosis with
ultrasound duplex after endovascular intervention in infrainguinal lesions. Ann Vasc Surg. 2011;25:454-460.
23. Tinder CN, Chavanpun JP, Bandyk DF, et al. Efficacy of duplex ultrasound surveillance after infrainguinal
vein bypass may be enhanced by identification of characteristics predictive of graft stenosis development. J
Vasc Surg. 2008;48:613-618.
24. Bandyk DF, Cato RF, Towne JB. A low flow velocity predicts failure of femoropopliteal and femorotibial
bypass grafts. Surgery. 1985;98:799-809.
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e-68
Doppler Ultrasound of Abdominal Vasculature
Ajay K. Singh
Rathachai Kaewlai
Doppler ultrasound (DUS) examination is a noninvasive means for evaluating the anatomy and blood-flow
dynamics of vascular aneurysms, stenoses, or occlusions. It can also guide the interventional radiologist during
needle or catheter placement. Understanding the strengths and weaknesses of this modality is crucial for optimal
clinical utilization.
Advancements in technology have significantly increased the current role of noninvasive vascular imaging in
minimally invasive treatment. DUS provides real-time imaging and physiologic information without exposing the
patient to ionizing radiation. This chapter describes six common indications for abdominal DUS related to
vascular interventional procedures, namely, abdominal aortic aneurysms (AAAs), transjugular intrahepatic
portosystemic shunts (TIPSs), liver transplantation, renal transplantation, and the interrogation of native renal
and visceral arteries.
Abdominal Aortic Aneurysm

1. AAA is the most common large-vessel aneurysm encountered in vascular practice. In the United States,
routine one-time ultrasound (US) screening is reimbursed for the diagnosis of AAA for men in the age group of 65
to 75 years, who are smokers or have first-degree relatives with AAA.
2. AAA is diagnosed when (a) there is a focal dilation, ≥3 cm or (b) the aortic diameter equals or exceeding 1.5
times its expected normal diameter (1). The majority of AAAs are infrarenal, fusiform, and “true” aneurysms
caused by degenerative changes in the aortic wall.
3. Patients with AAA of 4.0 cm or less, 4.1 to 4.5 cm, and 4.6 to 5.0 cm are advised to follow up at 24, 12, and 6
months, respectively. Patients with AAA of 5.1 to 5.5 cm may undergo repair or close follow-up at 3-month
intervals. An aneurysm larger than 5.5 cm requires intervention.
4. US is used to screen, confirm the diagnosis, and monitor the size of AAA (Fig. e-68.1).
a. In nonacute situation, 8 hours of fasting before abdominal DUS is required to reduce the amount of bowel gas.
b. The abdominal aorta is interrogated from the level of aortic hiatus to the bifurcation with visualization of
bilateral common iliac arteries. Due to the
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depth of the aorta from the anterior abdominal wall, a low-frequency curvilinear transducer is routinely used.
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FIGURE e-68.1 • Abdominal aortic aneurysm. Sagittal US view shows an aortic aneurysm with intraluminal
thrombus (arrow). Spectral waveform is identified in the lumen of the aorta.
c. The aorta and common iliac arteries are routinely measured in anteroposterior and transverse diameters from
its outer to outer wall. The aorta is measured at the level of the diaphragm, superior mesenteric artery (SMA)
origin, and just above the bifurcation. The distance (nonaneurysmal neck) from the renal artery or SMA origin to
the most proximal extent of the aneurysm is measured.
5. Lifelong follow-up imaging of aortic grafts or stent grafts is mandatory for detecting possible complications, the
two most frequent being endoleak and limb occlusion. Typical follow-up imaging after aortic stent-graft
implantation is performed at 1, 6, and 12 months and then at every 1-year interval. In most institutions, computed
tomographic angiography (CTA) is considered a gold standard for an evaluation after AAA repair; however, DUS
by experienced operators is helpful in patients who cannot receive iodinated contrast agents.
a. Five types of endoleak include type I (poor sealing of either end of the stent with the native aortic wall), type II
(retrograde filling of aneurysmal sac via an aortic branch), type III (leak through a defect or tear in the graft),
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type IV (seepage of blood into aneurysmal sac due to graft porosity), and type V (significant expansion of the
aneurysmal sac without visible leak).
b. Limb occlusion is recognized as a lack of flow in the limb(s) of the stent graft.
6. Compared with CTA, DUS has a wide range of sensitivity in detection of endoleak from 64% to 86% with a
pooled sensitivity of 77% (2). An endoleak is identified on DUS as color flow outside the endovascular stent graft
with a uniform, reproducible, color Doppler appearance that has spectral Doppler waveforms synchronous with
the cardiac cycle.
7. Contrast-enhanced US (CEUS) overcomes limitation of US and DUS by providing better delineation of the
AAA and detection of endoleak. It enhances characterization of endoleak with analysis of velocity and flow
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direction. In a meta-analysis (2), its pooled sensitivity was 98% (ranges, 90% to 99%) and pooled specificity was
88% (ranges, 78% to 94%). The European Federation of Societies for Ultrasound in Medicine and Biology
currently recommends CEUS for detection and characterization of endoleak and follow-up of known endoleak
(3).
Transjugular Intrahepatic Portosystemic Shunt

US is an extremely useful modality to evaluate the hepatic vasculature prior to and after TIPS placement.
1. Prior to the procedure, patency and flow in the portal, splenic, superior mesenteric, hepatic, and internal
jugular veins are documented with DUS. The location of the portal vein bifurcation is assessed; undetected
variant anatomy can increase the risk of portal vein perforation into the peritoneal cavity during the TIPS
procedure.
2. After TIPS placement, DUS is routinely performed within 24 to 48 hours, at 3 months, and then at every 6
months to assess shunts patency and function. The TIPS stent appears as two parallel curvilinear lines, with
corrugated appearance to the wall, connecting the hepatic and portal veins (Fig. e-68.2).
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Although a typical TIPS stent is 10 mm in diameter, its in vivo diameter is 8 to 9 mm due to surrounding hepatic
tissue recoil (4). The portal venous and hepatic venous ends of the stent are normally slightly flared and should
be within the lumen of hepatic and portal veins, respectively. A fabric-covered stent may contain some gas (air)
that causes shadowing for several days until the gas is absorbed. The spectral waveform within TIPS is
monophasic and slightly pulsatile. Normal peak systolic velocity (PSV) is similar throughout the shunt at 90 to
120 cm per second, but it should not be less than 50 to 60 cm per second.
FIGURE e-68.2 • Normal TIPS anatomy. Color DUS shows blood flow from the portal vein to the hepatic vein, in
the TIPS (arrow).
3. Criteria for the diagnosis of TIPS (shunt) stenosis include (Fig. e-68.3)
a. Visible narrowing of the shunt
b. Velocity less than 50 to 60 cm per second anywhere within the shunt
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FIGURE e-68.3 • TIPS stenosis. Spectral Doppler waveform shows elevated systolic velocity of 298 cm per
second at the hepatic vein end of the TIPS (crosshairs), suggesting stenosis.
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FIGURE e-68.4 • TIPS occlusion. Color DUS shows lack of blood flow in the shunt (arrow).
c. Increase in a peak velocity of greater than 100 cm per second in the narrowed segment compared with a
normal segment of the shunt
d. Continuous, nonpulsatile flow within the shunt
e. Slow portal venous velocity of less than 30 cm per second
4. The use of fabric-covered stent has reduced prevalence of anatomic defects in TIPS, especially stenoses
along the central portion of the TIPS.
5. TIPS occlusion (Fig. e-68.4) is critical to identify, as it requires urgent corrective intervention (5). Suspicion of
TIPS occlusion on DUS should be confirmed by angiography.
Liver Transplant Evaluation

Grayscale US is used for postoperative evaluation of liver transplantation to identify a hematoma, fluid
collections, hepatic infarction, or biliary obstruction. Doppler scanning is used to confirm patency of hepatic
arteries, portal veins, hepatic veins, and inferior vena cava (IVC).
1. Baseline DUS is performed within 24 to 48 hours of liver transplantation (6).
a. A normal hepatic artery has a sharp systolic upstroke with high continuous diastolic velocity and a resistive
index (RI) of 0.5 to 0.8. The systolic acceleration time is less than 0.1 second. In an early postoperative period,
RI may be elevated secondary to reperfusion edema.
b. A normal portal vein is easier to visualize because of its large size (Fig. e-68.5). Normal portal venous flow is
hepatopetal with a velocity of less than 50 cm per second.
c. Normal hepatic veins and IVC have a multiphasic flow pattern due to cardiac pulsation.
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FIGURE e-68.5 • Portal vein spectral Doppler waveforms. A normal portal venous (arrowhead) has flow with an
undulating waveform. mpv, main portal vein.
2. Vascular complications of liver transplantation

a. Thrombosis of hepatic artery typically occurs within the first 6 weeks to 3 months of surgery. DUS can
diagnose hepatic arterial thrombosis with a sensitivity of 60% to 80% (6), manifested by an absence of arterial
signal in the hepatic artery and its branches. Actual thrombus may be visualized on grayscale US.
b. Stenosis of hepatic artery usually occurs at the anastomotic site and is characterized by a high velocity
(greater than 200 cm per second or three times of prestenotic segment) at the point of stenosis with poststenotic
turbulence. The intrahepatic arteries may show tardus parvus waveform, a low RI of less than 0.5, and delayed
systolic acceleration time of greater than 0.1 second.
c. Pseudoaneurysm (PSA) of the hepatic artery may be seen on grayscale US as a round anechoic fluid
collection adjacent to the hepatic artery (6) (Fig. e-68.6). Intrahepatic PSAs are commonly related to biliary
interventions, but extrahepatic PSAs raise a possibility of mycotic infection. If it is not thrombosed, a to-and-fro
pattern waveform is seen within the aneurysm on DUS.
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FIGURE e-68.6 • Fusiform aneurysm of the common hepatic artery. US shows a complex cystic lesion at the
porta hepatis (arrow). Color DUS (not shown) revealed blood flow in the aneurysm with thrombus at the wall
(right of arrow).
d. Stenosis of the portal vein usually occurs at the donor-recipient anastomosis. Focal narrowing of portal vein,
aliasing, and increased flow velocity at the site of stenosis are typical findings on DUS. When the velocity
gradient increases three- to fourfold relative to a prestenotic segment, it is considered to be hemodynamically
significant (6). Thrombosis of the portal vein is characterized by no flow.
Renal Transplant Evaluation

1. Similar to liver transplant evaluation, grayscale US and DUS is used in postoperative period to identify
peritransplant fluid collection, hydronephrosis, patency and flow direction of renal artery, anastomosis, renal
vein, and evaluation of intrarenal arteries.
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2. Vascular complications of renal transplantation (7)
a. Renal artery stenosis frequently occurs at the anastomotic site, approximately 3 to 12 months after
transplantation. It is characterized by a high velocity (greater than 250 cm per second or 1.8 times of external
iliac artery) and focal aliasing at the point of stenosis. The intrarenal artery may show tardus-parvus waveform
and a low RI.
b. Renal artery thrombosis/infarction can occur at the main renal artery to segmental arteries. There is no
parenchymal flow of the entire transplant kidney on DUS if the main renal artery is completely occluded.
Segmental lack of parenchymal flow can be more difficult to detect. Power Doppler or CEUS improves the
detection rate.
c. Renal vein thrombosis is a rare complication. It often occurs within 2 weeks after transplantation. A
combination of direct visualization of thrombus in the main renal vein, lack of flow, or reversed diastolic flow is
diagnostic on DUS.
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3. Vascular complications after interventional procedures (7)
a. Arteriovenous fistula (AVF) commonly occurs after percutaneous biopsy of the transplant. There is focal
turbulent high-velocity and low-resistive waveforms with tissue reverberation artifact. On grayscale US, no
hypoechoic pocket is visualized unlike PSA. More than 70% of iatrogenic AVFs will regress spontaneously.
b. PSA appears as a round or oval anechoic/hypoechoic structure on grayscale US with swirling motion (yin-
yang sign) on DUS. Connection of the sac to the artery and width/length of the PSA neck should be assessed.
Renal Artery Evaluation

1. Normal renal arteries have a low-resistance waveform pattern with a broad systolic phase and continuous
forward flow throughout diastole. PSV, acceleration time, and RI are obtained at origin, proximal, mid, and distal
portions of each renal artery. Intrarenal arterial waveforms and RI are assessed within the segmental arteries in
the upper pole, midportion, and lower pole of the kidneys.
2. Approximately 20% to 30% of patients referred for Doppler evaluation are considered inappropriate subjects
due to technical reasons including obesity or arterial calcifications (8).
3. Renal artery stenosis (Fig. e-68.7) is manifested on DUS as an increase in PSV of greater than 180 to 200 cm
per second, renal/aortic ratio (PSV at stenotic portion divided by that of the aorta at the renal artery origin) of
greater than 3.3 or 3.5, prolonged acceleration time of more than 0.07 seconds, and poststenotic flow
disturbance. Dampening of intrarenal arterial waveform (tardus-parvus) is an indirect sign suggestive, but not
specific, of renal artery stenosis.
Visceral Artery Evaluation

1. Doppler examination of the splanchnic arteries is a useful method to diagnose stenoses and follow up patients
after intervention.
a. Abdominal aorta is measured at the level of mesenteric arteries for baseline velocities (PSV). PSVs of normal
adults are between 70 and 100 cm per second. PSVs are subsequently obtained at the origins, proximal and
midsegments of the celiac artery, SMA, and IMA.
b. The normal celiac artery shows (end-organ) low vascular resistance that does not differ before and after
meals.
c. The normal SMA shows a high intestinal vascular resistance in a preprandial state (Fig. e-68.8). There is a
triphasic waveform with a peak systolic component, low diastolic flow, and end-systolic reversal flow. There is
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significantly increased SMA flow in the postprandial period with increased systolic velocity, end-diastolic velocity,
and loss of its flow reversal.
d. Stenosis (Fig. e-68.8) is primarily diagnosed on US as elevation of PSV, mesenteric artery/aortic PSV ratio
(MAR) and presence of tardus-parvus waveforms. Focal area of luminal narrowing, color flow aliasing,
poststenotic turbulence, and presence of collateral vessels are helpful secondary signs.
(1) Threshold of hemodynamically significant stenosis of celiac artery is PSV of greater than 200 cm per second
and MAR of greater than 3 to 3.5.
(2) In the SMA, a PSV of 275 cm per second or greater is correlated with significant stenosis, with a sensitivity of
89% to 100% and a specificity of 92% to 98% (9). An MAR of 3 to 3.5 or greater is suggestive of a significant
SMA stenosis.
e. If all three vessels (celiac artery, SMA, IMA) show increased PSVs, this might be due to a high-output state.
On the other hand, low PSVs of all three vessels are suggestive of low-output state. High PSV of the entire
course of vessel might be compensatory flow due to occlusion/stenosis of adjacent mesenteric arteries (10).
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FIGURE e-68.7 • Renal artery stenosis. A: Color DUS along axis of the vessel shows renal artery (curved arrow)
located adjacent to renal vein. There is a suggestion of narrowing closer to its origin. K, kidney. B: Spectral
Doppler (cross-sectional orientation) of renal artery origin shows pulsus parvus et tardus pattern secondary to an
osteal stenosis.
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FIGURE e-68.8 • Superior mesenteric artery with a hemodynamically nonsignificant stenosis. A: Grayscale US
shows the SMA (curved arrow) arising off the proximal abdominal aorta. B: Spectral Doppler waveform shows
PSV of 176 cm per second and delayed systolic upstroke. The SMA-to-aortic systolic velocity ratio (2.2) was less
than 3, so it does not meet the criterion for a hemodynamically significant stenosis.
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References
1. Polak JF. Ultrasound assessment of the abdominal aorta. In: Pellerito J, Polak JF, eds. Introduction to
Vascular Ultrasonography. 6th ed. Philadelphia, PA: Elsevier Saunders; 2012;450-465.
2. Mirza TA, Karthikesalingam A, Jackson D, et al. Duplex ultrasound and contrast-enhanced ultrasound
versus computed tomography for the detection of endoleak after EVAR: systematic review and bivariate
meta-analysis. Eur J Vasc Endovasc Surg. 2010;39:418-428.
3. Piscaglia F, Nolsøe C, Dietrich CF, et al. The EFSUMB guidelines and recommendations on the clinical
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practice of contrast enhanced ultrasound (CEUS): update 2011 on nonhepatic applications. Ultraschall Med.
2012;33:33-59.
4. Brehmer WP, Saad WE. Dysfunctional transjugular intrahepatic portosystemic shunt: anatomic defects
and Doppler ultrasound evaluation. Ultrasound Clin. 2013;8:125-135.
5. Colombato L. The role of transjugular intrahepatic portosystemic shunt (TIPS) in the management of portal
hypertension. J Clin Gastroenterol . 2007;41:S344-S351.
6. Ackerman SJ, Irshad A, Lewis M. Update on the role of sonography in liver transplantation. Ultrasound
Clin. 2014;9:641-652.
7. Zarzour JG, Lockhart ME. Ultrasonography of the renal transplant. Ultrasound Clin. 2014;9:683-695.
8. Moukaddam H, Pollak J, Scoutt LM. Imaging renal artery stenosis. Ultrasound Clin. 2007;2:455-475.
9. Lim HK, Lee WJ, Kim SH, et al. Splanchnic arterial stenosis or occlusion: diagnosis at Doppler US.
Radiology. 1999;211:405-410.
10. Revzin MV, Pellerito JS. Ultrasonography assessment of the aorta and mesenteric arteries. Ultrasound
Clin. 2014;9:723-749.
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e-69
Color Doppler and Ultrasound Imaging of Peripheral Veins
Joseph F. Polak
Veins of the Lower Extremity

Indications
1. To evaluate patients with acute onset of lower extremity swelling or pain, raising the clinical suspicion of
acute deep vein thrombosis (DVT)
2. To monitor the veins of high-risk, asymptomatic patients. The definition of “high-risk” is extensive and
includes elderly, bedridden, postsurgery (especially those who have had hip replacement or neurosurgical
procedures) (1), or patients following trauma (2).
3. To establish a baseline study following the completion of anticoagulation. This will permit the detection of
recurrent episodes of DVT or onset of venous reflux (3).
4. To evaluate patients with dyspnea and suspected pulmonary embolism (4), although the diagnostic yield
is low
5. To monitor in-hospital quality control programs aimed at the prophylaxis of DVT, particularly in high-risk
groups of patients (5)
6. Preoperative mapping of the great and small saphenous veins
7. Detection and segmental analysis of venous reflux in patients with
a. Varicose veins
b. Recurrent varicose veins after intervention
c. Cutaneous ulceration
d. Serious venous stasis complaints with or without subcutaneous induration
Contraindications
Relative
1. Difficulty of the examination is a function of body habitus and the transducer used (5.0 MHz or 7.5 MHz).
2. Recent surgical or skin wounds along sites to be surveyed
3. Painful extremity that does not permit adequate application of pressure to the skin surface overlying the
vein segment that is being evaluated
1. No patient preparation is needed.
2. Intensive care patients can be examined with portable units.
3. Equipment
a. Inferior to the inguinal ligament, high-resolution B-mode imaging is performed with a linear array transducer
with color Doppler and duplex imaging capability. Transducer grayscale frequency is 5 MHz or above; Doppler
frequency is 3 MHz or above. Pressure is applied by pushing the transducer down on the skin in order to
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compress the underlying vein. Color Doppler imaging and Doppler waveform analysis are used for evaluating
blood flow patterns.
b. A sector or curved array transducer is used above the inguinal ligament, in the iliac veins, and inferior vena
cava (IVC). The imaging and Doppler frequencies are lower. The gain is set so that the lumen of a normal vessel
is free of internal echoes. The accompanying artery is used as a reference.
c. Color Doppler imaging is complementary to the compression maneuver and is useful in demonstrating blood
flow and detects nonobstructive thrombus in the IVC, iliac, thigh, and calf veins. It is also used to detect venous
reflux.
d. Tilt tables or reclining stretchers held in reverse Trendelenburg position (feet down) help to evaluate patients
who have difficulty moving and to passively distend the veins during the evaluation of venous reflux.
Detection of Deep Vein Thrombosis
Procedure
1. Compressibility of the vein walls is the most important and reproducible criterion to exclude the
presence of acute thrombus (Figs. e-69.1, e-69.2, e-69.3).
a. Interrogation of the veins should ideally begin at the level of the inguinal ligament, roughly at the groin
crease, and continue to include the calf veins.
b. Examination of the femoral veins: The patient is positioned supine with the leg to be examined in slight
external rotation. The patient's head/torso may be elevated 15 to 20 degrees (reverse Trendelenburg) to
facilitate venous filling. The examination includes Doppler interrogation of the common femoral and femoral
veins, including the proximal portion of the great saphenous vein at the saphenofemoral junction just below
the inguinal ligament.
c. The transducer is held transverse to the axis of the vein and centered on the vein segment as pressure is
applied on the skin to compress the vein walls. The walls of a normal vein segment collapse and appose
together with minimal pressure. The failure to coapt the vein walls with compression while the
accompanying artery is deformed is regarded as a positive finding for intraluminal thrombus.
d. The compression maneuver is performed along the length of the vein by having the operator displace the
transducer every 2 to 3 cm staying centered on the vein and then pressing on the skin.
e. The femoral vein may be difficult to compress because it passes through the adductor canal. This can be
the site of a false-positive study; adjunctive imaging with color Doppler imaging can help evaluate the
patency of the venous segment or confirm the presence of a thrombus.
f. The saphenofemoral junction may be difficult to compress. This area should be carefully examined
because thrombus in the great saphenous vein near
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the femoral junction may propagate into the common femoral vein, thereby becoming a deep vein thrombus.
Radiology Books
FIGURE e-69.1 • The compression maneuver is performed with the transducer held transverse to the vein.
Pressure is applied to the surface of the skin through the transducer. This is transmitted to the deeper
structures and causes the vein walls to collapse. On real-time imaging, repeating this maneuver causes the
vein to wink. The maneuver shown here was applied to the femoral vein, which lies deep to the artery. The
artery should not deform before the vein. On rare occasions, we have seen the artery collapse before the
vein in patients with a prominent sartorius muscle. Reorienting the transducer more medially on the inside of
the leg and repeating the compression maneuver then led to a normal response. (From Polak JF.
Peripheral Vascular Sonography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004, with
permission.)
g. The popliteal vein is examined with the leg slightly flexed. Alternatively, the patient can be imaged prone
with the calf elevated approximately 30 degrees, with a towel or pillow beneath the shin to prevent
spontaneous collapse of the vein. The patient can also be examined in the decubitus position.
h. The popliteal vein is compressed from the adductor hiatus to the level of the calf veins.
i. The transducer is occasionally placed over the anterior compartment between the tibia and fibula in order
to evaluate the paired anterior tibial veins. Isolated thrombosis of the anterior tibial veins is very rare.
j. The paired posterior tibial and peroneal veins are in the posterior compartment and can be found by
displacing the transducer medially and posterior to the tibia. The posterior tibial artery and accompanying
paired veins lie medial and posterior to the tibia. The peroneal artery and accompanying veins are located
deeper on top of the fibula.
k. The paired gastrocnemius veins accompany the gastrocnemius artery in the gastrocnemius muscle.
Compressibility is mainly used for the diagnosis of thrombosis.
l. The muscular (mostly soleal) veins lie within the deep muscles of the calf and typically communicate with
the peroneal and posterior tibial veins. Compressibility is mainly used for the diagnosis of thrombosis.
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FIGURE e-69.2 • Abnormal compression ultrasonography is defined as a failure to appose the walls of the
deep vein while pressure is applied onto the skin through the transducer. Sufficient pressure is exerted to
the extent that the artery wall deforms slightly. An ancillary finding to the presence of DVT is distension of
the vein. The additional presence of echogenic material in the vein lumen reinforces the diagnosis. (From
Polak JF. Peripheral Vascular Sonography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004,
with permission.)
FIGURE e-69.3 • Compression ultrasonography will also detect the presence of partly obstructing
thrombus. There is failure for the walls of the vein to completely oppose during the compression maneuver.
The vein is not distended. An echogenic structure need not be visualized in the vein lumen. (From Polak JF.
Peripheral Vascular Sonography. 2nd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2004, with
permission.)
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m. Compression of the calf veins may require more force than in the popliteal and femoral regions
depending on body position. As for the above-the-knee veins, a noncompressible, often dilated, vein
segment is diagnostic of venous thrombosis.
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2. Doppler waveforms are used to evaluate
a. Spontaneous venous blood flow. Doppler signals are easily detected in large veins but detection of blood
flow may require squeezing the calf to augment venous return in smaller veins.
b. Respiratory phasicity: cyclical variation in venous blood flow measured in the common femoral vein that
parallels the respiratory cycle. Continuous, nonphasic low-velocity venous blood flow is compatible with
proximal (pelvic or above) venous obstruction.
c. Venous augmentation: a transient increase in blood flow velocity caused by distal compression of the calf
and emptying of blood in the calf veins. A normal response indicates the absence of occlusion between the
point of compression and the location of the transducer.
3. Color Doppler imaging can be helpful when results of compression ultrasound are indeterminate or the
examination is compromised by technical factors such as large patient size, previous episodes of DVT, or
pain with attempted compression.
a. The color gain and sensitivity are set to enhance the detection of low-velocity blood flow.
b. Evaluation of the lower extremity veins is performed in the transverse or longitudinal planes.
c. The study is considered positive for thrombus when a loss of color Doppler signal is seen in the vessel
lumen and negative if the lumen is filled with color Doppler signals.
d. Chronic DVT can cause a narrowed, irregular color lumen with wall thickening or the presence of
numerous venous collateral channels.
4. Thrombus visualization within the lumen of the vein is the most specific criterion for the presence of
DVT. It has low sensitivity because the acoustic echogenicity of fresh thrombus can be close to that of
blood. Therefore, fresh thrombus may escape detection if only grayscale imaging is used.
Patients with positive calf vein thrombosis who are not treated with anticoagulation should be followed at a 5-to-
7-day interval to identify the propagation of clot into the popliteal vein (6,7). Similarly, patients with a negative
above-the-knee study should have a repeat study at 5 to 7 days in order to detect the 20% of calf vein thrombus
cases that extend into the popliteal (above-the-knee) vein (6,7).
Results
1. Compression ultrasound (not including calf veins) has high sensitivity and specificity when originally
correlated with the findings of ascending venography. Its diagnostic value is now based on outcomes
analysis and the low rate of DVT recurrence following a negative venous ultrasound examination (6,8,9).
2. Additional calf vein imaging requires an additional 5 to 10 minutes of examination time. In patients with
isolated calf vein symptoms and negative abovethe-knee ultrasound studies, the accuracy of calf vein
imaging is very high (above 95%) (10,11). The sensitivity for detecting isolated calf vein thrombus in
hospitalized asymptomatic and high-risk groups is highly variable, ranging from 13% to 85%.
3. Full length studies of the lower extremity have high accuracy when outcomes are evaluated at 3 months
(6,8,9). These are comparable to performing twopoint examinations (common femoral and popliteal vein
compression only) at presentation and then 5 to 7 days later (6).
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Complications (Rare)
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Dislodgment of blood clot during compression causing pulmonary embolism has been reported. It is not clear
whether these were instances of dislodgment caused by the examinations versus coincidental observation of
spontaneous thrombus dislodgment.
Saphenous Vein Mapping Prior to Infrainguinal Bypass Procedures

1. Equipment: linear array transducer frequency above 5 MHz transducer and color Doppler frequency 3
MHz or above
2. Place the limb to be scanned in a dependent position to maximize distention. The examination is
performed with the patient standing or in 30-degree reverse Trendelenburg position with the knee slightly
flexed (12,13).
3. Begin the examination at the saphenofemoral junction just below the inguinal ligament with the
transducer in transverse orientation (12,13). Grayscale imaging is mostly used, and color Doppler is added
as needed.
4. Keep the great saphenous vein centered beneath the transducer, which is kept perpendicular to the skin
surface. Follow the course of the vein, and, if needed, use a marker to draw the path of the vein on the skin
surface. Note the vein diameter, any duplication/tributaries, varicosities, and any abnormal-appearing
valves (12,13). Compression examination is performed to confirm vein patency.
5. The same procedure may be used for the small saphenous vein, which originates laterally at the ankle
and joins the popliteal vein at the popliteal fossa.
6. Proximal compression can be used to distend the veins (14).
Results
1. Mapping of the great saphenous vein reveals several anatomic variations: complete double venous
system, branching double system, and the standard single medial dominant trunk in the thigh with an
anterior dominant vein in the calf.
2. Veins are unsuitable for use as a graft in approximately 10% of instances and questionable in
another 10% of patients studied.
3. Good estimates of vein diameters are obtained in most cases (13,15).
Detection and Segmental Evaluation of Venous Reflux

1. Equipment: greater than 5 MHz grayscale imaging transducer with pulsed and color Doppler frequencies of 3
MHz or above
2. The upper leg is examined with the patient standing, ideally on a step stool with some means of support such
as a chair or orthopedic walker. An alternative is a stretcher in 20- to 30-degree reverse Trendelenburg. The calf
can be examined with the patient sitting, either with the leg dangling or supported by the examiner's thigh.
3. The saphenofemoral junction is identified and the Doppler sample gate placed in the common femoral vein just
above it and the response to a Valsalva maneuver is recorded. There should be minimal reversal of blood flow.
4. The Doppler response is then recorded in various venous segments following augmentation either by
compressing the calf by hand or using an automated inflator. The cuff is inflated for 1 to 3 seconds; the presence
of reflux is evaluated following cuff deflation. The duration of retrograde blood flow is recorded. Normal reversal
of blood flow can last up to 0.5 to 0.7 second.
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5. Recordings are made in the upper common femoral, the proximal femoral, the proximal deep femoral, the distal
femoral, and the upper popliteal and lower popliteal veins. It is also performed for the great saphenous vein 4 cm
from the saphenofemoral junction, the saphenous vein in the distal thigh and the upper calf. Other veins that may
be studied depending on the clinical situation are the small saphenous vein just below the saphenopopliteal
junction and the calf veins.
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6. Grayscale imaging is used to locate the perforating veins (perforators). The transducer is displaced in the
transverse plane along the superficial veins. The perforators course deep into the fascia and are difficult to
identify if they are normal. Their evaluation includes sampling of the direction of blood flow (normal is from the
skin into the deep veins) and measuring their diameter (normal is >2 mm; incompetent veins are almost always
present when the diameter reaches 3 mm).
7. Because the status of the deep veins is often unpredictable from the physical examination or clinical
presentation, a complete examination of the deep and superficial veins is recommended. The status of the deep
system can have profound effects in directing treatment of superficial venous reflux disease.
None
Results
1. Normal reversal of blood flow (reflux) is <0.5 seconds in the superficial system but can be up to 1 second
in the popliteal vein (16).
2. Venous incompetence can be segmental. This knowledge and careful evaluation of the affected
segments permit more targeted surgical and percutaneous interventions (17).
3. Superficial vein reflux and perforator incompetence contribute to the pathogenesis of venous ulceration
and both are easily documented by ultrasound.
4. Grayscale imaging and color Doppler imaging have been used to guide laser or radiofrequency venous
ablation, delimit injection sites for venous sclerotherapy, and evaluate the success of such treatments.
Complications
None
Veins of the Upper Extremity

Indications
1. Unexplained swelling of the upper extremity
2. Suspicion of venous thrombosis associated with a central venous catheter (18)
3. To evaluate patients with dyspnea and suspected pulmonary, although the diagnostic yield is variable
(19)
Contraindications
None
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None
Procedure
1. The patient is positioned supine or in slight Trendelenburg position to distend the upper extremity veins.
The jugular and subclavian veins are examined with the patient's arm at his or her side; axillary and brachial
veins are examined with the patient's arm slightly abducted, palm directed upward. The examiner is
positioned either at the patient's head or side.
2. Equipment: 5.0 MHz or above linear array transducer with color and pulse wave Doppler capability (3
MHz or above). Color Doppler is used intermittently during the examination because the presence of
thrombus causes a flow defect.
3. The examination begins at the jugular vein in the mid to upper neck. The vein is easily identified next to
the carotid artery. The vein is compressed. Color Doppler confirms patency of the vein. Doppler velocity
waveforms are used to
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confirm the presence of cardiac pulsatility and of cyclical respiratory variation. The vein is imaged in both
longitudinal and transverse orientations.
4. In the transverse orientation, the transducer is swept down the jugular vein to the clavicle. The common
carotid artery-brachiocephalic artery junction is encountered first. Then, caudad to the artery, the junction of
the jugular vein-brachiocephalic vein-subclavian vein is found. To reach this level, the transducer may have
to be acutely angled caudad and pressed into the supraclavicular fossa. The patient is told that firm
pressure may be needed and to expect some discomfort. This area is examined for the presence of
thrombus, and a color Doppler image is recorded.
5. The medial aspect of the upper arm is scanned with color Doppler and grayscale ultrasound.
Compression examination is performed as far into the axilla as can be reached. An infraclavicular approach
is used to image the segment of the axillary and subclavian vein not seen in the previous orientations.
6. While imaging over the subclavian vein in transverse orientation, the patient is asked to sniff vigorously.
A normal response is a decrease in vein diameter.
7. The presence of venous catheters is documented as well as their effect on the blood flow dynamics
within the vein.
None
Results
1. Compression examination, augmentation, and respiratory variation are similar to the evaluation of the
lower extremity (20,21). Cardiac pulsatility is a good indicator of central vein patency (20).
2. There is high accuracy when results of venous ultrasound are compared to venography.
Complications
None reported
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References
1. Davidson HC, D. Mazzu B, Gage BF, et al. Screening for deep venous thrombosis in asymptomatic
postoperative orthopedic patients using color Doppler sonography: analysis of prevalence and risk factors.
2. Schellong SM. Venous ultrasonography in symptomatic and asymptomatic patients: an updated review.
Curr Opin Pulm Med. 2008;14:374-380.
3. van Rij AM, Hill G, Krysa J, et al. Prospective study of natural history of deep vein thrombosis: early
predictors of poor late outcomes. Ann Vasc Surg. 2013;27:924-931.
4. Elias A, Colombier D, Victor G, et al. Diagnostic performance of complete lower limb venous ultrasound in
patients with clinically suspected acute pulmonary embolism. Thromb Haemost. 2004;91:187-195.
5. Bilimoria KY, Chung J, Ju MH, et al. Evaluation of surveillance bias and the validity of the venous
thromboembolism quality measure. JAMA. 2013;310:1482-1489.
6. Bernardi E, Camporese G, Büller HR, et al. Serial 2-point ultrasonography plus D-dimer vs whole-leg
color-coded Doppler ultrasonography for diagnosing suspected symptomatic deep vein thrombosis: a
randomized controlled trial. JAMA. 2008;300:1653-1659.
7. Birdwell BG, Raskob GE, Whitsett TL, et al. The clinical validity of normal compression ultrasonography in
outpatients suspected of having deep venous thrombosis. Ann Intern Med. 1998;128:1-7.
8. Cornuz J, Pearson SD, Polak J. Deep venous thrombosis: complete lower extremity venous US evaluation
in patients without known risk factors—outcome study. Radiology. 1999;211:637-641.
9. Schellong SM, Schwarz T, Halbritter K, et al. Complete compression ultrasonography of the leg veins as a
single test for the diagnosis of deep vein thrombosis. Thromb Haemost. 2003;89:228-234.
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10. Atri M, Herba MJ, Reinhold C, et al. Accuracy of sonography in the evaluation of calf deep vein
thrombosis in both postoperative surveillance and symptomatic patients. AJR Am J Roentgenol .
1996;166:1361-1367.
11. Simons GR, Skibo LK, Polak JF, et al. Utility of leg ultrasonography in suspected symptomatic isolated
calf deep venous thrombosis. Am J Med. 1995;99:43-47.
12. Seeger JM, Schmidt JH, Flynn TC. Preoperative saphenous and cephalic vein mapping as an adjunct to
reconstructive arterial surgery. Ann Surg. 1987;205:733-739.
13. van Dijk LC, Wittens CH, Pieterman H, et al. The value of pre-operative ultrasound mapping of the
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greater saphenous vein prior to ‘closed’ in situ bypass operations. Eur J Radiol . 1996;23:235-237.
14. Hoballah JJ, Corry DC, Rossley N, et al. Duplex saphenous vein mapping: venous occlusion and
dependent position facilitate imaging. Vasc Endovascular Surg. 2002;36:377-380.
15. Cruz CP, Eidt JF, Brown AT, et al. Correlation between preoperative and postoperative duplex vein
measurements of the greater saphenous vein used for infrainguinal arterial reconstruction. Vasc
Endovascular Surg. 2004;38:57-62.
16. Labropoulos N, Tiongson J, Pryor L, et al. Definition of venous reflux in lower-extremity veins. J Vasc
Surg. 2003;38:793-798.
17. García-Gimeno M, Rodríguez-Camarero S, Tagarro-Villalba S, et al. Reflux patterns and risk factors of
primary varicose veins' clinical severity. Phlebology. 2013;28:153-161.
18. Luciani A, Clement O, Halimi P, et al. Catheter-related upper extremity deep venous thrombosis in cancer
patients: a prospective study based on Doppler US. Radiology. 2001;220:655-660.
19. Prandoni P, Polistena P, Bernardi E, et al. Upper-extremity deep vein thrombosis. Risk factors, diagnosis,
and complications. Arch Intern Med. 1997;157:57-62.
20. Baarslag HJ, van Beek EJ, Koopman MM, et al. Prospective study of color duplex ultrasonography
compared with contrast venography in patients suspected of having deep venous thrombosis of the upper
extremities. Ann Intern Med. 2002;136:865-872.
21. Mustafa BO, Rathbun SW, Whitsett TL, et al. Sensitivity and specificity of ultrasonography in the
diagnosis of upper extremity deep vein thrombosis: a systematic review. Arch Intern Med. 2002;162:401-404.
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e-70
Magnetic Resonance Angiography
Nanda Deepa Thimmappa
Martin R. Prince
Just as with conventional angiography, it is essential to learn all aspects of the operation of magnetic resonance imaging (MRI) equipment to select the appropriate imaging coil and
sequences (see LearnMRI.org). It is important to evaluate patients prior to imaging in order to determine the specific clinical issues that need to be addressed, and to assess how
cooperative the patient is likely to be with suspending respiration and remaining still for the scans. It is especially critical to determine the extent of vascular anatomy to be examined
because it does not necessarily correspond to the traditional organ-based magnetic resonance (MR) anatomical regions. Technologists are often not familiar with the regions of
coverage required for vascular studies and need guidance from the radiologist.
1. Safety screening: Before accepting a patient for MRI, do a quick check for the major contraindications (e.g., pacemakers, cochlear implants, and brain aneurysm clips). The
technologist must screen for other less frequent contraindications, including metallic foreign bodies in the orbits and certain medical implants. Vena cava filters, especially if
nonferromagnetic and remote from the
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imaging site, do not generally pose a safety hazard, but they may create artifacts if included in the imaging field.
2. Nephrogenic systemic fibrosis (NSF): If the patient is an inpatient, check the serum creatinine and calculate the glomerular filtration rate (GFR) (visit www. MDRD.com for
GFR calculator). If GFR <30 mL per minute, avoid high doses of gadolinium (Gd) and consider noncontrast magnetic resonance angiography (MRA) techniques. Patients in acute
renal failure should not receive Gd until the serum creatinine recovers toward normalcy or hemodialysis is instituted. Outpatients should be asked if they are on dialysis or about to
begin dialysis. All dialysis patients should have the MR scheduled for just prior (within 24 hours) to the next dialysis treatment session. For patients at risk for NSF, the macrocyclic
agents such as Gadobutrol (Gadavist, Bayer, Berlin, Germany), Gadoteridol (ProHance, Bracco, Princeton, NJ) or Gadoterate Meglumine (Dotarem, Guerbet, Bloomington, IN) are
safer than the linear agents. Agents with biliary excretion in addition to renal excretion including Gadobenate Dimeglumine (MultiHance, Bracco, Princeton, NJ), Gadexetate
Disodium (Eovist, Bayer, Berlin, Germany), and Gadofosveset Trisodium (Ablavar, Lantheus Medical Imaging) also have fewer or no reported cases complicated by NSF.
Gadobenate Dimeglumine and Gadofosveset Trisodium are U.S. Food and Drug Administration (FDA)-approved for aorto-iliac MRA. Keep in mind, however, that Gadodiamide
(Omniscan, GE Healthcare, Princeton, NJ) has the lowest rate of allergic reactions and may be well suited for patients at risk of allergic reactions and outpatient imaging centers
with limited ability to handle a code situation.
3. Clothing: Remove all clothing (including bras) with metallic components such as zippers, snaps, etc. Have the patient wear a hospital gown. Remove hairpins and metallic
jewelry. Nonmagnetic gold and silver rings may be worn so they do not get lost, but they should not be near or within the field of interest. If there is a question about safety, metallic
paraphernalia should be tested with a small hand magnet.
4. Sedation: Patients with claustrophobia will benefit from diazepam (Valium) 5 to 10 mg by mouth (PO) or lorazepam (Xanax) 1 to 2 mg PO taken 20 to 30 minutes prior to MR
scanning. The patient should not be given the sedative until arriving at the scanner in case the facility is behind schedule. Sedated patients need a responsible adult escort to go
home.
5. Intravenous (IV) lines
a. For gadolinium-enhanced MRA (Gd-MRA), a right arm IV access is preferred because this provides the most direct route to the central circulation. It is acceptable to use a small-
gauge IV access (minimum 22 gauge or high flow 24 gauge) in the antecubital fossa, hand, or wrist. However, if the IV access is tenuous, consider using a nonionic, low-osmolar Gd
contrast preparation to avoid potential pain caused by extravasation of high-osmolar ionic Gd preparations.
b. For hand injection of Gd, use the Smart Set (Topspins, Ann Arbor, MI). This device has a valve mechanism to allow automatic switching from contrast infusion to saline flush
without excessive force or risk of breaking connections. It also has the optimum length, caliber, and fittings to allow easy IV injection of contrast by an operator outside the magnet.
Caution is urged with power injectors because they are prone to misadministration, extravasation, and a greater risk to the patient in the event of a contrast reaction compared to
hand injection because the pump is activated remotely from the control room.
6. Coil selection: Coil selection has to be optimized because the choice determines the available field-of-view (FOV) and the signal-to-noise ratio (SNR)—both of which significantly
affect image quality. Because of the complexity of coil selection, many radiologists leave this up to the discretion of the technologist. However, it is important to be aware of the basic
coil selection principles because
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technologists will generally pick the coil that makes the exam easiest to perform instead of one that produces the highest image quality.
a. Use the smallest possible coil that still covers the anatomy of interest.
b. Choose coils that are used routinely and reliable such as the head, knee, torso, and body coils. Keep in mind that circumferential coils with birdcage construction (head, body,
and knee coils) tend to have the most homogeneous sensitivity to MR signal and are unlikely to produce confusing bright or dark spots on the images.
c. When using coil arrays, make sure all elements are working properly. One bad element can reduce vascular signal locally giving the false impression of disease.
Procedure
It is essential to keep the examination time as short as possible so that the patient is able to tolerate holding still for the entire exam. Try to keep the total imaging time below 25
minutes so that the examination can be completed within 45 minutes.
1. Protocols
a. Scout sequences: When selecting protocols for MRA examinations, it is useful to start with a large-FOV, low-resolution scout sequence to guide the prescription of
subsequent smaller FOV sequences confined to the vascular anatomy of interest (1,2,3,4).
(1) Single-shot fast spin echo (SSFSE) (General Electric, Milwaukee, WI) or half-Fourier acquisitions with single-shot turbo-spin echo (HASTE) (Siemens, Erlangen, Germany)
are also useful as “black blood” scout sequences.
(2) Three-plane ungated steady state free precession (SSFP) is a very useful “bright-blood” localizer because it has high SNR and yet is fast enough to minimize motion artifact
and cover a large FOV with multiple slices in a short time.
b. Multiplanar images: Take advantage of the multiplanar imaging capability of MRI to optimize visualization of anatomy in as many different orientations as possible. For this
reason, try to have at least one sequence in each cardinal plane: axial, coronal, and sagittal.
c. Contrast mechanisms: MRI has numerous contrast mechanisms that can be optimized to see anatomy and pathology in various ways. Some of the most popular contrast
mechanisms for MRA studies include:
(1) T1-weighted (T1-W): high SNR with black blood
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(2) Proton density: higher SNR than T1-W and black blood
(3) T2-weighted (T2-W): tumors, inflammation, and other lesions are bright, whereas fast flowing blood is black. Slow flowing blood in hemangiomas or slow flow vascular
malformations may be bright. This sequence is usually performed with fat saturation.
(4) Short T1 inversion recovery (STIR): like T2-W with fat saturation but without the degradation due to field inhomogeneity. Veins and especially vascular malformations are
typically very bright due to slow flow.
(5) SSFSE or HASTE: These sequences are immune to motion artifacts.
(6) SSFP: High SNR, bright-blood MRA—prone to artifacts especially at larger FOV but the small FOV renal MRA implementations (InHance, timeslip, Native TrueFISP, B-
Trance) are often excellent
(7) Three-dimensional (3D) Gd-MRA: provides a robust bright-blood MRA sequence similar to conventional angiography—least prone to artifacts.
(8) Time-of-flight (TOF): bright-blood MRA sequence—subject to flow and motion artifacts. ECG gating reduces artifacts due to arterial pulsation.
(9) Cine-SSFP: SSFP images acquired multiple times during the cardiac cycle and displayed as a movie to show variations between systole and diastole
(10) Phase contrast-MRA (PC-MRA): allows quantification of intraluminal blood flow and demonstrates flow disturbances
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(11) Arterial spin labeling: Blood is excited proximal to the region of interest (ROI) and imaged after flowing into the ROI.
(12) Fresh blood imaging (Delta flow, native Space, Trance): Images gated to systole are subtracted from images gated to diastole to show arteries without Gd.
(13) “TimeSlip” (Inhance, B-Trance, native trueFISP): good for renal arteries in patients with fast blood flow. Gd injection is not necessary.
2. MRA pulse sequences
a. 3D Gd-MRA: This is the most robust sequence for evaluating vascular anatomy and pathology. Figure e-70.1 is a 3D Gd-MRA study from the abdominal aorta to the
proximal calf region. The image illustrates the ability of the technique to demonstrate bilateral common iliac and popliteal artery aneurysms. 3D Gd-MRA is performed similarly to
CT angiography by acquiring a 3D spoiled gradient echo (SPGR) pulse sequence during the arterial phase of a contrast bolus (5) or Time Resolved Imaging of Contrast
KineticS (TRICKS) during arterial and venous phases. Use the shortest possible repetition time (TR) and echo time (TE), while being careful not to make the bandwidth (BW)
too high. A flip-angle of about 30 degrees is good for the arterial phase but should be lower for venous and equilibrium phases when Gd concentration has diminished. The
bolus duration should equal half the scan duration—timed for maximum arterial Gd concentration “opacification” to coincide with acquisition of center of k-space. The contrast
dose should not exceed 0.1 mL per kg in any patient at risk of NSF (GFR <30). More advanced, state of the art MR scanners generally can produce high quality MRA with
lower Gd doses. Alternatively, higher quality MRA can be achieved using a blood pool contrast agent such as Gadofosveset Trisodium (Ablavar, Lantheus, Billerica, MA). This
contrast lingers in the blood for hours so it is excellent for venous imaging. Diagnostic MRA can be obtained up to 8 hours after the injection, for example, in patients who leave
before the exam is completed.
(1) Bolus timing for long acquisitions: For long acquisitions, lasting more than 100 seconds, timing is easy because errors of 10 to 15 seconds are small relative to the total
scan duration.
(a) Use sequential ordering of k-space, so that the center of the k-space is collected during the middle of the acquisition.
FIGURE e-70.1 • 3D Gd-MRA demonstrating bilateral common iliac and popliteal artery aneurysms.
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(b) Begin injecting the Gd just after initiating imaging. Finish the injection just after the midpoint of the acquisition, being careful to maintain the maximum injection rate for the
approximately 10 to 30 seconds prior to the middle of the acquisition. This will ensure a maximum arterial enhancement during the middle of the acquisition, when central k-
space data are collected.
(c) To ensure full use of the entire dose of contrast agent, it is useful to flush the IV tubing with 20 mL of normal saline.
(2) Bolus timing for fast (breath-hold) scans: For fast scans, less than 30 seconds in duration, contrast agent bolus timing is more critical and challenging. This is because
timing errors of 15 seconds can ruin a fast breath-hold scan. There are several approaches to determining the optimal bolus timing for these fast scans. The simplest, although
least successful approach, is to guess on the basis of patient's age, cardiac status, presence of aortic aneurysmal disease, and location of the IV access.
(a) For a breath-hold scan, lasting 30 to 40 seconds, of a reasonably healthy patient with an IV in the antecubital vein, a delay of approximately 10 to 12 seconds is appropriate.
Therefore, in this scenario, begin the injection, and then 10 seconds later, start imaging while the patient suspends breathing. If there is no convenient clock available to time
this delay, take advantage of the natural rhythm of the patient's respiration. One deep breath in followed by a deep breath out takes approximately 4 seconds. Two breaths are
8 seconds, followed by a deep breath in (10 seconds), which represents the optimum delay between start of injection and beginning of scanning.
(b) If a patient is older and has a history of cardiac or aortic aneurysm, add one or two extra breaths to the delay. Also, if the IV site is in the wrist, add an extra breath to the
delay.
(c) Alternatively, if the patient is a marathon runner or you are injecting via a central line, it may be suitable to use only 1.5 breaths of delay, or 6 seconds.
(d) A fast injection is necessary to keep the contrast agent as a concentrated bolus. However, if the injection is too vigorous, it may rupture the vein causing extravasation of
the contrast agent. Injecting by hand gives an adequate flow rate while minimizing risk of extravasation.
(3) Other bolus timing techniques: More sophisticated, reliable, and precise techniques for determining the contrast travel time are also available. These include:
(a) Using a test bolus to precisely measure the contrast travel time (6)
(b) Using an automatic pulse sequence that monitors signal in the aorta and then initiates imaging after contrast is detected arriving in the aorta (fluoroscopic triggering (7) or
automatic triggering (8)
(c) Imaging so rapidly that bolus timing is unimportant, for example, timeresolved MRA (9,10). These techniques are increasingly popular and are known as 3D TRICKS,
TWIST, and Keyhole. Advanced methods of oversampling the center of k-space which allow for 3D volumes to be acquired at subsecond temporal resolution are developing
rapidly including Vastly undersampled Isotropic Projection Reconstruction (VIPR) and spiral LAVA.
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b. Time-of-flight: The bright-blood effect acquired with this sequence can be maximized by:
(1) Acquiring images perpendicular to the vessel of interest (usually in the axial plane)
(2) Using thin slices
(3) Using a sufficiently long TR so there is time for inflow of fresh, unsaturated spins between pulses (typically 10 msec per 1 mm of slice thickness)
(4) Using gradient moment nulling (flow compensation)—pulsatility artifact can be minimized by electrocardiogram (ECG) gating or reducing the flip-angle.
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c. SSFP: This bright-blood sequence has revolutionized vascular imaging by utilizing “rewinder” gradients that obtain residual signal from each pulse and superimpose it on the
signal of the next pulse. This builds up the signal over multiple pulses to attain high SNR. Because blood is a fluid with long T2, high SNR can be accumulated over many
pulses without requiring inflow of unsaturated spins. Accurate “rewinding,” requires a short TR (<4 msec) and good field homogeneity. It may not work in the setting of metal
clips and other susceptibility sources. Image quality is improved with a localized shim of the magnetic field over the ROI. SSFP sequences can be used to acquire fast two-
dimensional (2D) ungated localizer scans or, with gating, to show vascular pulsation and flow variation over a cardiac cycle. In a 3D “breath-hold” or navigator mode, SSFP is
useful for coronary artery imaging. An ECG-gated 2D version, quiescent interval single shot (QISS), is excellent for imaging peripheral vascular disease.
d. Phase contrast: By adding additional gradient activity to the basic TOF technique, it is possible to obtain a phase shift that is proportional to velocity and then to reconstruct
phase images in which signal intensity is proportional to velocity. This technique can be implemented in various ways, all of which require setting a velocity encoding value
(VENC) to the estimated velocity of blood flow in the artery of interest.
e. TimeSlip (InHance, native trueFISP, B-TRANCE): In this technique, an inversion pulse is applied to an axial slab encompassing the kidneys. When background tissues
reach the null point, signal is readout using segmented gradient echo, SSFP, or other techniques. The long inversion times, typically 800 to 1,400 msec, allow ample time for
the inflow of unsaturated blood into the imaging volume. Extending the inversion slab inferior to the kidneys helps to suppress venous signals entering from below. More recent
implementations allow two inversion volumes which can be positioned to cover each entire kidney and the inferior vena cava (IVC) below the renal arteries to further enhance
inflow (Fig. e-70.2).
FIGURE e-70.2 • Axial high-resolution dynamic spiral LAVA (3D SPGR) sequence showing variant hepatic arterial anatomy. The right hepatic artery is replaced to the celiac
trunk, the left hepatic is replaced to the left gastric, and the middle hepatic artery supplying segment 4 arises separately from celiac artery.
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f. Double inversion recovery (DIR) is a T1-W black blood MRA sequence with breath holding and ECG gating. The inversion time is set to around 650 msec so that blood
will be at the null point and appear black on the images. Because the R-R interval is about the same duration as the optimal inversion time, the inversion pulses can be given
after a first ECG trigger and the readout performed on a second ECG trigger one R-R interval later. The first inversion pulse is applied to the entire volume of tissue within the
coil while the second inversion pulse is applied to the slice being imaged. In this way, the slice being imaged receives 360 degrees (no effect) while all blood outside the
imaging slice has a 180-degree inversion. Readout occurs after all in-slice blood has been replaced by nulled out-of-slice blood. DIR provides fine details of the boundary
between the lumen and the vessel wall and is especially useful for identification of subtle dissection flaps. DIR is usually a breath holding technique with one image per
acquisition. A more advanced version using a smaller inversion pulse can be performed within a single R-R interval to double the acquisition speed.
g. LAVA (liver accelerated volume acquisition, also VIBE, THRIVE) is a bright-blood technique that combines contrast-enhanced, multiphase imaging with high resolution,
large coverage, zero-filling interpolation, and uniform fat suppression. It is based on a 3D SPGR pulse sequence. LAVA acquires a stack of overlapping slices with high in-plane
resolution in one breath hold. The usual protocol repeats this acquisition three or more times. To shorten the duration of breath holding, parallel imaging is used with partial
Fourier data filling and short TR/TE. The lower flip angle, typically 10 to 15 degrees allows for greater tissue visualization compared to standard 3D contrast MRA acquired at
higher flip angles. It is particularly useful in imaging both the lumen and wall of arteries and the features of aneurysms, for example, presence of thrombus, sac diameter, and so
forth. It is also particularly useful for post Gd venous imaging where there is greater dilution of Gd contrast into the entire blood pool, for example, in identifying deep vein
thrombosis (DVT) in the legs.
h. Fresh Blood Imaging, Native Space, TRANCE, Deltaflow: a 3D, noncontrastenhanced MRA application for peripheral arterial imaging. It is based on cardiac-gated, 3D
fast-spin echo and acquires two echoes, one in diastole and the other in systole. Slow arterial flow during diastole results in bright arteries in the diastole images, while faster
arterial flow during systole results in dark arteries in the systole images. A subtraction of the systole images from diastole images provides arterial-only images with excellent
suppression of venous and background signal. Interleaved acquisition and parallel imaging with optimized k-space trajectory helps reduce motion misregistration and improve
vessel visualization respectively. In addition, the use of partial Fourier and coronal plane acquisition allows for considerably reduced scan time.
3. Postacquisition image processing
a. Zero padding: This is an excellent method of increasing reconstructed image resolution via interpolation. It involves filling out peripheral lines of k-space data with zeroes
prior to performing the Fourier transform. Although no additional time is required for data collection, the Fourier transform will reconstruct more images with a smaller spacing.
For example, with twofold zero padding, if the partition thickness is 3 mm, the Fourier transform will reconstruct additional images that also have a 3-mm slice thickness but at
1.5-mm spacing with 50% overlap. This helps eliminate volume-averaging artifact and creates smooth visualization of small vessels on the reformatted maximum intensity
projection (MIP) images. If available, twofold zero padding in the slice direction is recommended.
b. MR digital subtraction angiography (MRDSA): Image contrast can be improved by digital subtraction of precontrast image data from dynamic,
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arterial-phase, or venous-phase image data. This subtraction can be performed either slice by slice or prior to the Fourier transform by using a complex vector subtraction
method. The improvement in contrast achieved with DSA may reduce the Gd dose required. However, there must be no change in the patient position between the precontrast
and dynamic contrast-enhanced imaging. This requirement for no motion is easily met in the pelvis and legs, which can be sandbagged and strapped down. It is more difficult to
achieve this in the chest and abdomen, where respiratory, cardiac, and peristaltic motions are more difficult to avoid. More recently, removal of the brightest background tissue
signal, fat, has been accomplished using Dixon (11) and other fat-water separation methods (LAVA flex).
c. Multiplanar reconstructions: One approach to performing a subvolume MIP is to first load the entire 3D volume of arterial-phase image data into the computer workstation
3D analysis program. Display a coronal MIP image of the entire volume, an axial reformation, and an oblique view. On the coronal view, move the tracker location icon cranially
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and caudally while watching the axial reconstruction window to find the renal arteries. Display this subvolume of sagittal data as a MIP (Fig. e-70.3). Make this oblique MIP thick
enough to encompass most of the aorta. Be certain to align the axis of the subvolume MIP so that it is parallel to the origin of the vessel. Although the entire length of the vessel
may not be seen on this image, it will be an accurate
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representation of the vessel's origin, with no overlap from the aorta. This may then be repeated by moving the tracker icon on the axial image and watching the oblique view to
create a sagittal view of the celiac and superior mesenteric arteries. This will show the celiac and superior and inferior mesenteric arteries as well as the anterior and posterior
margins of the aorta, to best advantage.
FIGURE e-70.3 • Maximum intensity projection (a) and volume rendered (b) images demonstrate a tortuous aorta with a left common iliac artery aneurysm (arrow). Arrowheads
show focal atherosclerotic stenosis in common femoral arteries, and there is a severe focal stenosis of left internal iliac artery origin as well as proximal left superficial femoral
artery stenoses.
d. Volume rendering: This is a method of 3D visualization in which tissues can have different degrees of transparency allowing visualization through overlying structures. It
gives more of a 3D perspective than what is possible on MIPs (see Fig. e-70.3).
Standard MRA Examinations (Visit www.MRprotocols.com for details) (Table e-70.1)

1. Aortic arch and carotids: stroke, transient ischemic attack (TIA), great-vessel anatomy, anomalies
a. Coil: A neurovascular coil extending caudally, low enough to the chest to include the aortic arch, is ideal if available. If a neurovascular or head-neck coil is not available, use a
torso array coil with elements placed anterior and posterior to the upper chest and neck.
b. Axial 2D TOF imaging with superior saturation
c. Axial T1-W with fat saturation (optional for carotid dissection)
d. Coronal 3D Gd-MRA (arch to skull base)
2. Thoracic aorta: Rule out dissection, aneurysm, embolic source, coarctation, aortitis, and great-vessel anatomy/anomalies, pre/postop.
a. 3-plane ungated SSFP localizer
b. Axial black blood DIR
c. Sagittal cine-SSFP, oblique view of aortic arch (candy cane view), about 5 to 6 slices will cover the aorta, with one breath hold per slice.
d. Coronal cine-SSFP of ascending aorta, including aortic valve
e. Axial cine-SSFP in-plane view of aortic valve
f. Coronal 3D Gd-MRA with ECG gating
(1) To look for thoracic outlet syndrome, this can be performed as a coronal time resolved MRA with the arms elevated over the head using a half dose and enough phases to see
venous enhancement (˜20 at 5 seconds temporal resolution). Then repeat the time resolved MRA with the arms down along the patient's sides.
g. Post-Gd coronal and axial LAVA
3. Pulmonary artery: embolism, arteriovenous (AV) fistula, aneurysm, and pulmonary hypertension
a. 3-plane SSFP locator
b. Coronal 3D Gd-MRA of both lungs (single injection)
c. Post-Gd axial and coronal LAVA
4. Abdominal aorta (aneurysm): preoperative, pre-stent-graft, to monitor diameter, dissection.
a. 3-plane SSFP of SSFSE localizer: use large FOV (48 cm)
b. Coronal 3D Gd-MRA (see Fig. e-70.1)
c. Post-Gd axial and coronal LAVA
5. Renal artery: transplant donor/recipient, hypertension, renal failure, postoperative, and preangioplasty mapping of arterial anatomy
a. Timeslip, InHance, Native trueFISP, B-Trance—noncontrast renal MRA
b. Coronal 3D Gd-MRA
c. Axial 3D phase contrast (PC) imaging of renal arteries
d. Delayed coronal 3D SPGR imaging of collecting system, ureters, and bladder (MR urogram). Images can be improved with IV administration of Lasix (10 mg).
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Table e-70.1 Common Indications for MRA Exams
Aortic Celiac and

Arch and Thoracic Abdominal Peripheral Pulmonary Mesenteric Hepatic Venous
Carotids Aorta Aorta MRA Artery Renal Artery Arteries Arteries Imaging
Common Great- Dissection, Preoperative, Claudication, Embolism, Transplant Mesenteric Pre-SIRT DVT,
Indications vessel aneurysm, pre-stent rest pain, AV fistula, donor/recipient, ischemia, Mapping for stenosis. To
anatomy, aortitis, graft, nonhealing aneurysm, hypertension, renal preoperative mapping pre- distinguish
anomalies, embolic aneurysm, ulcer, and pulmonary failure, preangioplasty mapping of radio- between
stroke, TIA source, dissection, prior free-flap hypertension mapping of arterial mesenteric embolization acute and
coarctation, follow-up repair anatomy, postoperative vascular chronic
pre/postop follow-up anatomy, venous
preor postliver thrombosis
transplantation
Sequences Axial 2D Axial SSFP Coronal 3D Time- Coronal 3D Noncontrast renal MRA 3D MRCP Axial/Coronal Axial 2D
TOF and black Gd-MRA resolved Gd-MRA of (Timeslip/InHance/Native Timeslip, SSFSE TOF->
Axial T1- blood DIR Post-Gd axial MRA of both lungs trueFISP, B-Trance) InHance, Dynamic Intraluminal
W FS Sagittal and coronal symptomatic (single Coronal 3D Gd-MRA. Native high filling defect:
Coronal cine-SSFP LAVA foot and calf injection) Axial 3D PC Coronal 3D trueFISP temporal SSFP or 2D
3D Gd- (candy 3D bolus- Post-Gd SPGR Coronal 3D resolution PC MRA
MRA cane) chase MRA axial and (+/− Lasix 10 mg or 2 Gd-MRA LAVA (e.g., Dynamic
Coronal from coronal glasses fluids) of Post-Gd spiral/radial TRICKS
cine-SSFP diaphragm to LAVA. collecting system coronal and LAVA). Pre/Post Gd
Cine SSFP ankle with (MR urogram) axial LAVA Post-Gd axial/coronal
in aortic inflated blood coronal/axial LAVA
valve plane pressure LAVA Axial T2 FS
Coronal 3D cuffs on thigh
Gd-MRA to reduce
with ECG venous
gating contamination
Post-Gd
coronal
and axial
LAVA
MRA, magnetic resonance angiography; TIA, transient ischemic attack; AV, arteriovenous; SIRT, selective internal radiation therapy; DVT, deep vein thrombosis; 2D, two-
dimensional; TOF, time-of-flight; T1-W, T1-weighted; FS, fat saturated; 3D Gd-MRA, three-dimensional gadolinium MRA; SSFP, Steady State Free Precession; DIR, double
inversion recovery; ECG, electrocardiogram; LAVA, liver acquisition with volume acquisition; MR, magnetic resonance; MRCP, MR-cholangiopancreatography; FISP, fast imaging
with steady state precession; SSFSE, single shot fast-spin echo.
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6. Mesenteric artery: mesenteric ischemia, preoperative mapping of mesenteric vascular anatomy, pre- or post-liver transplantation. Use renal artery protocol (earlier), add MR-
cholangiopancreatography (MRCP) as well as post-Gd axial and coronal LAVA.
7. Celiac and hepatic arteries: pre-SIRT (Selective Internal Radiation Therapy) Mapping for radioembolization. Use a high temporal resolution dynamic 3D fast spoiled gradient
echo dynamic MRI sequence using spiral encoding in the imaging plane and Cartesian encoding along the slice direction (Fig. e-70.4). Post-Gd axial and coronal LAVA.
8. Peripheral MRA: claudication, rest pain, nonhealing ulcer, and prior free-flap repair
a. Time-resolved MRA of symptomatic foot and calf
b. 3D bolus-chase MRA from diaphragm to ankle, using blood pressure cuffs on thigh inflated to 50 to 60 mm Hg to reduce venous contamination
9. Veins of the extremities for DVT
a. Keep legs warm, with multiple blankets as needed, to maximize flow to legs; consider elevating ankles to enhance venous return.
b. Use three-plane ungated SSFP localizers and axial 2D TOF to image from above the iliac crest to below the knee. Do this in at least two acquisitions per station to avoid acquiring
poor-quality images at the inferior and superior extent of the image volume.
(1) Any region that has an intraluminal filling defect should be further imaged with SSFP or 2D PC MRA, with superior-to-inferior flow encoding, to determine if a filling defect on TOF
is real or a flow artifact. Adjust VENC (velocity encoding value) as follows: pelvis, 40 cm per second; thigh, 30 cm per second; calf, 20 cm per second.
(2) To distinguish between acute and chronic venous thrombosis, axial T2 (with fat saturation) and LAVA (3D T1 with fat saturation) post-Gd are helpful. Acute thrombosis stimulates
a perivenous inflammatory response that is bright on T2-W images and enhances with Gd contrast.
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FIGURE e-70.4 • Maximum intensity projection images of the noncontrast Inhance sequence showing renal artery and their branches up to third and fourth order (arrows).
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(3) Dynamic TRICKS: Twenty phases is typically performed to see both arterial and venous phases.
(4) Post-Gd axial and coronal LAVA, matrix size 512 × 192, with 3 to 5 mm slices, can be especially helpful in identifying subtle DVTs.
References
1. Potchen JE, Haacke EM, Siebert JE, et al. Magnetic Resonance Angiography: Concepts and Applications. St. Louis, MO: Mosby; 1993.
2. Anderson CM, Edelman RR, Turski PA. Clinical Magnetic Resonance Angiography. New York, NY: Raven Press; 1993.
3. Yucel EK. Magnetic Resonance Angiography: A Practical Approach. New York, NY: McGraw-Hill; 1995.
4. Higgins CB. Essentials of Cardiac Radiology and Imaging. Philadelphia, PA: JB Lippincott; 1992.
5. Prince MR, Grist TM, Debatin JF. 3D Contrast MR Angiography. 3rd ed. Heidelberg, Germany: Springer-Verlag; 2003.
6. McRobbie DW, Moore EA, Graves MJ, et al. MRI: From Picture to Proton. 2nd ed. Cambridge, United Kingdom: Cambridge University Press; 2007.
7. Alart IP, Bongartz GM, Marchal G. Magnetic Resonance Angiography. Berlin, Germany: Springer-Verlag; 2003.
8. Duerinckx AJ. Coronary Magnetic Resonance Angiography. New York, NY: Springer-Verlag; 2002.
9. Schneider G, Prince MR, Meaney JFM, et al. Magnetic Resonance Angiography: Techniques, Indications and Practical Applications. Milan, Italy: Springer; 2005.
10. Agrawal MD, Spincemaille P, Mennitt KW, et al. Improved hepatic arterial phase MRI with 3-second temporal resolution. J Magn Reson Imaging. 2013;37(5):1129-1136.
11. Dixon WT. Simple proton spectroscopic imaging. Radiology. 1984;153(1):189-194.
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e-71
Computed Tomographic Angiography
Michael L. Martin
As with catheter angiography, prior to imaging, it is essential to evaluate the patient to determine the
appropriateness of the examination, address any clinical issues that might impact the study, select the area to be
imaged, and assess how cooperative the patient is likely to be. Technologists not familiar with the regions of
coverage or bolus timing issues germane to vascular studies will need guidance from the radiologist.
Choose the Appropriate Modality

1. Use CTA instead of MRA when (1)
a. There is greater local expertise with computed tomographic angiography (CTA).
b. Patient is claustrophobic.
c. Implants are contraindicated in magnetic resonance (MR) (pacemaker, cochlear implant, etc.).
d. In-stent lumen evaluation is required.
e. Depiction of arterial calcification is desired (e.g., assessment for bypass graft site).
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2. Use MRA instead of CTA when
a. There is greater local expertise with magnetic resonance angiography (MRA).
b. Patient is allergic to iodinated contrast.
c. There is a desire to avoid ionizing radiation.
d. Excessive vessel calcification, especially small vessels, is observed or anticipated.
e. Endoleak is suspected, and the patient has an MR-compatible stent graft (2). Consider MRA when a
questioned endoleak is occult to other imaging modalities.
1. Contrast-induced nephropathy (CIN): Vasculopaths may have multiple risk factors for CIN; therefore,
determination of calculated glomerular filtration rate (GFR) and avoidance of dehydration are essential.
Screening guidelines and interventions to mitigate CIN are dealt with in Chapter 65.
a. If the GFR <30 mL per minute, consideration should be given to noncontrast MRA, CO2 angiography, or a
combination of techniques. CTA can be performed after intra-arterial injection of contrast diluted 1:10 or more
with normal saline, resulting in considerably lower contrast volumes (3). When possible, patients on dialysis
should have their CTA scheduled immediately prior to a dialysis treatment session.
2. Clothing: The patient should remove all clothing with metallic components from the area to be examined.
3. Sedation: Sedation is rarely necessary, but if given, sedated patients need a responsible adult escort.
4. Intravenous (IV) lines: A right arm IV access is preferred when evaluation of the thoracic aorta is part of the
study (including carotid CTA); otherwise, the site of puncture and size of cannula are chosen to allow an injection
rate of at least 4 mL per minute. A 20-gauge cannula in the antecubital fossa is commonly used.
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Procedure
This chapter describes general principles; imaging protocols are scanner-specific and will need to be
developed within an institution for each examination (4). CTA of all vascular beds can be performed with
any modern computed tomography (CT) scanner without additional hardware. Automated tube current
modulation is recommended to individualize radiation dose and decrease image noise (5). Submillimeter
(typically 0.6 mm) collimation should be utilized for all vascular territories to ensure adequate z-axis
resolution. Pulsation artifact in the ascending aorta can be largely eliminated through the use of cardiac-
gating techniques. This may increase the diagnostic accuracy in the depiction of subtle ascending aortic
disease though currently cardiac-gating is rarely used outside of this limited indication.
1. Scanning protocol
a. Scout sequence: A digital radiograph topogram is performed to define scanning area and to choose a
level for contrast detection for bolus-triggering.
b. Occasionally, an optional nonenhanced acquisition is performed. Nonenhanced imaging is indicated in
assessment for acute thoracic aortic syndromes, gastrointestinal (GI) bleeding, and endoleaks in patients
following endovascular aneurysm repair.
c. Test-bolus, if bolus-triggering is not used
d. CTA acquisition series
e. An optional “delayed phase” acquisition in the event of nonopacification of distal vessels or expectation
of delayed opacification (e.g., endoleak study, GI bleed studies)
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2. Contrast injection (6)
a. The intensity and time course of arterial enhancement are determined by the rate and duration of
injection; they are adjusted depending on the vascular bed to be studied.
b. One to 1.5 g of iodine injected per second usually results in adequate arterial enhancement for an
average-sized patient. Body weight-based adjustments of the injection flow rate and volume are
recommended if patient weighs >90 kg or <60 kg.
c. Typically, a two-phase IV injection with a power injector, iodinated contrast followed with a normal saline
“chaser,” is used to achieve more uniform arterial enhancement over time.
3. Contrast bolus timing (6,7)
a. Image acquisition must occur when opacification of target vessels is sufficient for luminal assessment and
is timed to coordinate with arterial opacification after IV contrast injection (contrast transit time).
b. The variability of contrast transit time (the time to arterial opacification after onset of IV contrast injection)
can be compensated for by using
(1) A test bolus injection—10 mL of contrast is injected, and serial images are acquired every second,
without table movement, with the region of interest (ROI) on the artery of interest immediately proximal to
the area to be examined. A contrast enhancement curve is generated, and the peak opacification time
calculated.
(2) Bolus-triggering techniques—automated detection of bolus arrival and triggering of scan acquisition
c. Depending on the region to be scanned, a further scan delay is added to ensure there is adequate
opacification of distal vessels at the end of image acquisition.
4. Post-acquisition image processing (4,5,8,9) Stored images from the examination should include at
least one series of twodimensional (2D) cross-sectional images. Interpretation of the CT angiographic study
is performed primarily through the review of these images. Axial reconstructed data with an effective slice
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thickness of 2.5 mm is typically adequate for thoracic, abdominal, and peripheral imaging. Submillimeter
reconstructed data sets are helpful for small vessel evaluation such as in the peripheral upper or lower
extremity arteries, intracranial region, or occasionally renal arteries.
More advanced image reconstruction methods are used mostly to confirm findings seen on cross-section,
further evaluate complex lesions or tortuous vascular segments, and summarize findings for referring
clinicians. Optimally, a standardized set of reformatted images is created for each examination type,
including at least one series mimicking conventional angiography.
a. Maximum intensity projection (MIP images): The MIP algorithm stacks pixels with attenuation values
above an arbitrary threshold from a set of slices into a composite image. The resulting images are similar to
a nonsubtracted catheter angiogram, unless osseous structures are removed from the data set prior to the
creation of the MIP image.
Limitations
(1) Image generation is time-consuming if bones have to be removed manually from the data set.
(2) Vessels may be inadvertently removed in the bone removal process, creating potential for misdiagnosis.
(3) The vessel lumen may be obscured by dense mural calcification or stents, especially in small vessels.
b. Volume rendering: Images are rendered of several MIP frames in which the viewpoint is slightly
changed from one to the other, thus, creating the illusion of three-dimensional (3D) volume. 3D rendering
provides a visually efficient display allowing fast interactive exploration of the large data sets of CTA. One
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can use interactive selection of the appropriate viewing angles to expose relevant vascular segments.
Adjustment of the opacity transfer function allows blending in or carving out of exquisite vascular detail.
Table e-71.1 Commonly Used Protocols for Standard Computed Tomographic

Angiography Examinations
All studies are performed with collimation of 64 × 0.6 mm, 120 kVp, and automated dose modulation.
Ioversol 320 contrast or equivalent is used for all computed tomography (CT) angiography studies.
For all studies, a 30-mL “chaser” of saline is given at the completion of contrast injection at the same
rate as contrast administration. Please note that imaging protocols are machine-specific. Alternative
protocols should be available from CT vendors. Numerous online sources for imaging protocols are
available including at http://www.ctisus.org/mdct64/protocols/protocols.html (by permission, Elliott K
Fishman, MD, Johns Hopkins University)
Scan Additional
Study Indication Range Contrast Trigger Delay Phases
Arch to Carotid Lesser 100 mL at Automated 4 sec N/A

vertex stenosis, curve of 5 mL/sec trigger off
dissection, aortic arch ascending
FMD, to cranial aorta—
vascular vertex 100 HU
malformation
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Pulmonary Pulmonary Thoracic 100 mL at Automated 7 sec N/A
artery embolism, AV apex to 5 mL/sec trigger off
fistula inferior main
costophrenic pulmonary
angle artery—
115 HU
Whole Dissection, Thoracic 120 mL at Automated 5 sec Noncontrast

aorta aneurysm, apex to 4 mL/sec trigger off through
acute groin ascending same range
thoracic aorta— for
aortic 100 HU suspected
syndrome, acute
aortitis, thoracic
embolic aortic
source syndrome
Thoracic Follow-up Thoracic 90 mL at 4 Automated 5 sec N/A

aorta study of apex to mL/sec trigger off
known inferior ascending
thoracic costophrenic aorta—
aortic angle 100 HU
pathology
Abdominal Aneurysm, Apex of 90 mL at 4 Automated 15 Venous

aorta mesenteric diaphragm mL/sec trigger off sec phase at
ischemia to groin aorta at 60-90 sec
T12—100 postcontrast
HU for acute
intestinal
ischemia
Renal Hypertension Diaphragm 90 mL at 4 Automated 12 N/A

arteries to iliac crest mL/sec trigger off sec
aorta at
T12—100
HU
GI Acute GI Apex of 120 mL at Automated 15 Noncontrast

bleeding bleeding diaphragm 4 mL/sec trigger off sec and venous
study to groin aorta at phase at 60
T12—100 sec through
HU same range
Post- Evaluation Thoracic 90 mL at 4 Automated 5 sec Optional

EVAR following apex to mL/sec trigger off noncontrast
(thoracic endovascular inferior ascending through
aorta) aneurysm costophrenic aorta— endograft
repair angle 100 HU ±60 sec
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postcontrast
through
endograft
Post- Evaluation Apex of 90 mL at 4 Automated 15 Optional

EVAR following diaphragm mL/sec trigger off sec noncontrast
(abdominal endovascular to groin aorta at through
aorta) aneurysm T12—100 endograft
repair HU ±60 sec
postcontrast
through
endograft
Lower Claudication, Apex of 120 mL at Automated 17 N/A

extremity limb- diaphragm 4 mL/sec trigger off sec
threatening to toes aorta at
ischemia, T12—100
evaluation HU
for free flap
graft
Upper Chronic or Affected arm 120 mL at Automated 6 sec N/A

extremity acute above head, 4 mL/sec trigger off
ischemia, lesser curve IV in ascending
penetrating of aortic unaffected aorta—
trauma arch to arm 100 HU
fingertips
FMD, fibromuscular dysplasia; AV, arteriovenous; N/A, not applicable; GI, gastrointestinal; EVAR,
endovascular aortic aneurysm repair; IV, intravenous.
Limitations
(1) Stents or calcifications essentially preclude assessment of the vessel lumen.
(2) Most PACS workstations do not display the color information on highresolution grayscale monitors.
c. Multiplanar reformations (MPR): Sagittal and/or coronal reformatting is especially helpful in pulmonary
and aortic examinations, and oblique MPRs for carotid CTA. Simultaneous viewing of orthogonal projections
in heavily calcified or stented vessels can be a useful means of assessing the vascular lumen. Curved
planar reformats (CPRFs), also called “centerline” reconstructions, are longitudinal cross-sections along a
predefined vascular centerline. CPRFs are another useful technique for evaluating the lumen in stented
vascular segments. Limitations: CPRFs work well in normal or minimally diseased vessels but can fail in
segments that are severely diseased.
References
1. Chan D, Anderson ME, Dolmatch BL. Imaging evaluation of lower extremity infrainguinal disease: role of
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the noninvasive vascular laboratory, computed tomography angiography, and magnetic resonance
angiography. Tech Vasc Interv Radiol . 2010;13:11-22.
2. van der Laan MJ, Bartels LW, Viergever MA, et al. Computed tomography versus magnetic resonance
imaging of endoleaks after EVAR. Eur J Vasc Endovasc Surg. 2006;32: 361-365.
3. Gandhi D, Pandey A, Ansari SA, et al. Multi-detector row CT angiography with direct intra-arterial contrast
injection for the evaluation of neurovascular disease: technique, applications, and initial experience. AJNR
Am J Neuroradiol . 2009;30:1054-1058.
4. Fleischmann D, Hallett RL, Rubin GD. CT angiography of peripheral arterial disease. J Vasc Interv Radiol .
2006;17:3-26.
5. Fuentes-Orrego JM, Pinho D, Kulkarni NM, et al. New and evolving concepts in CT for abdominal vascular
imaging. Radiographics. 2014;34:1363-1384.
6. Bae KT. Intravenous contrast medium administration and scan timing at CT: considerations and
approaches. Radiology. 2010;256:32-61.
7. Fleischmann D, Rubin GD. Quantification of intravenously administered contrast medium transit through
the peripheral arteries: implications for CT angiography. Radiology. 2005;236:1076-1082.
8. Rubin GD, Leipsic J, Joseph Schoepf U, et al. CT angiography after 20 years: a transformation in
cardiovascular disease characterization continues to advance. Radiology. 2014;271:633-652.
9. Koechl A, Kanitsar A, Lomoschitz E. Comprehensive assessment of peripheral arteries using multi-path

curved planar reformation of CTA datasets. Eur Radiol . 2003;13: 268-269.
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e-72
Radionuclide Evaluation for Interventional Radiologists
Don C. Yoo
Sabah S. Tumeh
Ventilation-Perfusion Pulmonary Scintigraphy

Indications
1. Acute chest pain in the absence of heart disease
2. Clinical suspicion of pulmonary embolism (PE), elevated D-dimer levels
3. Baseline and follow-up of patients at high risk for PE
4. In patients with severe lung disease such as chronic obstructive pulmonary disease (COPD) (1,2)
Precautions
1. Severe pulmonary hypertension (the only reported instances of death following infusion of 99mTc-labeled
macroaggregated albumin [MAA] have occurred in such cases). The dose (number of particles) should be
appropriately reduced.
2. Pregnant or pediatric patients: The radiation dose should be reduced to minimize exposure to the fetus and to
children.
3. Patients with known right to left shunts: The dose should be appropriately reduced.
4. Typically for dose reduction, the standard dose is decreased by a half.
1. Chest radiographs (CXRs) taken within 24 hours of performing the lung scan should be available. The CXR
should show clear lungs for an optimal ventilation/perfusion ([V with dot above]/[Q with dot above]) scan.
Significant airspace disease or consolidation can make it difficult to interpret [V with dot above]/[Q with dot
above] scans and can often result in intermediate probability studies. Therefore, if possible, checking the CXR
prior to performing a [V with dot above]/[Q with dot above] scan would be ideal.
2. If the patient has had prior [V with dot above]/[Q with dot above] scans, it is also important to review them
when interpreting the new study because chronic PE from uncanalized clot can have the same appearance as
acute clots (3).
Procedure
1. Labeling of MAA with 99mTc
2. Intravenous (IV) injection of 3 to 5 mCi (200,000 to 1,000,000 particles) 30 to 100 μm diameter with
patient supine and taking deep breaths
3. Images performed in the anterior, posterior, right lateral, left lateral, left posterior oblique, right posterior
oblique, right anterior oblique, and left anterior oblique projections (minimum counts/image 750,000)
4. If the perfusion images are normal or heterogeneous but show no large wedgeshaped defect, the
examination can be terminated because the probability of PE is very low.
Radiology Books
5. If the perfusion scan is abnormal and xenon-133 is going to be used for ventilation, the projection that
depicts the defects to the best advantage should be used to ventilate the patient. Radioxenon is introduced
while the patient takes a deep breath for a single breath image. This is followed by rebreathing for about 2
to 4 minutes into a closed system to achieve equilibrium of distribution of radioxenon in the lungs. The
patient then breaths into a tubing system connected to a radioxenon trapping container for washout images.
The length of the ventilation scan should be no less than 6 minutes.
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6. The initial image is acquired for 100,000 counts while the equilibrium and washout images are acquired
for 45 to 60 seconds each.
7. If 99mTc-labeled diethylenetriamine pentaacetic acid (DTPA) aerosol is used as the ventilation agent, this
scan should precede the perfusion scan. About 30 to 40 mCi of 99mTc are used to label the radioaerosol,
whereas about only 800 to 1,000 μCi are actually inhaled by the patient. The advantage of this technique is
the ability to acquire images in multiple projections and directly compare to the perfusion images. However,
in many patients who cannot take a deep initial breath, there is a high incidence of deposition of the
radioaerosol in the tracheobronchial tree, resulting in significant artifacts.
8. Lung scintigraphy for PE can also be performed using single-photon emission computed tomography
(SPECT)/computed tomography (CT), which can improve sensitivity. In one study, the sensitivity of SPECT
in four or five investigations was higher than that of planar [V with dot above]/[Q with dot above] imaging.
When planar [V with dot above]/[Q with dot above] scans are “intermediate” (20% to 80% chance of PE),
then SPECT/CT may increase the certainty of the presence or absence of PE. SPECT may further improve
the performance of [V with dot above]/[Q with dot above] imaging, but a larger prospective evaluation is
necessary (4).
Usually none is needed.
Results
1. Revised Prospective Investigation of Pulmonary Embolism Diagnosis (PIOPED) [V with dot above]/[Q
with dot above] scan interpretation criteria (1)
a. High probability: At least two segmental perfusion defects without ventilatory or CXR abnormality.
These could be divided into
(1) Two or more large (>75% of a segment) segmental perfusion defects without corresponding ventilation
or chest radiographic images abnormality
(2) One large segmental perfusion defect and two or more moderate-size (25% to 75% of a segment)
segmental perfusion defects without corresponding ventilation or CXR abnormality
(3) Four or more moderate-size segmental perfusion defects without corresponding ventilation or CXR
abnormality
b. Intermediate probability
(1) One moderate to less than two large segmental perfusion defects without corresponding ventilation or
CXR abnormality
(2) Corresponding [V with dot above]/[Q with dot above] defects and CXR parenchymal opacity in lower
lung zone
(3) Single moderate matched [V with dot above]/[Q with dot above] defects with normal CXR findings
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(4) Difficult to categorize as normal, low, or high probability
c. Low probability
(1) Multiple matched [V with dot above]/[Q with dot above] defects, regardless of size, with normal CXR
(2) Corresponding [V with dot above]/[Q with dot above] defects and CXR parenchymal opacity in upper or
middle lung zone
(3) Corresponding [V with dot above]/[Q with dot above] defects and large pleural effusion
(4) Any perfusion defects with substantially larger CXR abnormality
(5) Defects surrounded by normal-perfusion lung (stripe or rim sign)
(6) Single or multiple small (<25% of a segment) segmental perfusion defects with normal CXR
(7) Nonsegmental perfusion defects (round or non-wedge-shaped defects)
d. Normal: no perfusion defects; homogeneous distribution of radioactivity
2. Correlation of [V with dot above]/[Q with dot above] scan category (PIOPED) with the clinical likelihood of
PE (1)
3. The Biello categorization of [V with dot above]/[Q with dot above] scans for the probability of PE (5)
a. High probability
(1) Single large (>90% of a segment) [V with dot above]/[Q with dot above] mismatch
(2) Perfusion defect substantially larger than density on CXR
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(3) Multiple medium (25% to 90% of a segment) or large [V with dot above]/[Q with dot above] mismatches
without matched density on CXR
(1) Severe diffuse obstructive pulmonary disease with perfusion defects
(2) Perfusion defect same size as CXR abnormality
(3) Single medium [V with dot above]/[Q with dot above] mismatch
c. Low probability
(1) Small (25% of an anatomical segment) [V with dot above]/[Q with dot above] mismatch(es)
(2) [V with dot above]/[Q with dot above] mismatches without corresponding changes on CXR
(3) Perfusion defect substantially smaller than CXR density
d. Normal: normal perfusion
4. The McNeil categorization of [V with dot above]/[Q with dot above] scans for the probability of PE (6)
a. High probability
(1) Single [V with dot above]/[Q with dot above] mismatch, lobe or larger, with normal CXR
(2) Multiple [V with dot above]/[Q with dot above] mismatches, segmental or larger; CXR normal
(1) Mixed [V with dot above]/[Q with dot above] match and mismatch
(2) Perfusion defect with matched density on CXR
c. Low probability
(1) Single [V with dot above]/[Q with dot above] mismatch, segmental or subsegmental; CXR clear
(2) [V with dot above]/[Q with dot above] perfusion match(es) alone
(3) Multiple [V with dot above]/[Q with dot above] mismatches, subsegmental; CXR clear
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d. Normal: normal perfusion
5. The three sets of interpretation criteria were compared in 96 patients who underwent [V with dot
above]/[Q with dot above] scans with technetium perfusion and aerosol ventilation, CXR, and pulmonary
angiography (7).
a. The PIOPED criteria had the most favorable likelihood ratio for predicting an angiogram showing PEs.
However, they also had the most intermediate studies.
b. The McNeil criteria had the least favorable likelihood for predicting PEs on an angiogram.
c. The Biello and McNeil criteria showed the most favorable likelihood ratio for predicting an angiogram not
showing PEs.
Complications
1. The potential for embolization of albumin particles to sensitive small-vessel areas such as the brain exists
when there is an unsuspected anatomical right-to-left shunt.
2. Inadvertent intra-arterial injection of a large number of albumin particles could cause digital ischemia in
the hand or foot by blocking the capillary bed.
Gastrointestinal Bleeding Studies

Indications
1. Acute gastrointestinal hemorrhage (AGIH) distal to the gastric antrum (nasogastric [NG] tube aspirate
negative for blood)
2. Intermittent gastrointestinal hemorrhage
3. To determine the need for visceral angiography for the diagnosis and treatment of AGIH
Precautions/Limitations
1. Multiple prior transfusions and chronic dialysis (since in both cases there is poor red blood cell [RBC] labeling)
2. Pregnancy
3. Patients with bright red blood aspirated from the NG tube or with large and frequent hematochezia should
undergo endoscopy. If endoscopy is nondiagnostic, these patients should undergo emergency angiography for
diagnosis and treatment.
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None needed.
Procedure (8,9)
1. In vitro labeling of the patient's RBCs with 20 mCi of 99mTc pertechnetate
2. Dynamic flow study following a bolus injection of the radiopharmaceutical with images obtained at 5 seconds
per frame for 60 seconds
3. Cine scintigraphy, acquiring 60 consecutive images (15 minutes) at 15 seconds per frame (average 350,000
counts/15 seconds/frame), is performed. While the first 15 minutes' images are reviewed, a subsequent identical
Radiology Books
set of 60 images (15 minutes) is acquired. This sequence is performed for six 15-minute image sequences. Cine
scintigraphy has been shown to improve localization and detection of gastrointestinal bleeding (10).
4. Alternatively, cine scintigraphy can also be performed for a 1 hour period of time.
Results (8)
1. Sensitive for acute bleeding at rates above 0.1 mL per minute; can estimate bleeding rates and identify those
patients who are at higher risk for developing massive gastrointestinal hemorrhage, which requires more
aggressive therapy (11)
2. Detection of foci of hemorrhage in symptomatic cases (hematochezia, melena, chronic anemia) in up to 65% of
cases (8). Subacute hemorrhage is often confirmed on delayed (6 to 24 hours) scintigrams (12). Scintigraphic
localization of a site of bleeding was correct in 77% of cases.
3. Angiography is likely to be negative if the bleeding scan fails to show the bleeding focus.
Captopril-Enhanced Renal Scintigraphy for Diagnosis of Renovascular

Hypertension
Indications
1. To uncover hemodynamically significant renal artery stenosis (RAS) or other renal disorders that may be
the cause of hypertension
2. To obtain an estimate of the differential renal function
3. To stratify hypertensive patients into those who will and will not benefit from revascularization—either
surgical or with angioplasty (controversial)
Contraindications
Relative
1. Inability to discontinue the use of angiotensin-converting enzyme (ACE) inhibitor drugs in sufficient time
prior to the study
2. Inability of the patient to lie flat on the imaging table without movement for at least 30 minutes
1. Patients should be instructed to discontinue the use of ACE inhibitors for at least 48 hours (13,14).
2. If the patient cannot stop taking the ACE inhibitor, the patient should hold the morning dose and take it in the
nuclear medicine section 1 hour before the study.
3. All other non-ACE-inhibitor antihypertensive medications should be discontinued, (at least overnight) if
possible, to decrease the likelihood of a hypotensive response to captopril when it is administered before the
test. Unfortunately, this is often difficult to achieve on a practical basis.
4. Stop oral intake at 3 AM the night before the procedure.
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5. Establish IV access with normal saline running at a slow rate (15 to 20 mL per minute). The IV should be 18 to
20 gauge to allow for urgent volume expansion if a hypotensive response to captopril occurs.
6. A Foley catheter is used in patients with bladder-emptying problems or renal transplants.
Radiology Books
Procedure
There are several protocols for performing ACE-inhibition scintigraphy. Some studies are performed with
the glomerular agent 99mTc-DTPA and some with tubular agents such as 131I-labeled Hippuran (131I-HIP) or
99mTc-labeled mertiatide (MAG-3). Some investigators perform the baseline and ACE-inhibited scintigram
on different days and some on the same day. Two protocols are presented here, one with a tubular agent
and the other with a glomerular agent.
Tubular Agent (99mTc-MAG-3) (15)
1. An ACE-inhibition scintigram is performed. Enalaprilat (Vasotec, Merck Sharp and Dohme, West Point,
PA) 2.5 mg (0.04 mg per kg) is given over 5 minutes by slow IV drip. Blood pressure (BP) is monitored every
5 minutes. Ten minutes after the infusion, give 40 mg IV of furosemide (80 mg in renal insufficiency). The
dose of MAG-3 is 5 to 10 mCi given as a bolus IV injection.
2. Alternatively, 50 mg PO of captopril may be given and the patient waits for 1 hour, during which BP is
monitored. Then, furosemide (Lasix) is infused IV followed by injection of the radiopharmaceutical.
3. If the patient has a systolic BP of less than 140 mm Hg, do not administer IV enalaprilat and consider
decreasing the oral dose of captopril to 25 mg. There is no consensus on exactly how this decreased dose
will influence the sensitivity of the exam.
4. A 60-second, rapid-sequence flow image of 1 frame per second is acquired following injection, beginning
when activity is seen in the abdominal aorta on the persistence scope. A 20- to 30-minute acquisition is
performed at a frame rate of 20 to 30 seconds per frame. Whole kidney and cortical regions of interest are
drawn and time-activity curves constructed. Curves are analyzed for time to peak and residual cortical
activity (16), where:
5. If the examination is abnormal, it is repeated without captopril as a baseline.

Glomerular Agent (DTPA) (17)
1. The preparation of the patient is similar to that with a tubular agent. Fifty milligrams of captopril is
administered orally. BP is monitored every 15 minutes for 1 hour.
2. Lasix is infused intravenously, followed by 12 mCi of 99mTc-DTPA. Images are acquired in the posterior
projection at a rate of 1 frame per 20 second for 20 to 30 minutes with the patient supine.
3. Regions of interest over each kidney are defined, excluding pelvic activity. Renogram curves are plotted.
4. Time to peak activity is determined from the time-activity curves, and a split function index is calculated
from the radionuclide uptake between the second and third minute of the study.
5. If the examination is abnormal, it is repeated without captopril.
1. Check the patient's BP in the supine and sitting positions. If there is an orthostatic drop in systolic BP, the
patient should receive IV hydration and not be discharged until this is corrected.
2. Advise the patient to resume all medications as previously prescribed.
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Results
1. Proposed grading system for the renogram curves (18)
a. Grade 0: normal (Fig. e-72.1)
b. Grade 1: mild delay in upslope and maximal activity (Tmax) (6 minutes ≤Tmax ≤11 minutes), or excretory
phase (Fig. e-72.2)
c. Grade 2: delay in upslope and Tmax with evidence of an excretory phase (Fig. e-72.3)
d. Grade 3: delay in upslope and Tmax without evidence of an excretory phase; marked reduction or
absence of uptake (Fig. e-72.4)
2. Table e-72.1 shows the likelihood of a critical RAS based on comparison of baseline and postcaptopril
curves (18).
3. Using the tubular agent 131I-HIP, an RCA of 30% or greater had a sensitivity of 96% and a specificity of
95% for the detection of renovascular hypertension in patients with normal renal function (serum creatinine
>1.5 mg per dL) (14). It appears that the criteria for 131I-HIP may be applied to studies performed with
99mTc-MAG-3 (19).
4. In patients with RAS, the captopril-enhanced renogram has prognostic value in predicting which patients
will have a reduction in BP (cure or improvement) after percutaneous transluminal angioplasty (20). The
sensitivity of the test was 91% (53/58 patients) for all patients, 95% in patients with unilateral RAS (35/37
patients), and 86% in patients with bilateral RAS, bilaterally treated (18/21 patients). In 18 patients with a
negative captopril renogram, the BP improved in 5 and did not change in 13.
5. Hypotension during the exam may create the artifactual appearance of bilateral RAS. This renographic
diagnosis in a patient who was rendered hypotensive should be made with caution.
6. False-positive scans may be caused by a full urinary bladder from any cause. The full bladder delays the
emptying of the renal collecting system, causing prolonged evaluation of the renogram curve. Patients with
bladder-emptying problems should have a Foley catheter during the study to avoid false-positive results.
Radiology Books
FIGURE e-72.1 • Grade 0 renogram curve. (Adapted from Nally JV Jr, Chen C, Fine E, et al. Diagnostic
criteria of renovascular hypertension with captopril renography. A consensus statement. Am J Hypertens.
1991;4:749S-752S.)
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1991;4:749S-752S.)
FIGURE e-72.3 • Grade 2A and 2B renogram curves. (Adapted from Nally JV Jr, Chen C, Fine E, et al.
Diagnostic criteria of renovascular hypertension with captopril renography. A consensus statement. Am J
Hypertens. 1991;4:749S-752S.)
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1991;4:749S-752S.)
7. Patient motion artifact can cause spurious points on the renogram curve and can be a cause of a false-
positive scan. This is easily checked by comparing the position of the kidneys at 3 minutes and 20 minutes
in a composite image to determine motion artifact.
Complications
Profound hypotension may be induced with the use of ACE inhibitors. This usually occurs in the volume-
contracted patient and emphasizes the importance of adequate hydration and BP monitoring during this
exam.
Table e-72.1 Probability of Renal Artery Stenosis (RAS) Predicted by Change from
Baseline Renogram Grade to Captopril-Enhanced Renogram Grade
Baseline Postcaptopril
Grade 0 Grade 1 Grade 2A Grade 2B Grade 3
Grade 0 L H H H H
Grade 1 L I H H H
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Grade 2A L L I H H
Grade 2B L L L I H
Grade 3 L L L I I
Probability of RAS—L, low; I, Indeterminate; H, high.
Reprinted from Nally JV Jr, Chen C, Fine E, et al. Diagnostic criteria of renovascular hypertension
with captopril renography. A consensus statement. Am J Hypertens. 1991;4: 749S-752S, with
permission.
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Diuretic Renal Scintigraphy
Indications (21)
1. Differentiating obstructed from nonobstructed dilatation of the upper urinary tract
2. Evaluate the efficacy of treatment of obstructive uropathy.
3. Quantitate differential renal function to determine treatment.
Contraindications
Dehydration
1. Establish IV access with normal saline running at slow rate (15 to 20 mL per min).
2. Empty bladder. A Foley catheter should be used in patients with bladder-emptying problems.
Procedure
1. Radionuclide: 99mTc-MAG-3 is preferred to DTPA. Dose: 3 to 6 mCi. The parenchymal extraction of
MAG3 occurs during the first minute and peaks about 3 minutes after the bolus injection.
2. Furosemide: 1 mg per kg in infants, 0.5 mg in children, and 40 mg in adults. Diuretic effect starts 1 to 2
minutes after the injection of the furosemide.
3. Timing of injections: several protocols
a. Inject furosemide 20 minutes after the radionuclide.
b. Inject furosemide 15 minutes before the radionuclide.
c. Inject furosemide just before the radionuclide. This is the preferred method because it simplifies and
standardizes the procedure.
Hydrate appropriately.
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Results
1. Normal. No obstruction (similar to Fig. e-72.1).
2. Obstructed: long peak time (Tmax >6 minutes) and high retention (>50% at 20 minutes)
Limitations
2. Patient inability to hold still
References
1. Prospective Investigation of Pulmonary Embolism Diagnosis Investigators. Value of the
ventilation/perfusion scan in acute pulmonary embolism. Results of the prospective investigation of
pulmonary embolism diagnosis (PIOPED). JAMA. 1990;263:2753-2759.
2. Worsley DF, Alavi A, Palevsky HI. Role of radionuclide imaging in patients with suspected pulmonary
embolism. Radiol Clin North Am. 1993;31:849-858.
3. Parker JA, Coleman RE, Grady E, et al. SNM practice guideline for lung scintigraphy 4.0. J Nucl Med
Technol . 2012;40(1):57-65.
4. Stein PD, Freeman LM, Sostman HD, et al. SPECT in acute pulmonary embolism. J Nucl Med.
2009;50(12):1999-2007.
5. Biello DR. Radiological (scintigraphic) evaluation of patients with suspected pulmonary embolism. JAMA.
1987;257:3257-3259.
6. McNeil BJ. Ventilation-perfusion studies and the diagnosis of pulmonary embolism: concise
communication. J Nucl Med. 1980;21:319-323.
7. Webber MM, Gomes AS, Roe D, et al. Comparison of Biello, McNeil, and PIOPED criteria for the diagnosis
of pulmonary emboli on lung scans. AJR Am J Roentgenol . 1990;154: 975-981.
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8. McKusick KA, Froelich J, Callahan RJ, et al. 99mTc red blood cells for detection of gastrointestinal
bleeding: experience with 80 patients. AJR Am J Roentgenol . 1981;137:1113-1118.
9. Bunker SR, Brown JM, McAuley RJ, et al. Detection of gastrointestinal bleeding sites. Use of in vitro
technetium Tc99m-labeled RBCs. JAMA. 1982;247:789-792.
10. Maurer AH, Rodman MS, Vitti RA, et al. Gastrointestinal bleeding: improved localization with cine
scintigraphy. Radiology. 1992;185:187-192.
11. Smith R, Copely DJ, Bolen FH. 99mTc RBC scintigraphy: correlation of gastrointestinal bleeding rates
Radiology Books
with scintigraphic findings. AJR Am J Roentgenol . 1987;148:869-874.
12. Alavi A. Scintigraphic demonstration of acute gastrointestinal bleeding. Gastrointest Radiol . 1980;5:205-
208.
13. Sfakianakis GN, Georgiou M, Cavagnaro F, et al. Fast protocols for obstruction (diuretic renography) and
for renovascular hypertension (ACE inhibition). J Nucl Med Tech. 1992;20:193-206.
14. Blaufox MD. The role and rationale of nuclear medicine procedures in the differential diagnosis of
renovascular hypertension. Nucl Med Biol . 1991;18:583-587.
15. Sfakianakis GN, Bourgoignie JJ, Georgiou M, et al. Diagnosis of renovascular hypertension with ACE
inhibition scintigraphy. Radiol Clin North Am. 1993;31:831-848.
16. Erbslöh-Möller B, Dumas A, Roth D, et al. Furosemide-131I-hippuran renography after angiotensin-

converting enzyme inhibition for the diagnosis of renovascular hypertension. Am J Med. 1991;90:23-29.
17. Setaro JF, Chen CC, Hoffer PB, et al. Captopril renography in the diagnosis of renal artery stenosis and
the prediction of improvement with revascularization. The Yale Vascular Center experience. Am J Hypertens.
1991;4:698S-705S.
18. Nally JV Jr, Chen C, Fine E, et al. Diagnostic criteria of renovascular hypertension with captopril
renography. A consensus statement. Am J Hypertens. 1991;4:749S-752S.
19. Sfakianakis GN, Bourgoignie JJ. Renographic diagnosis of renovascular hypertension with angiotensin
converting enzyme inhibition and furosemide. Am J Hypertens. 1991;4:706S-710S.
20. Geyskes GG, de Bruyn AJ. Captopril renography and the effect of percutaneous transluminal angioplasty
on blood pressure in 94 patients with renal artery stenosis. Am J Hypertens. 1991;4:685S-689S.
21. Boubaker A, Prior JO, Meuwly JY, et al. Radionuclide investigations of the urinary tract in the era of
multimodality imaging. J Nucl Med. 2006;47(11):1819-1836.
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PET/CT for Oncologic Interventions
Don C. Yoo
Positron emission tomography (PET) uses 18F-fluorodeoxyglucose (18F-FDG), a molecular imaging agent, which
couples a fluorine radioisotope (18F) with a glucose analog (FDG), to show physiologically active tumor. When
administered intravenously, the radiopharmaceutical is transported into all cells of the body, which actively use
glucose (1). As most cancer cells have higher metabolic activity and accumulate more 18F-FDG compared to
normal cells, they are highlighted by comparison to less active cells. By fusing radionuclide PET images with
those from x-ray computed tomography (CT), PET/CT distinguishes purely anatomic findings on CT from active
tumor.
PET/CT Imaging with 18F-FDG

Indications
1. To plan an initial treatment strategy (formerly referred as diagnosis and initial staging). For all solid
tumors except in the following circumstances:
a. Prostate cancer
b. Cervical cancer—for assisting in diagnosis
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c. Breast cancer—for assisting in diagnosis and detection of regional nodal metastases
d. Melanoma—for detection of regional nodal metastases in newly diagnosed melanoma
Note: PET/CT can be performed for initial treatment strategy of suspected distant metastatic disease for
cervical, breast, and melanoma in high-risk patients.
2. Subsequent treatment strategy (formerly referred as restaging, detection of suspected recurrence, and
treatment monitoring)
a. Lifetime insurance limit—three FDG-PET scans are covered for oncologic indications.
Additional scans will be permitted at the discretion of Medicare Administrative Contractor (based on Centers
for Medicare & Medicaid Services Coverage Decision effective June 11, 2013) (2).
Contraindications
1. Elevated glucose levels above 200 mg per dL
The American College of Radiology (ACR) and the Society of Nuclear Medicine and Molecular Imaging
(SNMMI) both recommend checking glucose levels on all patients prior to administration of 18F-FDG (3,4).
SNMMI guidelines recommend that patients with glucose of greater than 150 to 200 mg per dL be
rescheduled, if possible, as hyperglycemia will dilute the FDG uptake by tumors through competitive
inhibition. Therefore, tumor uptake of 18F-FDG will be reduced in hyperglycemic states (4).
2. Subcutaneous insulin
Subcutaneous insulin should not be administered to a patient with diabetes with high glucose within 4
hours of a PET/CT scan as insulin will stimulate FDG uptake by skeletal muscle resulting in an altered
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biodistribution which can severely limit image interpretation (5).
Patient Preparation
1. Fasting: minimum fasting of 4 hours. Recent meal can result in a hyperinsulinemic response resulting in
altered biodistribution (3,5).
2. Limiting exercise: Strenuous activity for 24 hours prior to injection should be avoided to decrease muscle
uptake, which could limit interpretation (3,5).
3. Hydration with water is encouraged to promote urinary excretion and decrease whole-body radiation dose
(3,4,5).
4. Low-carbohydrate diet for 24 hours before the study should be considered to decrease the amount of blood
glucose at the time of injection (5).
Procedure
1. Current PET-CT systems essentially consist of a CT scanner and a PET scanner that are combined in
tandem allowing for sequential imaging. The scout image from the CT determines the extent of the imaged
area on the CT and PET portions of the study. Major vendors offer integrated PET-CT systems that
combine different models of dedicated PET scanners and CT scanners.
2. In terms of performing PET/CT scans, there is considerable variability in PET/CT imaging protocols.
a. For many PET/CT scans, the CT portion of the study is performed without contrast and at a low kilovolt
peak (kVp) and milliampere (mA) for attenuation correction and localization.
b. Some PET/CT scans will have the CT portion performed with both intravenous (IV) and oral contrast with
a high kVp and mA. Utilizing an automated milliampere protocol can help limit the radiation dose while
optimizing image quality.
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c. The dose of the FDG is weight based and can vary depending on the recommendations of the PET/CT
vendor. For an adult patient, the dose is typically 10 to 15 mCi (370 to 555 MBq) of 18F-FDG.
d. Imaging is typically performed at 60 to 75 minutes after injection to allow 18F-FDG to be taken up by
tumors and cleared from background soft tissue and blood pool (1).
PET/CT Tumor Treatment Assessment

PET/CT has a growing role in the evaluation of tumor response after transarterial chemoembolization (TACE)
and radiofrequency ablation (RFA).
It is important to have pretreatment PET/CT imaging to determine the baseline metabolic activity of the
neoplasm. In the liver, this is especially true for hepatocellular carcinoma, which can have variable amounts of
FDG avidity. In the lung, low-grade or well-differentiated cancers can have mild metabolic activity (6,7).
False-positive findings on PET/CT after image-guided interventions may be seen and are attributable to an
inflammatory response and tissue regeneration that occurs at the periphery of the treatment site, which could be
mistaken for active malignancy (6).
Hepatic Metastases and Hepatocellular Cancer

PET/CT scan can be useful for evaluation of residual or recurrent disease after TACE for hepatocellular
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carcinoma (HCC) and RFA of hepatic metastases.
For patients with HCC who are candidates for TACE, the degree of FDG-avidity in HCC prior to TACE can be an
independent prognostic factor for tumor progression with higher FDG-avidity associated with worse prognosis
(8).
PET/CT for detection of recurrent, HCC is not commonly performed as HCC can have variable amounts of FDG-
avidity. In a meta-analysis of eight studies for the use of PET/CT in detecting recurrent HCC, the pooled
sensitivity and specificity were 81.7% and 88.9%, respectively (9). Generally, the more poorly differentiated HCC
have more metabolic activity on PET/CT compared to well-differentiated HCC. PET/CT is not sensitive for
detection of low-grade HCC as the metabolic activity is low and is similar to hepatocytes (10).
However, for patients being treated with TACE, PET/CT can be valuable for evaluation of viable HCC after
TACE treatment and can be superior to contrast-enhanced CT. In a study of 73 patients with a total of 91 lesions
with HCCs after TACE, the overall diagnostic sensitivity, specificity, and accuracy for detecting viable tumor were
89.3%, 65.7%, and 80.2% for FDG PET/CT and 60.7%, 77%, and 67% for contrast-enhanced CT, respectively
(11).
PET/CT scans as early as 1 month after TACE may have prognostic value for patients with HCC treated with
TACE, and the degree of response can be measured with the change in standardized uptake value (SUV) to
determine residual viable tumor (12).
For patients having RFA of liver metastases, the expected finding after treatment is photopenia at the site,
surrounded by homogeneous liver activity. If there is a focal area of more intense activity than the surrounding
liver parenchyma, then that should be regarded as suspicious for residual malignancy (7).
Regenerative tissue in the treatment site can present as areas of focally increased uptake on PET/CT scans,
potentially resulting in a false-positive interpretation. It has been reported that tissue regeneration can be found
as early as 3 days after RFA (13). After 3 days to 6 months following treatment, there are varying degrees of
focal uptake on PET/CT that could be from intense inflammatory changes. Pathologic specimens after RFA of
liver metastases have shown inflammatory cells and fibroblasts appearing at the periphery of the ablation cavity
as a healing response, which could be mistaken for residual or recurrent malignancy (14). Therefore, early
PET/CT scans performed within 1 day may be helpful for determining RFA success of liver lesions
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because these scans do not typically show focal abnormalities from liver necrosis or inflammation such as can be
seen on CT or magnetic resonance (MRI) alone (15). If feasible, having the PET/CT scan performed within 24
hours may result in the fewest number of false-positive scans. False-positive results on PET/CT scans present
as a rim-like area of increased activity at the ablation site, as early as 2 days after RFA (16).
Lung Cancer
Detection of residual tumor and recurrence in patients treated with RFA of lung cancer can identify patients who
may benefit from reablation or other image-guided therapy (e.g., stereotactic body radiotherapy [SBRT]).
However, unlike for hepatic metastases, for which early posttreatment PET/CT scans are useful for assessing
treatment success, studies looking at the use of early PET/CT (in the first few days or at 1 month) after RFA of
lung cancers have not been shown to be effective for evaluating treatment success and detecting residual tumor.
Nevertheless, postablation PET/CT scans performed at 3 to 6 months after ablation do correlate with clinical
outcome at 1 year (17,18). There are variable appearances of the postablation cavity on follow-up PET/CT
scans performed between 1 and 4 months after RFA. Unfavorable responses suspicious for residual or recurrent
disease are characterized as focal or rim uptake with additional focal uptake in the same location as the original
tumor (19).
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More research will be necessary to determine the optimal imaging time of the initial PET/CT scan after RFA of
lung cancers; however, it is reasonable to wait 3 to 6 months to decrease the false-positive findings.
Bone Tumors
Although only a few, the majority of the studies and case reports for the use of PET/CT after RFA are on patients
treated for osteoid osteomas and osteoblastomas. The nidus of the osteoid osteoma is metabolically active on
PET/CT (20). In general, the malignant tumors demonstrated higher metabolic activity, but there was
considerable overall of metabolic activity between malignant and some benign tumors such as osteoid osteomas
and giant cell tumors, which can have high metabolic activity (21).
Renal Cell Cancer

PET/CT is not generally recommended for follow-up evaluation of renal cell cancers after RFA. Renal cell cancer
can have variable metabolic activity on PET/CT, but many renal cell cancers have low metabolic activity (22,23).
The background activity in the kidney on PET/CT performed with 18F-FDG can be high due to renal excretion of
tracer. The residual tracer activity in the kidney can obscure visualization of the metabolic activity of the renal cell
cancer. In one study, the sensitivity of PET/CT in detecting the primary renal cell cancer in 66 patients was only
60% compared to 91.7% for CT (22).
Although PET/CT is not helpful for detection of the primary renal cell cancer, it can be helpful in the evaluation of
metastatic disease and recurrence of renal cell cancer after nephrectomy. In a study evaluating recurrent or
metastatic renal cell carcinoma, PET/CT had a sensitivity of 71% and specificity of 75% (24). Another study
showed a sensitivity of 90% and specificity of 91% after nephrectomy in patients who were being evaluated for
recurrence of renal cell cancer or distant metastases (25).
Conclusion
The optimal time to perform the first follow-up PET/CT scan after image-guided treatment can be different
depending on the location of the tumor.
1. For HCC, a follow-up PET/CT as early as 1 month after TACE can be helpful to determine treatment
success. For liver metastases treated with RFA, a follow-up PET/CT as early as 1 to 2 days after treatment
can be helpful to determine treatment success.
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2. For lung cancers, early PET/CT scans have not been shown to be useful, and the initial follow-up
PET/CT after RFA should be performed in 3 to 6 months.
3. For bone tumors treated with RFA, no specific recommendations on the optimal time for follow-up can be
made due to limited literature; however, PET/CT scans may have a role in detection of residual or recurrent
malignancy especially in cases with equivocal MRI or CT scans.
4. For renal cell cancer treated with RFA, PET/CT is not recommended for follow-up due to the low
metabolic activity of many renal cell cancers and the high background activity of the kidneys.
5. The optimal imaging times for additional surveillance PET/CT scans have not been established. If there
is no evidence of residual malignancy, on the initial follow-up PET/CT, then it may be reasonable to wait 6
months or a year for the next follow-up PET/CT. If there is a questionable finding on the PET/CT, then a
follow-up PET/CT in 3 to 6 months or further evaluation with other imaging modality such as contrast-
enhanced CT or MRI should be considered.
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References
1. Basu S, Kwee TC, Surti S, et al. Fundamentals of PET and PET/CT imaging. Ann N Y Acad Sci .
2011;1228:1-18.
2. Centers for Medicare & Medicaid Services. Decision memo for positron emission tomography (FDG) for
solid tumors (CAG-00181R4). https://www.cms.gov/medicare-coverage-database/details/nca-
decisionmemo.aspx?NCAId=263. Accessed June 11, 2013.
3. American College of Radiology. ACR-SPR practice parameter for performing FDG-PET/CT in oncology.
American College of Radiology Web site.
http://www.acr.org/˜/media/71B746780F934F6D8A1BA5CCA5167EDB.pdf. Updated 2012. Accessed March
29, 2013.
4. Delbeke D, Coleman RE, Guiberteau MJ, et al. Procedure guideline for tumor imaging with 18F-FDG
PET/CT 1.0. J Nucl Med. 2006;47(5):885-895.
5. Shankar LK, Hoffman JM, Bacharach S, et al. Consensus recommendations for the use of 18F-FDG PET
as an indicator of therapeutic response in patients in National Cancer Institute Trials. J Nucl Med.
2006;47(6):1059-1066.
6. Avril N. 18F-FDG PET after radiofrequency ablation: is timing everything? J Nucl Med. 2006;47(8):1235-
1237.
7. Paudyal B, Oriuchi N, Paudyal P, et al. Early diagnosis of recurrent hepatocellular carcinoma with 18F-
FDG PET after radiofrequency ablation therapy. Oncol Rep. 2007;18(6):1469-1473.
8. Song MJ, Bae SH, Lee SW, et al. 18F-fluorodeoxyglucose PET/CT predicts tumour progression after
transarterial chemoembolization in hepatocellular carcinoma. Eur J Nucl Med Mol Imaging. 2013;40(6):865-
873.
9. Lin CY, Chen JH, Liang JA, et al. 18F-FDG PET or PET/CT for detecting extrahepatic metastases or
recurrent hepatocellular carcinoma: a systematic review and metaanalysis. Eur J Radiol . 2012;81(9):2417-
2422.
10. Yamamoto Y, Nishiyama Y, Kameyama R, et al. Detection of hepatocellular carcinoma using 11C-choline
PET: comparison with 18F-FDG PET. J Nucl Med. 2008;49(8):1245-1248.
11. Song HJ, Cheng JY, Hu SL, et al. Value of 18F-FDG PET/CT in detecting viable tumour and predicting
prognosis of hepatocellular carcinoma after TACE. Clin Radiol . 2015; 70(2):128-137.
12. Ma W, Jia J, Wang S, et al. The prognostic value of 18F-FDG PET/CT for hepatocellular carcinoma
treated with transarterial chemoembolization (TACE). Theranostics. 2014; 4(7):736-744.
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13. Antoch G, Freudenberg LS, Beyer T, et al. To enhance or not to enhance? 18F-FDG and CT contrast
agents in dual-modality 18F-FDG PET/CT. J Nucl Med. 2004;45(suppl 1): 56S-65S.
14. Liu ZY, Chang ZH, Lu ZM, et al. Early PET/CT after radiofrequency ablation in colorectal cancer liver
metastases: is it useful? Chin Med J (Engl). 2010;123(13):1690-1694.
15. Antoch G, Vogt FM, Veit P, et al. Assessment of liver tissue after radiofrequency ablation: findings with
different imaging procedures. J Nucl Med. 2005;46(3):520-525.
16. Veit P, Antoch G, Stergar H, et al. Detection of residual tumor after radiofrequency ablation of liver
metastasis with dual-modality PET/CT: initial results. Eur Radiol . 2006;16(1):80-87.
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17. Deandreis D, Leboulleux S, Dromain C, et al. Role of FDG PET/CT and chest CT in the follow-up of lung
lesions treated with radiofrequency ablation. Radiology. 2011;258(1): 270-276.
18. Yoo DC, Dupuy DE, Hillman SL, et al. Radiofrequency ablation of medically inoperable stage IA non-
small cell lung cancer: are early posttreatment PET findings predictive of treatment outcome? AJR Am J
Roentgenol . 2011;197(2):334-340.
19. Singnurkar A, Solomon SB, Gönen M, et al. 18F-FDG PET/CT for the prediction and detection of local
recurrence after radiofrequency ablation of malignant lung lesions. J Nucl Med. 2010;51(12):1833-1840.
20. Lim CH, Park YH, Lee SY, et al. F-18 FDG uptake in the nidus of an osteoid osteoma. Clin Nucl Med.
2007;32(8):628-630.
21. Aoki J, Watanabe H, Shinozaki T, et al. FDG PET of primary benign and malignant bone tumors:
standardized uptake value in 52 lesions. Radiology. 2001;219(3):774-777.
22. Kang DE, White RL Jr, Zuger JH, et al. Clinical use of fluorodeoxyglucose F 18 positron emission
tomography for detection of renal cell carcinoma. J Urol . 2004;171(5):1806-1809.
23. Miyakita H, Tokunaga M, Onda H, et al. Significance of 18F-fluorodeoxyglucose positron emission

tomography (FDG-PET) for detection of renal cell carcinoma and immunohistochemical glucose transporter 1
(GLUT-1) expression in the cancer. Int J Urol . 2002;9(1):15-18.
24. Jadvar H, Kherbache HM, Pinski JK, et al. Diagnostic role of [F-18]-FDG positron emission tomography
in restaging renal cell carcinoma. Clin Nephrol . 2003;60(6):395-400.
25. Kumar R, Shandal V, Shamim SA, et al. Role of FDG PET-CT in recurrent renal cell carcinoma. Nucl
Med Commun. 2010;31(10):844-850.
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e-74
Clinical Evaluation of the Cancer Patient
Karen Marshall
Robert J. Lewandowski
The evaluation and management of cancer patients is complex, requiring a comprehensive approach. Ideally, a
patient is presented at a dedicated tumor board and a multidisciplinary team determines the best treatment plan.
The interventional radiologist (IR) has the expertise to assess pre- or posttreatment imaging and should take an
active role in these conferences. Furthermore, the IR must gain and utilize knowledge regarding the outcomes of
all cancer therapies as well as the clinical management of these patients.
Patient Assessment
Candidates for interventional oncology (IO) therapies should be seen in consultation. At minimum, the following
information is required:
1. Method of diagnosis
a. Primary liver cancer (e.g., hepatocellular carcinoma [HCC])
(1) Diagnosis made by imaging or biopsy (1)
(a) In setting of cirrhosis, tumors >1 cm that demonstrate arterial enhancement and venous washout are HCC
(either CT or MRI).
(b) Tumors not meeting these criteria require biopsy.
b. Secondary liver cancer (e.g., metastatic colon cancer [mCRC])
(1) Diagnosis made by biopsy +/− positron emission tomography (PET)
2. Tumor burden/extent of disease (multiphasic, contrast-enhanced imaging optimal)
a. Primary liver cancer
(1) MRI preferable for HCC
(2) Patients most often have liver-only disease.
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Table e-74.1 Child-Pugh Score
Measure 1 point 2 points 3 points
Total bilirubin (mg/dL) <2 2-3 >3
Serum albumin (g/dL) >3.5 2.8-3.5 <2.8
INR <1.7 1.7-2.3 >2.3
Ascites None Mild Moderate to severe

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Hepatic encephalopathy None Medication suppressed Refractory
Childs Pugh A: 5-6 points

Childs Pugh B: 7-9 points
Childs Pugh C: 10-15 points
(3) Patients present with varying tumor morphologies:

(a) Solitary nodule versus multifocal disease
(b) Unilobar versus bilobar disease
(c) Mass-forming tumors versus infiltrative disease
(4) Vascular invasion not infrequent (about one-third have portal vein thrombosis [PVT])
b. Secondary liver cancer
(1) CT (triphasic) preferable for metastatic disease
(2) Candidates for IO therapies have liver-only or liver-dominant disease.
(a) Presence of liver metastases negatively impacts survival outcome.
(3) Patients most often have multifocal, bilobar disease at presentation.
3. Liver function (for those patients being considered for liver-directed therapy)
a. Primary liver cancer
(1) Liver function affected by underlying cirrhosis and tumor burden.
(2) Child-Pugh (CP) score most commonly employed (2) (Table e-74.1)
(3) Best candidates for IO therapies are CP A to CP B7.
(a) Patients with more advanced liver dysfunction might be candidates for IO therapy if selective treatments are
being considered or if patient is a transplant candidate.
b. Secondary liver cancer
(1) Liver function affected by prior systemic therapy and tumor burden
(a) Systemic therapies have negative impact on liver function.
(2) Typically evaluated by reviewing serum total bilirubin
(a) Serum albumin, platelets, and international normalized ratio (INR) are also important.
(3) Best candidates for IO therapies have normal liver functions.
4. Patient performance status
a. Assessed with the Eastern Cooperative Oncology Group (ECOG) system (3) (Table e-74.2)
(1) Better ECOG leads to better outcomes.
Table e-74.2 Eastern Cooperative Oncology Group Performance Status Classification
ECOG 0 Asymptomatic
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ECOG 1 Symptomatic (e.g., pain or fatigue) but completely ambulatory
ECOG 2 Symptomatic and unable to carry out work activities
ECOG 3 Symptomatic and spends >50% of day in bed
ECOG 4 Bedbound
ECOG 5 Death
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(2) IO treatment candidates have ECOG performance status ≤2.
(a) Patients should be out of bed >50% of the day.
b. Treatment history
(1) Primary liver cancer
(a) Most patients have not received HCC therapy.
(2) Secondary liver cancer
(a) Patients have typically had previous therapies.
i. Negatively impact performance status
ii. Negatively impacts liver function
1. Resection or external beam radiation
2. Systemic chemotherapies
(i) Fluorouracil (5FU): hepatotoxicity/nodular regenerative hyperplasia
(ii) 5FU and irinotecan: chemotherapy-associated steatohepatitis (CASH)
(iii) Oxaliplatin: hepatic sinusoidal obstruction/fibrosis
Patient Triage
1. Primary liver cancer (HCC)
a. Patients often treatment naive with few other treatment options
b. Tumor staged per the tumor, node, metastasis (TNM) system (4)
c. Most patients staged according to Barcelona Clinic Liver Cancer (BCLC) system (5)
(1) Utilizes CP score, ECOG status, and tumor burden
d. BCLC A patients (early disease)
(1) Curative therapies
(a) Transplant
i. Milan criteria (6)
1. One lesion <5 cm
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2. No greater than three tumors, all <3 cm
ii. Model for End-Stage Liver Disease (MELD) (7)
1. Baseline MELD: total bilirubin, creatinine, and INR
(i) Quantifies end-stage liver disease for transplant planning
(ii) Ranges from 9 (healthier) to 40 (gravely ill )
(iii) Online calculators available
2. MELD upgrade
(i) Automatic 22 points given for HCC >2 cm satisfying Milan criteria
(ii) Upgrade 3 points every 3 months (while within Milan) until transplanted
iii. Outcomes
1. 5-year survival >70%
2. Recurrence rate 5% to 15%
(b) Resection
i. Best candidates: CP A with normal portosystemic gradient and solitary tumor
ii. Outcomes
1. 5-year survival >70%
2. 5-year recurrence rate up to 80%
(c) Ablation
i. Best candidates have ≤3 tumors ≤3 cm in size.
1. Radiofrequency ablation considered gold standard
2. Ethanol ablation of value in small tumors (<2 cm)
3. Microwave employed for larger ablations or to mitigate heat sink effect
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ii. Outcomes
1. Similar to surgical resection
2. Preferred to resection when tumors ≤2 cm
e. BCLC B patients (intermediate disease)
(1) Conventional transarterial chemoembolization (cTACE) standard treatment based on prospective randomized
trials in 2002
(a) Radioembolization considered when more advanced tumor, including PVT
(b) Drug-eluting microsphere chemoembolization considered when more advanced liver disease
f. BCLC C patients (advanced disease)
(1) Sorafenib offers 2 to 3 months survival advantage over placebo.
(2) Radioembolization has comparable outcomes to Sorafenib.
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g. BCLC D patients (terminal disease)
(1) Hospice/supportive care
2. Secondary liver cancer
a. Candidates for IO therapy should have liver-only or liver-dominant disease.
(1) Prognosis worsens in these patients once metastatic disease identified.
(2) Patients typically have had prior therapies, and they have other treatment options.
b. mCRC
(1) Surgical resection for those with limited disease
(a) Ablation considered for those who are not operative candidates
(b) Portal vein embolization may facilitate resection if otherwise a surgical candidate but has a small future liver
remnant.
(2) Systemic therapy is the standard of care for first- and second-line treatment.
(a) FOLFOX—folinic acid, fluorouracil, oxaliplatin
(b) FOLFIRI—folinic acid, fluorouracil, irinotecan
(c) Median survival 20 to 24 months (first line) and 10 to 11 months (second line)
(d) Targeted agents
i. Bevacizumab is a vascular endothelial growth factor (VEGF) inhibitor that is combined with first- or second-line
therapy.
ii. kRAS (wild-type) tumors are susceptible to Cetuximab.
(3) Intra-arterial therapy
(a) Radioembolization in the salvage setting (failing FOLFOX and FOLFIRI)
i. Median survival 8 to 14.5 months
(b) Drug-eluting microspheres with irinotecan being evaluated
(c) Future direction
i. Combining radioembolization with first- or second-line chemotherapy
c. Metastatic neuroendocrine cancer
(1) Heterogeneous group of tumors/patients
(a) Originate in neural and endocrine structures
(b) Second or third originate in the gastrointestinal tract
(2) World Health Organization (WHO) classification system and suggested grading (8)
(a) Mitotic count and Ki-67 index
i. Low grade (Ki-67 index ≤2%)
ii. Intermediate grade (Ki-67 index 3% to 20%)
iii. High grade (Ki-67 index >20%)
(3) Treatment and prognosis based on staging
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(a) Low/intermediate grade
i. Curative surgery and/or debulking when possible
ii. Somatostatin analogues
iii. Targeted radiotherapy
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iv. Liver-directed (intra-arterial) therapy
1. Employed for progressive, bulky, or symptom-producing disease
(b) High grade
i. Chemotherapy
Patient Follow-up
1. All patients should be seen in follow-up to IO therapies.
a. Follow-up typically within 1 month of treatment
b. Clinical, imaging, and serologic assessment appropriate
2. Assess/manage side effects and complications.
a. Side effects managed with supportive care
b. Complications recognized and managed appropriately
3. Assess response to treatment.
a. Imaging
(1) Size of treated tumor measured
(a) Response evaluation criteria in solid tumors (RECIST)
(b) WHO
(2) Necrosis
(a) Modified RECIST (mRECIST)—quantitative measure
(b) European Association for the Study of Liver Disease (EASL)—qualitative measure
(3) Metabolic response
(a) PET imaging (when applicable)
(b) Magnetic resonance (MR) diffusion-weighted imaging
b. Serum tumor marker reduction (when applicable)
(1) HCC—alpha-fetoprotein (AFP)
(2) mCRC—carcinoembryonic antigen (CEA)
(3) Neuroendocrine—chromogranin A, serotonin, gastrin
4. Triage patients into appropriate next stages of management
a. Surveillance
b. Other appropriate treatment options
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5. Communication with referring physician(s)
a. Coordination of further treatment and/or continued surveillance
References
1. Bruix J, Sherman M; for the American Association for the Study of Liver Diseases. Management of
hepatocellular carcinoma: an update. Hepatology. 2011;53(3):1020-1022.
2. Cholongitas E, Papatheodoridis GV, Vangeli M, et al. Systematic review: the model for end-stage liver
disease—should it replace Child-Pugh's classification for assessing prognosis in cirrhosis? Aliment
Pharmacol Ther. 2005;22(11-12):1079-1089.
3. Oken MM, Creech RH, Tormey DC, et al. Toxicity and response criteria of the Eastern Cooperative
Oncology Group. Am J Clin Oncol . 1982;5(6):649-655.
4. Yao FY, Bass NM, Ascher NL, et al. Liver transplantation for hepatocellular carcinoma: lessons from the
first year under the Model of End-Stage Liver Disease (MELD) organ allocation policy. Liver Transpl .
2004;10(5):621-630.
5. Llovet JM, Fuster J, Bruix J. The Barcelona approach: diagnosis, staging, and treatment of hepatocellular
carcinoma. Liver Transpl . 2004;10(suppl 2):S115-S120.
6. Mazzaferro V, Regalia E, Doci R, et al. Liver transplantation for the treatment of small hepatocellular
carcinomas in patients with cirrhosis. N Engl J Med. 1996;334(11):693-699.
7. Kamath PS, Kim WR; for the Advanced Liver Disease Study Group. The model for end-stage liver disease
(MELD). Hepatology. 2007;45(3):797-805.
8. van Essen M, Sundin A, Krenning EP, et al. Neuroendocrine tumours: the role of imaging for diagnosis
and therapy. Nat Rev Endocrinol . 2014;10(2):102-114.
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e-75
Cancer Imaging for Interventional Radiologists
Ajay K. Singh
Rathachai Kaewlai
Interventional oncology is a rapidly emerging subfield within interventional radiology. Many interventional
radiologists are familiar with indications, contraindications, and techniques of diagnostic and therapeutic
procedures for patients with cancer. However, it is crucial for interventional radiologists to incorporate cancer
imaging into their practice because this can improve diagnostic accuracy, guide interventions, and enhance the
quality of consultation with referring physicians. This chapter provides an overview of imaging for common
cancers in the thorax and abdomen (solid organ), which interventional radiologists are most likely to encounter.
Lung Cancer
1. Lung cancer is the leading cause of cancer mortality, accounting for 25% of all cancer deaths in the United
States (1). There are two forms of lung cancer: small-cell and non-small cell lung cancer (NSCLC). NSCLC
accounts for approximately 75% of all lung cancers. Patients with NSCLC commonly present with local symptoms
caused by the primary tumor, in contrast with those of small-cell carcinoma who frequently present with extensive
locoregional spread and metastasis.
a. Chest radiography is usually the first-line imaging exam performed in patients suspected of having lung
cancer.
b. Chest computed tomography (CT), including scans through the adrenal glands, is the current standard for
staging newly diagnosed lung cancers. Magnetic resonance imaging (MRI) may be utilized in patients with
symptoms of Pancoast (apical) tumor, chest wall invasion, or spinal canal involvement.
c. Positron emission tomography (FDG-PET) is U.S. Food and Drug Administration (FDA)-approved for the
workup of lung cancer. It is useful to detect abnormalities not seen on CT, thereby improving staging.
d. Low-dose computed tomography (LDCT) has emerged as a reasonable screening tool for lung cancer, which
has shown to reduce lung cancer and all-cause mortality in at-risk individuals. In the National Lung Screening
Trial (NLST), LDCT reduced lung cancer-specific mortality by 20% (compared with those who had chest
radiography) at the expense of a high false positivity rate (24%). Individuals who might benefit from screening,
according to the NLST are of age 55 to 74 years, asymptomatic current or former smokers without prior history of
lung or other cancers (2).
2. Typical presentations of NSCLC on imaging studies include solitary pulmonary nodule/mass, central mass,
malignant pleural effusion, and metastasis. Approximately 20% to 30% of lung cancers present as solitary
pulmonary nodules (SPN) (3). Indicators of malignancy of SPN are size >3 cm and spiculated margins, although
malignant nodules can be small and have smooth margins. The presence of a cavity and lobulation cannot be
used to discriminate benign from malignant SPNs. Central tumors often present as a hilar mass, with distal lung
volume loss from collapse or consolidation. CT with contrast administration can be used to distinguish an
obstructing central tumor from distal collapse. Collapsed lung typically demonstrates avid enhancement, whereas
tumor enhancement is relatively minimal. Tumors may invade visceral pleura, chest
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wall, diaphragm, pericardium, main bronchus, or other mediastinal structures. Nodal metastasis may involve
ipsilateral peribronchial, hilar, mediastinal, or subcarinal lymph node groups and extends to the contralateral side
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in a later stage. NSCLC staging is based on tumor, node, metastases (TNM) classification, which has
therapeutic and prognostic implications.
3. Further management of an SPN depends on its size (<8 mm, ≥8 mm), morphology (solid, part-solid, nonsolid),
and clinical probability of malignancy. Serial CT follow-ups, positron emission tomography (PET), nonsurgical
biopsy, and surgical diagnosis are potential options (4).
4. Adenocarcinoma in situ and minimally invasive adenocarcinoma (formerly known as bronchioloalveolar
carcinoma [BAC]) are subtypes of adenocarcinoma (Fig. e-75.1). In contrast to other types of adenocarcinoma
that tend to invade and destroy lung parenchyma, they spread along the alveolar/bronchiolar wall framework (a
pattern called “lepidic growth”). They most commonly present as a solitary nodule, which may have ground-glass
appearance and may contain bubbly lucencies. Therefore, tumors have a very good prognosis when localized.
However, they may present with diffuse/multifocal consolidations or nodules.
5. Small-cell lung cancers usually present as central tumors. Tumors tend to occur at the main or lobar bronchi
with extensive peribronchial invasion and a large hilar or parahilar mass. Extensive mediastinal and hilar
lymphadenopathy is common. Small-cell lung cancer has a poor prognosis because most patients present with
metastasis at the time of diagnosis.
6. Radiofrequency ablation of lung cancer is generally used for early-stage cancers that are less than 3 cm in
diameter and few in number (one or two). It can also be used for pulmonary metastases and in patients who
refuse surgery or are poor surgical candidates.
FIGURE e-75.1 • Bronchogenic carcinoma. Axial CT shows a speculated nodule (arrowhead) located centrally in
the right upper lobe.
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Hepatocellular Carcinoma
1. Hepatocellular carcinoma (HCC) (Fig. e-75.2) is the most common primary malignancy of the liver that usually
occurs in patients with chronic liver disease such as cirrhosis, hemochromatosis, and glycogen storage disease.
In the United States, there has been an increasing incidence of HCC within the past 20 years, probably related
to chronic hepatitis C infection. HCC usually occurs in the sixth to seventh decades of life, or earlier in high-
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incidence areas such as Japan.
There are three major patterns of growth of HCC: solitary mass, multifocal masses, and diffusely infiltrating
mass. The diffuse infiltrative form may be difficult to diagnose especially in an underlying dysmorphic (cirrhotic)
liver.
a. On unenhanced CT, HCC is usually iso- or hypodense compared to the liver. With contrast administration, a
typical HCC enhances during the arterial phase and demonstrates rapid washout in venous phase with tumor
heterogeneity due to necrosis or hemorrhage. HCC has a propensity to invade adjacent vascular structures,
especially portal veins, resulting in hepatic vascular occlusion and abnormal hepatic perfusion (5).
b. On ultrasound, it usually has mixed echogenicity with or without a thin hypoechoic capsule. Tumor
hypervascularity may be demonstrated on color Doppler ultrasound.
c. On MRI, appearances of HCC are variable, but a typical lesion demonstrates T1 hypointensity, T2
hyperintensity, restricted diffusion, arterial enhancement, and rapid venous washout. With hepatobiliary-specific
contrast agent, a typical HCC demonstrates no uptake during the hepatobiliary phase (6).
2. Major differential diagnoses of HCC on imaging include nodular regenerative hyperplasia (regenerating
nodules), dysplastic nodule, cholangiocarcinoma, hypervascular metastasis, focal nodular hyperplasia (FNH),
and small hepatic hemangioma.
a. Imaging clues to the diagnosis of HCC include presence of background hepatic cirrhosis, enhancement during
the arterial phase of CT or MRI, rapid
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venous washout, lack of uptake on hepatobiliary phase MRI, satellite lesions, presence of lymphadenopathy, and
portal vein invasion.
FIGURE e-75.2 • Hepatocellular carcinoma. A: Postcontrast T1-weighted sequence shows an enhancing right
hepatic mass lesion (arrowhead) with direct extension into right portal vein (curved arrow). (continued)
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FIGURE e-75.2 • (Continued) B: Coronal CT reformation demonstrates a large right hepatic mass (arrowheads)
with portal vein thrombus (curved arrow) in a patient with cirrhosis. There is also mass (straight arrow) in the
lower chest wall from needle tract seeding.
b. Nodular regenerative hyperplasia and dysplastic nodules may be difficult to differentiate from HCC, although
they tend to be more homogeneously enhanced than HCC and show uptake of the hepatocyte-specific agent.
c. Cholangiocarcinoma is hypovascular and often demonstrates biliary ductal dilatation and may show adjacent
capsular retraction (if peripherally located) and delayed enhancement.
d. FNH typically has a signal characteristic similar to an adjacent liver tissue on unenhanced and delayed scans,
strong arterial enhancement, and uniform uptake of hepatocyte-specific agent.
3. Radiofrequency ablation of HCC is a useful treatment option (see Chapter 56) for patients who are not ideal
surgical candidates, refuse surgery, have recurrent tumors, or do not respond to conventional therapies.
Typically, liver tumors less than 3 cm in diameter and three or fewer in number respond best to radiofrequency
ablation. Radiofrequency ablation has been widely used for colorectal cancer metastases to the liver.
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Hepatic Metastasis
1. Metastasis is the most common malignancy of the liver and most frequently arises from colon, stomach,
pancreas, breast, and lung neoplasm. In children, liver metastases are commonly from neuroblastoma and Wilms
tumor. The natural history and prognosis depends on the primary tumor site (7).
Hepatic metastases are usually multiple, involving both lobes of the liver. They may be solitary, multiple, or
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diffusely infiltrative. The most common appearance of hepatic metastasis is multiple, well-defined lesions of
varying size from few millimeters to centimeters. CT is considered the preferred imaging method for the diagnosis
of hepatic metastasis. MRI is indicated as a problemsolving technique, or when CT is contraindicated. Imaging,
either with CT or MRI, during the portal venous phase of enhancement is essential for detection of most
metastases.
a. Hepatic metastases are commonly hypodense on contrast-enhanced CT.
b. On ultrasound, hepatic metastases are commonly hypoechoic.
c. On MRI, they are typically hypointense on T1-weighted images (T1-W) and hyperintense on T2-weighted
images (T2-W) with varying degrees of enhancement.
d. When hypervascular metastases are suspected, hepatic arterial phase CT/MRI images should be obtained
(8). Hypervascular metastasis demonstrates marked enhancement in late arterial phase images. Primary tumors
that may produce hypervascular metastasis include islet cell tumor, carcinoid tumor, thyroid, renal cell carcinoma,
and pheochromocytoma. Hypovascular metastasis is commonly due to primary epithelial malignancy. It shows
low attenuation center with rim enhancement.
e. Cystic metastasis is demonstrated as a hypodense mass with fluid attenuation containing mural nodules,
thickened wall, or septa. It is usually seen with metastasis from cystadenocarcinoma or sarcoma.
f. Hepatic metastases containing calcifications are usually due to mucinous adenocarcinoma, teratoma, or
treated disease.
g. For initial evaluation of colorectal liver metastasis that has many available local treatment options including
ablation, surgery, and chemotherapy, MRI is preferred to CT as the first-line imaging method because it provides
highest detection rate even for lesions smaller than 10 mm (9).
2. Chemoembolization and/or ablation of liver metastases may be an option for selected patients.
Renal Cell Carcinoma

1. Renal cell carcinoma (RCC) (Fig. e-75.3) is the most frequent malignant tumor of the kidneys, accounting for
85% of primary renal malignancies in adults. It is a tumor of the tubular epithelium, typically centered in the renal
cortex. It is usually unilateral but can be multifocal within the same kidney. About half of the patients are
asymptomatic when RCC is found incidentally on cross-sectional imaging.
RCC may invade the renal collecting system, simulating transitional cell carcinoma, and may cause
subcapsular/perinephric hemorrhage. Venous invasion is not uncommon, typically to the renal veins and inferior
vena cava. A tumor thrombus is distinguished from a bland thrombus by the presence of enhancement and
expansion of vascular lumen.
2. CT and MRI are both appropriate modalities for the detection and characterization of RCC.
a. On CT, the appearance of RCC ranges from a complex cyst to a solid, enhancing mass centered in the renal
cortex. If large, it may bulge the renal contour. Contrast enhancement is heterogeneous in large tumors,
homogeneous in small tumors, and typically less than that of adjacent renal parenchyma.
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FIGURE e-75.3 • Renal cell carcinoma. Contrast-enhanced CT shows a solid enhancing mass (straight arrow)
arising from the right kidney.
b. On MRI, RCC is usually isointense to renal parenchyma on T1-W and iso- to hyperintense on T2-W. The out
of phase may show loss of signal intensity due to cytoplasmic fat in the tumor. Enhancement characteristics on
MRI is similar to that of CT (10).
3. Major differential diagnoses for RCC are oncocytoma, metastasis, minimal-fat angiomyolipoma, lymphoma,
transitional cell carcinoma, and abscess. Most of these lesions are not distinguishable from RCC by imaging
alone. It should be noted that small, solid enhancing lesions in the renal parenchyma should be presumed to
represent RCC until proven otherwise. Patients with renal metastasis or lymphoma usually have primary disease
outside the kidneys. Transitional cell carcinoma usually presents on imaging as an infiltrating mass centered in
the renal pelvis. Patients with renal abscess may present with signs of infection.
4. Image-guided biopsy is performed for type III Bosniak cysts, metastases, lymphoma, or prior to radiofrequency
ablation. Radiofrequency ablation results are best for an RCC less than 3 cm in diameter, located away from the
renal hilum or major vessels.
Adrenal Metastasis
1. The adrenal gland is a common site of metastatic disease (Fig. e-75.4). Adrenal metastasis is often clinically
silent; however, large adrenal metastasis may produce adrenocortical insufficiency. The most frequent sites of
the primary malignancy include lung, breast, skin (melanoma), thyroid, kidney, and colon.
In patients with known malignancy, the differential diagnoses of adrenal soft tissue mass include adenoma and
metastasis. CT (with and without contrast) or MRI with in- and out-of-phase imaging can be utilized to distinguish
between the two entities.
a. Characteristics of adrenal metastasis on CT are well-defined, solid adrenal mass with soft tissue attenuation.
The mass may be round, oval, or irregular
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in shape and unilateral or bilateral in location. Large masses may contain internal necrosis or hemorrhage,
resulting in heterogeneous density. Density measurement of an adrenal mass of less than 10 HU is definitive of a
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lipidrich adenoma. On contrast-enhanced CT, adrenal metastasis is distinguished from adenoma by prolonged
washout of contrast. The washout value of less than 60% after 15 minutes (or less than 52% after 10 minutes) of
contrast administration indicates metastasis or atypical adenoma (11).
FIGURE e-75.4 • Adrenal metastases. A: Contrast-enhanced CT shows bilateral adrenal metastases (straight
arrows) from melanoma. B: Coronal CT reformation shows bilateral adrenal metastases (straight arrows) from
bronchogenic carcinoma.
b. On MRI, adrenal metastasis may have variable signal intensity based on its component. Metastasis with
internal hemorrhage or necrosis shows heterogeneous intensity on both T1-W and T2-W; metastasis without
hemorrhage or necrosis is homogeneous hypointense on T1-W and hyperintense on T2-W. Metastasis from
malignant melanoma has a characteristic high intensity on T1-W and T2-W. Fat-suppressed T1-W and out-of-
phase imaging provides differentiation of fat-containing adenoma from other adrenal masses (11).
Pancreatic Cancer
1. Pancreatic adenocarcinoma is the most common primary malignant tumor of the exocrine pancreas,
accounting for 75% of all pancreatic tumors (Fig. e-75.5). It is one of the most lethal cancers despite continued
efforts for early diagnosis and improvement in treatment options. CT is recommended as the first diagnostic
method to detect and stage pancreatic cancer, prior to endoscopic retrograde cholangiopancreatography
(ERCP). This is because of the ability of CT to show the biliary tree and pancreas, without obscuration from the
instrumentation in the bile duct. Pancreatic cancer is most frequently located at the head, neck, or uncinate
process of the pancreas, followed by body and tail (12). The average size, at the time of diagnosis, is about 2 to
3 cm.
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a. Typical CT findings on early phase of enhancement include an irregular, poorly defined, hypodense
pancreatic mass with obstruction of the pancreatic and/or common bile duct. Pancreatic cancer is usually less
enhanced than the remaining pancreas. In some cases, there may be focal enlargement,
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contour abnormality, or a focal loss of normal fat replacement of the pancreas suggestive of an underlying tumor.
Pancreatic and biliary ductal dilatation (double duct sign) serves as a secondary sign of obstructive pancreatic
head tumor. Even in the absence of visible tumor on CT, isolated pancreatic ductal dilatation at the body or tail
with parenchymal atrophy should raise a concern for an obstructing cancer. CT may show evidence of tumor
extension beyond the pancreas, vascular involvement, nodal, and hepatic metastasis.
FIGURE e-75.5 • Pancreatic carcinoma. Contrast-enhanced CT shows a large unresectable pancreatic mass
(straight arrow) involving the pancreatic body with invasion of the fat planes around the celiac artery
(arrowhead).
b. MRI, with magnetic resonance cholangiopancreatography (MRCP), is a valuable method to diagnose and
evaluate patients with pancreatic cancer. The pancreatic neoplasm is usually hypointense on T1-W and variable
intensity on T2-W. Lesions may be more conspicuous on fat-suppressed T1-W. On contrast-enhanced dynamic
MRI, pancreatic cancer has enhancement characteristics similar to that on CT. MRCP allows an evaluation of
level and degree of ductal obstruction (13).
2. These patients are often referred to interventional radiology for the management of biliary obstruction (see
Chapter 52).
References
1. Edwards BK, Noone AM, Mariotto AB, et al. Annual report to the nation on the status of cancer, 1975-
2010: featuring prevalence of comorbidity and impact on survival among persons with lung, colorectal,
breast, or prostate cancer. Cancer. 2014;120:1290-1314.
2. Aberle DR, Adams AM, Berg CD, et al. Reduced lung-cancer mortality with low-dose computed
tomographic screening. N Engl J Med. 2011;365:395-409.
3. Viggiano RW, Swensen SJ, Rosenow EC III. Evaluation and management of solitary and multiple
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pulmonary nodules. Clin Chest Med. 1992;13:83-95.
4. Gould MK, Donington J, Lynch WR, et al. Evaluation of individuals with pulmonary nodules: when is it lung
cancer? Diagnosis and management of lung cancer, 3rd ed: American College of Chest Physicians evidence-
based clinical guidelines. Chest. 2013; 143:e93S-e120S.
5. Murakami T, Kim T, Hori M, et al. Double arterial phase multi-detector row helical CT for detection of
hypervascular hepatocellular carcinoma [letter]. Radiology. 2003; 229(3): 931-932.
6. Baron RL, Peterson MS. From the RSNA refresher courses: screening the cirrhotic liver for hepatocellular
carcinoma with CT and MR imaging: opportunities and pitfalls. Radiographics. 2001;21:S117-S132.
7. Baker ME, Pelley R. Hepatic metastases: basic principles and implications for radiologists. Radiology.
1995;197:329-337.
8. Kanematsu M, Kondo H, Goshima S, et al. Imaging liver metastases: review and update. Eur J Radiol .
2006;58:217-228.
9. Ahn SS, Kim MJ, Lim JS, et al. Added value of gadoxetic acid-enhanced hepatobiliary phase MR imaging
in the diagnosis of hepatocellular carcinoma. Radiology. 2010;255:459-466.
10. Pedrosa I, Sun MR, Spencer M, et al. MR imaging of renal masses: correlation with findings at surgery
and pathologic analysis. Radiographics. 2008;28:985-1003.
11. Blake MA, Cronin CG, Boland GW. Adrenal imaging. AJR Am J Roentgenol . 2010;194: 1450-1460.
12. Tempero MA, Arnoletti JP, Behrman SW, et al. Pancreatic adenocarcinoma, version 2.2012: featured
updates to the NCCN guidelines. J Natl Compr Canc Netw. 2012;10: 703-713.
13. Barish MA, Soto JA. MR cholangiopancreatography: techniques and clinical applications. AJR Am J
Roentgenol . 1997;169:1295-1303.
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e-76
Pediatric Angiography
Manraj K.S. Heran
Preprocedural Preparation (1)

1. Elective procedures can be performed safely with a platelet count of >50,000 per μL, prothrombin time (PT)
<18 seconds, partial thromboplastin time (PTT) <32 seconds, and international normalized ratio (INR) <1.2, with
an INR <1.5 preferred for urgent cases.
2. Preprocedural antibiotic prophylaxis is rarely indicated (there may be exceptions, including children with
cardiac shunts, those with suspected infection in whom foreign bodies such as embolization coils will be
implanted, as well as end-organ embolization procedures with a potential for abscess formation).
3. Preprocedural assessment should include recording the child's height and weight.
4. Very young patients, those undergoing lengthy diagnostic and interventional procedures, including those
requiring intermittent breath holds, will likely require more aggressive sedation and possibly general anesthesia
via laryngeal mask or endotracheal intubation.
5. Maintain appropriate homeostatic and monitoring environment during the arteriographic procedure. Young
children, especially those under 2 years of age, are very susceptible to ambient temperature changes.
Therefore, temperature monitoring is recommended.
Procedure (1)
Pediatric vessels are often superficial, especially in the neonate or young infant, with the arteries much straighter
and having very little or no intrinsic vascular disease. Pediatric vessels tend to occlude more easily, primarily due
to the larger catheter-to-vessel ratio, especially in children <15 kg, coupled with a greater occurrence of
vasospasm and dissection. Lack of vessel tortuosity makes intraarterial navigation straightforward.
1. The standard arterial site is the common femoral artery. Uncommonly, other sites and approaches may be
required, including axillary, brachial, and umbilical access.
2. Use of ultrasound guidance is strongly advocated for obtaining access.
3. Dermatotomy should be done carefully to avoid injury to the vasculature which may lie immediately beneath
the skin.
4. Guidewire advancement should be effortless and is best monitored under fluoroscopy.
5. Micropuncture systems in both 4 Fr. and 5 Fr. are readily available and allow easy conversion of 0.018-in.
access to 0.035-in. or 0.038-in. guidewire systems.
6. Expert opinion advocates routine use of vascular sheaths, especially if several catheter exchanges, multiple
manipulations, or interventional procedures are expected.
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7. The smallest catheter that can accomplish the objectives of the study should be used. In most diagnostic
cases, 4 Fr. can be used for those >10 kg and 3 Fr. catheters are now increasingly available for those <10 kg.
8. Dedicated pediatric-length catheters are now available, as adult-type preshaped catheters may not have the
appropriate configuration or curvature for pediatric arteriography.
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9. Intraprocedural systemic heparinization can prevent vascular thrombosis, and its use is well accepted,
especially in arteriography performed on infants <10 to 15 kg. This is typically administered as a 75 to 100 IU per
kg intravenous (IV) bolus dose once vascular access is obtained.
10. As the younger child and infant are prone to volume overload and contrast nephrotoxicity, volume of injected
contrast medium and flush must be carefully monitored.
11. Tailoring the size of the syringes used during the case to the size of the patient can aid in minimizing
inadvertent phlebotomy or fluid overload.
12. Contrast dose should be limited to 4 to 5 mL per kg for neonatal arteriography, whereas 6 to 8 mL per kg
should be regarded as the maximum volume for pediatric patients beyond this age.
1. Manual compression of arterial puncture site for 10 minutes which does not obliterate the pulse
2. All attempts at manual hemostasis should be done gently. Avoid prolonged occlusive pressure to ensure
maintenance of perfusion to the distal extremity and to minimize the possibility of thrombosis of the access artery.
3. Generally speaking, use of closure devices is not recommended especially in infants and small children.
Complications
Although complications are not common during pediatric diagnostic arteriography, they can still occur
primarily in patients weighing less than 15 kg.
1. The most common adverse events are complications at the site of access, which are predominantly
vascular and are primarily in the neonate or infant population.
2. The risk of vascular access complication is proportional to sheath size, number of examinations, and
patient age.
3. The risk of thrombosis is higher in general, in the pediatric population, even greater in patients <15 kg
and in those where arterial interventions are performed using larger sheaths.
Prevention and Management of Complications

1. Ultrasound-assisted arterial access guidance decreases the number of attempts required and lessens
puncture site complications.
2. As return of palpable pulses distally can be a false indicator of vessel patency (due to vigorous collateral
vessel reconstitution of distal pulses), rapid determination of vasospasm versus access site thrombosis may
be made by duplex ultrasonography. Further management strategies are outlined elsewhere.
3. This is typically continued until pulses return or for 24 hours.
References
1. Heran MK, Marshalleck F, Temple M, et al. Joint quality improvement guidelines for pediatric arterial
access and arteriography: from the Societies of Interventional Radiology and Pediatric Radiology. J Vasc
Interv Radiol. 2010;40(2):237-250.
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Tables
Table e-76.1 Methods to Reduce Pediatric Patient Radiation
1. Minimization of total fluoroscopy exposure and arteriography run times
2. Progressive pulse fluoroscopy
3. Last image hold
4. Use of roadmapping
5. Use of filters
6. Appropriate shielding (including gonadal protection and other regions)
7. Optimal coning/collimation
8. Reduction in distance between the image receptor and the patient (reducing scattered radiation)
9. Optimally increase source-to-skin distance
10. Removal of grid when imaging neonates and small infants (for nondigital angiography units)
11. Use of digital magnification
12. Optimize patient cooperation (appropriate sedation, immobilization, distraction, etc.)
Table e-76.2 Warming Strategies for Procedures in Small Children
Conservation
Increase room temperature
Warm blankets
Plastic (cling) wrap
Convection
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Radiant heat from warming lamp
Warm air flow (Bair Hugger, Arizant Inc, East Prairie, MN)
Conduction
Warm saline bags
Chemical warming blanket (TransWarmer, Cooper Surgical Inc, Trumbull, CT)
Table e-76.3 Pediatric Contrast Allergy Oral Premedication Protocol
Number of Maximum
Medication Dosage Doses Timing Dose
Prednisone 0.5 3 13, 7, and 1 hr before 50 mg/dose

mg/kg procedure
Diphenhydramine 1.25 1 1 hr 50 mg
mg/kg
Table e-76.4 Common Medications Used during Arteriography
Medication Dose Indication
Nitroglycerin (glyceryl 1-3 μg/kg/dose IA, repeated up to 3 times Treatment of vasospasm

trinitrate)
Heparina 75-100 IU/kg IV Prevent arterial

thrombosis
Protamine 10 mg IV/1,000 IU heparinb Heparin reversal agent
Glucagon 20-300 μg/kg IV/IA (neonates) Decreases bowel motility

20-100 μg/kg, max 1 mg
Papaverine 1 mg/kg IA Treatment of vasospasm
Lidocaine 0.5 mL/kg (5 mg/kg) 1% (without Local anesthesia

epinephrine)
0.7 mL/kg (7 mg/kg) 1% (with
epinephrine)
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Bupivacaine 1 mL/kg (2.5 mg/kg) 0.25% Local anesthesia
IA, intra-arterial.
aTypically recommended when performing angiography on children <15 kg.
bDosing is often adjusted allowing for the half-life of administered heparin dose.
Table e-76.5 Injection Parameters (Suggested Rate in Milliliter per Second for Total Volume
in Milliliter) by Location and Patient Weight
Artery Patient Weight (in kg)
<10 10-20 20-50 >50
Aorta a 5-10 for 8-15 10-20 for 20-40 20-25 for 25-50
Celiac a 2-3 for 10-20 3-5 for 15-30 5-8 for 30-60
Splenic a 2-3 for 10-15 3-5 for 15-20 5-8 for 20-50
Hepatic a 2-3 for 5-10 3-5 for 10-15 5-8 for 15-25
SMA a 2-3 for 10-15 3-5 for 15-30 5-8 for 30-50
IMA a a 1-3 for 6-9 2-3 for 10-15
Renal a 2-4 for 3-5 3-5 for 6-9 5-8 for 10-15
Adrenal a a a a
Subclavian a 2-3 for 4-6 3-4 for 6-15 5-8 for 15-25
Common carotid a 2-3 for 3-5 4-6 for 5-10 6-8 for 10-15
Internal carotid a 1-2 for 3-5 2-4 for 5-8 4-5 for 6-10
External carotid a a a 2-3 for 6-9
Vertebral 2-5 for 4-6 4-7 for 6-9

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a a
SMA, superior mesenteric artery; IMA, inferior mesenteric artery.
aHand injection is recommended.
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e-77
Bronchial Artery Embolization
Manraj K.S. Heran
Bronchial artery embolization (BAE) was first reported in 1973 by Remy et al. as a treatment option for massive
and life-threatening hemoptysis (1). In 90% of the cases of massive hemoptysis, the culprit vascular bed is the
bronchial circulation rather than the pulmonary (5%) or nonbronchial systemic circulations (5%) (1,2,3). BAE is a
safe and extremely effective therapeutic option because, unlike surgery, BAE preserves pulmonary function.
Most patients with massive hemoptysis have poor pulmonary function, and they tend to be poor surgical
candidates. In addition, surgery carries a mortality rate of 7.1% to 18.2%, this increases to about 40% when
surgery is performed as an emergency (4).
Indications
1. BAE is considered first-line treatment for most cases of massive hemoptysis.
a. Life-threatening hemoptysis is defined as:
(1) Bleeding of 300 mL in 24 hours, or
(2) 100 mL daily for at least 3 days, or
(3) Minor bleeding with hemodynamic instability (5)
b. Most commonly, these patients suffer from diffuse interstitial lung disease, lung infection, or chronic
granulomatous disease.
c. Conditions associated with hemoptysis include:
(1) Cystic fibrosis
(2) Tuberculosis
(3) Bronchiectasis
(4) Interstitial pulmonary fibrosis
(5) Fungal infections such as aspergillosis
(6) Ruptured bronchial artery aneurysm
(7) Arteriovenous fistulae
(8) Neoplasms
(9) Behçet disease
(10) Cryptogenic
Contraindications
Absolute
None
Relative
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a. Uncorrectable coagulopathy
b. Renal insufficiency
c. Documented prior serious contrast reaction (see Chapter 64)
2. Presence of a major radiculomedullary artery (i.e., supply to the spinal cord) from the target artery is
considered a contraindication by some interventionalists, but others advocate embolization if a
microcatheter can be negotiated safely beyond the vessel of concern (6).
3. Congenital pulmonary artery stenosis (CPAS). In patients with CPAS, the bronchial circulation may
provide essential pulmonary parenchymal perfusion. Pediatric cardiology consultation is imperative before
BAE (3).
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1. Resuscitation
In the setting of life-threatening hemoptysis, it is essential to stabilize the patient's condition with measures
including:
a. Protecting the airway by keeping the bleeding side dependent, selective intubation of the uninvolved lung, and
use of a dual lumen tube to ventilate the lungs separately
b. Optimizing oxygenation
c. Correct underlying hypotension, coagulopathy, and electrolyte imbalance as needed.
2. Preprocedure assessment
a. Chest x-ray (CXR) may help in diagnosing and localizing an underlying source. CXR is a quick, noninvasive,
and widely available first step that can be diagnostic in 50% of cases (7).
b. Computed tomography (CT)/computed tomographic angiography (CTA) is the cornerstone of diagnosis. It is
likely to define the causative etiology and the location and the extent of the underlying pathology. CTA delineates
the origin and the course of both the bronchial and nonbronchial systemic arteries. Reconstructed images can
aid in a more thorough characterization of the thoracic vascular anatomy (8,9).
c. Bronchoscopy was considered the primary method for the diagnosis and localization of hemoptysis. Many
researchers currently suggest it may be less useful due to low detection rates because of excessive blood in the
bronchi and little added information to CT. In addition, the procedure is not without risk and may delay definitive
therapy (5).
a. Automated blood pressure
b. Electrocardiogram (ECG) and pulse oximetry
c. Ensure large-bore intravenous (IV) access and maintain fluid resuscitation.
Procedure
1. Moderate sedation is adequate for most patients. Although endotracheal intubation and general
anesthesia may be required, many patients experiencing hemoptysis requiring BAE have poor respiratory
function so this should be evaluated on a case-by-case basis.
2. Standard sterile preparation of groin area
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3. Obtain common femoral artery access with a 5 Fr. vascular sheath. A 4 Fr. vascular sheath can be used
in younger patients.
4. A 5 Fr. pigtail catheter is often used to perform descending thoracic aortography in the anteroposterior
projection, with the images carefully evaluated to determine the number and origin sites of the bronchial
arteries and detection of nonbronchial systemic arteries. This may not be necessary if preprocedure CTA
has been performed.
5. The pigtail catheter is exchanged for a 5 Fr. selective catheter (e.g., Mickelson or Special, Cook Medical
Inc, Bloomington, IN), and the descending thoracic aorta is interrogated for bronchial arteries in the vicinity
of the left mainstem bronchus on the frontal projection, between the T5 and T6 vertebra, starting on the
side of highest clinical suspicion.
6. Arterial abnormalities can include active extravasation, pseudoaneurysms/aneurysms, or most commonly,
abnormally increased vascularity (hypertrophy, tortuosity, and neovascularity) and shunting.
7. Anatomic considerations: Understanding anatomic variants of the bronchial circulation is critical to
technical success.
a. Bronchial circulation
(1) Four classic bronchial artery patterns have been described (Fig. e-77.1): two on the left and one on the
right (Type 1; 40%), one on the left and one
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on the right (Type 2; 21%), two on the left and two on the right (Type 3; 20%), and one on the left and two
on the right (Type 4; 9.7%) (2,10,11).
Radiology Books
FIGURE e-77.1 • Diagram illustrates the four most common patterns of bronchial artery anatomy. A: Type
1: single right bronchial artery, paired left bronchial artery. B: Type 2: single right bronchial artery, single
left bronchial artery. C: Type 3: paired right bronchial arteries, paired left bronchial arteries. D: Type 4:
paired right bronchial arteries, single left bronchial artery.
(2) Classically, there is a single right bronchial artery arising from an intercostal artery called an
“intercostobronchial trunk (ICBT),” and this comes from the posterolateral surface of the aorta. The left
bronchial as well as additional right bronchial arteries usually arise from the anterolateral surface.
(3) In one-third of cases, one bronchial artery can have an ectopic origin, most commonly from the caudal
surface of the aortic arch.
(4) Other sites of variant bronchial artery origin include costocervical, thyrocervical trunk, and the internal
mammary.
b. Nonbronchial circulation
(1) Common systemic sources include intercostal, thoracic, inferior phrenic, thyrocervical, vertebral, axillary,
subclavian, and internal mammary arteries (3).
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8. Coaxial microcatheters (e.g., Renegade [Boston Scientific, Natick, MA] and Progreat [Terumo Medical
Corp, Elkton, MD]) allow more secure purchase into the target bronchial artery, minimize the risk of
vasospasm, help avoid nontarget embolization of spinal cord arteries, and reduce the risk of reflux of
embolic agents into the spinal branches or aorta.
a. Special attention should be paid when negotiating an intercostobronchial trunk to manipulate the catheter
beyond the intercostal moiety that may give rise to a radiculomedullary branch to the anterior spinal artery.
When this artery is identified by angiography, extreme caution should be employed during injection of
particles to avoid reflux!
9. Nonbronchial systemic collaterals should be interrogated and treated concurrently. Early recurrence of
hemoptysis following a technically complete BAE of typically configured bronchial arteries should prompt
investigation of suspected systemic contribution.
10. Embolic choice and technique: There are several embolic materials currently available for BAE.
a. The two best studied are polyvinyl alcohol particles (PVA) (Contour, Boston Scientific, Natick, MA; Ivalon,
Cook Inc, Bloomington, IN; others) and Embosphere microspheres (Biosphere Medical, Rockland, MA).
b. The most common particle size ranges from 250 to 500 μm to prevent passage through
bronchopulmonary anastomoses, which may result in pulmonary infarction or systemic embolization.
c. Coil embolization of bronchial arteries should be avoided to preserve potential access for future BAE.
1. Intensive care unit (ICU) admission for patient with life-threatening hemoptysis. The length of ICU or hospital
admission depends on the patient's hemodynamic status and the presence of complications.
2. Routine postangiography care
a. Vital signs as per institutional routine
b. Access site inspected with each vital sign check
c. Pain control (e.g., acetaminophen)
d. Antiemetic therapy if needed (e.g., ondansetron)
3. Neurologic consultation when the patient exhibits any worrisome neurologic symptoms or signs
Results
1. Technical success is defined as the ability to visualize and catheterize the desired artery and deliver the
embolic agent until the flow is stopped. This is accomplished in more than 90% of cases (6).
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2. Clinical success
a. Massive hemoptysis can be successfully controlled through BAE in 98% of cases (1,12).
b. Recurrence rates can be highly variable, depending mainly on the etiology and the chronicity of
underlying disease.
c. Immediate recurrent hemoptysis in otherwise technically successful BAE indicates the need for repeat
catheter angiography with meticulous investigation for a nonbronchial systemic artery supply requiring
embolization.
d. Long-term recurrence is mainly due to recruitment of collateral vessels, recanalization of embolized
vessels, or progression of disease.
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Complications
1. General complications of angiography
a. Access site complications (e.g., hematoma, pseudoaneurysm, occlusion)
b. Contrast-related complications
2. Postembolization syndrome (e.g., pain, fever, nausea)
3. Specific complications
a. Spinal cord ischemia is the most serious complication associated with BAE, occurring in 1.4% to 6.5%
(1,2). This most feared complication results from nontarget embolization of the anterior spinal artery, which
courses along the anterior surface of the spinal cord and receives supply from up to eight anterior
segmental medullary arteries that have a characteristic “hairpin” configuration. The most prominent of these
is the artery of Adamkiewicz, which typically arises from an intercostal artery between T9 and T12 in 75% of
cases (left > right).
b. Dysphagia due to esophageal necrosis from embolization of esophageal branches, reported in 0.7% to
18.2%
c. Extremely rare complications—pulmonary infarction/transient cortical blindness (10)
References
1. Lorenz J, Sheth D, Patel J. Bronchial artery embolization. Semin Intervent Radiol . 2012; 29:155-160.
2. Yoon W, Kim JK, Kim YH, et al. Bronchial and nonbronchial systemic artery embolization for life-
threatening hemoptysis: a comprehensive review. Radiographics. 2002; 22:1395-1409.
3. Sidhu M, Wieseler K, Burdick TR, et al. Bronchial artery embolization for hemoptysis. Semin Intervent
Radiol . 2008;25:310-318.
4. Fernando HC, Stein M, Benfield JR, et al. Role of bronchial embolization in the management of
hemoptysis. Arch Surg. 1998;133:862-866.
5. Garcia-Olivé, Sanz-Santos J, Centeno C, et al. Results of bronchial artery embolization for the treatment of
hemoptysis caused by neoplasm. J Vasc Interv Radiol . 2014;25:221-228.
6. Valji K. Pulmonary and bronchial arteries. In: The Practice of Interventional Radiology: With Online Cases
and Videos. Philadelphia, PA: Elsevier; 2012:443-470.
7. Hirshberg B, Biran I, Glazer M, et al. Hemoptysis: etiology, evaluation, and outcome in a tertiary referral
hospital. Chest. 1997;112:440-444.
8. Savvidou D, Malagari K, Kampanarou M, et al. The role of multislice computed angiography of the
bronchial arteries before arterial embolization in patients with hemoptysis. Open J Med Imaging. 2014;4:133-
141.
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9. Yıldız AE, Arıyürek OM, Akpınar E, et al. Multidetector CT of bronchial and non-bronchial systemic
arteries. Diagn Interv Radiol . 2011;17:10-17.
10. Sopko DR, Smith TP. Bronchial artery embolization for hemoptysis. Semin Intervent Radiol . 2011;28:48-
62.
11. Morita Y, Takase K, Ichikawa H, et al. bronchial artery anatomy: preoperative 3D simulation with
multidetector CT. Radiology. 2010;255:934-943.
12. Cheng LF, Fung EPY, Hon TYW, et al. Bronchial artery embolization for acute massive haemoptysis:
retrospective study. J HK Coll Radiol . 2005;8:15-19.
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e-78
Tracheobronchial Stents
K. Pallav Kolli
Roy L. Gordon
Tracheobronchial stenosis can be treated by surgical resection and reanastomosis, balloon dilation, laser
therapy, or stenting (1,2,3). Surgical treatment of stenoses with end-to-end reanastomosis is only possible when
there is sufficient length of airway available and when the patient is in physical condition to survive repeat
surgery. Although endobronchial mechanical debulking and ablative techniques can successfully treat small
protrusions within the airway, they cannot effectively deal with circumferential lesions with long scarred
segments, with stenoses caused by extrinsic airway compression, with functional airway collapse, nor with
fistulae or air leaks. Expandable stents can be used in all these conditions.
Tubular silicone stents have been used to stent tracheobronchial stenosis; however, they have a thick wall that
reduces the cross-sectional diameter of the airway, are prone to migrate, and interfere with mucociliary
mechanisms leading to plugging of the stent with inspissated secretions. Expandable, bare metallic stents are
thinwalled and become incorporated into the bronchial wall or epithelialized, preventing migration and possibly
permitting ciliary activity to continue. Expandable metallic stents have other advantages. They offer a rapid and
effective means for opening narrowed airways, resulting in excellent relief of symptoms. Stents are well tolerated
by patients who become unaware of their presence shortly after placement. Expandable stents are delivered in
their nonexpanded state so that their delivery systems are of small caliber. They are generally flexible over-the-
wire systems allowing placement into second-order branches of the bronchial tree as well as into the trachea and
mainstem bronchi. Expandable stents can be placed using a flexible rather than a rigid bronchoscope. They can
even be placed over a guidewire without bronchoscopy.
This chapter focuses on expandable metallic stents that are often placed by interventional radiologists in patients
with benign strictures. Modifications of these techniques, in particular stent selection, may be necessary when
treating malignant obstructions with large endoluminal components or airway fistulae/leaks.
Indications
1. Expandable stents have been successfully used in both benign and malignant conditions in severely
symptomatic patients who have not been amenable to other forms of treatment (1,2). The decision to treat is
heavily based on the degree of the patient's symptoms. These stenoses may be (a) endoluminal, (b) in the
wall of the airway itself (intramural), or (c) a result of external compression.
a. Benign obstruction: post-lung transplantation anastomotic strictures, tracheal strictures following
prolonged intubation, postinfection inflammatory strictures, tracheomalacia, relapsing polychondritis,
Wegener granulomatosis, AIDS, external compression from benign mediastinal masses or fibrosis, and
airway collapse related to chronic obstructive pulmonary disease
b. Malignant obstruction : Malignant airway obstructions may arise from primary or metastatic tumors or
invaded lymph nodes. Stenting has been used for symptomatic palliation, regardless of tumor type, provided
a patent airway distal to the obstructed segment is present. Malignant obstructions associated with
prolonged (>2 weeks) lung collapse should be approached with caution because treatment may not result in
improvement and risks the release of infected secretions into other portions of the lungs.
2. Fistulae/air leaks: Small series have been published describing the use of covered and uncovered self-
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expanding metal stents in the management of tracheoesophageal fistulae and postoperative airway
dehiscence (4,5).
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Contraindications
1. High tracheal lesions where placement would result in the upper end of the stent being in the vocal cords
2. Presence of active inflammation of the airways
3. Absence of a patent distal landing site
1. Pulmonary function tests: These are helpful in evaluating patients' subjective symptoms and allowing objective
evaluation of pre- and posttreatment status (6).
2. Thin-slice computed tomography (CT): This study should be performed using a carefully developed protocol in
both inspiration and expiration and during forced vital capacity at the previously identified site of maximal
narrowing. The CT scan yields important three-dimensional airway anatomy for characterization of the lesion and
stent selection. Multiplanar reconstructions are especially helpful in assessing the extent of airway abnormality
and obtaining airway measurements. The dynamic changes can highlight airway collapse from malacia as well
as focal or diffuse air trapping distal to the narrowed segment.
3. Bronchoscopy in the conscious, freely breathing patient: Bronchoscopy performed at the time of stent
placement may underestimate the degree of functional narrowing because the patient is typically under general
anesthesia with positive pressure respiration.
4. Treatment of active inflammation
5. Coagulation studies
6. Review of previous studies
7. Preliminary selection of stent type, diameter, and length: No stent is ideal nor universally accepted for use in
the tracheobronchial tree. The ideal stent should be available in suitable lengths and diameters; be easy to see
fluoroscopically; be easy to place accurately; be resistant to migration, fracture, and permanent deformation;
should not block ciliary action or mucus clearance; should be easily removable; and should be well tolerated. No
single stent or stent category fulfills each of these criteria. Covered self-expanding metallic stents are generally
reserved for situations in which an air leak is present, although some operators favor them because they are less
difficult to remove than bare self-expanding metal stents and are better able to prevent tumor or granulation
tissue ingrowth.
8. Coordination of other involved medical services including an anesthesiologist who is typically responsible for
the periprocedural medical management of the patient as well as intraprocedural anesthesia and a pulmonologist
who performs bronchoscopy.
Anatomy
The important tracheobronchial anatomy is shown in Figure e-78.1.
1. In general, the structures are larger in men than in women, and there is some variation from patient to patient.
With increasing age, there is mild enlargement in tracheobronchial dimensions.
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2. The trachea is about 110 to 120 mm in length, extending from the larynx at about C6 to the carina at T5.
Typical diameters for man and woman tracheas, respectively, are coronal, 19.5 and 16.5 mm, and sagittal, 20.5
and 17.0 mm.
3. The right main stem bronchus is about 25 mm in length, about half the length of the left, and about 15 mm in
diameter.
4. The left main stem bronchus is about 50 mm long and 13 mm in diameter.
5. Major branch airways have diameters in the 6- to 12-mm range.
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FIGURE e-78.1 • Tracheobronchial anatomy.
Procedure
1. The procedure is performed on a fluoroscopy table, usually under general anesthesia, using an
endotracheal tube of 8.0- to 8.5-mm diameter. This allows optimal airway management and a controlled
atmosphere that is comfortable and safe for both the patient and the operators. Accurate stent placement is
best achieved under these conditions. Alternatively, the airway can be managed with a laryngeal mask
airway (LMA), which is an advantage when stenting in the trachea. Other operators use conscious sedation.
2. The bronchoscope is passed via a right-angled connector coaxially down the endotracheal tube. This
arrangement provides an air seal and allows simultaneous bronchoscopy and ventilation. A small adult-
sized scope is usually chosen. A large adult scope provides better vision and a large instrument channel if
biopsy is required but is less conveniently used through the smaller endotracheal tubes.
3. Bronchoscopy is performed to visualize the nature and extent of the lesions. Lesions seen at this time, in
a patient who is under general anesthesia and is being ventilated, may differ from and appear less serious
compared with lesions seen during spontaneous respiration in the normal state. Lesion length can be
measured by moving the bronchoscope in and out from one margin of the lesion to the other. These
findings are correlated with the preprocedure CT.
4. Landmarks such as the carina, vocal cords, and upper and lower limits of the lesion are marked directly
on the TV screen of the fluoroscope during combined fluoroscopy and bronchoscopy. This technique
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requires that patient does not move and that the fluoroscope is not moved. We have not used contrast
agents to delineate the bronchial anatomy because the contrast tends to make it very difficult to clearly see
the metal stents.
5. The endotracheal tube can be modified by cutting off the distal beveled tip and the balloon-bearing part
of the tube to facilitate the placement of stents that end high, close to the vocal cords. In these patients,
ventilation is maintained without the balloon cuff.
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6. A suitable stent is selected.
a. For tracheal lesions, we have used the self-expandable Wallstent (Boston Scientific, Natick, MA), which
is available in suitably large diameters and suitable lengths. It has some elasticity, is well tolerated, has
good radial strength, and has not caused perforations. We have avoided Gianturco Z-stents (Cook Medical
Inc, Bloomington, IN), which have been reported to cause fatal perforations into adjacent vessels, are prone
to mechanical breakage, and are also prone to ingrowth of granulation tissue and tumor. The Wallstent
shortens by some 40%, and so accurate placement may be more difficult. In situations such as the
presence of high lesions close to the vocal cords, where accurate placement is essential, we have
employed two Wallstents of the same length and diameter deployed coaxially. The distal limit of placement
is accurately fixed using the first Wallstent, reserving the second stent to fix the proximal limit. The proximal
limit is accurately fixed by deploying the second stent coaxially within the first stent. The distal end of the
first stent serves as a reference point. When the distal end of the second stent is deployed x centimeters
proximal to the distal end of the first stent, the proximal limit of the second stent will be x centimeters longer
than the proximal limit of the first stent, as shown in Figure e-78.2. Many operators use the nitinol Ultraflex
Stent (Boston Scientific, Natick, MA) in both its covered and bare forms (1,3). We have avoided using nitinol
stents where possible because of the propensity of nitinol to fracture as reported in the literature and
observed in our initial few patients.
b. For bronchial lesions, we used to use the balloon-expandable Palmaz stent (Cordis, New Brunswick,
NJ), which had the advantages of being available in a variety of short lengths as well as being easy to see
fluoroscopically and place accurately. It could be expanded until an excellent fit to the airway was obtained.
However, in three patients, Palmaz stents became crumpled up and deformed, and we have since
abandoned their use in the tracheobronchial tree (7). This experience has been reported by other
interventionalists. We now use Wallstents in the bronchi, although they can be difficult to place accurately
because of stent shortening.
c. In cases where we have to stent over the upper lobe bronchus, we used to use the Symphony stent
(Boston Scientific, Natick, MA). The Symphony is self-expandable and is constructed of a mesh with the
largest interstices of the available stents. We had good results with this stent, which is no longer in
production but does point to the desirable feature of large interstices. However, this stent is made of nitinol
and therefore prone to fracture particularly in the airways where the diameter of the stent changes
significantly with each respiration.
7. After the bronchoscope is removed, the selected stent is deployed over a guidewire. Alternatively, the
small bronchoscope can be used to watch deployment of the closest end of the stent, while the distal end is
watched on the fluoroscope. Fluoroscopy is used to monitor the positioning of the stent. If the stent
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is not fully distended, it is dilated utilizing a percutaneous transluminal angioplasty (PTA) balloon catheter
over the retained guidewire. A high-pressure balloon may be needed and sometimes even a cutting balloon
will be helpful prior to stent placement. The balloon is inflated with very dilute contrast agent and saline so
that, in the event of balloon rupture, full-strength contrast agent does not flood into the lung, causing
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pulmonary edema. The balloon is only briefly inflated with a mechanical inflator with a pressure gauge to
limit interference with air movement through the airways.
FIGURE e-78.2 • Overlapping coaxial stents of the same diameter and length.
FIGURE e-78.3 • Stenting of the carina.
8. Bronchoscopy is used to check satisfactory placement and allow aspiration of any blood or secretions.
9. Lesions involving the carina or other branch points in the main airways present special problems. We
attempt to position stents around the carina as shown in Figure e-78.3. We try to avoid covering the origin
of a branch airway.
10. Stenting in infants is problematic because the stents cannot grow to keep pace with the growth of the
infant. The stents are therefore only of temporary value and will require removal at a later stage. This may
be difficult and can be traumatic.
11. In cases where an air leak is present, use of a covered stent is indicated. Leaks at an airway
anastomosis have been successfully treated. We reserve covered stents for use in patients with air leaks
because the covering prevents ciliary action and mucus clearing and leads to more frequent stent plugging.
Patients appear to have greater difficulty clearing secretions when covered stents are in place.
1. Patients go from radiology to the postoperative recovery room for observation following their general
anesthesia, and most patients stay in the hospital overnight.
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2. Long-term follow-up includes repeat pulmonary function tests, chest X-ray, CT, and bronchoscopy as dictated
by the clinical status of the patient.
3. Restenting or endobronchial debulking/ablation may be required in some benign cases if there is mucosal
hyperplasia or granulation tissue, and in malignant cases where tumor extension or overgrowth has occurred.
Results
1. Institutional experience (University of California, San Francisco, CA) in 40 patients who underwent
tracheal and/or bronchial stenting for benign airway stenoses. Indications were post-lung transplant
stenosis (n = 13), post-intubation tracheal stenosis (n = 10), relapsing polychondritis (n = 3),
tracheobronchial malacia (n = 4), external tracheal compression (n = 4), Wegener granulomatosis (n = 1),
idiopathic inflammation (n = 2), and tuberculosis (n = 3). A variety of stents were used but most were
Wallstents. Follow-up, which ranged from 6 to 2,473 days, was performed by means of chart review for
deceased patients and by means of clinical visit or telephone interview for surviving patients. Survival,
primary patency, and assisted patency were estimated by using the Kaplan-Meier product limits method.
Initial technical success was achieved in all cases. Symptomatic improvement was present in 39 of 40
cases. At review, 15 patients were alive and had clinical improvement, 18 had died of comorbid causes, 1
had died of uncertain causes, 3 had undergone subsequent airway surgery, 2 had undergone airway stent
retrieval, and 1 was lost to follow-up. Survival at 1, 2, 3, 4, 5, and 6 years was 79%, 76%, 51%, 47%, 38%,
and 23%, respectively. Loss of primary patency was most rapid during the first year. With repeat
intervention, assisted patency was 90% at 6.8 years. We concluded that attrition of tracheobronchial stent
patency is most rapid during the first year, and a high rate of long-term patency can be achieved with
secondary interventions. Metallic airway stents are well tolerated and useful adjuncts for management of
select benign tracheobronchial stenoses (2).
2. The group from the Cleveland Clinic published their 6-year experience using self-expanding metallic
stents (SEMS) in 82 patients (1). There were 50 patients with neoplasia and 32 with benign strictures. They
had good symptom relief in over 70% of this heterogeneous patient group using either Wallstents or
Ultraflex stents. They concluded that a SEMS was a safe and effective treatment modality for malignant as
well as selected benign airway obstruction. They stress the importance of careful patient selection and that
stenting should be reserved for use in patients who are not good candidates for surgical or other treatment.
Surgeons involved with the removal of metallic stents stress that they are difficult to remove, are associated
with significant complications, require prospective bronchoscopic surveillance, and often further therapeutic
intervention. Therefore, endobronchial metallic stents should be considered only for selected patients with
large airway compromise secondary to benign airway diseases for which other medical comorbidities
contraindicate formal airway surgery (3).
3. When stents are used for palliation in malignant airway obstruction, published results are very dependent
on patient selection. It should be noted that covered stents have been used in most cases in published
series. Clinical success rates have ranged from 50% to 90% in published series.
Complications
1. Acute complications are uncommon but include bleeding, which is usually selflimiting, and stent
malposition. Stent malposition involving the vocal cords is a particularly serious situation because the
airway is left unprotected against aspiration. Additionally, phonation will be affected by a stent in this
position.
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2. Long-term complications include stent migration, deformation or breakage, erosion into adjacent vascular
structures, and stent blockage by secretions or overgrowth of reactive granulation tissue or malignant
tissue. These complications are not infrequent in the first year and often require repeat interventions. In
benign disease, the rate of intervention tends to decrease after the first year (2). If surgical repair is
possible, it is the preferred approach because of the reintervention rate associated with stents.
As more and more experience has been accrued using expandable stents for tracheobronchial stenoses, it
is clear that there is a significant complication rate which is particularly important in patients with benign
strictures. Expandable stents can only be removed with difficulty once they have become incorporated into
the lining of the airway, which occurs as soon as 8 weeks following placement (3). This can be traumatic
and they are usually left in place permanently, except in growing infants in whom successful removal has
been reported. “Covered” versions of typically used self-expanding metal stents retain uncovered distal and
proximal ends. Attempted removal of these stents after incorporation can be similarly traumatic. A newer
generation of completely covered expandable metallic stents is now available which are meant to be
removable (Alveolus Inc, Charlotte, NC). In our limited experience with these stents, we have been unable
to easily remove them (8). Other authors have been more successful, and it is clear that removal of a bare
stent is much more difficult and causes much more trauma than the removal of a covered stent.
Stents should only be used when no better alternative is available for the particular patient, but the
established value of stents should not be overlooked (3). On July 29, 2005, the U.S. Food and Drug
Administration (FDA) issued an advisory regarding the use of metallic stents in benign conditions (9). The
reader is strongly urged to refer to this advisory that is quoted in its original form in the appendix at the end
of this chapter.
Appendix
U.S. Food and Drug Administration. FDA public health notification: complications from metallic tracheal stents in
patients with benign airway disorders, 2005.
http://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/PublicHealth Notifications/ucm062115.htm.
This is to alert you to serious complications associated with the use of metallic tracheal stents in patients with
benign airway disorders, and to recommend specific actions to prevent or minimize the problem. This
notification includes all covered and uncovered metallic tracheal stents.
Nature of the Problem

This notification focuses on patients with benign airway disorders because use of metallic stents in this patient
population may preclude them from receiving future alternative therapies (such as tracheal surgical procedures
or placement of silicone stents) after a metallic stent is removed. This patient population has a greater risk of
serious complications than those with malignant disorders since the metallic tracheal stent is left in place
longer.
Our concern about complications from using metallic tracheal stents in patients with benign airway disorders
stems from a review of recently published literature, medical device reports that we have received, and
information from physicians. These complications include obstructive granulation tissue, stenosis at the ends
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of the stent, migration of the stent, mucous plugging, infection, and stent fracture. Although many of the medical
device reports received by the FDA are associated with stent fracture,
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we believe that other complications cited in the literature are a potential risk with both covered and uncovered
metallic tracheal stents.
Removal of metallic stents can also result in serious complications, including mucosal tears, severe bleeding,
re-obstruction, and respiratory failure with the need for postoperative mechanical ventilation, and tension
pneumothorax. If the stent is removed in pieces due to device failure or fracture during removal, this can lead to
unwanted permanent incorporation of retained stent fragments into tissue. Data evaluating the ability to safely
and effectively remove embedded metallic stents from the trachea have never been provided to or reviewed by
the FDA.
We recognize that metallic tracheal stents, when used appropriately on carefully selected patients, have
benefit. We are currently working with manufacturers to ensure that the labeling of these stents adequately
conveys the risks when they are used in patients with benign airway disorders.
Recommendations
Use metallic tracheal stents in patients with benign airway disorders only after thoroughly exploring all
other treatment options (such as tracheal surgical procedures or placement of silicone stents). Using
metallic tracheal stents as a bridge to other therapies is not recommended because removal of the
metallic stent can result in serious complications.
If a metallic tracheal stent is the only option for a patient, insertion should be done by a physician trained
or experienced in metallic tracheal stent procedures.
If removal is necessary, the procedure should be performed by a physician trained or experienced in
removing metallic tracheal stents.
Always review the labeling before using the device, especially the indications for use, warnings, and
precautions. Select patients carefully.
We urge you to be aware of the guidelines from professional organizations regarding recommended
provider skills and competency for these procedures (i.e., training requirements and clinical experience).
These guidelines include information about equipment, personnel, anesthesia and monitoring, techniques,
indications, contraindication, and risks.
Reporting Adverse Events to FDA

Prompt reporting of adverse events can improve FDA's understanding of and ability to communicate the risks
associated with devices, and assist in the identification of potential future problems. The FDA requires
hospitals and other user facilities to report deaths and serious injuries associated with the use of medical
devices. If you suspect that a reportable adverse event was related to the use of a metallic tracheal stent, you
should follow the reporting procedure established by your facility. When reporting the adverse event(s), you
should specify whether the metallic tracheal stent was originally placed for a benign or malignant disorder.
References
1. Saad CP, Murthy S, Krizmanich G, et al. Self-expandable metallic airway stents and flexible bronchoscopy:
long-term outcome analysis. Chest. 2003;124:1993-1999.
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2. Thornton RH, Gordon RL, Kerlan RK, et al. Outcomes of tracheobronchial stent placement for benign
disease. Radiology. 2006;240(1):273-282.
3. Madden BP, Loke TK, Sheth AC. Do expandable metallic airway stents have a role in the management of
patients with benign tracheobronchial disease? Ann Thorac Surg. 2006;82:274-278.
4. Shin JH, Song HY, Ko GY, et al. Esophagorespiratory fistula: long-term results of palliative treatment with
covered expandable metallic stents in 61 patients. Radiology. 2004;232:252-259.
5. Mughal MM, Gildea TR, Murthy S, et al. Short-term deployment of self-expanding metallic stents facilitates
healing of bronchial dehiscence. Am J Respir Crit Care Med. 2005;172(6):768-771.
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6. Gotway MB, Golden JA, LaBerge JM, et al. Benign tracheobronchial stenoses: changes in short-term and
long-term pulmonary function testing after expandable metallic stent placement. J Comput Assist Tomogr.
2002;26(4):564-572.
7. Perini S, Gordon RL, Golden JA, et al. Deformation and migration of Palmaz stents after placement in the
tracheobronchial tree. J Vasc Interv Radiol . 1999;10:209-215.
8. Tan JH, Fidelman N, Durack JC, et al. Management of recurrent airway strictures in lung transplant
recipients using AERO covered stents. J Vasc Interv Radiol . 2010;21(12): 1900-1904.
9. U.S. Food and Drug Administration. FDA public health notification: complications from metallic tracheal
stents in patients with benign airway disorders, 2005.
http://www.fda.gov/MedicalDevices/Safety/AlertsandNotices/PublicHealthNotifications/ucm062115.htm.
Accessed November 19, 2015.
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e-79
Esophageal Stents
Ho-Young Song
Ji Hoon Shin
Chang Jin Yoon
Fluoroscopic or endoscopic placement of a covered or bare expandable metallic stent is increasingly being used
for the treatment of malignant (1,2,3,4,5,6,7,8,9,10,11,12,13,14) and benign (15,16,17) esophageal strictures.
These stents are thought to provide superior mortality and morbidity benefits and more effective relief of
dysphagia when compared with other conventional esophageal prostheses.
Indications
1. Unresectable or inoperable esophagogastric neoplasms
2. Patients with resectable esophageal neoplasms who wish to avoid surgery
3. Patients who need nourishment prior to surgery or chemoradiation therapy
4. Esophagorespiratory fistula (ERF) due to a malignant tumor
5. Extraluminal compression by neoplasms or adenopathy
6. Benign esophageal strictures refractory to balloon dilation
Removal of placed stents (14,17,18) is indicated for (a) patients with complications after stent placement
such as severe pain, stent migration, or stent deformity; (b) patients with stent placement for the sole
purpose of nourishment prior to surgery or chemoradiation therapy; and (c) patients with a benign stricture
who only need temporary treatment.
Contraindications
Relative
1. Uncontrollable bleeding diathesis
2. Severely ill patients with a very limited life expectancy
3. Severe vocal cord palsy
4. Multiple obstructive lesions of the small bowel (e.g., peritoneal seeding)
5. Neoplasms involving the upper esophageal sphincter
2. Stop all oral intake for 8 hours before procedure.
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3. Check hematocrit, platelet count, prothrombin time (PT), and partial thromboplastin time (PTT) and correct as
necessary.
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4. Perform esophagography and/or endoscopy to assess location and length of the stricture.
Procedure
Stent Placement (Fig. e-79.1A-F)
1. A variety of instruments and techniques for stent placement have been developed
(2,3,4,5,6,7,8,9,10,11,12,13,19,20,21). Stents available in the United States are listed in Table e-79.1.
2. The pharynx is topically anesthetized (aerosol lidocaine spray), and conscious sedation is administered
according to institutional protocols.
3. Extending the patient's neck and placement of an oral airway may facilitate the procedure. Atropine may
be useful for managing vagal tone or copious secretions.
4. With the patient in the left anterior oblique position, a 0.035-in. stiff guidewire (Radifocus Guide Wire M,
Terumo Corp, Tokyo, Japan) is inserted—with or without the help of an angiographic catheter—through the
mouth across the stricture into the distal esophagus or stomach (Fig. e-79.1A).
5. A sizing catheter (S&G Biotech, Seongnam, South Korea) is passed over the guidewire to inject water-
soluble contrast medium and to measure the length of stricture (Fig. e-79.1B,C).
6. The location of the stricture is marked on the patient's skin under fluoroscopic control.
FIGURE e-79.1 • Technical steps in esophageal stent placement. A: Insertion of a guidewire through the
mouth across the stricture into the stomach. B,C: Measurement of the length of the stricture with use of a
sizing catheter. D: Insertion of a preloaded stent-delivery system over the guidewire across the stricture.
E,F: Deployment of the stent.
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Table e-79.1 Characteristics of Currently Available Esophageal Stents

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Unconstrained
Delivery Length Outer

Covered/Uncovered System (cm) Diameter Comment
Wallstent Covered 18 Fr. 10 20 mm Shortens on

Esophageal II 15 midstent deployment
(Boston 28 mm
Scientific/Medi-Tech, midstent
Natick, MA)
Ultraflex Esophageal Uncovered 20 Fr. 7 18 mm Distal or

Stent System (Boston 10 midstent proximal
Scientific/Medi-Tech, 12 23 mm release
Natick, MA) 15 proximal mechanisms
flare
Covered 10
20 Fr. 12 18 mm
midstent
15 23 mm 15 mm
proximal uncovered
flare at each end
23 mm
midstent
28 mm
proximal
flare (10-
and 12-
cm
lengths)
Cook-Z Stents (Cook Covered 24 Fr. 10 18 mm Inner

Medical Inc, 12 midstent diameter of
Bloomington, IN) 25 mm midstent is
proximal 16 mm.
and Polyethylene
distal covered
flare stainless
steel
14 Central
fixation
barbs
Stent
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covered to
ends
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7. The sizing catheter is removed, leaving the guidewire in place.
8. A preloaded stent-delivery system, whose proximal part is lubricated with jelly, is passed over the
guidewire into the esophagus and advanced until the distal end of the stent reaches beyond the stricture
(Fig. e-79.1D). If the stricture is too tight to accommodate the stent-delivery system, balloon predilation is
needed up to maximum 10 mm.
9. The position of the stent relative to the stricture is confirmed with contrast injection. Allow 1 to 2 cm of the
stent to extend beyond both ends of the lesion.
10. The introducing sheath is slowly withdrawn over the pusher in a continuous motion, freeing the stent to
expand within the stricture (Fig. e-79.1E,F). The delivery system and guidewire are then removed.
Stent Removal (Fig. e-79.2A-F)
1. To facilitate stent removal, nylon drawstrings are attached to the upper inner margin of a retrievable stent
(Taewoong Medical, Goyang, South Korea) (8,14,17).
2. After topical anesthesia of the pharynx with an aerosol spray, a 0.035-in. stiff guidewire (Radifocus Guide
Wire M) is introduced through the mouth and then across the stent into the distal esophagus or stomach
(Fig. e-79.2A).
3. A sheath with a dilator is passed down over the guidewire into the proximal stent lumen (Fig. e-79.2B).
FIGURE e-79.2 • Technical steps in stent removal. A: Insertion of a guidewire through the mouth across the
stent into the stomach. B: Introduction of a sheath with a dilator over the guidewire into the proximal stent
lumen. C: Replacement of the dilator with a hook catheter. D: Grasping the nylon thread with the hook. E:
Withdrawing the hook catheter into the sheath to collapse the proximal end of the stent. F: Pulling them
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together out of the esophagus.
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4. After the guidewire and the dilator are removed from the sheath, a hook catheter is introduced into the
sheath and advanced until its metal part passes through the sheath into the stent lumen (Fig. e-79.2C).
5. The sheath with the hook catheter is then pulled out of the stent so that its metal part hooks onto the
nylon thread (Fig. e-79.2D). Then the hook catheter is withdrawn through the sheath to collapse the
proximal stent when it reaches the sheath tip (Fig. e-79.2E).
6. The sheath, hook catheter, and stent are then pulled together out of the esophagus (Fig. e-79.2F).
Postplacement
1. Patients can be allowed a liquid diet 1 hour after the procedure. A patient with an ERF is restricted to food
until the 1-day follow-up esophagography.
2. Patients in whom the stent straddles the distal esophageal sphincter are advised to sleep in a semierect
position to minimize reflux and aspiration of gastric contents. Proton pump inhibitor (lansoprazole 15 mg) should
be used to reduce reflux through the stent.
3. Esophagography is performed 1 day after stent placement to verify the position and patency of the stent.
4. Diet can be advanced to soft and solid diet after confirmation of stent expansion and position.
5. Advise proper chewing of food and use of carbonated drinks to reduce risk of food impaction.
Postretrieval
1. Patients can be allowed a liquid diet 1 hour after the procedure.
2. Esophagography is performed just after stent removal to check any complications.
3. Diet can be advanced to soft and solid diet, if there are no issues.
Results
Malignant Esophageal Strictures
1. Overall success rates of 96% to 100% have been reported (3,4,5,6,7,8,9,10,11,12,13,14).
2. Covered stents have the disadvantage of stent migration, which reportedly leads to a recurrence of
dysphagia in 5% to 32% of patients.
3. Bare esophageal stents have relatively low migration rates (0% to 3%) due to fixation of the stent wires
within the tumor (7,9,10). However, bare stents are not suitable for the treatment of ERFs. In addition,
progressive tumor ingrowth through the openings between the wire filaments of bare stents tends to cause
progressive dysphagia.
4. In patients with ERF due to esophageal or bronchogenic carcinoma, covered stents have been reported
to completely seal off the fistula in 80% (18). However, the fistula reopened in 35%.
5. Temporary placement of a covered retrievable stent for 3 to 4 weeks, with concurrent radiation therapy
for malignant esophageal strictures, is reported to be more effective than permanent placement in reducing
delayed complications and related reinterventions (14).
Benign Esophageal Strictures
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1. The long-term results of permanent placement, of either covered or bare stents, have been considered
discouraging because of the high reported rates (40% to 100%) of late complications caused by stent
migration or the formation of a new stricture.
2. In 25 patients with retrievable stents (17), all could ingest solid food after placement as well as after
removal. However, the recurrence rate during the
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mean follow-up period of 13 (range, 2 to 25) months after stent removal was >50%. The patients with
recurrence were treated by means of repeat balloon dilation.
1. Esophageal perforation or fistula formation: 0% to 7%
(2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22) Delayed ERF can be managed by additional stent
replacement (4,18).
2. Bleeding: 0% to 19% (2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22)
The chance of massive bleeding is higher in patients who undergo radiation therapy after stent placement
(4).
3. Stent migration: 4% to 14% (2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22)
Stent removal in patients with stent migration seems not to be urgent not only because the migrated stent
can pass through the rectum but also because it can remain for a long time in the stomach without causing
symptoms (4,8,17). However, some authors have reported that a migrated stent causes complications such
as pain, ulcer, and obstruction (6,9).
4. Tumor ingrowth, overgrowth, or food impaction: 3% to 36%
Tumor overgrowth and ingrowth can be managed by the addition of another stent. An impacted food bolus
can be displaced into the stomach using a balloon catheter or an endoscope (4).
5. Granulation tissue formation: 0% to 13% (2,3,4,5,6,7,8,9,10,11,12,13,14)
The formation of granulation tissue is more common with stents placed for a benign stricture (17). In
patients with granulation tissue formation after stent placement, it is necessary to remove the stent not only
because this improves the condition but also because granulated tissue eventually causes recurrence of
dysphagia. An additional stent that overlaps the end of the first stent is useful for patients with malignant
stricture.
6. Tracheobronchial compression: 0% to 6% (2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22)
Tracheobronchial compression after esophageal stent placement can be managed by either
tracheobronchial stent placement (18) or removal of the esophageal stent.
7. Reflux
Gastroesophageal reflux is a problem in patients who have a stent in the lower one-third of the esophagus
bridging the gastroesophageal junction. The symptoms can be relieved by taking antacids, sleeping with the
head of the bed raised by approximately 30 degrees, and avoiding large meals before going to bed.
Gastroesophageal reflux can be prevented by using antireflux stents (11,12).
8. Reopening of ERF: 0% to 35% (2,3,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22)
The causes of reopening include stent occlusion (due to tumor overgrowth or ingrowth, food impaction, or
granulation tissue formation), stent migration, funnel phenomenon, and stent-cover disruption
(3,18,19,20,21). These conditions can be managed by stent replacement, saline irrigation, injection of
Radiology Books
tissue glue in the persistent space, or tracheobronchial stent placement (4,19,21).
9. Miscellaneous complications
A metallic stent placed in patients with cervical esophageal strictures can cause a foreign body sensation in
the throat (4). Other complications include mucosal prolapse into the stent and aspiration pneumonia in
patients with stent placement in the esophagogastric junction.
References
1. Adler DG. Esophageal stents: placement, complications, tips, and tricks [video]. Video J and Encyclopedia
GI Endosc. 2013;1(1):66-68.
2. Song HY, Choi KC, Cho BH, et al. Esophagogastric neoplasms: palliation with a modified Gianturco stent.
Radiology. 1991;180:349-354.
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3. Miyayama S, Matsui O, Kadoya M, et al. Malignant esophageal stricture and fistula: palliative treatment
with polyurethane-covered Gianturco stent. J Vasc Interv Radiol . 1995;6:243-248.
4. Song HY, Do YS, Han YM, et al. Covered, expandable esophageal metallic stent tubes: experiences in
119 patients. Radiology. 1994;193:689-695.
5. Hindy P, Hong J, Lam-Tsai Y, et al. A comprehensive review of esophageal stents. Gastroenterol Hepatol .
2012;8:526-534.
6. Knyrim K, Wagner HJ, Bethge N, et al. A controlled trial of an expansile metal stent for palliation of
esophageal obstruction due to inoperable cancer. N Engl J Med. 1993; 329:1302-1307.
7. Acunaş B, Rozanes I, Akpinar S, et al. Palliation of malignant esophageal strictures with self-expanding
nitinol stents: drawbacks and complications. Radiology. 1996;199: 648-652.
8. Song HY, Park SI, Jung HY, et al. Benign and malignant esophageal strictures: treatment with a
polyurethane-covered retrievable expandable metallic stent. Radiology. 1997;203:747-752.
9. Adam A, Ellul J, Watkinson AF, et al. Palliation of inoperable esophageal carcinoma: a prospective
randomized trial of laser therapy and stent placement. Radiology. 1997; 202:344-348.
10. Cwikiel W, Tranberg KG, Cwikiel M, et al. Malignant dysphagia: palliation with esophageal stents—long-
term results in 100 patients. Radiology. 1998;207:513-518.
11. Do YS, Choo SW, Suh SW, et al. Malignant esophagogastric junction obstruction: palliative treatment
with an antireflux valve stent. J Vasc Interv Radiol . 2001;12:647-651.
12. Laasch HU, Marriott A, Wilbraham L, et al. Effectiveness of open versus antireflux stents for palliation of
distal esophageal carcinoma and prevention of symptomatic gastroesophageal reflux. Radiology.
Radiology Books
2002;225:359-365.
13. Siersema PD, Hop WC, van Blankenstein M, et al. A comparison of 3 types of covered metal stents for
the palliation of patients with dysphagia caused by esophagogastric carcinoma: a prospective, randomized
study. Gastrointest Endosc. 2001;54:145-153.
14. Song HY, Lee DH, Seo TS, et al. Retrievable covered nitinol stents: experiences in 108 patients with
malignant esophageal strictures. J Vasc Interv Radiol . 2002;13:285-293.
15. Sharma P, Kozarek R; and the Practice Parameters Committee of American College of Gastroenterology.
Role of esophageal stents in benign and malignant disease. Am J Gastroenterol . 2010;105:258-273.
16. Song HY, Park SI, Do YS, et al. Expandable metallic stent placement in patients with benign esophageal
strictures: results of long-term follow-up. Radiology. 1997;203:131-136.
17. Song HY, Jung HY, Park SI, et al. Covered retrievable expandable nitinol stents in patients with benign
esophageal strictures: initial experience. Radiology. 2000;217: 551-557.
18. Shin JH, Song HY, Ko GY, et al. Esophagorespiratory fistula: long-term results of palliative treatment with
covered expandable metallic stents in 61 patients. Radiology. 2004;232:252-259.
19. Saxon RR, Barton RE, Katon RM, et al. Treatment of malignant esophagorespiratory fistulas with
silicone-covered metallic Z stents. J Vasc Interv Radiol . 1995;6:237-242.
20. Morgan RA, Ellul JP, Denton ER, et al. Malignant esophageal fistulas and perforations: management with
plastic-covered metallic endoprostheses. Radiology. 1997;204:527-532.
21. Kozarek RA, Raltz S, Brugge WR, et al. Prospective multicenter trial of esophageal Z-stent placement for
malignant dysphagia and tracheoesophageal fistula. Gastrointest Endosc. 1996;44:562-567.
22. Shin JH, Ko GY, Yoon HK, et al. Temporary stent placement during radiation therapy in patients with
malignant esophageal strictures: initial experience. Radiology. 2002; 225:162.
Radiology Books
e-80
Gastroduodenal Stent Placement
Jin Hyoung Kim
Ho-Young Song
Chang Jin Yoon
In 1991, Song et al. (1) described the first metallic gastric stent placement in a patient with a gastric outlet
obstruction due to recurrent gastric cancer after bypass surgery. The first covered metallic gastroduodenal stent
placement, through a surgical gastrostomy using local anesthesia, in a patient without prior bypass surgery was
also reported by Song et al. (2) in 1993. In 1995, Strecker et al. (3) published the first report of a transoral stent.
Since then, transoral placement of metallic stents has been increasingly used for safe nonsurgical palliation of
unresectable malignant gastroduodenal obstructions (4,5,6,7,8,9,10,11,12,13,14,15). The procedure is
performed either under fluoroscopic guidance alone or combined with endoscopic guidance. Transoral
placement has a higher clinical success rate, lower morbidity and mortality rates, and a shorter length of hospital
stay than surgery (16,17).
Indications
1. Documented unresectable malignancy resulting in gastroduodenal obstruction
a. Intrinsic tumors including stomach and duodenal cancers
b. Extrinsic gastroduodenal obstruction due to pancreatic malignancy, cholangiocarcinoma, malignant
lymphadenopathy, localized intraperitoneal metastasis, or lymphoma
c. Surgical gastroenteric anastomotic site
2. Patients whose life expectancy is more than 1 month
Contraindications
Relative
1. Mildly symptomatic patients
2. Clinical evidence of perforation, peritonitis, or severe coagulopathy
3. Multiple obstructive lesions of the small bowel (e.g., peritoneal seeding)
4. Severely ill patients with a very limited life expectancy
1. Obtain informed consent after explaining the procedure, its risks and benefits, and alternative therapies.
2. Insert a nasogastric tube at least 24 hours before the procedure to ensure adequate gastric emptying. An
empty stomach becomes cylindrical and permits easier catheter manipulation and advancement of the stent-
delivery device (18).
necessary.
Radiology Books
4. Barium studies and/or endoscopy to evaluate the site, severity, and length of the stricture
Procedure
1. A variety of bare or covered expandable metallic stents have been used in the treatment of malignant
gastroduodenal strictures: the Wallstent (Boston Scientific, Natick, MA), Ultraflex stent
(Microinvasive/Boston Scientific, Natick, MA), Gianturco Z-stent (Wilson-Cook, Winston-Salem, NC), Niti-S
stent (Taewoong Medical, Ilsan, South Korea), Hanaro stent (M.I. Tech, Pyeongtaek, South Korea),
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and dual gastroduodenal stent (S&G Biotech, Seongnam, South Korea). Various stent-delivery systems are
used, and they range in diameter from 3.8 to 28 Fr.
2. The procedure is performed under conscious sedation and analgesia (e.g., intravenous midazolam and
fentanyl) (19,20). The pharynx is anesthetized with 1% lidocaine spray.
3. Patients are placed in the right lateral decubitus position, and then a 0.035-in. exchange guidewire
(Radifocus M, Terumo, Tokyo, Japan) and a catheter (100 cm, 5 or 6 Fr.) are inserted through the mouth
across the stricture into the distal portion of the stomach or duodenum under fluoroscopic guidance (Fig. e-
80.1A). Looping of the catheter guidewire system can be reduced by use of a 12 or 18 Fr. guiding sheath
(21).
4. Once the catheter has passed beyond the stricture, water-soluble contrast medium is injected to
delineate the anatomy (Fig. e-80.1B).
5. When the catheter has been advanced into the proximal jejunum, the guidewire is replaced with a 260-cm
exchange length Amplatz Super Stiff wire (Meditech/Boston Scientific, Watertown, MA).
6. In very tight stenoses, predilation with a 10-mm balloon can be performed to allow easy passage of the
stent-delivery system (12,15,22). The stent is deployed under fluoroscopic guidance and should be 2 to 4
cm longer than the stricture to reduce the risk of tumor overgrowth (18) (Fig. e-80.1C,D).
7. In patients with a technical failure in negotiation of the guidewire through the stricture with fluoroscopic
guidance alone, combining endoscopic guidance should be considered.
8. In patients with a stricture longer than 10 cm, two or three stents can be placed in a stent-within-stent
fashion to achieve complete coverage of the stricture (15).
9. Once the stent is placed, balloon dilation is usually not required because most self-expanding stents will
gradually expand and reach their full diameter. However, if the stent expands less than half of its nominal
diameter, stent dilation may be performed (12,15).
Radiology Books
FIGURE e-80.1 • Technique of gastroduodenal stent placement. A: A catheter and a guidewire are inserted
into the gastroduodenal area and manipulated to pass through the obstruction. (continued)
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Radiology Books
FIGURE e-80.1 • (Continued) B: The distal end of the obstruction is delineated by injection of a small
amount of contrast medium. C: The wire is exchanged with a superstiff guidewire. The catheter is then
removed, and the stent-delivery system is advanced over the stiff guidewire. (continued)
1. Patients are advised to resume an oral intake of liquids within 24 hours after stent placement, later advancing
to a normal diet as tolerated (12).
2. A barium study is advised 1 day after stent placement to verify the position and patency of the stent.
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Radiology Books
FIGURE e-80.1 • (Continued) D: The stent is deployed in the obstruction.
3. Patients are not allowed a soft or a solid diet until the follow-up study proves full stent expansion (12).
4. Patients are advised to chew their food and to avoid high-fiber food in order to reduce the risk of food bolus
obstruction (18).
Results
Technical Success
1. Technical success is defined as the passing of a guidewire and the suitable placement of the stent.
Review of the literature on metallic stenting, using fluoroscopic or endoscopic guidance (10,15,23), reveals
that technical success is achieved in 97% to 98% of the patients with malignant gastroduodenal obstruction.
Complicated anatomy, severe stenosis, or acute angulation of a bowel loop may result in technical failure
(15,18).
2. Technical success rate varies with the site of lesion (15). For instance, stent placement at the site of
duodenal obstruction is technically more difficult than it is in the peripyloric region, not only because of
potential looping of the stent-delivery system in the distended stomach but also because of the curved
configuration of the duodenal C-loop (11,15). A stricture at a surgical anastomotic site (especially
gastrojejunostomy) is most challenging for stent placement (15).
Clinical Success
1. Clinical success is defined as relief of symptoms and/or improvement of oral intake obviating the need for
palliative surgery. Review of publications (10,15,23) on metallic stenting using fluoroscopic or endoscopic
guidance shows that clinical success is achieved in 84% to 94% of patients with malignant gastroduodenal
obstruction.
2. Some patients do not show an improvement in their symptoms after stent placement due to unrecognized
distal small bowel strictures (4,12,14,15), lack of propulsive peristalsis in a chronically obstructed stomach
(4,24), or functional gastric outlet obstruction from neural involvement by tumor (6).
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1. Perforation
Perforation is a life-threatening complication requiring an urgent surgical treatment (18)—despite its rarity (less
than 1%) (15,23). Perforation is usually caused by an erosion of the bare ends of the stent through the wall of
the intestine.
2. Bleeding
Bleeding after stent placement occurs rarely (<1%) (15,23) and can be managed with conservative treatment
only. However, significant bleeding may require arterial embolization (25).
3. Stent obstruction
Obstruction is the most common complication (14% to 17%) after stent placement and is caused by food
impaction, tumor ingrowth or overgrowth, or stent collapse (15,23). The impacted food can be successfully
removed endoscopically (15). Tumor ingrowth or overgrowth and stent collapse can be successfully treated by
coaxial placement of an additional stent (18,26).
4. Stent migration
Stent migration can be partial or complete and proximal or distal (14). Migration rate is higher with covered stents
(21% to 26%) (13,14) than in uncovered stents (0% to 11%) (2,27,28) and is associated with chemotherapy after
stent placement (15). Stent migration can be managed by insertion of an additional stent (15,18,23). The
migrated stent can be passed out through the rectum or can be caught in the intestine and leads to obstruction
requiring surgery (15,18,23).
Biliary obstruction rate after gastroduodenal stent placement ranges from 1.3% to 6% (10,15,23). There is a
continuous debate regarding the relationship between stent placement bridging the Ampulla of Vater and biliary
obstruction (11,12). Some authors have suggested limiting the use of covered stents in duodenal obstruction
because of this possibility (29). Alternatively, either an uncovered bare stent is used or external biliary
decompression is performed if covering the Ampulla is unavoidable (14).
6. Pain
Abdominal pain lasts for 24 to 72 hours after stent placement and usually diminishes spontaneously (18).
Continuous pain can be managed with analgesics (12,23,30).
References
1. Song HY, Choi KC, Cho BH, et al. Esophagogastric neoplasms: palliation with a modified gianturco stent.
Radiology. 1991;180:349-354.
2. Song HY, Yang DH, Kuhn JH, et al. Obstructing cancer of the gastric antrum: palliative treatment with
covered metallic stents. Radiology. 1993;187:357-358.
3. Strecker EP, Boos I, Husfeldt KJ. Malignant duodenal stenosis: palliation with peroral implantation of a
self-expanding nitinol stent. Radiology. 1995;196:349-351.
Radiology Books
4. Bessoud B, de Baere T, Denys A, et al. Malignant gastroduodenal obstruction: palliation with self-
expanding metallic stents. J Vasc Interv Radiol . 2005;16:247-253.
5. Strand DS, Thlick JE, Patrie JT et al. Gastroduodenal stents are associated with more durable patency as
compared to percutaneous endoscopic gastrojejunostomy in the palliation of malignant gastric outlet
obstruction. J Interv Gastroenterol . 2012;2: 150-154.
6. Baron TH, Harewood GC. Enteral self-expandable stents. Gastrointest Endosc. 2003;58:421-433.
7. Larssen L, Medhus AW, Körner H, et al. Long-term outcome of palliative treatment with self-expanding
metal stents for malignant obstructions of the GI tract. Scand J Gastroenterol . 2012;47:1505-1514.
8. Piesman M, Kozarek RA, Brandabur JJ, et al. Improved oral intake after palliative duodenal stenting for
malignant obstruction: a prospective multicenter clinical trial. Am J Gastroenterol . 2009;104:2404-2411.
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9. van Hooft JE, Uitdehaag MJ, Bruno MJ, et al. Efficacy and safety of the new WallFlex enteral stent in
palliative treatment of malignant gastric outlet obstruction (DUOFLEX study): a prospective multicenter study.
Gastrointest Endosc. 2009;69:1059-1066.
10. Telford JJ, Carr-Locke DD, Baron TH, et al. Palliation of patients with malignant gastric outlet obstruction
with the enteral Wallstent: outcomes from a multicenter study. Gastrointest Endosc. 2004;60:916-920.
11. Yoon CJ, Song HY, Shin JH, et al. Malignant duodenal obstructions: palliative treatment using self-
expandable nitinol stents. J Vasc Interv Radiol . 2006;17:319-326.
12. Song HY, Shin JH, Yoon CJ, et al. A dual expandable nitinol stent: experience in 102 patients with
malignant gastroduodenal strictures. J Vasc Interv Radiol . 2004;15: 1443-1449.
13. Park KB, Do YS, Kang WK, et al. Malignant obstruction of gastric outlet and duodenum: palliation with
flexible covered metallic stents. Radiology. 2001;219:679-683.
14. Jung GS, Song HY, Kang SG, et al. Malignant gastroduodenal obstructions: treatment by means of a
covered expandable metallic stent-initial experience. Radiology. 2000;216:758-763.
15. Kim JH, Song HY, Shin JH, et al. Metallic stent placement in the palliative treatment of malignant
gastroduodenal obstructions: prospective evaluation of results and factors influencing outcome in 213
patients. Gastrointest Endosc. 2007;66:256-264.
16. Lopera JE, Brazzini A, Gonzales A, et al. Gastroduodenal stent placement: current status. Radiographics.
2004;24:1561-1573.
17. Del Piano M, Ballarè M, Montino F, et al. Endoscopy or surgery for malignant GI outlet obstruction?
Gastrointest Endosc. 2005;61:421-426.
Radiology Books
18. Sabharwal T, Irani FG, Adam A. Quality assurance guidelines for placement of gastroduodenal stents.
Cardiovasc Intervent Radiol . 2007;30:1-5.
19. Zollikofer CL, Jost R, Schoch E, et al. Gastroduodenal and colonic stents. Semin Interv Radiol .
2001;18:265-280.
20. Lindsay JO, Andreyev HJ, Vlavianos P, et al. Self-expandable metal stents for the palliation of malignant
gastrointestinal obstruction in patients unsuitable for surgical bypass. Aliment Pharmacol Ther. 2004;19:901-
905.
21. Bae JI, Shin JH, Song HY, et al. Use of guiding sheaths in peroral fluoroscopic gastroduodenal stent
placement. Eur Radiol . 2005;15:2354-2358.
22. Morgan R, Adam A. Use of metallic stents and balloons in the esophagus and gastrointestinal tract. J
23. Dormann A, Meisner S, Verin N, et al. Self-expanding metal stents for gastroduodenal malignancies:
systematic review of their clinical effectiveness. Endoscopy. 2004;36: 543-550.
24. Pinto Pabón IT, Díaz LP, Ruiz De Adana JC, et al. Gastric and duodenal stents: follow-up and
complications. Cardiovasc Interv Radiol . 2001;24:147-153.
25. Lopera JE, Alvarez O, Castaño R, et al. Initial experience with Song's covered duodenal stent in the
treatment of malignant gastroduodenal obstruction. J Vasc Interv Radiol . 2001;12:1297-1303.
26. Kim JH, Song HY, Shin JH, et al. Stent collapse as a delayed complication of placement of a covered
gastroduodenal stent. AJR Am J Roentgenol . 2007;188:1495-1499.
27. Binkert CA, Jost R, Steiner A, et al. Benign and malignant stenoses of the stomach and duodenum:
treatment with self-expanding metallic endoprostheses. Radiology. 1996;199:335-338.
28. Feretis C, Benakis P, Dimopoulos C, et al. Palliation of malignant gastric outlet obstruction with self-
expanding metal stents. Endoscopy. 1996;28:225-228.
29. Yates MR III, Morgan DE, Baron TH. Palliation of malignant gastric and small intestinal strictures with
self-expandable metal stents. Endoscopy. 1998;30:266-272.
30. Tang T, Allison M, Dunkley I, et al. Enteral stenting in 21 patients with malignant gastroduodenal
obstruction. J R Soc Med. 2003;96:494-496.
Radiology Books
e-81
Colorectal Stent Placement
Jin Hyoung Kim
Ho-Young Song
Ji Hoon Shin
In 1992, Spinelli et al. (1) first described metallic stent placement within the colon for treatment of malignant large
bowel obstruction. Since then, metallic stents have been increasingly used for safe nonsurgical palliation for
unresectable malignant colorectal obstructions and as a bridge to surgery to allow stabilization of the patient's
condition (2,3,4,5,6,7,8,9,10,11,12,13,14,15,16). Because surgical decompression has been associated with
high morbidity and mortality, minimally invasive stent placement is preferred to open surgery (2,11,12,13).
Colorectal stent placement is performed via the transanal route under a fluoroscopic guidance alone or in
combination with endoscopy. Placement under conscious sedation is generally well tolerated by patients. The
procedure allows immediate large bowel decompression with rapid resolution of patients' symptoms and
restoration of normal intestinal transit (11,12).
Indications (2,17,18)
1. Temporary colonic decompression to allow stabilization of the patient's condition before curative surgery for
malignant or benign (rarely) colorectal obstructions
2. Palliative treatment in patients with inoperable malignant colorectal obstructions
3. Covered stent placement for colonic fistulae
Contraindications (2,15,17)
1. Clinical or imaging evidence of perforation or peritonitis
3. Multiple obstructive lesions of the small bowel
4. Extension of rectal cancer to the anal sphincter
5. Location of obstruction is far too proximal within the colon (antegrade approach via cecostomy has been
described).
6. Obstruction is too long.
2. Barium studies and/or endoscopy to evaluate the site, severity, and length of the stricture and perforation or
proximal synchronous stricture
3. Prophylactic antibiotics are not routinely recommended.
4. Perform cleansing enema to clear the distal colon.
necessary.
Radiology Books
Procedure (2,15,17,19)
1. A variety of bare or covered expandable metallic stents have been used in the treatment of malignant
colorectal strictures: the enteral WALLSTENT (Boston Scientific, Natick, MA), precision colonic Ultraflex stent
(Boston Scientific, Natick, MA), colonic Z-stent (Wilson-Cook, Winston-Salem, NC), WallFlex stent (Boston
Scientific, Natick, MA), Niti-S colorectal stent (Tae Woong Medical, Ilsan, South Korea), Memo-therm colonic
stent (C. R. Bard Inc, Billerica, MA), and dual colorectal stent (S&G Biotech, Seongnam, South Korea). Various
stent delivery systems are used, and they range in diameter from 10 to 31 Fr. Device is selected based on length
of obstruction and distance from anus.
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2. The procedure is performed under a conscious sedation.
3. Patients are placed in the left lateral decubitus position, and then a 0.035-in. exchange guidewire (Radifocus
M; Terumo, Tokyo, Japan) and a catheter (100 cm, 5 Fr. or 6 Fr.) are inserted through the anus, across the
obstruction, into the proximal part of the obstruction. Care is taken to avoid perforation of friable tumors (Fig. e-
81.1A).
4. If the guidewire cannot be negotiated through the stricture with fluoroscopic guidance alone, combining
endoscopic and fluoroscopic guidance at the same sitting may be attempted.
5. Once the catheter has passed beyond the stricture, water-soluble contrast medium is injected to delineate the
adjacent anatomy (Fig. e-81.1B).
6. The initial guidewire is replaced with a 260-cm exchange-length Amplatz superstiff guidewire
(Meditech/Boston Scientific, Watertown, MA) (Fig. e-81.1C).
7. In very tight stenoses, predilation with an 8- or a 10-mm balloon can be performed to allow easy passage of
the stent delivery system. The stent is deployed under fluoroscopic guidance and should be 4 to 6 cm longer
than the stricture to allow a sufficient margin of stent on either side of the obstruction.
8. Contrast injection is performed to rule out perforation and to assess stent position and patency.
Radiology Books
FIGURE e-81.1 • Technique for colorectal stent placement. A: A catheter and guidewire are inserted into the
rectosigmoidal segment and manipulated through the obstruction. B: The distal end of the obstruction is
delineated by injection of a small amount of contrast medium. C: The wire is exchanged with a superstiff
guidewire. The catheter is then removed and the stent delivery system is advanced over the stiff guidewire. D:
The stent is deployed overlapping the obstruction.
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9. A long stricture may require overlapping of stents (Fig. e-81.1D).
10. Once the stent is placed, balloon dilation is usually not required as most self-expanding stents will gradually
reach their full diameter. However, if the stent expands to less than one-third of its nominal diameter, balloon
dilation may be performed.
Postprocedure Management (2,15)

1. Rapid evacuation is to be expected. In about 6% of patients, obstruction is not relieved immediately and
further investigation of the cause is warranted.
2. A water-soluble enema examination is performed immediately or 1 day after the procedure to assess the
expansion and patency of the stent and possible complications.
3. For surgical resection candidates, medical treatment and bowel cleaning are administered.
4. Patients with unresectable disease are advised to consume a low-residue diet and mineral oil to decrease
possibility of stent obstruction due to impaction of feces.
Results
Radiology Books
Technical Success
1. Technical success is defined as the passing of a guidewire and the suitable placement of the stent.
Review of the literature on metallic stenting, using fluoroscopic or endoscopic guidance, suggests that
technical success is achieved in approximately 96% of the patients with malignant colorectal obstruction
(11,14,15).
2. Technical failure is most commonly due to an inability to pass a guidewire because of complete
obstruction or tortuous anatomy (11,15).
Clinical Success
1. Clinical success is defined as colonic decompression with resolution of obstructive symptoms within 48 or
72 hours after stent placement. Review of publications (11,14,15) on metallic stenting, using fluoroscopic or
endoscopic guidance, reveals clinical success in 92% to 96% of the patients with malignant colorectal
obstruction.
2. Some patients do not show an improvement in their symptoms after successful stent placement due to
incomplete stent expansion, extension of the tumor to the adjacent small bowel, or unrecognized obstruction
in another segment of the small or large bowel.

1. Perforation
Perforation is a serious complication, reported in approximately 4% of patients implanted with colorectal self-
expandable metallic stents (11). Perforation occurs usually within 30 days and may be related to excessive
manipulation of guidewires, pre- or poststent balloon dilation, stent wire penetration, severe obstruction, or
inexperience (11,15,20,21,22). The perforation site is either in the tumor bed or in the normal colon proximal to it.
The cause of perforation of the normal colon proximal to the tumor bed is pressure necrosis from the proximal
ends of bare stents (15). Surgical intervention with administration of antibiotics is required to manage such
perforation.
2. Stent obstruction
Obstruction is reported in approximately 12% of patients with stents placed for palliation and is caused by tumor
ingrowth or overgrowth, stent migration,
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or fecal impaction (12). Obstruction caused by tumor ingrowth or overgrowth, or a stent migration, can be
managed by coaxial placement of a second stent that overlaps the ends of the initial stent. Fecal impaction can
be treated by endoscopic clearance.
3. Stent migration
Stent migration is reported in approximately 11% of patients with stents placed for palliation (12). Bridge-to-
surgery patients have lower rates of stent migration because the stent remains in the colon for a shorter time.
Migration rates are higher with covered stents: 30% to 50% (22,23), compared with uncovered stent: 3% to 12%
(10,24,25). Other potential factors associated with stent migration include balloon dilation prior to stent
placement and the use of chemotherapy, radiation therapy, or laser treatment (10,15). Stents usually migrate
distally and can be expulsed through the rectum (10).
4. Other
Other reported complications include rectal bleeding, anal/abdominal pain, and tenesmus. These complications
are rare and can be managed by conservative treatment (11).
Radiology Books
References
1. Spinelli P, Dal Fante M, Mancini A. Self-expanding mesh stent for endoscopic palliation of rectal
obstructing tumors: a preliminary report. Surg Endosc. 1992;6:72-74.
2. Mauro MA, Koehler RE, Baron TH. Advances in gastrointestinal intervention: the treatment of
gastroduodenal and colorectal obstructions with metallic stents. Radiology. 2000;215:659-669.
3. Arnell T, Stamos MJ, Takahashi P, et al. Colonic stents in colorectal obstruction. Am Surg. 1998;64:986-
988.
4. Harris GJ, Senagore AJ, Lavery IC, et al. The management of neoplastic colorectal obstruction with
colonic endolumenal stenting devices. Am J Surg. 2001;181:499-506.
5. Geraghty J, Sarkar S, Cox T, et al. Management of large bowel obstruction with self-expanding metal
stents. A multicentre retrospective study of factors determining outcome. Colorectal Dis. 2014;16:476-483.
6. Abbott S, Eglinton TW, Ma Y, et al. Predictors of outcome in palliative colonic stent placement for
malignant obstruction. Br J Surg. 2014;101:121-126.
7. Lopera JE, De Gregorio MA. Fluoroscopic management of complications after colorectal stent placement.
Gut Liver. 2010;4(suppl 1):S9-S18.
8. de Gregorio MA, Laborda A, Tejero E, et al. Ten-year retrospective study of treatment of malignant colonic
obstructions with self-expandable stents. J Vasc Interv Radiol . 2011;22:870-878.
9. de Gregorio MA, Mainar A, Tejero E, et al. Acute colorectal obstruction: stent placement for palliative
treatment—results of a multicenter study. Radiology. 1998;209:117-120.
10. Sebastian S, Johnston S, Geoghegan T, et al. Pooled analysis of the efficacy and safety of self-
expanding metal stenting in malignant colorectal obstruction. Am J Gastroenterol . 2004;99:2051-2057.
11. Watt AM, Faragher IG, Griffin TT, et al. Self-expanding metallic stents for relieving malignant colorectal
obstruction: a systemic review. Ann Surg. 2007;246:24-30.
12. Fregonese D, Naspetti R, Ferrer S, et al. Ultraflex precision colonic stent placement as a bridge to
surgery in patients with malignant colon obstruction. Gastrointest Endosc. 2008;67:68-73.
13. Repici A, Fregonese D, Costamagna G, et al. Ultraflex precision colonic stent placement for palliation of
malignant colonic obstruction: a prospective multicenter study. Gastrointest Endosc. 2007;66:920-927.
14. Small AJ, Baron TH. Comparison of Wallstent and Ultraflex stents for palliation of malignant left-sided
colon obstruction: a retrospective, case-matched analysis. Gastrointest Endosc. 2008;67:478-488.
15. Song HY, Kim JH, Shin JH, et al. A dual-design expandable colorectal stent for malignant colorectal
Radiology Books
obstruction: results of a multicenter study. Endoscopy. 2007;39:448-454.
16. Repici A, De Caro G, Luigiano C, et al. WallFlex colonic stent placement for management of malignant
colonic obstruction: a prospective study at two centers. Gastrointest Endosc. 2008;67:77-84.
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17. Mauro MA, Murphy KPJ, Thomson KR, et al, eds. Image-Guided Interventions. Philadelphia, PA:
Saunders/Elsevier, 2008.
18. Small AJ, Young-Fadok TM, Baron TH. Expandable metal stent placement for benign colorectal
obstruction: outcomes for 23 cases. Surg Endosc. 2008;22:454-462.
19. Baron TH. Colonic stenting: technique, technology, and outcomes for malignant and benign disease.
Gastrointest Endosc Clin N Am. 2005;15:757-771.
20. van Hooft JE, Fockens P, Marinelli AW, et al. Early closure of a multicenter randomized clinical trial of
endoscopic stenting versus surgery for stage IV left-sided colorectal cancer. Endoscopy. 2008;40:184-191.
21. Suzuki N, Saunders BP, Thomas-Gibson S, et al. Colorectal stenting for malignant and benign disease:
outcomes in colorectal stenting. Dis Colon Rectum. 2004;47:1201-1207.
22. Choo IW, Do YS, Suh SW, et al. Malignant colorectal obstruction: treatment with a flexible covered stent.
Radiology. 1998;206:415-421.
23. Kang SG, Jung GS, Cho SG, et al. The efficacy of metallic stent placement in the treatment of colorectal
obstruction. Korean J Radiol . 2002;3:79-86.
24. Camúñez F, Echenagusia A, Simó G, et al. Malignant colorectal obstruction treated by means of self-
expanding metallic stents: effectiveness before surgery and in palliation. Radiology. 2000;216:492-297.
25. Law WL, Chu KW, Ho JWC, et al. Self-expanding metallic stent in the treatment of colonic obstruction
caused by advanced malignancies. Dis Colon Rectum. 2000;43:1522-1527.
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e-82
Retrieval of Intravascular Foreign Bodies
Aneeta Parthipun
Tarun Sabharwal
The majority of intravascular foreign bodies (FBs) are the result of iatrogenic complications. First-line treatment is
percutaneous radiologic extraction. Since its first description 50 years ago, there has been increased application
of these techniques correlating with the expansion of endovascular procedures generally (1). Early reports on FB
retrieval techniques focused on broken catheters, guidewires, and vena cava filters. The spectrum of
endoluminal foreign bodies requiring removal has broadened and now includes embolization coils, ruptured
angioplasty balloons, and endovascular stents.
Endovascular retrieval of FBs is generally an effective, safe technique, which avoids the need for major surgery.
Given the disparate group of potential FBs, retrieval strategies depend on the device and its position within the
vasculature. In the majority of cases, it is essential to retrieve the FB to prevent potentially life-threatening
complications including sepsis, thrombosis, clot embolism, arrhythmias, and vascular perforation (2).
Indications
1. Misplaced or fractured guidewire, catheter, pacemaker wire, and broken endovascular device fragments
2. Misplaced embolization coils (Fig. e-82.1)
3. Malpositioned arterial and venous stents
4. Inferior vena cava (IVC) filters including both routine and complicated removal particularly when the filter
tip is angled against the IVC wall, is discussed further elsewhere in the book.
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Radiology Books
FIGURE e-82.1 • Misplaced Nester coil (Cook Medical Inc, Bloomington, IN) during embolization of the renal
artery. The coil embolized and became lodged within the profunda femoris artery.
Contraindications
Absolute
Relative
Each individual case must be considered in regard to the benefits of the procedure in light of the risks
associated with endovascular retrieval, if in fact removal is necessary. The risk of surgical removal must
also be considered.
1. Extensive thrombus attached to the FB that will embolize on removal
2. Firmly embedded or adherent FB that might result in vessel wall perforation. A sturdy tug on the catheter
fragment after snaring may result in a life-threatening or hazardous vasculature tear. In such cases, surgery
as a primary treatment option may be more appropriate.
3. When structural damage to the heart or vascular system might result. Surgery may be required in patients
with FBs in high-risk sites.
4. The risk of a lengthy intervention should always be balanced against the risk of retaining the FB. If
several percutaneous endeavors to snare an FB fail and
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the object is small, then the possibility of added intervention may outweigh the prospective benefits.
Radiology Books
1. Review of all imaging, preferably in a multidisciplinary setting, to identify (a) the precise location of the FB and
(b) the vascular access most suitable for retrieval. Multiplanar reconstructed computed tomography (CT) is a
valuable tool for planning.
2. For intracardiac FB, assess the presence of tamponade, valve involvement, and arrhythmias.
3. Check to ensure the appropriate equipment is available (Fig. e-82.2). In certain cases, more than one retrieval
system or technique may be necessary to achieve successful removal (3).
4. Laboratory evaluation including complete blood count (CBC), clotting parameters, and renal function. The
international normalized ratio (INR) should be corrected to <1.5 seconds, and the platelet count corrected to
>75,000 per μL.
a. Ensure anticoagulants have been stopped, if appropriate. If the patient is at moderate risk of bleeding,
clopidogrel should be withheld for 5 days prior to the intervention. If the patient is at high risk of bleeding, then
both clopidogrel and aspirin should be withheld for 5 days.
5. Patients should be on nil per os (NPO) 6 to 8 hours prior to the procedure. No clear liquids should be
consumed for 3 to 4 hours prior to the procedure.
FIGURE e-82.2 • Devices used for foreign body retrieval. A: Single-loop snare (ONE Snare, Merit Medical,
South Jordan, UT). B: Triple-loop snare (EN Snare, Merit Medical, South Jordan, UT). C: Retrieval basket
(Cook Medical Inc, Bloomington, IN). D: Grasping Forceps (Cook Medical Inc, Bloomington, IN).
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6. Start intravenous fluids (150 mL per hour) to ensure adequate hydration of the patient. Monitor fluid status.
Renal dialysis patients may need coordination of dialysis. However, it is important to note that these cases often
require only small volumes of contrast.
7. Informed written consent
Radiology Books
Procedure
a. Appropriate vascular access is chosen to facilitate FB removal, commonly single access or a combination
of the common femoral artery or vein and the jugular vein. An appropriately sized sheath should be inserted
to allow for easy removal and avoid trauma at the exit site. A “buddy wire” or parallel wire introduced
outside the sheath may be beneficial to maintain vascular access when FB removal requires sheath
removal.
b. Intraprocedural anticoagulation. An intra-arterial or intravenous dose of 5,000 IU heparin is injected at the
beginning of the procedure. Thereafter, further doses of heparin may be required to maintain an activated
clotting time (ACT) of greater than 250 seconds.
c. Anesthesia. FB retrieval can often be performed under local anesthesia; however, as part of the planning
stage of the procedure and following consideration of the complexity of the individual case along with the
patients' clinical status, sedation or general anesthesia may be required.
2. Specific scenarios
a. FB with free end
(1) Manufactured loop snare. The most popular snare device is a single-loop snare such as Amplatz
GooseNeck Snare (ev3, Plymouth, MN) or the ONE Snare (Merit Medical Systems, South Jordan, UT) (Fig.
e-82.2A) manufactured in a range of sizes (diameters from 5 to 35 mm). There are also microsnares
(diameters from 2 to 7 mm). The chosen diameter should correspond to the target vessel diameter. The
snare is deployed through a guide catheter (which has a radiopaque marker). To use the snare:
(a) Place a guidewire next to the FB. This is an essential beginning point. If this is not achieved, the
retrieval of the FB will not be possible.
(b) Advance the guide catheter over the guidewire and then remove the guidewire.
(c) The snare is compressed within an introducer, which should be advanced into the guide catheter.
(d) Push the snare loop out of the guide catheter tip and rotate to enable the loop to fully form and open
completely. The snare loop can now be advanced, retracted, or manipulated in order to grasp the FB.
(e) When the FB is within the snare loop, keep the loop still with controlled traction while advancing the
guide catheter over the snare loop and the FB (Fig. e-82.3D,E).The controlled traction grips the FB and
tightens the snare.
(f) Pull the snare attached to the FB back into the access sheath while maintaining tension on the closed
snare loop (Fig. e-82.3F).
Alternatively, a triple-loop snare (EN Snare, Merit Medical Systems, South Jordan, UT) (Fig. e-82.2B) can
be used (sizes from 2 to 45 mm). This snare is particularly useful when working in a confined space, or
when there is difficulty in turning the snare.
(2) A homemade loop snare could be considered if manufactured snares are unavailable. These can be
fabricated using a 5 Fr. diagnostic headhunter or multipurpose catheter and a 0.018-in. heavy-duty wire,
bent in the middle to create an eccentric loop, and doubled back out through the catheter hub (4). Such
homemade snares are often not as effective as a manufactured snare device.
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(3) Retrieval baskets (Fig. e-82.2C) have been shown to be effective and may be able to grasp objects
that have avoided capture (5). These have a low profile (2.4 Fr.) and can therefore be passed down a
narrow guide catheter and access small diameter vessels. The basket provides a wide loop that is valuable
Radiology Books
to encompass the FB (6). The disadvantage of this device is that it is difficult to manipulate.
(4) Flexible grasping forceps (Fig. e-82.2D) have been shown to be effective adjuncts in difficult cases
(3). The forceps are 3 Fr. and can be inserted into a catheter that accepts a 0.038-in. guidewire. This
device is beneficial when operating in a restricted space. Forceps are more traumatic than snares because
they can potentially grasp the vessel wall adjacent to the FB and therefore often not the first choice device.
b. FB with no free end
(1) Create a free end that can then be snared. This can be done by hooking the shaft of the FB with a
pigtail catheter, reverse curve catheter, or tipdeflecting wire or catheter to double the FB on itself and move
it into a more favorable position.
(2) Flexible grasping forceps can be considered when a suitable free end cannot be created and particularly
when the FB lies perpendicular rather than parallel to the vessel.
(3) A triple-loop snare can sometimes be useful when there is no free end (embedded ureteric stent). In
such cases, the triple-loop snare can grasp the side of the FB enough to pull into a position that permits
removal with a grasping forceps.
c. Stent reposition/retrieval
(1) If a stent migrates or is otherwise unsuitably deployed, it is important to keep the wire through the stent
lumen. This will enable a balloon to be inflated inside or distal to the stent for manipulating it into a more
favorable position for retrieval or deployment at a “safe” site where it will cause minimal morbidity.
(2) For self-expanding stents that are flexible and easily compressible (Fig. e-82.4A-C), the free end can be
snared and withdrawn into the guiding catheter (7). Rigid balloon-expandable stents cannot be easily
retrieved in this manner unless they are unexpanded or only partially expanded. For large-diameter stents
that cannot be retrieved through the guiding catheter, the entire assembly may be retrieved through an
appropriately upsized long sheath.
d. Distal wire grab technique: A guidewire is passed through the FB. A microsnare (Fig. e-82.2A) is
passed parallel to the wire and past the FB. The microsnare is then used to snare the distal aspect of the
guidewire that traverse the FB. The FB is confined between the guidewire and the snare catheter (1).
e. Difficult IVC filter retrieval
Routine IVC filter removal is covered elsewhere in the text. The most common reason for difficult IVC filter
retrieval is significant tilt or abutment of the tip (hook) against the IVC wall, impeding engagement with a
snare (6). When retrieving the OptEase filter (Cordis Endovascular, Miami Lakes, FL), the buddy wire
technique is useful. A stiff guidewire is threaded via a femoral sheath through the filter body to better align
the device and free the hook for snaring. There are three main techniques to achieve the same for a
Günther Tulip or Celect filter (Cook Medical Inc, Bloomington, IN), attempted in the following order (4):
(1) Curved catheter-twist technique. A curved catheter is placed through the standard retrieval kit sheath
and twisted within the filter to dislodge the hook from the IVC wall, thereby allowing it to be snared.
(2) Modified snare technique. The snare is introduced using a 7 Fr. curvetipped catheter to allow
directional control toward the hook.
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Radiology Books
FIGURE e-82.3 • Loop snare technique for an IVC filter (Celect, Cook Medical Inc, Bloomington, IN) (shown
here) that is difficult to retrieve. A: A reverse curve (or pigtail) catheter is placed through a large sheath
(SH) and used to hook the filter struts. B: A guidewire (GW) is introduced through the catheter. C: The GW
tip is grasped with a loop snare via the same SH. D: The distal tip of GW is pulled back through the SH
outside of patient, (E) holding both ends and maintaining minimal tension on the looped GW, the sheath is
advanced over the filter, and (F) the entire assembly is removed as a unit once the filter is seated within the
sheath.
(3) Loop-snare technique (Fig. e-82.3A-F). Using right internal jugular (RIJ) vein access, a reverse curve
catheter, hooked through at least two struts of the filter, is used to advance an exchange-length wire with its
tip pointing upward toward the internal jugular (IJ) sheath. The wire tip is snared in the upper IVC and
withdrawn back through the sheath to form a loop (around the filter) with both ends of the wire accessible
outside. Then a long coaxial sheath (8 to 16 Fr.) can be advanced over both wires to encase the filter for
retrieval. Alternatively, a loop snare can be advanced over both wires to the filter to snare its hook,
simultaneously manipulating the wires and retrieving it into the sheath (8,9).
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Radiology Books
FIGURE e-82.4 • Retrieval of malpositioned stent. A: A stenosis is identified at the origin of left subclavian
artery (thin black arrow). B: Left anterior oblique (LAO) projection of 10 × 40 mm self-expanding stent is
displaced inferiorly into the aorta (black arrow) upon deployment. Note: The wire is maintained through the
stent. C: Proximal end of the stent has been snared and withdrawn into the sheath (short black arrow),
shown retracted into common iliac artery.
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1. Observation of access site, vital signs, and distal pulses for 4 to 6 hours following arterial access; shorter
observation for venous access as per protocol. When stable, oriented, ambulatory, and able to tolerate oral
intake, the patient can be discharged home accompanied by a responsible adult along with clear postoperative
instructions.
2. Following venous intervention, if high risk for thrombosis, consider heparin for 24 to 48 hours (4).
Radiology Books
3. Cardiac monitoring for risk of arrhythmia or tamponade should be performed in cases involving intracardiac FB
removal or manipulations in the cardiac chambers.
Results
1. Success rates for retrieval of FB range from 91% to 100% (7,10). Success rates of 100% have been
reported with homemade wire snares (11) and Dormia baskets (5). Failure is attributable to incorporation
into the vessel wall due to endothelialization.
2. A 97% success rate has been reported for difficult Günther Tulip IVC filter removal (4).
Complications
1. Distal embolization of FB into an irretrievable location
2. Perforation or damage to the vessel wall, particularly if the FB was firmly embedded requiring excessive
manipulation
3. Thromboembolism, from either thrombus associated with FB, or if procedure is prolonged and
complicated, intraprocedural thrombus formation
4. Transient arrhythmias may occur during removal of an FB from the pulmonary artery via the right
ventricle. Injury of the cardiac valves and chambers during retrieval of an intracardiac FB may result in
hemopericardium and tamponade. Cardiothoracic surgery should be on standby, for appropriate cases.
1. To manage an injured vessel when there is evidence of extravasation, inflation of an occlusion balloon
with a view to deployment of a covered stent may be appropriate. Surgical conversion may be required.
2. Consider surgical cut down at the access site if the FB is too large to be removed percutaneously.
3. Anticoagulation, if clinically significant thromboembolism occurs
4. Cardiology consult and arrhythmia monitoring and management after complicated intracardiac FB
retrieval
References
1. Woodhouse JB, Uberoi R. Techniques for intravascular foreign body retrieval. Cardiovasc Intervent
Radiol . 2013;36:888-897.
2. Prahlow JA, O'Bryant TJ, Barnard JJ. Cardiac perforation due to Wallstent embolization: a fatal
complication of the transjugular intrahepatic portosystemic shunt procedure. Radiology. 1997;205:170-172.
3. Egglin TK, Dickey KW, Rosenblatt M, et al. Retrieval of intravascular foreign bodies: experience in 32
cases. AJR Am J Roentgenol . 1995;164:1259-1264.
4. Van Ha TG, Vinokur O, Lorenz J, et al. Techniques used for difficult retrievals of the Günther Tulip inferior
vena cava filter: experience in 32 patients. J Vasc Interv Radiol . 2009;20:92-99.
Radiology Books
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5. Sheth R, Someshwar V, Warawdekar G. Percutaneous retrieval of misplaced intravascular foreign objects

with the Dormia basket: an effective solution. Cardiovasc Intervent Radiol . 2007;30:48-53.
6. Pfammatter T, Hechelhammer L, Pfiffner R. A “Buddy Wire” technique for successful OptEase filter
retrieval. J Vasc Interv Radiol . 2009;20:656-659.
7. Gabelmann A, Kramer S, Gorich J. Percutaneous retrieval of lost or misplaced intravascular objects. AJR
Am J Roentgenol . 2001;176:1509-1513.
8. Rubenstein L, Chun AK, Chew M, et al. Loop-snare technique for difficult inferior vena cava filter
retrievals. J Vasc Interv Radiol . 2007;18:1315-1318.
9. Kuo WT, Bostaph AS, Loh CT, et al. Retrieval of trapped Günther Tulip inferior vena cava filters: snare-
over-guidewire loop technique. J Vasc Interv Radiol . 2006;17: 1845-1849.
10. Koseoglu K, Pailar M, Oran I, et al. Retrieval of intravascular foreign bodies with goose neck snare. Eur J
Radiol . 2004;49:281-285.
11. Mallmann CV, Wolf KJ, Wacker FK. Retrieval of foreign bodies using a self-made wire snare. Acta
Radiol . 2008;49(10):1124-1128.
Radiology Books
e-83
Liver Transplant Management
Wael E.A. Saad
Interventional radiology plays an integral role in the care of patients after liver transplantation, which includes
percutaneous interventions for treatment of vascular complications. Complications of the hepatic artery include
hepatic artery stenosis (HAS), hepatic artery thrombosis (HAT), arterioportal fistula (APF), hepatic artery
pseudoaneurysm (HAP), and nonocclusive hepatic artery hypoperfusion syndrome (NOHAH). The consequence
of diminished hepatic artery flow is far more significant in hepatic transplants than native livers because the
biliary tree is totally reliant on the hepatic artery (1,2). Hepatic outflow obstruction can be caused by either
hepatic venous (HV) or inferior vena cava (IVC) stenosis/thrombosis, usually at an anastomosis. Portal inflow
may be compromised by portal vein stenosis (PVS) usually at the anastomosis, portal vein thrombosis (PVT),
and portal hypertension (3,4,5). On the rare occasion, portal vein inflow can be compromised by steal
phenomenon from competing portosystemic collaterals.
Nonvascular complications of liver transplants are discussed elsewhere in this handbook and are dominated by
postoperative fluid collections and biliary strictures or obstruction with similar indications, contraindications, end
points, and complications as in nontransplant patients.
Indications (1,2,6,7,8,9,10)
1. Angioplasty or stent placement to treat HAS or HAT
a. Hepatic graft dysfunction
b. Abnormal noninvasive imaging of the hepatic artery with or without hepatic graft dysfunction
2. Embolization of APFs
a. Symptomatic, for example, graft dysfunction, bleeding
b. Asymptomatic
(1) Rapidly growing
(2) Hemodynamic changes seen on Doppler ultrasound, for example, portal flow reversal
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3. Embolization of HAPs
a. Intrahepatic—all regardless of size
b. Extrahepatic—temporizing prior to surgery
4. Angioplasty or stent placement to treat hepatic, IVC, or PVT or thrombosis
a. Hepatic graft dysfunction
b. Abnormal noninvasive imaging of the venous structures with or without hepatic graft dysfunction
c. Mean pressure gradient across anastomosis of >5 mm Hg
Contraindications
Relative
Radiology Books
3. Prior severe allergic reaction to iodinated contrast material
a. Consider use of gadolinium or CO2.
4. Unstable patient
a. Consider anesthesia consultation for assistance in patient management during intervention.
1. Laboratory evaluation: Most patients will have had extensive blood testing. Ensure current complete blood
count (CBC), platelet count, renal and hepatic function tests, and international normalized ratio (INR) are
available. Correct platelet count to >50,000 and INR to <1.7 seconds when possible. It is preferred to transfuse
platelets during the procedure and not before because many of these patients sequester platelets due to their
large spleens.
2. No food by mouth except normal medications with a sip of water for at least 6 hours; clear liquids can be
consumed up to 2 hours prior to the procedure.
3. Evaluate prior surgical operative notes, in particular the surgical transplant anatomy.
4. Review prior imaging. Careful study of surgical anatomy and imaging reduces angiographic time and inventory
utilization (1).
Procedure
Hepatic Artery Interventions
a. Review noninvasive imaging (duplex ultrasound, computed tomographic angiography [CTA], or
magnetic resonance angiography [MRA]) prior to angiography, the gold standard for the diagnosis of
arterial abnormalities.
b. Right common femoral artery access is preferred in most cases. Patients with significant
atherosclerotic aortoiliac disease may require a long (20 to 30 cm) arterial sheath.
2. HAS or HAT
a. Arteriography
(1) Abdominal aortography can be performed; however, it may not be necessary if the patient has had
a prior CTA. If there is suspicion of a proximal stenosis, perform a lateral aortogram (1).
(2) A celiac angiogram must be performed to evaluate the hemodynamics of the celiac trunk and to
exclude an arterial steal syndrome. Nonfilling of the graft hepatic artery on a celiac angiogram does not
suffice for the diagnosis of HAT. There may be a critical HAS with preferential flow to other celiac
branches or arterial steal phenomena. A selective hepatic artery angiogram to confirm occlusion is
required.
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(3) Catheter selection for selective hepatic arteriography is based on the surgical hepatic artery
anatomy (1,8,9).
(a) Supraceliac direct aortohepatic conduit can usually be catheterized with a Cobra (C-2) catheter.
Radiology Books
(b) Infrarenal aortohepatic conduit off the aorta anteriorly and extending cephalad to the liver can be
catheterized with a vertebral or similar shaped catheter.
(c) Graft hepatic artery anastomosis to recipient hepatic artery or other branch off the celiac trunk is
the most common arterial anastomosis performed. An Sos Omni or C-2 Cobra catheter may be used.
(4) Collateral arteries should be documented. When intrahepatic arterial flow is demonstrated by
Doppler ultrasound but occlusion of the hepatic artery is seen on angiography, there is collateral
arterial supply (9).
(5) If HAS is seen, perform further imaging in multiple projections:
(a) To determine the angle orthogonal to the stenosis
(b) To assess the entire hepatic artery for tandem lesions, tortuosity, or kinking
b. Hepatic artery angioplasty/stent placement
(1) The hepatic artery is measured for angioplasty balloon or stent sizing.
(2) A 6 Fr. braided 45- to 70-cm sheath is advanced to the origin of the celiac axis or the proximal
aortohepatic conduit.
(3) Administer heparin—3,000 units intravenous (IV) and 1,000 units every 20 to 30 minutes thereafter.
(4) Proximal lesions can be managed using a 0.035-in. coaxial platform. Smaller tortuous arteries and
distal lesions usually require 0.014- to 0.018-in. platforms.
(5) Rather than primary stenting, the author prefers initial balloon angioplasty with stent placement
reserved for refractory lesions, or when there are complications.
(6) If there are tandem lesions, the distal stenosis is treated first unless the proximal lesion hinders
passage of the balloon. Predilation with an undersized balloon is often performed (11,12).
(7) A postangioplasty angiogram is done to assess results and exclude dissection or thrombus.
(8) If results are unsatisfactory or a complication results, a stent is placed.
(a) The author prefers 0.014-in. platforms with balloon-mounted low-profile stents.
(b) The femoral approach usually suffices, but uncommonly, a brachial approach is required.
(c) Always have nitroglycerine in the room ready during balloon angioplasty and/or stenting because
vasospasm is not uncommon and can be detrimental leading to HAS and predisposing to hepatic
artery dissection with wire and catheter manipulation.
3. Arterioportal fistulas (2,13)
a. Perform selective hepatic arteriography; however, seeing the fistulous tract is rare. Angiographic
signs of a hemodynamically significant APF include:
(1) Filling of a portal venous radical in the early arterial phase
(2) Nonvisualization of the distal arterial branches (sump effect)
b. Microcatheters are used to get as selective as possible into the hepatic arterial branches, to reduce
the risk of inducing HAT, and to minimize damage to normal liver.
c. Microcoils tailored to the size of the involved artery are deployed. Ideally, complete obliteration is the
end point; however, enough occlusion to reduce flow into the PV will often suffice.
d. A hepatic arteriogram should be repeated to look for additional fistulas. Obliterating a dominant
fistula may unmask others. The additional sites may be occluded in this or subsequent sessions. The
mindset should be analogous
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to managing complex vascular malformations, that is, the more one does in any single session, the
Radiology Books
greater the risk of complication—especially HAT and segmental ischemia of the graft.
4. Pseudoaneurysms (14,15,16)
a. Spontaneous extrahepatic pseudoaneurysms are usually contained ruptures of mycotic aneurysms
and require prompt open surgery. Stent grafts have a role in stabilizing and temporizing bleeding prior
to surgery.
b. Iatrogenic extrahepatic or major branch pseudoaneurysms from balloon angioplasty can be treated
with stent grafts or balloon tamponade.
c. Intrahepatic pseudoaneurysms of any size should be treated with superselective coil embolization,
either sac obliteration or occlusion of the involved segmental artery distal and proximal to the
pseudoaneurysm.
d. If endovascular access to an intrahepatic pseudoaneurysm is not possible or the pseudoaneurysm
persists after embolization, direct percutaneous therapy should be considered (15).
(1) An ultrasound-guided 21-gauge needle puncture is performed and thrombin and/or microcoils can
be deposited.
(2) An angiography/fluoroscopy-guided gun-site technique can also be used with or without ultrasound
for deeper lesions or if there is concern of injury to larger vessels.
5. NOHAH (2,6,7)
a. NOHAH is hepatic arterial hypoperfusion (slow flow) in the setting of a patent hepatic artery.
(1) It has many causes including increased resistance of the arterial bed of the liver relative to the
spleen. It also may be a response (by reducing hepatic arterial flow) to hyperdynamic (increased)
portal flow. It is not necessarily a simple “arterial steal phenomenon”.
(2) There are two types: splenohepatic (82% to 88%) and gastroduodenalhepatic (12% to 18%).
b. A celiac arteriogram is required for diagnoses.
c. Splenohepatic steal syndromes can be treated by proximal splenic artery coil embolization to reduce
splenic arterial flow or placement of an hourglass stent graft. Surgical options include splenectomy
(6,7).
d. Gastroduodenalhepatic steal syndromes can be treated with coil embolization of the gastroduodenal
artery (GDA). It is imperative to perform a superior mesenteric artery (SMA) angiogram and lateral
aortogram to rule out SMA stenosis or occlusion prior to embolization of the GDA. Untreated SMA
stenosis would be a contraindication to GDA embolization.
Venous Outflow Interventions

1. Anastomotic IVC stenosis or occlusion (10,17)
a. Obtain venous access with a micropuncture set. The right common femoral vein is preferred over
the transjugular approach particularly when dealing with an IVC stenosis close to the cavoatrial
junction.
b. A long vascular sheath with a side arm allowing continuous flushing is inserted.
c. Through a coaxial pigtail catheter, a cavogram is performed in both anteroposterior (AP) and lateral
projections.
d. Pressure gradient measurements are the gold standard for diagnosing IVC stenosis. The author
uses a 4- to 5-mm Hg gradient as the threshold for treatment.
e. The stenosis is traversed with a 0.035-in. wire. A Glidewire may be necessary for a tight stenosis.
Radiology Books
f. If there is significant thrombus, mechanical and possibly pharmaceutical thrombolysis is performed
over 12 to 48 hours before proceeding to angioplasty. If there is minimal or no thrombus, heparin
(1,000 to 3,000 units IV) is given. Some operators would give heparin routinely, but a minority do not in
the absence of any baseline thrombus.
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g. Balloon dilation is performed starting with a 10-mm balloon and then increasing the diameter
incrementally by 2 mm to 110% of the adjacent normal caval diameter.
h. With prolonged balloon inflation, the blood pressure may drop significantly due to a reduction in
venous return.
i. Postangioplasty pressures are recorded. Reduction of the pressure gradient to less than 5 mm Hg is
considered successful.
j. If there is immediate intraprocedural recoil or the cava has restenosed within 1 to 3 months from a
prior venoplasty, a stent is deployed. The author prefers PALMAZ stents (Johnson & Johnson Cordis,
Miami, FL) oversized to 110% to 120% of the IVC diameter to reduce the risk of migration.
k. Catheters and guidewires are removed and hemostasis is achieved.
2. Hepatic vein stenosis or occlusion (10,17)
a. Puncture the right internal jugular vein using a micropuncture set and insert a vascular sheath with a
side arm hooked to continuous flush.
b. Selectively catheterize the hepatic vein using a 5 Fr. catheter. A vertebral, multipurpose (MPA) or C-
2 Cobra catheter can be used.
c. If the stenosis is too tight to be crossed from the IVC, a transhepatic approach can be attempted
using a 22-gauge Chiba needle. Once the hepatic vein is accessed, a 0.018-in. wire is passed into the
vein. After crossing the stenosis, it is engaged with a snare inserted through the jugular vein, and
pulled through into the IVC. The procedure is continued via the transjugular approach. This reduces
the risk of capsular bleeding.
(1) If the wire cannot be passed into the IVC, insert a 4 Fr. sheath over the 0.018-in. wire then
exchange it for a 0.035-in. Glidewire that can be used in a more forceful attempt to enter the IVC.
(2) Some operators will perform the whole venoplasty from a transhepatic approach.
d. Venography and pressure gradients are performed.
e. If there is significant thrombus, mechanical and possibly pharmaceutical thrombolysis is performed
over 12 to 48 hours before proceeding to angioplasty. If there is minimal or no thrombus, heparin
(1,000 to 3,000 units IV) is given.
f. Balloon dilation is performed starting with a 6- to 8-mm balloon and the diameter is increased
incrementally by 2 mm to 110% of the adjacent normal venous diameter.
(1) When there are simultaneous stenoses of both hepatic vein and IVC, kissing venoplasty or stent
placement is required.
(2) The hepatic vein is accessed from the jugular and/or transhepatic approach and the IVC accessed
from the transjugular and/or femoral approach.
g. After venoplasty, venography and pressure measurements are repeated. A reduction of the
pressure gradient to less than 5 mm Hg is considered successful.
h. Immediate recoil or a persistent gradient above 5 mm Hg may warrant stent placement.
(1) The most traditional stent to be used is the self-expanding WALLSTENT (Boston Scientific
Corporation, Natick, MA); however, it requires larger delivery systems than new generation stents.
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(2) If accurate deployment is needed, balloon expandable stents may be used.
(3) Stent sizes for adult whole grafts should be 12 to 14 mm and for adult split grafts 10 to 12 mm. In
pediatric cases, a 7- to 8-mm balloon expandable stent should be used at the minimum. A diameter of 8
mm should take a pediatric liver transplant patient to adolescence/adulthood and when the patient is of
adult size, they can be expanded further.
i. There are cases where repair of both the hepatic outflow disease and transjugular intrahepatic
portosystemic shunt (TIPS) are considered. The
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author performs the lower risk hepatic venous outflow management first. If a hepatic vein stent is
necessary because of postangioplasty recoil, it should be placed carefully to ensure that it will not
hinder subsequent TIPS. Repair of the hepatic veins alone may improve the portal hypertension
sufficiently that no further treatment is necessary.
j. The catheters and sheaths are removed, and hemostasis is achieved.
Portal Venous Interventions

1. Portal venous anastomotic stenosis
a. Access:
(1) Transjugular access when (3):
(a) Coagulopathy is observed.
(b) PVT and thrombolysis is contemplated.
(c) An extrahepatic anastomotic stenosis is observed.
The portal vein is accessed in the same manner as for a TIPS procedure except that it is optimal to
puncture the hepatic vein slightly deeper into the liver and access the portal vein slightly more distant
from the porta hepatis. This is to maximize the distance from the portal access site to the target lesion.
(2) Direct percutaneous transhepatic access (3,4,5)
(a) This is the approach of choice for the author because access is in-line with the long axis of the
portal vein. It allows easier manipulation of devices across the lesion particularly when there is a tight
stenosis.
(b) Transhepatic access does not preclude and may even aid an additional transhepatic approach.
(c) The approach is favored over transjugular access when:
i. The intrahepatic portal radicals are small.
ii. The target stenosis is close to the porta hepatis (typical of split liver grafts).
iii. The anastomotic stenosis is at the branch point of the right anterior and right posterior portal vein
branches in split right lobe hepatic grafts. In this instance, a kissing balloon/stent technique is used,
requiring two separate transhepatic portal access sites.
(d) The principal disadvantage is an increased risk of bleeding, particularly if thrombolytics are
administered for PVT or the patient is coagulopathic.
b. Once secure access is achieved, a portal venogram is performed and pressure gradients assessed.
The author uses a 5-mm Hg gradient as the cutoff for significant stenosis.
c. The stenosis is traversed with a 0.035-in. wire, and 3,000 units of heparin are administered
intravenously.
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d. If there is significant thrombus, the vein is cleared with mechanical and possibly pharmaceutical
thrombolysis over 12 to 48 hours before proceeding to angioplasty.
e. Balloon dilation is performed starting with a 7- to 8-mm balloon, and the diameter is increased
incrementally by 2 mm to 110% of the adjacent normal portal vein diameter.
f. If there is immediate recoil (or >30% residual stenosis), a stent is deployed.
(1) Balloon-expandable or, more commonly, self-expanding stents can be used.
(2) If feasible, the operator should avoid placement of a stent extending proximally (upstream) into the
mesenteric-splenic confluence.
g. Perform a postdilation venogram and pressure measurement.
h. If an anastomotic stenosis is at the branch point of the right anterior and right posterior portal vein
branches in a split right lobe hepatic graft, kissing balloon/stent technique is required. This requires
two separate transhepatic portal access sites. The kissing technique ensures the balloons/stents
support one another, avoiding occlusion of the adjacent portal vein branch.
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i. If access is via the transhepatic route, it is optimal to obtain an activated clotting time (ACT)
assessment prior to withdrawing the catheters. When the ACT is <180 seconds, it is usually safe to
remove the transhepatic sheath with embolization of the tract.
j. The sheath is pulled out of the portal vein while puffing contrast.
k. Once into the parenchymal tract, 6- to 8-mm diameter coils are packed in the tract as the sheath is
pulled out. Some physicians embolize the tract with contrast impregnated Gelfoam torpedoes, with or
without coil deposition.
l. PVS recurring within 6 months after angioplasty should be treated by stent placement.
2. PVT (3,18)
a. Transhepatic or transjugular access into the portal vein is achieved, and a portal venogram is
performed to evaluate the extent of the thrombus.
b. After baseline inflow and outflow evaluation, mechanical thrombolysis can be performed followed by
thrombolytic infusion.
c. Tissue plasminogen activator (tPA) can be instilled at 0.5 mg per hour (5 to 10 mg of tPA diluted in
500 mL of normal saline, infused at 25 to 50 mL per hour).
d. Venography is performed in 12 to 24 hours. The thrombolytic infusion is continued for a maximum of
36 to 48 hours.
e. Patient monitoring is performed as for arterial thrombolysis.
f. If portal vein branches remain clogged with thrombus despite adequate thrombolysis, a TIPS is
created to improve outflow.
(1) TIPS also allows more aggressive mechanical thrombolytic techniques to be utilized. These include
the use of a Fogarty catheter to pull recalcitrant thrombus from the main portal vein into the TIPS
where it can be fragmented with a mechanical thrombectomy device such as the Arrow-Trerotola
percutaneous thrombolytic device (PTD) (Arrow International, Inc, Reading, PA).
g. Once portal venous flow is reestablished, a PVS may be uncovered. Angioplasty and/or stent
placement is required.
Portal Hypertension (3,4,5,18,19)
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TIPS have the same indications, contraindications, procedural steps, end points, and complications as TIPS
in nontransplanted patients. Technical considerations specific to transplant livers include:
1. Hepatic venous stenosis may result in elevated portosystemic gradient and graft dysfunction. In the
author's opinion, the hepatic vein stenosis should be treated and TIPS performed only if hepatic dysfunction
persists.
2. Difficulties in accessing the hepatic veins can be encountered due to altered postsurgical anatomy
(especially left lobe split grafts) and hepatic venous stenosis. Careful preprocedure analysis of cross-
sectional imaging is essential.
3. Serum levels of immunosuppressant drugs should be monitored because they may rise precipitously after
successful TIPS and induce encephalopathy.
1. Postprocedure monitoring
a. Routine postangiographic management for femoral access
b. Transhepatic access
(1) Bed rest depends on the patient's anticoagulation status and the size of transhepatic sheath required. At the
least, the patient should be on bed rest for 4 hours.
(2) Access sites are checked within 12 to 24 hours for bleeding or discharge (biliary or purulent).
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(3) Observe the patient for signs and symptoms of intra-abdominal bleeding, including increased abdominal girth.
Serial hematocrits are obtained to monitor occult bleeding.
2. Postprocedure hydration is administered depending on contrast volume used and patient's volume status. In
cases of severe IVC stenosis, patients may exhibit postobstructive diuresis. Adequate hydration and patient
reassurance are required.
3. If stents have been deployed, anticoagulation (starting with heparin converting to Coumadin) and antiplatelet
therapy (aspirin or clopidogrel) should continue for 6 months postprocedure (1,2,8).
4. Noninvasive imaging
a. Following arterial interventions for APF and/or HAS/HAT, baseline Doppler ultrasound is performed within 24
to 48 hours and should be repeated at 1, 3, 6, and 12 months, or as clinically indicated.
b. Following embolization of APFs or HAPs, Doppler ultrasound and/or CTA is performed within 24 to 48 hours.
c. Doppler ultrasound following interventions for NOHAH should show increased arterial velocities and
normalization of the arterial waveform within the hepatic artery, normalization of high resistance index, and
reduced portal vein velocities (2,6,7).
d. Following hepatic, IVC, or portal venous intervention, follow-up Doppler ultrasound and magnetic resonance
(MR) imaging should be performed at 1 month postprocedure.
5. Clinical and laboratory follow-up is conducted to assess resolution of graft dysfunction (including ascites).
Results (1,3,8,10,11,12,13,17,18,20)
1. HAS/HAT: Technical success rates for HAS are 81% to 93% for angioplasty and 100% for stent placement.
Technical success is decreased if there are multiple HASs, hepatic artery kinking, or inexperienced operators
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(8). One-year patency rates are 44% to 65% after angioplasty and 53% to 55% after stent placement, with
restenosis in 32% and 31% to 41%, and HAT in 19% and 8% to 14%, respectively.
2. Hepatopulmonary syndrome/arterioportal fistula (HPS/APF): Only anecdotal reports are available following
embolization in liver transplantation. Technical success rates are high.
3. Hepatic vein/inferior vena cava (HV/IVC) stenosis: Technical success rates for angioplasty of HV and IVC
stenosis are 94% to 100%. One-year patency rates for HV angioplasty are 60%. Recurrent stenosis is frequent
and requires repeated dilation or stent placement. One-year patency for IVC angioplasty and stent placement is
40% and 91% to 100%, respectively. Resolution of symptoms is achieved in 73% to 89% of cases.
4. PVS: Technical success rates for balloon dilation and/or stent placement for PVS is 74% to 100%. One- to
three-year patency for portal venous angioplasty and/or stent placement is approximately 36% to 67%.
5. PVT: Data for technical success rates and long-term results after portal vein thrombolysis in transplant
recipients are limited. Anecdotal case reports of portal vein patency exceeding 2 years have been reported.
Complications/Management (1,8,10,11,12,13,17,20)
1. Hepatic artery spasm. Spasm is the most common complication of arterial intervention and when neglected
may evolve into HAT. Hepatic artery spasm should be treated promptly with vasodilators. Aliquots of 100 to 200
μg of nitroglycerine
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are injected intra-arterially, to be repeated as necessary as long as the diastolic pressure is above 70 mm Hg.
Heparin may also be administered to prevent HAT. Repeat angiography is performed until the spasm is relieved.
In refractory cases, papaverine can be infused overnight along with therapeutic anticoagulation and the patient is
returned for a second look angiogram in 12 to 24 hours.
2. Hepatic artery dissection (particularly in cases of sharp arterial turns and kinks)
a. If flow-limiting, stent placement is required. Prolonged balloon inflation to tack a dissection flap is not advised
because the hepatic artery is prone to spasm and thrombosis.
b. Non-flow-limiting dissection may be treated with anticoagulation.
3. HAT (likely secondary to dissection). It may be difficult to differentiate severe spasm from arterial dissection
from HAT, and all three may coexist. Intraprocedural HAT (as opposed to delayed postsurgical thrombosis that is
rarely treated by transcatheter means) is managed by immediately injecting 1 to 3 mg of tPA. Some operators
may infuse abciximab (ReoPro). Refractory HAT can be treated with transcatheter thrombolysis and
anticoagulation overnight with a secondlook angiogram next day, or surgical revascularization.
4. Arterial rupture. Arterial rupture can be managed with stent grafts or may need emergent surgery. Balloon
tamponade usually leads to partial or complete HAT.
5. Hypotension due to occlusion of venous return or arrhythmia. Hypotension can usually be resolved by
deflating the balloon and administering bolus IV fluids. Arrhythmias are usually resolved by stopping the inducing
maneuver.
6. Stent migration. Depending on position, a migrated stent may be stabilized by balloon dilation or anchoring
with an overlapping stent. Stents occasionally can be moved to a more optimal position for deployment or
removed with a snare. A stent that has migrated to the heart usually requires open heart surgery. If the stent has
passed through the right heart intact, deploying it in the pulmonary artery may be possible.
7. Bleeding (especially from the transhepatic puncture site). If intra-abdominal bleeding occurs, correct
coagulopathy and obtain a surgical consult.
Radiology Books
8. PVT following balloon angioplasty. Iatrogenic PVT should be treated promptly and vigorously with balloon
maceration, bolus thrombolytics, and anticoagulation.
References
1. Saad WE. Management of hepatic artery steno-occlusive complications after liver transplantation. Tech
2. Saad WE. Management of nonocclusive hepatic artery complications after liver transplantation. Tech Vasc
Interv Radiol . 2007;10:221-232.
3. Woo DH, LaBerge JM, Gordon RL, et al. Management of portal venous complications after liver
transplantation. Tech Vasc Interv Radiol . 2007;10:233-239.
4. Funaki B, Rosenblum J, Leef J, et al. Percutaneous treatment of portal venous stenosis in children and
adolescents with segmental hepatic transplants: long-term results. Radiology. 2000;215:147-151.
5. Ko GY, Sung KB, Yoon HK, et al. Early posttransplantation portal vein stenosis following living donor liver
transplantation: percutaneous transhepatic primary stent placement. Liver Transpl . 2007;13:530-536.
6. Saad WE. Nonocclusive hepatic artery hypoperfusion syndrome (splenic steal syndrome) in liver
transplant recipients. Semin Intervent Radiol . 2012;29(2):140-146.
7. Saad WE, Anderson CL, Kowarschik M, et al. Quantifying increased hepatic arterial flow with test balloon
occlusion of the splenic artery in the liver transplant recipients with suspected splenic steal syndrome:
quantitative digitally subtracted angiography correlation with arterial Doppler parameters. Vasc Endovascular
Surg. 2012;46(5): 384-392.
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8. Saad WE, Davies MG, Sahler LG, et al. Hepatic artery stenosis in liver transplant recipients: primary
treatment with percutaneous transluminal angioplasty. J Vasc Interv Radiol . 2005;16:795-805.
9. Saad WE, Orloff MC, Davies MG, et al. Postliver transplantation vascular and biliary surgical anatomy.
Tech Vasc Interv Radiol . 2007;10:172-190.
10. Darcy MD. Management of venous outflow complications after liver transplantation. Tech Vasc Interv
Radiol . 2007;10:240-245.
11. Kodama Y, Sakuhara Y, Abo D, et al. Percutaneous transluminal angioplasty for hepatic artery stenosis
after living donor liver transplantation. Liver Transpl . 2006;12:465-469.
12. Ueno T, Jones G, Martin A, et al. Clinical outcomes from hepatic artery stenting in liver transplantation.
Liver Transpl . 2006;12:422-427.
13. Saad WE, Davies MG, Rubens DJ, et al. Endoluminal management of arterioportal fistulae in liver
Radiology Books
transplant recipients: a single-center experience. Vasc Endovasc Surg. 2006;40:451-459.
14. Saad WE, Davies MG, Ryan CK, et al. Incidence of arterial injuries detected by arteriography following
percutaneous right-lobe ultrasound-guided core liver biopsies in human subjects. Am J Gastroenterol .
2006;101:2641-2645.
15. Marshall MM, Muiesan P, Srinivasan P, et al. Hepatic artery pseudoaneurysms following liver
transplantation: incidence, presenting features and management. Clin Radiol . 2001;56:579-587.
16. Saad WE, Dasgupta N, Lippert AJ, et al. Extrahepatic pseudoaneurysms and ruptures of the hepatic
artery in liver transplant recipients: endovascular management and a new iatrogenic etiology. Cardiovasc
17. Wang SL, Sze DY, Busque S, et al. Treatment of hepatic venous outflow obstruction after piggyback liver
transplantation. Radiology. 2005;236:352-359.
18. Ueda M, Egawa H, Ogawa K, et al. Portal vein complications in the long-term course after pediatric living
donor liver transplantation. Transplant Proc. 2005;37:1138-1140.
19. Saad WE, Darwish WM, Davies MG, et al. Transjugular intrahepatic portosystemic shunts in liver
transplant recipients: technical analysis and clinical outcome. AJR Am J Roentgenol . 2013;200(1):210-218.
20. Denys AL, Qanadli SD, Durand F, et al. Feasibility and effectiveness of using coronary stents in the
treatment of hepatic artery stenosis after orthotopic liver transplantation: preliminary report. AJR Am J
Roentgenol . 2002;178:1175-1179.
Radiology Books
e-84
Selective Salpingography and Fallopian Tube Recanalization
Lindsay Machan
Indications
Diagnostic Selective Salpingography (1,2)
1. Clarification of poor filling of fallopian tube on hysterosalpingogram (HSG)
a. Technically inadequate HSG
b. Tubal spasm
c. True obstruction
d. Tubal disorder such as salpingitis isthmica nodosa (SIN)
2. Discordance between HSG and laparoscopy
3. Discordance between HSG and clinical diagnosis
4. Patient not pregnant after surgical anastomosis
5. Prior to fluoroscopic-guided insertion of tubal occlusion device (3)
6. Proximal tubal obstruction for recanalization
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Therapeutic Fallopian Tube Recanalization (4)
1. Infertility due to proximal fallopian tube occlusion (20% to 40% of female infertility is due to tubal disease)
2. Reocclusion after surgical reversal of tubal ligation (5)
Contraindications
Absolute
1. Active pelvic infection
Relative
1. Severe tubal or peritubal pathology not amenable to laparoscopic or surgical repair
2. Distal tubal occlusion (may be performed in conjunction with laparoscopic repair distal tube)
3. Intrauterine adhesions (severe)
4. Anaphylactoid reactions to radiographic contrast media (consider using gadolinium)
1. Evaluation by infertility specialist or gynecologist including verification of unprotected intercourse for at least 6
months
2. Pelvic ultrasound and laparoscopy optional
3. HSG (can be at the same session)
Radiology Books
Patient Education
1. Ideally performed with the patient's partner present. Inquiry into other male or female factors contributing to
fertility allows a more accurate assessment of the probability of pregnancy. The procedure should be described
as (a) defining more precisely the anatomy of the fallopian tubes and (b) a possible nonoperative alternative or
adjunct to tubal surgery or assisted fertility procedures. The rarity of occurrence and clinical sequelae of
procedural complications such as tubal perforation or infection should be discussed.
2. The unlikely possibility of a tubal pregnancy should be stressed, and the patient should be advised to visit her
gynecologist as soon as she misses a period and has a positive pregnancy test.
3. Approximately 25% of tubes opened by fallopian tube recanalization will reocclude by 6 months; thus, if the
patient is not pregnant at that time, the tubes should be reevaluated and reopened (once more) if necessary.
Patient Preparation
1. Schedule procedure during first 5 days after menstrual bleeding has stopped. This is an outpatient procedure.
2. Prophylactic antibiotics (doxycycline 100 mg PO bid) are started on the evening prior to or the morning of the
procedure and continued for 3 to 5 days postprocedure.
4. Devices: needed for two separate functions. Can be in prepackaged kits (e.g., FluoroSet, Cook Medical Inc,
Bloomington, IN).
a. Cervical cannulation. A cannula that can be fixed to the cervix allowing opacification of the uterine cavity and
has a central port large enough for coaxial passage of a catheter for fallopian tube catheterization is necessary.
Generally, these devices have an acorn or balloon tip and are fixed to the cervix by a vacuum cup, endocervical
balloon, or tenaculum.
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b. Fallopian tube catheterization. This requires a 4 Fr. or 5 Fr. angled catheter for selective salpingography and
for recanalization, a 0.035-in. hydrophilic guidewire, or far less frequently, a 3 Fr. straight catheter/0.018-in.
guidewire.
Procedure (2,6)
1. Start a peripheral intravenous (IV) ( Note: Some physicians will do this procedure with oral nonsteroidal anti-
inflammatory drugs [NSAIDs] only).
2. Place patient in lithotomy position. Foam padding to elevate the patient's pelvis from the x-ray table and
comfortable foam pads beneath the knees are preferable to stirrups.
3. Premedicate with midazolam (Versed) 2 mg IV and Fentanyl 100 μg IV (make sure someone can drive the
patient home following the procedure). Distention of the uterine cavity may be very uncomfortable for some
women, so significant amounts of sedation may be required.
4. Utilize sterile technique for preparation of perineum (chlorhexidine scrub, drape).
5. Insert vaginal speculum and scrub the cervix.
6. Cannulate cervix with an introducing catheter and perform HSG.
7. If the HSG confirms proximal tubal occlusion, insert a multipurpose-shaped 4 Fr. or 5 Fr. catheter coaxially
through the introducing catheter and selectively catheterize the ostium of the occluded tube. Inject contrast
medium selectively into the tubal ostium only until tubal spill or occlusion confirmed.
Radiology Books
8. If selective ostial injection confirms proximal tubal occlusion, there are two methods to recanalize the tube:
a. Use a 0.035-in. angled hydrophilic guidewire to probe and recanalize the tubal occlusion. After this wire is
successfully manipulated past the tubal obstruction, it is removed and distal tubal patency is checked by ostial
injection through the multipurpose-shaped catheter.
b. Insert a 3 Fr. catheter and 0.018-in. guidewire coaxially through the multipurpose catheter and probe the
obstruction with the guidewire. Once the 0.018-in. guidewire is successfully manipulated past the obstruction, the
3 Fr. catheter is gently passed over the guidewire, the guidewire is withdrawn, and contrast medium is injected
through the 3 Fr. catheter.
9. After manipulations are completed on one side, the procedure is repeated in the contralateral occluded
fallopian tube.
10. Optional: A final HSG is performed through the introducing catheter in the cervix to document tubal patency.
If the initial tube opened does not appear patent, this is most likely spasm and not an indication to attempt to
reopen it.
11. Two of the more frequently encountered technical difficulties are
a. Difficulty cannulating the cervix. This usually occurs because of poor visualization. Use of a lighted speculum
(e.g. KleenSpec [Welch Allyn, Skaneateles Falls, NY]) or a large metal speculum may help. Gently applying a
tenaculum to the 12 o'clock position of the cervix greatly facilitates cannulation and subsequent manipulations.
b. Difficulty advancing the catheter into a cornu. There are significant normal variations in uterine orientation and
the guidewire/catheter may preferentially go into one cornual region. This can be overcome by firm traction on
the cervix to straighten the uterus, use of a hydrophilic-coated wire, or use of a preformed curved catheter (e.g.,
multipurpose or Kumpe).
1. Observe patient for 60 minutes. Discharge, if stable, to a responsible adult who can accompany her home.
2. Advise patient that vaginal spotting and pelvic cramping are normal for 1 to 2 days.
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3. Patient to use pads rather than tampons as needed until next cycle and to avoid intercourse for 1 day
Complications
1. Tubal perforation (2%: no clinical sequelae)
2. Ectopic pregnancy (1% to 5%)
3. Pelvic infection (<1%)
4. Radiation exposure
Results (7,8)
The patients described in published series constitute a diverse group, and some authors have reported statistics
per patient, whereas others have reported success rates per tube attempted.
Technical Success
1. Idiopathic proximal fallopian tube obstruction—71% to 100% of tubes attempted
2. Occlusion after surgical anastomosis for reversal of tubal ligation—44% to 77% (5)
Radiology Books
3. SIN—77% to 82% of tubes but technically more challenging (9)
Pregnancy
The average reported pregnancy rate is 30% (range 9% to 73%) with median procedure to conception intervals
of 4.4 to 16.2 months. The wide variations reflect other factors contributory to infertility, including patient age,
associated distal tubal disease, and disorders of ovulation or sperm production.
References
1. Lopera J, Suri R, Kroma GM, et al. Role of interventional procedures in obstetrics/gynecology. Radiol Clin
North Am. 2013;51(6):1049-1066.
2. Thurmond AS. Fallopian tube catheterization. Semin Intervent Radiol . 2008;25(4): 425-431.
3. McSwain H, Brodie MF. Fallopian tube occlusion, an alternative to tubal ligation. Tech Vasc Interv Radiol .
2006;9(1):24-29.
4. Papaioannou S, Afnan M, Sharif K. The role of selective salpingography and tubal catheterization in the
management of the infertile couple. Curr Opin Obstet Gynecol . 2004;16(4):325-329.
5. Houston JG, Anderson D, Mills J, et al. Fluoroscopically guided transcervical fallopian tube recanalization
of post-sterilization reversal mid-tubal obstructions. Cardiovasc Intervent Radiol . 2000;23:173-176.
6. Al-Omari M, Al-Mnayyis A, Obeidat N, et al. Fallopian tube recanalisation using dedicated radiographic
tubal assessment set in angiography suite. J Med Imaging Radiat Oncol . 2014;58(4):415-421.
7. Anil G, Tay KH, Loh SF, et al. Fluoroscopy-guided, transcervical, selective salpingography and fallopian
tube recanalisation. J Obstet Gynaecol . 2011;31(8):746-750.
8. Al-Jaroudi D, Herba MJ, Tulandi T. Reproductive performance after selective tubal catheterization. J
Minim Invasive Gynecol . 2005;12:150-152.
9. Houston JG, Machan LS. Salpingitis isthmica nodosa: technical success and outcome of fluoroscopic
transcervical fallopian tube recanalization. Cardiovasc Intervent Radiol . 1998;21:31-35.
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e-85
Abnormal Placentation: Minimizing Surgical Blood Loss
Susan Kiernan O'Horo
Obstetrical hemorrhage remains a leading cause of maternal morbidity and mortality in the United States,
affecting up to 18% of deliveries. It is commonly defined as blood loss exceeding 500 mL (1). The most common
etiology of primary hemorrhage (defined as hemorrhage within 24 hours of delivery) is uterine atony, whereas
secondary hemorrhage is usually attributable to retained products or, less commonly, arterial pseudoaneurysm.
Interventional radiologists (IRs) developed uterine artery embolization (UAE) to control deep pelvic bleeding and
have used embolization to effectively control postpartum hemorrhage (PPH) since it was first described in
1979(1).
Placental abnormalities may be increasing given the increase in advanced reproductive technologies, twin births,
and cesarean sections (2). Placental abnormalities are divided by the depth of invasion into the uterine wall, with
an accreta, the least invasive, and percreta, the most invasive. The prevalence of placental abnormalities is
estimated at 1 per 500 pregnancies (2). The risks of abnormal placentation are life-threatening and include
hemorrhage, infection, hysterectomy, and death. The IR is increasingly asked to help mitigate these risks with
the placement of bilateral internal iliac artery (IIA) occlusion balloon catheters in an effort to reduce blood loss
(3). Although the efficacy of this procedure is controversial, it may allow uterine conservation in women in whom
the diagnosis of accreta is equivocal or to reduce intraoperative blood loss during cesarean hysterectomy.
Cesarean hysterectomy is the traditional treatment for placental implantation anomalies.
Indications
1. Embolization for PPH unresponsive to conservative measures
2. Prophylactic IIA balloon occlusion
a. Control of hemorrhage during planned cesarean hysterectomy for known placental abnormality
b. Control of hemorrhage in women who have suspected placental abnormality prior to either cesarean
hysterectomy or where possible uterine artery embolization
Contraindications
1. Contraindications include those of general angiography
a. Severe contrast allergy
b. Connective tissue disorder
d. Uncontrolled coagulopathy
2. When the patient is already in an operative unit and too unstable to travel, hysterectomy may be more
expeditious and save the patient's life.
1. PPH
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a. Informed consent obtained from the patient and/or her health care proxy.
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b. Foley catheter placement
c. Pedal pulses marked
d. Consideration for anesthesia assistance
2. Prophylactic IIA balloon occlusion
a. Clinic evaluation for a full explanation of the procedure, its risks, possible benefits, alternatives, and informed
consent. Anesthesia consultation may also be appropriate.
b. Admission the morning of delivery
c. Baseline labs including a type and cross and complete blood count
d. Nil per os (NPO) after midnight the night before
e. Epidural anesthesia by anesthesiology
f. Foley catheter placement
g. Placement of pneumatic boots (sequential compression devices) for deep vein thrombosis (DVT) prevention
h. Pedal pulses marked
Procedure
1. PPH
a. The right common femoral artery (CFA) is accessed and a 5 Fr. sheath placed and connected to a
heparin flush.
b. Using fluoroscopy, a flush catheter is advanced into the aorta, and a pelvic arteriogram is performed.
c. Typically, the contralateral (left) IIA is selected first with either a 4 Fr. or 5 Fr.
Cobra or Roberts uterine catheter (RUC). An arteriogram of the IIA is performed to define the uterine arterial
anatomy and identify any and all bleeding sources whether from the uterine artery or other pelvic arterial
vessels.
(1) With uterine atony, it is uncommon to see active extravasation. Embolization is performed in the absence
of any angiography finding when there is a clinical indication of hemorrhage.
d. Typically, the left uterine artery is selected and arteriography performed.
The Roberts uterine catheter or Cobra 2 catheter can be used to engage the origin; however, care should
be taken to avoid spasm because these patients often receive vasoconstrictors during resuscitation. A
smaller catheter is preferable, and if not, a microcatheter may be used if superselective catheterization is
required.
e. Embolization is performed on the left uterine artery.
(1) Embolization is typically performed with absorbable gelatin sponge (Gelfoam) either as slurry (macerated
with dilute contrast) or as a pledget because the goal is to induce a temporary, reversible ischemia.
Embolization is performed to stasis.
(2) If a pseudoaneurysm is seen, consideration should be given to superselective coil embolization.
f. Similarly, the right IIA and uterine artery is interrogated, selected, and embolized to stasis.
g. The sheath is removed if the patient is not coagulopathic, and manual compression used to achieve
Radiology Books
hemostasis.
2. Technique of prophylactic balloon occlusion
a. Attention should first be given to the fluoroscopy unit and parameters adjusted to minimize the radiation
dose to the fetus and mother.
b. Access is gained to the bilateral CFAs, and appropriately sized sheaths are placed to accommodate
occlusion balloons (6 to 7 Fr.). Each sheath is labelled and attached to a heparin flush.
c. Each IIA is selected from the contralateral access using a Cobra catheter.
Contrast injection confirms location with the IIA, and exchange is made for an appropriate-sized compliant
occlusion balloon catheter, typically 8.5 mm.
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d. Placement of catheters within the bilateral IIA (or anterior division of the IIA) is confirmed with hand
contrast injection and should demonstrate free flow to the uterus with the balloons uninflated.
e. Individually, test the balloons for the optimal inflation volume. Correct placement should be confirmed by
stasis of contrast or occlusion of flow with inflation and forward flow with deflation. It is extremely important
to deflate and leave the balloons uninflated until the fetus is delivered. Inflation will limit blood flow to the
placenta and fetus.
f. After balloons are deflated, store and reference an image to document correct position. Connect occlusion
catheters to pressurized saline infusions and label for site and side.
g. After the fetus is delivered and the umbilical cord is clamped or cut, the IR should inflate the balloons.
Excellent attending-to-attending communication is paramount. Documentation should occur that pedal
pulses are unchanged. Pedal pulses are monitored and documented at least every 5 minutes by nursing
staff. Loss of pedal pulses suggests displacement of the catheters into the common or external iliac artery
or access site thrombosis. Alternatively, a pulse oximeter can be placed on the bilateral toes for ongoing
monitoring of displacement or nontarget vessel occlusion.
h. The placenta is removed by the obstetrician, and hemostasis is achieved. If hysterectomy is planned, it is
typically performed with balloons inflated.
i. Pedal pulses are monitored during this period to ensure the balloons are not displaced during uterine
manipulation. If bleeding occurs, check the position of the occlusion balloons with fluoroscopy and compare
to the reference image. This may be difficult when it requires the image intensifier to be brought into the
surgical field at an inconvenient time.
j. Balloon catheters should be left inflated until hemostasis is achieved.
Following hemostasis, the catheters are deflated and removed. Alternatively, for patients who do
hemorrhage and desire conservative therapy, uterine artery embolization, as described earlier, can be
performed.
k. Bilateral CFA sheaths are removed as soon as possible and knee immobilizers are placed.
1. Patient is transferred to the recovery room and monitored for postpartum and postangiography complications
largely related to access site complications.
2. Patients are seen in follow-up on the first postprocedure to check the access site and assay the results of their
intervention.
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Results
1. UAE for PPH
UAE for PPH was initially described in 1979 (1), and the results replicated in several large retrospective
series. In recent studies, technical success was 90% to 100% (1,4,5). Clinical success largely depended on
how this was defined and the study population selected. Ganguli et al. (1) achieved a clinical success of
98% for primary PPH when success was defined as avoidance of hysterectomy. A clinical success rate of
89.7% was achieved by Lee et al. (4) when it was defined as the avoidance of any surgical intervention and
repeat embolization. Of note, 85% of these patients had primary PPH. Similar clinical results were obtained
by Lee et al. (5) in 2012.
With regard to secondary PPH, Ganguli et al. (1) reported 23.6% of patients who had secondary PPH had
cesarean sections. For secondary PPH, embolization was also highly clinically successful in 94% of
patients. Pseudoaneurysms are
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uncommon causes of PPH but are important to recognize. Dohan et al. (6) specifically studied PPH
attributable to pseudoaneurysms. These authors retrospectively evaluated 588 women for PPH and found a
prevalence of 3.06% for pseudoaneurysms. Sixty-seven percent were treated with Gelfoam alone and 28%
coils + / − Gelfoam. They reported a 94% clinical success rate. Of the patients who had pseudoaneurysms,
61% had cesarean sections. In a separate study, pseudoaneurysms were present in 3.9% (3/76) of patients
but 100% of the patients had undergone operative delivery (1). Similarly, Lee et al. (5) also described an
overall prevalence of 2.7% of pseudoaneurysms. Although pseudoaneurysms have been treated with many
different embolic agents, superselective coils embolization is thought to be most effective (1).
2. Prophylactic balloon occlusion of the IIA for placental abnormalities
Placement of IIA balloon occlusion catheters, in the setting of well-defined or suspected placental
abnormalities, has been described mostly in small case series and retrospective analyses. Dilauro et al. (3)
reviewed the literature in this area and found that technical success was high (100%) across all reports.
Clinical success, measured by hysterectomy rates, length of stay, blood loss volume, and transfusion rates,
is somewhat difficult to compare as techniques and patient selection varied considerably between
institutions. Some authors have suggested that there is no difference in clinical success (7), whereas others
have reported improved clinical outcomes (8).
Complications
1. Potential complications of both UAE and prophylactic balloon occlusion include general complications of
angiography and complications related to massive hemorrhage. In their series, Kim et al. (9) describe two
deaths and five patients who suffered strokes and multisystem organ failure from hypovolemic shock.
2. Specific complications of UAE for PPH
a. Nontarget embolization
b. Endometritis
c. DVT
d. Postembolization syndrome
3. Specific complications of prophylactic balloon occlusion
a. Access site thrombosis requiring surgical thrombectomy. Dilauro and colleagues' (3) analysis of 132
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patients found 7 who had thromboembolic complications for an overall rate of 5%.
b. Pseudoaneurysm formation at the location of balloon inflation
Complications post UAE for PPH can be mitigated by maintaining an active clinical presence in the patients'
care particularly while they are in the hospital. The access site and pulse exam should be monitored. The
patient and referring service counseled about postembolization syndrome signs and symptoms because it
may be mistaken for endometritis or other infections.
Described complications related to prophylactic balloon placement can be mitigated by marking and actively
monitoring pedal pulses during the case. This will most easily detect displacement and inflation of the
occlusion balloon in a nontarget artery. Thrombolysis is not an option, and surgical thrombectomy may be
necessary if thrombosis does occur. The pregnant patient is often hypercoagulable, so using the smallest
sheath and balloon combination to achieve the effect is desirable. A heparin flush to both the sheath and
the balloon catheter (when not inflated) is a must. It is important that compliant balloons are used and that
these balloons are neither over- nor underinflated. The volume of fluid to adequately
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inflate the balloons must be carefully titrated to observe stasis of flow. Again, great caution must be
exercised to not inflate the balloons (with the exception of each individually at the test occlusion) before the
fetus is delivered. Both balloons should never be inflated simultaneously until the fetus is delivered.
References
1. Ganguli S, Stecker MS, Pyne D, et al. Uterine artery embolization in the treatment of postpartum uterine
hemorrhage. J Vasc Interv Radiol . 2011;22(2):169-176.
2. Gonsalves M, Belli A. The role of interventional radiology in obstetric hemorrhage. Cardiovasc Intervent
Radiol . 2010;33:887-895.
3. Dilauro MD, Dason S, Athreya S. Prophylactic balloon occlusion of internal iliac arteries in women with
placenta accreta: literature review and analysis. Clin Radiol . 2012;67:515-520.
4. Lee HJ, Jeon GS, Kim MD, et al. Usefulness of pelvic arterial embolization in cesarean section compared
with vaginal delivery in 176 patients. J Vasc Interv Radiol . 2013;24:103-109.
5. Lee HY, Shin JH, Kim J, et al. Primary postpartum hemorrhage: outcome of pelvic arterial embolization in
251 patients at a single institution. Radiology. 2012;264(3):903-909.
6. Dohan A, Soyer P, Subhani A, et al. Postpartum hemorrhage resulting from pelvic pseudoaneurysm: a
retrospective analysis of 588 consecutive cases treated by arterial embolization. Cardiovasc Interv Radiol .
2013;36:1247-1255.
7. Shrivastava V, Nageotte M, Major C, et al. Case-control comparison of cesarean hysterectomy with and
without prophylactic placement of intravascular balloon catheters for placenta accreta. Am J Obstet Gynecol .
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2007;197:402.e1-402.e5.
8. Tan CH, Tay KH, Sheah K, et al. Perioperative endovascular internal iliac artery occlusion balloon
placement in management of placenta accreta. AJR Am J Roentgenol . 2007;189:1158-1163.
9. Kim YJ, Yoon CJ, Seong NJ, et al. Failed pelvic arterial embolization for postpartum hemorrhage: clinical
outcomes and predictive factors. J Vasc Interv Radiol . 2013;24:703-709.
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e-86
Peritoneal Dialysis
Peter B. Hathaway
Peritoneal dialysis (PD) is a form of permanent renal replacement therapy that utilizes the semipermeable
properties of the peritoneal membrane to remove excess metabolic solutes and fluid. PD requires the
implantation of a catheter into the peritoneal space to facilitate filling and drainage of a dextrose- and
electrolytecontaining fluid, termed dialysate. Efficient PD requires near-complete drainage of indwelling dialysate
with each fluid exchange. Meticulous attention to catheter site planning and procedural detail can improve
outcomes by optimizing catheter performance and reducing the risk of treatment failure.
Indications
1. End-stage renal failure (1)
2. Acute renal failure—infrequently used
3. Nonrenal indications—rare (e.g., congestive heart failure [CHF]) (2)
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Contraindications (1,3)
Absolute
1. Documented loss of peritoneal membrane function
2. Extensive peritoneal adhesions (“frozen abdomen”)
3. Patient who is physically or mentally incapable of performing PD
4. Uncorrectable hernias or body wall defects
5. Women starting the third trimester of pregnancy
Relative
1. Fresh intra-abdominal foreign bodies
2. Peritoneal leaks
3. Body size limitations
4. Intolerance to PD volumes
5. Inflammatory or ischemic bowel disease
6. Active abdominal wall or skin infections
7. Morbid obesity (in short individuals)
8. Severe malnutrition
9. Ostomy
10. Frequent episodes of diverticulitis
11. Homelessness
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1. Clinical evaluation is recommended prior to elective PD catheter placement. Examine the abdomen with the
patient both supine and upright to locate the catheter exit site away from skin folds or the belt line.
2. Preprocedural imaging is not generally needed.
3. Anticoagulants and antiplatelet medications are stopped for an appropriate interval prior to the procedure.
International normalized ratio (INR) < 1.5 recommended (4).
4. A bowel preparation is recommended if there is a history of constipation.
5. The patient should empty their bladder before entering the procedure area.
Procedure (5)
1. Prophylactic antibiotics. A single dose of intravenous (IV) cephalosporin, or vancomycin if cephalosporin-
allergic, is given.
2. Preoperative site marking
a. Careful site planning is recommended to ensure proper catheter placement.
b. PD catheters are most often placed to the left of midline. Placement opposite the site of dominant surgical
scars may help to avoid adhesions.
c. Site planning is assisted with the use of a nonsterile catheter or plastic template laid on the surface of the
abdomen. With the patient in the recumbent position, the superior border of the symphysis pubis is palpated and
marked with indelible marker. The upper border of the catheter coil is then aligned with the mark (Fig. e-86.1).
d. Ultrasound can be performed to identify the location of the rectus abdominis muscle and inferior epigastric
artery.
3. Catheter selection and preparation
a. Double-cuffed, internally coiled PD catheters (Merit Medical, South Jordan, UT; Covidien/Medtronic,
Minneapolis, MN) are most commonly used. A preformed bend between the cuffs (“swan neck”) has the benefit
of creating a downward facing exit site, reducing the risk of migration and exit site infection.
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Radiology Books
FIGURE e-86.1 • Technique of abdominal site marking. The upper border of the catheter coil is aligned with the
upper margin of the symphysis pubis (curved arrow). The anticipated positions of the deep (small arrow) and
superficial cuffs (large arrow) are then marked. The exit site should be located away from skin folds and the belt
line. (From Abdel-Aal AK, Dybbro P, Hathaway P, et al. Best practices consensus protocol for peritoneal dialysis
catheter placement by interventional radiologists. Perit Dial Int. 2014;34:481-493, with permission.)
b. Longer or shorter coil-to-cuff length catheters can be used to compensate for large or small body habitus.
c. The catheter is prepared by flushing and placing into a bowl filled with sterile saline. The polyester cuffs are
manually compressed to extrude trapped air that may impede tissue ingrowth.
4. Sedation: moderate sedation (e.g., IV midazolam and fentanyl)
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5. Incision
a. Sterile skin preparation. The tissues are anesthetized down to the peritoneum under ultrasound. A horizontal
incision is made at the marked location; a 4- to 6-cm incision is useful when placing a swan neck-type catheter.
The tissue tract is bluntly dissected from the incision down to the rectus muscle.
6. Accessing the peritoneum
a. A variety of needles can be used for peritoneal access, including a 21-gauge blunt trocar style needle with a
diamond tip stylet, 21-gauge Chiba needle, 21-gauge micropuncture needle, blunt-tip 18-gauge Hawkins-Adkins
needle, or Veress-type needle.
b. The needle is advanced in a caudal orientation under ultrasound guidance through the rectus abdominis
Radiology Books
muscle and gently pushed against the peritoneal surface until the needle penetrates with a loss of resistance.
c. Nonionic contrast media (iodine, 300 mg per mL) is injected through the needle under fluoroscopy to confirm
intraperitoneal access.
d. The needle is exchanged for a stiff hydrophilic guidewire. Manipulation under fluoroscopy with an angled 5 Fr.
angiographic catheter (e.g., Kumpe), and intermittent injections of nonionic contrast are often needed to achieve
wire access into the posterior pelvic cul-de-sac.
7. Catheter insertion
a. An appropriately sized peel-away sheath is introduced over the wire under contralateral oblique fluoroscopy.
b. The catheter is inserted through the sheath over the guidewire without a stiffener. The catheter coil is formed
deep in the pelvic cul-de-sac to avoid the greater omentum and reduce the risk of catheter migration or
obstruction.
c. The peel-away sheath is removed while gently advancing the deep cuff toward its intended final position. The
guidewire is then removed.
8. Cuff implantation. A free-floating cuff in the subcutaneous layer increases the risk of leakage and should be
avoided. The traditional surgical method requires implantation of the cuff within the rectus muscle or in the
properitoneal space, but published series of percutaneous placements indicate a low incidence of leakage when
the cuff is firmly seated against the surface of the anterior rectus fascia (6,7,8). A stable deep cuff position is
established by downward pressure of the subcutaneous tissues on the catheter swan neck created during
layered suture closure, or the cuff may be secured to the rectus fascia with an anchoring stitch (Vicryl, Ethicon,
Somerville, NJ). Intramuscular cuff placement can be aided with the use of a dedicated instrument (Cuff-
Implantor tool, Merit Medical, South Jordan, UT), if desired.
9. Tunneling. The exit tunnel is bluntly dissected in a downward vertical orientation. A skin incision 1 to 2 mm
smaller than the catheter diameter is made at the exit site. A stainless steel or plastic tunneler is used to pull the
catheter through the tunnel and out the exit site, taking care not to unseat the deep cuff. The orientation of the
longitudinal stripe on the catheter is checked to ensure there is no axial twist within the tunnel.
10. Fluid exchange. A luer-locking hub is attached to the end of the catheter. Catheter function is confirmed with
the instillation and free drainage of up to 1 L warmed saline or dialysate. Because of supine positioning, it is
unusual to retrieve the entire infused volume.
11. Closure. The subcutaneous tissues and dermis are closed using layered or interrupted absorbable suture
(e.g., 3-0 Vicryl). The epidermis is approximated with Steri-Strips. To avoid skin infection and irritation, the
catheter is not sutured at the exit site.
12. Catheter flush. After drainage of fluid, the catheter is flushed with 10-mL heparin 100 units per mL and
capped.
13. Bandaging
a. An absorbent dressing is placed over the catheter and incisions. One or two adhesive strips can be used to
attach the coiled catheter and transfer set to
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the skin under the dressing. Because the dressing will remain in place for up to 7 days, hypoallergenic tape
(Medipore, 3M, Minneapolis, MN) is used instead of a clear adhesive dressing to prevent skin irritation.
b. Tubular netting is stretched around the abdomen to help stabilize the dressing (Elastic Net, Medline,
Mundelein, IL).
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1. Routine postsedation recovery and monitoring
2. PD is delayed for 2 weeks to allow for cuff incorporation.
3. The catheter is flushed by the PD nurse and rebandaged after 1 week.
Results
Technical success of percutaneous PD catheter placement is 96% to 99% (6,7,8).
Complications
Procedural Complications
1. Bowel perforation (9): 1%
2. Major bleeding (9): < 1%
3. Infection (9): < 1%
Late Complications
1. Infection
a. Peritonitis: 0.6 episodes per year at risk (10)
b. Tunnel and exit site infection: 0.83 episodes per year at risk (10)
2. Inadequate dialysis and ultrafiltration failure: together with peritonitis accounts for up to 35% patient
dropout from PD in the first year (11)
3. Extruded cuff
4. Leaks and hernias: Pericatheter leaks often resolve after cessation of PD for 1 to 2 weeks.
5. Noninfectious catheter malfunction: causes for up to 20% of transfers from PD to HD (1)
References
1. National Kidney Foundation. KDOQI clinical practice guidelines for peritoneal dialysis adequacy (2006).
https://www.kidney.org/sites/default/files/docs/12-50-0210_jag_dcp_guidelines-pd_oct06_sectionb_ofc.pdf.
Accessed December 12, 2015.
2. Sotirakopoulos NG, Kalogiannidou IM, Tersi ME, et al. Peritoneal dialysis for patients suffering from
severe heart failure. Clin Nephrol . 2011;76:124-129.
3. Shetty A, Oreopoulos DG. Peritoneal dialysis: its indications and contraindications. Dial Transplant.
2000;29:71-77.
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2012;23:727-736.
5. Abdel-Aal AK, Dybbro P, Hathaway P, et al. Best practices consensus protocol for peritoneal dialysis
catheter placement by interventional radiologists. Perit Dial Int. 2014;34:481-493.
6. Maher E, Wolley MJ, Abbas SA, et al. Fluoroscopic versus laparoscopic implantation of peritoneal dialysis
catheters: a retrospective cohort study. J Vasc Interv Radiol . 2014;25:895-903.
7. Voss D, Hawkins S, Poole G, et al. Radiological versus surgical implantation of first catheter for peritoneal
dialysis: a randomized non-inferiority trial. Nephrol Dial Transplant. 2012;27:4196-4204.
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8. Reddy C, Dybbro PE, Guest S. Fluoroscopically guided percutaneous peritoneal dialysis catheter
placement: single center experience and review of the literature. Ren Fail . 2010;32:294-299.
9. Peppelenbosch A, van Kuijk WH, Bouvy ND, et al. Peritoneal dialysis catheter placement technique and
complications. NDT Plus. 2008;1:iv23-iv28.
10. Li PK, Szeto CC, Piraino B, et al. Peritoneal dialysis-related infections recommendations: 2010 update.
Perit Dial Int. 2010;30:393-423.
11. Chaudhary K. Peritoneal dialysis drop-out: causes and prevention strategies. Int J Nephrol . 2011;
2011:434608.
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Management of Recurrent Ascites
Maye M. Chan
David A. Rosenthal
Ascites occurs in the terminal stages of many malignancies. Its presence severely affects the patient's remaining
quality of life by causing pain, limited mobility, difficulty breathing, nausea, vomiting, early satiety, lower extremity
edema, and frequent trips to a hospital for treatment. The goal of management of malignant ascites is palliation,
improvement in quality of life, and increased independence. Health care providers can help the patient and family
choose a treatment option that best fits the patient's wishes. Safe and effective treatment options discussed here
include paracentesis and tunneled peritoneal catheters.
Paracentesis is a procedure in which a needle is directed into the peritoneal cavity and fluid is removed.
Although the procedure may be performed at bedside, image guidance with ultrasound improves both results and
safety. Diagnostic paracentesis refers to the removal of small quantity of fluid for analysis; therapeutic
paracentesis is performed to alleviate symptoms. Tunneled peritoneal catheters are placed to allow home
drainage by the patient or caregiver. Nontunneled drainage catheters and peritoneovenous shunts may also be
appropriate management strategies.
Patients are referred for tunneled peritoneal drainage catheters either from their oncologist or an inpatient
physician; however, the decision to place a tunneled catheter is often first suggested by the provider performing
multiple therapeutic paracentesis procedures. Selection of patients for tunneled peritoneal drainage catheters
includes the following patient characteristics:
1. Accepting of catheter and semipermanent status of catheter
2. Motivated to learn a new skill
3. Compliant with medical regimens
4. Amenable to home care follow-up
5. Has a caregiver available for assistance
Indications
Paracentesis
1. Evaluation of new or preexisting ascites
2. Management of symptomatic ascites
3. Drainage of small or loculated fluid collections
Tunneled Peritoneal Catheters
1. Palliation of symptoms caused by recurrent ascites
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Contraindications
Absolute
Radiology Books
1. Hemodynamically unstable patient
3. Rarely, a lack of safe pathway to drain fluid
Relative for Tunneled Peritoneal Catheters specifically
1. Active infection
2. Life expectancy of days
3. Loculated collections
4. An uncooperative patient or a patient with an inability to understand or comply with medical treatment
1. Evaluate patient history, physical examination, and prior imaging studies.
2. For elective procedures when medically appropriate (1)
a. Interrupt oral and intravenous (IV) anticoagulation.
b. Interrupt antiplatelet medication other than aspirin and nonsteroidal antiinflammatory drugs (NSAIDs).
3. Preprocedure laboratory testing is typically not performed for paracentesis unless there is a history of bleeding
diatheses, severe liver dysfunction, and/or the patient is anticoagulated. It is performed routinely prior to
peritoneal catheter placement.
a. An international normalized ratio (INR) is recommended for patients on warfarin. Consideration can be given
for reversal with vitamin K and/or fresh frozen plasma.
(1) Correct the INR to < 2.0 for paracentesis.
(2) Correct the INR to < 1.7 for peritoneal catheter placement.
b. Activated partial thromboplastin time (APTT) is recommended for patients receiving IV unfractionated heparin.
c. Platelet transfusion is recommended for counts under 50,000 per μL.
4. IV access is required for
a. Colloid replacement following large volume paracentesis (> 5 L). Usually, a liter of saline is administered over
the encounter.
b. Following removal of 5 or more liters of ascites, particularly in patients with portal hypertension or cirrhosis, an
albumin solution of 6 to 8 g per L of fluid can be administered to prevent hypovolemia, hyponatremia, or renal
impairment (2).
c. Antibiotic administration prior to tunneled peritoneal catheter. A cephalosporin is recommended for coverage of
skin organisms or clindamycin (600 mg) in penicillin-allergic populations.
d. Sedation. Image-guided paracentesis is well tolerated when performed under local anesthesia. Peritoneal
catheters are typically performed with sedation. When providing sedation, hospital diet guidelines for sedation
are followed.
5. Discuss with the patient or health care proxy the procedure indications, risks and benefits, and alternative
options. Obtain consent. Introduction to the care and maintenance of a peritoneal catheter can occur through a
detailed discussion by the operator at the time of consent or with the use of helpful digital presentations provided
by the device manufacturer, which demonstrate the necessary care.
6. Determine appropriate tests for fluid characterization at the time of initial paracentesis
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a. Albumin. Useful to obtain serum to ascites albumin gradient (SAAG) score. SAAG = (ascites albumin value) -
(serum albumin value) (3)
(1) SAAG ≥1.1 g per dL predicts portal hypertension (HTN) and a nonperitoneal cause for ascites.
(2) SAAG ≤ 1.1 g per dL indicates that patient does not have portal HTN.
b. Cell count and differential. Corrected neutrophil count of ≥250 per mm3 is suggestive of infection.
c. Total protein
(1) Exudate process if the total protein concentration is ≥2.5 or 3 g per dL
(2) Transudate process if total protein concentration is ≤2.5 or 3 g per dL
d. Lactate dehydrogenase (LDH) concentration. LDH ratio is obtained measuring ascites fluid
concentration/serum concentration. It is approximately 0.4 in uncomplicated ascites. The ratio approaches 1.0 in
the setting of infection, bowel perforation, or malignancy.
e. Glucose. Suspect infectious or malignant causes of ascites if concentration of glucose in ascites fluid is lower
than blood serum concentration. Suspect bowel perforation if glucose concentration is undetectable.
f. Gram stain and culture. Helpful for identifying bacteria in ascites to direct treatment
g. Amylase. The ascites fluid concentration-serum ratio of amylase is approximately 0.4 in uncomplicated ascites.
It rises above this level in the setting of pancreatic leak or bowel perforation.
h. Bilirubin. Ascites fluid concentration greater than serum bilirubin is suggestive of biliary or bowel perforation
into ascites.
i. Triglycerides. If greater than 200 to 1,000 mg per dL, suggests chylous ascites
j. Acid-fast bacilli (AFB) stain and culture for detection of tuberculous peritonitis
k. Cytology. Demonstrates malignant cells in patients with peritoneal carcinomatosis related to malignancy
l. Serum pro-brain natriuretic peptide concentration. Median levels (6,100 pg per mL) in heart failure patients are
higher than levels (165.7 pg per mL) in cirrhotic patients (4).
Procedure
Paracentesis
1. Perform safety pause (time-out) with the patient and nurse/assistant.
2. Position the patient supine on the examination table. Evaluate the patient's abdomen for surgical scars
because these areas may contain tethered bowel to the peritoneal wall risking inadvertent bowel
perforation.
3. Perform preprocedure ultrasound and choose the largest pocket of fluid that can be safely accessed.
Confirm there are no vessels (e.g., inferior epigastric artery) in the intended path of the needle. Determine
the length of needle required to enter into the peritoneum and mark the skin (Fig. e-87.1).
4. Sterilize the skin with 2% chlorhexidine gluconate and 70% isopropyl alcohol (ChloraPrep, CareFusion,
San Diego, CA) and drape the intended procedure site.
5. Apply a sterile cover over the ultrasound machine and probe. Anesthetize the skin with 1% lidocaine with
a 22-gauge needle. Under ultrasound guidance, direct the needle up to the peritoneum without puncturing it
and infuse lidocaine while withdrawing the needle.
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6. Create a 3- to 5-mm skin nick and advance a paracentesis (sheathed) needle into the peritoneal cavity.
7. Attach a syringe and remove an appropriate volume of fluid for diagnostic testing (200 mL or more for
cytologic testing). Then connect the sheath to a vacuum container using a valved connector tubing.
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FIGURE e-87.1 • Potential access sites for paracentesis. The lower lateral Xs indicate the location of the
left and right iliac spine. The suggested access site for paracentesis is located in the areas 3 cm medial to
the iliac spine and 3 cm superior. The access sites are depicted in the area surrounded by the black dots
on either left or right side.
8. Reposition the patient as necessary to encourage complete drainage. You may also apply gentle
contralateral abdominal pressure to facilitate drainage.
9. Images of the initial ultrasound evaluation, the puncture, and the abdomen at completion are saved.
10. Remove the catheter and apply a dry sterile dressing.
Tunneled Peritoneal Catheter Placement
1. Intraperitoneal fluid is visualized by ultrasound and the site prepared as for paracentesis. The preferred
access site is in an upper quadrant.
2. After local anesthesia, with approximately 5 mL of 1% to 2% lidocaine, access is gained with an 18-gauge
sheathed needle under real-time sonographic guidance.
3. A floppy guidewire is passed into the peritoneal space under fluoroscopic guidance. The procedure kit
includes a short 0.035-in. wire that also can be used.
4. A 5 Fr. Berenstein catheter (AngioDynamics, Latham, NY) is placed and the wire removed.
5. The catheter tunnel exit site is selected in a cranial and medial location relative to the access site.
6. A subcutaneous tunnel is created from the exit site to the access site. The catheter's polyester cuff is
positioned 1 to 2 cm from the exit site (Fig. e-87.2).
7. A stiff 0.038-in. Amplatz (Cook Medical Inc, Bloomington, IN) wire is placed through the Berenstein
catheter under fluoroscopic guidance.
8. A 16 Fr., 15-cm peel-away sheath is placed. Serial dilation is occasionally performed.
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Rarely, a 16 Fr. × 30-cm peel-away sheath is used to ensure that optimal catheter position is achieved if
adhesions are present or if only a small pocket is accessible.
9. The wire and dilator are removed.
10. PleurX (CareFusion, San Diego, CA) was the first U.S. Food and Drug Administration (FDA)-approved
peritoneal catheter. It is a 15.5 Fr., 66-cm long silicone
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catheter with 30 side holes, a one-way valve mechanism, and a polyester cuff. Occasionally, the catheters
are trimmed shorter when the full length is redundant because of presumed intraperitoneal adhesions.
FIGURE e-87.2 • PleurX peritoneal catheter placement.
11. The catheter is inserted through the sheath and the sheath removed. Fluoroscopic confirmation of
catheter position is obtained. It is important to ensure that all side holes are within the peritoneal cavity and
not in the tunnel.
12. The catheter is connected to the drainage system tubing and then to wall suction or glass vacuum
bottle.
13. The access site is closed using a figure-of-8 technique with a 2-0 Vicryl (Ethicon, Johnson & Johnson,
New Brunswick, NJ) absorbable suture in the deep dermal layer or fascia, 4-0 Vicryl subcuticular suture,
and 2-octyl cyanoacrylate adhesive (Dermabond) (Ethicon, Johnson & Johnson, New Brunswick, NJ) for
the skin.
14. The catheter is secured at the exit site with 2-0 Prolene (Ethicon Johnson & Johnson, New Brunswick,
NJ) nonabsorbable suture, usually in a modified purse-string fashion, to prevent leaking.
15. Following therapeutic paracentesis, a sterile cap is applied. A foam pad is placed on the skin, the
catheter coiled on the pad and covered with gauze. A clear bandage that is provided in the procedure kit is
placed, as illustrated in Figure e-87.3.
16. A supine abdominal film or spot image is obtained in the procedure room.
17. After placement, the catheters are ready for subsequent drainage by nursing staff, the patient, or other
caregivers who are trained in use of the device. The fluid is drained by connecting the PleurX catheter to
the proprietary tubing and 1-L plastic drainage bottles or wall suction.
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1. Document in the postprocedure note the quality and quantity of fluid removed.
a. Uncomplicated ascites: clear or translucent yellow
b. Infected fluid: turbid/cloudy
c. Slightly elevated triglycerides or cirrhosis: opalescent
d. High triglyceride concentration exceeding serum concentrations (chylous ascites): milky
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FIGURE e-87.3 • Dressing application.
e. Traumatic tap, cirrhosis, or malignancy: pink or bloody

f. High bilirubin (e.g., ruptured gallbladder or perforated duodenal ulcer): brown
g. Bowel perforation: feculent
2. Anticoagulation can be resumed 24 hours postprocedure barring any bleeding complications or may be
restarted earlier in patients at high risk for thromboembolic events.
3. Following paracentesis, the patient can be transported to a recovery area or back to the hospital floor. Monitor
patient for hemodynamic changes with 30-minute vital signs for 1 hour, particularly if large volume paracentesis
is performed. Monitor paracentesis site for signs of bleeding, infection, or ascites fluid leak.
4. Following peritoneal catheter placement, the patient can be discharged home or returned to his or her room
after recovery from sedation and catheter monitoring for complications. Discharge instructions for catheter care
are reviewed and home care supplies obtained, along with instructions on how to obtain drainage kits for
subsequent use.
a. Initial drainage is usually recommended within 2 days of the procedure to prevent pressure buildup around the
catheter, which can result in leakage.
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b. Insurance forms for the drainage kits are faxed to the medical supply company.
c. Clinical information is provided to the visiting nurse agency as required.
d. Dressings are changed at the time of each paracentesis. The dressing should be covered with a waterproof
covering while showering.
e. Interventional radiology (IR) clinic follow-up is generally not required.
f. It is worth reassuring patients and referring clinicians that if ascites is no longer produced, it is a simple
bedside procedure to remove the catheter.
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Results
Ultrasound-guided paracentesis is a safe procedure and when performed for appropriate indications help to
identify the etiology of ascites and facilitate appropriate treatment of infected ascites (5). It is also
associated with reduced mortality especially in hospitalized patients with cirrhosis and ascites (6).
The safety and efficacy of tunneled peritoneal catheters have been demonstrated in numerous studies with
small numbers of patients (7,8,9). Lungren et al. (9) has reported on the largest series of patients to date,
188 patients receiving tunneled peritoneal catheters for refractory ascites. They reported a 7% minor
complication rate including leakage and catheter malfunction. Peritonitis rates reported by Rosenberg et al.
(7) in a series of 40 patients and Courtney et al. (8) in a series of 34 patients were 2.5 and 2.9%,
respectively. In the later study, 85% of patients were free of catheter interventions at 12 weeks.

Paracentesis (10)
1. Ascites fluid leak following paracentesis from the access site is the most common complication (5%).
a. Dermabond or suture may be applied to the paracentesis needle site. An ostomy bag may be applied over
paracentesis site as a temporizing measure.
2. Bleeding (< 1%)
a. If a vessel is inadvertently lacerated, a figure-of-eight suture around the needle entry site can be done to
control the bleeding.
b. Laparotomy to control the hemorrhage is rarely needed.
3. Bowel perforation or peritonitis from paracentesis needle is rare (< 1%).
a. Treatment is not indicated unless patient develops clinical signs of infection.
4. Mortality from paracentesis is exceedingly rare and dependent on the preprocedure condition of patient.
Peritoneal Catheter
1. Leakage at the exit site. Leakage is the most common complication of peritoneal catheters and is usually due
to inadequate drainage (3%). Leakage often resolves with more frequent drainages, sometimes daily. The
dressing must be changed frequently to prevent skin irritation. We have found this to be a rare problem with our
current technique of access site closure and explicit instructions to drain within 1 or 2 days of placement and
every other or every 2 days subsequently for the first 2 weeks. Drainage frequency is then adjusted according to
symptoms.
Radiology Books
2. Catheter malfunction. Defined as inadequate or incomplete drainage; caused by catheter occlusion or fluid
loculation preventing drainage. Tissue plasminogen activator (tPA) has been used to lyse fibrinous blockages in
abscess drains in the abdomen and chest. tPA lysis of blocked peritoneal catheters appears to have some
success with little risk (8).
3. Development of loculated fluid collections (3% to 4%). Fluid loculation may be a cause of catheter
“malfunction.” Loculations occur as disease progresses and shortly before death. No intervention is done in the
majority of cases where loculations prevent normal function of the PleurX catheter other than checking patency
of the catheter by instilling saline and attempting to aspirate fluid. If no significant fluid is present on bedside
ultrasound and minimal fluid is being drained, catheter removal is recommended.
4. Infection including skin infection and peritonitis. Removing a catheter when large volume of ascites continues
to be produced should not be done for minor skin infection or minimally symptomatic peritonitis. In most cases,
infection
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will resolve with antibiotics. Cellulitis occurs in about 3% of patients without requiring catheter removal. Removal
may result in prolonged leakage of peritoneal fluid, which is very irritating to the skin. Cather removal for infection
occurs rarely (< 1%).
5. Renal failure from acute fluid loss in patient with existing renal impairment due to dehydration/hypovolemia (<
1%)
References
2012;23:727-736.
2. Runyon BA. Introduction to the revised American Association for the Study of Liver Diseases Practice
Guideline management of adult patients with ascites due to cirrhosis 2012. Hepatology. 2013;57(4):1651-
1653.
3. Runyon BA, Montano AA, Akriviadis EA, et al. The serum-ascites albumin gradient is superior to the
exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med. 1992;117(3):215-220.
4. Sheer TA, Joo E, Runyon BA. Usefulness of serum N-terminal-ProBNP in distinguishing ascites due to
cirrhosis from ascites due to heart failure. J Clin Gastroenterol . 2010;44(1):e23-e26.
5. Grabau CM, Crago SF, Hoff LK, et al. Performance standards for therapeutic abdominal paracentesis.
Hepatology. 2004;40(2):484-488.
6. Orman ES, Hayashi PH, Bataller R, et al. Paracentesis is associated with reduced mortality in patients
hospitalized with cirrhosis and ascites. Clin Gastroenterol Hepatol . 2014;12(3):496-503.
7. Rosenberg S, Courtney A, Nemcek AA Jr, et al. Comparison of percutaneous management techniques for
recurrent malignant ascites. J Vasc Interv Radiol . 2004;15:1129-1131.
8. Courtney A, Nemcek AA Jr, Rosenberg S, et al. Prospective evaluation of the PleurX catheter when used
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to treat recurrent ascites associated with malignancy. J Vasc Interv Radiol . 2008;19;1723-1731.
9. Lungren MP, Kim CY, Stewart JK, et al. Tunneled peritoneal drainage catheter placement for refractory
ascites: single-center experience in 188 patients, J Vasc Interv Radiol . 2013;24:1303-1308.
10. De Gottardi A, Thévenot T, Spahr L, et al. Risk of complications after abdominal paracentesis in cirrhotic
patients: a prospective study. Clin Gastroenterol Hepatol . 2009;7(8):906-909.
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The Whitaker Test
David W. Hunter
The Whitaker test is used to differentiate residual or recurrent upper renal collecting system obstruction from
dilatation secondary to permanent changes in musculature, when other less invasive imaging tests are equivocal
(1). It remains a useful test today, particularly in the evaluation of renal obstruction following percutaneous or
surgical intervention, often in transplant kidneys. Adaption of a similar concept to the biliary system for the
evaluation of benign strictures expands its role (2).
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Urinary Whitaker—Ureteral Perfusion Challenge
The Whitaker test involves an injection of dilute contrast into the collecting system, combined with intermittent
measurement of pressures in the bladder and collecting system. An increase of pressure in the collecting system
to a value greater than 15 cm of water above the bladder pressure indicates obstruction. The site of the
obstruction can usually be determined by careful fluoroscopic analysis. An increase of pressure in the bladder
that is transmitted to the collecting system indicates reflux, and the degree of elevation is a rough measure of
lack of bladder compliance.
Indications
1. A patient with a dilated collecting system, dilated ureter, or both in whom it is unclear if there is an
obstruction or in whom the location, anatomy, and severity of the obstruction has not been adequately
defined
2. A patient with a percutaneous nephrostomy catheter in place after stricture dilation and for whom a
determination needs to be made whether the stricture is resolved and the nephrostomy tube can be
removed
Contraindications
1. Uncorrectable coagulopathy if a new puncture into the collecting system is required
2. Urinary tract infection—untreated or unresponsive to treatment
1. Urinary obstruction is first evaluated by one or more noninvasive tests including ultrasound, computed
tomography (CT), and a diuresis renogram. In children in whom vesicoureteral reflux may be present, a voiding
cystogram should be performed prior to the Whitaker procedure.
3. Testing in adults can be performed with conscious sedation. Pediatric patients may require general
anesthesia. Follow institutional guidelines in preparation for sedation and anesthesia.
Procedure
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1. Set up the pressure measurement equipment as demonstrated in Figure e-88.1 (3). Measurements are
faster and easier when made with two channel hemodynamic
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monitoring equipment rather than manometers. For pressure conversion, 1 cm H2O = 0.736 mm Hg.
FIGURE e-88.1 • Equipment setup for the urinary Whitaker test: (a) power injector; (b) threeway stopcocks;
(c) connecting tubing; (d) manometers or transducers positioned so that the zero point is at the level of the
kidney and bladder, respectively; (e) 22-gauge needle; (f) Foley catheter; and (g) Christmas tree adapter.
2. Establish intravenous (IV) access for the administration of sedation if needed.

3. Using sterile technique, place a catheter into the urinary bladder and empty it. An appropriately sized
Foley balloon catheter (10 to 16 Fr.) can be used in an adult or older child, and a pediatric feeding tube can
be used in an infant. After the bladder is empty and the study is ready to begin, the end of the bladder
catheter is connected to a manometer or pressure transducer through a threeway stopcock, which can be
used to empty the bladder if needed.
4. Place the patient prone to establish access to the renal collecting system. There are three methods that
can be used to perfuse and monitor pressures in the collecting system.
a. A single 22-gauge needle, or the 3 Fr. catheter from a triaxial set in which 3 to 4 extra side holes have
been created near the tip, is placed in the collecting system. The needle tip should not touch the wall.
Smooth rise and fall of the pressure tracing with breathing is a good indicator that the needle tip is free in
the collecting system. A three-way stopcock is attached to the hub of the needle with one channel attached
to the infusion pump and one to the pressure-measuring device. Every 2 minutes, the infusion is interrupted
by rotation of the stopcock to allow a pressure measurement.
b. Two 22-gauge needles, or a double-lumen needle or catheter, are placed within the renal collecting
system. One lumen is used to measure pressures and the other is used for a continuous, uninterrupted
infusion.
c. In patients with a nephrostomy tube, the tube can be used in the same manner as a single needle
system.
5. Position the transducers or manometers so that the “0” point is at the level of the collecting system for the
renal monitor and the level of the bladder for the bladder monitor.
6. Record the resting (empty) bladder and collecting system pressures, which are normally below 10 cm of
water (7 mm Hg) and should be roughly equal.
7. Begin the infusion of dilute contrast (contrast:saline ratio, 1:2 or 1:3) at 10 mL per minute in adults or
older children and 5 mL per minute in infants and children less than 5 years of age. The infusion requires an
infusion pump.
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8. Continuous infusion of contrast allows fluoroscopy and spot films to be taken to show the progress of the
infusion. Areas of narrowing are well demonstrated as well as the strength, integrity, and frequency of
peristalsis. Pressure measurements and images are taken from the start of the infusion but may only start to
rise and reflect the actual physiologic status of the urinary tract after the renal pelvis and ureter are fully
distended and the flow of fluid being pumped into the renal pelvis is equal to the amount of fluid leaving it.
9. Simultaneous collecting system and bladder pressures are measured at least every 2 minutes for a
minimum of 20 minutes or until a steady state is reached. In some cases of visually significant stenoses that
have equivocal pressure-flow studies, increasing the infusion rate to as high as 20 mL per minute may
evoke an obstructive pressure gradient. Physiologically normal maximum flow rates are closer to 10 mL per
minute, and therefore, a flow rate of 20 mL per minute may evoke a falsely positive response (4). In cases of
neurogenic bladder, possible vesicoureteral reflux, following reimplantation of ureters, or any possible
cause of decreased bladder compliance, it is important to continue pressure measurements until the bladder
is fully distended.
1. Following the completion of the study, the needle(s) may be removed. If the study has demonstrated an
obstruction, and the needle has been placed through an
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appropriate posterolateral calyx, the needle may be used to place a percutaneous nephrostomy drain.
2. If a nephrostomy tube is placed, the patient may need to be admitted overnight for pain control or observation
of hematuria. However, if the urine is clear, appropriate teaching about tube and dressing management has been
completed, and pain is adequately controlled with oral pain medication, the patient may be discharged to home.
The patient is given an appointment to return to clinic within 1 to 2 weeks, and a postprocedure phone call is
made the following day.
3. If the access is removed, the patient is observed for 2 hours and then discharged if there are no complications
such as worsening flank pain or hematuria.
Results
1. A collecting system to bladder pressure gradient of less than 15 cm of water (11 mm Hg) is normal. A
gradient greater than 22 cm of water (16 mm Hg) is abnormal (5).
2. A gradient between 15 and 22 cm of water is indeterminate. Increasing the infusion rate to 20 mL per
minute may resolve the indeterminate case (4).
3. A positive study correctly predicts the outcome of intervention in only 77% of cases, which is one of the
reasons that the Whitaker test is only used to resolve discrepancies between noninvasive tests (6).
4. Fluoroscopic documentation of the site of obstruction and the quality of peristalsis is critical to the
determination of the appropriate intervention.
5. Historically, careful evaluation of the pressure measurements, including the amount of elevation and the
relative timing of the changes of pressures in the bladder and collecting system, has also been used to
determine if there were problems with either reflux or bladder compliance (5,7). The accuracy and specificity
of the test in these situations, however, is only of significant value if it corroborates other clinical or
laboratory evaluations.
Radiology Books
Complications
1. Infection. Although this is always a consideration for any invasive procedure, it is an infrequent problem
for a brief and minimally invasive procedure such as this. The major infection concern is unrecognized
urinary tract infection. A urinary tract infection is a common problem in patients with any degree of
obstruction or in whom a nephrostomy tube has been in place for over 72 hours. If pressure is applied to an
infected collecting system, the chance of developing septicemia and potentially clinical sepsis is high. To
avoid this problem, get a urine analysis and culture prior to undertaking a Whitaker test, especially if a
nephrostomy tube is in place.
2. Bleeding. This is only a problem if a new needle puncture is made and usually involves only mild and
transient hematuria. Avoiding this complication requires meticulous puncture technique using careful
ultrasound guidance to obtain access through a posterolateral calyx. In addition, bleeding problems can be
decreased if the “one needle” technique is used employing a smaller caliber (22 gauge) needle. The major
problem with hematuria is that blood clots can block the needle or the ureter rendering the test results
useless. If obvious bleeding occurs, the test should be stopped, the needle removed, and the patient
observed until hematuria begins to clear. The test can be rescheduled for any time after 3 to 4 days.
3. Extravasation of contrast. Because the test is performed with frequent fluoroscopic checks, extravasation
should be detected early and the test stopped. It is usually of no consequence. The finding of extravasation
is a priori evidence that some type of obstruction exists unless there have been technical issues with needle
placement. In most cases, therefore, a nephrostomy tube is placed if it was not already in place. External
drainage allows rapid healing.
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Biliary Whitaker—Biliary Manometric Perfusion Test
The biliary manometric perfusion test involves an escalating injection of dilute (30% to 50%) contrast in the
biliary system, combined with intermittent measurement of pressures in the biliary system. The normal maximum
pressure in the biliary system is 20 cm of water (15 mm Hg). Above that level, production of bile is decreased and
cellular function is impaired. An increase of pressure in the biliary system to a value greater than 20 cm of water
indicates obstruction. In addition, even if the pressures have not increased to 20 cm of water, the development of
nausea, vomiting, right upper quadrant pain, or chills should also be considered a “failure” and treated as
residual obstruction (8).
Indications
1. A patient who has had percutaneous or surgical treatment of a benign biliary stricture and in whom a
decision is being made as to the advisability of removing the percutaneous drainage catheter
Contraindications
1. Untreated or unresponsive cholangitis
2. Testing can be performed with or without conscious sedation; institutional guidelines are followed if conscious
Radiology Books
sedation is used.
3. Administer IV antibiotics within 1 hour of the start of the procedure.
Procedure
1. Set up the pressure measurement equipment in a similar fashion to the equipment that would be used to
measure pressures in the collecting system during a urinary Whitaker test.
2. Using sterile technique, replace the preexisting internal-external biliary catheter with an identical size
(same outer diameter) short catheter with one or two side holes near the tip, or a vascular sheath. The tip of
the catheter or sheath must be above the level of the treated stenosis. Make sure that the bile ducts are
empty and clear of debris.
3. Connect one port of a three-way stopcock to the pressure transducer and the second port to the power
injector. Flush all tubing with sterile saline or the dilute contrast mixture to clear out any air.
4. Place the zero point of the transducer or manometer at the level of the midaxillary line.
5. Measure the baseline intrahepatic pressure.
6. Infuse 30% to 50% diluted contrast material into the biliary tree as follows:
a. 2 mL per minute for 5 minutes
b. 4 mL per minute for 5 minutes
c. 8 mL per minute for 5 minutes
d. 15 mL per minute for 3 minutes, or 5 minutes if this is the final infusion
e. 20 mL per minute for 2 minutes (optional because the value of this above normal flow rate has not been
determined)
7. Alternatively, because it has not been tested to the same degree as the above protocol, a simpler
alternative infusion protocol can be used of 10 mL per minute for 20 minutes taking pressures every 2
minutes. This mimics the urinary Whitaker test.
8. Perform a pressure assessment every 5 minutes at the end of each infusion.
9. If the pressure at the end of each infusion is < 20 cm of water and no complications are experienced,
continue to next level of infusion.
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10. If the pressure increases to > 20 cm of water, the study is abnormal and warrants repeat dilation and
continued long-term drainage.
11. Perform intermittent fluoroscopy and spot filming to verify the sheath position and to visualize any areas
of narrowing.
1. If the test is normal, the catheter is removed and the patient is observed for 2 to 4 hours and then discharged.
2. If the test is abnormal, repeat dilation is performed and a new, hopefully larger, internal-external catheter is
placed. The patient is observed for 2 to 4 hours and then discharged.
3. Studies on patients with surgical or percutaneous treatment of benign biliary strictures demonstrate that
strictures will recur in approximately 20% of treated patients who are declared a “success” based on clinical or
manometric testing (2). It has not been possible to predict which patients will recur or when, so periodic, chronic
follow-up is needed.
Radiology Books
Results
1. A pressure increase to a level > 20 cm of water (15 mm Hg) is considered positive for obstruction.
2. Biliary manometry was equally successful to a clinical trial of an upstream “capped tube” in terms of
being able to predict treatment success or failure. Follow-up to 6 years showed that the Kaplan-Meier
survival curves showed that the probability of patency at 0, 2, 4, and 6 years after treatment was 1.0, 0.96,
0.78, and 0.59 after passing a biliary manometric perfusion test and 1.0, 0.91, 0.78, and 0.78, after passing
a clinical “capping” trial (p > .10) (2).
Complications
1. If the test is performed in an infected biliary system, the increase in pressure can cause bacteremia and
sepsis. If an infection is suspected, a biliary Gram stain and culture should be obtained 48 hours before the
manometric test.
References
1. Johnston RB, Porter C. The Whitaker test. Urol J. 2014;11:1727-1730.
2. Savader SJ, Cameron JL, Lillemoe KD, et al. The biliary manometric perfusion test and clinical trial—long-
term predictive value of success after treatment of bile duct strictures: ten-year experience. J Vasc Interv
Radiol . 1998;9:976-985.
3. Whitaker RH. The Whitaker test. Urol Clin North Am. 1979;6:529-539.
4. Pfister RC, Newhouse JH, Yoder IC. Effect of flow rates on ureteral perfusion results. Am J Roentgenol .
1980;135:209.
5. Whitaker RH. An evaluation of 170 diagnostic pressure flow studies of the upper urinary tract. J Urol .
1979;121:602-604.
6. Lupton EW, George NJ. The Whitaker test: 35 years on. BJU Int. 2010;105:94-100.
7. Witherow RO, Whitaker RH. The predictive accuracy of antegrade pressure flow studies in equivocal
upper tract obstruction. Br J Urol . 1981;53:496-499.
8. Cerna M, Thomas RP, Köcher M, et al. Manometric perfusion test in biliary strictures treatment.
Hepatogastroenterology. 2012;59(117):1354-1358. doi:10.5754/hge11095.
Radiology Books
e-89
Angiographic Contrast Media
Michael A. Bettmann
Patient Evaluation Prior to Contrast Administration: Areas Requiring Specific

Attention (1,2,3,4)
1. Consider the risk/benefit ratio. Obvious but essential. Is the procedure to be performed optimal for the patient,
in his or her current clinical status? That is, can ultrasound (US), a radionuclide study, magnetic resonance
imaging (MRI)/magnetic resonance angiography (MRA), or computed tomography (CT) (particularly if it can be
done without a contrast agent) be performed instead?
2. There are NO absolute contraindications to the use of an iodinated contrast agent. Several cautions, however,
are important, in regard to the following issues:
a. Should a contrast agent be administered?
b. Are there any significant risk factors?
c. Is administration of a contrast agent likely to be safe?
d. What class of agent should be given?
3. Relevant history, to determine whether or not there is an increase in the risk of a contrast reaction.
a. Has there been prior contrast administration? Concern: Many reported prior “reactions to contrast” are
actually not contrast-related, but a true reaction does increase the risk (by 10% to 20%) of a recurrent contrast
reaction.
(1) If so, did a reaction occur?
(2) What did the reaction specifically consist of? Many “reactions” are a reflection of anxiety about the procedure
or a physiologic response (e.g., nausea, hot feeling) rather than an actual reaction to the contrast agent.
(3) Which specific contrast agent was used?
b. Are there any active, serious allergies (e.g., anaphylaxis to multiple medications)? Concern: increased risk of a
contrast reaction. A history of shellfish allergy does NOT increase the risk of a reaction to iodinated contrast
agents.
c. Is there active asthma that currently requires treatment? Concern: worsened bronchospasm secondary to
contrast or perhaps to anxiety
d. Is there significant cardiac disease (e.g., pulmonary hypertension, class III-IV congestive heart failure [CHF],
class III-IV angina, tight aortic stenosis)? Concern: acute cardiac decompensation secondary to volume load
e. There is a theoretical concern about those with cerebrovascular disease because of decreased cerebral
perfusion with hypotension, although there are no clinical studies that suggest that this is a real risk.
f. Is there a history or risk of renal dysfunction (urinary tract disease, paraproteinemia, or diabetes mellitus)? Is
the patient on any nephrotoxic medications or metformin? (see Chapter 65). Concerns: With renal disease (+/−
diabetes), there is risk of contrast-induced nephropathy (CIN); with paraproteinemia, concern is acute renal
failure. If the patient is on metformin AND has renal dysfunction, concern is lactic acidosis.
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4. Physical examination
a. Assess patient's ability to understand and cooperate with examination.
b. Assess level of anxiety.
c. Assess level of hydration.
d. Obtain baseline vital signs.
5. Laboratory assessment
a. Blood urea nitrogen (BUN) and creatinine (Cr) only if there is concern about renal function (e.g., history of
renal stone, benign prostatic hyperplasia [BPH], bladder prolapse, recurrent urinary tract infections [UTIs]),
diabetes mellitus; patient on metformin (elevated serum Cr remains an absolute contraindication to the use of this
common medication).
b. Complete blood count (CBC) and urinalysis (for proteinuria, specific gravity) if there is concern about
hydration, general status
c. For concerns regarding bleeding risk of procedure, practical parameters for an interventional procedure are an
adequate platelet count and activated partial thromboplastin time (APTT) and international normalized ratio (INR)
within normal limits. Not a limitation to contrast administration in itself (e.g., with CT)
6. Informed consent is necessary prior to any invasive procedure that carries “significant risk”; what constitutes
significant risk is somewhat subjective. It is widely accepted that specific informed consent for contrast
administration is NOT necessary. Most centers, however, do utilize a patient information sheet that asks for
relevant information from patients (this is reviewed, and as appropriate, brought to the attention of the
responsible physician). This sheet obtains relevant history and risk factors, indicates the risks, and gives the
patient the opportunity to ask any questions:
a. Tailor consent to examination but include risks of contrast administration and the greater risks of conscious
sedation and of the procedure itself.
b. Physician should be available to answer questions.
c. Risk of severe, life-threatening contrast reaction is less than 1:10,000. Risk of direct mortality from a contrast
agent is substantially less than 1:120,000.
Principles for Angiographic Contrast Agent Administration (1,2,3,4,5,6,7)

1. Minimize the volume of contrast/iodine as much as possible, without compromising image quality and
diagnostic information. Although an increase in volume and iodine content usually improves image quality, it may
NOT add useful information, or may actually obscure certain lesions (i.e., prevent observation of detail through a
vessel). Also, increased volume may add risk in patients with limited cardiac output or renal failure. Increased
iodine concentration (e.g., 300 mgI per mL vs. 350 mgI per mL) increases osmolality, which may increase risk as
well.
2. Conversely, in the absence of specific risks (heart failure, renal dysfunction), contrast volume itself is not a
limitation: There is no direct relationship between increased volume of contrast and adverse events.
3. Emergency equipment to treat reactions, such as cardiopulmonary arrest, as well as personnel fully trained to
use this equipment (advanced cardiac life support [ACLS] certification or the equivalent) must be readily
available.
4. There are three basic kinds of contrast agents, all based on a tri-iodinated benzene ring (1,6):
a. High-osmolality contrast agents (HOCA) are very safe and less expensive than the other two categories. They
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were widely used parenterally for over 40 years and are extremely safe but have the highest incidence of minor
side effects (e.g., pain and heat, nausea, urticaria); they are now infrequently used. They are monomers (i.e., a
single fully substituted 6 carbon ring) with an osmolality of 1,200 to 2,000 mOsm per kg, depending primarily on
iodine content but also on the specific formulation. All are ionic (i.e., in solution, they dissociate to an anion and a
cation) of the three classes.
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b. Low-osmolality contrast agents (LOCA) have an osmolality of 450 to 600 mOsm per kg, depending on iodine
content and specific formulation. All but one are nonionic (i.e., nondissociating) monomers. Ioxaglate (Hexabrix,
Guerbet, Villepinte, France) is an ionic dimer. It is rarely used in the United States currently. As a class LOCA
cause less pain and heat and have fewer minor side effects but have similar overall mortality risk. They are less
nephrotoxic in patients with compromised renal function. LOCA are almost universally used preferentially to
HOCA for most intravenous (IV) and intraarterial (IA) (including intracoronary) contrast administration.
c. Isotonic contrast agents. Only one, iodixanol (Visipaque, GE Healthcare, Princeton, NJ), is currently available
in most of the world. It is available in formulations with an iodine content of 280 or 320 mgI per mL; both have an
osmolality equal to that of blood (about 280 mOsm per kg). It causes almost no discomfort on injection and fewer
cardiac alterations. It may be associated with a lower risk of CIN but a higher risk of delayed cutaneous
reactions. Cost is generally about twice that of most LOCA.
Reactions to Intravascular Contrast Agents

1. Incidence varies with route of administration, presence or absence of specific risk factors, and the type of
agent. Incidence also depends on definition used for “reaction,” “complication,” or “adverse event”
(1,2,3,4,5,6,7,8,9,10):
a. Life-threatening reactions occur in fewer than 1 in 1,000 patients (probably < 1:10,000).
b. Mortality associated with contrast injections is usually primarily related to underlying health factors (severe
CHF, major trauma, general debilitation). Mortality does rarely occur in otherwise generally healthy patients, in
fewer than 1:120,000 cases.
2. Risk factors for reactions
a. General reactions: prior contrast reaction, significant allergies, impaired cardiac function/limited cardiac
reserve, blood-brain barrier breakdown, marked anxiety (1,2,9,10,11)
A prior reaction is the best single predictor of a contrast reaction, but the correlation is poor: Incidence of
reactions in patients with a prior reaction is 8% to 25% (2).
A contrast reaction is NOT an “allergy”—it is an idiosyncratic reaction. This is supported by three facts: (a) the
contrast molecules are almost certainly too small (at about 800 D) to act as antigens; (b) no antibodies to
contrast agents have ever been found; and (c) by definition, if a patient has a true allergy, reexposure to the
allergen will always cause a reaction of similar or greater severity, and this is clearly not the case. The
significance of this is twofold. Many patients do not receive contrast because they have erroneously been
labelled as “allergic to contrast,” and this may compromise their care. Second, most such patients can receive
contrast safely. Delay of an exam to administer corticosteroids may have detrimental effects if the exam is truly
necessary and will only prevent minor, NOT major adverse events (1,2,12).
b. Renal reactions: renal failure, poor renal perfusion, marked volume depletion Risk increases in those with
diabetes mellitus (1,13,14,15) or with other nephrotoxic risk factors (medications, poor renal perfusion, major
surgery) (see Chapter 65).
c. Bronchospasm: active asthma
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d. Acute pulmonary edema: heart failure, acute or chronic
Steps to Prevent Contrast Reactions

1. Obtain a good history (general health, prior contrast administration with any associated adverse events and
specific agent used, renal status). It is not rare
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that what is called a “prior contrast reaction” or even a “contrast allergy” is in fact not an accurate diagnosis (8).
A careful history and review of records is imperative, particularly in those patients who were thought to have had
a prior contrast-related adverse event.
2. Minimize patient anxiety (8,11,16).
a. Explain procedure clearly. Obtain fully informed consent (only for invasive procedures and, preferably, for
patients with a history of a prior reaction to a contrast agent) and highlight symptoms likely to occur (e.g.,
discomfort, heat) but attempt to minimize unfounded/unlikely concerns. This is most important in patients who are
particularly anxious and in those who are particularly ill.
b. Use anxiolytic (e.g., midazolam, diazepam) and analgesic (e.g., fentanyl) medications prophylactically as
necessary, with careful monitoring (see Chapter e-94). It is easier to prevent pain and anxiety before they occur
than it is to treat them once present.
3. Contrast agent selection (Table e-89.1)
a. Although HOCA are safe, effective, and inexpensive, LOCA are generally used for all parenteral
administrations because they cause less discomfort and have a lower incidence of reactions (although this is
true solely for minor, non-life-threatening reactions). HOCA can be used for nonvascular purposes, such as
nephrostograms, percutaneous biliary drain or gastrostomy tube placements, or abscess injections.
Table e-89.1 Intravascular Iodinated Contrast Agents
Iodine
Trade Name Content Osmolality
Class Generic Name (Vendor) (mg/mL) (mOsm/μg)
High 1. Sodium and/or Hypaque (Nycomed- 141 633

osmolality— methylglucamine diatrizoate Amersham) 282 1,415
ionic 370 2,016
Renografin (Bracco) 141 644

282 1,404
370 1,940
2. Sodium and/or Conray 202 1,000

methylglucamine (Mallinckrodt) 282 1,400
iothalamate 400 2,100
Low 1. Sodium meglumine Hexabrix 320 602

osmolality— ioxaglate (Mallinckrodt,
ionic Guerbet)
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—nonionic 2. Ioversol Optiray 160 355
monomeric (Mallinckrodt) 320 680
350 702
3 Iohexol Omnipaque 240 520

(Nycomed- 300 672
Amersham) 350 844
4. Iopamidol Isovue (Bracco) 200 413

300 616
370 796
5. Iopromide Optivist (Berlex, 300 605

Schering) 370 780
6. Ioxilan Oxilan (Cook) 300 585

350 695
Nonionic
dimer
7. Iodixanol Visipaque (GE 270 290

Healthcare) 320 290
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Contrast agents are available with a wide range of iodine concentrations. Use one that has the lowest iodine
content that will allow satisfactory images; a lower iodine content means a smaller osmotic load. For CT and
angiography, the usual range is 280 to 400 mgI per mL, depending on injection site relative to area to be imaged.
Iodixanol, because it is nonionic as well as isotonic to blood, is particularly useful for exams that may be painful,
such as external carotid or peripheral arterial injections. Because it is also associated with minimal or no
sensations (e.g., warmth) on injection, it may also be useful in particularly anxious patients.
b. If the patient has a documented prior severe reaction (e.g., cardiopulmonary collapse, laryngeal edema)
(1) Reassure the patient that such a reaction is unlikely to recur (1,2,5,8).
(2) Ensure patent IV access.
(3) Ensure the availability of personnel trained in resuscitation (ACLS); consider anesthesia standby.
(4) Try to use a different contrast agent than that used previously. Consider using the isotonic agent (nonionic
dimer); based on current usage patterns, this specific contrast agent is unlikely to have been used previously.
4. Contrast reaction prophylaxis
a. There is NO clear evidence that any regimen prevents severe reactions. Steroid pretreatment, although
widely used, only decreases the incidence of mild reactions (1,2,5,12,17,18,19).
b. Low-osmolality (specifically nonionic) contrast agents reduce the risk of recurrence of mild reactions, but there
is no evidence to suggest that they prevent severe reactions (2,5).
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c. Reassurance is paramount.
d. The only pretreatment regimen proven effective to date (in preventing minor reactions) is methylprednisolone
32 mg by mouth (PO), 12 and 2 hours prior to contrast use (12). Note: This study dealt only with IV contrast in
patients without a prior reaction. It was too small to examine whether or not steroids prevented severe reactions,
although administration did decrease the incidence of minor, non-life-threatening reactions. Concurrent use of
specific H1- and H2-blockers has also been recommended (16), but proof of efficacy has not been shown. There
are data showing that administration of steroids 3 hours or less prior to contrast administration does not provide
a protective effect even for minor reactions (12).
5. CIN (see Chapter 65 for a more comprehensive discussion)
a. Clinically significant renal dysfunction due to the use of any iodinated contrast agent is essentially limited to
patients with preexisting renal compromise (1,14,15). There is a debate as to whether the risk is lower, or if it
even exists, with IV contrast injection (19)—but the risk is clearly a concern with intra-arterial and intracardiac
injections.
b. In patients with renal dysfunction, risk is increased with
(1) Diabetes mellitus
(2) Increasing age
(3) Increasing volume of contrast
c. Multiple myeloma and other paraproteinemias lead to renal failure through a combination of dehydration and
protein precipitation in tubules, a different mechanism from contrast-related failure (CIN). This renal failure is
likely preventable with good hydration (before, during, and after exam).
d. CIN prophylaxis
(1) Ensure adequate hydration before, during, and after procedure (optimally, good PO intake + IV normal saline,
1 mL/kg/h, for 12 hours pre-angiography and 12 hours postangiography) (20,21,22).
(2) Limit volume of contrast.
(3) Consider isotonic agent, especially for patients over age 70 as well as those with estimated glomerular
filtration rate (eGFR) < 50 mL per minute.
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(4) Consider alternative imaging examinations.
(5) Avoid other risk factors (e.g., surgery, dehydration, high-dose nonsteroidal anti-inflammatory drugs [NSAIDs],
gentamicin).
(6) Consider N-acetylcysteine (600 or preferably, 1,200 mg PO twice on the day prior to and twice on the day of
contrast administration) (23,24) with or without sodium bicarbonate (3 vials in 1,000 mL D5W, 3 mL per kg over 1
hour prior to contrast and 1 mL/kg/h over 6 hours after contrast) (25,26). Alternatively, statin therapy may be
useful (27).
e. The use of metformin and metformin-containing compounds is a special situation (28). Although metformin is
contraindicated in any patients with compromised renal function, this is not universally recognized. Current
recommendations are that metformin should be stopped at the time contrast is administered and restarted after
48 hours. Reevaluation of renal function is necessary only if there is concern that it has deteriorated.
Alternatives to Iodinated Contrast Agents

1. Consider alternative modalities that would not require a contrast agent. These include US, radionuclide
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studies, and MRI without contrast.
2. Carbon dioxide (29,30)
This is useful as an alternative for arterial injections below the diaphragm and has also been used safely for
inferior vena cavography and for peripheral venous injections (see Chapter 2). On injection, CO2 rapidly
dissolves and is eliminated during first pass in the lungs, without alterations in blood gas parameters.
Advantages: No volume constraints. No adverse renal effects. Cost is minimal. Quality of information obtained is
equivalent to that achieved with iodinated contrast agent use.
Disadvantages: requires some expertise for effective use. Because differences in density between CO2 and
surrounding structures are less than with iodinated contrast agents, quality of images depends heavily on high-
quality digital subtraction and may be limited. Not useful in patients who cannot effectively cooperate during
digital subtraction angiography (DSA). Carbon dioxide may have cerebral toxicity, so it should not be used if
there may be reflux into cerebral vasculature (i.e., arterial injection above the diaphragm; venous injection in the
presence of a potential right-to-left communication, such as patent foramen ovale [PFO]).
3. Use of magnetic resonance (MR) contrast agents (see Chapter e-70) was previously considered, but it is now
widely held (although still not entirely clearly defined) that gadolinium (Gd)-based contrast agents should not be
used in patients with significant renal dysfunction, due to the risk of nephrogenic systemic fibrosis (NSF) which
may be fatal. The occurrence appears to be associated with particular types of Gd-based agents, those with less
tightly bound Gd, and such agents should be avoided in all patients with eGFR < 30 and used with great caution
in patients with eGFR 30 to 60 mL/min/m2 (1,13,31,32).
References
1. Bettmann MA. Frequently asked questions: iodinated contrast agents. Radiographics.
2004;24(suppl1):S3-S10.
2. Bettmann MA, Heeren T, Greenfield A, et al. Adverse events with radiographic contrast agents: results of
the SCVIR Contrast Agent Registry. Radiology. 1997;203:611-620.
3. Spring DB, Bettmann MA, Barken HE. Nonfatal adverse reactions to iodinated contrast media:
spontaneous reporting to the U.S. Food and Drug Administration, 1978-1994. Radiology. 1997;204:325-332.
4. Spring DB, Bettmann MA, Barkan HE. Deaths related to iodinated contrast media reported spontaneously
to the U.S. Food and Drug Administration, 1978-1994: effect of the availability of low-osmolality contrast
media. Radiology. 1997;204:333-337.
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5. Kopp AF, Mortele KJ, Cho YD, et al. Prevalence of acute reactions to iopromide: postmarketing
surveillance study of 74,717 patients. Acta Radiol . 2008;49(8):902-911.
6. Li X, Chen J, Zhang L, et al. Clinical observation of the adverse drug reactions caused by non-ionic
iodinated contrast media: results from 109,255 cases who underwent enhanced CT examination in
Chongqing, China. Br J Radiol . 2015;88(1047):20140491.
7. Bettmann MA. Contrast media: safety, viscosity, and volume. Europ Radiol . 2005;15(suppl 4):D62-D64.
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8. Bush WH Jr, Krecke KN, King BF Jr, et al, eds. Radiology Life Support. New York, NY: Oxford University
Press; 1999.
9. Mammarappallil JG, Hiatt KD, Vincent W, et al. How accurate is the label “allergic to iodinated contrast
agents”? [published online ahead of print January 13, 2015]. Acta Radiol . 2015.
doi:10.1177/0284185114568049.
10. Lawrence V, Matthai W, Hartmaier S. Comparative safety of high-osmolality and low-osmolality

radiographic contrast agents. Report of a multidisciplinary working group. Invest Radiol . 1992;27:2-28.
11. Podrid PJ. Role of higher nervous activity in ventricular arrhythmia and sudden cardiac death:
implications for alternative antiarrhythmic therapy. Ann N Y Acad Sci . 1984;432:296-313.
12. Lasser EC, Berry CC, Talner LB, et al. Pretreatment with corticosteroids to alleviate reactions to
intravenous contrast material. N Engl J Med. 1987;317:845-849.
13. American College of Radiology. ACR Manual on Iodinated Contrast Agents. 6th ed. Reston, VA:
American College of Radiology; 2008. http//www.ACR.org. Accessed November 22, 2015.
14. Rudnick MR, Goldfarb S, Wexler L, et al. Nephrotoxicity of ionic and nonionic contrast media in 1196
patients: a randomized trial. Kidney Int. 1995;47:254-261.
15. Bettmann MA. Contrast medium-induced nephropathy: critical review of the existing clinical evidence.
Nephrol Dial Transplant. 2005;20(suppl 1):i12-i17.
16. Samuel MA. Neurogenic heart disease: a unifying hypothesis. Am J Cardiol . 1987;60:15J-19J.
17. Meth MJ, Maibach HI. Current understanding of contrast media reactions and implications for clinical
management. Drug Saf. 2006;29(2):133-141.
18. Kolbe AB, Hartman RP, Hoskin TL, et al. Premedication of patients for prior urticarial reaction to
iodinated contrast medium. Abdom Imaging. 2014;39(2):432-437.
19. Diogo LP, Bahlis LF, Carvalhal GF. Computerized tomography contrast induced nephropathy (CIN)
among adult inpatients. J Bras Nefrol . 2014;36(4):446-450.
20. Bader BD, Berger ED, Heede MB, et al. What is the best hydration regimen to prevent contrast media-
induced nephrotoxicity? Clin Nephrol . 2004;62:1-7.
21. Taylor AJ, Hotchkiss D, Morse RW, et al. PREPARED: Preparation for Angiography in Renal
Dysfunction: a randomized trial of inpatient vs outpatient hydration protocols for cardiac catheterization in
mild-to-moderate renal dysfunction. Chest. 1998;114:1570-1574.
22. Mueller C, Buerkle G, Buettner HJ, et al. Prevention of contrast media-associated nephropathy:
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randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch
Intern Med. 2002;162:329-336.
23. Kim BJ, Sung KC, Kim BS, et al. Effect of N-acetylcysteine on cystatin C-based renal function after
elective coronary angiography (ENABLE Study): a prospective, randomized trial. Int J Cardiol .
2010;138(3):239-245.
24. Trivedi H, Daram S, Szabo A, et al. High-dose N-acetylcysteine for the prevention of contrast-induced
nephropathy. Am J Med. 2009;122(9):874.e9-874.e15.
25. Navaneethan SD, Singh S, Appasamy S, et al. Sodium bicarbonate therapy of contrastinduced
nephropathy: a systematic review and meta-analysis. Am J Kidney Dis. 2009;53(4):617-627.
26. Zoungas S, Ninomiya T, Huxley R, et al. Systematic review: sodium bicarbonate treatment regimens for
the prevention of contrast-induced nephropathy. Ann Intern Med. 2009;151(9):631-638.
27. Chyou AC, Thodge A, Feldman DN, et al. Statins in the prevention of contrast-induced nephropathy. Curr
Treat Options Cardiovasc Med. 2015;17(4):375.
28. Bettmann MA. Use of intravenous contrast agents in patients receiving metformininvited response.
Radiology. 2002;225:312.
29. Giordano A, Messina S, Polimeno M, et al. Peripheral diagnostic and interventional procedures using an
automated injection system for carbon dioxide (CO2): case series and learning curve. Heart Lung Vessel .
2015;7(1):18-26.
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30. Scalise F, Novelli E, Auguadro C, et al. Automated carbon dioxide digital angiography for lower-limb
arterial disease evaluation: safety assessment and comparison with standard iodinated contrast media
angiography. J Invasive Cardiol . 2015;27(1):20-26.
31. Perez-Rodriguez J, Lai S, Ehst BD, et al. Nephrogenic systemic fibrosis: incidence, associations, and
effect of risk factor assessment—report of 33 cases. Radiology. 2009;250(2):371-377.
32. Nandwana SB, Moreno CC, Osipow MT, et al. Gadobenate dimeglumine administration and nephrogenic
systemic fibrosis: is there a real risk in patients with impaired renal function? Radiology. 2015;276:741-747.
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e-90
Angiographic Equipment Selection and Configuration
Keith J. Strauss
J. Anthony Seibert
Imaging Equipment for Angiography

Equipment should be tailored to the needs of patients imaged in the angiography suite. A review of the major
imaging components is presented in the following text. The basic management of these components, for
example, optimization of radiographic techniques used during the acquisition of images from the production of x-
rays, is briefly discussed.
Generators
1. Purpose
The generator provides electrical energy from which x-rays are generated. It also controls the production of x-
rays.
2. Image acquisition controls
Good image quality requires precise control of the production of x-rays. Lower dose fluoroscopy should be used
during catheter placement, whereas a higher dose fluoroscopic mode may be needed for critical positioning of
wires and catheters. A radiographic mode is typically provided to create higher quality images for interpretive and
archival quality.
a. Tube voltage (measured in units of kVp, kilovoltage peak) determines the kinetic energy of the electrons
reaching the anode of the x-ray tube, the energy level of each x-ray in the beam, and the penetrating capability of
the x-ray beam. The relative frequency of photoelectric effect and Compton-scattering photon interactions in
tissue, determined by x-ray energy, affects both patient radiation dose and subject contrast in the image. The x-
ray tube potential should be in the 60 to 80 kVp range to match the effective energy of the x-rays to the k-edge of
iodine which improves subject contrast. Tube voltages less than 60 kVp lead to excessive patient radiation dose
and should be avoided (1).
b. The tube current (measured in units of milliamperes, mA) determines the flow of electrons from the cathode to
the anode of the x-ray tube, which determines the quantity of photons in the beam. The total energy in the beam
depends on the number of photons (mA) and the energy carried by each photon (kVp). Tube currents range from
10 to 1,000 mA depending on the size of the selected focal spot size (2).
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c. The pulse width (measured in units of milliseconds) is the duration of the exposure. The pulse width should
range between 3 msec and 10 msec to adequately freeze motion during imaging. The maximum pulse width for
children should not exceed 6 msec (1). The maximum tube current is used to minimize the pulse width when
imaging large patients. Small tube currents are used with small body parts to maintain kVp values greater than
60 to avoid excessive patient radiation dose.
d. The pulse rate (pulses per second) is the rate at which images are created. This rate should be proportional
to the rate of motion of imaged anatomic structures. Capturing the sequence of motion of rapidly moving objects
is called temporal resolution. Fluoroscopic pulse rates range from 30 images per second (pediatric interventional
imaging) to 1 to 4 images per second (nonvascular studies). Angiographic pulse rates range from 0.5 to 6 images
per second (1). Lower frame rates reduce radiation dose to patients and staff.
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e. The size of the focal spot (measured in millimeters) determines the geometric unsharpness in the image,
which determines resolution in the image. A smaller focal spot size provides sharper vessel borders, but this
improvement must be balanced against less sharpness due to motion that results from the longer pulse widths
required by the reduced tube current of the smaller focal spot.
f. Beam filtration is the thickness of filter material inserted in the x-ray beam prior to the patient. Added filtration
removes low energy photons from the beam, reduces the patient's radiation dose, and improves image quality if
the tube voltage is reduced to generate a more monoenergetic x-ray beam (3,4). Typical filters range from 0.1 to
0.9 mm of copper. Some manufacturers have chosen to use filter materials other than aluminum such as k-edge
(higher z) materials.
g. Dose rate (μGy per image) at the image receptor determines the total number of information carriers used to
create the image. An increase in kVp, mA, or pulse width increases the number of photons, reduces image noise
due to quantum mottle, and increases the radiation dose rate to the patient.
3. Design
The mid- to high-frequency inverter is the most common generator design due to its low manufacturing cost and
compact design.
a. Reproducibility and linearity of x-ray production are improved due to closedloop regulation of the tube current
and high voltage, with response as rapid as 0.2 millisecond (2).
b. Automatic recalibration of the x-ray tube as it ages maintains accurate values of the radiographic technique
factors.
c. Eighty to 100 kW of power is necessary to penetrate large patients in oblique projections with a low tube
voltage, high tube current, and short exposure time. These factors are necessary to visualize small vessels with
minimal motion artifacts during rapid image acquisition sequences (3).
4. Hierarchy of adjustment of image acquisition controls
a. When more or less radiation is required at the image receptor due to changes in the thickness of the patient,
the generator should follow the sequence below.
(1) Adjust tube current. If additional adjustment is required, the generator should next,
(2) Adjust the pulse width. If additional changes are needed, the generator should next,
(3) Adjust the tube voltage. The tube voltage is adjusted last to maintain appropriate contrast levels in the image.
b. These acquisition parameters are unique as a function of
(1) Type of angiographic study
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(2) Size of the patient
(3) Fluoroscopic mode versus image archive. These two modes utilize radiation doses at the image receptor that
differ by at least a factor of 100 (1).
5. Configuration of acquisition parameters
Currently, no manufacturer's “state-of-the-art imagers” automatically provide a sufficient range of radiation output
to properly image both the largest and smallest patients (1). In some cases, anatomic program capabilities of the
generator allow the selection of appropriate combinations of the image acquisition controls to overcome this
deficiency.
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6. Control console display
Ideally, the control panel should provide a real-time display of all of the acquisition parameters during exposure
of the patient. This feature allows the technologist to monitor the performance of the imager during the
progression of the examination with respect to the size of the patient on the table.
X-ray Tubes
1. Basic design
The primary components of the x-ray tube consist of a tungsten filament cathode and a spinning anode disk with
a tungsten surface. Electrons are boiled off the filament, accelerated to the anode by the tube potential, and
stopped by the tungsten surface of the anode. This process converts approximately 1% of the kinetic energy
(energy of motion) of the electrons to x-ray energy. The remaining energy is converted to heat at the point of
collision on the tungsten anode.
2. Focal spot sizes
a. Multiple focal spot sizes are provided.
(1) Small spot: 0.4 to 0.6 mm with a kW rating of 30 to 50
(2) Large spot: 0.8 to 1.2 mm with a kW rating of 75 to 100
(3) Third spot: 0.3 mm with a kW rating of 10 to 20
b. The choice of focal spots must balance the need for minimal geometric unsharpness (small spot) against the
need for minimal motion unsharpness (large spot). The following nominal focal spot sizes are recommended:
(1) Contact arteriography (magnification factors < 1.4) (1)
0.3 mm: infants and toddlers
0.4 to 0.6 mm: children up to small teenagers
0.7 to 1.0 mm: small to large adults
(2) For magnification arteriography
0.2 mm or 0.3 mm for 2 × magnification
0.1 mm for greater than 2 × magnification
3. Anode
a. The anode of the x-ray tube has a large heat load rating to allow the serial imaging techniques required in
angiography. This is achieved by
(1) Reducing the anode angle
(2) Enlarging the length of the focal track traced out by the electron collisions on the spinning anode surface
(diameter of anode)
(3) Increasing the size of the focal spot
b. The smallest anode angle that provides full coverage of the image receptor by the x-ray field should be
chosen. For example, anode angles of 11, 9, and 7 degrees allow coverage of 15-in., 12-in., or 9-in. image
receptors, respectively, with a typical source-to-image receptor distance (SID) of 100 cm (3).
c. Some manufacturers have increased the focal track diameter to 8 in. with advanced bearings at a lower speed
of rotation (3,000 rpm). This increases loading and reduces the rotor noise. Rotor noise can be stressful during
difficult, lengthy cases.
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4. Collimation assembly
A collimator assembly is attached to the x-ray tube port from which the x-rays are emitted. This assembly
contains adjustable beam blocking blades, selectable beam filters, and adjustable wedge filters (3).
a. The adjustable beam blocking blades shape and limit the area of the x-ray beam at the entrance plane to the
patient. Newer units provide (additional cost option) a graphical display of the position of the collimator blades in
the field of view while the operator positions the blades. This allows reduction of the area of the x-ray field
without radiation to the patient.
b. Adjustable wedge filters reduce intense radiation areas in the beam to improve image quality and reduce
patient dose. A graphical display, as described earlier, may be provided to eliminate additional patient dose
during the adjustment of the position of these wedges.
c. Although thicker filters have a greater impact on patient dose reduction, the filter thickness must be reduced
as the patient size increases to deliver a sufficient number of photons to the image receptor. Most new
equipment automatically selects the largest available filter thickness that allows proper penetration of the patient.
This frees the operator from managing this image acquisition parameter.
Patient Tables
1. Pedestal base
Patient tables are typically floor mounted on a pedestal base. Manufacturers, in response to the growing girth of
the largest patients, continue to increase the weight capacity of the tables.
2. Tabletop composition
Carbon fiber tabletops provide the strength required to support an adult cantilevered from the pedestal support
while minimizing the attenuation of the diagnostic x-rays.
3. Tabletop dimensions
The length of the tabletop must accommodate the tallest patient. The width must accommodate the patient but
be narrow enough to allow adjacency of the image receptor to the exit plane of the patient during lateral imaging.
4. Tabletop motions
a. Vertical motion: Motorized vertical motion sufficient to position any part of the patient's body at the vertical
isocenter of the imaging plane is necessary.
b. Float: The level tabletop must “float” when electromagnets are released to allow axial and transverse motion
of the tabletop.
c. Stepping: The tabletop must shift (step) parallel to the axial axis of the patient with the moving bolus of
contrast to allow lower extremity angiography. This feature is typically an additional cost option.
d. Tilt: The tabletop tilt ± 15 degrees with respect to level to properly support some interventional procedures (3).
This feature is typically an additional cost option.
e. Cradle rotation: The tabletop may rotate the patient about the patient's axial axis when supine. This feature is
typically an additional cost option. It is typically used when the interventional unit is installed in the operating
room.
Gantry Stands
1. X-ray tube/image receptor alignment
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The gantry stand supports both the x-ray tube housing and the image receptor/imaging chain. The alignment of
the central ray of the x-ray beam to the center
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of the image receptor is maintained while the angle of the central ray changes within either the coronal or
transverse plane of the patient's body.
2. Linear movement of image receptor
Movement of the image receptor parallel to the central ray is accomplished by providing a variable SID of at least
90 to 120 cm (3). This allows the positioning of the input plane of the image receptor close to the exit plane of the
patient to minimize geometric unsharpness in the image and to minimize the patient radiation dose.
3. Basic rotational design
While a number of different designs of the gantry are still present in the field (4), the majority of new equipment
uses a C-arm geometry to achieve angulation in one dimension. When the x-ray tube and image receptor are
rotated on a “C” within a C, both components are rotated about a true pivot point called the isocenter, with a
fixed SID. These two design criteria are required to allow accurate rotational angiography and the production of
cone beam computed tomography (CT) images from the angiographic device.
4. Single plane configuration
Single plane gantry stands are typically mounted from ceiling supported rails. This maximizes the travel of the
gantry to/from the pedestal mounted patient table. This allows the gantry to be parked well away from the patient
table in the case of emergency. Most manufacturers also offer their single plane gantry configuration mounted to
a fixed location on the floor.
5. Biplane configuration
Biplane configurations, with the lateral plane assembly mounted on ceiling rails, are necessary for
neuroangiography of adults and most angiography studies performed on children due to the child's limited
tolerance of iodine contrast media (4). A biplane configuration forces the frontal plane assembly to be mounted
on the floor.
6. Robot configuration
At least one manufacturer (5) offers the x-ray tube and image receptor C configuration mounted on a
programmable “robot” gantry. The robot is modified from automotive manufacturing. Robots allow more flexible,
accurate, reproducible, and rapid motions of the C-arm support. Although this technology should increase the
flexibility and applications of the imager, it also significantly increases the cost of the imaging system.
7. Rotational motions
In addition to imaging with the x-ray tube and image receptor stationary, C-arm gantries with a true isocenter
allows two types of rotational angiography:
a. Rotational angiography is created by rotating the x-ray tube and image receptor about the isocenter, pulsing
the x-ray beam, and collecting a series of two-dimensional (2D) images. The projected view on playback rotates
about the patient anatomy at the isocenter.
b. Cone-beam CT uses the same acquisition protocol described earlier. The projection images use “cone beam”
reconstruction algorithms to create tomographic slices through the volume. The quality of the tomographic
images is not on par with those acquired with conventional CT scanners but can be obtained without
transporting the patient to a CT scanner. A gantry rotation of ˜200 degrees in 3 to 5 seconds is required.
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Displays
1. Number of monitors
a. Single plane configuration: Multiple individual monitors are necessary to adequately view the progression of
the examination.
(1) One monitor provides live fluoroscopy.
(2) One monitor provides road maps, which are fluoroscopic images created with a limited amount of contrast
media to illustrate the vasculature tree.
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(3) One monitor displays patient images from other modalities, for example, three-dimensional, magnetic
resonance imaging (MRI), CT, ultrasound (US), or plain radiographs.
(4) One monitor displays the patient's real-time physiologic monitoring data.
b. Biplane configuration: When two planes of imaging are produced simultaneously, one needs a minimum of
two, more typically four additional monitors.
(1) Six total monitors: The two additional monitors relative to the description earlier are used for live fluoroscopy
and roadmaps of the lateral plane.
(2) Eight total monitors: The additional monitors are available to allow some combination of 3D, MRI, CT, US
images, or plain radiographs to be displayed simultaneously.
c. An alternative is one large (˜60 in.) diagonal monitor. This single monitor is driven by multiple computer-driven
inputs to allow the simultaneous presentation of the previously described images. The display system is
calibrated with multiple hanging protocols, each one specifically designed to a different operator's preferences
for different types of clinical examinations.
2. Types of monitors
Liquid crystal display (LCD) flat-panel monitors are preferred due to their superior image quality and lack of bulk.
The matrix size of individual monitors must be sufficient to display interventional images in full resolution (1,000 ×
1,000 matrix). This matrix size allows display of all but plain radiographs at full resolution.
3. Support carriage
a. The support carriage is ceiling mounted on a long set of rails. A transverse set of rails or a long arm mounted
on pivot allows movement of the carriage parallel to or transverse to the axis of the patient.
b. Transport of the carriage is designed so that it may be placed on the left side, right side, or the foot end of the
patient. The access point of the catheter into the patient's vasculature determines the correct location of the
carriage for a given examination.
4. Patient dose display
Newer equipment displays two types of patient dose information on the monitor carriage (6). See Chapter e-99.
a. Air kerma is a quantitative indication of the ability of the x-ray machine to produce radiation at a specified
location from the focal spot. Air kerma, measured in units of mGy, is the cumulative radiation delivered to the
entrance plane of the patient's skin (minus backscatter) during the examination. Medical physicists use this dose
metric to estimate the risk of a deterministic radiation injury, for example, skin burn, to the patient.
b. The interventional reference point (IRP) (7) is the assumed entrance plane location for a typical adult relative
to the focal spot of the imager. This point is 15 cm toward the focal spot from the isocenter along the central ray
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of the x-ray beam.
c. The IRP is a poor indicator of the entrance plane of pediatric patients. Inverse square law corrections are
necessary as a function of patient thickness.
d. Dose-area product (DAP) or kerma-area product (KAP) is the product of the air kerma and area of the x-ray
beam at the entrance plane of the patient. Medical physicists use this dose metric to estimate the risk of a
stochastic radiation injury, for example, cancer induction, to the patient.
e. Patient dose monitoring
Some state radiation control programs require hospitals to develop patient dose monitoring programs that rely
heavily on the displayed dose indices. The displayed KAP or air kerma values are correct to ± 35%. If these
displayed dose indices are used to estimate cumulative patient dose, a medical physicist should develop
calibration factors to be applied to the displayed values.
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Contrast Injector
1. Mounting
The contrast injector arm can be ceiling suspended or mounted on the patient table. The injector control unit can
either be mounted on a pedestal in the procedure room or rack-mounted in the control area.
2. Control parameters
Injection volume, peak injection rate, and acceleration to peak rate are adjustable. A mechanical stop on the
volume injected is an important safety feature.
3. Programming
Programming options allow the injector, table motion, and x-ray generator to be synchronized.
Image Chain
1. Image chain
The image receptor converts the x-ray pattern in space that exited the patient to an intensified light image.
Traditionally, the image chain has consisted of an image intensifier (II) coupled to a charge-coupled device
(CCD) television camera that sends a video signal to the television monitor. Today, a flat-panel detector has
replaced the II and TV camera on newer fluoroscopic interventional imagers. Regardless of the type of image
receptor used, the imaging chain should (8):
a. Provide fields of view (FOV) from 10 to 45 cm with typically four or more electronically selectable FOV. The
smaller FOV (magnification modes) improve high-contrast resolution at the expense of increased patient dose
because typically the dose rate is proportional to 1/FOV.
b. Acquire images at a 1,024 × 1,024 matrix size, to allow adequate visualization of small vessels, catheters, and
guide wires. The 1,024 matrix must be available at maximum frame rates of 6 and 30 frames per second,
respectively, for radiographic and fluoroscopic imaging.
c. Allow equal horizontal and vertical resolution: Up to 3 line-pairs per millimeter should be resolved with a 10 to
13 cm FOV (9).
d. Adjust the radiation dose at the image receptor in response to changes in operator-selected dose settings, in
selected FOV, filter thickness placed in the x-ray beam, or pulse rates during fluoroscopy (1).
e. Provide a last-image-hold or “freeze-frame” mode on most digital TV systems, significantly reducing
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fluoroscopy time and patient and personnel radiation dose.
f. Provide a last fluoro-loop-store-replay mode allowing the most recent sequence of fluoroscopic images to be
stored to disc and replayed, allowing further review of the fluoroscopic sequence without additional radiation to
the patient and staff.
2. Image intensifier/CCD TV camera
a. The II was developed as an image receptor to create a visual image of the exit x-ray pattern in space with
sufficient intensity to be viewed in daylight conditions by the human eye (10).
b. The II creates
(1) A light image, followed by conversion to
(2) An electronic image that can be amplified, followed by conversion back to a
(3) Light image
c. The output of II is coupled to a CCD TV camera that converts the light image to an electronic video signal that
is converted back into a light image at a display monitor.
d. The solid state CCD TV camera has replaced analog TV cameras due to its improved temporal stability and
reduced electronic noise (11).
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e. Despite these abilities, this imaging chain has the following shortcomings (11):
(1) The spherically shaped input phosphor of the II suffers from pincushion distortion creating distance
measurement errors in the periphery of the FOV as high as 15%.
(2) Interaction of the II with the earth's magnetic field leads to “S”-shaped distortion particularly during rotational
angiography.
(3) Vignetting, the loss of light intensity at the periphery of the FOV, results in nonuniform brightness.
(4) Veiling glare, a light scattering event, reduces overall image contrast.
(5) The limited dynamic range of the TV camera leads to saturation of video signals which can diminish imaged
quality.
3. Flat-panel detector
X-ray detectors using thin-film transistor (TFT) arrays are divided into indirect and direct x-ray conversion,
depending on how the x-ray-induced charge is produced.
a. All active-matrix TFT substrates consist of amorphous silicon (a-Si). Main components include (see Fig. e-
90.1):
(1) TFT (electronic switch)
(2) Charge collection electrodes
(3) Storage capacitors
(4) Interconnections including gate lines and drain lines
b. During an x-ray exposure
(1) TFT switch is closed. Charge builds in each DEL capacitor proportional to the incident x-ray fluence.
(2) Activation of the TFT switch after the exposure allows charge to flow from the source (storage capacitor) to
the signal amplifier along each column drain line.
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FIGURE e-90.1 • The active matrix flat-panel imager (AMFPI) TFT array is composed of an amorphous silicon
substrate, on which various electronic components are layered. This device converts x-ray energy to an
electronic signal. Components in each detector element include a transistor (electronic switch), a charge
collection electrode to capture x-ray-induced charges, and a storage capacitor. Globally, each TFT in the array is
connected by gate lines along rows (the “on-off” control of the TFT), drain lines along columns (connecting the
storage capacitor to the charge amplifiers), and the charge amplifiers connected to each of the columns in the
array. The charge amplifier output is a voltage amplitude that corresponds to the x-ray energy absorbed locally in
the image receptor and is digitized with an analog-to-digital converter (ADC) to create an integer value in the
image array at the same position.
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(3) Banks of amplifiers amplify the collected charge and digitize the voltage signals in parallel from each row of
the detector matrix.
c. Electronic components, described in 3.a.1-3., occupy a substantial fraction of the DEL. Because they are
insensitive to x-ray interactions, they reduce the overall collection efficiency of x-ray-induced charge.
(1) Fill-factor is the term describing the ratio of the active charge collection area to the total area of the DEL (11).
(2) A small area DEL improves spatial resolution but diminishes the fill-factor because the area required for the
electronic components remains unchanged.
(3) Large-FOV detectors for general fluoroscopy have a DEL spacing (pitch) of approximately 100 to 140 μm,
depending on the manufacturer.
(4) Because the fill-factor is as little as 40% to 50% for 100 μm DELs; this size
DEL is the smallest detector sampling pitch currently available.
(5) The maximum spatial resolution is determined by the detector aperture and sampling pitch, which is on the
order of 140 μm for large FOV (40 × 40 cm) detector.
d. Indirect x-ray conversion TFT arrays use a scintillator to convert x-rays to light, with optical coupling of the
phosphor layer to the active matrix, Figure e-90.2A.
(1) Light photons from the scintillator fall on the photodiode within each DEL, producing a corresponding charge
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that is stored locally.
(2) Technologic advances are improving fill-factor penalties by using microlens arrays to focus light into the
active area, or by layering a continuous photodiode component directly on the TFT array with underlying
electronics.
(3) TFT detectors with photodiodes are more labor intensive to manufacture with greater probability for errors
compared to TFT detectors without photodiodes (11).
e. Direct x-ray conversion TFT arrays use a semiconductor that produces electron-hole pairs in proportion to the
incident x-ray intensity, converting absorbed x-ray energy directly into charge (Fig. e-90.2B).
(1) Amorphous selenium (a-Se) is layered between two electrodes connected to the bias voltage and a dielectric
layer.
(2) Ion pairs are collected under a high voltage to reduce charge recombination and lateral spread during transit.
(3) Reduced spreading of the information carriers (holes and electrons) improves spatial resolution.
(4) Fill-factor issues are diminished because the electrical potential field lines can bend and direct charge to the
collection electrode that is smaller than the DEL (11).
f. Various size flat panel detectors (23 × 23 cm, 30 × 40 cm, 43 × 43 cm FOV) are available from manufacturers.
(1) Both indirect (CsI scintillator) and direct (a-Se semiconductor) x-ray conversion detectors are used for
fluoroscopy and interventional procedures.
(2) Recent design improvements provide the ability to acquire 30 frames per second with minimal lag and good
image quality for both real-time fluoroscopy and spot radiographs (11).
(3) Sampling pitch and DEL area dimensions of approximately 150 to 250 μm are typical for fluoroscopic
detectors.
g. Selecting a different FOV requires changes to the area of the DEL.
(1) DEL binning may be implemented, where 3 × 3 binning of DELs occurs with the large FOV (e.g., 150 to 450
μm effective DEL dimension), 2 × 2 binning with an intermediate FOV, and no binning with the smallest FOV to fit
the image matrix onto the display (typically a 1,000 × 1,000 matrix).
(2) Some manufacturers send the full fidelity image from the detector to the display electronics where the image
pixels are binned prior to display.
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FIGURE e-90.2 • Indirect- and direct-conversion AMFPI cross-sections. A: A structured phosphor, cesium iodide
(CsI), is used with the indirect TFT detector. The scintillator thickness can be increased to increase absorption
efficiency without a corresponding loss of spatial resolution, due to the internal reflection of light within each
vertically oriented crystal. B: The direct conversion process results in essentially no lateral spread of induced x-
ray charge due to the high voltage placed across the semiconductor material.
h. Superior noise suppression is obtained with the detector-binning mode (large FOV) at the expense of spatial
resolution, which is improved by not performing binning (small FOV).
(1) As less binning of the DELs results in less averaging of the information carriers, the exposure rate increases
in an attempt to maintain signal-to-noise ratio (SNR) through automatic exposure control feedback.
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(2) The fluoroscopy automatic exposure rate control should be calibrated to deliver a linear, inverse relationship
with FOV (1) to maintain adequate SNR.
i. Flat-panel TFT arrays have both advantages and disadvantages.
(1) Fast electronics, low-lag converters, wide exposure latitude, minimal image distortion, a small profile allowing
better patient access, and a square FOV are some typically listed advantages (11).
(2) The three disadvantages of flat-panel detectors are a poorer detective quantum efficiency (DQE) at lower
exposure levels during fluoroscopy, cost of manufacturing, and longevity of the image receptor.
Image Data Processing

Image processing involves a number of steps, from the preprocessing correction of detector imperfections to the
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postprocessing manipulation of image contrast and spatial resolution enhancement. Achieving the optimal image
requires proper tuning during implementation and acceptance testing.
1. Preprocessing
All digital detectors have preprocessing algorithms applied periodically to the raw, uncorrected data.
a. The initial step (12) corrects nonfunctional or partially functional detector elements and row/column defects
within the TFT.
(1) A uniform exposure is made on the detector.
(2) DEL responses adjacent to defects are determined, and bilinear interpolation is used to determine a
substitute value.
(a) Nonfunctional areas of the detector are eliminated.
(b) Correlated noise patterns are introduced that locally reduces spatial resolution.
(3) Currently, there are no standards for digital detectors in terms of number of defects, their location, and the
number of adjacent or clustered defects.
b. Step 2 performs a 2D flat-field correction.
(1) A low-quantum-noise image that reveals gain and structure variations is obtained, inverted, and normalized to
represent the characteristic variations of the detector response.
(2) Corrections are obtained on raw images by first subtracting the offset image and then multiplying the
normalized flat-field image, the net result being the corrected output image.
(3) At this stage in preprocessing, corrections for detector defect, structure, and gain variations have been made.
c. The large exposure latitude produces a low-contrast image that is diagnostically inadequate.
(1) Step 3 identifies clinically relevant information on the raw image and produces a normalized, scaled image
over a predetermined bit range (usually 10 bits or 12 bits).
(2) Collimator borders are determined, and a histogram (frequency distribution of pixel values) within the
collimated area is constructed.
(3) The shape of the histogram distribution depends on the anatomy and is independent of the incident exposure
(12).
(4) A computer matching algorithm calculates the best fit between the measured and derived shapes, from which
the minimum and maximum values of useful anatomic information is determined, in addition to the median.
(5) The median value is used to determine overall amplification of the image data and to reallocate the
information over the fixed bit depth of the output image.
(6) Final output of the detector is the defect corrected, digitally scaled digital imaging and communication in
medicine (DICOM) “for processing” image (13) ready for spatial and contrast enhancement.
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2. Postprocessing
Postprocessing to improve contrast and spatial resolution often makes the difference between an acceptable and
unacceptable image from the radiologist's perspective and results in the DICOM “for presentation” image (13).
a. Algorithms that change the subject contrast of the image in a variable, regionally specific way to allow
simultaneous viewing in underpenetrated and overpenetrated regions of the image (see Fig. e-90.3) include:
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(1) Dynamic range control
(2) Multiscale, multifrequency processing (14)
(3) Tonescale processing
(4) Contrast-limited adaptive histogram equalization
These algorithms reduce the dynamic range in areas of high absorption (e.g., mediastinum) and increase
dynamic range in areas of low absorption (e.g., lungs).
b. High-contrast spatial resolution enhancement is used to compensate for the limited spatial resolution of digital
detectors.
(1) Sharpening kernels
(2) Harmonization
(3) Frequency-based filtering algorithms are applied to the image data. A generic way to improve sharpness of
an image subtracts a slightly blurred version from the original image (Fig. e-90.4). This difference image, which
emphasizes the higher-spatial-frequency content, is added back to the original, resulting in an edge-enhanced
image.
FIGURE e-90.3 • Effects of image processing. A: Suboptimally processed “for presentation” image exemplifies
washed-out contrast. B: Window and level adjustments are applied to the image to display anatomy in the low
transmission subdiaphragm and mediastinal areas, saturating the lung areas. C: Window and level adjustments
are applied to improve contrast in the high transmission lung areas, thresholding contrast in the subdiaphragm
area. D: Contrast-limited adaptive histogram equalization processing uses adaptive methods to enhance local
contrast in local areas that are globally equalized over the total image area.
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FIGURE e-90.4 • Generic algorithm for spatial resolution enhancement. A: The original image, unenhanced. B:
Original image blurred producing an image of lower spatial frequency content. C: High-frequency difference
image obtained by the subtraction of the blurred image from the original image. D: Edge-enhanced image is
created by the addition of the normalized difference image to the original image, producing the spatially
enhanced image.
c. Perceived quantum mottle (noise) in the image can be reduced with spatial frequency processing involving
smoothing kernels that average out highfrequency noise, albeit at the loss of spatial resolution.
3. Other processing
a. Digital subtraction angiography (DSA) images render contrast filled vessels in the image more conspicuous.
(1) A noncontrast mask image is subtracted from a series of images containing contrast.
(2) Background structures are removed from the difference image leaving only the contrast filled vasculature.
(3) Because the dynamic range of the subtracted image is reduced by the removal of background anatomy, the
image can be amplified to improve the visualization of the vasculature.
(4) This amplification increases the perceived noise in the image.
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FIGURE e-90.5 • A dual-energy image dataset consists of two images, one obtained at low (60) kVp and another
obtained at high (120) kVp. A: The high-energy composite image is shown here. B: Energy-weighted subtraction
produces a “soft-tissue only” and (C) a “bone-only” image set; the conspicuity of the lesion can be increased
with the removal of structured “anatomic noise.”
(5) Increasing the radiation dose at the image receptor 10-fold reduces the perceived noise to acceptable levels
but results in relative high radiation doses to the patient.
b. Dual energy radiography (DER) techniques allow the selective removal of anatomy from the image.
(1) DER uses the energy-dependent attenuation characteristics of bone, soft tissue, and fat (Fig. e-90.5) (15).
(2) Bone (calcium) x-ray attenuation varies more rapidly with effective beam energy than soft tissues due to the
photoelectric effect.
(3) Two projection images are acquired at high and low effective energy in rapid sequential fashion (60 kVp
followed by 120 kVp).
(4) Differences in the relative attenuation of tissues will occur in the subtracted image pairs.
(a) One of the images can be “weighted” to zero-out the soft tissue signals in the subtracted pair, leaving a bone
residual image, Figure e-90.5C.
(b) The opposite weighting results in only soft tissue components in the difference image (Fig. e-90.5B).
(5) Although the dose of DER chest imaging is somewhat greater (up to 2×) compared to a conventional single-
energy radiograph, increased benefits of removing structures likely outweighs the added risks of the larger dose
to the patient.
c. Rotational 3D angiography and intraoperative 3D image guidance (Fig. e-90.6), represent the process of
generating volumetric, multiplanar slices of the patient's anatomy (16,17,18).
(1) Projection images are acquired with a C-arm flat-panel detector rotating over a ˜200-degree arc around the
patient during an interventional procedure.
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FIGURE e-90.6 • A and B are images of the C-arm gantry in two positions during its approximately 200 degrees
of rotation about the cylindrical phantom sitting on the table of the fluoroscope. In image A, the image receptor is
on the left while the x-ray tube and collimator assembly are on the right. Images C and D are anteroposterior (AP)
and lateral (LAT) projection images acquired with cone-beam geometry of an anthropomorphic spine phantom.
Images E and F are tomographic reconstructions at two different levels of the lumbar spine within the scanned
volume. Please note the presence of significant artifacts at the periphery of the anatomy in the tomographic
reconstructions.
(2) Image data are reconstructed into tomographic images using cone beam algorithms, scatter reduction
strategies, and small as possible FOV.
(3) The resulting voxel data can be viewed in multiple planes (axial, sagittal, coronal) with multiplanar
reformatting.
(4) Radiation dose depends on patient size because automatic exposure control systems attempt to maintain
signal to noise; dose is typically
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less than a multidetector helical CT scan but with less image quality (contrast).
(5) Use of cone beam CT has shown to reduce the need for fluoroscopy, potentially reducing overall patient
dose; this is countered by easy access to CT imaging and requires analysis of physician practice patterns.
Acceptance Testing and Quality Control

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1. Establishment of initial baseline performance indicators and periodic quality control testing is crucial to
maintaining high-quality images at the proper dose to the patient. One must follow specific manufacturer-
recommended procedures as well as independent procedures and standards.
2. Overexposing a patient significantly, with no outward sign of doing so, is a major concern. The American
College of Radiology (ACR) has recently published practice guidelines specifically for digital radiography (19,20).
These documents contain a significant number of recommendations from the medical physics perspective and
should aid in the effective and safe use of digital radiography devices.
References
1. Strauss, KJ. Pediatric interventional radiography equipment: safety considerations. Pediatr Radiol .
2006;36(suppl 2):126-135.
2. Ammann E, Wiede G. Generators and tubes in interventional radiology. In: Balter S, Shope TB, eds.
Syllabus: A Categorical Course in Physics: Physical and Technical Aspects of Angiography and
Interventional Radiology. Oak Brook, IL: Radiology Society of North America; 1995:59-74.
3. Rauch PL, Strauss KJ. X-ray generator, tube, collimator, positioner, and table. In: Nickoloff EL, Strauss KJ,
eds. Syllabus: Categorical Course in Diagnostic Radiology Physics: Cardiac Catheterization Imaging. Oak
Brook, IL: Radiology Society of North America; 1998:61-82.
4. Strauss KJ. Cardiac catheterization equipment requirements: pediatric catheterization laboratory

considerations. In: Nickoloff EL, Strauss KJ, eds. Syllabus: A Categorical Course in Diagnostic Radiology
Physics: Cardiac Catheterization Imaging. Oak Brook, IL: Radiology Society of North America; 1998:105-
119.
5. Freiherr G. Siemens robot revolutionizes interventional imaging. Diagnostic Imaging. 2007.
6. Balter S. Methods for measuring fluoroscopic skin dose. Pediatr Radiol . 2006;36 (suppl 2):136-140.
7. International Electrotechnical Commission. International Electrotechnical Commission Report 60601:

Medical Electrical Equipment—Part 2-43: Particular Requirements for the Safety of X-Ray Equipment for
Interventional Procedures. Geneva, Switzerland: International Electrotechnical Commission 2000.
8. Belanger B, Boudry J. Management of pediatric radiation dose using GE fluoroscopic equipment. Pediatr
Radiol . 2006;36(suppl 2):204-211.
9. Blume H. The imaging chain. In: Nickoloff EL, Strauss KJ, eds. Syllabus: A Categorical Course in
Diagnostic Radiology Physics: Cardiac Catheterization Imaging. Oak Brook, IL: Radiology Society of North
America; 1998:83-103.
10. Coltman JW. Fluoroscopic image brightening by electronic means. Radiology. 1948;51(3):359-367.
11. Seibert JA. Flat-panel detectors: how much better are they? Pediatr Radiol . 2006;36 (suppl 2):173-181.
Radiology Books
12. Seibert JA. Digital radiographic image presentation: pre-processing methods. In: Samei E, Flynn MJ, eds.
Syllabus: A Categorical Course in Diagnostic Radiology Physics—Advances in Digital Radiography. Oak
Brook, IL: Radiology Society of North America; 2003:147-151.
13. Clunie D. DICOM implementations for digital radiography. In: Samei E, Flynn MJ, eds. Syllabus: A
Categorical Course in Diagnostic Radiology Physics—Advances in Digital Radiography. Oak Brook, IL:
Radiology Society of North America; 2003:163-172.
14. Ogoda M, Hishinuma K, Yamada M, et al. Unsharp masking technique using multiresolution analysis for
computed radiography image enhancement. J Digit Imaging. 1997;10(3):185-189.
15. MacMahon H. Dual-energy and temporal subtraction digital chest radiography. In: Samei E, Flynn MJ,
eds. Syllabus: Categorical Course in Diagnostic Radiology Physics—Advances in Digital Radiography.
Oak Brook, IL: Radiology Society of North America; 2003:181-188.
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16. Jaffray DA, Siewerdsen JH. Cone-beam computed tomography with a flat-panel imager: initial
performance characterization. Med Phys. 2000;27(6):1311-1323.
17. Siewerdsen JH, Jaffray DA. Optimization of x-ray imaging geometry (with specific application to flat-panel
cone-beam computed tomography). Med Phys. 2000;27(8):1903-1914.
18. Orth RC, Wallace MJ, Kuo MD. C-arm cone-beam CT: general principles and technical considerations for
use in interventional radiology. J Vasc Interv Radiol . 2008;19(6):814-820.
19. Krupinski EA, Williams MB, Andriole K, et al. Digital radiography image quality: image processing and
display. J Am Coll Radiol . 2007;4(6):389-400.
20. Williams MB, Krupinski EA, Strauss KJ, et al. Digital radiography image quality: image acquisition. J Am
Coll Radiol . 2007;4(6):371-388.
Suggested Readings
Bushberg JT, Seibert JA, Leidholdt EM, et al. The Essential Physics of Medical Imaging. 3rd ed.
Philadelphia, PA: Lippincott Williams & Wilkins; 2012.
Godfrey DJ, Das SK, Wolbarst AB, eds. Advances in Medical Physics 2014. Madison, WI: Medical Physics;
2014.
Wolbarst AB, Capasso P, Godfrey DJ, et al eds. Advances in Medical Physics 2012. Madison, WI: Medical
Physics; 2012.
Wolbarst AB, Mossman KL, Hendee WR, eds. Advances in Medical Physics 2008. Madison, WI: Medical
Physics; 2008.
Radiology Books
Wolbarst AB, Zamenhof RG, Hendee WR, eds. Advances in Medical Physics 2006. Madison, WI: Medical
Physics; 2006.
Radiology Books
e-91
Standard Angiography/Interventional Procedure Tray Contents
Petra Clark
Please refer to Chapter e-100, Infection Control and Sterile Technique in Interventional Radiology.
Procedure Tray Content

Safety needles should be used at all times. Types of needles and their uses are listed in Table e-91.1.
Table e-91.1 Needles and Their Uses
Size (No.) Use
25-gauge × 5/8 in. (1) Lidocaine injection, skin/superficial
22-gauge × 1 in. (1) Lidocaine injection, deep
18-gauge × 1 in. (1) Aspiration of lidocaine from vial
18-gauge × 1-in. filter needle (1) Aspiration of medications from glass ampules
Single wall 18-gauge × 2 3/4 in. (1) Percutaneous arterial access (may be added later to
(Open cannula needle with a cutting or interventional tray on table)
beveled edge)
Seldinger 18-gauge two-piece needle Percutaneous arterial or venous access
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Please see useful syringe types in Table e-91.2.
Table e-91.2 Syringe Type
Type (No.) Use
Luer lock, 10 mL (2) Flush/hand contrast injection
Luer lock, 20 mL (3) Flush
Fingertip-control Luer lock, Local anesthesia

10 mL (1)
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Transparent medication Affix one by one to each medication added to syringes and bowls on
labels the procedure table
Sterile Table Equipment (Number Needed)

1. Stopcock, plastic one-way (snap flow-switch), for flow control for proximal end of catheter (1)
2. Safety scalpel, no. 11 blade, for skin incision (1)
3. Hemostat, 5-in. curved mosquito, for dividing skin and superficial soft tissues (1)
4. Closed intravascular flush administration set with three-way stopcock to gravity drainage waste reservoir
system (1)
5. Closed contrast administration set with three-way stopcock piggybacked to three-way stopcock of
intravascular flush set (1)
6. Large basin with sterile solution for wire/catheter placement (1)
7. Sharps container/sharps pad for disposal of sharp objects (1)
8. Small cup for mixing solutions/contrast media (1)
9. Sponges (gauze), 4 in. × 4 in. (20)
10. Sterile cloth towels for draping around access site (9)
11. Sterile backed table covers (2): one for the procedure table and the other for the prep stand
12. Sterile femoral artery fenestrated drapes with contrast absorption barrier for angiography kit (1) or sterile
fenestrated drape (1) with large sterile drape sheet (1) for interventional kit
13. Sterile impervious surgical gowns (1,2)
14. Sterile towel clips (3)
15. Sterile set up covers (3): one each for the procedure table, prep table, and solution stand
Note: The use of setup covers should be restricted to situations when there is a risk that the sterile field may be
contaminated by personnel and activities required during the periprocedural period. Ideally, sterile tables should
be set up immediately prior to use.
16. Sterile plastic bouffant hats to cover image intensifier, lead shields, and table controls
Solutions (for Flush/Irrigation)

1. Flush: 500 mL normal saline (NS) with 500 units heparin (1 bag) for intravascular flushing of the angiographic
catheter
2. Irrigation: 500 mL irrigating saline with 500 units heparin (1 bag) for large basin
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Table e-91.3 shows some useful antiseptic washes and scrubs.
Table e-91.3 Antiseptic Scrubs/Preps
Antiseptic Use
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ChloraPrep To prep
procedure site
OR
Betadine scrub sticks (3) To wash

procedure site,
and
Betadine prep stick To paint

procedure site
If patient is allergic to Betadine and ChloraPrep, a bactericidal soap solution is

recommended, that is, Hibiclens or green soap.
Personal Protective Equipment

Personal protective equipment should be available for all team members to use during invasive procedures.
This includes:
1. Sterile and nonsterile gloves (latex free). Sterile indicator gloves are recommended to be worn under the
sterile outer gloves.
2. Impervious gowns
3. Face shields
4. Eye shields
Suggested Readings
Association of Perioperative Registered Nurses. Recommended practices for surgical attire. In: Perioperative
Standards and Recommended Practices. Denver, CO: Association of peri-Operative Registered Nurses;
2012:73-75.
Association of Perioperative Registered Nurses. Standards practices for maintaining a sterile field. In:
Perioperative Standards and Recommended Practices. Denver, CO: Association of periOperative
Registered Nurses; 2012:87-94.
Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health. NIOSH
Alert: Preventing Occupational Exposures to Antineoplastic and Other Hazardous Drugs in Health Care
Settings. Atlanta, GA: Centers for Disease Control and Prevention; 2004.
Radiology Books
e-92
Needles, Guidewires, Catheters, and Stents
David W. Trost
An understanding of needles, guidewires, catheters (vascular and nonvascular), balloons, and stents with
respect to their material and dimensional characteristics is very important because of how these devices are
made and measured and how these scales relate to one another and the device's general physical behavior.
Dimensional scales of gauge, French, inches, and millimeter are commonly used to measure the diameter of
interventional devices, causing confusion even
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among seasoned practitioners. Needles are measured in gauge, guidewires in inches, catheters in French, and
balloons and stents in millimeters. The gauge (Birmingham Wire Gauge, developed in the 1800s) specifies the
outer diameter (OD) of the needle, with smaller diameters counter intuitively having higher values. French size,
developed by the French medical instrument-maker, Joseph-Frédéric-Benoît Charrière, refers to the outer
circumference a device, with one French size equaling approximately 0.33 mm (e.g., 3 Fr. OD ˜1.0 mm OD).
Inches and millimeters are self-explanatory and refer to the nominal OD (or length) of a device. Sizing scale
conversions are outlined in Table e-92.1.
The internal diameter (ID) will vary with the thickness of the wall of the device. Because the introduction of these
devices into the body requires sliding one through another, it is essential to know the relationships of these
measuring standards. The rule of thumb is that 19 gauge, 3 Fr., 0.038 in., and 1 mm are all about the same
size. The ID of devices in not standardized but varies with specifications for the device. Some devices are
labeled by the French size of the device they accommodate; sheaths and guiding catheters are labeled in this
manner. Sometimes, even devices that should fit through each other based on the labeling may not do so due to
variances in manufacturing tolerances. For example, a sheath 5 Fr. labeling should accept a 5 Fr. catheter. If the
catheter is at the upper limits of its manufacturing tolerances and the sheath is at the lower limits of its
tolerances, then the system might not fit. This is rare but can happen, especially when the manufacturers are
different. Other factors that can affect the fit are dry blood or contrast on a catheter or guidewire, which can
distort dimensions or create excessive friction. This is especially important with small-diameter devices, which
have tighter tolerances. Hydrophiliccoated devices must always be kept wet in order for them to perform
properly.
Table e-92.1 Sizing Scale Conversions
Gauge Inches mm Fr.
27 0.016 — —
26 0.018 — —
25 0.020 — —
23 0.025 — —
Radiology Books
21 0.032 — —
20 0.035 — —
0.038 1 3
19 0.042 — —
18 0.050 — —
0.053 1.35 4
0.066 1.67 5
0.079 2 6
0.092 2.3 7
0.105 2.7 8
0.118 3.0 9
0.131 3.3 10
0.144 3.7 11
0.158 4.0 12
0.184 4.7 14
0.210 5.3 16
0.236 6.0 18
0.263 6.7 20
0.288 7.3 22
0.315 8.0 24
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FIGURE e-92.1 • Biopsy needles and their tip configurations. (From Gazelle GS, Haaga JR. Biopsy needle
characteristics. Cardiovasc Intervent Radiol . 1991;14:12-16, with permission.)
Needles
Although the basic concept of a needle is simple, there are many permutations of the basic design that are
optimized for specific tasks. Almost every procedure that is performed by the interventionalist begins with the
choice of a specific needle.
The concept of “form follows function” really applies to needle design. Needles, generally made from surgical
stainless steel, come in many sizes and lengths. Short squat needles do not bend when introduced into soft
tissue, but thin longer ones can bend and miss deeper targets unless guided properly. Needles are generally
hollow, may be filled with an inner removable trocar, and are categorized broadly for access or biopsy.
Access needles usually have a wedge-shaped tip or a trocar (simple-pointed) tip. The OD is specified by its
gauge, whereas the ID varies with the wall thickness. In general, a 19-gauge needle will accept a 0.035-in.
guidewire, and a 21-gauge needle accepts a 0.018-in. guidewire. Access needles are used to enter structures
such as blood vessels (see Fig. 1.2), organs, and collections. They are designed to penetrate soft tissue to the
desired target and then allow injection of fluid, usually contrast, or allow the passage of a guidewire, once the
trocar is removed.
Biopsy needles are designed to remove tissue for microbiologic or pathologic analysis (see Fig. e-92.1). There
are fine needle aspiration (FNA) needles and core biopsy needles. FNA needles (20 to 25 gauge) are produced
with different tip configurations to facilitate removal of cells. They can often transgress bowel with impunity.
These needles may be placed through a guiding needle. Chiba (wedge tip), Westcott (side-cutting notch), and
Franseen (serrated tip) are the more popular designs. Core biopsy needles are designed to cut out a piece of
tissue and retain it in the device. These devices are usually spring-loaded and do not require suction. They also
are frequently placed through an outer guiding needle.
Guidewires
The common guidewires used in interventional radiology are constructed of a fine wire tightly wound around a
stiff inner “mandrel” core wire. These wires are made in a variety of sizes and lengths but usually range from
0.010 to
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0.038 in. in diameter and 40 to 300 cm in length. The outside of the guidewire is frequently coated with Teflon to
reduce friction and may be impregnated with heparin to reduce thrombogenicity. The inner core provides the
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rigidity of the wire. This inner core, or mandrel wire, is tapered starting at a variable distance from the tip, toward
the introduction end of the guidewire. Varying the taper and the distance that the core extends toward the end of
the guidewire allows the designer to vary tip flexibility and the transition to a softer segment toward the tip. Some
wires have tapered cores at each end of the wire, allowing either end to be used for introduction. Frequently,
these wires have a straight end and a J-shaped end. Some wires have movable cores so that the flexibility of the
tip can be changed at will. Most guidewires have an extra fine “safety” wire running the full length to prevent the
outer wire coil from uncoiling and breaking off.
Some guidewires are specially made to enhance their “torquability,” that is, the ability to translate a rotational
movement of the wire on the outside to the tip inside the patient. These wires can be “steered” into the desired
location in the body.
Most guidewires are constructed of steel; however, other materials such as nitinol, enhance the wire's resistance
to kinking. Platinum and gold can be added to the tip to provide for better radiopacity. Some guidewires have
coatings to make them more slippery. Most of these coatings are hydrophilic and only work when they are wet.
Flexible-tip standard wires are generally used for routine percutaneous introduction of catheters. Tip flexibility
allows the wire to buckle easily in the vessel to avoid wall damage. However, one must be aware that even a
very flexible guidewire is very stiff and traumatic when it first exits the tip of the catheter. Exchange wires are
usually longer versions of standard wires, which have enough length between the target site and external end so
that a new catheter may be introduced without losing wire purchase internally.
Specialty wires, such as those used with microcatheters, have solid torquable hydrophilic shafts with radiopaque
soft tips. These wires are designed with distal segments that vary greatly in length and in flexibility. The tips can
have a fixed shape or be shapable.
Tip-deflecting wires allow the softer tip of the catheter to bend to a set radius when an external handle is
activated. These wires are useful for steering catheters (e.g., through the right heart) or to facilitate foreign body
retrieval.
Guidewire Handling
Most guidewires are fragile and can be very expensive. The cost of a guidewire ranges from $10 to several
hundred dollars depending on its design and the construction materials. Care should be taken to preserve their
useful life as long as possible. Guidewires should be wiped with a saline-soaked gauze or lint-free pad after each
introduction into the body. The buildup of blood clot, fibrin, or dried contrast can render the wire useless by
causing it to stick inside catheters, or worse, causing emboli. The guidewire should be stored loosely coiled in a
bowl of heparinized (5,000 units per L) saline to help prevent thrombus formation.
Vascular Catheters
Catheters are designed for safe and efficient cannulation of vessel orifices. Efficient cannulation is determined by
the shape of the catheter and its “torquability.” The ability to retain shape and torquability and to sustain injection
pressures safely is in turn determined by the characteristics of the materials from which the catheter is
manufactured (Table e-92.2).
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Table e-92.2 Material Characteristics of Catheters
Catheters Material Characteristics
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Polyurethanes (PU) Soft unbraided tip; stainless steel braided body; provides for good torque
control, but wall is thicker and internal diameter is smaller; unbraided
catheters available
Highest coefficient of friction between catheter surface and tissues, and
catheter and guidewire
Polyethylenes (PE) Commonly used plastic. Soft and flexible but stiffer than unbraided
catheters (i.e., better torsional rigidity), therefore better torque. Coefficient
of friction much less than PU
When unbraided, follows tight corners well
Polypropylenes Good memory: less likely to lose shape at body temperature. Lower
coefficient of friction than PU
Teflons Stiff, good memory, lowest coefficient of friction; material strength allows for
manufacture of thin-walled (large inner bore, small outer caliber) catheters.
May kink easily if bent too sharply
Nylon Combined with PU for manufacture of high-flow 4-5 Fr. catheters
Balloon percutaneous Balloon material characteristics

transluminal angioplasty
(PTA) catheters
Irradiated PE Sustains high pressure without stretching
Polyurethane (PU) Dimension changes with repeated inflation; bursts easily
Polyvinylchloride Tends to stretch, low dilating force but follows bends well
Determination of Flow Rate and Bursting Pressure

1. Flow rate is calculated by the Hagen-Poiseuille equation
where Δ P = pressure drop across catheter, r = radius, L = catheter length, and μ = viscosity contrast at room
temperature. Flow rate varies with internal radius to the fourth power and is inversely proportional to the length.
Flow rates increase linearly with lower viscosity contrast.
2. Catheter bursting pressure is calculated as
P = T (t / r)
where T = tensile strength of catheter material, t = wall thickness, and r = internal radius. Thicker walls and
smaller internal diameters make stronger catheters.
Catheters: Technical Facts and Precautions

1. There is no standard color coding corresponding to a catheter French size.
Radiology Books
2. Watch for weak points in catheter (holes, etc.). Catheters usually burst at the hub, where pressure limits are
exceeded first; however, catheters can burst inside the patient if they have been kinked or stressed in other
ways. Do not use a catheter that has had kink in it. This typically occurs if the sterile pouches have been folded
or during removal of the catheter from the packaging.
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3. Watch for “lack of fit” (between catheters/sheaths/wire).
a. Catheters of the same French size may accept different size wires. The French size refers to the OD of the
catheter; the ID can vary due to the construction of the catheter. Check the manufacturers' specifications for
details on a particular catheter.
b. Recommended manufacturing tolerances for 5 Fr. catheters are ± 0.3 Fr. on diameter and ± 5% in length.
c. Dimensional discrepancy can exist between products from the same manufacturer.
d. Noncompatible equipment can prolong procedures of cause breakage, increasing risk to the patient.
4. Watch for leakage, separation, or both at connections.
5. The radiopacity of catheters depends on impregnation with barium sulfate.
Some catheters are not very radiopaque (because either size, material, or manufacturing process does not allow
proper barium sulfate impregnation).
6. Catheters are not normally bonded with heparin. Thrombogenicity of catheters is minimized by improving the
smoothness of the catheter surface. The ability to make the surface smooth depends on the catheter material
(including additives) and the manufacturing process. Significant factors in thrombus formation are the relative
size of the catheter's OD with respect to the vessel's ID and the indwelling time. An occlusive catheter will almost
always result in an intravascular thrombus. Never leave any catheter within the body longer than it is needed for
diagnosis or treatment.
7. Catheters should be double-flushed (after removing the wire) and single-flushed every 3 minutes when in the
artery (and on removal if needed again). Doubleflush technique:
a. Use one syringe to aspirate blood and thrombus from the catheter and discard it safely.
b. Use a second syringe with fresh heparinized saline to aspirate a little blood and forward-flush briskly to clear
the catheter.
c. Shut off the stopcock while still flushing forward.
8. Teflon-coated wires have smoother surfaces, reducing friction and thrombogenicity.
9. The likelihood of infection increases with the amount of time a catheter is left in the body.
Nonvascular Catheters
Catheters and stents of various materials and designs are commercially available for nonvascular use (e.g.,
biliary, urinary, and gastrointestinal tracts), for purposes such as access (enteral feeding), drainage, or stenting.
The catheter material is designed to be soft and kink-resistant.
Drainage Catheters
Drainage of a collecting system, a duct, a hollow viscus, or a fluid collection will require approximately the same
type of tube. The materials are similar, as are the retention systems. There are many retention systems, but the
most popular one is the Cope loop, which allows the distal segment of the catheter to be locked into a loop by
pulling back on a suture (at the outer hub), which is tied to the distal inner end of the catheter (see Figs. 53.1
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and 53.4). The fixed loop is relatively hard to withdraw through the access hole. There are other modifications of
the basic Cope loop designed for organ specific drainage (see Chapters 47, 50, 51, and 53). Side holes can be
present solely at the distal loop for drainage of collections or both distally and more proximally in the shaft to
bridge obstructions, for example, distal biliary obstruction. A nephroureteral stent is simply a Cope loop catheter
where the distal segment (loop-end) is elongated to pass down the ureter into the bladder (see Figure 53.2). The
Cope loop type of catheter works well for most situations,
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but sometimes, specialized catheters are needed. There are many of these devices, but they differ only in
material and suture-locking mechanisms. These catheters are usually placed with a stiff metal or semiflexible
plastic stiffener to facilitate placement. Drainage tubes are sometimes mounted on a trocar needle for single
puncture placement. Viscous or particulate-laden collections frequently cannot be drained through the typical 6
to 14 Fr. Cope drains. Larger lumens and side holes are needed. Larger vinyl drains have over-the-wire dilator
introducers, large side holes, and lumens, allowing drainage of such collections.
Enteral Drainage Catheters

In addition to specific products commercially available for percutaneous placement, Foley catheters or loop
nephrostomy catheters of a large size may also be used for feeding and/or suction drainage.
Gastrostomy, Gastrojejunostomy, and Jejunostomy Catheters

1. Locking Cope loop-type catheters (various manufacturers): 6 to 14 Fr., 25 to 35 cm in length, with multiple
side ports with locking Cope-type loop
2. Pull-type gastrostomy tubes (various manufacturers): 15 to 28 Fr. The same gastrostomy tubes that are
commonly placed by endoscopists can be used. These tubes can be converted for jejunal feeding with a coaxial
catheter system.
3. Deutsch gastrostomy set (Cook Medical Inc, Bloomington, IN): 16 Fr., 25-cm long radiopaque polyurethane
catheter with Cope loop style tip supplied with enteral feeding adapters.
4. MIC gastroenteric tube (Halyard Health, Alpharetta, GA): This is a silicone duallumen design that allows
gastric and jejunal access. Available in a variety of sizes for adult and pediatric use. They use a balloon in the
stomach for retention.
5. MIC jejunostomy tube (Halyard Health, Alpharetta, GA): 14 to 24 Fr. (even sizes) with a 28-mL balloon; for
surgical placement or replacement of surgically placed jejunal tubes. These tubes use a balloon for retention.
6. Low-profile or button gastrostomies or gastrojejunostomies. These tubes are similar to the previously
mentioned tube 4 and 5, but they are designed with a proximal disk designed to be left flush with the skin
surface. They are accessed with a special locking adapter. These tubes must be sized to the correct length from
the retention balloon to the skin disk to properly fit the patient.
Dilatation Balloons
Dilatation balloons are usually thought of as angioplasty devices for dilating vascular obstructions; however,
such devices are useful elsewhere such as the biliary or genitourinary systems. They can be used to dilate
parenchymal tracts in place of a tapered dilator or to displace adjacent critical structures during ablation
procedures. Balloons are sized by their nominal diameter and length at full dilatation. They come on various
catheter-shaft lengths and in over-the-wire or rapid-exchange configurations. Most dilatation balloons are
constructed from noncompliant plastics allowing the expansion diameter to be equal along the balloon's length
and transferring pressure uniformally to lesion. Excessive compliance is a dangerous quality for angioplasty
balloon because this would risk bulging out beyond the ends the lesion and traumatizing the adjacent normal
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diameter vessel wall segments. All balloons have a two pressures ratings specified in atmospheres (ATM). The
nominal pressure is the number of ATM needed to expand the balloon to its stated diameter. The burst pressure
is the maximum pressure at which the inflated balloon ruptures. The manufacturer usually supplies a table, which
shows the balloon diameter at various pressures. The more noncompliant a balloon is, the less the change in
diameter once the nominal pressure is reached. Balloon catheters come on a variety of shaft lengths and IDs that
can accommodate various guidewires (e.g., 0.035 in., 0.018 in., or 0.014 in.). With an over-the-wire
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configuration, the shaft's inner lumen runs through the entire length of the catheter, and injections can be made
through it. Rapid-exchange balloon catheters have “monorail” wire lumen configurations, where this lumen runs
only over a short segment along the distal end of the catheter. This allows long balloon catheters to be
exchanged over wires that are only slightly longer than them, but they must be introduced through larger guiding
catheters or sheaths.
Balloons should be inflated with dilute non-blood-tinged contrast for visualization. Any blood that enters the
inflation lumen may clog the lumen and prevent subsequent inflation or deflation of the balloon.
Compliant balloons are available and are useful for occluding vessels (e.g., Swan-Ganz catheters while
measuring pulmonary artery wedge pressures) or for dilating stent grafts to ensure good wall apposition, without
placing undue pressure on the vessel wall. Compliant balloons are designed to mold to the vessel contour and to
not exert excessive pressure at any one point.
Stents
There are many U.S. Food and Drug Administration (FDA)-approved metallic stents, which are made of various
metals and come in a wide range of sizes. There are two basic types: self-expanding and non-self-expanding
(balloon inflatable).
Most self-expanding stents are made of nitinol (a nickel-titanium memory alloy), which allows delivery through
low-profile systems when they are constrained.
Once unconstrained within the vessel lumen, they strive to reach their rated nominal diameter, and if outward
expansion is resisted, they will continue to exert an outward radial force. Self-expanding stents are flexible,
conform well to tortuous anatomy, and are available in various diameters (5 to 14 mm) and lengths (at full
deployment). Most self-expanding stents shorten by a predictable amount when fully expanded. The Wallstent
(Boston Scientific, Natick, MA) is a self-expanding stent that shortens significantly during deployment, but it is a
very useful device because it comes in large sizes (up to 24 mm) and exerts a high radial force where needed.
The manufacturer supplies a chart, which estimates the length of the stent at various deployment diameters.
Balloon-expandible stents are mounted on balloon catheters, allowing expansion to the balloon's rated diameter.
Balloon-expandible stents do not shorten very much upon expansion; however, the stent should not be
overdilated because this can result excessive shortening and poor radial support at the edges of a lesion.
Balloon-expandible stents exert a higher radial force than self-expanding stents. They can also straighten
adjacent tortuosity if inappropriately sized. They should not be deployed in areas of the body that can flex (e.g.,
adjacent to limb joints) where they can be compressed or crushed completely. Self-expanding stents are
preferred in these segments.
Stent Grafts
Stent grafts are metallic stents covered graft material—usually a polymer or a synthetic fabric. They can be
balloon-expandable or self-expanding, ranging in diameter from a few millimeters to 4 cm. The delivery systems
for stent grafts are much larger than for bare metal stents due to the bulk added by the graft material.
Radiology Books
Suggested Readings
Geshwind JF, Dake MD, eds. Abrams' Angiography: Interventional Radiology. 3rd ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2014.
Kadir S. Atlas of Normal and Variant Anatomy. Philadelphia, PA: WB Saunders; 1994.
Mauro MA, Murphy K, Thomson K, et al, eds. Image-Guided Interventions. 2nd ed. Philadelphia, PA:
Elsevier; 2014.
Radiology Books
e-93
Embolization Materials
Siobhan M. Flanagan
Olga Duran-Castro
Jafar Golzarian
Therapeutic embolization is defined as the deliberate introduction of occluding material into a blood vessel in
order to reduce or obstruct blood flow. Several factors determine the selection of an embolic material. One of the
most important factors is the degree of permanence desired; therefore, agents are often classified as temporary
or permanent agents (Table e-93.1). After a traumatic injury, a temporary agent is often used because it allows
healing of an otherwise normal vessel to occur before blood flow is reestablished. Conversely, in a patient with
an arteriovenous fistula, permanent vascular occlusion is required in order to achieve the therapeutic endpoint.
Another consideration is the desired location or level of occlusion. When treating an arteriovenous malformation,
agents which occlude flow at the level of the nidus are needed. A more proximal occlusive agent would be
needed for procedures such as gastroduodenal artery occlusion prior to radioembolization. Finally, there are
important characteristics of each embolic agent with which the interventionist should be familiar. These include
size, radiopacity, material composition, mechanism of occlusion, and biologic behavior.
Indications for Embolization (1)

1. Occlusion of vascular abnormalities which have potential to cause adverse health effects (e.g., congenital or
acquired aneurysm, pseudoaneurysm, vascular malformation)
2. Treatment of acute or recurrent hemorrhage
3. Devascularization of benign or malignant tumors for palliation or to reduce operative blood loss
4. Ablation of non-neoplastic tissue causing adverse health effects (e.g., hypersplenism, varicocele)
5. Flow redistribution to protect normal tissue (e.g., gastroduodenal artery and right gastric artery embolization in
hepatic artery chemoembolization or radioembolization) or to facilitate subsequent treatment (e.g., right portal
vein embolization to induce left lobe hypertrophy prior to surgical resection)
6. Management of endoleak
7. Targeted delivery of drug or other agents (e.g., chemotherapy, beta emitting spheres)
Mechanical Occlusive Devices

1. Coils
Coils are made from either stainless steel or platinum and are available in a wide variety of sizes. They may have
fibers placed at right angles to the long axis of the coil, or coatings such as hydrogel, to increase the surface
area and thereby increase the speed and permanence of thrombosis. Coils rely on mechanical obstruction,
platelet activation, and the patient's own clotting cascade to fully occlude vessels. Therefore, in the setting of
thrombocytopenia and coagulopathy, the efficacy of coil embolization is compromised. Tight coil packing is
therefore important to achievement of arterial occlusion and reduction of early recanalization. All coils are
permanent devices and should be used when permanent occlusion is desired. When larger nonterminal vessels
are occluded with coils, there is relatively rapid formation of collateral arteries. These collateral vessels bypass
the point of occlusion and perfuse the distal vascular bed, although at a lower pressure than that prior to
embolization.
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Table e-93.1 Characteristics of Embolic Agents
Embolic Duration Vessel Size Mechanism Technical Notes

Agent of Action of Action
Gelfoam Temporary Small to medium Flow Shapeable, occlusive effect

obstruction lasts for several weeks
Avitene Temporary — Flow Vessel recanalizes within 8

obstruction weeks
Coils Permanent Small to large Flow Can size to vessel

obstruction
Vascular Permanent Medium to large Flow Can size to vessel

plugs obstruction
Detachable Permanent Medium to large Flow May deflate over time

balloons obstruction
PVA Permanent Small Flow May clog catheter compared

obstruction to spheres
Embolic Permanent Small Flow Uniform, less catheter

spheres obstruction clogging issues compared to
PVA
Drug eluting Permanent Small Flow Tumor treated via ischemic

particles obstruction effect and local drug
deposition
Glue Permanent Capillary to large, Flow Forms to vessels and can

conforms to vessel obstruction penetrate distally
lumen
Onyx Permanent Capillary to large, Flow Forms to vessels

conforms to vessel obstruction Requires occlusion balloon to
lumen form pushable cast and
prevent reflux
Alcohol Permanent Capillary to large Thrombosis Only requires small aliquots to

be effective
Ethanolamine Permanent Capillary to large Thrombosis Less penetrating effect

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compared to alcohol
Sclerosants Permanent Capillary to medium Sclerosant Best for use in venous

(Sotradecol, structures
etc.)
PVA, polyvinyl alcohol.
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Coil stability is essential to prevent nontarget embolization. Stability can be aided by the following:
a. Use of a guiding catheter
b. Coil oversizing. Oversizing is essential to minimize the risk of dislodgment. However, this should be weighed
against the negative effect that an elongated and incompletely formed coil has on hemostasis. Oversizing by
approximately 15% has been suggested in arteries (1). A greater degree of oversizing is required in veins.
Certain coils such as the AZUR Peripheral HydroCoil (Terumo Medical Corp, Somerset, NJ) do not require
oversizing.
c. Detachable coils. Detachable coil designs allow the operator to test the stability of the coil before detaching,
which is preferred in high-risk situations or those in which the embolization target is in close proximity to an
arterial branch whose patency is desired. Detachable coils can be released by electrolytic or mechanical
detachment, or by degradation of a polymer adhesive.
In a high-flow situation such as arteriovenous fistula, embolization can be performed using detachable coils with
the double microcatheter technique. After placing the first microcatheter at the desired level of deployment in the
target vessel, a coil can be delivered but not detached. It is used to prevent migration of more proximal coils
delivered through the second microcatheter. The distal coil can be detached or retracted at the end of the
procedure (2).
d. Coil anchoring technique. The use of anchoring techniques using coils or other devices can help achieve the
stable deployment of coils into a large vessel with high flow or high wall compliance. Coil anchoring devices
include both purpose-built commercial devices and modifications of existing designs (e.g., coil cages) (3). Coil
anchoring devices are particularly useful for occlusion of large arteriovenous fistulae in the lungs and large
portosystemic collaterals.
(1) The Amplatz spider (Cook Medical Inc, Bloomington, IN) is a stainless-steel, self-expanding metallic device
that can be introduced through a guiding catheter or vascular sheath. It prevents the movement of coils and
allows rapid occlusion of the vessel. One modification allows the spider to be screwed onto a threaded guidewire
before loading into the catheter, which allows it to be retrieved and repositioned to ensure accurate placement.
(2) Retrievable coil anchors offer the advantage of improved safety due to the ability to retrieve and redeploy
suboptimally placed devices. They are also intended to enhance occlusive efficacy by allowing a high density of
occlusive material without compromising the self-anchoring capability of the nested coils.
As new coil products become available, each product boasts desirable features compared with its predecessors.
For example, the Ruby coil (Penumbra Inc, Alameda, CA) offers a high volume coil that can be easily delivered
through a high flow microcatheter. It can be used in a variety of situations, most notably when aneurysmal
packing is needed (4). Many other coils are available in different sizes and shapes that can be used in smaller
microcatheters to reach more distal vessels in cases such as gastrointestinal (GI) bleeding. The amount of fibers,
volume of the metal, and radial force can affect tractability, packing, and delivery. Those qualities can affect coil
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selection based on the clinical scenario.
2. Vascular plugs
Vascular plugs are permanent occlusive devices which consist of self-expanding nitinol mesh in a three-
dimensional (3D) disc geometry. The Amplatzer Vascular Plug (AVP) (St. Jude Medical, St. Paul, Minnesota, MN)
is available in four versions (AVP I, II, III, and IV). These plugs vary by the number of mesh layers, the shape and
number of lobes, diameter range, unconstrained length, and the length of time to achieve vessel occlusion. Each
plug has radiopaque platinum
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marking bands, is attached to a delivery wire by a microscrew, and must be deployed through either a guide
catheter or sheath (5 to 9 Fr.). The maximal length of the delivery system is 100 cm for plugs I and II and 120 cm
for plug III. AVP I has a single mesh layer, single lobe design which is well suited for a short landing zone due to
its short unconstrained length (7 to 8 mm). The AVP IV is available in 4- to 8-mm sizes and can be deployed
using a 0.038-in. guidewirecompatible braided diagnostic catheter no longer than 125 cm. Due to the low profile
and flexible design of the AVP IV, it is well suited for use in tortuous vessels. Plugs should be oversized relative
to the target vessel diameter by 30% to 50% as recommended by the manufacturer. The devices are deployed
by unscrewing the lock in a counterclockwise direction; therefore, precise positioning and repositioning can be
achieved.
In general, due to their compact design, the relatively large surface area, and tight nitinol mesh structure, plugs
should be considered when single-step occlusion of a larger vessel or branch is desired, or when an initial plug
is needed to act as a scaffold for subsequent coil embolization. Various applications include occlusion of internal
iliac arteries prior to the deployment of aortoiliac stent grafts, exclusion of visceral arterial aneurysms, and
treatment of ascending aortic pseudoaneurysms or emergency embolization of active bleeding (5).
A new generation of plugs are available or under evaluation. The microvascular plug (ev3 Endovascular Inc,
Covidien, Plymouth, MN ) has become popular due to its ease of use. This plug can be deployed through a
microcatheter into vessels up to 5 to 7 mm in diameter. They are partially covered, allowing immediate occlusion
of the target vessels. Larger devices are becoming available that can be used through 0.038-in. lumen diagnostic
catheters. The release technique is electrical or mechanical.
3. Balloons
Detachable balloons were on the market in the United States several years ago but were recalled due to
manufacturing problems and difficulties with placement. The use of these devices has been replaced by the use
of detachable coils or plugs.
Particulate Embolic Agents

Particulate embolic agents are typically used for the embolization of tumor and tumor-related symptoms such as
mass effect or tumoral hemorrhage in addition to the treatment of certain hemorrhagic conditions not caused by a
mass. In general, these agents are administered from a selective position within the arterial supply of the target
organ and are subsequently deposited in a flow-directed manner to the area of desired treatment. Embolic
particles differ in available size ranges, uniformity of size and shape, tendency to aggregate, especially
nonspherical PVA, and compressibility. More compressible particles in theory will result in more distal
embolization. Particulate embolic agents tend to be classified as resorbable or nonresorbable.
1. Gelfoam
Gelfoam (Upjohn Co, Kalamazoo, MI) is a water-insoluble, hemostatic agent prepared from purifiedpork skin
gelatin. It was the first embolic particle used in humans and induces hemostasis by hastening clot development
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and providing structural support to the thrombus. Gelfoam is used when a temporary effect is desired, such as to
stop traumatic bleeding or to devascularize a lesion prior to surgical removal. Gelfoam is usually resorbed
completely with little tissue reaction. The rapidity and degree of resorption depends on the amount used, degree
of saturation with blood, and site at which it is used. The treated vessel typically recanalizes within a few weeks.
Gelfoam can be prepared and shaped in numerous ways, depending on the indication for embolization.
“Torpedoes” can be created by tightly rolling small
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strips of Gelfoam and injecting them through a catheter placed at, or slightly proximal to, the level of intended
embolization. Gelfoam torpedoes are also useful in the embolization of needle or catheter tracts. Alternatively,
less selective embolization can be performed with Gelfoam slurry. The slurry can be created by cutting a sheet
into strips or squares, which can be loaded into a syringe connected via a three-way stopcock to another syringe
filled with contrast. The materials are pumped back and forth between the syringes to create a suspension of
smaller Gelfoam particles (1). Gelfoam powder is no longer commercially available.
2. Avitene (Davol Inc, Cranston, RI) is a microfibrillar collagen which was previously more often used in practice.
It is available in powder and sheet form. In arteries embolized with Avitene, moderate recanalization occurs by 2
weeks and total recanalization by 2 months. It is a useful agent for tumor necrosis and organ ablation because it
can be delivered through a microcatheter.
3. Polyvinyl alcohol
PVA has historically been used in cements, packaging materials, water-resistant adhesives, cosmetics, and
household sponges. The original PVA embolic particles (Cook Medical Inc, Bloomington, IN; Boston Scientific,
Natick, MA) are still in use. They are irregularly shaped shavings from PVA blocks or sheets and are available in
sizes from 50 to 1200 μm. PVA is also supplied in the form of microspheres (Contour SE, Boston Scientific,
Natick, MA). PVA particles produce mechanical occlusion of the vessel, activate thrombin, and induce fibroblast
ingrowth, all of which leads to relatively permanent vessel occlusion. Although the permanence of PVA as an
embolic agent is well established, it is also clear that the occlusion caused by PVA particles is not always
permanent. Proposed mechanisms for recanalization include angiogenesis and capillary regrowth caused by
vascular proliferation inside the organized thrombus. In addition, resorption of the thrombus found among clumps
of PVA in the lumen of an embolized vessel can occur after the resolution of inflammation (6).
PVA particles are distributed dry or in solution and are prepared by mixing in a solution of contrast and saline.
PVA particles tend to clump, leading to occlusion of vessels that are larger than the diameter of the individual
particles. As a result, these particles can be used to occlude a large range of vessel diameters from arterioles to
larger arteries. The level of occlusion can be controlled to some degree by the dilution of the particles. There are
several maneuvers that can reduce clumping:
a. In the mixing vial
(1) Particles are mixed in a solution containing 40% contrast. This mixture should maintain suspension of the
particles in solution and prevent flocculation.
(2) The use of highly diluted particles is essential to prevent catheter occlusion or clumping, which may result in
proximal embolization. Dilute the particles in a 40-mL solution of contrast and saline. After the first syringe is
used, add another 10-mL solution to the bowl to maintain or increase dilution. Occasionally, this process
continues up to a final solution of 70 to 80 mL per vial of 1 mL PVA particles.
b. In the syringe immediately prior to injection
(1) A 10-mL or 20-mL syringe is used to aspirate the particles mixed with contrast and saline from the mixing vial
and serves as a reservoir and is connected to the middle hub of a three-way stopcock. A 3-mL or 5-mL syringe is
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then connected to the end hub of the three-way stopcock (in line with the microcatheter), and the syringes are
aspirated back and forth to mix the particles.
(2) Another method uses a 3-mL non-Luer lock syringe. After aspirating the solution from the reservoir syringe,
the injection syringe is rotated continuously during the slow injection of the particles to prevent precipitation and
clogging.
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4. Spherical embolics (“microspheres”)
Compared to conventional PVA particles, the principal advantages of spherical embolic agents are ease of
injection and reduced aggregation. The end result is a more predictable level of occlusion with less clogging of
catheters. Several spherical embolic agents have been developed. Embosphere microspheres (Merit Medical
Systems, South Jordan, UT) were the first microspheres to be used in patients and are biocompatible,
hydrophilic, nonresorbable, precisely calibrated trisacryl gelatin particles. Embospheres are U.S. Food and Drug
Administration (FDA)-approved for use in the embolization of hypervascular tumors and uterine fibroids.
EmboGold Microspheres (Merit Medical, South Jordan, UT) are made from trisacryl cross-linked with gelatin
impregnated with 2% elemental gold for visibility. Currently, there are additional embolic agents available
including Contour SE PVA microsphere (Boston Scientific, Natick, MA); Bead Block PVA-based hydrogel
microsphere (Biocompatibles UK Ltd, Surrey, United Kingdom); QuadraSphere (Merit Medical, South Jordan,
UT) super absorbing polymer microspheres; and Embozene hydrogel microspheres covered with Polyzene-F
coating (CeloNova BioSciences Inc, San Antonio, TX).
Microspheres are available in size ranging from 40 to 1,200 μm and are supplied in apyrogenic sterile sodium
chloride solution. There are physical and mechanical differences between each of the spherical embolic agents
that can significantly influence clinical outcomes. For any given embolization procedure, each type of
microsphere differs in the size of particles used and angiographic endpoint. It is essential to be familiar with the
specific idiosyncrasies of each type of spherical embolic agent prior to use (6).
a. Injection technique for spherical embolic agents
(1) The syringe containing the particles and a 3- to 5-mL syringe with contrast material are connected to a three-
way stopcock. The contrast is aspirated into the particle syringe, and after 3 to 5 minutes, a uniform suspension
is obtained. Once mixed, this solution can be injected easily and slowly. There is no need to perform the back
and forth aspiration as for PVA particles. In fact, this maneuver is not recommended because it might damage the
spheres.
(2) In the authors' experience, there can still be some clumping with spherical particles so that a 10-mL or 20-mL
contrast solution to create greater dilution may be used.
(3) The injection technique of embolic particles is of paramount importance. Flow-directed injection of particles
respects the physiology of the circulation and allows for deposition of particles preferentially to the tumor even
with a catheter in a non-superselective location. Forceful injection can result not only in vessel damage or reflux
but in some situations may also provoke the opening of vascular anastomoses with subsequent nontarget
embolization.
5. Drug-eluting particles
Drug-eluting microspheres offer the possibility of simultaneous embolization with sustained controlled drug
release. The electric charge of particles can be used to temporarily bind medications with an opposite charge.
After the beads are delivered, the drug elutes over time. To date, the beads have been most commonly loaded
with chemotherapeutic agents although in theory any watersoluble biologically active agent could be delivered
(7). Currently these beads are provided unloaded and the physician loads by soaking in his or her medication of
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choice.
a. DC Bead (Biocompatibles UK Ltd, Surrey, United Kingdom) are produced from biocompatible,
nonbiodegradable PVA hydrogel that has been modified with sulphonate groups to allow for the controlled
loading and delivery of a chemotherapeutic drug. Doxorubicin-loaded beads (DEBDOX) have been used for the
treatment of hepatocellular carcinoma and Irinotecan-loaded beads (DEBIRI) for the palliative treatment of
metastatic colorectal cancer.
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b. QuadraSphere microspheres (Merit Medical, South Jordan, UT) are superabsorbent polymer (SAP)
microspheres that are biocompatible, hydrophilic, nonresorbable, acrylic copolymer microspheres that can
absorb up to 64 times their dry-state volume. SAP microspheres can be loaded with doxorubicin or cisplatin and
to date have been largely used for the treatment of hepatocellular carcinoma. These beads are marketed in
Europe as HepaSphere.
c. Embozene tandem particles (CeloNova, BioSciences Inc, San Antonio, TX) are spherical, biocompatible,
nonresorbable, hydrogel microspheres coated with an inorganic prefluorinated polymer. They are available in a
range of sizes suitable for embolic therapy. They may be loaded with drugs such as doxorubicin or irinotecan
and subsequently embolized. They can elute a local, controlled, sustained dose of a drug to the targeted tumor.
The theoretical advantages of drug-loaded particles include a higher local concentration of the therapeutic agent
resulting in less systemic adverse effects, longer exposure of the target to the therapeutic agent, and the
potential to use drugs that are potentially toxic if injected systemically.
In the field of particulate embolization, the trend is toward the development of resorbable, loadable, and visible
microspheres to improve the outcome.
Liquid Embolic Agents

1. Glue
Glue (cyanoacrylate) is a fast and efficient, nonresorbable, nonradiopaque liquid embolic material. Liquid
monomeric cyanoacrylate is converted to a solid long-chain polymer immediately on contact with anionic
substances such as plasma, blood cells, endothelium, or saline. The reaction proceeds so rapidly that the glue
will solidify in a catheter unless a substance is added that extends the polymerization time. The most commonly
used agent is Lipiodol, ethiodized oil (Guerbet LLC, Bloomington, IN) typically in cyanoacrylate to oil ratios
ranging from 1:5 to 2:5 depending on length of time needed until polymerization. Some operators also add
powdered tantalum to increase radiopacity and facilitate visualization during injection, which is particularly useful
for intracranial procedures. It is critical that this preparation takes place in an ion-free environment to prevent
premature polymerization, preferably on a separate side table from that used for the remainder of the
angiographic procedure. The bolus of glue is introduced into the catheter after it has been flushed with 5%
dextrose solution (D5W) and is pushed out of the catheter with another bolus of D5W. The catheter is typically
changed after each injection.
Histopathologic studies of glue demonstrate that cyanoacrylate provokes a more intense inflammatory reaction
than that caused by PVA and involves the wall of the vessel and the adjacent interstitial areas. This inflammatory
reaction ultimately leads to vessel necrosis, fibrous ingrowth, and permanent occlusion (8). The most common
application of glue is the treatment of vascular malformations, particularly intracranial, although it has been
applied throughout the body for virtually every embolic indication. Risks of using cyanoacrylates include rapid
polymerization and reflux resulting in gluing the catheter in place or feeding vessel occlusion without the desired
nidal penetration. If the polymerization time is too long, the cyanoacrylate can pass into the venous circulation,
resulting in pulmonary emboli.
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2. Onyx
Onyx (ev3 Endovascular Inc, Covidien, Plymouth, MN) is a biocompatible liquid embolic agent. It is an ethylene
vinyl alcohol copolymer dissolved in various concentrations of dimethyl sulfoxide (DMSO) and opacified with
micronized tantalum powder. When this mixture contacts aqueous media such as blood, the DMSO rapidly
diffuses away, resulting in in situ precipitation and solidification of the polymer. It forms a soft elastic embolus
without adhesion to the
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vascular wall or the catheter. The polymerization process is mainly influenced by the amount of ethylene vinyl
alcohol (EVOH) in the mixture. Onyx comes in two different preparations which differ in the concentration of
EVOH, Onyx 18 with 6% EVOH and Onyx 34 with 8% EVOH. The lower the concentration of EVOH, the less
viscous the solution, and the longer it will take to precipitate. The lower concentration Onyx will penetrate more
distally into the treated vessel .
Because the polymer will solidify on contact with aqueous media, the delivery catheter must be preflushed with
DMSO. A DMSO-compatible catheter is required (e.g., Rebar, Echelon) (ev3 Endovascular Inc, Covidien,
Plymouth, MN). Onyx is nonadhesive, allowing for easy removal of the delivery catheter and of the polymer itself.
As opposed to glue, there is no concern for catheter adherence to the embolic material which can cause difficulty
in removing the catheter from the patient. Unfortunately, Onyx is quite expensive. It is primarily used for
intracranial aneurysms; however, in peripheral embolization, it has been successfully used for both the treatment
of aortic graft endoleak and high flow vascular malformations (9).
3. Alcohol
Absolute alcohol is a very effective embolization agent; however, it must be used with great care. It can be
injected via an intravascular route or direct percutaneous puncture. Upon contact with the vessel wall, ethanol
denudes the endothelium, which leads to thrombosis and eventual fibrosis. In addition, ethanol induces further
thrombosis as it contacts blood. Both actions lead to complete permanent vascular occlusion. This effective
occlusion can be used from an intra-arterial approach for tumor or organ ablation, particularly renal embolization.
In the hands of a very skilled practitioner, it can be used in the treatment of vascular malformations. Despite its
efficacy, it is important to consider the risk of toxicity and adverse effects of alcohol.
a. The principal disadvantage of absolute alcohol is the risk of necrosis of neighboring tissues including nerves
or skin (10). Methods to decrease the risk of nontarget embolization include:
(1) Controlling reflux with occlusion balloons
(2) Using in vascular beds without significant collaterals (e.g., kidney)
(3) Precisely defining the anatomy of the vessels to be occluded including assessment of supply to normal
tissues
(4) Placing the catheter in as selective a position as possible
(5) Using the smallest volume likely to achieve the intended effect, usually in small aliquots
(6) Occluding venous outflow to isolate the target vascular bed
(7) Opacifying ethanol with tantalum powder or Ethiodol to improve visualization
b. The risk of systemic toxicity increases with doses above 1 mL per kg or if the total volume exceeds 60 mL.
The patient must be monitored closely, including continuous vital sign assessment. Some practitioners advocate
the use of pulmonary artery pressure monitoring during procedures involving ethanol.
4. Ethanolamine oleate
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Ethanolamine oleate (Ethamolin 5%, QOL Medical, Kirkland, WA) is a mixture of 5% ethanolamine oleate (a
synthetic mixture of ethanolamine and oleic acid) and Ethiodol (ratio 5:1 to 5:2). The oleic acid causes intimal
irritation, which leads to an inflammatory response which ultimately causes mural necrosis, thrombosis, and
fibrosis. Compared with ethanol, ethanolamine has less penetrative effect, so it may be safer to use in situations
where vascular structures are in proximity to nerves. Ethanolamine has been used predominantly for venous
sclerosis, including treatment of gastroesophageal varices and venous malformations, as well as for cyst
sclerosis.
Approximately 50% of the oleic acid may combine with serum proteins within 30 minutes and can cause renal
toxicity in association with a marked intravascular
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hemolysis, hemoglobinuria, and hepatotoxicity. Prophylactic haptoglobin may be helpful during and after the
injection to reduce nephrotoxicity (11).
5. Other sclerosing agents
Technically, all liquid embolic agents can be considered sclerosants; however, the term is usually applied to low-
viscosity agents used predominately in venous disease. Each agent has also been used with varying success in
other types of embolization and cyst ablation. Properties of the most commonly used sclerosants will be
described, but other agents such as hypertonic dextrose, bleomycin, acetic acid, triamcinolone, and methyl
methacrylate have been or are being used, in some cases with spectacular results.
a. Sodium tetradecyl sulfate (Sotradecol, AngioDynamics, Latham, NY;
Thrombotect, Omega, Montréal, Canada) is an anionic surfactant widely used for sclerosis of esophageal
varices, varicose veins, and venous malformations. It is an anionic detergent containing 2% benzyl alcohol. It
causes intimal inflammation and thrombus formation and subsequent formation of fibrous tissue resulting in
vessel occlusion. It is not as effective as other agents in the treatment of high-flow vascular malformations but
can be used in low-flow lesions. It can be injected in liquid form or can be mixed with room air or carbon dioxide
to form a foam consistency. Although toxicities such as urticaria, anaphylaxis, hemolysis, and hematuria can be
seen with larger doses, it is generally a very safe, easy-to-use agent with low morbidity.
b. Polidocanol (Aethoxysclerol, Kreussler, Wiesbaden, Germany) is a nonionic surfactant sclerosant that was
first developed as an anesthetic. It causes vascular injury through endothelial overhydration. The agent's
attractive anesthetic properties make it nearly painless. Its use is primarily restricted to venous disease.
c. Sodium morrhuate (Scleromate 5%, Glenwood LLC, Englewood, NJ) is an irritant and sclerosing agent
composed of a sodium salt of fatty acids in cod liver oil. This agent has been used in the treatment of varicose
veins and venous malformations; however, it has been reported to be 1.5 to 4 times less effective than sodium
tetradecyl sulfate.
d. Ethibloc (Ethicon, Norderstedt, Germany) consists of a solution of zein, sodium amidotrizoate, oleum
papaveris, and propylene glycol. It is derived from corn gluten and forms hard shells used in coatings of foods
and pharmaceutical products. Ethibloc has been used effectively for the treatment of venous, lymphatic, and
arteriovenous malformations. It requires approximately 10 to 15 minutes to solidify into a viscous solution,
allowing it to remain static within the target lesion to cause intravascular thrombosis, necrosis, and fibrosis (12).
References
1. Golzarian J, Sun S, Sharafuddin MJ. Vascular Embolotherapy: A Comprehensive Approach. Volume 1:
General Principles, Chest, Abdomen, and Great Vessels. Heidelberg, Germany: Springer; 2006.
Radiology Books
2. Greben CR, Setton A, Putterman D, et al. Double microcatheter single vascular access embolization
technique for complex peripheral vascular pathology. Vasc Endovascular Surg. 2010;44:217-222.
3. Wilson MW, Gordon RL, LaBerge JM, et al. Intravascular occluding device using a modified Gianturco
stent as a coil cage. J Vasc Interv Radiol . 2000;11:221-224.
4. Golzarian J, Patel P, Beasley, R. Clinical techniques utilizing the Ruby embolization coil. Endovascular
Today. 2014;1-4.
5. Laganà D, Carrafiello G, Mangini M, et al. Indications for the use of the Amplatzer vascular plug in
interventional radiology. Radiol Med. 2008;113(5):707-718.
6. Laurent A. Microspheres and nonspherical particles for embolization. Tech Vasc Interv Radiol .
2007;10(4):248-256.
7. Liapi E, Geschwind JF. Intra-arterial therapies for hepatocellular carcinoma: where do we stand? Ann Surg
Oncol . 2010;17:1234-1246.
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8. Howington JU, Kerber CW, Hopkins LN. Liquid embolic agents in the treatment of intracranial
arteriovenous malformations. Neurosurg Clin N Am. 2005;16:355-363.
9. Rosen RJ, Nassiri N, Drury JE. Interventional management of high-flow vascular malformations. Tech
10. Do YS, Yakes WF, Shin SW, et al. Ethanol embolization of arteriovenous malformations: interim results.
Radiology. 2005;235:674-682.
11. Kaji N, Kurita M, Ozaki M, et al. Experience of sclerotherapy and embolosclerotherapy using
ethanolamine oleate for vascular malformations of the head and neck. Scand J Plast Reconstr Surg Hand
Surg. 2009;43:126-136.
12. Loffroy R, Guiu B, Cercueil JP, et al. Endovascular therapeutic embolisation: an overview of occluding
agents and their effects on embolised tissues. Curr Vasc Pharmacol . 2009;7:250-263.
Radiology Books
e-94
Commonly Used Medications
Mikhail C.S.S. Higgins
Krishna Kandarpa
Michael A. Bettmann
Analgesics
Lidocaine Hydrochloride (Xylocaine)
Mode of Action
Stabilizes neuronal membrane, preventing initiation and conduction of nerve impulses
Indications
1. Local anesthesia of skin and subcutaneous tissue, at skin puncture site prior to catheterization
2. Peripheral and central neural blockade
3. Locoregional analgesia such as during transarterial chemoembolization
Contraindications
1. Known history of hypersensitivity to amide-type local anesthetics or components of the injectable
formulation. Consider infiltration with procaine-type local anesthetic or with sterile normal saline alone.
2. Use with caution if there is inflammation or sepsis, or both, at proposed site of injection.
Adverse Reactions
1. Drowsiness is an early sign of high blood level of lidocaine due to inadvertent intravascular administration or
rapid absorption of the drug.
2. Nervousness, dizziness, blurred vision, tremors, seizures (usually of short duration), and possibly respiratory
arrest
3. Hypotension, bradycardia, and cardiovascular depression are dangerous late signs.
4. Intra-articular infusion is associated with chondrolysis post-arthroscopic/surgical intervention.
Preparation
1. For local subcutaneous infiltration: 1% to 4% solution, maximum dose 7 mg per kg with epinephrine, 4.5 mg
per kg without, up to 300 mg (30 mL of 1% solution)
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2. For use with chemoembolization: Use 2% Xylocaine solution which has 20 mg per mL of anhydrous active
lidocaine hydrochloride (HCl). Mix 10 mL of 2% Xylocaine (without epinephrine) in 100 mL contrast, giving one
an effective concentration of 2 mg per mL.
Dosage and Method
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1. Percutaneous infiltration: Start with small subcutaneous/intracutaneous wheal and then subcutaneous
infiltration, with aspiration prior to each injection to avoid intravascular injection. Addition of epinephrine aids in
limiting dispersion of the lidocaine.
2. As additive to contrast: See item 2 in “Preparation”
Kinetics
Metabolized by the liver and excreted by the kidney. Local anesthetic effect and duration depends on volume
and concentration infiltrated. Plasma half-life is approximately 2 hours.
Reversal
Treatment of toxic manifestations: Maintain patent airway and ventilation. Support circulatory system with
intravenous (IV) fluids and vasopressors as required. Treat convulsions as necessary.
Opioids (see Table e-94.1)

Butorphanol Tartrate (Stadol)
Mode of Action
Potent synthetic phenanthrene type opioid agonist-antagonist analgesic, with antagonist activity 1/40 that of
naloxone
Indications
1. Sedation: with notably milder respiratory response than opioids; analgesia, with less elevation in biliary
tract pressures and greater reduction (vs. opioid agonists) of smooth muscle tone, providing potential
advantages in gastrointestinal (GI) procedures
Contraindications
1. Hypersensitivity to drug
2. Stadol should be avoided in individuals who are dependent on narcotics as symptoms of withdrawal may
occur.
3. Once Stadol has been administered, the effects on an opioid agonist (e.g., morphine) are unpredictable
due to its weak antagonistic effect at the supraspinal narcotic receptors.
Table e-94.1 Relative Opioid Potency (Equivalent Parenteral Dose)
Agonists
MSO4 10 mg
Methadone 10 mg
Hydromorphone (Dilaudid) 1.5 mg
Fentanyl 1.00-200 μg
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Levorphanol 2 mg
Codeine 130 mg
Meperidine (Demerol) 75-100 mg
Agonist-Antagonists
Nalbuphine (Nubain) 10 mg
Dezocine (Dalgan) 10 mg
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Adverse Reactions
1. Sedation (40% of patients), nausea (6%), diaphoresis (6%)
2. Respiratory depression (2 mg Stadol = 10 mg morphine); however, the magnitude of respiratory depression
does not increase beyond a dose of 4 mg.
3. Increases load on the heart and therefore should be avoided, if possible, in patients with acute myocardial
infarctions (MIs) and patients with ventricular or coronary insufficiency
Preparation
Available in 1-mL disposable syringe, with 2 mg per mL
Dosage and Method

1. Premedication may be given on floor: 1 to 2 mg Stadol intramuscular (IM) with
25 to 50 mg Vistaril IM.
2. Titration to desired effect in angiography suite: Administer 0.5 mg IV slowly and every 15 minutes (while
assessing patient's response) up to a dose of 2 mg.
3. After adequate analgesia has been established, additional 0.5 mg increments of
Stadol may be given every 30 minutes up to a total of 6 mg, depending on the patient's size, age, and level of
debilitation.
4. It is difficult to “catch up” with pain; thus, adequate pre- or early administration of medication is the key.
Kinetics
Rapid onset of action (10 minutes) and early peak analgesia (30 minutes) following IV administration. Duration of
action is 3 to 4 hours.
Reversal
1. Naloxone (Narcan): 0.1 to 0.2 mg per dose over 2 to 3 minutes; titrate to desired effect (adequate ventilation,
alertness).
2. General supportive therapy including oxygen, IV fluids, and vasopressors, as necessary
Radiology Books
Fentanyl Citrate (Sublimaze)
Mode of Action
Short-acting synthetic opioid with rapid onset of action
Indications
1. Analgesia: 50 to 100 times the analgesic potency of morphine at same dose, with generally acceptable
cardiovascular effects
2. Sedation (primarily in combination with specific sedative medication)
Contraindications
1. Known intolerance to the drug
2. Avoid in patients using monoamine oxidase (MAO) inhibitors.
3. Use with caution in patients predisposed to respiratory depression such as those who are comatose,
have a head injury or brain tumor, or have significant respiratory compromise.
Adverse Reactions
1. Respiratory depression (peaks at 5 to 15 minutes). Administer O2 by nasal cannula and use capnography
during procedure.
2. Bradycardia (depends on dose and rate of injection; prophylactic atropine prevents bradycardia)
3. Nausea
4. Dizziness
5. Bronchoconstriction and laryngospasm
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6. Muscle rigidity causing stiff-chest syndrome: occurs with rapid injection especially in elderly patients. Muscle
relaxants are useful for treatment.
7. Hypertension resulting from administration in patients receiving MAO inhibitors within 14 days (managed by
use of vasodilators and β-blockers)
Preparation
Available in 2-mL and 5-mL ampules (both: 50 μg per mL)
Dosage and Method

1. Load: 25 to 100 μg IV over 1 to 2 minutes
2. Maintenance: 25 to 100 μg every 30 minutes (as needed for pain control)
3. Maximum dose: 3 μg/kg/h
4. Equivalence: 100 μg fentanyl = 10 mg morphine = 100 mg meperidine
5. Monitor vital signs. Hold maintenance dose if there is any change in blood pressure or heart rate > 20%, or if
respiratory rate is < 10 breaths per minute.
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6. Decrease dosage appropriately for elderly and debilitated patients.
Kinetics
When administered intravenously, onset of action is immediate (2 to 5 minutes), but maximum analgesia and
respiratory depression take several minutes (about 15 minutes). Duration of action for single IV dose of 100 μg
(0.1 mg or 2 mL) is 30 to 60 minutes.
Reversal
1. Respiratory support with oxygen administration and maintenance of patent airway
2. General supportive care
alertness without significant pain or discomfort).
4. Note: The duration of respiratory depression following overdosage may exceed duration of action of the
narcotic antagonist. Continue capnography monitoring until full reversal.
Meperidine Hydrochloride (Demerol)

Mode of Action
A synthetic opioid analgesic
Indications
1. Analgesia in setting of moderate to severe pain
2. Shivering
Contraindications
1. Hypersensitivity to drug
2. Concomitant MAO-inhibitor therapy (potential life-threatening hypertension and hyperthermia can occur)
3. Concomitant use of other narcotic or of alcohol
4. Use with extreme caution in patients with asthma or other respiratory conditions and those susceptible to
increased intracranial pressure.
5. Pregnancy, peripartum state, or nursing mother
Adverse Reactions
1. Tachycardia following IV injection (anticholinergic effect)
2. Respiratory depression (effect equal to morphine sulfate)
3. May lower seizure threshold
4. Light-headedness, dizziness, sedation, nausea, vomiting, and sweating, although less than with morphine
sulfate
5. Orthostatic hypotension, similar to morphine sulfate
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6. Lesser rise in biliary pressure than morphine sulfate
Radiology Books
7. Urinary retention (rare)
8. Urticaria, drug rash (rare)
Preparation
Available in 100-mg injectable cartridge needle
Dosage and Method

1. Titrate up to 0.5 to 1.0 mg per kg. During the procedure, fractional doses (10 mg) may be repeated every 30
minutes to 1 hour as needed by the patient. Meperidine has a shorter duration and one-tenth the analgesic
potency of morphine sulfate.
2. As premedication: 50 to 100 mg IM, 30 to 45 minutes before procedure
Kinetics
Onset of action (3 to 5 minutes after IV injection) is slightly more rapid than morphine sulfate and duration is
slightly shorter (2 to 4 hours). Redistribution half-life is about 7 minutes; elimination half-life is about 4 hours.
Metabolized by the liver.
Reversal
1. Maintain adequate airway.
2. General supportive therapy and monitoring
alertness).
4. Oxygen, IV fluids, vasopressors as needed
Morphine Sulfate (MSO4)
Mode of Action
Phenanthrene narcotic analgesic, naturally occurring opiate
Indications
1. Analgesia
2. Sedation
Contraindications
1. Allergy to morphine or other opiates
2. Acute bronchial asthma
3. Upper airway obstruction
5. Hepatic insufficiency: results in poor metabolization and prolonged duration of drug effect
6. Nursing mothers
Adverse Reactions
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1. Respiratory depression (reduces brainstem response to carbon dioxide)
2. Convulsions (high IV dose)
3. Nausea and vomiting
4. Causes rise in common bile duct pressure, decrease in gastric emptying, decreased colonic tone,
bronchoconstriction, and urinary retention
5. Orthostatic hypotension without significant change in cardiac rate, rhythm, or output
Preparation
Multiple, generally as 1 mg per mL. Available in disposable syringe as 10 mg per 10 mL
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Dosage and Method
1. Give 2 to 3 mg IV per dose, slowly over 1 minute (titrate monitoring vital signs; maximum dose, 10 mg per hour
for a 70-kg patient or not to exceed total dose of 0.2 mg per kg).
2. Hold maintenance dose if there is any change in blood pressure or heart rate > 20%, or if respiration rate is <
10 breaths per minute.
3. As premedication: 1 mg per 10 kg IM. Administer with extreme caution in elderly or debilitated patients.
Kinetics
1. Rapid onset of action (5 to 7 minutes) with peak analgesia about 20 minutes after IV injection
2. Analgesia and respiratory depression last several hours depending on dose (3 to 4 hours).
3. Elimination half-life: 1.5 to 2.0 hours. Major metabolic pathway is via conjugation with glucuronic acid in the
liver. Ninety percent of intravenously administered morphine is eliminated via the urine in 24 hours.
4. About 10% of the administered dose is eliminated in the feces.
Reversal
1. Maintain adequate airway.
2. General supportive measures: Monitor vital signs, fluid input/output.
3. Naloxone (Narcan): 0.1 to 0.2 mg/dose over 2 to 3 minutes; titrate to desired effect (adequate ventilation,
alertness without undue pain). Duration of effect is 30 to 45 minutes; therefore, patient must be monitored for 1 to
2 hours.
Nalbuphine Hydrochloride (Nubain)

Mode of Action
Potent synthetic phenanthrene opioid narcotic agonist-antagonist analgesic
Indications
Analgesia and sedation (with less elevation of biliary pressure than fentanyl and butorphanol)
Contraindications
1. Known hypersensitivity
Radiology Books
2. Contains metabisulfite and may cause allergic-type reaction in patients with sulfite sensitivity and
asthmatics
Adverse Reactions
1. Excessive sedation
3. Dizziness
4. Restlessness
5. Limited analgesia
6. Reversal of analgesia produced by other opioids.
7. In nondependent patients, may show additive effect with other narcotics; reduce dose of drugs.
8. Respiratory depression. Use in low doses and cautiously in patients with respiratory problems.
9. Bradycardia
Preparation
Available in 1-mL ampules at 10 mg per mL
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Dosage and Method
1. Give 5 to 10 mg IM, or
2. Give 1 to 3 mg IV.
3. Maximum recommended for pain relief is 10 mg for a 70-kg adult. May be repeated every 3 to 6 hours.
Kinetics
Onset of action is within 5 minutes of IV injection, and 15 minutes of IM or subcutaneous (SC) injection. Plasma
half-life: 5 hours. Duration of analgesia: 3 to 6 hours. Metabolized in the liver, excreted by the kidneys.
Reversal
1. Naloxone or nalmefene (Selincro)
2. Resuscitative equipment must be available.
3. Oxygen and supportive measures
Antibiotics
Current indications and doses for antibiotic prophylaxis in interventional procedures are listed in Table e-94.2.
Anticoagulants
Heparin
Mode of Action
Multiple interactions. Main action is reversible combination with antithrombin III to inactivate thrombin, a
coagulation protein, thus preventing conversion of fibrinogen to fibrin; does not directly lyse existing clot. Also
affects multiple other coagulation factors (e.g., Factor Xa) and platelets.
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Indications
1. Prophylaxis and treatment of venous thromboembolism
2. Periprocedural anticoagulation (e.g., during percutaneous angioplasty and stenting, immature fistula
evaluation, and arterial or venous thrombolysis)
Contraindications
1. Heparin-induced thrombocytopenia (HIT) is defined as a 50% decrease in platelet count. Incidence: 10%
to 20%. This is thrombocytopenia without significant associated symptoms, and heparin may be continued
with caution.
2. Heparin-induced thrombocytopenia with thrombosis (HITT): 5% to 10% incidence, often with longer use.
An immune-mediated, allergic reaction requiring cessation of heparin use. Antibodies may disappear after 1
year, so heparin may be cautiously restarted. Can be characterized by uncontrollable bleeding and diffuse
thrombosis.
3. Hemophilia
4. Bacterial endocarditis
5. Excessive ethanol intake
Adverse Reactions (see above)

1. Hemorrhage (3% to 8% of patients)
2. Acute thrombocytopenia
3. Systemic hypotension
4. Hypersensitivity, chills, fever, urticaria (2% to 5% of patients)
5. Vasospastic reactions
6. Osteoporosis and symptomatic vertebral fracture (2% to 3% of patients, with prolonged use)
7. Anaphylactic shock (rare)
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Table e-94.2 Recommended Antibiotic Prophylaxis in Interventional Radiologic Procedures
Recommended Adult Dosage

Procedure Suspected Organism(s) Drug and Duration
Vascular system
Diagnostic None None —

angiography
Interventional None None —

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(angioplasty, certain
embolizations,
infusion, etc.)
Biliary tract
No clinical infection Enterobacteriaceae (includes Cefazolin 1 g IV/IM before

suspected Escherichia coli, Klebsiella, and q8h for 48
Enterobacter), enterococcus, hours
Pseudomonas, Clostridium
or
Cefoperazone 2 g IV/IM before

and q12h for 48
hours
Clinical infection Same as above Cefoperazone 2 g IV/IM before

suspected (or other third- and q12h
generation (based on
cephalosporin) results of Gram
stain and
culture)a
or
Ampicillin plus 2 g IV before

and q6h (based
on results of
Gram stain and
culture)a
Gentamicin 1.5 mg/kg IV

before and
q8ha,b
Outpatient procedure Same as above Ceftriaxone 1 g IV/IM (single

dose)
Genitourinary systemb
No clinical infection None Cefazolin 1 g IV/IM before

suspected and q8h for 48
hours
or
Radiology Books
Cefoperazone 2 g IV/IM before
and q12h for 48
hours
Clinical infection Enterobacteriaceae (includes E. Ampicillin plus 2 g IV before

suspected coli, Klebsiella, Proteus, and q6h (based
Enterobacter), enterococcus, on results of
Pseudomonas aeruginosa Gram stain and
culture)a
Gentamicin 1.5 mg/kg IV

before and
q8ha,b
or
Ticarcillin or Consult product

other insert
ureidopenicillin
Drainage of fluid
collection
Tap of “clear” fluid None None —

collection (renal or
hepatic cyst,
lymphocele)
Known or suspected Enteric gramnegative bacteria, Cefoxitin 2 g IV before

abscess enterococcus, Bacteriaceae and q6h (based
fragilis, other anaerobes on results of
Gram stain and
culture)a
or
Cefotetan 1 g IV before
and q12ha
or
Gentamicin plus 1.5 mg/kg IV

metronidazole before and
q8ha,b
500 mg IV
before and q6ha
Radiology Books
or
Gentamicin plus 1.5 mg/kg IV

clindamycin before and
q8ha,b
900 mg IV
before and q8ha
Endocarditis prophylaxisc
Biliary, genitourinary, Enterococcus Ampicillind plus 2 g IV before

or gastrointestinal gentamicin and q8h in for
procedures that are 48 hours
not considered 1.5 mg/kg IV
“clean” before and q8h
for 48 hoursb
a These drugs are recommended as prophylaxis. Specific therapy should be instituted when clinically
indicated and when results of cultures are available, in consultation with referring clinical staff.
b Dose may require modification in the presence of renal insufficiency. Consult product insert.
c Endocarditis prophylaxis recommended for the following cardiac conditions: prosthetic cardiac valves
(including biosynthetic valves), most congenital cardiac malformations, surgically constructed systemic-
pulmonary shunts, rheumatic or other valvular dysfunction, idiopathic hypertrophic subaortic stenosis
(IHSS), previous history of bacterial endocarditis, and mitral valve prolapse with insufficiency.
d When patient has penicillin allergy, substitute vancomycin, 1 g IV before and q12h for 48 hours.
Modified from Spies JB, Rosen RJ, Lebowitz AS. Antibiotic prophylaxis in vascular and interventional
radiology: a rational approach. Radiology. 1988;166:381-387.
Preparation
Mix 50,000 units of heparin in 500 mL of normal saline (NS) or 5% dextrose solution (D5W) (100 IU per mL) or in
50 mL D5W or NS (1,000 IU per mL).
Dosage and Method (Continuous IV Infusion)

1. Bolus: 5,000 U IV (2,500 to 5,000 U IV if < 70 kg)
2. Infuse: 800 to 1,500 U per hour (reduce rates for older patients, especially females)
3. Maintain activated partial thromboplastin time (APTT) at 1.5 to 2.5 times normal (normal = 25 to 35 seconds).
Check APTT at 4 hours, then every 2 to 4 hours until therapeutic, and then four times per day (qid).
4. If using activated clotting time (ACT) during an intravascular procedure, adequate IV heparin should be
administered (per above protocol) to achieve a minimum ACT of 300 seconds. In most cases, the ACT is
maintained at 300 to 400 seconds by giving additional boluses as needed. ACT is less precise than APTT and
lacks high correlation with it.
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Kinetics
1. Onset: immediate (30 minutes to maximum activity)
2. Duration: 60 to 90 minutes in normal people (cleared by reticuloendothelial cells of the liver)
Reversal
To reverse heparin's anticoagulant effect:
1. Prior to a planned procedure: Preferably stop infusion for 3 to 6 hours (or about three half-lives) and check
anticoagulation status before the starting procedure.
2. After completion of an intravascular procedure: Administer IV protamine sulfate 10 mg per 1,000 U of heparin
given during the procedure (drip slowly; use cautiously in diabetics taking neutral protamine Hagedorn [NPH]
insulin; very high incidence of allergy to protamine among these patients, with possible anaphylaxis in up to
50%). Check if desired anticoagulation reversal has been achieved.
Warfarin Sodium (Coumadin)

Mode of Action
Inhibits hepatic synthesis of clotting factors II, VII, IX, and X, thereby preventing clot formation or extension of
formed clot; does not directly lyse existing clot
Indication
Long-term anticoagulation (oral administration)
Absolute Contraindications
1. High risk for serious hemorrhage
2. Patient who abuses alcohol or drugs or who is at risk of hemorrhage from serious trauma (e.g., elderly,
infirm patients or those with balance disorders)
3. Pregnancy (crosses placenta, potential teratogen)
4. Lactating mother who breastfeeds infant
Relative Contraindication
Noncompliant patient
Adverse Effects
1. Hemorrhage (3% of cases)
2. Hypersensitivity (rare)
3. Severe cutaneous reaction (rare but may be irreversible and fatal)
Preparation
Available for oral administration: 2 mg, 2.5 mg, 5 mg, 7.5 mg, and 10 mg. Dose is individually titrated to
therapeutic prothrombin time (PT) or, more usually, international normalized ratio (INR): 2 to 3 for deep vein
thrombosis (DVT)/pulmonary embolism (PE) treatment, 3 to 4 for atrial fibrillation (AF) prophylaxis, artificial
cardiac prosthesis. Concomitant administration of heparin will affect PT.
Kinetics
1. Onset of action after loading dose: 2 to 7 days for fully effective anticoagulation
2. Duration: 4 to 5 days
3. Half-life: 2.5 days. Metabolites are primarily excreted through the urine.
Reversal
1. If an intravascular procedure is contemplated, it is best to discontinue Coumadin 3 to 5 days prior to an
invasive procedure. If necessary, IV heparin may be given instead of Coumadin until 3 to 6 hours prior to the
procedure. Acceptable INR for intravascular procedures is < 2.0.
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2. Alternatively, prothrombin complex concentrate, fresh frozen plasma, or activated Factor VII may be given to
urgently normalize INR. The onset is fast, and duration of action is limited. Nota bene: These will not generally
lower INR below 1.5
3. Another option is to administer vitamin K, 25 to 50 mg IM, 4 hours prior to the procedure. Both onset of action
and duration are prolonged. Unfortunately, it may take 1 to 3 weeks to reestablish acceptable anticoagulation
with Coumadin after vitamin K reversal.
Newer Anticoagulants
Three categories: low-molecular-weight heparins (LMW heparins), synthetic direct factor inhibitors, and direct
thrombin inhibitors. LMW heparins include enoxaparin (Lovenox), fondaparinux (Arixtra), and danaparoid.
I. LMW Heparins
These include Enoxaparin and Fondaparinux.
Mode of Action
1. Enoxaparin acts by irreversibly combining with Factor Xa.
2. Fondaparinux acts by reversibly combining solely with antithrombin III (ATIII).
Contraindications
Absolute and relative contraindications are generally the same as with heparin, with the exception that
HITT, an allergic phenomenon, is less common because the molecules are smaller and may not include the
specific antigenic component of heparin. Prior HITT may not, therefore, be an absolute contraindication.
Adverse Reactions
1. Generally the same as with heparin, although HITT, as noted, is less common.
2. Other bleeding complications also tend to be less common because the mode of action is more specific than
for the parent compound.
Administration
Parenterally: every 12 (enoxaparin) or 24 (fondaparinux) hours
Monitoring
Tests are less commonly available for measuring the effect of LMW heparins. They can generally be
administered on a weight-based dosing schedule, and monitoring is not necessary. Efficacy, in general,
both for prophylaxis and for treatment, for example, of DVT, is equivalent to that of high-molecular-weight
(HMW) heparin or HMW heparin followed by warfarin.
II. Direct Thrombin Inhibitors

These include Argatroban, bivalirudin (Angiomax), dabigatran, desirudin, hirudin, lepirudin (Refludan),
melagatran, and ximelagatran (Exantra).
Mode of Action
Direct inhibition of the action of thrombin
Indications
Anticoagulation for patients, particularly for short term, who have a contraindication to heparin use
(generally, heparin allergy). Most common use is during hemodialysis or for initial treatment of DVT or PE.
Kinetics and Monitoring

These medications have a short half-life/short duration of action (< 30 minutes), so they must be
administered by IV infusion, with the exception of ximelagatran (oral), melagatran, and desirudin (SC). No
specific tests for measuring efficacy are
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currently available. These medications must be administered on a weight-based schedule. Although they
may affect PT or APTT secondarily, their duration of action is short, so it is generally safe to proceed with
interventional procedures after the infusion has been stopped for several half-lives (i.e., 2 hours). For
bivalirudin, patients with renal impairment are monitored with the ACT, with > 300 seconds indicating
adequate anticoagulation. Monitoring is not usually indicated for ximelagatran or melagatran.
Antiemetics
Although many agents are available, none are universally effective. Some, specifically the 5-HT3 receptor
antagonists, are more effective when given prophylactically than for treatment of established nausea or vomiting.
Common agents are
1. Prochlorperazine (Compazine), a phenothiazine derivative: 2.5 to 10 g IV/IM or by mouth (PO)/per rectum (pr)
2. Hydroxyzine (Atarax, Vistaril): 12.5 to 100 mg PO/IM
3. Promethazine (Phenergan): 12.5 to 25 mg PO/pr
4. Perphenazine (Trilafon)
5. Thiethylperazine (Torecan)
6. Meclizine (Antivert)
7. 5-HT3 receptor antagonists:
a. Ondansetron (Zofran): 4 to 24 mg PO, IM or IV, qid, or two times per day (bid)
b. Granisetron (Kytril): 1 to 2 mg PO or IV, qid, or bid
Hydroxyzine (Vistaril)
Mode of Action
Acts on subcortical central nervous system (CNS)
Indications
1. Prevention of nausea and vomiting
2. Sedation
3. Decreasing apprehension
Contraindications
1. Known hypersensitivity
2. Pregnancy
Adverse Reactions
1. Excessive sedation
2. Dry mouth
3. Potentiates CNS depressants (narcotics, barbiturates, alcohol). It is prudent to avoid concomitant CNS
depressants (e.g., meperidine). If absolutely necessary, reduce their dose by 50% and use with extreme caution.
4. Counteracts pressor effect of epinephrine.
Preparation
IM solution: unit-dose vials of 50 mg per mL (1 mL fill) and 100 mg per 2 mL (2 mL fill)
Dosage and Method

Give 25 to 100 mg IM; must be injected deep within the body of a large muscle (e.g., upper outer quadrant of the
buttock or midlateral thigh). SC injection will cause tissue damage. Avoid inadvertent IV and intra-arterial (IA)
injection.
Kinetics
Rapidly absorbed following IM injection
P.822
Reversal
1. Supportive
2. No specific antidote
Anti-inflammatories
Ketorolac Tromethamine (Toradol)
Mode of Action
A nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic effects; inhibits synthesis of
prostaglandins
Indication
Only parenteral NSAID. Short-term management of pain. Best given before onset of pain. Pain control, for
postsurgical/postprocedural pain, is equal to that of opiates with fewer adverse effects. Analgesia without
respiratory depression; can be used with opioids (meperidine and morphine) (see e-Table 94.2).
Contraindications
1. Not approved for use in obstetric or pediatric patients
2. Known hypersensitivity or prior reaction to aspirin and other NSAIDs
Adverse Reactions
1. Reversible platelet dysfunction (24 to 48 hours after drug is discontinued) and may prolong bleeding time
2. Side effects additive with other NSAIDs
3. With long-term use
a. Gastritis and peptic ulceration
b. Inhibition of renal autoregulation (use with caution in patients with renal impairment)
Preparation
Supplied as 15 mg per mL and 30 mg per mL in 1-mL syringe, or 30 mg per mL in 2-mL syringe
Dosage and Method

For short-term use only. Should not be administered for > 72 hours.
1. Give 30 to 60 mg IM loading dose followed by half of loading dose (15 to 30 mg) every 6 hours, as needed.
2. Toradol 10 mg IM gives equivalent pain relief of meperidine 50 mg or morphine 6 mg, generally with less
drowsiness, nausea, and vomiting than morphine.
Kinetics
With IV administration, initial onset of analgesia is about 10 minutes. Time to peak plasma level (proportional to
dosage) is about 30 to 60 minutes, and peak analgesia occurs about 45 to 90 minutes later. Primarily renal
excretion.
Reversal
Supportive measures
Glucocorticoids (Corticosteroids)
Include dexamethasone, prednisone, prednisolone, methylprednisolone (Medrol or Solu-Medrol), cortisone,
hydrocortisone, and others
Mode of Action
Potent anti-inflammatory
P.823
Indication
Prophylaxis against contrast and drug hypersensitivity reactions (Multiple other indications are not listed
here.)
Contraindications
1. Hypersensitivity to compounding components (e.g., tartrazine sensitivity, which may occur in patients with
aspirin hypersensitivity)
2. Systemic fungal infections, active tuberculosis
Adverse Reactions
Depend on dosage and duration of treatment
1. Hyperglycemia
2. Hypertension
3. Fluid and sodium retention
4. Allergic, anaphylactic, and hypersensitivity reactions have been reported following oral as well as parenteral
therapy.
Preparation
1. Medrol is available in 2-, 4-, 8-, 16-, 24-, and 32-mg tablets.
2. Solu-Medrol is available in powder form for IV and IM use.
Dosage and Method (for Medrol)

Give 32 mg PO 12 and then 2 hours prior to contrast administration (administration at 2 hours alone provided no
prophylaxis).
Kinetics
Readily absorbed through the GI tract and metabolized by naturally occurring steroid metabolism pathways
Reversal
1. Supportive measures
2. Long-term therapy should be gradually tapered.
Antiplatelet Agents
Abciximab (ReoPro)
Mode of Action
Abciximab, the Fab fragment of the chimeric (human-murine) monoclonal antibody 7E3, binds to the glycoprotein
(GP) IIb/IIIa receptor on human platelets and inhibits aggregation.
Indication
U.S. Food and Drug Administration (FDA)-approved for use as an adjunct in percutaneous coronary
interventions (PCIs), and for patients with unstable angina not responding to conventional medical therapy,
when PCI is planned within 24 hours. Abciximab is intended for use with concomitant aspirin and heparin
therapy.
Contraindications
1. As with thrombolytic agents, all reasons for potential adverse bleeding should be excluded (refer to
Chapter 14 and “Thrombolytic Agents” section in the following text).
2. Administration of oral anticoagulant therapy within 7 days unless PT less than 1.2 times control
3. Thrombocytopenia (platelet count < 100,000 cells per μL)
4. Presumed or documented history of vasculitis
5. Pregnant or nursing female (relative)
P.824
Adverse Reactions
1. Bleeding (risk may be higher with concomitant use of thrombolytic, anticoagulant, or other antiplatelet agents)
2. Thrombocytopenia (usually occurs within first 24 hours)
3. Hypersensitivity reactions (possible on readministration)
Preparation
Supplied in a 5-mL single-use vial at a concentration of 2 mg per mL (total drug per vial = 10 mg). IV bolus and
infusion doses should be mixed and filtered as specified by the manufacturer. The drug should not be shaken or
frozen. Mixed solution may be stored at 2°C to 8°C for up to 24 hours.
Dosage and Method

1. A platelet count, PT, APTT, and ACT (if applicable) should be obtained to rule out preexisting abnormalities.
2. A bolus dose of 0.25 mg per kg IV is recommended 10 to 60 minutes prior to coronary intervention. For
peripheral interventions, including thrombolytic therapy, the abciximab bolus dose is usually given following the
diagnostic angiogram and after the decision to treat has been made. The bolus is immediately followed by a
continuous infusion dose of 0.125 μg/kg/min (not to exceed a maximum of 10 μg per minute) for the next 12
hours. Heparin is given at subtherapeutic levels (IV bolus of 2,000 U, followed by infusion at 500 U per hour).
3. A platelet count should be obtained at 2 to 4 hours and at 24 hours (or prior to discharge, whichever is sooner)
following the bolus.
Kinetics
Abciximab rapidly binds to platelet receptors. Its initial plasma half-life is 10 minutes, followed by a second phase
half-life of 30 minutes. At recommended doses, 80% of the receptor sites are blocked and the median bleeding
time increases to over 30 minutes (baseline = 5 minutes) for the duration of the infusion. At the termination of
infusion, the plasma concentration drops rapidly, and platelet function returns gradually. Bleeding time returns to
below 12 minutes within 12 to 24 hours of termination of infusion in most patients. Platelet aggregation studies
begin to normalize in 24 to 48 hours.
Reversal
1. With major bleeding, stop abciximab and heparin simultaneously.
2. For properly documented thrombocytopenia, discontinue abciximab, consider stopping heparin and aspirin,
and consider platelet transfusion for severe thrombocytopenia (< 50,000 cells per μL).
Acetylsalicylic Acid (Aspirin)*

Mode of Action
Blocks cyclooxygenase (COX), thus blocking the formation of the prostaglandin precursor cycloendoperoxides
from arachidonic acid. Acts primarily on COX-1 but also on COX-2 (as well as at other sites).
1. Low dose (e.g., 81 mg qid): acts primarily to block platelet production of thromboxane A2, a potent platelet-
aggregating agent and vasoconstrictor
2. High dose (e.g., 325 to 1,000 mg qid): reversibly inhibits formation of endothelial prostacyclin, a platelet
antiaggregant and vasodilator, in addition to blocking thromboxane production irreversibly
Indication
Platelet inhibition during and after percutaneous transluminal (balloon) angioplasty
(PTA) or vascular stent placement
P.825
1. Active bleeding (aspirin prolongs bleeding time)
2. Known aspirin allergy or hypersensitivity
1. Hepatic or renal insufficiency
2. Hypoprothrombinemia or other bleeding disorder
Adverse Reactions
1. Bleeding (< 7% of patients)
2. GI distress (20% of patients)
3. Disturbed acid-base balance (toxic doses)
Preparation
Available as tablets and in various other formulations
Dosage and Method

Prior to PTA: 85 to 325 mg PO the night before and on the morning of the procedure
Kinetics
Aspirin is cleared from the body within a few hours (mainly through the kidney), but its effect on platelets is
irreversible and lasts for the lifetime of the platelet (8 to 10 days). Plasma half-life = 15 minutes but is dose-
dependent and depends on urine pH as well.
Reversal
Discontinue drug and treat according to severity of symptoms.
Clopidogrel Bisulfate (Plavix)

Mode of Action
A thienopyridine class drug, it is activated in the liver by P450 cytochromes (including CYP2C19). In the active
form, it inhibits adenosine diphosphate (ADP)-induced platelet aggregation by irreversibly binding to platelet
membrane P2Y receptor, thereby inhibiting platelet aggregation. Up to 14% of patients are deficient in the
cytochrome which activates the drug and may have limited response to it.
Indication
Reduction of atherosclerotic events (MI, stroke, and vascular death) in patients with atherosclerosis
documented by recent stroke, recent MI, or established peripheral arterial disease
To prevent platelet-based thrombotic events after cardiovascular interventions.
Contraindications
1. Hypersensitivity
2. Active pathological bleeding such as peptic ulcer or intracranial hemorrhage
Adverse Reactions (Incidence data from the CAPRIE Trial)

1. Bleeding: GI hemorrhage, 2%; intracranial hemorrhage, 0.4%
2. Neutropenia/agranulocytosis
3. GI symptoms (nonhemorrhagic): 27.1%
4. Rash: 15.8%
5. Thrombotic thrombocytopenic purpura (TTP) has been reported sometimes after a short exposure (<2 weeks).
6. Known genetic variant of the drug-metabolizing enzyme CYP2C19-clopidogrel may be ineffective in these
patients.
P.826
Preparation
Supplied as a 75-mg tablet
Dosage and Method

The recommended dosage is oral administration of 75 mg daily with or without food. No dosage adjustment is
required for elderly patients or those with renal disease. Usually begun 4 to 24 hours prior to a high-risk
cardiovascular intervention. May be given as a loading dose of 300 to 600 mg.
Kinetics
Dose-dependent inhibition of platelet aggregation can be seen 2 hours after a single oral dose. With continued
administration, steady state is reached between days 3 and 7, with inhibition level between 40% and 60%.
Platelet aggregation and bleeding time gradually return to baseline values after treatment is discontinued,
generally in about 5 days.
Reversal
Binding to the platelet ADP receptor is nonreversible. Platelet transfusion is necessary to reverse the effect.
Eptifibatide (Integrilin)
Mode of Action
Eptifibatide is a cyclic heptapeptide that reversibly inhibits platelet aggregation by blocking the binding of
fibrinogen, von Willebrand factor, and other adhesive ligands to the GPIIb/IIIa receptor.
Indication
FDA-approved for indications similar to abciximab (see preceding text)
Contraindications
1. As with thrombolytic agents, all reasons for potential adverse bleeding should be excluded (refer to
Chapter 14 and “Thrombolytic Agents” section in the following text).
2. Concurrent therapy with another GPIIa/IIIb inhibitor
3. Thrombocytopenia (platelet count < 100,000 cells per μL)
4. Elevated serum creatinine (Cr) (relative; adjust dose per package insert for serum Cr greater than 2 mg
per dL)
5. Renal dialysis
6. Administration of oral anticoagulant therapy within 7 days, unless PT less than 1.2 times control
7. Presumed or documented history of vasculitis
8. Pregnant or nursing female (relative)
Adverse Reactions
1. Bleeding (risk may be higher in the elderly and with concomitant use of thrombolytic, anticoagulant, or other
antiplatelet agents)
2. Rare allergic reactions
Preparation
Eptifibatide (Integrilin) is supplied in 10-mL vials containing 20 mg of drug and 100-mL vials containing 75 mg of
drug. Vials should be protected from light and refrigerated at 2°C to 8°C. Drug should be reconstituted per
manufacturer's instructions.
Dosage and Method

1. A platelet count, PT, APTT, and ACT (if applicable) should be obtained to rule out preexisting abnormalities.
P.827
2. Usually administered as a 180 μg per kg slow IV bolus over 1 to 2 minutes, followed by an IV infusion at 2
μg/kg/min, adjusted down to 1 μg/kg/min for patients with serum Cr levels between 2 mg and 4 mg per dL, for up
to 24 hours. Longer infusions may be considered in individual cases. A second IV bolus of 180 μg per kg may be
considered 10 minutes following the first one. Heparin doses should be curtailed.
3. Because the reported incidence of thrombocytopenia with eptifibatide is no greater than with placebo, only
routine platelet counts need be obtained during therapy.
Kinetics
Plasma elimination half-life is about 2.5 hours. At recommended doses, a steadystate level is reached in 4 to 6
hours, with bleeding time prolonged about fivefold and greater than 90% inhibition of platelet aggregation. Both
platelet inhibition and bleeding time decrease rapidly within 4 to 6 hours of discontinuation of the infusion.
Clearance is equal by both renal and nonrenal routes.
Reversal
With major bleeding, stop eptifibatide and heparin simultaneously.
Sedatives
I. Benzodiazepines
Diazepam (Valium)
Mode of Action
A commonly used benzodiazepine that probably increases the responsiveness of brain receptors to the inhibitory
neurotransmitter γ-aminobutyric acid
Indications
1. Sedation
2. Induction of anterograde amnesia
3. Treatment of seizures
Contraindications
1. Known hypersensitivity to the drug
2. Acute narrow-angle glaucoma
3. Untreated open-angle glaucoma
Adverse Reactions
1. Drowsiness, fatigue, ataxia. Watch for mental status changes, especially in the elderly.
2. Respiratory depression may occur with large IV doses, especially in patients with chronic obstructive
pulmonary disease.
3. Has additive effect with other CNS depressants (especially opioids)
4. Because it is lipophilic, it causes pain and possible thrombophlebitis on peripheral venous injection.
Preparation
Available in 10-mL vials, 2-mL ampules, and 2-mL disposable syringes; also 2-, 5-, and 10-mg tablets
Dosage and Method
1. Premedication: 5 to 10 mg PO. Premedication of elderly patients prior to arrival at the angiography suite is not
recommended. Give 2 to 3 mg IV over 1 minute (maintenance 2 to 3 mg IV every 20 to 30 minutes, monitoring
vital signs; maximum recommended dose 10 mg per hour for a 2-hour study). Use lower doses for elderly
patients.
2. Toxic convulsions: up to 10 mg IV to therapeutic effect
P.828
Kinetics
Onset of action is within 2 to 3 minutes after IV injection (up to 1 hour after oral dose). Duration up to 6 to 10
hours. Sedative effects are long lived but amnestic effects are not (1 to 30 minutes). Distribution half-life: 1 to 2
hours. Elimination half-life: 24 to 48 hours. Liver dysfunction and aging retard metabolization. Metabolites are
excreted through the kidney.
Reversal
1. General supportive measures: Monitor vital signs.
2. Maintain IV fluids and airway.
3. Hypotension may be treated with levarterenol (Levophed) or metaraminol (Aramine).
4. Physostigmine (Antilirium) 1 mg IV slowly or aminophylline 1 to 2 mg per kg IV can reverse the CNS
depression.
5. Flumazenil is a specific benzodiazepine antagonist that has undergone extensive clinical trials. One to 10 mg
will reverse the CNS and respiratory depressant effects of benzodiazepines. Additional doses may be required 1
to 2 hours later.
Midazolam (Versed)
Mode of Action
A short-acting benzodiazepine CNS depressant. As other benzodiazepines, binds to specific γ-aminobutyric acid
(GABA) receptors sites. Midazolam has anxiolytic, hypnotic, muscle relaxant, anterograde amnestic, and
anticonvulsant properties. The potency is approximately 3 to 4 times that of diazepam (Valium). Unlike diazepam,
it is hydrophilic, not lipophilic, so pain on peripheral venous injection is much less likely.
Indications
Induction of conscious sedation and amnesia during angiographic or interventional procedures
1. Known hypersensitivity to the drug
2. Acute narrow-angle glaucoma (benzodiazepines in general); however, treated open-angle glaucoma is
not a contraindication.
3. Acute alcohol/drug intoxication and shock
1. Pregnancy—potential hazard to the fetus and neonatal CNS depression (midazolam is not recommended
for obstetrical use, especially in the first trimester)
2. Nursing mother
3. Increased sensitivity to the drug and slower elimination occur in the elderly.
Adverse Reactions
1. Fluctuations in vital signs, including serious cardiopulmonary events. Apnea is more likely to occur with higher
dose and speed of injection.
2. During conscious IV sedation, hypotension can occur with concomitant narcotic premedication (e.g.,
meperidine).
3. With IV administration, a greater than 1% incidence of the following has been reported: hiccups, nausea,
vomiting, coughing, oversedation, headache, drowsiness.
4. Patients with chronic obstructive pulmonary disease are extremely sensitive to the respiratory depressant
effect of this drug.
5. Profound and prolonged amnesia can occur.
6. Paradoxical reactions, with anxiety, seizure-like muscle movements may occur with any benzodiazepines
P.829
Preparation
1. Available in 1-, 2-, 5-, and 10-mL vials at 5 mg midazolam per mL. Also 2-mL Tel-E-Ject (Roche Labs, Nutley,
NJ) disposable syringe (5 mg per mL).
2. Midazolam can be diluted in D5W, NS, or Ringer lactate solution to two to five times the original volume for
titration of the dose.
Dosage and Method

Administer only if continuous cardiac and respiratory monitoring are available.
1. For IV conscious sedation (incidence of venous irritation and thrombophlebitis is significantly less than for
diazepam)
a. Initial titration dose given immediately prior to procedure: Average healthy adult, 1.0 to 2.0 mg (0.035 mg per
kg) given over 2 to 3 minutes; debilitated or elderly adult, 0.5 to 1.5 mg given over 2 to 3 minutes. With the given
doses, cardiovascular depression and clinical evidence of respiratory depression are usually minimal. End point
of titration should be slurred speech.
b. If further sedation is needed, wait 2 minutes and, if the vital signs are stable, the dosage may be titrated in
small increments (25%) of the initial dose.
c. Dose to maintain sedation is 25% of the initial dose required to obtain that level of sedation.
d. Total recommended dose for an average healthy adult: 0.1 to 0.15 mg per kg
e. Narcotic medication (e.g., fentanyl, meperidine, morphine sulfate) is often concomitantly administered. If this is
done, the dosage of midazolam should be lowered by 25% to 30%. In patients who are debilitated or older than
60 years, dosage should be cut by 50% and rate and frequency of administration should be slower. Drug effect
is prolonged in the elderly.
f. For obese patients, single IV dose may be determined by true body weight, but continuous infusion and
maintenance should be based on ideal body weight.
2. If used for outpatient procedures
a. The patient should be instructed not to operate vehicles or machinery until the next day.
b. Postprocedure instructions should be written or given to accompanying responsible adult.
Kinetics
1. Onset of action is rapid (1 to 2 minutes), and duration of action is short (30 minutes) following an IV (5 mg)
dose. Plasma elimination half-life: 2 to 4 hours (normal healthy patients). Elimination half-life is about 10-fold less
than diazepam.
2. About 45% to 57% of the dose is excreted in urine as a major (conjugated) metabolite. The elimination half-life
is increased 1.5 to 2 times in patients with chronic renal failure and 2 to 3 times in those with congestive heart
failure. Hepatic dysfunction does not appear to affect the elimination half-life when small IV doses (5 mg) are
administered.
Reversal
1. Manifestations of overdosage: sedation, somnolence, confusion, diminished reflexes, and so forth (similar to
other benzodiazepines)
2. Monitor vital signs—especially early signs of apnea (this can result in hypoxic cardiac arrest).
3. Oxygen and equipment to maintain airway patency should be immediately available.
4. General supportive measures, including patent IV access
5. Hypotension is treated with IV fluid infusion, Trendelenburg position, and vasopressors.
6. Midazolam-induced sedation may be reversed with physostigmine 1 mg IV administered over 2 minutes (for
adults). Atropine sulfate is an antagonist for physostigmine up to 2 mg.
7. Respiratory depressant effects of midazolam cannot be reversed by naloxone (Narcan).
P.830
Lorazepam (Ativan)
Very similar to other benzodiazepines, with short to medium duration of action, good anxiolytic efficacy, but high
addictive potential. Not lipophilic. Longer duration of sedation (12 to 24 hours) than diazepam or midazolam, thus
not useful for procedure-related sedation.
Alprazolam (Xanax)
Another benzodiazepine-class sedative used primarily for acute anxiety as well as anxiety disorders and for
nausea related to chemotherapy; rapid onset of action (< 1 hour) and peak activity (1 to 2 hours)
II. Antihistamines
Diphenhydramine (Benadryl)
Mode of Action
Histamine (H1 and H2), receptor blockade, and CNS depression
Indications
1. Moderate sedation
2. Treatment of contrast-induced pruritus or urticaria
3. Antiemetic
4. Precontrast prophylaxis in high-risk patients (controversial)
5. Anticholinergic (decreased secretions and bronchodilation)
Contraindications
1. Hypersensitivity to drug or chemically similar antihistamines
2. Should not be used to treat lower respiratory tract symptoms including asthma, in conjunction with MAO
inhibitors or in nursing mothers
Adverse Reactions
1. Sedation, sleepiness, dizziness, distorted coordination
2. Epigastric distress
3. Thickening of bronchial secretions
4. Urinary retention
5. Urticaria/drug rash/chills/dry mouth
6. Paradoxical reactions
Preparation
Available in 1-mL disposable syringe at 50 mg and as 25 mg tablets
Dosage and Method

Give 25 to 50 mg PO, IV, or IM. Maximum dose during 2-hour study should be limited to 100 mg.
Kinetics
Onset of action after oral dose: 30 to 60 minutes. After IV administration: 5 to 10 minutes. Duration of activity
(average PO dose): 4 to 6 hours. Metabolites formed in the liver are excreted within 24 hours.
Reversal
1. General supportive measures: Monitor vital signs, fluid intake, and output.
2. If drug is administered orally, induce vomiting or consider gastric lavage.
3. Maintain IV line.
4. Vasopressors for hypotension
5. Do not use stimulants.
P.831
Thrombolytic Agents
Streptokinase (Streptase)
Mode of Action
Streptokinase first forms a complex with plasminogen. This complex then converts unbound plasminogen to
plasmin. Plasmin is an enzyme that degrades fibrinogen and fibrin.
Indication
Fibrinolysis. Streptase is now rarely used, although it is FDA-approved for treatment of acute MI, PE, DVT,
or arterial or venous embolism.
Contraindication
2. Recent (2 months) cerebral vascular accident (CVA), intracranial, or intraspinal surgery
3. Intracranial neoplasm
4. Known recent streptococcal infection or streptokinase use may predispose to allergic reactions.
Antibodies may exist in patients with recent streptococcal infection or prior treatment with streptokinase so
that, if used, higher doses may be needed in these patients, but one is cautioned to avoid using this drug in
such cases.
Adverse Reactions
1. Bleeding
2. Allergic reactions: Minor: itching, urticaria, flushing, nausea, headache, musculoskeletal pain, breathing
difficulty; major: bronchospasm, periorbital swelling, angioneurotic edema. Mild and moderate allergic reactions
are treated with antihistamines or corticosteroids, or both. With severe allergic reactions, discontinue
streptokinase and treat with IV adrenergics, antihistamines, and corticosteroids as clinically indicated.
3. Fever
Preparation
Streptase is available in vials of 250,000 units or 1,500,000 units and is reconstituted using sterile water.
Dosage and Method (for Peripheral Arterial Thrombolysis)

1. Bolus (into thrombus): 50,000 IU
2. Infuse: 5,000 IU per hour for 12 hours and then 2,500 IU per hour for duration of therapy.
3. Systemically heparinize patient to prevent clot formation around catheter (maintain PTT at 40 to 50 seconds).
Kinetics
Two to 6 hours in serum. Plasminogen and fibrinogen levels may be decreased for longer.
Reversal
Fresh frozen plasma
Reteplase (Retavase, Rapilysin)

Mode of Action
A recombinant, non-glycosylated form of human tissue plasminogen activator (tPA), causes fibrin-enhanced
conversion of plasminogen to plasmin. It is less fibrin-specific than recombinant tissue plasminogen activator (rt-
PA, Activase), and reportedly diffuses more easily through the thrombus.
P.832
Indication
Thrombolysis
2. Recent (2 months) CVA, intracranial, or intraspinal surgery
3. Intracranial neoplasm
4. See Chapter 14 for relative contraindications.
Dosage and Method

Retavase is not FDA-approved for use in the peripheral arteries. No optimal dosing regimen exists. An initial
(optional) intrathrombic lacing dose of 2 to 5 U is recommended. The currently recommended dose of IA infusion
is 0.5 U per hour for arteries and 1.0 U per hour for veins. Although no maximum dose has been established, it is
wise to not exceed 24 U within 24 hours. Concomitant subtherapeutic IV heparin may be used. Caution: Usual
dose for acute MI is 10 IU, but usual dose for rt-PA is 100 mg. Because Retavase contains no antibacterial
preservatives, it has to be reconstituted immediately prior to use. Nevertheless, the drug can be diluted with NS
to 0.02 U per mL, and it remains biologically active for around 24 hours.
Adverse Reactions
1. Bleeding
2. Mild hypersensitivity reactions
Reversal
1. Stop infusion of Retavase (plasma half-life is 13 to 16 minutes; cleared primarily by the liver and kidneys) and
heparin if used simultaneously.
2. Fresh frozen plasma
Tissue Plasminogen Activator (Activase, Alteplase)

Mode of Action
A recombinant human tPA, produced by DNA technology, catalyzes plasminogen conversion to plasmin, with
high specificity for fibrin-bound plasminogen
Indication
Fibrinolysis (approved for use in management of acute MI, acute massive PE, and acute ischemic stroke)
Contraindications
Same as for other thrombolytic drugs (see “Streptokinase (Streptase)” section)
Adverse Reactions
1. Bleeding
2. Mild hypersensitivity reactions
3. Fever
Preparation
Activase is available as a sterile, lyophilized powder in 50-mg vacuum vials. The solution must be prepared
immediately before use. When reconstituted with the supplied volume of sterile water (no preservatives,
nonbacteriostatic), a solution at a concentration of 1 mg per mL (pH of 7.3) is obtained. Mix by gentle swirling.
Large bubbles (from foaming) are dissipated when the solution is left to stand for a few minutes. The solution
may be kept for approximately 8 hours at room temperature. The concentration may be reduced (0.2 mg per mL
is the minimal concentration recommended by the manufacturer) by adding the appropriate
P.833
volume of NS or D5W. Further dilution will cause precipitation of the drug and its adherence to the plastic bag
and IV tubing, reducing the total delivered dose.
Dosage and Method

1. rt-PA is not FDA-approved for IA use in the peripheral arteries. No optimal dosing regimen exists.
2. An initial (optional) intrathrombic lacing dose of 5 to 10 mg is recommended. Previously, weight-based doses
of 0.05 to 0.1 mg/kg/h were used for continuous infusion. However, the current recommended dose for IA
infusion is 0.5 to 1.0 mg per hour, up to a maximal dose of 50 mg for the entire treatment. Concomitant
subtherapeutic IV heparin may be used.
Kinetics
Activase is cleared rapidly (50% within 5 minutes) from the plasma, primarily by the liver.
Reversal
1. Stop infusion of Activase and heparin simultaneously (if used).
2. Fresh frozen plasma
Urokinase
Mode of Action
Urokinase (UK) is an enzyme that directly converts plasminogen to plasmin. Plasmin is a fibrinolytic enzyme that
degrades fibrinogen and fibrin. Not commonly used in the United States now.
Indication
Thrombolysis
Contraindications
Same as for other thrombolytic drugs (see “Streptokinase (Streptase)” section).
Adverse Reactions
1. Bleeding
2. Mild bronchospasm or skin rash (serious allergic reactions are rare)
3. Fever (2% to 3% of patients receiving UK; treat fever with acetaminophen, not aspirin)
Preparation
Reconstitute UK with nonbacteriostatic sterile H2O; standard preparation is 750,000 IU of UK in 250 mL D 5 W
or NS (concentration = 3,000 IU per mL). Supplied in vials of 250,000 IU, containing 25 mg mannitol and 45 mg
sodium chloride.
Dosage and Method

For peripheral arterial thrombolysis: IA infusion
1. Lace (into thrombus): 30,000 to 60,000 IU
2. Infuse: 4,000 IU per minute for 2 hours (80 mL per hour), then 2,000 IU per minute for 2 hours (40 mL per
hour), and then 1,000 IU per minute for 8 hours (20 mL per hour). Continue at this rate with periodic angiographic
monitoring (see Chapter 14).
3. Systemically heparinize patient to prevent clot formation around catheter (maintain PTT at 40 to 50 seconds).
Kinetics
Serum half-life of 20 minutes or less (cleared by liver) but may also decrease plasma plasminogen and fibrinogen
levels for 12 to 24 hours
P.834
Reversal
Fresh frozen plasma
Vasoconstrictors
Vasopressin (Pitressin)
Mode of Action
Causes smooth muscle contraction in the GI tract and vascular bed (capillaries, small arterioles, vessels); short
acting, rapid response
Indications
IA infusion for the control of GI bleeding. Decreases flow in mesenteric, gastric, and splenic arteries but
increases flow in hepatic arteries.
Contraindications
1. Anaphylaxis or hypersensitivity to the drug
2. Chronic nephritis with elevated blood urea nitrogen
3. Angina pectoris
Adverse Reactions
1. When using vasopressin, watch for hypertension, angina, and CNS symptoms.
2. Vasopressin has an antidiuretic hormone (ADH) effect due to increased water resorption by the renal tubules.
3. Local or systemic allergic reactions: anaphylaxis, cardiac arrest, or shock, or a combination of these
4. Abdominal cramps, nausea and vomiting, diaphoresis, urticaria, bronchial constriction, vertigo, and “pounding”
head
Preparation
Prepare vasopressin solution as follows: Vasopressin (Pitressin) is supplied in ampules of 10 U or 20 U per 0.5
mL or 1.0 mL. Mix 100 U of vasopressin in 500 mL of NS or D5W (0.2 U per mL), or in a more concentrated form
of 200 U per 500 mL of solution (0.4 U per mL).
Dosage and Method

Infuse with a constant arterial infusion pump at an initial rate of 60 mL per hour (0.2 U per minute). Protocol for GI
bleeding—see Chapter 10.
Kinetics
Rapid onset of action (20 to 40 minutes) is noted when used to stop GI bleeds. Duration of action is on the order
of minutes unless continuous infusion is given.
Reversal
Spontaneous recovery from side effects such as blanching of skin, abdominal cramps, and nausea within
minutes after the infusion is stopped
Vasodilators
Nifedipine (Procardia)
Mode of Action
Calcium (slow) channel blocker relaxes and prevents arterial spasm (decreases peripheral vascular resistance
and increases flow to distal bed)
Indication
As a vasodilator during angioplasty to prevent or treat vasospasm caused by catheter or wire manipulation
P.835
Contraindication
Known hypersensitivity
Adverse Reactions
Watch for hypotension. Generally, there are few problems with a one-time 10-mg dose.
Preparation
Supplied as 10-mg capsule
Dosage and Method

During peripheral angioplasty: 10 mg PO or sublingual (puncture hole in capsule and squeeze contents
sublingually and then ask patient to swallow capsule)
Kinetics
Plasma half-life: 2 hours. Approximately 80% of this drug and its metabolites are excreted by the kidney.
Clearance may be prolonged with impaired renal function.
Reversal
Cardiovascular support: Monitor vital signs, elevate extremities, monitor fluid input and output, and adjust as
necessary. Vasoconstrictors may be beneficial.
Nitroglycerin (Nitro-Bid IV)

Mode of Action
Relaxes vascular smooth muscle; a short-acting, postcapillary vasodilator
Indications
1. Vasodilator during PTA to prevent or treat vasospasm caused by catheter or wire manipulation
2. Palliation and/or prevention of angina pectoris or MI
Contraindications
1. Known hypersensitivity to nitroglycerin or known idiosyncratic reaction to organic nitrates
2. Hypotension
3. Increased intracranial pressure due to trauma or hemorrhage
4. Constrictive pericarditis or pericardial tamponade
Adverse Reactions
1. Headache (2% of patients)
2. Tachycardia, nausea, vomiting, retrosternal discomfort, palpitation (< 1%)
Preparation
Available as 15 mg in 150 mL of D5W (100 μg per mL). Prepare, store, and administer in glass containers.
Protect from light until use. Usually available as 1 mg vial (1,000 μg) in 1 mL volume; add 1 mg (1 mL) to 9 mL
NS, for a final concentration of 100 μg per mL.
Dosage and Method

1. During angioplasty: 100 to 200 μg (bolus directly into artery that is to undergo angioplasty)
2. For angina pectoris: 0.3 mg sublingually, as needed, or 20 μg per minute IV infusion, increase to effect;
monitor for hypotension.
Kinetics
Rapid onset of action and short duration of effect. Plasma half-life: 1 to 4 minutes
P.836
Reversal
Cardiovascular support: Monitor vital signs, elevate extremities, monitor fluid input and output, and adjust as
necessary.
Tolazoline Hydrochloride (Priscoline)

Mode of Action
Direct peripheral vasodilator (α-blocker), decreases peripheral resistance, and increases venous capacitance; no
longer commercially available in the United States and Canada
Indications
1. Useful during peripheral arteriography to elicit hyperemic pressure gradients
2. To better visualize the portal venous system (in noncirrhotics) during visceral arteriography or peripheral
vessels in extremity arteriography
Contraindications
1. Hypersensitivity to the drug
2. Patients with mitral stenosis, coronary artery disease, and arrhythmias
Adverse Reactions
1. Systemic hypotension
2. Tachycardia
4. Skin flushing
5. Oliguria
Preparation
Previously available in 4-mL ampules at 25 mg per mL (off the market in the United States and Canada)
Dosage and Method

Historically, 25 mg IA (diluted) were administered over the course of 2 minutes prior to contrast injection.
Kinetics
Rapid onset of action and peak activity
Reversal
1. Trendelenburg position
2. IV fluids
3. General supportive measures: Monitor vital signs and fluid intake/output.
4. Do not use epinephrine or norepinephrine to reverse hypotension due to priscoline overdosage—further
reduction in blood pressure and subsequent exaggerated rebound may occur.
Miscellaneous
Atropine
Mode of Action
A muscarinic cholinergic blocking agent
Indications
1. During vasovagal reaction for bradycardia (pulse < 60 beats per minute and systolic blood pressure
[BP] < 90 mm Hg) in patients, otherwise, normotensive with normal heart rate
2. Given for severe bradycardia and atrioventricular (A-V) block other than complete heart block
(increases sinus rate and A-V conduction)
P.837
3. Decreases GI muscle tone and potential benefit during transhepatic biliary drainage procedures
Contraindications
1. Narrow-angle glaucoma
2. Adhesions between iris and lens
3. Severe heart disease
4. Prostatism
Adverse Reactions
1. Dry mouth
2. Diminished respiratory secretions; relaxes bronchial smooth muscle
3. Urinary retention
4. Blurred vision
5. Aggravation of glaucoma
6. Sedation and confusion
Preparation
Atropine sulfate injection, USP: 10-mL (1 mg) prefilled syringe (0.1 mg per mL) for
IV, IM, or SC use
Dosage and Method
1. Give 0.5 to 1 mg every 5 minutes up to 2 mg or pulse greater than or equal to 60 beats per minute.
2. A dose of 0.4 mg IV may be used to prophylactically counteract bradycardia during intracoronary contrast
injection.
Kinetics
Plasma half-life: about 2.5 hours; most are excreted in the urine within 12 hours.
Reversal
Large doses are not indicated for the purposes outlined earlier. However, should delirium or coma result
from inadvertent administration of a large dose, physostigmine may be administered via slow IV injection (1
to 4 mg in adults, 0.5 mg in children).
Epinephrine (1:1,000 or 1:10,000)
Mode of Action
The relative composition of α- and β-adrenergic receptors in a vascular bed determines its overall response
to epinephrine. As a potent α- and β-adrenergic agonist, in the visceral and renal arteries, epinephrine is a
vasoconstrictor. As a vasoconstrictor, it increases heart rate, blood pressure, ventricular contractility,
myocardial oxygen consumption, and systemic vascular resistance.
Indications
To treat life-threatening cardiac arrest anaphylaxis or bronchospasm
Contraindications
1. Individuals with organic brain damage
2. Narrow-angle glaucoma
3. Use with caution in patients with cardiovascular disease, hypertension, and diabetes
Adverse Reactions
1. Palpitations
2. Respiratory difficulty
3. Dizziness
4. Headache
5. Anxiety
6. Ventricular arrhythmias
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Preparation
Use prefilled 1:1,000 (1,000 μg epinephrine per mL) or 1:10,000 (100 μg per mL) syringe.
Dosage and Method
1. Anaphylaxis: 0.15 to 0.3 mL of 1:1,000 or 1.5 to 3 mL of 1:10,000 epinephrine IA or IV
2. Cardiac arrest: Administer 1 to 3 mL of 1:10,000 IA or IV, via airway or intracatheter, to effect.
3. Astman: 0.3 to 0.5 mL of 1:1,000 subcutaneously
Kinetics
Rapid onset (seconds) and short duration (minutes) when administered parenterally. When administered
subcutaneously, onset is rapid but action may be prolonged (hours).
Reversal
1. Because epinephrine is rapidly inactivated, treatment of acute toxicity (increase in arterial and venous
blood pressure may cause cerebrovascular hemorrhage) is mainly supportive.
2. If necessary, a rapidly acting α-adrenergic blocking agent such as phentolamine may be used to
counteract the pressor effect.
3. If necessary, a rapidly acting β-blocker (e.g., esmolol) can decrease the bradycardia.
Glucagon
Mode of Action
1. Relaxation of smooth muscles of stomach, duodenum, small bowel, and colon
2. Stimulates conversion in the liver of glycogen to glucose
Indication
Used to decrease bowel peristaltic activity during digital subtraction arteriography or gastrostomy tube
placement
Contraindications
1. Hypersensitivity to the drug
2. Use with caution in patients with diabetes, insulinomas (can cause hypoglycemia), or
pheochromocytomas (can cause severe hypertension).
Adverse Reactions
2. Possible hypokalemia
Preparation
Dissolve lyophilized glucagon in diluting solution provided.
Dosage and Method
Give 0.5 to 1.0 mg IV a few minutes prior to study.
Kinetics
When administered intravenously, the time of onset of action for a 0.5-mg dose is 1 minute and the duration
of effect is 9 to 17 minutes. Plasma half-life: 3 to 6 minutes
Reversal
1. Hypoglycemia should be treated with oral or IV glucose and other supportive measures.
2. Hypertension (in patients with pheochromocytomas) may require 5 to 10 mg IV of phentolamine mesylate.
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Naloxone Hydrochloride (Narcan)
Mode of Action
Opioid antagonist with complete or partial reversal of the opioid effects of the drugs noted below by
competing for the same receptor sites
Indication
Reversal of narcotic overdosage from opiates including morphine sulfate (Duramorph), meperidine
(Demerol), butorphanol (Stadol), and fentanyl (Sublimaze).
Contraindications
1. Known sensitivity to the drug
2. Use with care in the very old and very young.
Adverse Reactions
Abrupt reversal of narcotic depression resulting in nausea, vomiting, diaphoresis, tachycardia, ventricular
arrhythmias, elevated blood pressure, and tremulousness
Preparation
Available in 1-mL ampule (or disposable prefilled syringe) at 0.4 mg per mL
Dosage and Method
1. Postprocedural narcotic depression: 0.1 to 0.2 mg IV over 2 minutes, at 2- to 3-minute intervals until
desired degree of reversal—adequate ventilation and alertness without undue pain—is achieved. Because
the duration of reversal is about 45 minutes, the patient must be monitored closely for 1 to 2 hours and
given repeat doses of Narcan as indicated.
2. Narcotic overdosage: 0.4 to 2.0 mg IV; repeat at 2- to 3-minute intervals, up to 10 mg total dose (If no
response, question narcotic overdose as cause of problem.)
Kinetics
1. Onset of action 1 to 2 minutes after IV administration. Duration varies with dose (45 minutes at 0.4 mg per
70 kg).
2. Serum half-life in adults is approximately 1 hour. Naloxone is metabolized in the liver by glucuronide
conjugation and is excreted in the urine.
Reversal
There is no clinical experience with Narcan overdosage in humans.
Suggested Readings
O'Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the management of ST-elevation
myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines. J Am Coll Cardiol . 2013;61(4):e78-e140.
Oppenheimer J, Ray CE Jr, Kondo KL. Miscellaneous pharmaceutical agents in interventional radiology.
Semin Intervent Radiol . 2010;27(4):422-430.
Sutcliffe JA, Briggs JH, Little MW, et al. Antibiotics in interventional radiology. Clin Radiol. 2015;70(3):223-
234. doi:10.1016/j.crad.2014.09.021.
Tuite C, Rosenberg EJ. Sedation and analgesia in interventional radiology. Semin Intervent Radiol .
2005;22(2):114-120.
Venkatesan AM, Kundu S, Sacks D, et al. Practice guidelines for adult antibiotic prophylaxis during vascular
and interventional radiology procedures. Written by the Standards of Practice Committee for the Society of
Interventional Radiology and endorsed by the Cardiovascular Interventional Radiological Society of Europe
and Canadian Interventional Radiology Association. J Vasc Intervent Radiol . 2010;21(11):1611-1630.
e-95
Risk Management
Sarah D. Cohn
The practice of radiology has been no less affected by the developments in the professional liability field than
any other specialty. Studies reported in 1990 (delay in diagnosis of breast cancer) (1) and in 1992 (delay in
diagnosis of lung cancer) (2) indicated that failure to diagnose cancer continued to be a significant claim area for
radiologists. In 2002, the Physicians Insurers Association of America (PIAA) studied 450 paid malpractice claims
involving failure to diagnose breast cancer; in these cases, the most commonly named defendant was the
interpreting radiologist. The average malpractice payment in these cases was $438,047 (3). These older data
continue to be updated. In 2013, a study of causes of medical malpractice suits against radiologists in the United
States was published (4); it analyzed credentialing data from 8,401 radiologists. Results showed that error in
diagnosis of breast cancer remained the most frequent malpractice case allegation, followed by failure to
diagnose nonvertebral fractures and spinal fractures. After error in diagnosis, procedural complications (only of
procedures actually performed by the defendant radiologist) were the most frequent, although much less
common. Liability concerns also seem to continue to influence the practice choices made by radiology house
staff (5,6).
A recent study found that the likelihood of a radiologist being a named defendant in:
At least one lawsuit is 50% by age 60, but both the frequency and average number of
lawsuits varies widely by state of residence and sex. Among resolved suits, the percentage
of cases in which payment was made to the plaintiff differs markedly by state, as do
median and mean award amount. (7)
Litigation risks attributed to radiology in general and interventional radiology in particular are not limited to the
United States. A study published in 2012 examined malpractice insurance claims against interventional
radiologists in Italy between 1993 and 2006. The data were derived from the files of the Italian Society of Medical
Radiology. Although the absolute number of claims was not large (n = 98), the numbers increased over the
years, and in 21 cases, the event was said to have caused the patient's death. The most frequent cause of claim
was complications “after interventional procedures on the vascular district” (8).
Although it is not possible to prevent injury and claims, it is possible to create an environment in which patients
understand their risks and in which any claim brought is less likely to be successful.
Credentialing of Interventional Radiologists

1. Interventional radiology procedures are most often done in hospitals, but regardless of where they take place,
appropriate credentialing of the physician must occur.
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2. Many private practices hiring interventional radiologists delegate this assessment to the hospital where
privileges are requested. In fact, the hospital has a legal corporate responsibility to avoid negligence in
credentialing.
a. In addition to checking other required matters, such as training, licensure, malpractice insurance, and claims
data, hospitals and practices should check references. Specifically, the person providing the reference should be
given explicit information about what procedures or categories of procedures are to be done and asked about the
applicant's training and competence in these procedures.
b. Hospitals will be found liable if they credential an interventional radiologist or other physician without any
practice restrictions that would have been required had the medical staff office made the appropriate inquiries.
3. Many physicians are reluctant to be completely honest in the provision of references. They worry about
professional repercussions or that the applicant will sue for defamation of character.
a. In order to prevent suit and to protect reference writers, hospitals require their applicants to sign a broad
waiver of liability to protect those who provide information about a practitioner. A copy of this waiver should be
provided or may be requested before a reference is written.
b. In addition to the waiver, states also provide a “qualified immunity” to reference writers: that is, if the reference
is provided in good faith, there will be no liability.
c. Regardless of the legal risks, it remains important to be honest, balanced, and complete in reference writing—
it may cause patients harm to release problem physicians to other practices without appropriate supervision.
4. Interventional radiology practices should track complications, morbidity, and mortality for recredentialing. Care
provided by individuals that exceeds expected complication rates should be reviewed to determine if retraining,
extra assistance, or other mechanisms are needed.
Informed Consent
1. Once the radiologist is appropriately credentialed, the law requires that consent for the procedure be obtained
from the patient or family, except in an emergency. In fact, early interventional radiology procedures were
involved in some of the cases in which the consent doctrine developed.
2. One of the earliest of these more modern cases was decided in 1957 (Salgo v Leland Stanford Jr. University
Board of Trustees). The plaintiff was a 55-year-old man who was experiencing symptoms of vascular
insufficiency in his legs. He was referred to a surgeon who felt that the patient might have a blockage in the aorta
and advised an aortogram. The patient agreed to the procedure. The court's opinion states that the aortogram
was done under general anesthesia. The surgeon inserted a needle and penetrated the wall of the aorta; the
stylet was removed, contrast was injected directly into the aorta and films were taken. The films showed a
blockage in the descending aorta below the renal arteries; further contrast was injected to define the extent of
the blockage. The procedure was without apparent complication. However, when the patient awoke, his lower
extremities were paralyzed and remained so. Subsequently, he sued. Experts who testified in the case differed:
The plaintiff's expert testified that the needle was in the wrong place when the contrast was injected, whereas
the defense expert stated that the contrast could have affected the spinal cord even if it were in the aorta. A jury
awarded the plaintiff $250,000, which the judge reduced to $215,355. The defendants appealed. Among other
things, the plaintiff testified that he was not informed about the procedure; the physicians acknowledged that
they had not warned him of the possible dangers. The court held that the physician need not discuss every risk
no matter how remote but must
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disclose facts that are “ necessary to form the basis of an intelligent consent by the patient to the proposed
treatment.” The verdict was reversed (on other grounds), and a new trial was ordered (9).
3. The process of obtaining consent should not be viewed as a clerical task. Although the actual discussion can
be delegated to a nurse or resident (if the hospital policies permit such delegation), the radiologist who performs
the procedure remains responsible for the adequacy of the consent. Some patients may request to audiotape or
videotape the consent discussion. The physician may refuse this request and should do so if the taping may alter
the interactive nature of the consent discussion. To the greatest extent possible, language used in the consent
discussion and on the consent form should be language that is understandable to the patient.
4. The law requires that the following categories of information be disclosed and discussed:
a. Name of procedure
b. Potential benefits
c. Reasonable alternatives including no treatment with risks and benefits
d. Potential risks of the proposed procedure
5. Not all potential risks need to be discussed. In general, it is advisable to discuss those risks that
a. Are statistically more common but less likely to be life-threatening, such as bleeding and infection
b. Although rare, but significant, such as death or loss of a body part or function
c. Are important for this patient or procedure, such as coil or embolic material migration
6. The consent note does not need to detail every risk but should be written before the procedure and use
“ including but not limited to” language in noting the matters discussed. In all cases, it is important not to be
perceived as promising or guaranteeing any particular result.
7. In a genuine emergency, such as a patient in whom the radiologist will embolize an artery for acute life-
threatening hemorrhage, consent is not required. A note should document the emergency; consent after the
procedure should not be sought.
8. A few cases in the legal literature also document that a competent patient is entitled to refuse recommended
treatment but that refusal also must be “informed.” Therefore, if a patient refuses therapy recommended by an
interventional radiologist, or accepts therapy that is not as highly recommended, the radiologist must document
that discussion. This note should include information about the warning the patient was given regarding the risks
that could or are likely to be incurred from having refused the recommended therapy.
Clinical Research
1. Clinical trials using human subjects are generally subject to certain federal protections. The Institutional
Review Board that reviews studies does so to assure the institution(s) participating that the rights of human
subjects are protected. Research consent forms are usually more extensive than those used in nonresearch
contexts. In addition to the discussion of risks, benefits, and alternatives required in nonresearch procedures, the
following items are required for research studies:
a. A statement that the study involves research, an explanation of the purpose and the expected duration of the
subject's participation, and a description of the procedures, including which procedures are investigational
b. A statement describing the extent to which patient-identifiable records will be maintained and may be
examined by the sponsor of the research, the U.S. Food and Drug Administration (FDA), and others
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c. For research involving more than minimal risk, an explanation as to whether medical treatment and
compensation are available for a research-related injury, or where information may be obtained.
d. A statement that participation in the research is voluntary and may be discontinued at any time
e. A statement that refusal to participate or withdrawal will not cause the subject to incur a penalty or lose
benefits to which he or she was otherwise entitled
f. Identification of a person to contact for information about research subject rights and about research-related
injuries
g. In some cases, it may also be necessary to inform the subject of extra health care costs that may be incurred
by participation in the research as well as other matters.
2. Interventional radiologists who perform clinical research are often using a research technique or procedure to
attempt to provide clinical benefit. It is important that the radiologist not inflate the potential benefits or minimize
the potential risks in these consent discussions.
3. Reporting the results of radiology studies done purely for research, not diagnostic or therapeutic, purposes is
somewhat controversial . The consent form must be clear about what will be reported to the patient, if anything.
However, regardless of what the consent form says, there is a duty to report findings of clinical significance.
This duty is an extension of law that developed long ago. We take for granted that the radiologist must report
abnormalities noted on films even if the findings were incidental to the purpose of the examination. However, as
recently as 1969, a radiologist argued that, although he had noted an opacity in the area of the patient's right
kidney, he was not required to report it since the lumbosacral spine series was ordered because the patient was
complaining of low back pain. The radiologist lost the case (10). An extensive review on the subject of incidental
findings in research was published in 2008 and concluded among other things that “as imaging research
technologies become more powerful, the incidental finding problem will grow” (11).
4. There is no obligation to report findings from a research scan when the radiologist does not know the
significance. However, if a magnetic resonance imaging (MRI) of the brain is done on a normal healthy control
and a mass is noted, that information must be transmitted back to the patient's physician, usually through the
principal investigator of the study.
Incidental Findings
1. Incidental findings, which are traditionally defined as “results that arise that are outside the original purpose for
which the test or procedure was conducted” (12), have created clinical, legal, and ethical challenges for
clinicians in general, and radiologists in particular.
2. A recent Presidential Commission studying incidental findings concluded the following:
Professional representative groups should develop guidelines that categorize the findings
likely to arise from each diagnostic modality; develop best practices for managing incident
and secondary findings … as professional organizations … determine that certain findings
are sufficiently significant and actionable to merit disclosure, a number of findings—
previously considered anticipatable incidental findings—are likely to become actively
sought secondary findings. The transition from unanticipated incidental findings to
anticipated or secondary findings allows for more information to be provided to potential
recipients and therefore facilitates more meaningful consent …. (13)
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3. In the meantime, there are very few reported professional liability cases that call into question how incidental
findings were handled. In one example, decided by the Supreme Court of Rhode Island in 2006, a patient was
seen by a neurologist complaining of weakness in his legs. An MRI was done and was reported as showing
“evidence of moderate hypertrophy of adenoidal soft tissue … clinical correlation is recommended.” The
neurologist felt that the finding was associated with a viral illness and did not require follow-up. Two years later,
the patient was diagnosed with nasopharyngeal cancer and claimed that the incidental finding required referral to
an otolaryngologist and caused a delay in diagnosis. A jury found for the defendant and the Rhode Island
Supreme Court affirmed (14).
Drugs versus Medical Devices

1. The FDA regulates both pharmaceuticals and medical devices. The definition of a medical device is very
broad and includes devices as diverse as thermometers and vascular stents.
2. Although a drug company is not permitted to advertise or promote a pharmaceutical for an off-label use, it is
quite legal for a physician to prescribe a drug for an off-label use and this occurs often.
3. Medical devices are regulated more strictly. In general, a physician is not permitted to use a device for an off-
label indication, absent research authority. Some authorities define an “off-label” indication very narrowly. That
is, if a stent is approved for an interventional radiologist to use in the carotid artery, it may not be used in other
vessels until approved for that use. Others believe that a stent approved for vascular use may be used
elsewhere in the vascular system. This conflict remains unresolved legally and should be considered particularly
when interventional medical devices are used. At the least, the radiologist should know what the device is
approved for, so an informed decision can be made.
4. Hospitals must report (to the device manufacturer, the FDA, or both) medical device malfunctions. A medical
device that malfunctions during use or is removed from a patient due to malfunction should be retained for
examination by hospital medical engineers or by the device manufacturer. Nondestructive testing is advisable,
particularly if the patient has suffered harm and suit is possible.
Retention of Films and Medical Records

1. It is the obligation of the radiologist and the department or practice to retain films (hard copy or electronic
storage) at least as long as required by the relevant state law, which varies among the states. Despite legal
storage requirements, it is prudent to retain films that are more frequently involved in claims: mammograms,
chest films, obstetric studies, and so forth.
2. Typically, retention requirements for paper records (reports) are longer than for films.
3. Now that it is possible to store digital images, the incidences of lost films are likely to decline.
4. It is not uncommon for interventional and other radiologists who note an interesting study to remove the most
interesting images and place them in a personal teaching file. This practice damages the defensibility of
professional liability actions. Original films should remain in the custody of the practice or hospital (Note: Health
Insurance Portability and Accountability Act [HIPAA] Regulations); de-identified copies or digital images may be
used for teaching.
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Professional Liability
1. Professional liability is a type of negligence action. The doctrines developed in England and were brought to
the United States with the rest of the general legal system, arriving about 1840 (15). Most of the principles are
found in case law, not in statutes. The statute that defines the outer time limit after the negligent act during which
a suit may be brought (the statute of limitations) is one exception to the judge-made law rule.
2. There are four elements that the plaintiff must prove in order to prevail in a professional liability action
against a health care provider:
a. The first is the existence of a physician-patient relationship. This relationship is rarely disputed when the care
has occurred in the hospital or office context. The relationship will generally be found to exist even if a colleague
is unexpectedly called to assist during an interventional or other procedure. The existence of a physician-patient
relationship requires that the physician use reasonable care in the care of the patient.
b. The second element that must be proven is the standard of care applicable. The standard is that standard
that was applicable at the time the incident took place, not the standard when the case was filed or later tried.
(1) The devices and techniques in use by interventional radiologists have changed rapidly over the past years.
As a result, it is prudent to retain policies, documents, and procedural information for at least 7 years after they
change. Otherwise, it is difficult for radiologists and their lawyers to reconstruct when a particular coil, for
example, was brought into use.
(2) The standard of care for interventional radiology is set not by courts, judges, or juries but by other
interventional radiologists. They may base their opinions on the literature (in which nearly every viewpoint
possible will be represented), professional guidelines from the Society of Interventional Radiology or American
College of Radiology and other groups, and personal opinion and experience.
(3) Because courts long ago recognized that juries did not have enough knowledge to evaluate the
appropriateness of physician practice, expert testimony for the plaintiff is required in nearly all cases (other than
cases involving injuries such as a fall from radiology table, or a brachial plexus injury sustained as a positioning
injury). The defense naturally also uses expert testimony to defend itself.
3. The third element the plaintiff must prove is causation: that is, that the alleged omission or commission
proximately caused damage. It is possible to find a physician negligent, but where negligence is not a proximate
cause of injuries (16).
4. The fourth element to be proven is damages.
5. The law governing professional liability has expanded in past years to permit patients to make claims for
injuries that were not compensable in the past. Because judges make most of the law in this area, plaintiffs'
lawyers make new claims and wait for courts to rule on them. If courts accept them, then new law is made in that
state, although other states may not yet have accepted that cause of action.
6. One area in which this is occurring in interventional diagnostic imaging has to do with clinical research.
Attorneys for plaintiffs are currently attempting to claim in some cases that the standard of care requires referral
to another facility so that the plaintiff could have participated in a clinical trial of a new, and supposedly better,
device or procedure. Because by definition, a research protocol is testing for safety and effectiveness, courts
have thus far rejected these claims. However, when interventional radiologists testify that a device under
evaluation was better, safer, or more effective than standard approved therapy, courts may begin to expand
liability.
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References
1. Physician Insurers Association of America. Breast Cancer Study. Rockville, MD: Physician Insurers
Association of America; 1990.
2. Physician Insurers Association of America. Lung Cancer Study. Rockville, MD: Physician Insurers
3. Physician Insurers Association of America. Breast Cancer Study. Rockville, MD: Physician Insurers
4. Whang JS, Baker SR, Patel R, et al. The causes of medical malpractice suits against radiologists in the
United States. Radiology. 2013;266:548-554.
5. Bassett LW, Bent C, Sayre JW, et al. Breast imaging training and attitudes: update survey of senior
radiology residents. AJR Am J Roentgenol . 2011;197:263-269.
6. Bassett LW, Monsees BS, Smith RA, et al. Survey of radiology residents: breast imaging training and
attitudes. Radiology. 2003;227:862-869.
7. Baker SR, Whang JS, Luk L, et al. The demography of medical malpractice suits against radiologists.
Radiology. 2013;266:539-547.
8. Magnavita N, Fileni A, Mirk P, et al. Malpractice claims in interventional radiology: frequency,

characteristics and protective measures. Radiol Med. 2013;118:504-517.
9. Salgo v Leland Stanford Jr. University Board of Trustees, 317 P2d 170 (1957).
10. Capuano v Jacobs, 305 NYS2d 837 (1969).
11. Wolf SM, Lawrenz FP, Nelson CA, et al. Managing incidental findings in human subjects research:
analysis and recommendations. J Law Med Ethics. 2008;36:219-248.
12. Presidential Commission for the Study of Bioethical Issues. Anticipate and communicate: ethical
management of incidental and secondary findings in the clinical, research, and direct-to-consumer contexts.
(December 2013 report of the Presidential Commission for the Study of Bioethical Issues). Am J Epidemiol .
2014;180:562-564.
13. Presidential Commission, supra; p. 6-7.
14. Riley v Stone, 900 A2d 1087 (RI 2006).
15. Mohr JC. American medical malpractice litigation in historical perspective. JAMA. 2000;283:1731-1737.
16. Estate of Swan v Balan, 956 A2d 1222 (DE 2008).

e-96
QA/QI General Principles
Michael A. Bruno
Hani H. Abujudeh
In 1999, the Institute of Medicine (IOM) released its first report on medical errors and their management entitled
To Err Is Human: Building a Safer Health System. This seminal publication exposed a previously unappreciated
epidemic of serious and often lethal medical mistakes leading to the present “Quality and Safety Revolution” in
health care. The report estimated, for example, that in the calendar year of 1997, at least 44,000 and possibly as
many as 98,000 hospitalized Americans died as a result of errors or negligent care. The new IOM data on the
magnitude of this problem came as a surprise to the medical profession and, to the public, revealed a shortfall of
effective data gathering on medical errors. With little related research or experience to draw on, physicians and
other health care professionals looked to other industries for guidance, specifically to those where safety was a
primary consideration, and whose operations required systematic and comprehensive data gathering, analyses
of risk factors, and optimization of “best practices” to minimize errors. Notably, the nuclear power and aviation
industries, among others, have had an extensive literature in quality optimization and safety management for
decades.
P.847
In more than 16 years since the IOM report was issued, quality and safety has developed as a field of
scholarship and practice in its own right, spurred on by a second IOM monograph, Crossing the Quality Chasm:
A New Health System for the 21st Century, published in 2001, which established much of the agenda for the
fledgling quality movement. Since that time, governmental and nongovernmental agencies have been developed
and lavishly funded to support research into quality improvement methodologies and best practices as well as
the development of metrics and standards for health care and dissemination of quality improvement data
throughout the health care industry. Governmental health care reform efforts including the Affordable Care Act
(ObamaCare) have cantered on the methodologies and concept of continuous quality improvement (CQI)
borrowed from other industries and incorporated these as an underlying structural feature of health care reform.
Indeed, the application of CQI concepts and methods from industry to health care has, in turn, spawned a new
subindustry, with widespread revolutionary ramifications from hospital review and accreditation to professional
training and certification, including maintenance of certification, and as a basis for stratifying payments made to
physicians and hospitals for medical services rendered. A parallel premium placed on transparency and
openness is leading to various quality measures being available to patients and payers as they decide where
and from whom health care services should be obtained in the local marketplace. The overarching importance of
quality and safety and its escalating impact to the health care industry and economy will only continue to grow as
health care reform progresses in the years and decades ahead.
Creating a “Culture of Safety and Quality”

As the model for quality management shifted away from a punitive response to errors (with perverse incentives
for hiding errors) to an analytical and nonpunitive approach (which facilitates discovery of errors), radiology
departments have embraced the concept of the “Culture of Safety and Quality,” by adopting a few overarching
goals originally proposed by the IOM. The goal is to promote health care practices that are
1. Safe: protecting patients from injury and avoidable complications—a first priority
2. Effective: evidence-based practice, including refraining from providing services with no benefit to the patient
(e.g., overutilization of imaging)
3. Efficient: Quality practices avoid waste, including that of people's ideas and energy.
4. Equitable: Care is not dependent on patient's ability to pay or other circumstantial issues.
5. Timely: reduction of access and wait times, and other avoidable delays, that overlap both patient safety and
customer satisfaction issues
6. Patient-centered: an altruistic approach to health care, focusing on the needs and well-being of the patient as
the sole priority and not on the needs of the system, institution, or caregivers
As other risk-prone industries have already discovered, achieving success in grand safety goals requires an
open discussion of errors and untoward events. To achieve this, it is necessary to foster a “blameless culture,”
based on an environment of mutual trust and focused primarily on optimizing service quality and patient safety.
Experience has shown that an environment free of recrimination permits a truly open exchange of information,
including the rapid and open reporting of adverse incidents, thereby allowing for a rapid elimination of risks to
patients. Such a change represents a 180-degree paradigm shift from a traditional medical culture that previously
sought to assign and apportion blame for every transgression—one that demanded a perhaps unrealistic
perfection of practitioners. This type of perfectionist thinking, which recurs periodically is to be resisted, but it has
its roots in fears of litigation and the practice of “defensive medicine,” which has led to an overreliance on
technologies and procedures that inadvertently subject patients to further risks of errors and complications.
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Levels of Quality Management—Basic Concepts and Vocabulary
The vocabulary of CQI, which has been part of the industrial lexicon for decades, is now common in radiology:
1. Quality control : sets minimum standards of quality
2. Quality assurance: focuses on methods to measure and assure that the minimum quality standards are met
3. Quality improvement: a more labor-intensive and proactive, analytical process by which underlying issues
impacting the quality and safety of clinical practices are analyzed, improved, and acted on as needed.
National- and Local-Level Quality and Safety Initiatives

The need for improvement in the quality and safety of health care services has been addressed at multiple levels
and organizations:
1. The Joint Commission (TJC): annually revises a list (see National Patient Safety Goals in Appendix section)
of specific patient safety issues, based on expert consensus, and requires adherence from hospitals seeking
accreditation
2. The Institute for Healthcare Improvement (IHI): a for-profit organization; helps member hospitals develop and
achieve their quality program goals
3. The Blue Ridge Group: a “think tank” of influential nonphysicians from government, industry, and academia
considers the “Quality and Safety” movement a key part of overall health care reform.
4. The Leap Frog Group: a coalition of more than 150 health care purchasers highlights three main areas for
quality improvement: computerized physician order entry (CPOE), evidence-based hospital referral (HER), ICU
physician staffing
5. The Centers for Medicare and Medicaid Services (CMS): has dramatically altered the payment schema in
U.S. health care in recent years, increasingly utilizing Pay for Performance criteria, including both rewards and
penalties, linking payment to physicians and hospitals to demonstrated achievement selected, measurable
quality goals. This also has created a significant bureaucratic burden, which is contributing to a wave of
consolidations of practice entities nationwide.
6. The Agency for Healthcare Research and Quality (AHRQ): The AHRQ of the U.S. Department of Health and
Human Services is a governmental agency providing resources, such as an extensive library of “quality toolkits”
available online for physicians and health systems to conduct quality improvement initiatives, as well as serving
as a repository for a large pool of research funding.
7. The Patient-Centered Outcomes Research Institute (PCORI): A foundation established by the U.S. Congress
to support quality-related research and clinical improvement programs nationwide. PCORI is a significant source
of funding for quality-related health care research.
Performance Improvement Tools, Resources, and Methods

1. Just-in-Time Training: delivers training when needed, to maximize effectiveness
2. Team Building: programs designed to enhance cohesion of dedicated work units
3. Plan-Do-Check-Act (PDCA) process: basic process of CQI implementation
4. Dashboard Data Analysis: a graphic display of the status of various quality metrics allows for evaluation of
initiatives and timely corrections
5. Root Cause Analysis (RCA) process: a traditional method for analyzing “sentinel adverse events” and
assigning a “root cause(s)” for the occurrence
6. Flow charts: a graphical tool for logical charting of the processes involved in the delivery of services; may
reveal where interventions are most needed or potentially most effective
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7. Cause-and-Effect Diagrams: self-explanatory; a conventional business tool
8. Lean Six Sigma: resulting from the fusion of Six Sigma, which is a statistical approach to business and/or
quality management problems (fewer than four defects in a million) and data analysis, and Lean, an industrial
practice that focuses on reducing waste inherent in processes by creating “more value with less work.” Wastes
are typically: Defects, Overproduction, Waiting, Transporting, Movement, Inappropriate Processing, and
Inventory. This is growing in impact throughout health care and, in many leading institutions, is the predominate
methodology for quality improvement projects.
9. Human Factors Engineering: design of machine interfaces to work more intuitively and effectively with the
humans
10. Ergonomics and Environmental Controls
11. Health Care Failure Mode and Effects Analysis (HCFMEA): A procedure, also derived from manufacturing,
for analyzing potential risks for classification by severity or determination of the effect of failure on the larger
system
Appendix
The 2015 Joint Commission National Patient Safety Goals and Universal Protocol (Adapted from The Joint
Commission on Accreditation of Healthcare Organizations [JCAHO] website).
Goal 1. Improve the accuracy of patient identification.
Goal 2. Improve the effectiveness of communication among caregivers. For radiology, specific recommendations
include such things as guidelines for providing verbal or telephonic reporting of critical test results, such as
having the person receiving the information record and “read-back” the test result, using only standardized
abbreviations, acronyms or symbols, and so forth.
Goals 3-5. Improve the safety of using medications: Identify and, at a minimum, annually review a list of look-
alike/sound-alike drugs used by the organization, and take action to prevent errors involving the interchange of
these drugs, especially anticoagulants.
Goal 6. Improve the safety of clinical alarm systems.
Goals 7-14. Reduce the risk of health care-associated infections.
Goal 15. Identify patients at risk for suicide.
And the Universal Protocol (3 parts):
UP01.01.01 Conduct a preprocedure verification process.
UP01.02.01 Mark the procedure site.
UP01.03.01 A time-out is performed before the procedure.
Suggested Readings
Abujudeh HH, Bruno MA, eds. Quality and Safety in Radiology. New York, NY: Oxford University Press;
2012.
Agency for Healthcare Research and Quality. http://www.ahrq.gov. Accessed November 15, 2015.
Blue Ridge Academic Health Care Group. Health Care Quality and Safety in the Academic Center.
http://www.healthcarecan.ca/wp-content/uploads/2014/11/Blue-Ridge-Academic-Health-Group-2007-
Report.pdf. Accessed November 15, 2015.
Bruno MA, Nagy P. Fundamentals of quality and safety in diagnostic radiology. J Am Coll Radiol .
2014;11(12):1115-1120.
Donchin Y, Gopher D, Olin M, et al. A look into the nature and causes of human errors in the intensive care
unit. Crit Care Med. 1995;23(2):294-300.
Institute for Healthcare Improvement. http://www.ihi.org. Accessed November 15, 2015.
Institute of Medicine. Crossing the Quality Chasm: A New Health System for the 21st Century. Washington,
DC: National Academy Press; 2001.
Kohn LT, Corrigan JM, Donaldson MS, eds. To Err Is Human: Building a Safer Health System. Washington,
DC: National Academy Press; 1999.
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Patient-Centered Outcomes Research Institute. http://www.pcori.org/. Accessed November 15, 2015.
Reason JT. Human Error. New York, NY: Cambridge University Press; 1990.
Reason JT. Managing the Risks of Organizational Accidents. Hampshire, United Kingdom: Ashgate; 1997.
Thrall JH. Quality and safety revolution in health care. Radiology. 2004;233:3-6.
Wong BM, Etchells EE, Kuper A, et al. Teaching quality improvement and patient safety to trainees: a
systematic review. Acad Med. 2010;85(9):1425-1439.
e-97
Quality Improvement Strategies in Interventional Radiology
Gloria M. Salazar
Hani H. Abujudeh
Introduction
In medicine, delivering improvements in the quality and safety of health care remains a challenge, with an
increased focus on reducing unnecessary variation, eliminating preventable errors, and improving safety in care
delivery. Quality is defined by the Institute of Medicine (IOM) as care that is safe, patient-centered, equitable,
timely, and efficient (1). Poor care delivery results from suboptimal implementation or execution (noncompliance)
of safe practices to reduce errors. In interventional radiology (IR), there are several opportunities to address
these issues with process improvement projects (2). Most of the safe practices within IR were systematically
developed by consensus and evidence-based conclusions (“Society of Interventional Radiology Clinical Practice
Guidelines”) to provide clinical indicators that assist in optimal medical decision making (3).
Development of quality improvement (QI) safety strategies in IR has been described with different approaches,
and this chapter will describe an overview of safe care delivery domains that are relevant to IR and types of
indicators of quality that can be used in IR QI strategies.
Defining Clinical Indicators for QI

Indicators for performance and outcome measurement allow the quality of care and services to be measured.
Measurements serve many purposes such as benchmarking; setting priorities; supporting accountability,
regulation, and accreditation; and supporting QI and the patient's choice of providers. Clinical indicators are
considered the basis for QI in health care, and it is essential to understand their definitions, characteristics, and
categories (4).
Appropriate development and selection of clinical indicators are needed for systematic evaluation of patients'
care. Indicators can be expressed as numbers, rates, or averages, and include measures of structure, process,
and outcome for general or specific disease processes. Examples of rate-based indicators include hospital-
acquired bacteremia and catheter-related infections. Examples for sentinel indicators that are generally used for
risk management purposes include wrong site procedures, postprocedural deaths, and unexpected death after
ambulatory procedures (4). The following are characteristics of an ideal clinical indicator: It is based on best
available evidence with agreed definitions used for comparative studies, valid and reliable, optimally specific and
sensitive, and is relevant to clinical practice (4). In IR, most of the clinical indicators are derived from consensus
documents produced and published by the Society of Interventional Radiology (SIR) (3).
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Structural indicators describe the amount of resources used by a specific health care system, for example,
proportion of specialists to other doctors, access to technologies or specific units, and the use of clinical
guidelines that should be periodically revised.
Process indicators assess what the provider did for the patients and how well it was done. It can measure
activities and tasks in patient episodes of care. Examples include proportion of patients treated according to
clinical guidelines, proportion of patients with myocardial infarction who receives thrombolysis, and proportion of
patients assessed by a doctor within 24 hours of referral. In order for a process indicator to be valid, it must be
previously demonstrated to produce a better outcome (4).
Outcome indicators measure the effects of care on the health status of patients and populations. Outcomes can
be expressed as the five Ds: death, disease, discomfort, disability, and dissatisfaction. Examples of such
indicators include mortality, morbidity, functional status, health status measures, work status, quality of life
(QOL), and patient satisfaction (4).
More recently, provider-level quality performance measures that address the end-user needs (patients, families,
consumers, and payers) have been described. These measures are yet to be tested and can be classified
according to IOM domains. Some examples include patient experience scores, hospital 30-day readmission,
adverse event rate, rate of same day access, and so forth (5).
In IR, most of the clinical indicators are defined in the SIR Quality Improvement Guidelines documents (3). In
addition, there are many therapies developed in IR that affect patient QOL. There are validated tools that define
QOL outcomes metrics that can be used in clinical trials and QI projects (6). However, there is still need for
validation of process/outcomes metrics in IR that can be utilized as standard of care in IR. Table e-97.1 refers to
some of examples of clinical indicators that have been described in IR, and some of which are yet to be
validated.
Clinical Indicators in IR
SIR has recommended instituting important procedure-specific aspects of care such as appropriateness, safety,
and efficacy through the Quality Improvement Guidelines documents (3). SIR documents address important
aspects of procedural care including appropriateness, efficacy and safety, and evaluation with indicator
thresholds for specific procedures. When appropriateness of indications or success rates (technical and clinical)
are below the minimum threshold, or when complication rates exceed a maximum threshold, a review should be
performed to determine causes and to implement changes as necessary (3). The next sections describe
indicators that relate to care delivery in IR with respect to procedural complications and safety indicators.
Table e-97.1 Potential Clinical Indicators in Interventional Radiology
IOM Quality
Metric Dimension Domain Examples
Adverse event rate Safe Outcome Complication rates per SIR guidelines for
specific procedures (3)
Safe practices Effective Process Adherence to universal protocol to avoid

implementation wrong site procedures per SIR guidelines (15)
Functional health Effective Outcome Functional Assessment of Cancer Therapy

outcome scores (FACT) scale (6)
Hospital 30-day Effective Outcomes —

readmission rate (23)
Adapted from Meyer GS, Nelson EC, Pryor DB, et al. More quality measures versus measuring what
matters: a call for balance and parsimony. BMJ Qual Saf. 2012;21:964-968.
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Indicators for Specific Procedures

Indicators thresholds may be used to assess the efficacy of ongoing improvement programs. The SIR QI
guidelines have recommended instituting important procedure-specific aspects of care such as
appropriateness, safety, and efficacy. Indications (appropriateness) and potential complications for specific
procedures are presented elsewhere in this book. Universal complication thresholds are very difficult to
determine as they may be influenced by baseline patient population characteristics and referral patterns.
Therefore, each institution may have to customize recommended thresholds for its own QI program. SIR
thresholds are reported in the following text for more recent documents published for high-volume
procedures in our specialty.
Indications for diagnostic arteriography (7) have been described for pulmonary, spinal, bronchial, aorta,
abdominal visceral, renal, pelvic, and extremity arteriography (7). When fewer than 95% (SIR threshold) of
the procedures are for these indications, the department must review the process of patient selection. The
overall procedure threshold for major complications is 1.0%, and complications are divided into three
groups: access site, systemic, and catheter-induced, and the thresholds for major adverse events. Access
site-related complications thresholds are as follows: hematoma (3%), occlusion (1%), and
pseudoaneurysm/arteriovenous fistula formation (0.2%). Systemic complications have reported thresholds
for major adverse events of 1% and includes major contrast reactions (5%) and contrast agent-induced
nephropathy (5%).
Catheter-induced complications reported major adverse event thresholds are distal emboli (0.5%), arterial
dissection/subintimal passage (1%), and subintimal injection of contrast (1%).
2. Central venous access
The indications for central venous access (8) have been described elsewhere in this book. Success rate
thresholds for central venous access placement in the adult population are 95% for internal jugular
approach and 90% for subclavian vein and translumbar approaches for peripherally inserted central
catheters (PICC) and peripherally implanted ports (8). The overall procedure threshold recommended for
major complications related to image-guided central venous access (subclavian, jugular, and peripheral
approaches) is 3%. Specific major complications thresholds for venous access via subclavian and jugular
approaches are pneumothorax (4%), hemothorax (2%), hematoma (4%), perforation (2%), air embolism
(2%), wound dehiscence (2%), procedure-induced sepsis (2%), and thrombosis (8%). Specific major
complications thresholds for peripheral PICC and ports are pneumothorax/hemothorax (0%), hematoma
(2%), wound dehiscence (2%), phlebitis (8%), arterial injury (1%), thrombosis (6%), and procedure-induced
sepsis (2%) (8).
3. Inferior vena cava filters
Absolute and relative indications for filter placement (9) have been described elsewhere. Technical success
for placement is expected to be 97%; therefore, the threshold for review of technical failures is 3%.
Complication thresholds include filter embolization (1%), access site thrombosis/occlusion (3%),
deployment outside target area (0%), and death (<1%). Trackable events are also described for filters that
are left in the inferior vena cava (IVC) for permanent indications, which can be utilized as performance
indicators for QI projects in IR. These include IVC penetration, filter movement, filter fracture, recurrent
pulmonary embolism, access site thrombus, and insertion problems (9).
4. Transcatheter embolization
Overall technical and clinical success thresholds range from 85% to 95% for different embolization (10)
procedures. Overall major complication threshold for general procedures is 6%. Specific major
complications for general procedural thresholds are sepsis
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(1%), abscess (1%), target ischemia (4%), nontarget embolization (2.5%), hemorrhage (1%), spinal
infarction (1%), and procedure-related death (1%). Overall major complication threshold for splenic
embolization is 15%, and specific thresholds are abscess/sepsis (5%), pneumonia (8%), pleural effusion
(4%), and death (2%). Overall major complication threshold for portal vein embolization is 6%, and specific
thresholds are abscess (1%), cholangitis (1%), main or left portal vein occlusion (1%), pneumothorax (1%),
portal hypertension (1%), subcapsular hematoma (1%), and death (2%) (10).
General Safety Indicators

In general, safety parameters that are considered important for radiology include radiology-generated infections,
medication errors rates, patient falls, contrast material-induced nephropathy, critical test reporting, specimen
labeling errors, universal protocol, hand hygiene, medication reconciliation, and correct image labeling (11).
Due to the variety of procedures performed in IR, there are different parameters to be used in continuous
monitoring of patient safety for vascular and nonvascular procedures, as recommended by the SIR Clinical
Practice Guidelines documents. These guidelines support optimization of patients' quality of care,
standardization of clinical practices, and the development of quality and safety programs. Procedural
complications are rate-based outcomes metrics that can be utilized to evaluate performance of care and ideally
should be linked to evidence-based clinical processes. When specific thresholds for complications are reached,
a reevaluation of cases and safety processes/structures linked to that specific procedure is recommended. In this
setting, safe practices implementation metrics that evaluate effectiveness of care delivery (appropriateness of
indications, hand hygiene compliance, periprocedural antibiotic use, etc.) can be used for QI to aim at
improvement of outcomes or reduction of complications. For example, catheter-related bloodstream infection is
considered an outcome indicator for central venous line placement. There are five evidence-based process
metrics (hand hygiene, full-barrier precaution during insertion, chlorhexidine use, avoiding femoral access, and
removing unnecessary catheters) that are identified as having the greatest impact on catheter-related
bloodstream infections and are recommended by the Centers for Disease Control and Prevention (CDC).
Pronovost et al. (12) demonstrated that safety outcome indicators (catheter-associated infections) can be
modified by improving staff compliance with evidence-based guidelines (safety processes recommended by
CDC) with the combination of multiple interventions including the utilization of a procedural checklist. Similarly in
IR, safety processes of care can be developed with the use of practices implementation metrics which have been
endorsed by societal guidelines including adherence to infection control practices (13), catheter-related
infections (14), prevention of “wrong site, wrong procedure, and wrong person surgery” (15), and medication
labeling (16). The SIR-endorsed sterile technique guidelines (13) include several process metrics that affect
periprocedural infection rates including time to table preparation, room turn over, gowning and downing, hand
hygiene, and so forth. Compliance with universal protocol (UP) (preprocedural verification/side/site marking and
time-out) is a metric associated with preprocedure verification to avoid wrong site procedures, and it has been
demonstrated to address issues with wrong site/procedure and person surgery in the surgical literature with
improved perisurgical outcomes (17).
QI Projects: Where to Focus?

In IR, every aspect of patient care presents with opportunities for improvement; therefore, developing a list of QI
initiatives may be challenging. Some publications address these challenges and provide a framework for
prioritization and tools to determine which processes you can focus on first and how to maximize the return in
clinical improvements (2,18). Data analysis with Pareto charts can help prioritization by identification of high
volume processes.
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Topics in IR can be focused on care delivery, patient-centered care issues, and care coordination. Within care
delivery, there are several opportunities for example on patient safety (reducing preventable
errors/complications), improving compliance with The Joint Commission (JC) practices, and reducing catheter-
related infections. Patient-centered care topics include reducing waiting times for appointments, improving
patient satisfaction scores, and access to information. Care coordination topics are complex and in the hospital
setting; a recent QI study focused on improved communication between caregivers was shown to reduce
preventable errors in inpatient care (19).
The following section describes some QI strategies for safety in care delivery.
Safety QI Strategies
QI projects on safe care delivery can affect processes (compliance with safe evidence-based practices) or
outcomes (adverse events and complication rates). In the United States, most of the safety guidelines are
mandated by the JC, with recommendations for best practices, ongoing assessment of clinical outcomes, and
voluntary reporting of serious events. The SIR has been proactive, adapting the JC guidelines to produce
standards of practice for different procedures, thereby establishing risk management strategies to improve safety
and quality in IR (15). These guidelines can be employed at various stages of patient care (preprocedural
verification, indications and complication thresholds, and clinical outcomes) and at different levels of care
delivery (physician qualification, nursing protocols, technologist training standards, and necessary resources).
QI initiatives that focused on patient safety may be challenging to develop because some of its indicators may
occur at very low incidence, for example, in the case of wrong site procedures, but these processes can still be
studied in the form of sentinel indicators as metrics. In the surgical literature, implementation of UP has shown to
decrease rates of deaths, complications, and surgical site infections (17) and provide the basis for
implementation of safe practices in procedural areas.
The SIR guidelines recommended that institutional thresholds are determined for compliance with UP as part of
QI program (15). Once evidence-based standard processes are implemented in IR units, compliance with
guidelines can be improved with interventions, which include physician education, introduction of checklists, and
so forth.
A recent study described the implementation of training, checklists, and simulation to promote the creation of
highly reliable procedural teams for implementation of UP in IR (20). The authors utilized a validated safety
attitudes questionnaires (Teamwork and Safety Climate Survey) to evaluate the results of the educational
program, in addition to reported safety events that included near-misses. The results of an 18-month period
study demonstrated that perception of safety climate improved 25%, and perception of the teamwork climate
decreased 5.4% in IR, while there is ongoing reluctance to document near-misses (20). This study highlights the
importance of cultural changes to achieve patient safety goals through implementation of UP and that long-term
efforts are needed to maintain QI projects in this topic.
Reduction of Preventable Adverse Events

Recording, root-cause analyses, reporting, and corrective actions are all important for preventing recurrence of
adverse events; however, most of these tools are reactive and much focus is needed to use prospective tools to
decrease errors (2). The SIR Task Force on Medical Errors has adopted a previously published (21) list of
possible causes of preventable adverse events (Table e-97.2) that can be used for the development of QI
projects aimed at avoiding these risks, by focusing on
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the creation of standardized protocol and checklists that can be evaluated prospectively. For example, a recent
study on implementation of hand-offs program to reduce serious medical errors secondary to miscommunications
demonstrated a reduction preventable events without a negative effect on workflow (19).
Table e-97.2 Possible Causes of Preventable Adverse Events
Before procedure
1. Necessary equipment not available for a case

2. Incomplete necessary history or examination
3. Predisposition for hemorrhage is not known because of insufficient documentation or inadequate
history
4. Patient ate before a procedure requiring an empty stomach
5. Wrong patient sent from ward
6. Patient allergies not checked
7. Vitals signs and/or patient assessment not done before sedation or procedure
8. No consent before the procedure
During procedure
1. Procedure performed on the wrong patient, side, or organ

2. Wrong patient is indicated on monitor and/or fluoroscopy equipment
3. Handed the wrong equipment during a case
4. Handed equipment incorrectly during a case
5. Asked for wrong equipment
6. Incorrect medication or dose of medication given (by operator or nurse)
7. Medication on procedure table incorrectly labeled or not labeled
8. Administration of medication to patient with a known allergy to the drug
9. Fluid overload due to high intravenous fluid administration rate
10. Stopcock blows off during power injection
11. Contrast medium injected but no images are obtained
12. Images are obtained but contrast medium injector did not inject
13. Patient falls off stretcher or table during transfer or procedure
Procedure-specific
1. Performance of pulmonary arteriography in a patient with known left bundle branch block
2. Placement of IVC filter in gonadal vein or hepatic vein
3. Embolization of bronchial artery without recognition of the artery of Adamkiewicz—risk of cord
ischemia
4. Ureteral stent deployed with tip in the renal parenchyma or coiled in the ureter
5. Excessive oversizing of balloon or stent in artery with risk of rupture
6. Perforation of renal capsule with a guidewire during renal intervention
7. Radiofrequency ablation in a patient with a pacemaker
8. Intra-arterial placement of a venous access device
9. Placement of nitinol stent or filter in a patient with nickel allergy
10. Injecting CO2 in a patient with a right-to-left shunt
Postprocedure
1. Attempt an arterial line placement in a patient undergoing thrombolytic therapy

2. Inadequate postprocedural monitoring or instructions, leading to delayed therapy of a substantial
postprocedural complication, for example, infection after uterine artery embolization, pneumothorax
after lung biopsy, neurologic complication of lytic therapy
3. Images incorrectly labeled
4. Official report with correct dictation in incorrect patient
5. Official report with incorrect dictation in correct patient
6. Patient and/or family is not advised of a high radiation dose to skin and appropriate follow-up
Adapted from Miller DL. Safety in interventional radiology. J Vasc Interv Radiol . 2007;18:1-3.
Retrospective review of preventable events is also a valuable approach to understand the causes of technical
procedural failures. A recent study evaluating preventable causes of nondiagnostic adrenal vein sampling utilized
failure mode analysis to review causes of noncatheterization of venous sampling procedures (22). The authors
found that failure modes included diluted sample from correctly identified vein, vessel misidentified as adrenal
vein, failure to locate an adrenal vein, cosyntropin stimulation failure, and laboratory error.
Conclusion
Safe IR practice requires continuous measuring, monitoring, evaluation, and refinement based on clinical
indicators representing various aspects of patient care. Establishing QI projects is critical for maintaining a
high service quality and for establishing credibility among professional peers and patients alike clinical
indicators are the basis for implementation of QI projects to improve care delivery in IR (see Chapter e-98).
References
1. Institute of Medicine. Crossing the Quality Chasm: A New Health System for the 21st Century.
Washington, DC: National Academies Press; 2001.
2. Duncan JR. Strategies for improving safety and quality in interventional radiology. J Vasc Interv Radiol .
2008;19:3-7.
3. Cardella JF, Kundu S, Miller DL, et al. Society of Interventional Radiology clinical practice guidelines. J
Vasc Interv Radiol . 2009;20:S189-S191.
4. Mainz J. Defining and classifying clinical indicators for quality improvement. Int J Qual Health Care.
2003;15:523-530.
5. Meyer GS, Nelson EC, Pryor DB, et al. More quality measures versus measuring what matters: a call for
balance and parsimony. BMJ Qual Saf. 2012;21:964-968.
6. Monsky WL, Khorsand D, Nolan T, et al. Quality of life assessment in interventional radiology. Acad
Radiol . 2014;21:407-414.
7. Dariushnia SR, Gill AE, Martin LG, et al. Quality improvement guidelines for diagnostic arteriography. J
8. Dariushnia SR, Wallace MJ, Siddigi NH, et al. Quality improvement guidelines for central venous access. J
9. Caplin DM, Nikolic B, Kalva SP, et al. Quality improvement guidelines for the performance of inferior vena
cava filter placement for the prevention of pulmonary embolism. J Vasc Interv Radiol . 2011;22:1499-1506.
10. Angle JF, Siddigi NH, Wallace MJ, et al. Quality improvement guidelines for percutaneous transcatheter
embolization: Society of Interventional Radiology Standards of Practice Committee. J Vasc Interv Radiol .
2010;21:1479-1486.
11. Johnson CD, Krecke KN, Miranda R, et al. Quality initiatives: developing a radiology quality and safety
program: a primer. Radiographics. 2009;29:951-959.
12. Pronovost P, Needham D, Berenholtz S, et al. An intervention to decrease catheter-related bloodstream

infections in the ICU. New Engl J Med. 2006;355:2725-2732.
13. Chan D, Downing D, Keough CE, et al. Joint Practice Guideline for Sterile Technique during Vascular
and Interventional Radiology Procedures: from the Society of Interventional Radiology, Association of
Interventional Radiology Standards of Practice Committee, and endorsed by the Cardiovascular
Interv Radiol . 2012;23:1603-1612.
14. Miller DL, O'Grady NP. Guidelines for the prevention of intravascular catheter-related infections:
recommendations relevant to interventional radiology for venous catheter placement and maintenance. J
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15. Angle JF, Nemcek AA Jr, Cohen AM, et al. Quality improvement guidelines for preventing wrong site,
wrong procedure, and wrong person errors: application of The Joint Commission “Universal Protocol for
Preventing Wrong Site, Wrong Procedure, Wrong Person Surgery” to the practice of interventional radiology.
16. Statler JD, Towbin RB, Ronsivalle JA, et al. Recommendations for the implementation of Joint
Commission guidelines for labeling medications. J Vasc Interv Radiol . 2009;20:S251-S255.
17. Haynes AB, Weiser TG, Berry WR, et al. A Surgical safety checklist to reduce morbidity and mortality in a
global population. N Engl J Med. 2009;360:491-499.
18. Sridhar S, Duncan, JR. Strategies for choosing process improvement projects. J Vasc Interv Radiol .
2008;19:471-477.
19. Starmer AJ, Spector ND, Srivastava R, et al. Changes in medical errors after implementation of a handoff
program. N Engl J Med. 2014;371:1803-1812.
20. Ross J, Wolf D, Reece K. Highly reliable procedural teams: the journey to spread the universal protocol
in diagnostic imaging. Perm J. 2014;18:33-37.
21. Miller DL. Safety in interventional radiology. J Vasc Interv Radiol . 2007;18:1-3.
22. Trerotola SO, Asmar M, Yan Y, et al. Failure mode analysis in adrenal vein sampling: a single-center
experience. J Vasc Interv Radiol . 2014;25:1611-1619.
23. Prabhakar AM, Harvey HB, Oklu R. Thirty-day hospital re-admissions: a metric that matters. J Vasc Interv
Radiol . 2013;24:1509-1511.
e-98
PQI Projects
Mohammad Mansouri
Hani H. Abujudeh
To maintain an American Board of Radiology (ABR) certificate, radiologists are required to complete parts I to IV
of the Maintenance of Certificate (MOC). Part I, Professional Standing, requires the possession of an
unrestricted medical license. Part II, Lifelong Learning and Self-Assessment, requires the credits for continuing
medical education (CME) each year. Part III, Cognitive Expertise, requires passing an examination with several
selected modules in clinical skills and one module, which is designated by the ABR testing as noninterpretative
skills.
Part IV, Practice Quality Improvement (PQI), needs the completion of PQI projects. The number of required PQI
projects to be completed was defined for the 10-year MOC cycle and is dependent on the starting date.
Candidates must complete at least one PQI project in the previous 3 years. Note that continuous certification
began with certificates issued after 2012 and therefore affects all current radiology residents.
PQI projects can be accomplished as an individual, a group, or an institutional/organizational level (1). This
chapter can be used as a guide to fulfill the practice quality improvement (QI) requirement in interventional
radiology.
Individual PQI Projects

In some settings, one may not be able to perform PQI as a group or may have subspecialty PQI requirements
that are not shared by practice associates. In these situations, individual PQI participation is appropriate.
Individual PQI projects may be sponsored or self-designed.
Sponsored PQI projects, including registries, may be performed by individuals or groups. Sponsored projects
are often concerned in significant, common radiologic care issues. These projects have role in improving
practice and also an understanding the effects of QI efforts on a national level. Examples include
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“RADPEER,” “Dose Index Registry,” “General Radiology Improvement Database,” or “CT Colonography
Registry” (Table e-98.1).
Self-designed projects are suited for individual PQI participants. Such projects do not require approval for use;
however, certain rules in construction and execution of these projects must be followed. Although these
projects are self-designed, documentation with record keeping is necessary. Examples include “optimizing
radiation use during fluoroscopic procedures” or “reducing door-to-puncture times for intra-arterial stroke
therapy.”
The following presents a step-by-step process for project selection, development, and completion, the PDSA
cycle, which is continued until the project is concluded (2).
Baseline PDSA Cycle (Cycle No. 1)

1. Plan. Determine the area of interest that you consider to be in need of and have the potential for improvement,
which is relevant to your practice and amenable to repeated measurements. Topic should be challenging and
address the existing gaps in your practice. You can consider improving your own interventional radiology
practice to a safer, timelier, more efficient, more effective, more patient-centered, or more equitable practice.
Then devise an appropriate measure to gauge the issue you have selected. Set a desired level of performance
in your practice. Note if you predict that your goal will be met on initial measurement, this might not be
considered as suitable topic for a QI project. Then devise a plan or process for collecting the data (Table e-
98.2).
2. Do
Set your plan in motion.

Make baseline measurements in an unbiased manner for appropriate number of cases.
Collect your data.
3. Study. Assess your baseline data and compare the data with both the predicted result and the desired target.
If the results did not meet your performance goal, determine root causes and factors, which you attribute the
results. The team needs to retrospectively investigate the problem and explore all possible causes until the true
root cause can be established. After identifying the root cause, attempts are made to identify corrective
measures. However, if the results met the desired performance level, institute a plan to sustain the gain and
remeasure at appropriate intervals.
4. Act. Consider what can be done to address the root causes for not achieving the performance target.
Implement your improvement plan before remeasurement (Table e-98.3).
Post-PQI Project PDSA Cycle (Cycle No. 2)

Apply the improvement plan and repeat the cycle. Set the new measurements in an appropriate number of
cases/data points and analyze the remeasurement data. Determine whether the project goal has been met or
whether additional action is needed. The PDSA cycle can be repeated until the goal is met or until an end point
is otherwise determined. If you reached your desired goal, make the improvement process routine and perform
intermittent PDSA cycle to sustain the improvement.
Group PQI Projects

Based on the ABR, the group is defined as “Two or more diagnostic radiologists, radiation oncologists, or
medical physicists of the same or different disciplines, sharing a common central organizational structure, who
work together to provide patient care, regardless of individual contractual affiliations or relationships. These
diagnostic radiologists, radiation oncologists, or medical physicists may provide services at single or multiple
facilities or locations in a variety of clinical settings, including hospitals, offices, or patient-imaging centers.”
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Table e-98.1 Comparison of Dose Index Registry as an Example of National Radiology Data
Registry and “RADPEER”
RADPEER Dose Index Registry
Prior data 6 months 6 months

needed
Radiologists Processing fee of $50 For physicians at facilities that

must RADPEER group ID number register on or after July 15, 2014, in
submit to RADPEER physician ID number addition to NRDR participation fees:
ACR A signed RADPEER Practice Quality ACR member rate: $199 per
Improvement (PQI) AGREEMENT physician per year.
affirming that the radiologist intends to Nonmember rate: $299 per
use RADPEER as a PQI project. This physician per year
includes confirmation from the NRDR participation fee schedule:
Department Chair/Chief, since he or she There is a one-time facility
will be participating in his or her registration fee of $500 for NRDR.
performance improvement plan. In addition, there is an annual fee
based on the number of radiologists
practicing at a facility and the
number of sites included in a facility
(from $500 to $10,000).
Choose a single person at facility to
be the Facility Administrator.
Multicenter facilities will need to
register “master” and “child”
facilities.
Send ACR a signed copy of the
NRDR Participation Agreement by
email (nrdr@acr.org), fax, or mail.
Submit data to the selected
databases.
Submit payment.
ACR will Acknowledgment of PQI agreement and The ACR will verify that the facility
provide 6-month baseline PQI report has participated in dose index
Due date of subsequent PQI report (9 registry during the baseline and
months from date of baseline report) post-implementation data collection
periods.
If the facility has supplied the
information listed earlier to the ACR
and has responded adequately to
any requests for resolution of data
anomalies, the ACR will notify the
ABR and the facility by e-mail that
the project has been successfully
completed.
Diplomates must sign on to their
ABR personal database at
www.abronline.org in order to
officially attest to their participation
in the project.
At Signed RADPEER PQI Check List A statement of how closely the

completion Baseline and follow-up PQI report target measure was approximated.
of data Practice Improvement Plan
collection,
the
radiologist
will submit
to the ACR.
Notes RADPEER can only be used as a project The project cannot be repeated by
if there are discrepancies at either the the same participants for additional
individual or group level. If there are no PQI credit.
discrepancies, please choose another
project.
ACR, American College of Radiology; NRDR, National Radiology Data Registry; ABR, American Board
of Radiology.
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Table e-98.2 Examples of Planning Quality Improvement Projects
IVC Filter Retrieval Reduction of Incomplete Requests of

Improvement Specimens Sent to Pathology
What is the To improve inferior vena cava To reduce the incidence of incomplete
overall goal of (IVC) filter retrieval rates in requests of specimens sent to pathology to
the project? patients who had them placed for ZERO
temporary indications
What is the Retrieval rates are reported to be Significant variation exists in the process for
gap in quality low 15%-20% in the radiological specimens' reconciliation in IR. There is lack of
of care that literature, and there are risks of consistency in the specimen labeling process.
your project having IVC filters implanted for We had an overall incidence of 2% of
aims to long-term when is no longer incomplete requisitions of specimens sent to
address? clinically indicated. pathology in IR.
What is the Patients who underwent IVC filter Patients who undergo IR-guided procedures
target placement for temporary with specimens sent to the pathology
population that indications department
will be
studied?
What is the Inclusion of “IVC filter” as an 1. Preprocedure: Include specimen labeling

intervention active problem in the electronic reconciliation as part of the briefing. 2.
that will be medical record Postprocedure: A second team member will
studied? check the specimen labels prior to delivery.
What is the 18 months 9 months

anticipated
project
duration?
What is the Retrieval rates for IVC filter placed Percentage of errors per month
baseline for temporary indications
measurement?
What will be Will be the baseline rates Will be based on our historical baseline data
the
comparison
group?
How will the Will review the percentage of Compliance with the intervention will be
intervention be patients who had the problem list evaluated with observation of 30 procedures
evaluated? updated with newly placed IVC per month.
filters
Group participation in PQI is well suited to address systems-based problems, thus is considered as an important
option. Group participation may also be more convenient for administrative purposes, especially in interventional
radiology with a higher incidence of patients' complaints related to interventional procedures than diagnostic
examinations (6).
The main feature of group PQI, comparing to individual projects, is the requirement of group meetings to ensure
meaningful participation of members in the process. Group meetings enhance productive interactions among the
participants in performing quality measurements and assessments and implementing practice improvement
actions relevant to the system in which the participants practice.
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Table e-98.3 Examples of PDSA in Quality Improvement Projects
Radiation Optimizing Radiation Use during Reducing Door-to-

Protection of Fluoroscopic Procedures (4) Puncture Times for Intra-
Patients in arterial Stroke Therapy
Interventional (5)
Radiology (3)
Plan Plan to assess the Plan to collect, analyze, and Plan to retrospectively
status of radiation feedback patient exposure during identify delays to the
doses imparted to fluoroscopic procedures. Collect neurointerventional suite
patients and check if data from radiology information after patients' arrival to
they are within system database, audio and video emergency department.
international recording systems in interventional Data on sources of delay
standards. Gather radiology suite to assess are gathered. It was
data from communication and radiation use, deemed that a major source
interventional rooms and dose reports from of delay was the late
and dosimetry. interventional angiographic system. activation of key team
Investigate the Based on measurements, set the members. The sequential
frequency of best interventional radiology suite activation of the
procedures for as a target and compare with the multidisciplinary team
patients, patient others. Plan to reduce patient members also was another
doses, and availability radiation exposure while source of delay. Plan to
of staff protection. maintaining overall system implement process changes
Plan to implement performance at a single center. to reduce the overall door-
changes to reduce to-puncture time interval.
the possible
increases in radiation
doses.
Do Adopt standards of Standardize existing imaging Early neurointerventional

safety for protection. protocols. Modify the settings in activation system is
Change the existing the rooms with lower performance implemented. The
protocols to the to the target level and collect the neurointerventional fellow is
standards to reduce data. alerted before imaging
the patients' dose acquisition to ready the
without comprising on suite and assemble all
image quality. Now, necessary team members in
collect the data. parallel with the completion
of imaging and treatment
decision making. Collect
data.
Study Comparing data Data show that novices have delay Data reveals documenting
collected from in decision making to step off the time delays is not enough
previous phase pedal and terminate the because some data for
shows patients are fluoroscopic sequence. In contrast patients is missing. High
not perfectly of experts, they also spend time on case-to-case variability
protected from considering nonproductive reflects the lack of
radiation. Causes branches of decision tree. standardized approach. To
include lack of routine quantify exact source of
measurement of dose delay, data collection
values and should be anchored by key
documentation in time points during patient
medical records, lack triage and treatment
of attention to dose including patient arrival,
quantities, and start of neuroimaging,
standards of patient neurointerventional suite
safety not fully arrival, and groin puncture.
adopted.
Act Dosimetry should Improve planning skills and A formal process of

become routine for execution for novices. documenting time delays is
patients. Protocols Predetermined selection of the necessary. A unique
should be adopted to cues. Finding feedback channels protocol to be implemented.
educate staff, in order that do not require fluoroscopy, for Data to be gathered in key
to pay attention to example, watching the back of the time points.
dose quantities and guidewire or monitoring tactile
manage the dose cues.
acquired. Standards
should be optimized
for the department.
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Standards for Group PQI Process
For the group PQI process, leader of the group must be identified. This will facilitate group affairs such as
scheduling meetings; taking attendance and keeping minutes of meetings; and coordinating data collection,
analysis, and review as well as improvement planning and implementation.
Participants' names must be documented beside the title and description of the project as well as start and end
dates. Each group member is required to attend at least three meetings with minutes kept for each participant.
These meetings are mandatory whether the project is society-sponsored, registry, or group-designed.
Participants must have access to all of the documentation, including meeting minutes and any additional relevant
data. Group members must participate meaningfully in the project, and when a PQI project is completed, they are
required to write a paragraph of self-reflection, stating how the project positively impacted their own practice
and/or patients.
Leader needs to sign off the project before receiving ABR MOC Part 4 credit. After completing the project, each
radiologist participant will receive individual credit from the ABR. Attestation is needed to be completed through
participant's account.
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Standards for Group PQI Project
Preferred projects in group PQI are nationally endorsed ones that include measures directly related to patient
care. The goals and measures of any project should be relevant to each physician's practice, with the potential
to improve care.
Society-sponsored, preapproved PQI projects, including registries, if the project is relevant to the group's
practice, may be useful. Following the title of each project, details such as goals and metrics are discussed.
The society-sponsored projects can be used as a framework for designing a group PQI initiative that is more
pertinent to a particular group's clinical practice.
Group-designed PQI projects are designed by the group to address a gap in quality or safety in their daily
practice. Although approval is not required, certain standards in construction, design, and execution of the
project must be met. Documentation of process is necessary.
Group-Designed Project Criteria

Baseline PDSA Cycle (Cycle No. 1)
1. Plan. Identify project area, measure, and target (Group PQI Meeting No. 1).
As mentioned earlier, the purpose of PQI is to improve challenging issues or gaps in your practice. Select the
area that your group judge to be in need of improvement. Decide on a systems-based challenge that is relevant
to your practice. Decide the measurements your group needs to determine the current performance and your
future improvement. Create a data collection form to record the measurements. Determine a desired target to
evaluate your status after the project has been completed. Predict the baseline measurement results to adjust
your perception with reality during data analysis.
2. Do. Data collection, act your plan. Take baseline measurements in an unbiased manner for appropriate
number of cases.
3. Study. Analyze your data (Group PQI Meeting No. 2).
Arrange a meeting to assess the baseline data collected, discuss the implications of the results for the practice,
and determine the root causes of failure to achieve your desired target. Compare results with your predictions in
Plan phase.
4. Act. Action plan to improve performance (Group PQI Meeting No. 3). If you have met your measure target,
plan to sustain the improvements and terminate this project because it was not challenging. Select another topic
and proceed with a new project. If you have not met your measure target, determine the potential root causes for
not achieving target. Proceed to PDSA Cycle No. 2.
Post-PQI Project PDSA Cycle (Cycle No. 2)

After implementation of the baseline cycle, conduct a second PDSA cycle to assess the degree of any gain
achieved.
1. Plan. Implement your plan and discuss data collection process with members.
2. Do. Collect data. Set plan in motion.
3. Study. Analyze remeasurement data. Root causes for lack of achievement.
4. Act. Decision point of project (Group PQI Meeting No. 4)
Analyze the postimprovement cycle data. Assess if you have met your target.
a. If so, select another appropriate project to start, while maintaining the gains you achieved. Perform PDSA
cycles intermittently to assure maintenance of the achievements.
b. If not, continue with your project. Use the PDSA cycle(s) continuously to reach the target, or otherwise
determine an end point.
5. Self-reflection. After the project is finalized, each group member must prepare a short statement, indicating
how the project positively affected his or her practice and/or patients.
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Institution/Health Care Organization Practice Quality Improvement Projects
PQI projects can be implemented in some leading U.S. health care institutions. In health care organizations,
performance assessment is especially critical for the development of best practices that can lead to improved
outcomes in patient care (7). Features of institutional PQI projects include standards listed in group PQI
participation, with the addition of further structure as discussed in the following text. Institutional projects mostly
provide effective, intrasystem, and system-wide QI programs. Besides, these projects enhance collaboration of
different health care providers in projects of mutual interest. Institutional PQI projects feature effective participant
training, dissemination of QI principles, investment in key personnel and infrastructure, and demonstration of
outcomes. Institutions may also consider establishment of a “Just Culture” and to do root cause analyses as an
institutional PQI project (8). Also, quality improvements due to new developments in simulation technologies with
the highest impact in interventional radiology can become an area of interest for organizations (9).
Potential institutional sponsors include hospitals, health care systems, academic medical centers, medical
societies, health plans, payers, and accountable care organizations (ACOs). In some instances, leading
departments with proper infrastructure and a prior success in QI activity can guide the other departments in an
institution, leading to broad multidisciplinary collaboration.
Institutional PQI projects demand active collaboration of physicians in the design and/or implementation of the
project, such as team meetings, data analysis, implementation training, collection, submission, and review of
project data and also implementation of interventions to improve care.
The Hawthorne Effect

The “Hawthorne effect” (or the “observer effect”) is a modification of one's behavior that results from increased
attention to the problem under consideration. For example, Goodson et al. (10) reported improvement in breast
examination quality by focusing clinician attention, even without retraining in technique. A “quality improvement
curve,” described by Abujudeh et al. (11), showed an initial increase in incidence of reporting of patients' falls
(attributed to the Hawthorne effect), followed by a brief plateau phase, and finally, the effect of quality
improvement initiatives, seen possibly as a sustained true decline in the incidence of the falls (12). Thus, raising
the awareness to quality issues potentially can itself improve behaviors. PQI projects enhance this effect by
formalizing the process.
References
1. American Board of Radiology. Maintenance of Certification Part IV: ABR guide to practice quality
improvement 2014. http://www.theabr.org/sites/all/themes/abr-media/pdf/moc-dr-pqiguides.pdf. Accessed
December 24, 2014.
2. Abujudeh HH, Bruno MA, eds. Quality and Safety in Radiology. New York, NY: Oxford University Press;
2012.
3. Rehani MM, Ciraj-Bjelac O, Al-Naemi HM, et al. Radiation protection of patients in diagnostic and
interventional radiology in Asian countries: impact of an IAEA project. Eur J Radiol . 2012;81:e982-e989.
4. Duncan JR, Street M, Strother M, et al. Optimizing radiation use during fluoroscopic procedures: a quality
and safety improvement project. J Am Coll Radiol . 2013;10(11): 847-853.
5. Mehta BP, Leslie-Mazwi TM, Chandra RV, et al. Reducing door-to-puncture times for intra-arterial stroke
therapy: a pilot quality improvement project. J Am Heart Assoc. 2014;3:e000963.
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6. Salazar G, Quencer K, Aran S, et al. Patient satisfaction in radiology: qualitative analysis of written
complaints generated over a 10-year period in an academic medical center. J Am Coll Radiol . 2013;10:513-
517.
7. Abujudeh HH, Kaewlai R, Asfaw BA, et al. Quality initiatives: key performance indicators for measuring and
improving radiology department performance. Radiographics. 2010;30:571-580.
8. Abujudeh HH. “Just culture”: is radiology ready? J Am Coll Radiol . 2015;12(1):4-5.
9. Sabir SH, Aran S, Abujudeh HH. Simulation-based training in radiology. J Am Coll Radiol . 2014;11:512-
517.
10. Goodson WH III, Hunt TK, Plotnik JN, et al. Optimization of clinical breast examination. Am J Med.
2010;123(4):329-334.
11. Abujudeh HH, Aran S, Daftari Besheli L, et al. Outpatient falls prevention program outcome: an increase,
a plateau, and a decrease in incident reports. AJR Am J Roentgenol . 2014;203(3):620-626.
12. Bruno MA. The “Abujudeh curve” in radiology quality and safety research. AJR Am J Roentgenol .
2015;204(5):W606.
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Radiation Safety in Interventional Radiology
Donald L. Miller
Primary Safety Principles

1. Scatter radiation is the main source of exposure to the operator (1). Anything that reduces the patient's
radiation dose will reduce scatter and therefore reduce operator dose as well.
2. Remember TIDS: Time, Intensity, Distance, Shielding
a. Time: Limit the amount of fluoroscopy time. Use fluoroscopy only to observe objects in motion. Use last-
image-hold images or stored fluoroscopy loops as much as possible.
b. Intensity: Use the lowest fluoroscopic dose rate that yields adequate image quality. Know what the dose rate
is. Use the lowest digital acquisition rate that provides the necessary information. Remain aware of the patient
dose throughout the procedure.
c. Distance: Stay as far away from the primary beam and from the x-ray tube as possible.
d. Shielding: Wear appropriate personal protective equipment (aprons and eyewear).
3. Treat radiation like you treat iodine. Use radiation the same way that you use iodinated contrast material—
give as much as necessary, but no more; do not give it without a good reason. As the dose increases, be more
aggressive in managing its use. In particularly sensitive patients, try to limit radiation dose as much as possible.
Radiation Biology and Radiation Effects

1. Mechanism of radiation effects
a. Indirect: interaction of a photon with an atom or molecule; formation of a reactive free radical that then
interacts with DNA. The most common interaction is with water to form a hydroxyl radical.
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b. Direct: physical interaction of a photon with DNA (less common)
c. DNA damage is usually repaired within 24 hours (2). As opposed to singlestrand DNA breaks, double-strand
DNA breaks are more often repaired incorrectly. Incorrect repair can result in point mutations, chromosome
translocations, or gene fusions.
d. Repopulation of cells that are damaged beyond repair and die can take several months (2).
2. Types of radiation effects
a. Stochastic: The result of unrepaired or incorrectly repaired DNA damage in a single cell. With time,
descendants of this cell may result in a cancer. The current model used for stochastic risk is the “linear no
threshold” (LNT) model, a conservative model designed for radiation protection purposes. This states that
stochastic risk increases linearly as dose increases, and injury severity is independent of dose. The actual risk
is unknown for effective doses <100 mSv (3,4). (Effective dose is defined in the following text, under “Radiation
Dose Measurement” section.) An analogy for the LNT model is a lottery with only one “prize” (cancer); you could
win if you buy only one ticket (small amount of radiation), but you are more likely to win if you buy lots of tickets.
In the end, you either win the entire prize (develop cancer) or lose. Unlike a lottery, the chance of getting the
“prize” increases the longer you hold your “ticket.” For patients exposed at a very young age, lifetime risk is
increased, both because their lifetimes are longer and because the risk of induction of certain cancers (leukemia
and thyroid, skin, breast, and brain cancer) is greater for young patients (5).
b. Tissue reactions (deterministic effects): Large numbers of cells are damaged beyond repair and die,
resulting in injury (typically to skin and subcutaneous tissues in interventional radiology procedures). Patients
who undergo interventional procedures may be at risk for injuries ranging from transient mild erythema to skin
necrosis and bone necrosis. Radiation-induced tissue reactions are unlikely below an absorbed dose to the skin
(threshold) of 2 Gy; serious skin effects are unlikely below a skin dose of 5 Gy (2). The threshold dose
demonstrates biologic variability. The most severe injuries are typically seen only after very high skin doses (>10
Gy). Sunburn is an exact analogy with regard to threshold and severity; you can stay out in the sun for a period
of time with no ill effects, but after that time (the threshold), you are certain to develop a sunburn. How long you
can stay out in the sun safely varies from person to person. The severity of the sunburn will increase the longer
you are exposed to the sun.
Radiation Dose Measurement

All measurements of patient dose contain some degree of uncertainty related to variations in instrument
response with changes in beam energy, dose rate, and collimator size. To accommodate these uncertainties,
displayed cumulative air kerma values, for example, are permitted to deviate from the actual value by ±35% (6).
1. Skin dose: Ideally should be estimated and mapped during procedures with the potential for high-radiation
dose, but at present, this capability is not generally available on most fluoroscopes. The highest dose to any
point on the skin surface, or peak skin dose (PSD) measured in Gy, determines the severity of a radiation-
induced skin injury.
2. Cumulative air kerma (synonyms: reference dose, reference point dose, reference point air kerma,
reference air kerma, RPDose, Ka,r, cumulative dose, CD): Indicated in mGy or Gy and displayed automatically on
all fluoroscopic equipment sold in the United States since mid-2006. It is the dose at the patient entrance
reference point (PERP). For C-arm units, the PERP is located along the
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central ray of the x-ray beam, 15 cm back from the isocenter (the central point about which the C-arm rotates)
toward the x-ray tube. Cumulative air kerma is not the same as the skin dose; reference air kerma is usually
greater than PSD. When PSD estimates are not available, cumulative air kerma may be used as a guide to
indicate when patient follow-up is necessary to detect possible tissue reactions (7,8).
3. Kerma-area product (synonyms: KAP, PKA, air kerma-area product, dose-area product, DAP): The product of
the radiation dose and the area of the irradiated field, with the unit of Gy·cm2. It does not change with distance
from the x-ray tube. It is a good measure of the total energy delivered to the patient, and therefore, a good
estimator of the risk of a stochastic effect. It is not a good indicator of the risk of a tissue reaction.
4. Fluoroscopy time: Commonly used in the past, primarily because it was easy to measure and widely
available. Fluoroscopy time, measured in minutes, does not reflect the effects of fluoroscopic dose rate and does
not include the radiation dose from radiography such as digital subtraction angiography (DSA). It is a poor
indicator of patient radiation dose. For this reason, fluoroscopic units that display fluoroscopy time as the only
dose metric should not be used for complex, high-dose interventional procedures (8).
5. Effective dose: The whole body dose that is equal—in terms of the risk of a stochastic effect—to the
estimated dose delivered to a portion of the body. Effective dose (E) is measured in sievert. It must be
calculated; it cannot be measured directly. Calculations incorporate potential errors from estimation because the
stochastic risk depends on both the number of interactions that occur in a given volume of tissue and the
specific sensitivity (based on cell composition, mitotic activity, and other tissue- and host-specific factors) of that
tissue. These calculations must be made for the volume affected by the primary beam as well as for the effects
of scatter radiation throughout the rest of the body. Current techniques use computer simulation based on a
“model” body and statistical simulations of the radiation exposure. This limits their applicability for individuals and
gives only a gross approximation of E. In many online radiation risk “calculators,” E is derived using formulas
designed for radiation protection purposes that introduce additional sources of error because they do not
consider the individual's age or gender. The bottom line is that E is useful in estimating stochastic risk for
populations and for comparing relative radiation doses from different procedures, but it is not useful (and is not
recommended) for individual patients (4,9).
6. Patient radiation dose metrics should be recorded in the medical record for every interventional radiology
fluoroscopic procedure. Every available dose metric should be recorded (10).
Protecting the Patient (8,11)

Proper technique is essential for managing radiation dose.
1. Equipment positioning
a. Maximize source-to-skin distance: Reduce skin dose by keeping the skin as far away from the tube as
possible (raise the table as high as is comfortable for the operator).
b. Minimize source-to-image receptor distance: Keep the image receptor (flat panel or image intensifier) as
close to the patient as possible.
2. Equipment settings
a. Collimate: Reducing the size of the radiation field decreases scatter to the patient and the operator, improves
image quality, and helps with dose-spreading (see the following text).
b. Minimize fluoroscopy dose rate: Use dose-reducing pulsed fluoroscopy whenever possible. Reduce both
the fluoroscopy pulse rate and the dose per
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pulse to the lowest values that still yield adequate image quality for the clinical task. In most circumstances,
fluoroscopy at 7.5 or 15 pulses per second and “low” or “normal” dose yields acceptable image quality.
3. Operator technique
a. Control the number of images: Modern fluoroscopic units make it very easy to perform DSA continuously at
2 images per second or faster for prolonged periods of time. Excessive numbers of images add radiation dose
but provide no additional information. Each image should provide useful information for diagnosis or
documentation. See Chapter 1 for suggested arteriographic image acquisition programs.
b. Use fluoroscopy only to observe motion in real time: Last-image-hold fluoroscopy images and stored
fluoroscopy loops can be used to review image findings seen on fluoroscopy without adding additional patient
dose.
c. Avoid magnification when possible: Magnification often requires a higher fluoroscopic dose rate.
d. Use dose spreading to minimize skin dose: 5- to 10-degree angulation of the tube, either left to right or
craniocaudal, in conjunction with tight collimation, will move the radiation field on the patient's skin and help
prevent a “hot spot” where the skin dose exceeds the threshold for radiation-induced skin effects. However, this
must be planned and performed from the beginning of the case (12).
Patient Radiation Management (7,8,11)

1. Before the procedure: Be aware of the factors that predispose to radiation injury, either due to a lowered
threshold for deterministic effects or to the likelihood of administering a relatively high-radiation dose.
a. Diseases: ataxia-telangiectasia, collagen vascular diseases, diabetes mellitus
b. Obesity (13)
c. High-dose procedures: embolization, transjugular intrahepatic portosystemic shunt (TIPS) creation,
angioplasty, or vascular stent placement in the abdomen or pelvis (8)
d. Previous radiation to the same skin entrance site
e. Pediatric patients (stochastic risk)
2. During the procedure: Be aware of the radiation dose at all times but especially after the cumulative air
kerma exceeds 3 Gy.
a. Optimize radiation dose: Use the least amount of radiation possible that provides adequate image quality for
the clinical purpose.
b. If the cumulative air kerma approaches or exceeds 5 Gy, consider limiting further radiation or postponing a
nonessential portion of the procedure.
3. After the procedure: Be aware of the amount of radiation used and institute follow-up if necessary.
a. Record radiation dose metrics in the medical record.
b. If the cumulative air kerma exceeds 5 Gy, institute a follow-up plan and inform the patient to inspect the
skin at the beam entrance site at 2 to 4 weeks postprocedure (8,14).
c. Obtain follow-up from the patient; assume that any skin effects at the site of the entrance beam that conform
to the radiation field are because of the radiation unless proved otherwise.
Protecting the Operator (1,8,15)

Generally, controlling patient radiation dose reduces scatter and limits operator dose (1). This is a win-win
situation: Reducing the patient's dose also reduces your dose.
1. Personal protective equipment
a. Apron: A properly fitted apron that provides adequate coverage at the neck and arm holes is essential, both
for radiation protection and for ergonomic
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reasons (to prevent cervical and lumbar spine injury from long-term use). If the operator's back will be turned
away from the beam, a wrap-around apron that shields the back is required. For women especially, if the
armholes are too large, portions of the breast may not be protected adequately. The lead equivalent thickness of
the apron may be mandated by state or local regulations; if not, it can be chosen to match the wearer's level of
exposure. The most common thickness is 0.5 mm lead equivalent, which attenuates 97% to 99% of the incident
radiation.
b. Eyewear: The lens of the eye is more sensitive to radiation than previously thought (16). Operators are at a
risk for cataract formation. Leaded eye-glasses are necessary when ceiling-mounted shields cannot be used.
Eyewear with side shields is essential, both for radiation protection and for splash protection.
c. Lead gloves: Radiation-attenuating surgical gloves may have some value if the operator's hands must be
near the primary beam. Mild to moderate radiation attenuation must be balanced against possible increases in
procedure time because of the reduced dexterity. These gloves not only do not protect hands placed in the
primary beam but, in this situation, they cause also an increase in dose to the patient, the operator, and the
operator's hands because of the effects of the automatic brightness control in the fluoroscopic unit (8).
2. Mobile shielding
a. Table-mounted: Flexible leaded shielding suspended from the side of the table blocks scatter radiation from
below the table and protects the operator's legs. Movable floor-standing shields may be used for the same
purpose but can be less convenient.
b. Ceiling-mounted: A clear leaded shield suspended from the ceiling on a movable boom attenuates scatter
directed toward the operator's head and neck. Some form of eye protection is still required for protection against
splashes.
c. Shielding on the patient: Radiation-attenuating, sterile disposable pads are commercially available and can
be used to decrease the scatter radiation to the patient or the operator (1). They must be kept out of the primary
beam.
3. Positioning
a. Keep as far away from the primary beam as possible. Keep your hands out of the primary beam. For
vertebral augmentation procedures, use an instrument when positioning needles and a cement injector with a
long tube. For angiography, use a power injector instead of hand injection whenever possible. Step out of the
procedure room when performing DSA.
b. Position the tube away from yourself. Scatter radiation is distributed asymmetrically, with much more on
the tube side of the patient than on the image receptor side. Position the frontal plane so that the tube is below
the table to protect your upper body. If possible, position the lateral plane so that the tube is on the opposite side
of the patient from you. Fluoroscopic units with the tube fixed over the table should not be used for interventional
procedures.
References
1. Miller DL, Vañó E, Bartal G, et al. Occupational radiation protection in interventional radiology: a joint
guideline of the Cardiovascular and Interventional Radiology Society of Europe and the Society of
Interventional Radiology. J Vasc Interv Radiol . 2010;33:230-239.
2. Balter S, Hopewell JW, Miller DL, et al. Fluoroscopically guided interventional procedures: a review of
radiation effects on patients' skin and hair. Radiology. 2010;254:326-341.
3. Hendee WR, O'Connor MK. Radiation risks of medical imaging: separating fact from fantasy. Radiology.
2012;264:312-321.
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4. Hendee WR; for the International Organization for Medical Physics. Policy statement of the International
Organization for Medical Physics. Radiology. 2013;267:326-327.
5. United Nations Scientific Committee on the Effect of Atomic Radiation. Sources, effects and risks of
ionizing radiation. UNSCEAR 2013 Report. Volume II. Scientific Annex B. Effects of radiation exposure of
children. New York, NY: United Nations; 2013.
6. U.S. Food and Drug Administration. Performance standards for ionizing radiation emitting products.
Fluoroscopic equipment. 21 CFR 1020.32.
7. Stecker MS, Balter S, Towbin RB, et al. Guidelines for patient radiation dose management. J Vasc Interv
Radiol . 2009;20:S263-S273.
8. National Council on Radiation Protection and Measurements. Radiation Dose Management for
Fluoroscopically Guided Interventional Medical Procedures. NCRP Report No. 168. Bethesda, MD:
National Council on Radiation Protection and Measurements; 2010.
9. Harrison JD, Streffer C. The ICRP protection quantities, equivalent and effective dose: their basis and
application. Radiat Prot Dosimetry. 2007;127:12-18.
10. Miller DL, Balter S, Dixon RG, et al. Quality improvement guidelines for recording patient radiation dose
in the medical record for fluoroscopically guided procedures. J Vasc Interv Radiol . 2012;23:11-18.
11. Miller DL, Balter S, Schueler BA, et al. Clinical radiation management for fluoroscopically guided
interventional procedures. Radiology. 2010;257:321-332.
12. Pasciak AS, Jones AK. Does “spreading” skin dose by rotating the C-arm during an intervention work? J
13. Bryk SG, Censullo ML, Wagner LK, et al. Endovascular and interventional procedures in obese patients:
a review of procedural technique modifications and radiation management. J Vasc Interv Radiol . 2006;17:27-
33.
14. Steele JR, Jones AK, Ninan EP. Quality initiatives: establishing an interventional radiology patient
radiation safety program. Radiographics. 2012;32:277-287.
15. Schueler BA, Balter S, Miller DL. Radiation protection tools in interventional radiology. J Am Coll Radiol .
2012;9:844-845.
16. Vano E, Kleiman NJ, Duran A, et al. Radiation-associated lens opacities in catheterization personnel:
results of a survey and direct assessments. J Vasc Interv Radiol . 2013;24:197-204.
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Infection Control and Sterile Technique in Interventional
Radiology
Daniel Chan
Sterile technique in the context of medical and surgical procedures refers to the process used to prevent
contamination of wounds and other sites by organisms that can cause infection. The goal of sterile technique is
the prevention of surgical site infections (SSIs).
There are over 51.4 million surgical procedures performed each year. SSIs are the third most frequently reported
nosocomial infections which contribute to increased health care costs. Understanding and adhering to sterile
technique guidelines plays an integral first-line role in the prevention of SSIs. Prevention of SSIs in the
interventional suite focuses primarily on adherence to aseptic practices related to personnel attire, proper hand
hygiene, gowning, gloving, prepping, draping, maintaining a sterile field, and sanitation of the interventional
radiology (IR) suite.
Sterile technique is the first line of defense in prevention of SSIs and practices have existed since the time of
Joseph Lister, the father of modern surgery. Whereas
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some sterile technique processes may seem intuitive, an organized process and commitment to accepted
practices is imperative. Effective incorporation of sterile technique and infection control practices requires a
multidisciplinary and cooperative approach.
Definitions
1. Surgical site infection
The Centers for Disease Control and Prevention (CDC) define an SSI as an infection at the site of surgery
within 30 days of an operation or within 1 year of an operation if a foreign body is implanted as part of the
surgery. The CDC has further classified an SSI into either incisional or organ/space. Contamination with an
organism is the precursor for SSIs. For most SSIs, the source of pathogens is the endogenous flora of the
patient's skin, mucous membranes, or hollow viscera. Exogenous sources of SSIs pathogens include
surgical personnel, the operating room environment, all tools, instruments, and materials brought into the
sterile field during a procedure. The most common organisms involved in SSIs are Staphylococcus aureus,
coagulase-negative staphylococci, Enterococcus species, and Escherichia coli .
2. Interventional radiology scope—procedures, environments, and modalities
IR procedures can be classified as vascular and nonvascular interventions. Procedures are performed with
different imaging modalities, in various environments at the bedside or in procedure suites. Different
environments include an ultrasound, computed tomography (CT), or magnetic resonance imaging (MRI)
suite, or most commonly an angiographic suite. Multiple imaging modalities are utilized concomitantly, for
example, ultrasound to obtain vascular access in the angiography suite. Each specific modality and
environment has its unique instruments and special considerations.
Bedside procedures include but are not limited to vascular access procedures, drainage procedures, and
biopsies, frequently performed with ultrasound guidance which incorporates the imaging unit and probes
within the sterile field. Procedures involving the CT or MRI suites need to take into account the appropriate
space needed to maintain a sterile field between the patient and equipment. For example, there should be
an assessment to provide appropriate clearance of needles and catheters during scanning. The image
intensifier of an angiographic unit or portable C-arm in an operating room or office-based environment is
incorporated in the sterile field. Multiple accessory units (e.g., ultrasound, generators) are also within the
sterile field including their various cords, probes, and attachments.
3. Procedure classification—sterile and clean procedures
The National Academy of Sciences/National Research Council has divided surgical wounds into four
classes: clean, clean-contaminated, contaminated, and dirty. Each confers a different risk of infection.
a. Clean: A procedure is regarded as clean if the gastrointestinal tract, genitourinary tract, or respiratory
tract is not entered; if inflammation is not evident; and if there is no break in aseptic technique. Examples
include:
(1) Vascular procedures: angiography, angioplasty, thrombolysis, stent and endograft placement,
embolization including uterine artery and chemoembolization of liver tumors, central venous access, inferior
vena cava filter placement, and transjugular intrahepatic portosystemic shunt (TIPS) revision
(2) Nonvascular procedures: vertebroplasty/kyphoplasty and percutaneous biopsy
b. Clean-contaminated: A procedure is regarded as clean-contaminated if the gastrointestinal, biliary, or
genitourinary tract is entered; if inflammation is not evident; and there is no break in aseptic technique.
Examples include:
(1) Vascular procedures: TIPS creation
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(2) Nonvascular procedures: transrectal or transgastric percutaneous biopsy, percutaneous gastrostomy or
gastrojejunostomy tube placement, genitourinary procedures, tumor ablation, liver and biliary procedures
c. Contaminated: A procedure is regarded as contaminated if entry into an inflamed or colonized
gastrointestinal or genitourinary tract without frank pus or if a major break in aseptic technique occurs.
Examples include:
(1) Nonvascular procedures: presumed infected genitourinary and biliary procedures
d. Dirty: A procedure is regarded as dirty if it involves entering an infected purulent site such as an abscess,
a clinically infected biliary or genitourinary site, or perforated viscus. Examples include:
(1) Nonvascular procedures: abscess drainage
Aseptic Technique and Environmental Controls

1. Prepping, draping, and maintaining a sterile field
a. Control of traffic
(1) The interventional suite is not sterile. Organisms are present in the air, on dust particles, and on dirt in the
environment. The procedure table, walls, floors, cabinets, IR equipment, and other stationary fixtures in the suite
may harbor microorganisms and therefore are potential sources of infection.
(2) The interventional suite should be treated as an “operating room-like” environment. The IR suite should be
restricted to essential personnel only. The personnel who work in this clinical area need to be trained to follow
strict aseptic practices and use proper procedure room attire.
(3) The doors to the IR suite should remain closed during procedures and between procedures to decrease the
risk of transmission of infective microorganism into the suite and potentially onto the sterile field and patient.
(4) Other ancillary personnel (e.g., anesthesia respiratory, intensive care unit [ICU] personnel, and medical
personnel in training) who are required to be in the suite during the procedure must also follow requirements for
proper attire and aseptic practices.
(5) Non-IR personnel who need access the clinical area must be redirected via another route other than through
the procedural suite. If personnel need to enter the IR suite, they must don surgical attire, hats, and masks.
b. Room turnover and cross-contamination
(1) Any item that has been in contact with blood, tissue, or bodily fluids potentially is contaminated with infectious
pathogenic microorganisms. The interventional procedure suite and work surfaces should be properly cleaned
and disinfected after every procedure to decrease the amount of dust and microorganisms.
(2) Patient devices (e.g., arm holders) and areas around the procedure table must be cleaned prior to the next
procedure to decrease the chance of cross-contamination.
(3) The floors in the procedure suite may or may not be visibly soiled with blood or bodily fluids but are required
to be properly cleaned and disinfected between every procedure.
(4) Immediately after use, disposable supplies should be discarded in designated waste containers. All regulated
medical waste should be placed into red bags and designated sharp containers. In this regard, all personnel
performing the procedure must be protective of each other and employ safety techniques such returning needles
and sharps (no capping) to their proper designated containers on the procedure table.
(5) Linen and team members' protective clothing soiled with body fluids are to be handled as little as possible to
prevent contamination of the person
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handling the linen. Gloves should be worn whenever handling soiled linen. Soiled linen must be placed into the
designated linen receptacle.
(6) At the conclusion of the day's schedule, all surfaces and equipment must be thoroughly cleaned.
c. The sterile field
The creation of the sterile field in the IR suite incorporates the surgical drapes, sterile supplies, and
instrumentation. All items introduced to a sterile field should be sterile and introduced by a method that maintains
the items sterility and integrity.
(1) Items should be inspected for
(a) Expiration dates, if applicable. If an item is expired, it should not be used. The item should be discarded,
reprocessed, if suitable and recommended by the manufacturer, or returned to the company for credit. It is
advisable to inspect and rotate inventory to prevent the expiration of sterile supplies.
(b) Package integrity (holes, tears, etc.)
(c) Sterile processing indicators (ensuring the proper parameters for sterilization have been met)
(d) Internal package contents that meet the consumer's expectations and the manufacturer's guarantee (sterile
device degradation)
(2) According to the CDC, sterile gowns and drapes are used to create a barrier between the surgical field and
potential sources of bacteria. Wide variations in draping products, patient populations, and limited study data and
study design make it difficult to understand the relationship between sterile draping and surgical site wound
infections.
(a) Draping materials and the size of the drape should be determined by the anticipated procedure.
(b) All invasive procedures should be performed using sterile instruments and supplies. The team should
practice aseptic technique when opening and dispensing supplies to the sterile field. Sterile items should be
handed to or placed gently and securely on the sterile field. Opening sterile supplies in wrapped, peel pouched,
or rigid containers should be away from the individual, and the sterile item should not rub over the outer,
unsterile, adhesive edges. Unsterile arms or hands should not pass over the sterile field. A safe distance should
remain between the sterile field and the individual who is performing patient care. Establishing patterns of
movement around the sterile field and keeping sterile areas in view can reduce accidental contamination.
d. Back table preparation
(1) There is often pre-preparation of a “back” table in IR procedures. The table usually contains the initial sterile
instruments, devices, and containers. During the course of a procedure, the table is often used to place
additional sterile instruments, equipment, medications, and devices. Although there is a lack of evidence and
consensus regarding certain guidelines regarding the back table, the following recommendations were made in
recent multisociety guidelines:
(2) The recommended time frame between preparation and the use of the back table is <1 hour, preferably
immediately before the procedure.
(3) The person or persons preparing the back table need to be wearing sterile gowns and adhere to sterile
technique guidelines.
(4) The recommended location for preparation of the back table is only inside the IR suite in which it is intended
to be used. The table must remain in an environment in which it can be continuously monitored to be sure no
breaks in sterility occur.
(5) A new table meant for a different procedure cannot be prepared in a room that is currently being used for a
procedure.
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(6) A cover drape extending over the edges of the sterile pre-prepared back table is not recommended. It is
preferable that no table cover be used. Any cover placed over the sterile pre-prepared back table should not
extend over any edge of the table.
2. Personnel—attire, hand hygiene, gowning, and gloving
a. Proper attire
(1) The purpose of surgical attire is to promote a high level of cleanliness and hygiene within designated
environments. The surgical attire is designed to interfere with the passage of microorganisms from personnel to
the patient and the IR environment and from patient to personnel.
(2) Hospital-laundered (provided) surgical attire (scrubs) must be worn in the procedure suite and should not be
worn outside the department or the hospital—refer to your hospital/departmental policy. Fresh scrubs should be
worn each day. Staff who are required to wear hospital-laundered surgical attire who need to go outside the
building should change out of their attire before leaving the building or change into new surgical attire before
returning to the IR procedure suite. Surgical attire should be changed or removed when it becomes visibly soiled
or wet.
(3) Hair is a gross contaminant harboring bacteria. Hair attracts bacteria and shedding of hair is in proportion to
its length, oiliness, and curliness. Covering the hair with a hat helps to prevent introducing contaminants. Hats
must be the first item of apparel donned prior to entering the procedural suite. Hats are usually disposable
(single use). Reusable cloth hats should be laundered when soiled and between each wearing. The use of
disposable hats is preferred. Hats should be removed and deposited in a designated receptacle when leaving
the procedure suite. During invasive procedures, hair covers (hats) must be worn to ensure that all hair is
completely covered.
(4) A surgical mask must be worn to cover nose and mouth completely. Masks should conform to the nose to
provide a secure fit. The mask should be tied securely at the back of the head and the bottom ties at the nape of
the neck to prevent venting, which can allow for unfiltered air to escape. A surgical mask is either on or off; it
should never be allowed to dangle around the neck where it can become heavily contaminated with
microorganisms. Masks with face shields or protective eyewear with side shields must be worn when splashes,
sprays, splattering of blood, or other body fluids is anticipated. Masks should be removed and discarded after
use and when they become wet or soiled. Masks that have been worn are contaminated with droplet nuclei.
Handling the mask after use can transfer microorganisms from the mask to the hands. Masks should be disposed
in a designated receptacle prior to leaving the suite. Hands should be washed after mask removal.
(5) Sterile gowns must be worn when aerosolization or splattering of blood or other body fluids is anticipated.
Gowns must not permit passage of blood or body fluids.
(6) Gloves are worn when direct contact with blood and/or body fluids is expected, but the patient must be
screened for latex allergies. The use of gloves does not replace the need for hand hygiene.
b. Hand hygiene
(1) Hand hygiene requires washing hands with either plain or antimicrobial soap and water or the application of
an alcohol-based skin rub. When hands are visibly soiled, or contaminated with proteinaceous material, hand
washing must be done preceding application of an alcohol-based hand rub.
(2) Surgical hand scrub is performed immediately prior to gowning and gloving in preparation of a procedure.
Traditional antimicrobial scrub agents
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are detergent-based products containing alcohol, iodine, or chlorhexidine gluconate. The purpose of the surgical
hand scrub is to remove dirt, skin oils, and transient microorganisms. This process reduces the amount of
residing microorganisms on the nails, hands, and lower arms to as low a level as possible and to prevent growth
of microorganisms for as long as possible by mechanical washing and use of chemical agents. The purpose of
the surgical hand scrub is to prevent the transfer of microorganisms from personnel to patients, from patients to
personnel, and from patient to patient.
(3) Fingernails should be short and clean. Long nails may puncture protective gloves or potentially scratch a
patient during patient handling or transfer. Health care workers who wear artificial nails are more likely to harbor
gram-negative pathogens on their fingertips than those who have natural nails. Wearing nail polish or chipped
nail polish leads to greater numbers of bacteria than natural nails or freshly polished nails.
(4) Use of alcohol-based hand rubs are common and have been shown to save time and reduce costs. There
are studies that also show they can be more effective than products used in the traditional scrub method.
Alcohol-based hand rub products, however, do not take the place of washing and mechanical action when hands
are visibly soiled or contaminated with proteinaceous material.
c. Gowning and gloving procedure
(1) After the hand scrub procedure has been performed, the hands and arms must be thoroughly dried before the
gown is donned. If the hands and arms are not thoroughly dried, contamination of the gown may occur with
strike-through from organisms contained in moisture on the skin.
(2) The sterile gown must be constructed of material that provides a barrier to prevent the passage of
microorganisms from the interventional team to the patient and from the patient to the interventional team. The
gown material should provide a protective barrier for microorganisms and fluids. The gowns should be durable
and resistant to tears, punctures, and abrasions and lint-free.
(3) Sterile gloves are a barrier that is intended to prevent passage of microorganisms from the scrubbed person
to the patient and from the patient to the scrubbed person.
(4) Sterile gloves should be selected according to desired durability, size, and compatibility. Latex-free gloves
should be used when personnel or the patient have latex allergies.
(5) Wearing a second pair of gloves over the first pair is known as “double gloving.” Double gloving has been
shown to reduce hand contact with the patient's blood and/or body fluids during procedures.
Suggested Readings
Ad Hoc Committee of the Committee on Trauma, National Research Council. Postoperative wound infection:
the influence of ultraviolet radiation of the operating room and various other factors. Ann Surg.
1964;160(suppl 2):1-192.
Association for the Advancement of Medical Instrumentation. ANSI/AAMI 2006—Comprehensive Guide to

Steam Sterilization and Sterility Assurance in Health Care Facilities. Arlington, VA: Association for the
Advancement of Medical Instrumentation; 2006:24, 36, 73.
Association of Perioperative Registered Nurses. Recommended Practices for Maintaining a Sterile Field.
Colorado, CO: Association of Perioperative Registered Nurses; 2008: 565-573.
Association of Perioperative Registered Nurses. Recommended practices for maintaining a sterile field. In:
Standards, Recommended Practices, and Guidelines. Denver, CO: Association of Perioperative Registered
Nurses; 2008:614-615.
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Chambers CE, Eisenhauer MD, McNicol LB, et al. Infection control guidelines for the cardiac catheterization
laboratory: society guidelines revisited. Catheter Cardiovasc Interv. 2006;67:78-86.
Chan D, Downing D, Keough CE, et al. Joint practice guideline for sterile technique during vascular and
interventional radiology procedures: from the Society of Interventional Radiology, Association of
Interventional Radiology Standards of Practice Committee, and Endorsed by the Cardiovascular
Interv Radiol . 2012;23(12):1603-1612.
Dalstrom DJ, Venkatarayappa I, Manternach AL, et al. Time-dependent contamination of opened sterile
operating-room trays. J Bone Joint Surg Am. 2008;90:1022-1025.
Herron DM, Gagner M, Kenyon TL, et al. The minimally invasive surgical suite enters the 21st century. Surg
Endosc. 2001;15:415-422.
Katzen BT, Becker GJ, Mascioli CA, et al. Creation of a modified angiography (endovascular) suite for
transluminal endograft placement and combined interventional-surgical procedures. J Vasc Interv Radiol .
1996;7:161-167.
O'Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the prevention of intravascular catheter-related
infections. Centers for Disease Control and Prevention. MMWR Recomm Rep. 2002;51(RR-10):1-29.
Sikkink CJ, Reijnen MM, Zeebregts CJ. The creation of the optimal dedicated endovascular suite. Eur J Vasc
Endovasc Surg. 2008;35:198-204.
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Nursing Management during Angiography and Interventional
Procedures
Evelyn P. Wempe
DéAnn O. McNamara
Krishna Kandarpa
The objective of this chapter is to offer guidelines for developing clinical standards of practice related to nursing
care and management of patients during all phases of interventional radiology (IR) procedures. Although the
emphasis here is on nursing, all members of the IR patient care team should be knowledgeable and familiar with
each patient's individual circumstances. The Joint Commission provides National Patient Safety Goals which are
directed toward improvement in patient safety, organizational performance, documentation, and quality of care. It
is the IR nurse's professional responsibility to demonstrate competency, collegiality, and patient advocacy. Good
practice requires a culture of commitment to patient safety, effective communication, efficiency, and teamwork.
The IR nurse must maintain patient privacy and ensure confidentiality, safe transportation of patients, adherence
to departmental policies regarding safe attire, infection control, and other safety practices in the procedural area
and throughout the patient's care.
Preprocedure Nursing Considerations

In preparation for an IR procedure, the nurse must thoroughly review the patient's case, clinical history,
presentation, and indication for the procedure—working to ensure safe conditions for the patient's care. Although
the workflow and patient movement through the continuum of care differs for inpatients and outpatients (OPs),
those who undergo OP or same-day admit procedures require the same workup as inpatients. For all patients,
the preparation begins with a review of the chart for preprocedural nursing assessment and development of a
plan of care.
For OPs in particular, the nurse should be familiar with the case prior to conducting preprocedure phone screen,
which is best accomplished 72 to 48 hours in advance in order to address all needs. The OP phone screen
familiarizes the nurse with the patient and provides an opportunity to educate the patient about the procedure
and what to expect upon arrival to the department and to address the patient's concerns. The nurse should
1. Follow established criteria at time of scheduling the procedure to determine whether the patient is a candidate
for phone screen, or if an appointment for face-to-face evaluation is needed, and whether an anesthesia consult
may be necessary.
2. Hospital policy regarding allowing a family member to provide/receive information about the patient within the
context of the preprocedure phone call must be followed.
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Procedure-Specific Considerations
1. Review chart, history, indication for procedure.
2. Review of systems: conducted by the nurse to learn of any clinical conditions that may require additional
attention. This can be done during a phone screen prior to the day of the procedure.
a. Cardiovascular: coronary artery disease (CAD), congestive heart failure (CHF), valvular disease, arrhythmia
b. Respiratory: cystic fibrosis, asthma obstructive sleep apnea, use of continuous positive airway pressure
(CPAP), noninvasive positive-pressure ventilation (NPPV), or bilevel positive airway pressure (BIPAP), O2
requirements, artificial airway
c. Gastrointestinal (GI): dietary restrictions/requirements, nutrition/metabolic screening
(1) Diarrhea, dental problems, difficulty swallowing, persistent nausea/vomiting (N/V), appetite, weight loss/gain,
bone marrow transplant (BMT), tube feeds, total parenteral nutrition (TPN), end-stage diseases, esophageal
disease/surgery, major burn/trauma, major GI or oral surgery, myocardial infarction (MI)/stroke, diabetes, surgical
patient more than 70 years old, pressure ulcer
d. Genitourinary: problems with urination, anuria, ostomy, suprapubic Foley catheter
e. Reproductive/sexual health: female; last menstrual period (LMP), pregnancy, breastfeeding
f. Tubes/lines/drains: such as percutaneous nephrostomy tubes, biliary tubes, abscess drains, blood
suction/drains, chest tubes, peritoneal abscess drains
g. Skin assessment: rashes, open wounds/sore, discoloration, redness, itchiness
h. Musculoskeletal : difficulty walking, moving extremities, assistive devices for walking, Morse Falls Scale,
deteriorating/debilitating conditions affecting mobility
i. Internal/external devices: pacemaker/defibrillator, joint/valve, piercings/tattoos, medication patches,
subcutaneous ports, external catheters
j. Pain: current, chronic, new onset; location, character duration, frequency scores per hospital policy
k. Assistive/prosthetic devices: dentures, glasses/contacts, hearing aids, crutches/cane, walker
l. Past anesthesia/sedation history: IR procedures are routinely performed under moderate sedation or some
form of anesthesia (monitored anesthesia care [MAC] or general anesthesia). It is important for the nurse to be
familiar with patient's existing documented history and physical (H&P), including surgical history in which
anesthesia was utilized:
(1) Head/neck surgery/cancer
(2) Prior complications with anesthesia
(3) Blood relatives who have anesthesia complications (malignant hyperthermia [MH])
(4) Postoperative nausea/vomiting
(5) Difficult intubation/extubation
(6) Ability to lie flat for duration of pre-, intra-, and postprocedure as appropriate
(7) Claustrophobia
(8) Previous history/problems tolerating procedural sedation—agents/amounts from previous experiences
3. Preprocedure laboratory testing: Blood work is necessary with numerous IR procedures. Patients need to be
instructed if any preprocedure blood work is needed to be drawn and the rationale for the needed blood work.
Oftentimes, evaluation of renal function is mandatory for procedures where contrast is necessary. Additionally,
other factors, such as coagulation status, need to be known for determining
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risk of bleeding. Patients requiring blood work should be told to have it done few days prior to the procedure
when possible to avoid delays the day of the procedure. When of childbearing age, may require testing at least 7
days prior to the procedure
4. Allergies: known allergies with description of types of reactions; past reactions involving contrast, severity, and
interventions. Patients with known contrast reactions may be premedicated with steroids, antihistamines, and H2
antagonists. It is important for the IR nurse conducting the intake screen to inquire if the patient has had a
“breakthrough” reaction after receiving premedication; this information must be communicated to the IR provider.
5. Medications: It is important to review the patient's current prescription medications because some of them may
be contraindications for the procedure, if not stopped or managed appropriately. Patients should bring a list of
their medications with them. Hospital policy regarding patients bringing medications from home for use in hospital
should be known by the nurse.
a. Anticoagulants—increased risk of bleeding during IR procedure. Patients should be informed well in advance
to “hold” medications in preparation to undergo a procedure.
b. Nonsteroidal anti-inflammatories (NSAIDs)—in general, do not cause significant bleeding problems except in
patients with existing coagulopathies, hemophilia, von Willebrand disease, or severe thrombocytopenia.
Paradoxically, NSAIDs tend to diminish the antiplatelet effect of aspirin when given concomitantly and therefore
should not be given to patients receiving aspirin therapy for cardiovascular disease.
c. Diabetic agents—insulin regimen or oral agent administration for control of glucose needs to be known, to
provide instructions on when to self-administer these prior to the procedure. Additionally, metformin instructions
“to hold for 48 hours postadministration of contrast” should be explained to the patient.
d. Cardiac and antihypertensives
e. Thyroid medications
f. Inhalers/prednisone
6. Discharge planning: Planning for the discharge should begin prior to the procedure.
a. Transportation: Special consideration for transportation, indicated hospital admission, or home health care
should be discussed with the patient at the time of the phone screening. For OPs who will be going home after
meeting postprocedure discharge criteria, it is important to plan for traveling home with a responsible companion
especially if moderate sedation or MAC/general anesthesia was utilized for the procedure.
b. Psychosocial support: Undergoing an IR procedure can be a very stressful time for the patient. It is important
to inquire about the patient's sources of emotional support. Family and caregivers should be involved in the
patient's care if agreeable. The nurse should screen for depression, anxiety, self-harm, suicide, and domestic
abuse. Special needs should be taken into consideration (e.g., language, cultural/psychosocial, physical,
spiritual). Address and facilitate practices related to religion, culture, or alternative/complementary therapies that
will need to be integrated as part of the care as appropriate.
c. Behavioral screening: Risks for tobacco use, alcohol use (Clinical Institute Withdrawal Assessment [CIWA]
score), and drug use should be inquired about additional support needed to assist the patient.
d. Patient education: The nurse conducting the preprocedure screen has an opportunity to educate the patient
on what to expect upon arrival on the day of the procedure including parking, registration process, preprocedure
nursing process, consenting, and meeting with the members of the IR team.
e. Advance care directives (ACD): Indicate whether copy is in medical record or status, otherwise. Offer
information regarding ACD and whether patient accepted or refused the information.
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7. Instructions for date of service: Patient instructions in preparation for an upcoming procedure are important to
ensure optimization and decrease possibility of having to be rescheduled. Instructions should include:
a. Home medications on hold
b. Home medications which can be taken with a sip of water (i.e., antihypertensives such a β-blocker)
c. Explanation of nil per os (NPO) 6 hours prior to the procedure when moderate sedation, MAC, or general
anesthesia is to be utilized
d. Transportation back home needs to be via companion or caregiver
e. Preprocedures for specific imaging/interventions and personal belongings.
Please see checklist below, which can be tailored for OP or inpatient (IP) use:
Preprocedure Nursing Evaluation Checklist
Outpatient Phone Screen □ Patient Chart Review □
Labs □ H&P □ Signed Requisition □
Patient Name_____________________________ MRN_____________________________
Home Phone No.__________________ Cell Phone No._________________________
Planned Procedure______________________________________________________
Date________________________ Arrival Time_____________________________
If □ to be arranged (TBA) or □ Labs needed, patient is instructed to report/register in admissions 30 minutes
early.
Patient or responsible person giving interview_________________________________
COMMUNICATION: Patient able to speak and understand ENGLISH □ Yes □ No
Primary Language_______________________________________________________
INTERPRETER Services □ Yes □ No Confirm No._______________________________
CONSENT: Patient legally competent to give CONSENT? □ Yes □ No
If No, who will accompany patient to give CONSENT?____________________________
Relationship to Patient________________________ Phone#_____________________
TRANSPORTATION: Ride and Caregiver (stay if necessary) arranged? □ Yes □ No
Transitional Care Facility or Rehab (if applicable)
Name__________________________________________ Phone#________________
Outside Facility electrocardiogram (ECG), Labs, H&P, reviewed □ Yes □ No
Patient will be transported by ambulance? □ Yes □ No
AMBULANCE Company____________________________ Phone#________________
ALLERGIES & CONTRAST REACTIONS:
Any known drug allergies? □ Yes □ No
Specify:__________________________________________________________
CONTRAST REACTION: History of contrast reaction? □ Yes □ No
If yes, what kind of reaction?______________________________________________
IR/Radiologist notified of PRIOR contrast reaction_____________________________
Plan for current Contrast Administration:_____________________________________
OTHER PRECAUTIONS □ Yes □ No
Specify:__________________________________________________________
MEDICATION LIST: Reviewed with patient □ Patient bringing home medications □
Patient taking an ANTICOAGULANT: □ Yes □ No
Patient instructions provided: □ Yes □ No
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Is patient DIABETIC □ Yes □ No
Is patient on Glucophage and undergoing a contrast study? □ Yes □ No
If Yes, instructions provided: □ Yes □ No
Is patient on Insulin? □ Yes □ No
If yes, instructions given? □ Yes □ No
ANESTHESIA
DIFFICULT AIRWAY □ Yes □ No
Postoperative Nausea and Vomiting (PONV) □ Yes □ No
Previous Head/Neck Surgery □ Yes □ No
Respiratory Problems____________________________________________________
History with Sedation Agents:______________________________________________
Medications for pain or anxiety □ Yes □ No
Medication/Doses______________________________________________________
SLEEP APNEA: Does patient have a history of sleep apnea? □ Yes □ No
If Yes, patient instructed to bring BIPAP machine? □ Yes □ No
Weight__________________________Height_____________________________
Do you have difficulty breathing when lying flat? □ Yes □ No
Claustrophobia □ Yes □ No
Arrange Anesthesia Support □ Yes □ No
Anesthesia Consult □ Yes □ No
VENOUS ACCESS CASES:
Does patient have history of central venous catheter? □ Yes □ No
□ RIGHT SIDE □ LEFT SIDE □ BILATERAL TYPE:
_____________________________________________________________
TUBES/DRAINS/LINES: Foley, Ostomy, etc.____________________________________
INTERNAL/EXTERNAL DEVICES:
List:_________________________________________________________________
LAB WORK:
Is patient's creatinine greater than 1.3 AND undergoing a contrast study? □ Yes □ No
If yes, name of MD/PA notified_____________________________________________
Is platelet count greater than 50,000 and INR ≤1.5? □ Yes □ No
Are labs current and within acceptable range for the procedure ordered? □ Yes □ No
If Radioembo/Chemoembo Preprocedure Liver Function Tests (LFTs) ordered □
Transjugular liver biopsy: Obtain order for Complete Blood Count (CBC) and Clot to
Blood Bank (BB) □
Nephrostomy or Biliary Drain Capping □ Check with MD to order necessary labs □
LMP if applicable_______________________________________________________
TRANSFUSION:
If blood products are needed prior to procedure, name of person notified____________
Plan, if needed, to address issue:___________________________________________
POSTPROCEDURE CARE:
Does patient currently have Home Care Services? □ Yes □ No
Is Home Care needed postprocedure? □ Yes □ No
If Yes, Name and Phone # of person contacted:_________________________________
Plan_________________________________________________________________
Recent Travel__________________________________________________________
Anything else you would like to share about your personal health history/status?_______
_____________________________________________________
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PATIENT INSTRUCTIONS:
□ NPO 6 hours before the procedure except for sips of clear liquids to take oral medications.
□ Avoid bringing valuables, jewelry, or money to the hospital. Wear comfortable clothing.
□ Take all regular oral antihyperglycemics, cardiac, antihypertensives, anti-anxiety, and pain medications.
□ Patient reminded to bring medication list and/or bottles of any medications necessary during stay.
□ Patient understands procedure process including possibility of extended wait or delay.
□ Length of time expected to be in hospital
□ DIRECTIONS TO Hospital/ Family Waiting Area
Website information for further information related to the hospital, maps, parking options, hotels, etc. Patient
given telephone number to contact IR Nurse with any questions or concerns:
Personal Protective Equipment (PPE) Complete □ Date___________ RN Completing
PPE___________________________________________________
Comments____________________________________________________________
Procedure Preparation Protocol for Nurses

The day of the procedure can be stressful for the patient and family members. It is important for the registered
nurse caring for the patient to provide a calm environment and reassurance. The nurse caring for patients
undergoing IR procedures should consider patient's condition and plans to optimize procedural candidacy,
minimize patient pain and anxiety, and involve the patient and family in all phases of care.
Nursing Preprocedure Interaction with the Patient

The plan for nursing care should prescribe goals for actual or potential patient problems noted in the nursing
diagnosis.
1. Preprocedure teaching should include a review of written instructions using “Teach Back” technique with
return demonstration of learning. Ideally, this should be done during the preprocedure or preadmission patient
assessment.
a. Adjustment of medications as indicated by procedure-specific guidelines. Instruct OPs about their regular daily
medications per radiologist orders. Arrange for patient medications to be available during periprocedural period.
Some institutions allow patients to bring their own labeled medications to be taken during this time.
b. History of contrast allergies must be carefully reviewed. Consider pretreatment with corticosteroids in
consultation with the radiologist. Provide the patient with necessary prescriptions. Review written instructions
with the patient.
c. Modify diet as needed. Procedures requiring sedation or intravascular contrast will require NPO (e.g., no solid
foods for 6 hours, encourage clear liquids for 2 hours prior to procedure, patient may continue to take prescribed
medications with sips of water up to time of procedure). Encourage patients to hydrate orally and avoid alcoholic
beverages the day before the exam. A late dinner or bedtime snack will help minimize morning hunger.
d. Instruct patients to report the onset of a cold, flu, or fever.
e. Instruct OPs to arrange for a responsible adult to drive them home and stay with them the evening following
the procedure.
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f. Inform patient of physical anticipated activity restrictions after the procedure.
g. Describe procedure process, environment, and expected activities of procedure to staff.
h. Orient the patient to the use of pain and sedation scales.
2. Instruct the patient about the “time out/safety pause” for identification and procedure verification. The patient
should be actively involved in the identification and procedure verification process. Patients should wear a
hospital wristband on admission to the department if one has not been previously issued.
3. Confirm procedure consent for completeness. The consent form should include patient identification; the
planned procedure including site, side, level, and sedation plan. The consent form must be dated and signed by
both patient and clinician who obtained consent.
4. Review preadmission nursing assessment, medical history, results of labs and tests, physical exam, and the
rationale for sedation and analgesia.
5. Verify that all elements of preprocedural patient preparation have been completed: pretreatments or
premedication, NPO and time of last meal, medications brought in from home, and OP discharge arrangements
completed.
Physician Evaluation
Each patient must have a targeted H&P, completed by the physician, which includes the following basic
elements: chief complaint, history of present illness, previous medical and surgical history, allergies, medications,
social history, family history, review of systems, physical examination, vital signs laboratories and imaging
results, impression, and plan. At a minimum, the physical exam should include head, eyes, ears, nose, and throat
(HEENT); lungs; heart; abdomen; neurologic; and extremities. As appropriate to patient, the physical exam
should extend to neck, back and thorax, breast, pelvic, rectal, and integument. Other considerations should
include:
1. Location of symptoms because it relates to planning access and positioning for the procedure
2. Infectious disease precautions
3. Intraprocedural consideration of patient comorbidities: cardiovascular status (CHF, previous MI, heart-valve
disease, angina); pulmonary status: chronic obstructive pulmonary disease (COPD), pulmonary hypertension
(PHTN), asthma, cystic fibrosis, bronchitis; cancer; neurologic status; metabolic status: periprocedural
management of blood glucose for diabetic patients
Interphysician Interaction and Coordination of Care

All medications must be reviewed and signed off by the physician and pharmacist. The referring physician and IR
must have a plan to balance the risks of medications given in the periprocedure period, considering:
1. Laboratory abnormalities relative to baseline health, volume status, organ function, and bleeding risk
2. Contrast reactions and other allergies
3. Glucose management: including adjusting insulin and metformin doses (along with a plan to follow renal
function)
4. Anticoagulants: the postprocedure risk of bleeding versus risk of thrombosis is considered when to stop and
restart periprocedural anticoagulants
5. Cardiac medications: antihypertensives and antiarrhythmics
6. Pain and narcotic medications, along with adverse reactions to sedation and analgesia, should be evaluated
along with a plan for sedation and pain control in the periprocedure period.
7. Type and cross for blood potential product needs
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Nursing Reassessment on Day of Procedure

The role of the IR nurse in patient assessment includes review of completed medical physical exam and the
performance of a focused assessment immediately prior to the procedure. The following issues should be
considered for most interventional radiology procedures:
1. Potential for impaired gas exchange
2. Potential for aspiration
3. Potential for related airway obstruction
4. Potential for adverse reactions to medications including contrast agents, sedatives, and analgesics
5. Pain
6. Anxiety related to fear of the procedure and/or fear of the outcome
7. Fluid volume deficit and/or overload
8. Alteration in circulation
9. Alteration in mobility
10. Potential for bleeding
11. Potential for emboli/thrombosis
12. Potential for infection
13. Potential for injury
14. Knowledge deficit (i.e., regarding planned procedure, recovery care, and management of equipment or
supplies postprocedure)
15. Potential urinary retention
16. Potential confusion/altered or loss of consciousness
A complete nursing assessment should include:
1. Brief physical examination
a. Skin condition
b. Baseline vital signs including O2 saturation, capnography, and blood pressure (BP) in both arms if
possible. Caution: Do not place BP cuff on affected limb of a patient who has had breast surgery, has a
hemodialysis (HD) fistula, an implant, or injury to the extremity.
c. Airway: breath sounds, respiratory pattern, rate, and depth. In anticipation of potential intubation and/or
positive pressure ventilation, evaluate head and neck range of motion and note presence of nasal
oropharyngeal abnormalities, craniofacial abnormalities, dental apparatus, and condition of dentition.
d. Height and weight: Consider habitus relative to weight limitations and gantry sizes per indicated imaging
equipment and weight-based medication doses.
2. Complete pain assessment; specify location, duration, frequency, and intensity. Assessment is conducted
considering anesthetic approach(s) including:
a. Local, regional, MAC, general anesthesia, and/or procedural sedation
b. Type of pain anticipated (e.g., ischemic, biliary or renal colic, pressure)
c. Baseline pain assessment per institutional policy scale
d. Document level of patient anxiety and sedation.
3. Analgesia and sedation plan: Document American Society of Anesthesiologists (ASA) Physical Status
Category Score. Assess and document capacity of patient to adapt to
a. Comorbidities associated with the procedure
b. Duration of the procedure
c. Physical positioning required by procedure
d. Discomfort associated with the procedure
e. Assure appropriate consults with anesthesia and/or other medical disciplines have been completed.
Some institutions encourage any team member to request an anesthesia consult at their discretion.
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Nursing Preparation of the Procedure Room
1. Procedure room fully stocked with any equipment and supplies anticipated for the procedure: suction
equipment and catheters, bite blocks, intubation kit, airways and masks, and self-inflating positive pressure
oxygen supply system capable of delivering 90% oxygen at 15 L per minute flow rate.
2. Monitoring equipment: cardiac monitor, automated BP unit and sphygmomanometer with multiple cuff sizes,
invasive pressure monitor, stethoscope, pulse oximeter, capnograph, and pressure transducers.
3. Procedure medications: Assure that all medications needed for the procedure are available, for example,
antibiotics, anticoagulants, local anesthetics, and heparinized saline flushes. Ideally, medications should be
reviewed, maintained, and dispensed by pharmacy services. Medications should be provided in predetermined
unit dosages and made available in either pharmacy stocked procedure kits and/or automated medication
dispensing machines. If medications are stocked in the procedure room, they should be checked daily for
completeness of stock by par level, expiration date, dose/concentration, and route of administration. The Joint
Commission (TJC) Medication Management Standards requires specific conditions regarding storage and
management of medications. Drugs for the management of potential adverse events (e.g., contrast reactions,
emergency reversal of sedatives and analgesics, agents for the management of hypo/hypertensive events, and
first-line emergency care drugs such as atropine, epinephrine) should be readily available.
4. Emergency cart and resuscitation equipment: Emergency code cart should be properly checked daily and
restocked per institutional protocol. Cardiac defibrillator should be configured for battery operation and reviewed
for anteroposterior defibrillation and cardioversion and external cardiac pacing features.
Nursing Preparation of the Patient

1. Check for functional intravenous (IV) line (18-gauge or 20-gauge Angiocath). If not present, place before
procedure.
2. Institute cardiac, oxygen saturation, and capnography continuous monitoring and document baseline heart
rate, rhythm, oxygen saturation, and validate endtidal CO2.
3. Assess and document baseline vital signs, sedation scale, and pain scale.
4. If items such as Foley catheter, pneumoboots (sequential compression devices), a warming or cooling
blankets are required for the procedure, place them before positioning and draping for the procedure.
5. Prepare and calibrate equipment for intravascular pressure measurements as applicable.
6. Discuss patient positioning requirements for the planned procedure with the radiologist and technologist.
7. Discuss sedation and analgesia plan. Document the patient's response (e.g., sedation scale, pain scale, vital
signs, oxygen saturation, capnography, presence of protective reflexes, and adequacy of respiration).
Intraprocedural Nursing Care Considerations

Please see Chapter 61, Universal Protocol in Interventional Radiology. Document vital signs per current ASA
guidelines and in accordance with hospital policy related to procedural sedation, after each contrast injection,
and prior to the administration of medications. Current standards for moderate procedural sedation require
physiologic parameters to be documented every 5 minutes continuously
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for at least 30 minutes following the last dose of sedation and until the patient returns to baseline.
1. Physiologic monitoring
a. Continuous cardiac monitoring: Note rate, rhythm, conduction abnormalities, and the presence of ischemic
changes. This is especially important if cardiac chambers are traversed. Inform the operating physician
immediately of all changes. A transvenous cardiac wire and pacemaker and/or external cardiac pacemaker
should be immediately available for patients at risk for conduction abnormalities.
b. Intravascular pressure monitoring as needed for continuity of care and for the management of hypo- and
hypertensive events.
c. Temperature of skin, axillary or deep cavity, at least recorded preprocedure and prior to discharge.
Temperature should also be monitored as indicated during prolonged procedures. Consider potential for
malignant hyperthermia in general anesthesia cases.
2. Maintaining fluid balance
a. Hourly documentation of intake and output
b. Hourly calculation of IV contrast load per kilogram of body weight. Observe for intolerance to contrast (e.g.,
chemotoxic and osmotoxic effects, tachycardia, tremors, shortness of breath, pulmonary edema).
c. Administer a sufficient amount of isotonic IV fluids to maintain normal fluid and electrolyte balance. Where not
contraindicated, normal saline or Ringer lactate is preferable for procedures in which IV contrast media are used.
3. Continuous surveillance of respiratory status
a. Visually assess and document the following per institutional policy: position of head to ensure airway patency;
skin color and other indicators of respiratory status as appropriate (i.e., nail beds, mucosa, etc.) respiratory rate,
rhythm, and depth; continuous pulse oximetry; and capnography.
b. Capnography: monitors patient's ventilatory status by measuring exhaled carbon dioxide and gives an earlier
sign of depressed ventilation than blood oxygen saturation alone. Capnography provides a mechanism of early
identification and intervention for unanticipated patient ventilatory and/or cardiac response due to O2
desaturation and hypoxia. Administration of supplemental oxygen delays identification of oxygen desaturation
when the patient experiences decreased respiratory rate or apnea. For this reason, pulse oximetry alone is
insufficient to detect ventilation problems as it may delay crucial and timely intervention.
4. Prevention and early detection of spasm, thrombosis, embolism, hemorrhage, and dissection
a. Assess and document condition of distal extremity used for intravascular access and document color,
sensation, motion, temperature, and capillary refill every 10 minutes.
b. Assess vascular access distal extremity pulses every 10 minutes.
c. Continuous surveillance of the distal extremity (subjected to intervention as in items “a” and “b” above).
d. Monitor for signs of bleeding: hematoma formation, hypotension and reflexive tachycardia, cold clammy skin,
pale mucous membranes, and alterations in consciousness.
5. Physical support
a. Proper anatomic positioning: Support all joints and place all extremities in a nondependent position, provide
lumbar support, position thorax and abdomen to maximize airway, and maintain maximal tidal volume with
respiration. Minimize pressure points (e.g., heels, knees, shoulders, elbows) with additional padding.
b. Protect patient from exposure to cold. Minimize saturation of drapes with fluids and blood; the layering of
blankets is preferred to one heavy blanket.
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Keep the patient covered as much as possible while prepping and draping. Place absorbent under pads while
patient uses bedpan or urinal. Discuss the need for a Foley with the radiologist in anticipation of a lengthy
procedure.
c. Offer bedpan or urinal frequently.
d. Assist patient to move unrestricted extremities as frequently as possible.
e. Moisten lips and mouth as needed.
6. Psychosocial support
a. Explain all procedures and activities.
b. Provide consistent reinforcement and elicit patient's cooperation.
c. Utilize diversion techniques, progressive muscle relaxation, and modeling to assist patient to cope with rigors
of the procedure.
d. Provide patient (and when possible, family) with frequent progress reports.
e. Keep the noise level in the procedure room to a minimum. Avoid inadvertent arousal of patients who are
sleeping following sedation.
f. The patient's need for dignity, privacy, and emotional support should be met continuously throughout the
duration of his or her stay in the department.
7. Sedation and analgesia: When necessary, consult with an anesthesiologist who can recommend specific
strategies for the clinical management of patients receiving sedation and analgesia.
a. Institute sedation and analgesia plan as ordered by the radiologist.
b. Explain the goals of the plan to the patient. Contract with the patient regarding what to expect and how to
participate in pain management. Use a pain scale and a sedation scale as a guide for nurse-patient collaboration
in the assessment of the efficacy of the treatment plan.
c. Institute patient monitoring and documentation as described previously and per the approved hospital and
departmental standards.
d. Verify that OPs have written home care instructions (including precautions that should be taken following
sedation) and a responsible adult who can take them home.
e. Patient monitoring must include the following until 30 minutes after the last dose of sedation and until the
patient returns to baseline is transferred to a properly monitored level of care.
Postprocedure Nursing Considerations

Plan for monitoring patient in accordance with the procedure performed. Maintain patient comfort during the
postprocedure phase: Include appropriate consideration for pain control and PONV. Postprocedure scoring
system and discharge criteria should be developed as approved by the moderate procedural sedation policy for
the institution.
Communications with Floor Nurses/Handoff Report

Following the completion of the procedure, the nurse must have handoff communication with the receiving nurse
on the floor, who should have an opportunity to ask questions and clarify concerns. The content of this handoff
communication should be agreed on between nursing administration and the IR division's nurses and be an
established institutional policy. The Joint Commission recommends standardized communication that allows for
feedback between caregivers.
Discharge
Reassessment of the patient is conducted as follows: (a) reconsideration of the nursing evaluation, (b) revision
of goals, and (c) modification and implementation of the follow-up nursing care plan. Patient and family
participation is included in the development of the nursing care plan.
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Discharge criteria. Ensure discharge criteria are met prior to discharge per hospital organization policy.
1. Provisions for short- and long-term follow-up are identified. OP discharge plans are written and reviewed with
patient and family.
2. Continuity of patient care is ensured via the immediate implementation and documentation of the
postprocedure orders, verbal and written nursing reports, and transfer note.
Suggested Readings
American Nurses Association; Association for Radiologic and Imaging Nursing. Scope and Standards of
Practice: Radiologic and Imaging Nursing. Silver Spring, MD: American Nurses Association; 2013.
American Society of Anesthesiologists. Standards, guidelines, statements and other documents.

http://www.asahq.org/ForMembers/Standards-Guidelines-and-Statements.aspx. Accessed July 3, 2015.
Association for Radiologic and Imaging Nursing. http://www.arinursing.org/. Accessed July 3, 2015.
Baerlocher MO, Nikolic B, Silberzweig JE, et al. Society of Interventional Radiology position statement on
recent change to the ASA's moderate sedation standards: capnography. J Vasc Interv Radiol . 2013;24:939-
940.
Duncan K. Orientation Manual for Radiologic and Imaging Nursing. 2nd ed. Herndon, VA: Association for
Radiologic & Imaging Nursing; 2015.
Fetzer S. Postoperative nausea and vomiting. In: Schick L, Windle P, eds. Perianesthesia Nursing Core
Curriculum: Preprocedure, Phase I and Phase II PACU Nursing. 2nd ed. St. Louis, MO: Saunders Elsevier;
2010.
Gross K, eds. Core Curriculum for Radiologic and Imaging Nursing. 3rd ed. Hillsborough, NJ: Association
for Radiologic and Imaging Nursing; 2014.
Patel IJ, Davidson JC, Nikolic B, et al. Consensus guidelines for periprocedural management of coagulation
status and hemostasis risk in percutaneous image-guided interventions. J Vasc Interv Radiol . 2012;23:727-
736.
Putrycus B, Ross J. Certification Review for Perianesthesia Nursing. 3rd ed. St. Louis, MO: Saunders
Elsevier; 2013.
Radiologic Nursing Certification Board. http://certifiedradiologynurse.org/en/. Accessed July 3, 2015.
Smouse B. Clinical management issues in interventional radiology. Semin Intervent Radiol . 2006;23(4):319-
328.
Sousa M. Management and leadership: educating and orienting the radiology nurse of the future. J Radiol
Nurs. 2011;30(3):135-136.
e-102
Organization and Operation of the Interventional Radiology Clinic
Evelyn P. Wempe
Richard Foley
DéAnn O. McNamara
Critical to the success of a clinically based interventional radiology (IR) practice is the establishment of the
ambulatory IR clinic. Due to the complex diagnostic and therapeutic procedures that the specialty offers, along
with involved patient medical histories, the IR clinic setting offers the opportunity for providers to evaluate,
manage, and provide follow-up care to patients.
Having an IR clinic promotes the provider-patient relationship, which is fundamental to the practice of medicine.
Establishing trust and effective communication
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between the patient and the health care provider improves clinical outcomes and patient compliance (1).
Additionally, the clinic visit offers the opportunity to provide patient and family education regarding the procedure,
identify patient needs, develop a plan of care, and coordinate any preprocedure workup. Establishing and
operating a clinic requires hard work by the entire IR team, with the trade-off of enhancing both the patient
experience and quality of care.
Clinical Considerations
1. Scheduling
a. New patient visits. Patients being seen in the IR clinic for the first time should be scheduled for 1 hour. This
allows sufficient time to obtain the necessary information as it relates to the patient and the clinical presentation
for which consultation is sought. The initial visit includes a comprehensive examination, pertinent history and
physical examination, and explanation of the intended procedure including risks, benefits, and potential
complications. Oftentimes, patients arrive to the clinic having researched their condition and potential treatment
options. They will be well informed and have pertinent questions that require multifaceted explanations. It is
important to provide a relaxed environment where the exchange of information can occur between patient and
provider.
b. Established patients. Follow-up visits for patients that are known to the practice are typically scheduled for 30
minutes. Routinely, these visits are postprocedure evaluations and problem-focused. These visits provide the
continuity of care that reinforces the specialty's responsibility and accountability in the longitudinal care of
patients undergoing invasive procedures.
2. Clinical assessment
a. Comprehensive examination. Clinical assessment of the patient includes performing a comprehensive exam,
which includes a thorough history and physical examination, a review of diagnostic imaging and blood work, and
a review of pertinent medical records.
b. A comprehensive exam should include the following:
(1) Chief complaint
(2) History of present illness
(3) Past medical history
(4) Past surgical history
(5) Social history
(6) Allergies
(7) Medications
(8) Review of systems
(9) Physical examination
(10) Review of imaging studies
(11) Assessment/impression
(12) Plan of care
c. Assessment may identify other clinical problems not related to the chief complaint (2). The IR provider brings a
unique perspective that can lend valuable insight into the cause of the problem and treatment options.
d. Certain clinical conditions and management issues are not within the realm of the IR specialty and should be
referred to the appropriate specialty. The IR provider needs to recognize his or her scope of practice and refer
when appropriate to provide optimum patient care.
3. Plan of care
By the conclusion of the patient's visit, a plan of care should be created and documented by the IR provider. If
the plan of care involves undergoing a procedure, the IR provider will need to identify the procedure to be
performed and the rationale. The plan of care also identifies any preprocedure workup required.
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4. Coordination of care
a. Preprocedure planning. The clinic visit offers the opportunity for patients to have any preprocedure workup
coordinated prior to being discharged from the clinic. Patients may require updated blood work, additional
imaging, or an additional clinical visit with the anesthesia team, primary care provider (PCP), or a specialty
provider in order to prepare optimally for the procedure.
(1) Procedure scheduling. Communication between the IR clinic staff and the facility in which the procedure is to
be performed should take place during the patient's clinic discharge process. A date and time should be provided
to the patient. Insurance considerations need to be addressed at the time of scheduling to ensure a realistic date
is provided to avoid delay of treatment.
(2) Blood work/imaging workup. Preprocedure blood work or additional diagnostic imaging needs to be ordered
and arranged. It is important for the patient to be scheduled for all specified testing prior to the date of the
procedure and within an acceptable time frame to avoid cancellation or rescheduling of the procedure.
(3) Anesthesia or specialist clearance. Coordination of future visits for patients requiring anesthesia evaluation
or preprocedural evaluation by a PCP or specialist needs to be completed to ensure the recommendations are
communicated to the IR provider prior to the anticipated date of the procedure.
5. Patient education
The IR clinic setting is an ideal location for patient education. Providers have the opportunity to educate patients
on what to expect prior to, during, and after a procedure is performed in IR. Discussion of the procedure and
symptom management is important in helping to lessen the anxiety of patients. The clinic visit offers the chance
for the IR provider to explain and review imaging results with patients. This provides a visual understanding to
the patient about pertinent findings prior to a procedure or imaging evidence of results after having undergone an
IR procedure.
6. Provider communication
Communication regarding the patient's plan of care should occur between the IR provider and the patient's other
providers who are involved in the management of the clinical condition for which IR services are being
requested, including the PCP. Communication of patient's care should be done in a timely manner. A letter to the
referring provider outlining the clinical findings and recommendations is one method of communication. A follow-
up phone call to the referring practitioner is appropriate if issues of concern are noted.
Operational Considerations
The success of an IR clinic depends on the organization and management of its operations. Considerations
involving the operations of an IR clinic are dependent on its location and accessibility, staffing, physical layout,
and functionality.
1. Staffing considerations
a. Ancillary support. The IR clinic should be staffed with sufficient ancillary staff to assist with the daily workflow.
Roles include front desk personnel, procedure schedulers, and insurance coders.
b. Management. A supervisor/office manager is necessary to oversee the daily operational needs of the clinic
such as staffing, budget, payroll, and equipment and supply ordering. In addition, management has the
opportunity to network, market, and promote IR services to surrounding community practices.
c. Clinical staff. The clinical staff in the IR clinic is fundamental to the patient's experience.
(1) Medical assistants can escort patients to exam rooms, take vital signs, and assist with any patient care issues
and, with proper certification and competency validation, may assist the clinical team by setting up and facilitating
procedures as appropriate.
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(2) Registered nurses oversee patients' charts in preparation for their visit, oversee the daily clinic flow of
patients, perform dressing changes, administer medications, make referrals, and provide patient education and
other skilled care as warranted.
(3) An advanced registered nurse practitioner (ARNP) or physician's assistant (PA), with proper credentialing and
state licensing, can complete histories and physicals, write prescriptions as appropriate for state regulations,
write orders, and coordinate the patient's care (3).
d. Multidisciplinary consultants. Multidisciplinary consultation support may be required from radiology, vascular
surgery, vascular medicine, cardiology, oncology, neurovascular surgery, or other specialist as appropriate to
evaluate patients in the clinic.
2. Infrastructure and clinic design
a. Convenience and proximity
(1) IR clinics established in proximity to the IR procedural environment offer the IR provider the convenience of
being able to plan a clinic schedule around their procedure schedule.
(2) IR clinics not associated with a surrounding hospital need to consider the obligation for referral of patients to
a specific hospital.
b. Consider and promote amenities
(1) Parking for the IR clinic should be convenient and handicapped accessible.
(2) Easy directions to the clinic should be available for patients to use as a reference.
(3) Adequate signage should be displayed throughout the clinic area discussing providers, procedures, or other
information relevant to the practice.
(4) Diagnostic testing should be available in close proximity to the clinic with adequate directions and signage.
c. The reception area
(1) The reception area should create a welcoming first impression where patients have easy access to the
reception staff.
(2) Seating should be comfortable, of an adequate amount, and should accommodate wheelchairs.
(3) Patient education and reading material should be available in the reception area including education videos.
(4) Use washable or one-time-use toys in clinics where pediatric patients are expected or children accompany
adults to clinic. An infection control policy for toy use needs to be created.
(5) Television, if appropriate
d. Exam room(s)
(1) Multiple exam rooms promote efficient workflows.
(2) The space requirement for exam rooms needs to accommodate for necessary equipment, furniture, and
computer workstation for documentation and viewing/explaining image findings.
(3) When designing the room, consider the following:
(a) Lighting
(b) Seating capacity for practitioner, patient, and family/caregivers
(c) Desk and counter space
(d) Exam table with privacy curtain to separate exam area from consult area
(e) Sink and hand disinfectant containers
(f) An integrated wall mounted system that includes a stethoscope, sphygmomanometer, ophthalmoscope,
otoscope, and thermometer
(g) Weight scale and tape measure for measuring abdominal girth, leg sizes, or other pertinent body parts
(h) Doppler ultrasound equipment
(i) Linen—gown, pillows, sheets
(j) Dressings for wound care
P.892
e. Other requirements
(1) Dictation/workroom for providers
(2) Workstation for dictation, whether using an electronic or paper medical record
(3) Paper forms, including consent forms, if an electronic record is not used or a component of the
documentation is not yet electronic
(4) Picture archiving and communication system (PACS) or other workstation for review of imaging
(5) Storage for supplies, equipment, and medications
(6) Patient and staff bathrooms
3. Documentation
Documentation of the patient's clinic visit needs to outline the history and physical exam performed, review of
existing blood work and imaging, assessment, and plan of care including recommendation for procedure and/or
further workup. Computerized medical records or standardized forms may be used. Consider a secure electronic
method of documentation, dictation/transcription that eases the IR workflow (4). Ensure application of Health
Insurance Portability and Accountability Act (HIPAA)-compliant guidelines for patient confidentiality and privacy.
4. Billing
a. The IR clinic needs to have an established billing system. Billing can be handled through the clinic's qualified
coding staff, or the clinic can hire an outside billing company to oversee the billing.
b. Medical coders must be knowledgeable with Medicare regulations for billing provider services. Evaluation and
Management (E&M) codes are updated annually and outlined in specified codebooks. Examples of these include
the Current Procedural Terminology (CPT) and International Classification of Diseases, 10th revision (ICD-10)
codebooks. The staff overseeing the billing should be familiar with the latest codes to accurately bill properly.
c. A list of contracted managed care companies should be available to the staff. Prior to scheduling any clinic
visit, patient's insurance company should be contacted to verify plan participation.
d. Consider a comprehensive billing process, which includes documentation of the clinic visit to substantiate the
billed service.
Clinic Resources
• Duncan K. ed. Orientation Manual for Radiologic and Imaging Nursing. Herndon, VA: Association for
Radiologic & Imaging Nursing; 2015.
• Gross K, ed. Core Curriculum for Radiologic and Imaging Nursing, 3rd ed. Hillsborough, NJ: Association
for Radiologic & Imaging Nursing; 2014.
• American Nurses Association. Radiologic and Imaging Nursing: Scope and Standards of Practice. Silver
Spring, MA: American Nurses Association; 2013.
• American Medical Association. Current Procedural Coding Expert. Chicago, IL: American Medical
Association; 2014.
• Centers for Disease Control and Prevention. International classification of diseases, tenth revision, clinical
modification (ICD-10-CM). http://www.cdc.gov/nchs/icd/icd10cm.htm. Accessed November 27, 2015.
References
1. Siskin GP, Bagla S, Sansivero GE, et al. The interventional radiology clinic: key ingredients for success. J
2. Brook BS, Black JH III. Clinical vascular examination. In: Mauro MA, Murphy K, Thompson K, et al, eds.
Image-Guided Interventions. Volume I. Philadelphia, PA: Saunders Elsevier; 2008:17-25.
3. Taylor K, Sansivero GE, Ray CE Jr. The role of the nurse practitioner in interventional radiology. J Vasc
Interv Radiol . 2012;23:347-350.
4. Gassert G, Durham J, Cain M, et al. Interventional radiology workflow management in the electronic
medical record. J Digit Imaging. 2014;27:314-320.
e-103
Outpatient Drainage—Catheter Care
Susan Benveniste
Maye M. Chan
DéAnn O. McNamara
Initial Biliary Catheter Placement

When endoscopic biliary drainage is not possible, decompression or diversion of the biliary tract is achieved by
accessing the biliary system percutaneously to drain bile (1). Ideally, side holes of the biliary drain are positioned
proximal and distal to the lesion so bile can drain internally utilizing an internal-external drainage catheter. In
cases where an obstruction or injury cannot be crossed, the tube is positioned proximal (upstream) to the
obstruction which allows for decompression utilizing an external drain.
1. Postprocedure management
a. Patients are typically admitted for observation following placement of a biliary catheter.
b. Pain is typical postprocedure. When severe, it may lead to hypoventilation. Although most patients respond to
oral pain medication, some may require intravenous (IV) pain management or a nerve block if the drain is placed
intercostal.
c. Although bleeding is usually self-limited, intra- and extrahepatic bleeding is possible due to the vascularity of
the liver. Bile drainage should be monitored. Following drain placement, blood stained bile is expected and
should clear within 24 to 48 hours. When drainage appears to be bright red blood, a hematocrit is obtained.
Careful monitoring of the patient's hemodynamic status is essential, especially in the first 24-hour period. It is
unusual for bleeding to require transfusion, but persistent bleeding may indicate an arterial or portal vein injury.
Resuscitation of the patient and arteriography may be required.
d. While the patient is administered appropriate prophylactic antibiotic within 60 minutes of procedure start time,
fever or rigors can occur immediately postprocedure as a result of transient bacteremia. The patient should be
treated symptomatically and monitored for progression to cholangitis and sepsis, all of which would require
immediate treatment with a plan for increased level of care. Rapid resolution of bacteremia through appropriate
antibiotics and supportive care for cholangitis permits transition to oral antibiotic administration and decreased
hospital stay.
e. Bile peritonitis can occur if even a small amount of bile leaks around the tube into the peritoneal space during
tube placement. This can result in severe, acute pain which typically requires IV narcotics. It may last several
days.
2. Instructions for biliary tube care
a. External drainage catheters and their attached bag should be considered a closed system and precautions
should be taken to prevent bacteria from being introduced retrograde. Unless instructed to cap the tube, by the
health care provider, the tubing should not be disconnected from the drainage bag. Always clean hands with
soap and water, or an alcohol-based sanitizer before and after tube care. Depending on the physician's
preference and the patient's clinical status, the tube may be flushed with 10 mL of normal saline to keep the tube
patent by removing biliary debris which can build up in the lumen and cause an obstruction. When flushing is
planned, a coupling device with a port access, such as a three-way stopcock or Y-connector, is left between the
catheter and the drainage bag (Fig. e-103.1).
P.894
FIGURE e-103.1 • Flushing your catheter. (From Your Nephrostomy Catheter. Patient Education. Brigham and
Women's Hospital; 2011, with permission.) (continued)
P.895
FIGURE e-103.1 • (Continued)
P.896
FIGURE e-103.1 • (Continued)
P.897
b. Prior to flushing, clean the access port with alcohol. When flushing biliary tubes, do not aspirate. Aspiration
introduces bacteria from the intestine, colonizing the bile. Signs of biliary drain obstruction or displacement
include resistance, pain, or pericatheter leaking when flushing.
c. The dressing should be changed routinely to keep the skin clean and dry. Dressing changes should use clean
technique to prevent introduction of bacteria into the biliary system. When changing the dressing, inspect the
tube insertion site as well as the surrounding skin for signs of infection or local irritation. The skin can be washed
with a clean gauze and water. The skin should be dry before reapplying clean dressing to cover the site.
d. The tube may be secured at the insertion site with a suture, or it may be stabilized with various drain securing
devices. The patient needs to be aware of how the anchor works in order to recognize displacement of the
catheter.
e. Biliary tube insertion site and dressing must remain dry and clean to reduce the likelihood of infection.
(1) They should never be submerged in standing water. For this reason, tub baths and swimming are to be
avoided.
(2) For the first 48 hours, the patient is instructed to refrain from showering and to maintain integrity of the
dressing. Afterward, patients may be instructed to cover the site and dressing with plastic wrap prior to
showering. It must be noted that, currently, there is a lack of literature to suggest a difference between the
practices of allowing the patient to shower with the tube site exposed versus covered.
3. Follow-up care
a. If attempts to cross the lesion are not successful, the biliary catheter will be placed to external drainage. It may
be beneficial for the patient to return in 2 to 7 days for a repeat attempt to cross the lesion. In some situations,
depending on the patient's diagnosis, the biliary tube may need to be left permanently to external drainage.
Long-term external drainage may lead to electrolyte disturbances; oral or IV replacement of fluid and electrolytes
is required.
b. After initial placement of a biliary catheter across an obstruction, the internal-external drainage catheter is
typically attached to a bag to permit external drainage for 24 hours prior. This is thought to help prevent
cholangitis. After optimal decompression of the biliary system, the tube can be capped to allow internal biliary
drainage.
c. The biliary tube should be checked and changed every 2 to 3 months. Patients should be seen sooner if they
develop problems. Changing the tube is usually an outpatient procedure. The procedure is typically not as
painful as the initial tube placement, and patients can often be discharged the same day with the tube capped.
d. Prophylactic IV antibiotics are usually administered prior to the tube change, but there remains a risk of
developing bacteremia and/or biliary sepsis postprocedure. If this occurs, the patient's tube should be opened to
external drainage and the situation assessed for the severity of symptoms. A fever less than 101°F may typically
be treated with antipyretic medication and observed. Fever greater than 101°F suggests cholangitis and requires
appropriate antibiotic therapy and supportive care which may include hospitalization (2).
Initial Nephrostomy Tube Placement

Percutaneous nephrostomy tubes may be indicated to provide access for endourologic procedures or for
treatment of an obstruction or injury of the renal collecting system (3). Urine may be drained externally to
decompress an obstructed system or divert urine away from a ureteral injury or fistula. If the obstruction or injury
can
P.898
be crossed, a nephroureteral tube can be passed through the ureter to the bladder, which allows the urine to
drain internally.
a. The placement of a nephrostomy tube may be done on an outpatient basis if there are no other medical
reasons that require admission to the hospital.
b. If the nephrostomy tube is placed for decompression due to an obstruction, related to a stone, or pregnancy,
the tube will remain to external drainage until the source of the obstruction is resolved.
c. If the obstruction is related to external compression of the ureter, benign or malignant, ureteral stricture, or
ureteral injury, an attempt may be made to cross the lesion and place a nephroureteral stent. This tube will
terminate in the bladder, thus allowing the urine to drain internally. The external portion of the tube may then
remain capped.
d. The patient is observed for potential acute complications related to the procedure.
(1) Postprocedure pain is typically attributed to the passage of a catheter through the skin, subcutaneous
tissues, and muscles to access the kidney. Although some pain may be expected and can typically be treated
with oral agents, escalating pain is atypical and requires evaluation. If the patient's preprocedural pain was
related to hydronephrosis, this may continue for a few hours, but sometimes the patient may feel relief
immediately after the drain is placed.
(2) Although bleeding is usually self-limited, intra- and extraparenchymal bleeding is possible. The urine drainage
should be monitored closely. Initially, the drainage will be bloody, but this should clear over 48 hours. The
nephrostomy tube may need to be flushed with normal saline per physician preference to assure patency of the
tube. Large amounts of bright red blood may be cause for concern and requires further evaluation, often
angiography.
(3) Although the patient is administered appropriate prophylactic antibiotic within 60 minutes of the procedure
start time, fever or rigors related to transient bacteremia can still occur immediately postprocedure. The patient
should be treated symptomatically and monitored closely for urosepsis, which would necessitate urgent
treatment with a plan for an increased level of care.
3. Instructions for nephrostomy tube care
a. Meticulous care of the nephrostomy and nephroureteral tubes are critical in order to maintain patency and
reduce the rate of infection in the system. It is important to keep nephrostomy drainage a closed system and as
clean as possible. Stress the importance of
(1) Hand hygiene prior to tube care
(2) Cleaning the access port with alcohol prior to flushing. Depending on the physician's preference and the
patient's clinical status, the tube may be flushed with 10 mL of normal saline to keep the tube patent by removing
debris which can build up in the lumen and cause an obstruction. When flushing is planned, a coupling device
with a port access, such as a three-way stopcock or Y-connector, is left between the catheter and the drainage
bag (Fig. e-103.1). Choosing the Y-connector may provide the following benefits, particularly for patients who
have bilateral nephrostomy tubes:
(a) Less uncomfortable than rigid stopcock when lying or sitting
(b) Decrease likelihood of skin injury from lying on top of the coupling device. Consider The Joint Commission's
National Patient Safety Goal 14.01.01 related to pressure ulcer prevention.
(c) Easier for patients to understand and perform proper flushing
i. For most patients, the tubing extends long enough for the patient to reach the flushing port more easily than
the stopcock.
P.899
ii. Once the clamp is closed, the tube can only flush toward the nephrostomy tube, rather than toward the bag;
this may increase the likelihood that the tube will remain patent.
b. Patient condition and physician preference. The tube may be flushed with normal saline to maintain patency
depending on patient condition and physician preference.
c. Dressings should be changed routinely according to physician preference. Dressing should use clean
technique. When changing the dressing, the tube insertion site as well as the surrounding skin should be
inspected for signs of infection or local irritation. The skin can be washed with clean gauze and water. The skin
should be dry prior to reapplying a clean dressing.
d. Nephrostomy tubes should not be submerged in standing water due to risk of infection (i.e., tubs or
swimming). After 48 hours, showering is permitted similar to biliary catheters.
e. Supplies should include a Foley bag to allow for greater volume capacity for night drainage.
4. Follow-up care
a. If an initial attempt to cross the lesion is not successful, a nephrostomy tube must be placed to external
drainage. After external drainage and decompression of the system, the patient may return for a second attempt
to cross the lesion.
b. In the case of a ureteral stricture, the patient may need to return for serial ureteroplasty procedures and
sequential upsizing of stents to allow for remodeling of the stricture around the stent until the stricture remains
open.
c. If the patient has a nephroureteral stent, with the external portion capped off, the patient will need to be
supplied with a drainage bag and instructions how to attach it, should the patient experience signs or symptoms
of obstruction or infection.
d. Nephrostomy catheters and nephroureteral stents are typically exchanged every 3 months. Catheter
exchanges are typically an outpatient procedure and performed as outpatients. A single dose of antibiotics is
typically administered.
Abscess Drainage Catheter Care

The symptomatic patient who presents with imaging studies demonstrating drainable fluid collection(s) is a
candidate for image-guided percutaneous drainage and placement of an abscess drainage catheter(s). The fluid
collections are fully aspirated at the time of procedure, and the fluid is sent off for further diagnostic testing (e.g.,
Gram stain, culture and sensitivities, creatinine, triglycerides, bilirubin, amylase and lipase) to guide further
management. Image-guided drainage and placement of a catheter for abscesses and other abnormal fluid
collections have resulted in reduced mortality and morbidity, reduced hospital costs and length of stay (4).
a. Hospital admission or overnight observation is advisable whenever a potentially infected fluid collection is
drained in order to continue preprocedure IV antibiotics and observe for postprocedure bacteremia or sepsis.
b. Select patients who are very compliant and in good physical condition can sometimes be discharged the
following day and followed closely as outpatients.
c. Postprocedure orders include, at a minimum, monitoring vital signs and recording catheter output.
d. Careful access planning usually minimizes the risk of bleeding, unless drainage is of abdominal viscera such
as the liver, kidney, or spleen where it is less predictable.
2. Instructions for abscess tube care
a. The abscess drainage catheter is typically a looped (pigtail) catheter secured by an internal locking
mechanism. The size of the catheter (8 to 14 Fr.) can vary based on the size and viscosity of the fluid collection
being drained.
P.900
b. The catheter is secured to the skin by a fixation device and/or suture. Avoid kinking or excessive bending of
the catheter when securing it to the fixation device to encourage effective drainage. Ensure the abscess
drainage catheter is always oriented to facilitate drainage by gravity.
c. The catheter is attached to a three-way stopcock/MicroClave (needleless Luer access) and connector tubing
to an external collection bag. The external collection bag is secured to the patient's body or clothing to avoid
traction on the catheter (Fig. e-103.2).
d. Abscess drainage catheters are typically flushed with 10 mL of sterile normal saline every 8 hours to maintain
patency and to irrigate the cavity (particularly for viscous collections). The size of the fluid cavity and catheter
lumen is considered when flush orders are implemented to avoid over distending the fluid cavity.
e. Wash your hands thoroughly with soap and water. The sterile cap attached to a three-way stopcock wiped
with alcohol facilitates sterile technique during catheter irrigation. Attach a sterile prefilled 10-mL normal saline
syringe to the sterile cap. Turn the three-way stopcock valve, so 5 mL of normal saline may be flushed toward
the catheter. Then turn the three-way stopcock valve the opposite direction and flush 5 mL of normal saline
toward the external collection bag. Return the valve to its original position to allow drainage of fluid into the
external collection bag.
f. Aspiration and irrigation through the abscess catheter may be required to break down suspected or known
loculations to encourage complete drainage of fluid.
g. Catheter output and drainage quality should be recorded daily. Be sure that the quantity of irrigant used to
flush the catheter is not included in daily output measurements.
h. Change the dressing and/or fixation device when soiled or loose.
i. The connector tubing and external bag should be changed when drainage output becomes minimal so that the
quality of the fluid can be accurately assessed. This would aid in the determination of abscess resolution for
catheter removal.
3. Follow-up care
a. Catheter removal is often advisable 48 hours following placement for low volume collections appearing
nonpurulent at the time of catheter placement with negative Gram stain and no growth on microbiology cultures.
b. For infected fluid collections, catheter removal is considered when:
(1) Patients exhibit clinical signs of improvement and are afebrile.
(2) The quality of the drainage appears nonpurulent.
(3) There is no associated fistula (5).
(4) The volume of drainage is less than 20 mL per day.
(a) For deep pelvic abscess drained via transgluteal, transrectal, or transvaginal, some have advocated the daily
required output should be less than 10 mL a day (5).
c. Persistent output of greater than 40 mL per day despite complete drainage of fluid cavity is suggestive of a
fistula from biliary, pancreatic, gastrointestinal, or lymphatic source. A contrast injection through the existing
catheter under fluoroscopy may be performed to confirm the source of persistent drainage and to direct further
intervention (6).
d. Repeat imaging prior to catheter removal may be prudent to ensure correct catheter position and to ensure
complete resolution of abscess. If drainage of the abscess was incomplete due to loculations and/or
hyperviscosity, exchange of current catheter for larger lumen catheter or instillation of a fibrinolytic agent such as
tissue plasminogen activator (tPA) can be considered and administered by the medical team (7). Depending on
the size of the abscess, 4 mg of tPA diluted in 10 to 30 mL of normal saline is used. The catheter is then capped
and mixture is removed after an hour. This may be repeated three times.
P.901
FIGURE e-103.2 • Components of abscess drainage catheter and drainage bag. (With permission by Dr. Paul
Shyn, MD/Maye Chan, PA-C, Brigham and Women's Hospital, Cross Sectional Interventional Drainage Catheter
Pamphlet.)
P.902
e. Premature removal of abscess drainage catheter may result in recurrence necessitating repeat drainage
and/or hospitalization.
f. Malfunctioning encrusted or occluded catheter(s) may require exchange for a new catheter. Dislodged
catheters may require exchange or replacement.
g. As the abscess cavity collapses, patients may report increased discomfort and minor leakage of clear fluid
around the catheter site when attempting to flush the catheter. Decreasing the flush amount to maintain patency
of the catheter can be considered until patient can be evaluated.
h. Routine catheter exchange is recommended to prevent degradation of catheter integrity every 6 months.
Please check specific catheter's manufacturer's recommendation for routine changes.
General Discharge Planning and Education

1. Stable patients without clinical signs of infection may be discharged with a drainage catheter in place.
a. Antibiotic therapy may be prescribed as appropriate to the clinical situation.
b. The risk of bleeding postprocedure versus risk of thrombosis is considered when restarting anticoagulants.
Typically, anticoagulants can be resumed within 24 hours. Earlier anticoagulation may be required for a patient
with higher risk of thrombosis. The referring physician and interventional radiologist must collaborate to create a
plan to balance these risks (8).
2. An assessment of the patient's ability to care for a drainage catheter at home is a priority in discharge
planning. This assessment includes family members who may be assisting in the patient's care.
3. Tube care instructions should be written and reviewed with the patient and any caregiver before discharge. To
assure the patient and caregiver is prepared to manage the tube, it is best to require they demonstrate tube care.
This will allow for any questions or problems to be addressed.
4. Home care services, if needed, should be in place before the patient is discharged.
5. The patient will need to be discharged with adequate supplies to last until home care services are available.
The patient should always be sent home with an extra drainage bag and instructions how to attach it for external
drainage, should the patient have any signs or symptoms of obstruction or infection.
6. If the tube requires flushing, “Y” connection tubing or a three-way stopcock should be added to the drainage
system to assure that flushing can be done while maintaining a closed system. Provision for saline for flushing
needs to be arranged.
7. Ensure that the patient has telephone numbers to reach a health care professional 24 hours a day with any
questions and concerns. These numbers should be included in the discharge instructions.
8. The patient should be instructed to contact the interventional radiology (IR) service for the following urgent
situations representing symptoms of infection, tube dysfunction, and/or the need for urgent tube replacement:
a. Fever of 101°F or greater and/or shaking chills
b. Resistance or pain with flushing
c. Leakage around the tube at the exit site
d. Nausea/vomiting
e. A change in the quality or quantity of drainage
f. The tube pulls back or falls out
g. Redness, pain, swelling, or purulent drainage at the tube exit site
h. The stitch comes out
i. New or increased pain related to the drain
P.903
References
1. Saad WE, Wallace MJ, Wojak JC, et al. Quality improvement guidelines for percutaneous transhepatic
cholangiography, biliary drainage, and percutaneous cholecystostomy. J Vasc Interv Radiol . 2010;21:789-
795.
2. Mosler, P. Management of acute cholangitis. Gastroenterol Hepatol (N Y). 2011;7(2):121-123.
3. Ramchandani P, Cardella JF, Grassi CJ, et al. Quality improvement guidelines for percutaneous
nephrostomy. J Vasc Interv Radiol . 2003;14:S277-S281.
4. Wallace MJ, Chin KW, Fletcher TB, et al. Quality improvement guidelines for percutaneous
drainage/aspiration of abscess and fluid collections. J Vasc Interv Radiol . 2010;21:431-435.
5. Charles, HW. Abscess drainage. Semin Intervent Radiol . 2012;29(4):325-336.
6. Golfieri R, Cappelli A, Giampalma E, et al. CT-guided percutaneous pelvic abscess drainage in Crohn's
disease. Tech Coloproctol . 2006;10(2):99-105.
7. Beland MD, Gervais DA, Levis DA, et al. Complex abdominal and pelvic abscesses: efficacy of adjunctive
tissue-type plasminogen activator for drainage. Radiology. 2008;247:567-573.
2012;23:727-736.

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Editors

Krishna Kandarpa MD, PhD

Sun Ho Ahn, MD, FSIR

Ronald S. Arellano, MD, FSIR

Jamie B. Arton, MHS, PA-C

Susan Benveniste, BSN, RN, CRN

Michael A. Bettmann, MD, FACR, FSIR

Daniel B. Brown, MD, FSIR

Michael A. Bruno, MS, MD, FACR

Francisco Cesar Carnevale, MD, PhD

Maye M. Chan, PA-C

John Chung, MD, FRCPC

Petra Clark, MS, CNS-AG, RN, CRN

Timothy W.I. Clark, MD, FSIR

Sarah D. Cohn, RN, JD, FACNM

Anne M. Covey, MD, FSIR

Laura Crocetti, MD, PhD, EBIR

André Moreira de Assis, MD

Joseph P. Erinjeri, MD, PhD

Khashayar Farsad, MD, PhD

Ripal T. Gandhi, MD, FSVM

Christos S. Georgiades, MD, PhD, FSIR

Jafar Golzarian, MD, FSIR

Rulon L. Hardman, MD, PhD

Ziv J. Haskal, MD, FSIR, FAHA, FACR

Claudia I. Henschke, PhD, MD

Manraj K.S. Heran, MD, FRCPC

Mikhail C.S.S. Higgins, MD, MPH

Stephen G.F. Ho, MD, FRCPC

David W. Hunter, MD, FSIR, FACR

M. Fuad Jan, MBBS, MD, FACC, FACCP

D. Thor Johnson, MD, PhD

Michele H. Johnson, MD, FACR

S. Lowell Kahn, MD, MBA

John A. Kaufman, MD, MS, FSIR

Jin Hyoung Kim, MD, PhD

Sebastian Kos, EBIR, FCIRSE

David A. Kumpe, MD, FSIR

Riccardo Lencioni, MD, FSIR, EBIR

Robert J. Lewandowski, MD, FSIR

David Li, MD, PhD

Leonard J. Lind, MD, FCCM

David M. Liu, MD, FRCPC, FSIR

Robert A. Lookstein, MD, FSIR, FAHA

Karen Marshall, RN, BSN

Alan H. Matsumoto, MD, FACR, FSIR, FAHA

Ellen McKeon-Levine, RN, BSN

DéAnn O. McNamara, MS, ACNP-BC, CRN

Donald L. Miller, MD, FSIR, FACR

Robert J. Min, MD, MBA

Jennifer P. Montgomery, MD, PhD

Airton Mota Moreira, MD, PhD

Peter L. Munk, MDCM, FRCPC, FSIR

Kieran Murphy, MB, FRCPC, FSIR

Susan Kiernan O'Horo, MD, MPH, FSIR

Aneeta Parthipun, MBBS, BSc (Hons), FRCR

Aalpen A. Patel, MD, FSIR

Parag J. Patel, MD, MS

Edward F. Patz Jr., MD