Operative Techniques in Vascular Surgery

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Operative techniques in vascular surgery / editor, Ronald L. Dalman ; editor-in-chief, Michael W. Mulholland.
p. ; cm.
Includes bibliographical references and index.
ISBN 978-1-4511-9020-5 (alk. paper)
I. Dalman, Ronald L., editor. II. Mulholland, Michael W., editor. III. Operative techniques in surgery. Contained in (work): IV.
Operative techniques in transplantation surgery. Contained in (work):
[DNLM: 1. Vascular Surgical Procedures—methods. 2. Carotid Arteries—surgery. 3. Vascular Diseases—surgery. WG 170]
RD120.7
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Dedication
The love and support of my wife, Jocelyn J. Dunn MD, continues to enable all my professional
accomplishments.
—Ronald L. Dalman
Contributing Authors
Georges E. Al Khoury, MD
Assistant Professor of Surgery
Department of Surgery
Division of Vascular Surgery
University of Pittsburg School of Medicine
Pittsburgh, Pennsylvania
George J. Arnaoutakis, MD
Fellow in Cardiothoracic Surgery
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
Ramin E. Beygui, MD, FACS

Associate Professor
Department of Cardiothoracic Surgery
Stanford University
Stanford, California
Elizabeth Blazick, MD
Fellow
Division of Vascular and Endovascular Surgery
Massachusetts General Hospital
Boston, Massachusetts
Danielle E. Cafasso, DO
Tripler Army Medical Center
Honolulu, Hawaii
Rabih A. Chaer, MD
Associate Professor of Surgery
University of Pittsburgh School of Medicine
Venita Chandra, MD
Clinical Assistant Professor
Stanford University School of Medicine
James Chang, MD
Chief
Division of Plastic and Reconstructive Surgery
Professor of Surgery and Orthopedic Surgery
Stanford University Medical Center
Roberto Chiesa, MD
Scientific Institute Ospedale San Raffaele
Chair of Vascular Surgery
School of Medicine
Vita-Salute San Raffaele University
Milan, Italy
Efrem Civilini, MD
School of Medicine
Milan, Italy
Mark F. Conrad, MD
Massachusetts General Hospital
Boston, Massachusetts
Ronald L. Dalman, MD
Chidester Professor of Surgery
Division Chief of Vascular Surgery
Scott M. Damrauer, MD
Instructor in Surgery
Fellow
Division of Vascular Surgery and Endovascular Therapy
Hospital of the University of Pennsylvania
Philadelphia, Pennsylvania
Narasimham L. Dasika, MD
Associate Professor of Radiology
Department of Radiology
Division of Vascular and Interventional Radiology
University of Michigan Health System
Ann Arbor, Michigan
Brian G. DeRubertis, MD
David Geffen School of Medicine at University of California, Los Angeles
Los Angeles, California
Michael J. Englesbe, MD
University of Michigan Medical School
Ann Arbor, Michigan
Julie Ann Freischlag, MD

William Steward Halsted Professor
Chair
The Johns Hopkins Hospital
Johns Hopkins Medical Institutions
Baltimore, Maryland
Michael G. Galvez, MD
Resident
Division of Plastic and Reconstructive Surgery
Sung Wan Ham, MD

Vascular Surgery Fellow
Vascular Surgery Division
University of Southern California
Los Angeles County Medical Center
E. John Harris, Jr., MD

Professor of Surgery
Grace Huang, MD
Resident
Surgery
Los Angeles County Medical Center
Zhen S. Huang, MD
Fellow in Vascular and Endovascular Surgery
Department of Vascular and Endovascular Surgery
New York-Presbyterian Hospital
Weill Cornell Medical Center
New York, New York
Nathan Itoga, MD
Vascular Surgery Resident
Geetha Jeyabalan, MD
University of Pittsburgh Medical Center
Karina S. Kanamori, MD
Clinical Research Fellow
Mayo Clinic
Rochester, Minnesota
Sharon C. Kiang, MD
Department of General Surgery
Ronald Reagan UCLA Medical Center
Alexander Kulik, MD, MPH, FRCSC

Cardiovascular Surgeon
Lynn Heart & Vascular Institute
Boca Raton Regional Hospital
Affiliate Associate Professor
Charles E. Schmidt College of Medicine
Florida Atlantic University
Boca Raton, Florida
Gregory J. Landry, MD
Knight Cardiovascular Institute
Oregon Health & Science University
Portland, Oregon
Cheong J. Lee, MD
Medical College of Wisconsin
Milwaukee, Wisconsin
Jason T. Lee, MD
Associate Professor of Vascular Surgery
Peter H. U. Lee, MD, MPH

Clinical Instructor
Department of Cardiothoracic Surgery
Stanford University
W. Anthony Lee, MD, FACS

Director
Endovascular Program
Lynn Heart & Vascular Institute
Boca Raton Regional Hospital
Boca Raton, Florida
Amit K. Mathur, MD
Clinical Lecturer
Transplant Fellow
Section of Transplantation Surgery
Ann Arbor, Michigan
Germano Melissano, MD
School of Medicine
Milan, Italy
Matthew Mell, MD
Joseph L. Mills, Sr., MD

Chief
Co-Director
Southern Arizona Limb Salvage Alliance
University of Arizona Health Sciences Center
Tucson, Arizona
Mark D. Morasch, MD, FACS

Vascular Surgeon
Heart and Vascular Center
St. Vincent Healthcare
Billings, Montana
Gustavo S. Oderich, MD
Director
Endovascular Therapy
Director
Edward Rogers Clinical Research Fellowship
Mayo Clinic
Rochester, Minnesota
F. Gallardo Pedrajas, MD
Consultant Angiology and Vascular Surgery
Hospital University of Santiago
Santiago de Compostela
Compostela, Spain
Thomas Reifsnyder, MD
Assistant Professor
Chief
Vascular Laboratory
Johns Hopkins Bayview Medical Center
Johns Hopkins Medical Institutions
Baltimore, Maryland
Enrico Rinaldi, MD
School of Medicine
Milan, Italy
Darren B. Schneider, MD
Chief of Vascular and Endovascular Surgery
Weill Cornell Medical College
New York-Presbyterian Hospital
Weill Cornell Medical Center
New York, New York
Peter A. Schneider, MD
Division of Vascular Therapy
Hawaii Permanente Medical Group
Kaiser Foundation Hospital
Honolulu, Hawaii
Benjamin W. Starnes, MD, FACS

Professor and Chief of Vascular Surgery
University of Washington
Seattle, Washington
Robert W. Thompson, MD
Radiology
Cell Biology
Physiology
Vice Chair for Research
Director
Washington University Thoracic Outlet Syndrome Center
Barnes-Jewish Hospital
Washington University School of Medicine
St. Louis, Missouri
Brant W. Ullery, MD
Stanford, Carolina
Vinit N. Varu, MD
Ranjith Vellody, MD
Assistant Professor of Radiology
Division of Vascular and Interventional Radiology
Department of Radiology
Ann Arbor, Michigan
Chandu Vemuri, MD
Fellow in Vascular Surgery
Barnes-Jewish Hospital
St. Louis, Missouri
Fred Weaver, MD, MMM

Chief
Division of Vascular Surgery and Endovascular Therapy
Keck Hospital
Edward Y. Woo, MD
Director
Regional Vascular Program
MedStar Washington Hospital Center
Chief
Vascular Surgery
MedStar Georgetown University Hospital
Washington, DC
Mohamed A. Zayed, MD, PhD, RPVI

Section of Vascular Surgery
St. Louis, Missouri
Luke X. Zhan, MD, PhD

Resident
Southern Arizona Limb Salvage Alliance
Tucson, Arizona
Wei Zhou, MD
Stanford University
Chief
Vascular Surgery
VA Palo Alto Health Care System
Palo Alto, California
Series Preface
Operative therapy is complex, technically demanding, and rapidly evolving. Although there are a
number of standard textbooks that cover aspects of general, thoracic, vascular, or transplant surgery,
Operative Techniques in Surgery is unique in offering a comprehensive treatment of contemporary
procedures. Open operations, laparoscopic procedures, and newly described robotic approaches are
all included. Where alternative or complementary approaches exist, all are provided. The scope and
ambition of the project is one of a kind.
The series is organized anatomically in sections covering thoracic surgery, upper gastrointestinal
surgery, hepato-pancreatico-biliary surgery, and colorectal surgery. Breast surgery, endocrine
surgery, and topics related to surgical oncology are included in a separate volume. Modern
approaches to vascular surgery and transplantation surgery are also covered in separate volumes.
The series editors are renowned surgeons with expertise in their respective fields. Each is a
leader in the discipline of surgery, each recognized for superb surgical judgment and outstanding
operative skill. Breast surgery, endocrine procedures, and surgical oncology topics were edited by
Dr. Michael Sabel of the University of Michigan. Thoracic and upper gastrointestinal surgery topics
were edited by Dr. Mary Hawn of the University of Alabama at Birmingham, with Dr. Steven Hughes
of the University of Florida directing the volume on hepato-pancreatico-biliary surgery. Dr. Daniel
Albo of Baylor College of Medicine directed the volume dedicated to colorectal surgery. Dr. Ronald
Dalman of Stanford University edited topics related to vascular surgery, including both open and
endovascular approaches. The discipline of transplantation surgery is represented by Dr. Michael
Englesbe of the University of Michigan. In turn, the editors have recruited contributors that are world-
renowned; the resulting volumes have a distinctly international flavor.
Surgery is a visual discipline. Operative Techniques in Surgery is lavishly illustrated with a
compelling combination of line art and intraoperative photography. The illustrated material was all
executed by a single source, Body Scientific International, to provide a uniform style emphasizing
clarity and strong, clean lines. Intraoperative photographs are taken from the perspective of the
operating surgeon so that operations might be visualized as they would be performed. The result is
visually striking, often beautiful. The accompanying text is intentionally spare, with a focus on crucial
operative details and important aspects of postoperative management.
The series is designed for surgeons at all levels of practice, from surgical residents to advanced
practice fellows to surgeons of wide experience. The incredible pace at which surgical technique
evolves means that the volumes will offer new insights and novel approaches to all surgeons.
Operative Techniques in Surgery would be possible only at Wolters Kluwer Health, an
organization of unique vision, organization, and talent. Brian Brown, executive editor, Keith
Donnellan, acquisitions editor, and Brendan Huffman, product development editor, deserve special
recognition for vision and perseverance.
Michael W. Mulholland, MD, PhD
Preface
The pace of innovation in vascular surgery continues to accelerate. Driven by surgeons and industry
alike, catheter-based, image-guided intervention, coupled with minimally invasive or “hybrid”
exposures, are both revolutionizing care of the vascular patient. The surgeon-authors featured herein
represent the vanguard of this movement—leveraging all the advantages inherent in new technology
while maintaining fidelity with the fundamental principles of open surgery.
As part of the series Operative Techniques in Surgery, this atlas was created to provide a
comprehensive reference for practicing surgeons looking to incorporate new skills in vascular
disease management as well as trainees at all levels looking for expert guidance. Familiarity of the
reader with endovascular skills as well as a representative range of device options for arterial and
venous intervention are assumed—those interested in more background should consult a fundamental
reference first.
Successful completion of this project was enabled by the steady and encouraging guidance of the
series editor, Dr. Michael W. Mulholland, and the professional editorial and project management
staff at Wolters Kluwer Health, especially Brendan Huffman and Keith Donnellan. Dr. Jason Lee
provided invaluable structural guidance and contributor recommendations. On behalf of everyone
involved on this project, it is our shared hope that the thousands of hours of operative insights
condensed in this edition will inspire the next generation of vascular specialists.
Ronald L. Dalman, MD
Contents
Contributing Authors
Series Preface
Preface
Section I Cerebrovascular Arterial Surgery/Intervention
1 Arch and Great Vessel Reconstruction with Debranching Techniques

W. Anthony Lee and Alexander Kulik
2 Extrathoracic Revascularization (Carotid–Carotid, Carotid–Subclavian
Bypass and Transposition)
Edward Y. Woo and Scott M. Damrauer
3 Carotid Surgery: Interposition/Endarterectomy (Including
Eversion)/Ligation
Vinit N. Varu and Wei Zhou
4 Carotid Surgery: Bifurcation Stenting with Distal Protection
Zhen S. Huang and Darren B. Schneider
5 Carotid Surgery: Distal Exposure and Control Techniques and Complication
Management
Cheong J. Lee
6 Vertebral Transposition Techniques and Stenting
Mark D. Morasch
Section II Management of the Thoracic Outlet

7 Neurogenic Thoracic Outlet Syndrome Exposure and Decompression:
Supraclavicular
Robert W. Thompson and Chandu Vemuri
8 Neurogenic Thoracic Outlet Syndrome Exposure and Decompression:
Transaxillary
George J. Arnaoutakis, Thomas Reifsnyder, and Julie Ann Freischlag
9 Venous and Arterial Thoracic Outlet Syndrome
Jason T. Lee
Section III Upper Extremity Reconstruction/Revascularization

10 Proximal to the Wrist: Upper Extremity Reconstruction/Revascularization
Mohamed A. Zayed and Ronald L. Dalman
11 Distal to the Wrist: Upper Extremity Revascularization and Reconstruction
Michael G. Galvez and James Chang
Section IV Thoracic Aorta Distal to the Pericardium

12 Exposure and Open Surgical Reconstruction in the Chest: The
Thoracoabdominal Aorta
Germano Melissano, Efrem Civilini, Enrico Rinaldi, and Roberto Chiesa
13 Thoracic Aortic Stent Graft Repair for Aneurysm, Dissection, and
Traumatic Transection
Brant W. Ullery and Jason T. Lee
14 Exposure and Open Surgical Management at the Diaphragm
Peter H. U. Lee and Ramin E. Beygui
Section V Hybrid, Open and Endovascular Approaches to the

Suprarenal Abdominal Aorta
15 Retroperitoneal Aortic Exposure

Matthew Mell
16 Hybrid Revascularization Strategies for Visceral/Renal Arteries
Benjamin W. Starnes
17 Snorkel/Chimney and Periscope Visceral Revascularization during Complex
Endovascular Aneurysm Repair
Jason T. Lee and Ronald L. Dalman
18 Branched and Fenestrated Endovascular Stent Graft Techniques
Gustavo S. Oderich and Karina S. Kanamori
Section VI Celiac, Mesenteric, Splenic, Hepatic and Renal
Artery Disease Management
19 Stenting, Endografting, and Embolization Techniques: Celiac, Mesenteric,

Splenic, Hepatic, and Renal Artery Disease Management
Mohamed A. Zayed and Ronald L. Dalman
20 Visceral Reconstruction to Facilitate Cancer Management: Celiac,
Mesenteric, Splenic, Hepatic and Renal Artery Disease Management
Mohamed A. Zayed and E. John Harris, Jr.
21 Hepatic- and Splenic-Based Renal Revascularization
Fred Weaver, Sung Wan Ham, and Grace Huang
Section VII The Abdominal Aorta and Iliac Arterial System

22 Advanced Aneurysm Management Techniques: Open Surgical Anatomy
and Repair
Elizabeth Blazick and Mark F. Conrad
23 Advanced Aortic Aneurysm Management: Endovascular Aneurysm Repair
—Standard and Emergency Management
Vinit N. Varu and Ronald L. Dalman
24 Advanced Aneurysm Management Techniques: Management of Internal
Iliac Aneurysm Disease
W. Anthony Lee
25 Occlusive Disease Management: Isolated Femoral Reconstruction,
Aortofemoral Open Reconstruction, and Aortoiliac Reconstruction with
Femoral Crossover for Limb Salvage
Nathan Itoga and E. John Harris, Jr.
26 Occlusive Disease Management: Iliac Angioplasty and Femoral
Endarterectomy
Venita Chandra
Section VIII Infrainguinal Arterial Disease Management/Limb

Salvage Strategies
27 Management of the Infected Femoral Graft

Matthew Mell
28 Surgical Exposure of the Lower Extremity Arteries
Luke X. Zhan and Joseph L. Mills, Sr.
29 Percutaneous Femoral–Popliteal Reconstruction Techniques: Reentry
Devices
Danielle E. Cafasso and Peter A. Schneider
30 Percutaneous Femoral–Popliteal Reconstruction Techniques: Antegrade
Approaches
F. Gallardo Pedrajas and Peter A. Schneider
31 Maximizing Vein Conduit for Autogenous Bypass
Gregory J. Landry
32 Tibial Interventions: Tibial-Specific Angioplasty Considerations and
Retrograde Approaches
Georges E. Al Khoury and Rabih A. Chaer
33 Perimalleolar Bypass and Hybrid Techniques
Geetha Jeyabalan and Rabih A. Chaer
Section IX Surgical Management of Venous Disease

34 Acute Iliofemoral Deep Vein Thrombosis and May-Thurner Syndrome:
Surgical and Interventional Management
Sharon C. Kiang and Brian G. DeRubertis
35 Transjugular Intrahepatic Portosystemic Shunt
Ranjith Vellody and Narasimham L. Dasika
36 Surgery for Portal Hypertension in Children and Adults
Michael J. Englesbe and Amit K. Mathur
Index
Arch and Great Vessel Reconstruction with
Chapter 1 Debranching Techniques
W. Anthony Lee Alexander Kulik
DEFINITION
■
An aortic arch aneurysm is defined as dilation of the aortic arch to greater than 5 cm in diameter.
Rarely occurring in isolation, aneurysms of the aortic arch are often extensions of aneurysms
present in the ascending or descending aorta. Causes of aortic arch aneurysms included
atherosclerotic degeneration, cystic medial degeneration, aortic dissection, congenital aortopathy
(i.e., bicuspid aortic valve), penetrating aortic ulcer, previous traumatic transection (chronic
pseudoaneurysm), and previously repaired aortic coarctation (postsurgical pseudoaneurysm).
Aortic arch aneurysms have traditionally been repaired with graft replacement of the aorta, with or
without an elephant trunk, using cardiopulmonary bypass and deep hypothermic circulatory arrest.
With the advent of thoracic endovascular aortic repair (TEVAR), debranching of the
brachiocephalic vessels is a recently developed technique that takes advantage of the reduced
surgical trauma associated with stent grafting.1 Debranching functionally extends the proximal
landing zone by repositioning the inflow of the brachiocephalic arteries toward the proximal
ascending aorta. This facilitates endovascular stent graft repair of the aortic aneurysm by allowing
stent coverage across the ostia of the arch vessels, producing a stable and fixed proximal landing
zone in the ascending aorta.
PATIENT HISTORY AND PHYSICAL FINDINGS

■
Aortic arch aneurysms are usually diagnosed as incidental findings noted on imaging studies, such as
a chest x-ray or computed tomography (CT) scan, to evaluate other concurrent medical conditions.
■
Most patients have no symptoms from their aneurysms. Symptoms, if they exist, may include chest or
back pain from aneurysmal growth or those associated with compression of adjacent structures
(i.e., trachea, esophagus). Hoarseness may develop from stretching of the left recurrent laryngeal
nerve (Ortner’s syndrome). Acute chest or back pain, with or without signs of shock, should raise
the suspicion of impending aortic rupture and/or acute aortic dissection. Additional details
regarding a patient’s past medical history should be gathered, including a history of previous
coronary intervention, previous cardiac surgery, known valvular heart disease, previous aneurysm
surgery, or a family history of aortopathy.
■
The physical examination is often unremarkable. However, attention should be directed to the
presence of aortic valve insufficiency (diastolic murmur, widened pulse pressure), previous
surgical incisions, and the presence of concomitant peripheral vascular disease.
IMAGING AND OTHER DIAGNOSTIC STUDIES

■
Although a routine chest x-ray may be the first imaging test to note an aortic arch abnormality,
further imaging is necessary, including a CT scan of the aorta (FIG 1) and an echocardiogram.
■
An arterial phase CT angiogram should evaluate the entire length of the aorta, from the level of the
skull base proximally to the femoral heads distally, to ensure visualization of the vertebral and
iliofemoral arteries, respectively. The CT images are then processed using 3D imaging software
for case planning and device selection. A magnetic resonance imaging (MRI) or a noncontrast CT
scan will not suffice.
■
A transthoracic (2D) echocardiogram should be performed to assess left and right ventricular
function and to exclude the presence of significant valvular heart disease.
■
Strong consideration should be given to evaluating the anatomy of the coronary arteries in the
preoperative period. A CT coronary angiogram may be an option for younger patients or those
with complex proximal aortic dissection. However, if there is a strong suspicion of coronary
disease, then a preoperative conventional coronary angiogram should be performed, including
those patients older than 40 years of age and those with a history of smoking.
SURGICAL MANAGEMENT
Preoperative Planning
■
Indications for repair of an aortic arch aneurysm include large aneurysmal size (>5.5 cm), rapid
growth (>0.5 cm per year), the presence of chest pain or back pain unexplained by other causes,
and compression of adjacent organs (esophagus, trachea, or left main bronchus).2
■
More aggressive size criteria may be applied for patients with Marfan’s syndrome (repair at 4.5 to
5 cm). However, stent graft outcomes appear less favorable in patients with connective tissue
disease, and therefore, alternative surgical techniques (such as conventional aortic replacement
surgery) should be considered.2
■
The presence of significant concurrent cardiac disease may alter the surgical approach. Should
significant coronary artery or valvular heart disease be identified in the preoperative period,
consideration may be given to performing concomitant coronary artery bypass grafting (CABG) or
valve replacement at the time of the aortic debranching procedure.
■
During the second stage of the arch repair, stent graft deployment in the distal ascending aorta may
require the placement of a guidewire across the aortic valve into the left ventricular cavity. The
presence of a mechanical aortic prosthetic valve, through which a guidewire and the delivery
system cannot safely be placed, may require a single-stage approach with deployment of the stent
graft at the time of debranching (see endovascular second stage). A bioprosthetic valve in the
aortic position may allow for careful transvalvular introduction of devices, with preference to
bovine pericardial valves over porcine valves.
■
Selection of the ideal treatment strategy for repair of an aortic arch aneurysm remains controversial
and is dictated by surgical experience and local area expertise. Aortic arch debranching and stent
graft completion is an appealing repair option that avoids a thoracotomy incision and may avert the
use of cardiopulmonary bypass and circulatory arrest. These types of hybrid procedures may be
performed either as single- or two-stage repairs. However, conventional open replacement of the
entire aortic arch,3,4 or replacement of the ascending aorta and proximal arch with the creation of
an elephant trunk followed by stent graft completion,1,5 should be considered as clinically
indicated.
■
Debranching of the aortic arch off the ascending aorta may not be applicable for a patient with an
aortic arch aneurysm who has previously undergone cardiac surgery and who is too high-risk for
consideration of redo sternotomy. In this case, an alternative option would include extra-anatomic
debranching of the aortic arch (carotid–carotid, carotid–subclavian) followed by stent graft repair
of the arch, with or without innominate artery chimney (snorkel) stenting.6
■
The preoperative CT scan requires careful review before undertaking an aortic arch debranching
operation. Arch branch anatomy and appropriate landing zones need to be identified proximal and
distal to the arch aneurysm, with criteria similar to those that apply for stent graft repair of a
descending thoracic aortic aneurysm. Anatomic variations of the aortic arch anatomy may require
modification of the debranching procedure. These include a bovine aortic arch (common trunk of
the innominate and left common carotid), arch origin of left vertebral artery, and an aberrant right
subclavian artery.
■
The ascending aorta is typically 6 to 7 cm in length from the sinotubular junction to the innominate
artery. Placement of the proximal inflow anastomosis as low as possible on the ascending aorta
(just distal to the sinotubular junction) will result in an optimal 3- to 4-cm proximal landing zone
for the stent graft repair. The largest currently available thoracic stent grafts are 42 to 46 mm in
diameter. To provide a safe and durable proximal landing zone and avoid a proximal type I
endoleak, we recommend replacement of an ascending aorta that is extremely short or if its
diameter is 36 mm or larger. Open replacement of the ascending aorta would be performed at the
time of the arch debranching procedure, with implantation of an aortic graft 34 mm or smaller.
■
The size of the iliofemoral arteries is worth noting on the preoperative CT study. The external iliac
arteries need to be larger than 7 mm in diameter to provide adequate vascular access to deliver the
stent graft devices during the second stage. An iliac artery conduit may be needed if the
iliofemoral arteries are extremely small or in the presence of severe calcification and occlusive
disease. Alternatively, a single-stage antegrade introduction of the stent graft from the ascending
aorta may be performed (see endovascular second stage) to avoid access problems from a
retrograde iliofemoral approach.
■
The diameters of the brachiocephalic arteries are measured on the preoperative CT scan to
determine the interposition graft sizes for the debranching procedure. Most frequently, the size of
the graft chosen for the innominate artery branch is 10 to 14 mm, with 6- to 8-mm grafts usually
used for the left carotid and left subclavian arteries.
■
Cerebral oximetry monitoring may be helpful for the aortic debranching procedure to monitor brain
perfusion before and after clamping of the brachiocephalic arteries. For the second-stage
endovascular procedure, cerebrospinal fluid (CSF) drains are placed preoperatively to reduce the
risk of spinal cord ischemia if a significant length of the descending thoracic aorta is to be
covered.
Positioning
■
For the arch debranching procedure, patients are positioned supine just as they are during standard
cardiac surgical operations. Prepping is performed from the neck to the knees, with draping higher
than usual to strategically provide access to the lower neck. The head may be turned slightly to the
right to facilitate extension of the sternotomy incision proximally along the left
sternocleidomastoid muscle.
TECHNIQUES
AORTIC ARCH DEBRANCHING

■
Although some advocate the use of a right thoracotomy incision or upper hemisternotomy, we prefer
to expose the ascending aorta through a conventional sternotomy incision. This provides optimal
visualization and control. The pericardium is incised and retracted.
■
The ascending aorta is carefully mobilized to facilitate later placement of a proximally positioned
side-biting clamp. The space between the left side of the aorta and the pulmonary artery is
dissected, with small vessels cauterized or clipped and divided. The ascending aorta is mobilized
proximally down to the level of the aortic root (sinotubular junction) to enable identification (and
avoid injury) to the right coronary artery.
■
The brachiocephalic arteries are circumferentially exposed. The innominate vein is mobilized and
retracted with an umbilical tape to facilitate exposure of the arch vessels (FIG 2). Uncommonly,
the innominate vein requires ligation and division to aid in arch exposure. The left subclavian
artery is often more posterior than expected, and exposure of this artery may be difficult. In these
circumstances, the sternotomy incision may be extended superiorly and leftward along the
sternocleidomastoid muscle. Alternatively, innominate and left carotid debranching may be
combined with a left carotid-subclavian bypass/transposition procedure, through a standard
supraclavicular approach, obviating the need to expose the left subclavian artery through the
sternotomy.
■
Although a preformed bifurcated or multilimb graft may be used, these occupy a large footprint and
reduce the length available for the ascending aortic landing zone. Instead, we prefer to construct a
Y-graft by sewing a beveled smaller Dacron graft end-to-side to larger Dacron graft (FIG 3). The
graft sizes are selected based on the measured diameters from the preoperative CT scan.
Typically, a 10- or 12-mm graft is used for the innominate artery, and a 6- or 8-mm graft is used
for the left carotid artery.
■
Heparin is administered to achieve an activated clotting time (ACT) of 200 seconds. The blood
pressure is lowered to 90 mmHg systolic, and an aortic side-biting clamp is placed on the right
anterolateral side (convexity) of the ascending aorta, as low as possible, with care not to
compromise the right coronary artery. A retraction suture in the right atrial appendage may be
needed to facilitate proximal aortic exposure. Consideration may be given to performing this and
subsequent steps in the operation with cardiopulmonary bypass to provide optimal hemodynamic
control during clamp application and removal and to improve brain protection with systemic
cooling in the range of 32°C to 34°C.
■
The proximal end of the larger (10 or 12 mm) graft is cut to the appropriate length so the Y-graft
easily reaches the arch vessels. The graft is beveled and sewn end-to-side to the ascending aorta
with a running 3-0 or 4-0 polypropylene suture (FIG 4). BioGlue may be applied to further support
the anastomosis. The aortic clamp is gently released. A large clip may be placed across the heel of
the anastomosis. This will help visualize the origin of the debranching graft from the ascending
aorta and precisely define the proximal landing zone without the need for contrast during the
second-stage endovascular procedure.
■
The innominate artery is transected, and the proximal end is oversewn with two layers of 4-0
polypropylene. The distal large end of the Y-graft is then tunneled underneath the innominate vein
and sewn end-to-end to the innominate artery with running 5-0 polypropylene (FIG 5).
■
Next, the left common carotid artery is transected, and the proximal end of the carotid artery is
oversewn with 4-0 polypropylene. The distal smaller end of the Y-graft is tunneled underneath the
innominate vein and sewn end-to-end to the carotid artery with running 5-0 polypropylene (FIG 6).
■
At this point, a decision needs to be made regarding the debranching strategy for the left subclavian
artery. Indications for left subclavian revascularization are controversial. Routine versus selective
strategies may be adopted.7 If the left subclavian artery needs to be revascularized but cannot
safely be exposed, a carotid–subclavian bypass can be performed as previously mentioned. If the
subclavian artery can be exposed, the distal anastomosis is created first using a 6- or 8-mm Dacron
graft anastomosed either end-to-end to the transected artery or end-to-side (functional end-to-end)
followed by ligation of the proximal artery in continuity. A side-biting clamp is then placed along
the carotid graft, and the subclavian graft is sutured end-to-side to the carotid graft with 5-0
polypropylene suture (FIG 7).
■
Protamine is administered to reverse the heparin, and hemostasis is ensured. The grafts should lie
tension free within the mediastinum. The pericardium may be partially closed over the grafts, with
care to avoid compression of the graft branches. Chest tubes are positioned, and the sternum is
closed routinely. After the sternum is closed, the blood pressure should be assessed in each arm
and cerebral oximetry monitored to confirm adequate perfusion through the graft branches and the
absence of graft compression.
ENDOVASCULAR SECOND STAGE

■
The endovascular second stage of the arch repair is conducted in a fairly similar manner to that of
stent graft repair of a descending thoracic aortic aneurysm, as described in Chapter 13 (Thoracic
Endografting).
■
The timing of the endovascular repair as a single versus staged approach remains controversial. We
prefer to delay the second stage depending on the clinical scenario. It can range from a few days
(same hospitalization) to several weeks (separate admission) to allow the patient to recover from
the first procedure. This reduces the overall physiologic stress on the patient.
■
Although we favor delivery of the stent graft in a retrograde manner from the iliofemoral arteries, in
cases of a mechanical aortic valve or severe iliofemoral occlusive disease, single-stage antegrade
deployment should be considered. The technical variations for these less common situations are
beyond the scope of the present chapter.
■
The site of insertion of the endovascular graft delivery system is decided based on the size and
quality of the access vessels. In general, the grafts are delivered through the common femoral
artery, whereas an iliac conduit may be required for very small or diseased iliofemoral arteries.
■
The delivery guidewire is placed in the left ventricle during the endovascular procedure to provide
sufficient proximal rail support for the endovascular graft.
■
The proximal stent graft is deployed in the ascending aorta just distal to the origin of the debranching
graft. During deployment, it is useful to lower the blood pressure using one of a variety of
pharmacologic, ventricular pacing or atrial inflow occlusion techniques.8
PEARLS AND PITFALLS

Indication ■ The preoperative CT angiogram should be reviewed in detail to
ensure the patient is a suitable candidate for aortic arch repair
with debranching and stent grafting, including appropriate landing
zones proximally and distally and adequate vascular access.
Proximal type I endoleak ■ To optimize the length of the proximal landing zone and prevent a
type I endoleak, the debranching graft should be placed as low as
possible on the ascending aorta. Preemptive replacement of the
ascending aorta should be performed if it is extremely short or its
diameter is >34 mm.
Mechanical aortic prosthesis ■ After aortic debranching, the endovascular graft delivery system
may have to cross the aortic valve. Although transvalvular
placement of a large sheath is relatively safe for native and
bioprosthetic valves, it is contraindicated for a mechanical aortic
valve. Antegrade stent graft deployment at the time of debranching
should be considered in the presence of a mechanical prosthesis.
Injury to right coronary ■ Care should be taken when applying the side-biting clamp low on
artery the ascending aorta to avoid occlusion or injury to the right
coronary artery.
Ascending aortic dissection ■ The systolic blood pressure should be lowered to <90 mmHg
when applying the side-biting clamp on the ascending aorta to
prevent injury and dissection of an already fragile and diseased
aorta.
Left subclavian artery ■ If the left subclavian artery is not easily accessible via the
sternotomy incision (large rotated aortic arch aneurysm), then
debranching of this artery can be performed via carotid–
subclavian bypass.
Compression and kinking of ■ Ideally, the main debranching graft should lie along the right side
debranching grafts of the ascending aorta to avoid compression by the sternum after
chest closure. The graft branches should lie tension free, with care
taken to avoid kinking at the time of pericardial and chest wall
closure.
POSTOPERATIVE CARE
■
Following the debranching procedure, patients are monitored in a cardiovascular surgical intensive
care unit for 48 hours, with a focus on neurologic status, applying standard postoperative cardiac
surgery protocols.
■
Chest tubes are typically removed 2 days after the debranching operation.
■
If a patient is recovering well after debranching without complication and has stable renal function,
then the stent graft completion can be performed 3 to 5 days postoperatively. In the event of a
major complication requiring extended recovery, the patient may be discharged to a rehabilitation
center. The stent graft procedure can be delayed for a few weeks. However, up to 25% of patients
may not return for their second stage.
■
Following the second-stage stent graft procedure, the blood pressure is augmented with fluid and
vasopressor support to achieve a target systolic blood pressure of 140 to 160 mmHg for 48 hours
to optimize spinal cord perfusion.
■
CSF drains are left open for 24 hours following stent grafting. Drainage is limited to less than 15 mL
per hour or less than 350 mL per day to avoid the potential risk of subdural hemorrhage. In the
absence of spinal cord injury, CSF drains are then clamped for 12 hours and subsequently
removed.
■
Follow-up CT angiograms of the aorta are performed at 1 and 6 months after the stent graft
procedure, and then yearly thereafter.
OUTCOMES
■
In the authors’ experience of 37 aortic arch debranching procedures,1 rates of spinal cord injury,
stroke, and 30-day mortality were 0%, 10.8%, and 16.2%, respectively. The incidence of
proximal type I endoleak was 3.7% at 1 and 12 months. Survival at 1 and 12 months was
86.5±5.6% and 71.6±8.5%, respectively. Freedom from undergoing any secondary surgical
procedure after stent graft completion at 1 and 12 months was 71.0±7.8% and 52.8±10%,
respectively.
■
A recent systematic review of aortic arch debranching summarized the clinical outcomes of 27
published studies including a total of 642 patients.9 Reporting results similar to those of the
authors’ experience1; the review noted rates of spinal cord injury, stroke, and 30-day mortality of
4.3%, 7.3%, and 11.9%, respectively. In this review, a trend existed between higher surgical
volume and lower neurologic complications, with stroke rates of 9.6% and 6.5% in low-volume
and high-volume case series, respectively.9
■
In another review article that included 18 studies and data from 195 patients, the technical success
rate following aortic arch debranching and stent graft repair was reported at 86%. The most
common reason for technical failure was endoleak (9%).10
COMPLICATIONS
■
Reopening for bleeding
■
Stroke or transient ischemic attack (TIA)
■
Spinal cord ischemic injury
■
Ascending aortic dissection
■
Endoleak
■
Iliofemoral artery injury
■
Mortality
REFERENCES
1. Lee CW, Beaver TM, Klodell CT Jr, et al. Arch debranching versus elephant trunk procedures for hybrid repair of thoracic aortic
pathologies. Ann Thorac Surg. 2011;91(2):465–471.
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. Circulation. 2010;121(13):e266–e369.
3. Kulik A, Castner CF, Kouchoukos NT. Outcomes after total aortic arch replacement with right axillary artery cannulation and a
presewn multibranched graft. Ann Thorac Surg. 2011;92(3):889–897.
4. Sundt TM 3rd, Orszulak TA, Cook DJ, et al. Improving results of open arch replacement. Ann Thorac Surg. 2008;86(3):787–796;
discussion 787–796.
5. Milewski RK, Szeto WY, Pochettino A, et al. Have hybrid procedures replaced open aortic arch reconstruction in high-risk
patients? A comparative study of elective open arch debranching with endovascular stent graft placement and conventional elective
open total and distal aortic arch reconstruction. J Thorac Cardiovasc Surg. 2010;140(3):590–597.
6. Yang J, Xiong J, Liu X, et al. Endovascular chimney technique of aortic arch pathologies: a systematic review. Ann Vasc Surg.
2012;26(7):1014–1021.
7. 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(5):1155–1158.
8. Lee WA, Martin TD, Gravenstein N. Partial right atrial inflow occlusion for controlled systemic hypotension during thoracic
endovascular aortic repair. J Vasc Surg. 2008;48(2):494–498.
9. 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(6):1286–1300, 1300.e1–1300.e2.
10. Antoniou GA, El Sakka K, Hamady M, et al. Hybrid treatment of complex aortic arch disease with supra-aortic debranching and
endovascular stent graft repair. Eur J Vasc Endovasc Surg. 2010;39(6):683–690.
Extrathoracic Revascularization (Carotid–Carotid,
Chapter 2 Carotid–Subclavian Bypass and Transposition)
Edward Y. Woo Scott M. Damrauer
DEFINITION
■
Extrathoracic revascularization, including carotid–subclavian and carotid–carotid bypass, involves
the bypass of the proximal great vessels outside of the chest. Initially described for treatment of
cerebrovascular and upper extremity occlusive disease, these procedures are commonly now
employed to create a proximal seal zone for endovascular treatment of thoracic aortic disease by
“debranching” the aortic arch.
■
Carotid–subclavian bypass is accomplished by inserting a graft conduit between the mid-common
carotid artery to the ipsilateral subclavian artery.
■
Subclavian artery transposition is a potential alternative to carotid–subclavian bypass requiring
division of the subclavian artery proximal to the vertebral artery and transposing it to the
ipsilateral common carotid artery. It is an efficient way to revascularize the subclavian artery
without the use of prosthetic conduit.1
■
Carotid–carotid bypass provides flow from one common carotid artery to the contralateral common
carotid artery.
■
When carotid–carotid bypass is performed in a right-to-left manner and in conjunction with carotid–
subclavian bypass, the blood flow to the left brain can be preserved while allowing for extension
of the proximal thoracic endovascular aortic repair (TEVAR) seal zone to cover the left common
carotid artery.

■
The history should focus on neurologic symptoms that may indicate the presence of symptomatic
cerebrovascular disease. Previous head and neck or carotid surgery should be noted, as well as a
history of head, neck, or upper chest region external beam radiation therapy, as these may
significantly increase the complexity of the procedure.
■
The directed physical exam should be focused on detection of underlying vascular disease that may
complicate planned intervention. Bilateral upper extremity blood pressures should be obtained; a
difference of greater than 10 mmHg indicates the potential presence of preexisting occlusive
disease. Likewise, the presence of carotid bruits, delayed carotid upstrokes, or abnormal upper
extremity pulses suggests arterial occlusive disease that should be delineated prior to
extrathoracic reconstruction or bypass of the great vessels.
■
Special attention should be directed toward the cranial nerves and voice, especially in patients with
prior cervical surgical procedures. Indirect laryngoscopy should be performed preoperatively in
patients with hoarseness or in whom a preexisting vocal cord or cranial nerve deficit has been
noted.
■
Neck mobility and the presence of cervical spinal disease should be assessed, as neck extension and
rotation is essential for adequate operative exposure. Patients with relative neck immobility may
be poorly suited for these procedures.

■
Carotid duplex scanning should be used to identify patients with carotid artery stenosis prior to
planned bypass procedures. Failure to identify and address stenoses at the carotid bifurcation may
lead to postoperative steal phenomenon and neurologic sequelae. Manipulation of the diseased
carotid artery may also increase the risk of periprocedural stroke. In these circumstances,
concomitant or staged carotid intervention may be warranted.
■
Computed tomographic (CT) angiography of the aortic arch and proximal carotid arteries provides
the anatomic detail necessary to safely perform carotid–subclavian bypass, subclavian artery
transposition, or carotid–carotid bypass. This study is complementary to duplex scanning, as it
provides anatomic rather than hemodynamic assessment and images vessels equally well inside
and outside the chest. CT scanning also visualizes the course of the subclavian artery in
relationship to the clavicle, as its course may also be distorted by a large arch aneurysm.
SURGICAL MANAGEMENT
■
Neuromonitoring is a useful adjunct to ensure adequacy of cerebral perfusion from the contralateral
cerebral circulation when the ipsilateral common carotid artery is clamped. Numerous modalities
exist for neuromonitoring, including electroencephalography (EEG), transcranial Doppler, near-
infrared spectroscopy, and stump pressure measurement. An indwelling carotid shunt may be
placed to improve ipsilateral blood flow when monitoring indicates cerebral perfusion is
inadequate. This problem occurs infrequently, as only the common carotid is occluded, but
preparations should be made for shunting procedures when indicated. Alternatively, as with
carotid endarterectomy (CEA), in the absence of neuromonitoring, shunts may be placed
prophylactically to preserve carotid flow in all cases.
■
Invasive continuous arterial pressure monitoring is routinely employed, with line placement dictated
by the laterality of the procedure. Keeping in mind the potential need to occlude the subclavian
artery for the reconstruction, the arterial line should be placed in the contralateral limb or in a
femoral artery.
Positioning
■
The patient is positioned supine with the head rotated away from the operative side. A pneumatic
pillow is placed under the shoulders to allow for neck extension. Careful attention must be paid to
achieve maximum neck extension while still supporting the occiput. The bed is placed in a semi-
Fowler’s position to reduce venous pressure and minimize bleeding.
■
For carotid–carotid bypass, the head is positioned midline to facilitate bilateral dissection.
TECHNIQUES
CAROTID–SUBCLAVIAN BYPASS
Exposure of the Subclavian Artery
■
The incision is extended from the lateral aspect of the clavicular head of the sternocleidomastoid
(SCM) muscle laterally across the supraclavicular fossa. This is further developed through the
subcutaneous tissue and platysma with electrocautery. If the external jugular vein is encountered, it
should be ligated and divided.
■
Sufficient clavicular head of the SCM is divided to allow for adequate medial exposure. Up to one-
half of the sternal head of the SCM can also be divided if also needed, but this is rarely necessary.
The scalene fat pad is then visualized and divided. It is preferable to divide this near its inferior
border so that most of the fat pad can be preserved and reclosed to cover the reconstruction. Care
must be taken to identify and preserve the phrenic nerve as it courses over the anterior scalene
muscle deep to the fat pad. The thoracic duct is easily identified. If it is injured or in the way, it
should be ligated to prevent significant morbidity from a postoperative lymphatic leak.
■
Once the fat pad has been mobilized, the anterior scalene muscle is divided to reveal the underlying
subclavian artery (FIG 1). It is best to divide the muscle slowly and in layers to prevent injury to
the underlying vessel. The subclavian artery is dissected circumferentially and controlled with
vessel loops. Care must be taken when manipulating this vessel, as the subclavian artery is
significantly more fragile and prone to injury than lower extremity arteries of comparable diameter
(e.g., femoral or popliteal). Depending on the method of reconstruction and location of the planned
anastomosis, the thyrocervical trunk, inferior mammary, and vertebral arteries may need to be
controlled separately (FIG 2).
Exposure of Carotid Artery

■
In the medial aspect of the wound, the lateral border of the internal jugular vein is identified and
sharply defined. The vein is retracted posteriorly and the carotid sheath is entered from the lateral
posterior margin. Care must be taken to identify the vagus nerve early, as its usual posterior
position places it immediately in the field of dissection as the sheath is opened from this approach.
■
The common carotid artery is dissected circumferentially (FIG 3). Only 5 cm of artery needs to be
isolated in order to obtain control and perform the anastomosis. The dissection should stay
proximal to the carotid bulb, which minimizes risk of cerebral embolization and injury to more
proximal nerves.
Bypass
■
Either Dacron or polytetrafluoroethylene (PTFE) can be used as conduits for extrathoracic bypass
with no difference in outcomes.2 Autogenous vein grafts should be avoided, however, as their
long-term patency is inferior to prosthetic in this location.3 We favor Dacron given the size ranges
available and the relative resistance of the graft to kinking over the short distance of the
reconstruction.
■
Prior to arterial clamping, systemic anticoagulation is achieved with intravenous heparin
administration. The activated clotting time (ACT) should be monitored and additional heparin
administered throughout the procedure to maintain adequate anticoagulation.
■
The subclavian anastomosis is performed first. Arterial control (vessel loops or clamps) is obtained
and the vessel is opened with a longitudinal arteriotomy. The anastomosis should be fashioned in
the position most favorable to the planned graft. The graft is beveled and trimmed so that the graft
lies at an approximately 60-degree angle to the artery. A running Prolene suture is used to perform
the anastomosis with completion of the back wall first. Once the anastomosis is complete, the graft
is clamped and flow restored to the arm by unclamping the subclavian artery. It is useful to flush
through the graft to remove any debris prior to opening to the arm. The graft should also be flushed
with heparinized saline and clamped near the anastomosis to avoid any thrombosis of the stagnant
blood column within the graft. If repairs are needed, control is restored and pledgeted sutures are
used to avoid injury to the fragile artery.
■
The graft is tailored to the appropriate length to prevent redundancy and kinking, and beveled so that
the heel of the anastomosis will lie proximally on the carotid artery. As the common carotid artery
is clamped, special attention must be directed to neuromonitoring; significantly diminished
cerebral perfusion, although very uncommon, mandates shunt placement at this stage of the
procedure. A longitudinal arteriotomy is performed and the proximal anastomosis completed with
running Prolene suture, again starting with the back wall (FIGS 4 and 5).
■
The final sequence of clamp removal is important to prevent embolism to the brain. Proximal
subclavian artery control is again obtained, and the clamp is removed from the graft. The proximal
carotid clamp is then removed to allow “flushing” down the arm rather than to the brain. After a
few cardiac cycles, the distal carotid clamp is also removed. The proximal subclavian artery is
then released as well.
■
When performed in anticipation of thoracic aortic stent grafting, the subclavian artery must be
ligated proximal to the origin of the vertebral artery. This can involve dissection deep into the
mediastinum and carries an inherent risk of catastrophic bleeding. Alternatively, the proximal
subclavian artery can be controlled by placement of an intraarterial occlusion device (e.g.,
Amplatzer), either during the carotid–subclavian bypass or at the time of subsequent stent graft
placement via a left brachial approach.4
Closure
■
If a pneumatic pillow was used to provide exposure, it is deflated prior to wound closure in order to
reduce neck extension and assist in allowing the wound to be closed without tension.
■
A closed suction drain is left in the deep wound and brought out through a separate stab incision.
■
In order to provide coverage for the graft, the scalene fat pad is returned to its anatomic location and
sutured in place. The SCM is reapproximated with running absorbable sutures.
■
The platysma and subcutaneous tissues are closed in separate layers in a running fashion and the skin
is reapproximated with a running dermal suture.
SUBCLAVIAN ARTERY TRANSPOSITION

Exposure
■
The subclavian artery is exposed, as described in the previous section, for carotid–subclavian
bypass. The dissection must be carried proximal to the vertebral artery and enough artery must be
exposed proximally to allow sufficient length for the anastomosis as well as control the proximal
stump. This can often be difficult as an aortic aneurysm can occupy a significant portion of the
mediastinum limiting vessel manipulation.
■
The carotid artery is exposed in the same manner as described in the previous section.
Division of the Subclavian Artery
■
Systemic heparin is administered, and maximum arterial length is obtained by advancing a Cooley
clamp as deeply as possible into the mediastinum along the subclavian artery. A distal atraumatic
clamp is then applied, typically in the midsubclavian artery, with the more proximal branches
individually controlled with vessel loops. There must be adequate distance between the proximal
clamp and the vertebral artery to allow for proximal control, transposition, and anastomosis. Prior
to transection, pledgeted 5-0 Prolene stay sutures are placed on each side of the proximal artery to
ensure that if clamp control is lost for any reason, the open artery does not retract into the
mediastinum (FIG 6).
■
The proximal subclavian artery is oversewn by extending the stay sutures across the stump.
Hemostasis is confirmed by slowly releasing clamp control while maintaining traction on the stay
sutures. Only once hemostasis is rigorously ensured are the sutures divided and the proximal
subclavian artery allowed to retract into the mediastinum.
Carotid–Subclavian Anastomosis
■
The subclavian artery, having been freed circumferentially, is then mobilized toward the carotid
artery. It may be tunneled anterior or posterior to the internal jugular vein depending on the length
of the artery and patient-specific anatomy. The carotid artery is then clamped proximally and
distally and the anastomosis performed in the standard running fashion. Prior control of the
subclavian artery is maintained (FIG 7). As the anastomosis is completed, the unclamping
sequence should be repeated as described in the preceding section to prevent inadvertent air or
particulate embolization to the brain.
Closure
■
As described in the section on carotid–subclavian bypass, the wound is closed in multiple layers
over a closed suction drain placed through a separate stab incision.
CAROTID–CAROTID BYPASS
Exposure of the Bilateral Carotid Arteries
■
Bilateral incisions are made over the anterior border of the SCM at the base of the neck. The
subcutaneous tissues and platysma are divided and the anterior border of the SCM is identified.
■
The SCM is mobilized laterally by carrying the dissection down toward the internal jugular vein;
this exposes the carotid sheath. Any bridging veins encountered can be divided; however, the
entire dissection should be below the level of the facial vein, as this marks the carotid bifurcation.
For this procedure, there is no need to risk injury to adjacent structures by exposing the carotid
bifurcation. To obtain sufficient proximal exposure, the omohyoid muscle may need to be divided
bilaterally.
■
The carotid sheath is entered sharply on its anterior surface. The vagus nerve must be identified
within the carotid sheath and protected as the common carotid artery is exposed and controlled.
Graft Tunneling and Anastomosis
■
Once the bilateral common carotid arteries are sufficiently exposed and controlled, the appropriate
graft tunnel can be created. Tunneling is achieved via blunt finger dissection from both sides of the
neck. The graft may be tunneled either between the trachea and esophagus or behind the esophagus,
depending on patient habitus and surgeon preference (FIG 8). Care must obviously be taken to
avoid injuries to these critical structures. Placement of an orogastric or nasogastric tube prior to
creation of the dissection plane can be helpful for identifying the esophagus.
■
Once the tunnel has been developed, the graft is passed and patient systemically anticoagulated with
intravenous heparin administration.
■
The anastomoses are performed in the standard running fashion; either one may be performed first.
Careful attention must be paid to neuromonitoring as the carotid artery is clamped.
■
Once the first anastomosis is complete, the graft is clamped and carotid artery flow restored on that
side. Prior to removing the distal carotid artery clamp, the distal artery can be back-bled and the
proximal artery flushed out the open graft. As with the subclavian artery, the graft should be
flushed with heparinized saline and clamped close to the anastomosis to avoid a long stagnant
column of blood within the prosthetic graft.
■
The contralateral anastomosis is then performed in the same fashion (FIG 9). The graft should be
flushed with heparinized saline and the graft, proximal carotid artery, and distal carotid artery
should be vigorously flushed prior to completion.
Closure
■
Hemostasis is obtained. The neck wounds are closed in layers, first taking care to reapproximate the
SCM in its anatomic position with interrupted absorbable sutures.
■
A closed suction drain is left in each wound.
■
The platysma and subcutaneous tissues are closed with running absorbable sutures and the skin
reapproximated with a running deep dermal suture.
PEARLS AND PITFALLS

Positioning ■ When inflating the pneumatic pillow, care must be taken to ensure
that the occiput is adequately supported. Failure to adequately
support the head may result in cervical spine and
neurologicinjuries.
Thoracic duct ■ Great care must be taken to avoid injuring the thoracic duct when
exposing the subclavian artery. All lymphatic tissue encountered
should be ligated before being divided as the ensuing lymphatic
leak can be quite troublesome for the patient and the surgeon.
Subclavian artery control ■ The subclavian artery can be controlled either with vessel loops
or with atraumatic vascular clamps, depending on which helps to
better deliver the artery into the wound without unduetension.
Subclavian artery ■ The subclavian artery is exceedingly friable and should be
anastomosis handled carefully. Given the exposure, it may be easier to
parachute the anastomosis rather than fix the suture line at the heel
of theanastomosis.
Positioning vis-à-vis the ■ Depending on the habitus of the individual patient, the graft may
internal jugular vein lie better tunneled either above or below the internal jugular vein.
It is prudent to explore both options prior to creating and
completing the carotid anastomosis.
Proximal subclavian control ■ The use of stay sutures on the proximal subclavian artery in
during transposition subclavian artery transposition is crucial. Once the stay suture on
the proximal end of the artery is released, the artery retracts deep
into the mediastinum and is not retrievable. Uncontrolled bleeding
may be disastrous and lead to fatal complications. As such, the
proximal oversewed subclavian artery must be hemostatic prior to
release of the stay sutures. Stay suture safety is ensured by
placement of pledgeted sutures at either end of the subclavian
closure.
Common carotid artery ■ It is not necessary and not advisable to expose or manipulate the
exposure carotid bulb or bifurcation in performing any of these
reconstructions unless a concomitant CEA is necessary or the
bifurcation is situated low in the neck. These procedures are
performed on the common carotid artery, and exposing the
bifurcation only increases the risk of cranial nerve injury and
stroke.
Closure ■ The pneumatic pillow should be deflated prior to closure to assist
in bringing the tissue together without tension.
POSTOPERATIVE CARE
■
Careful attention should be paid to both systolic and mean arterial blood pressure in the
postoperative period. Invasive arterial monitoring is usually maintained for the first 24 hours.
When carotid–subclavian bypass or subclavian artery transposition is performed, blood pressure
should be monitored in the contralateral arm.
■
Neurologic status and distal pulses should be followed closely in the postoperative period. Any
pulse changes need to be rigorously investigated as they may indicate the presence of either graft
occlusion or distal embolization.
■
When carotid–subclavian bypass, where the proximal subclavian artery is not ligated, is performed
as a debranching procedure prior to thoracic aortic stent grafting, the timing of the endovascular
procedure is important. In these patients who tend not to have concomitant occlusive disease, there
is competitive flow via the native circulation, putting the newly placed graft at risk of thrombosis.
In the absence of complications or other mitigating circumstances, the endovascular aortic
procedure should be performed within 3 to 5 days of the debranching bypass.
■
Patients should be placed on aspirin therapy and followed at regular intervals with duplex
ultrasonography.
OUTCOMES
■
Recent review of the American College of Surgeons National Surgical Quality Improvement
Program (ACS-NSQIP) database from 2005 to 2010 demonstrates that extrathoracic
revascularization carries a 3.5% risk of stroke and 3.3% risk of death in the immediate
perioperative period.5 Over this time period, 918 procedures were performed, with 10% of them
as part of a staged approach to thoracic aortic stent grafting.
■
Carotid–subclavian bypass has excellent durability. In a series of 284 consecutive patients, Takach
and colleagues2 reported 5-, 10-, and 15-year primary patency rates of 94%, 88%, and 86%,
respectively. These results have subsequently been replicated by other large, multiple-decade
series.6 Subclavian artery transposition has similarly outstanding long-term patency, with rates as
high as 99% reported at 5 years.6,7
■
Symptom-free survival following revascularization is likewise excellent, with long-term results
approaching 88% to 99% at 5 years.6,7
COMPLICATIONS
■
The thoracic duct lies at the medial aspect of the field of dissection when dissecting in the
supraclavicular fossa. This can be easily injured and remain undetected during the course of the
operation. Continued or milky drainage is a clear sign of duct injury. The oral administration of
cream can be used to promote chyle flow, and if a leak is present, will promptly increase drain
output. When this occurs, the closed suction drain should be left in place, the patient kept fasting,
and parenteral nutrition instituted. With conservative management, some of these injuries may
close without further intervention. The complete management of this complication is beyond the
scope of this text; however, it should be mentioned that reexploration of the wound in the early
period is relatively straightforward and may represent the best way to resolve the problem. Late
reexploration can be fraught with difficulty finding the leak as the tissue becomes fixed. A muscle
flap may then be needed to close the space. The main concern with a persistent leak is the potential
for graft infection. Unfortunately, early wound reexploration significantly increases the risk of
prosthetic graft infection as well.
■
The vagus, phrenic, and recurrent laryngeal nerves, as well as the brachial plexus, can all be injured
as a result of carotid and subclavian artery exposure. Most injuries are due to traction rather than
transection, and conservative therapy will generally resolve symptoms over the course of months
to a year. In the case of a staged bilateral subclavian revascularization, it is important to ensure
that any vagus or phrenic nerve injury has resolved prior to contralateral intervention, as bilateral
injuries can lead to tracheal obstruction and acute respiratory failure.
■
Although uncommon, significant bleeding from the wound should mandate reexploration. More
commonly, minor wound hematomas may develop that can be observed. Judgment regarding the
need for reexploration of a neck hematoma is similar to that required during any other neck
procedure.
■
Infection of the wound can be devastating if prosthetic is involved. Local cellulitis should be treated
aggressively with early institution of antibiotics in order to prevent deeper infection. Upon
removal of the drain, it is important that the drain site does not continue to leak, as continued
leakage may act as an entry point for bacterial contamination. Simple suture closure should resolve
this. Prosthetic graft infection necessitates graft removal, which is extremely difficult and beyond
the scope of this chapter.
■
Although uncommon, stroke is a complication of any carotid procedure. Taking the precautions
outlined previously in this chapter should minimize these risks.
REFERENCES
1. Morasch MD. Technique for subclavian to carotid transposition, tips, and tricks. J Vasc Surg. 2009;49(1):251–254.
2. Takach TJ, Duncan JM, Livesay JJ, et al. Contemporary relevancy of carotid-subclavian bypass defined by an experience spanning
five decades. Ann Vasc Surg. 2011;25(7):895–901.
3. Ziomek S, Quiñones-Baldrich WJ, Busuttil RW, et al. The superiority of synthetic arterial grafts over autologous veins in carotid-
subclavian bypass. J Vasc Surg. 1986;3(1):140–145.
4. Woo EY, Bavaria JE, Pochettino A, et al. Techniques for preserving vertebral artery perfusion during thoracic aortic stent grafting
requiring aortic arch landing. Vasc Endovascular Surg. 2006;40(5):367–373.
5. Madenci AL, Ozaki CK, Belkin M, et al. Carotid-subclavian bypass and subclavian-carotid transposition in the thoracic
endovascular aortic repair era. J Vasc Surg. 2013;57(5):1275–1282.
6. Cinà CS, Safar HA, Laganà A, et al. Subclavian carotid transposition and bypass grafting: consecutive cohort study and systematic
review. J Vasc Surg. 2002;35(3):422–429.
7. Berguer R, Morasch MD, Kline RA, et al. Cervical reconstruction of the supra-aortic trunks: a 16-year experience. J Vasc Surg.
1999;29(2):239–246; discussion 246–248.
Carotid Surgery: Interposition/Endarterectomy
Chapter 3 (Including Eversion)/Ligation
Vinit N. Varu Wei Zhou
DEFINITION
■
Stroke is the leading cause of disability in the United States and Western Europe and the third
leading cause of death behind coronary artery disease and cancer.
■
Pivotal studies have shown the efficacy of carotid endarterectomy (CEA) in stroke prevention in
both symptomatic and asymptomatic patients with internal carotid artery (ICA) stenosis versus
medical therapy alone.1,2
■
CEA is defined as the surgical excision of atherosclerotic lesions of the intima and tunica media of
the carotid artery.
■
Occasionally, ICA ligation and/or interposition bypass may be indicated for stroke prevention.

■
Patients may be entirely asymptomatic and still benefit from carotid intervention to prevent long-
term stroke. In the United States, most CEA procedures are performed on asymptomatic patients.
Symptoms of cerebroembolic disease originating from the carotid bifurcation, when present, may
include dysarthria, dysphasia, aphasia, hemiparesis, or hemisensory deficit or amaurosis fugax.
Symptoms that resolve within 24 hours are defined as transient ischemic attacks (TIAs) regardless
of severity; symptoms that persist past the first day constitute a stroke.
■
For patients at risk for cerebroembolic disease, a thorough vascular history is obtained including
modifiable risk factors such as smoking, hyperlipidemia, hypertension, and diabetes management.
Prior to surgery, single-agent antiplatelet therapy is initiated and continued indefinitely following
intervention. Blood pressure control at or below 140 mmHg systolic and 90 mmHg diastolic is the
single most important medical intervention to reduce stroke risk.3 Sufficient β-blockade to
stabilize resting heart rate at 60 bpm is also instituted prior to surgery to limit perioperative
myocardial oxygen demand unless contraindicated.4
■
Cervical auscultation is performed in both the supraclavicular and mandibular regions. Bruits
appreciated at the mandibular angle usually indicate ICA or bifurcation disease. More proximal
bruits may indicate common carotid artery (CCA) disease or radiating heart sounds.
■
A full neurologic assessment including mental status, speech, facial symmetry, and extremity strength
must be obtained and documented prior to surgery.

■
All patients exhibiting symptoms of carotid territory ischemia need appropriate vascular imaging
studies. Screening is not recommended to detect asymptomatic disease in the general population;
patients with appropriate risk factors, or those with a bruit on physical exam should be evaluated
when clinical circumstances warrant.
■
Carotid duplex ultrasound provides a reliable and accurate noninvasive tool to identify predicted
stenosis and is the initial diagnostic study of choice. Peak systolic velocity (PSV) higher than 125
cm per second predicts angiographic stenosis more than 50% and higher than 230 cm per second
predicts more than 70% stenosis. However, a combination of PSV, end diastolic velocity, and the
PSV ratio of ICA to CCA is more accurate in estimating significant carotid stenosis. In general,
end diastolic velocity higher than100 cm per second correlates to more than 80% carotid stenosis.
■
When duplex imaging is not definitive, as is the case in the setting of extensive carotid bifurcation
calcification, additional cross-sectional imaging (computed tomography angiography [CTA] or
magnetic resonance angiography [MRA]) may be necessary to quantify the degree of stenosis.
When accurate velocity information is obtainable, duplex imaging provides the most accurate and
physiologically relevant estimates of percent diameter reduction.
SURGICAL MANAGEMENT
Indications
Endarterectomy
■
The Society for Vascular Surgery recommends that neurologically symptomatic patients with greater
than 50% stenosis or asymptomatic patients with greater than 60% stenosis should be offered CEA
to reduce risk of recurrent or initial stroke, respectively. Endarterectomy is appropriate for
patients with at least a 3- to 5-year life expectancy with perioperative stroke/death rates less than
3%. In all other circumstances, optimal medical therapy is preferred.5
■
Surgical endarterectomy is the procedure of choice for good-risk surgical patients with normal
cervical anatomy. For selected high-risk patients, such as those with tracheal stoma, previously
radiated neck, prior cranial nerve injury, or lesions proximal to the clavicle or distal to C2
vertebral body, transcatheter angioplasty and stenting is generally the preferred approach.5
Indications and technical guidelines for carotid angioplasty and stenting procedures are discussed
in Chapter 4.
Carotid Artery Interposition Bypass
■
Reconstruction for extensive bifurcation disease, injury to the bifurcation during endarterectomy, or
aggressive restenosis following previous intervention (endarterectomy or stent placement) is best
accomplished by carotid resection and interposition grafting. Other indications include the
following:
■
Significant diffuse CCA and ICA disease
■
Radiation-induced stenosis or other forms of arteritis involving long arterial segments
■
Aneurysms (degenerative or traumatic) and invasive carotid body tumors.
Ligation
■
Ligation and resection of the proximal ICA may be indicated in the setting of carotid stump
syndrome, when persistent distal embolization from the “cul-de-sac” of the occluded ICA may
reflux into collateral pathways, such as through the ophthalmic artery into the distal ICA.
■
Similar outcomes are achieved with general anesthesia or regional anesthesia.
■
Use of shunt during CEA is dependent on operator preference. Most surgeons either shunt
selectively or use a shunt for all cases. Some surgeons never shunt.6 Surgeons should develop the
methods they feel most comfortable with to optimize outcome. Objective measures that may
influence shunt usage include stump pressure measurement, electroencephalographic monitoring,
and transcranial Doppler assessment. Data supporting use of these adjuvants is inconsistent, and
none is considered standard of care nationally.
■
Optimal neck extension is obtained by placing a towel or gel roll behind the scapula. The head is
rotated contralateral to the operative side. In older patients, often with limited neck movement or
prior cervical fusions, padding and shay positioning must be sufficient to support the neck to
prevent hyperextension injury. The chin, angle of the mandible, lower earlobe, and sternal angle
are prepped and preliminarily draped within the operative field. The bed itself can be flexed with
the head in relative extension to aid in positioning (FIG 1).
■
Arterial blood pressure monitoring is necessary for optimal anesthetic management. Bladder
catheterization is performed if the procedure is expected to extend beyond 2 hours. If
endarterectomy is performed with regional anesthesia, an audible squeeze device is placed in the
patient’s contralateral hand for indirect neurologic monitoring. Preoperative antibiotics are
administered routinely.
■
Aspirin therapy is initiated well in advance of surgery and continued throughout the perioperative
period. Evidence suggests that statin therapy, initiated preoperatively, reduces postoperative
neurologic events and mortality.7
TECHNIQUES
CAROTID ENDARTERECTOMY—PATCH ANGIOPLASTY

Incision
■
The skin incision is optimally placed along the anterior border of the sternocleidomastoid muscle.
This should be curved posterolaterally near the angle of the mandible to avoid dissection into the
parotid gland.
■
Alternatively, a more transverse incision can be made at the level of the carotid bifurcation.
Although providing an improved cosmetic result, exposure of the distal ICA may be compromised
with this approach (FIG 2).
Carotid Exposure and Control

■
As the incision is extended through the platysma muscle, the anterior border of the
sternocleidomastoid muscle is visualized and retracted posterolaterally. The greater auricular
nerve should be identified and protected at the superior extent of the incision.
■
Following fascial incision, the facial vein is identified and securely ligated. This vein usually
transverses the CCA near the bifurcation. Failure to adequately secure this vein may lead to
bleeding and airway compromise during postoperative cough spells or Valsalva maneuvers.
■
Within the carotid sheath, the vagus nerve usually extends posterior to, and parallel with, the artery
and vein. However, this position relative to the other contents of the carotid sheath may vary, and
the vagus should always be identified and protected in the course of the dissection. The ansa
cervicalis nerve is commonly much smaller than the vagus and runs anterior to the carotid
bifurcation. When completely isolated, the proximal ansa arises from the ipsilateral hypoglossal
(XII) cranial nerve. The ansa cervicalis can be divided to improve exposure if necessary or
mobilized sufficiently to be gently retracted out of the operative field.
■
The CCA is circumferentially dissected from surrounding structures in sufficient length to provide
adequate exposure for proximal clamping and control. The CCA is optimally controlled by
placement of an appropriately sized, atraumatic vascular clamp such as a Gregory profunda clamp.
The ratchet should be engaged only to the minimal amount necessary to control bleeding to prevent
intimal injury and dissection at the site of clamp placement.
■
Following common carotid control, the dissection is extended cranially and posteriorly along the
posterolateral border of the ICA. Development of the dissection plane posterolaterally along the
proximal ICA minimizes risk of hypoglossal nerve injury. This dissection is also performed with
minimal displacement and instrumentation of the ICA to reduce intraoperative embolization risk
(FIG 3).
■
To complete the necessary exposure, the external carotid artery (ECA) is dissected and mobilized to
at least the level of the superior thyroidal artery. The superior laryngeal nerve may also be
encountered posterior to the carotid bifurcation in this area.
■
Following dissection, and prior to clamp placement, sufficient unfractionated heparin is
administered intravenously to obtain an activated clotting time (ACT) of more than 200 seconds.
With normal circulation times, this is usually accomplished within 2 or 3 minutes of injection.
■
Clamping of ICA is performed first, followed by control of the external and common carotid
arteries. This sequence is followed to minimize embolization risk associated with clamping. When
necessary, measurement of ICA stump pressure is obtained at this juncture by cannulation of the
carotid bifurcation and selective removal of the internal carotid clamp.
Conventional Endarterectomy
■
The arteriotomy is initiated in a soft, uninvolved proximal segment of the CCA and extended
cephalad with Potts scissors. It should be positioned on the anterior-lateral surface of the ICA to
avoid the flow divider. (FIG 4A).
■
When an indwelling shunt is indicated or required, the distal tapered end is carefully inserted into
the ICA under direct vision. We prefer the Pruitt-Inahara shunt, which has pilot balloons at both
ends to maintain shunt position and hemostasis. Once the distal end is inserted, the distal balloon is
inflated with less than 1 mL of air until the “pop-off” balloon inflates on the pilot tube. Familiarity
with this shunt prior to insertion is essential; if the inflation override cuff covers the “pop-off”
balloon on the pilot tube, overinflation may injure or rupture the distal ICA. Following distal ICA
cannulation and balloon inflation, the shunt is back-bled to confirm luminal placement and decant
air. With the shunt actively back-bleeding, the proximal end is inserted into the CCA followed by
proximal clamp removal into the unobstructed lumen. The proximal pilot tube is inflated with the
provided syringe until the cuff is palpable in the CCA, after which a prepositioned Rumel
tourniquet is gently cinched around the artery. When performed quickly, with concurrent digital
control of the CCA following clamp removal and prior to shunt insertion, minimal bleeding ensues.
When saline is applied to the shunt tubing, pulsatile flow is appreciable with handheld Doppler
insonation.
■
At the site of maximal atherosclerotic disease in the CCA, the Penfield knife is employed to identify
and develop the appropriate endarterectomy plane within the medial layer. When the correct plane
is identified, the plaque is easily and rapidly elevated from the underlying adventitia. In areas
containing intraplaque hemorrhage, inflammation may increase adherence of the plaque to the
adventitia, and care should be taken not to extend the dissection plane into the adventitia itself.
■
At the distal extent plaque, sufficient exposure should be present to create a defined endpoint,
allowing placement of tacking sutures if necessary, ensuring that no further potentially mobile
plaque remains. It is essential to “feather” the plaque at the distal endpoint to minimize risk for
distal dissection or thrombus accumulation. If the plaque extends past the point where feathering is
feasible, a distal endpoint should be determined and created sharply with scissors or a no. 15
blade (FIG 4B). Tacking sutures, placed circumferentially, can control distal plaque at the
transection site. Care should be taken, however, to place the minimal number of sutures necessary
to prevent dissection, or consider extending the arteriotomy and endarterectomy to identify a more
suitable termination site. Successful suture placement requires circumferential dissection and
optimal visualization.
■
Once the distal endpoint is determined, residual plaque is removed from the ECA by eversion into
the CCA and circumferential dissection and traction. Sufficient back-bleeding is performed to
remove any luminal debris within the ECA.
■
Direct visualization of the endarterectomy bed following plaque removal commonly identifies
loosely attached residual medial elements. These are best removed with fine forceps under
magnification. Complete removal is facilitated by continuous irrigation to identify mobile medial
elements. Integrity of the distal and proximal endpoints is also verified using this technique.
Patch Placement
■
An appropriately sized bovine pericardial or Finesse Dacron knitted polyester patch is selected and
trimmed as necessary for closure-assisted angioplasty. Both bovine pericardial and polyester
patches have chirality considerations; one surface is preferred for luminal apposition. Please
consult the accompanying instructions for use prior to implantation. Closure is secured with
running 6-0 polypropylene suture initiated at the cephalad extent of the arteriotomy and continued
proximally along the long axis of the patch.
■
After 90% or more of the circumference of the patch is secured, flushing is accomplished by
sequential clamp removal and luminal irrigation with heparinized saline. Closure is then
completed prior to restoration of flow.
■
The declamping sequence is of critical importance. The CCA is released first, followed by the ECA
clamp. After several cardiac cycles have ensued, the distal ICA is released (FIG 4C).
■
We perform intraoperative completion duplex imaging of the endarterectomy site as well as the
proximal and distal carotid arteries, with purpose-designed, miniaturized 7 MHz probes.
Completion duplex scanning is quick, efficient, highly reproducible, and effective at identifying
significant residual luminal defects. Detailed description of the characteristics of significant
luminal defects identified by completion ultrasonography are beyond the scope of this chapter.
Intraoperative insonation is not possible through extruded polytetrafluoroethylene (ePTFE) patches
and should not be attempted.
Closure
■
Following adequate duplex imaging and endpoint determination, anticoagulation is reversed with
protamine sulfate. Some practitioners are reluctant to reverse anticoagulation due to uncertainty
regarding thrombogenicity at the endarterectomy site. In our experience, technical issues at the
endarterectomy site are most predictive of postoperative neurologic events, and these are
efficiently identified and corrected, when present, with completion ultrasonography. Following
reversal, the entire wound is inspected for venous or arterial bleeding. The entirety of the patch
angioplasty suture line is reinspected for periodicity of suture placement and potential leaks.
Reinforcing sutures are applied liberally as needed to ensure hemostasis, but with experience and
even suture spacing, the need for additional sutures should be rare. Bleeding lymph nodes should
be sutured and removed from the operative field. Confirmation of hemostasis, the platysma is
reapproximated with running absorbable suture followed by skin closure. We usually also perform
a Valsalva maneuver to identify occult venous injuries that may not be apparent with positive
pressure ventilation prior to closure.
CAROTID ENDARTERECTOMY—EVERSION
Incision
■
See section under Carotid Endarterectomy—Patch Angioplasty.
Dissection and Control of the Carotid Artery
■
Eversion endarterectomy
■
An oblique or circumferential incision is made at the junction of the bulbous portion of the ICA and
CCA (FIG 5A).
■
The ICA adventitia is grasped with fine forceps and everted away, as gentle traction is placed on the
plaque within the artery. This maneuver is extended distally until the feathered endpoint identifies
itself. Tacking sutures are not possible using this approach, which can be a deterrent to adoption
by surgeons trained with conventional endarterectomy. Common and external carotid plaque is
subsequently removed by the Penfield knife as indicated. The proximal CCA arteriotomy may be
extended as needed to ensure complete removal.
■
Common and external carotid plaque is subsequently removed by the Penfield knife as indicated.
The proximal CCA arteriotomy may be extended as possible to ensure complete removal (FIG
5B).
Anastomosis
■
The ICA is reverted and anastomosed end-to-end to the proximal CCA (FIG 5C).
■
If redundant residual ICA is present following plaque removal, the ICA spatulation is extended, as
is the CCA arteriotomy, and the two ends are further advanced over each other prior to closure.
Alternatively, a portion of the redundant ICA may also be excised.
Closure
■
CAROTID ARTERY INTERPOSITION BYPASS

Incision
■
■
■
Although reversed autogenous vein is the preferred conduit, when available, ePTFE provides a
suitable alternative when necessary.8
Anastomosis
■
The diseased segment of the carotid artery is resected. Commonly, the ECA is oversewn as well.
■
End-to-end anastomoses are performed in standard fashion. Prior to completion, flushing maneuvers
are done to evacuate particular matter or residual air (FIG 6).
Closure
■
CAROTID ARTERY LIGATION (CAROTID STUMP SYNDROME)

Incision
■
■
Endarterectomy
■
The technique is similar to that for standard ICA endarterectomy, the difference being the
arteriotomy being carried out on the distal CCA into the ECA (FIG 7A).
■
The thrombosed ICA is resected, ideally in line with the common and external carotid arteriotomies.
Closure is accomplished via patch angioplasty (FIG 7B,C).
Closure
■
PEARLS AND PITFALLS

Incision ■ On table duplex scanning optimizes incision placement,
particularly for transverse exposure.
Identifying the vagus nerve ■ Vagus nerve is located posterolateral to the carotid artery, within
and hypoglossal nerve the carotid sheath and between carotid artery and internal jugular
vein. Hypoglossal nerve typically crosses ICA anteroinferiorly to
posterosuperiorly. Following the ansa cervicalis will lead to
hypoglossal nerve.
Clamping ■ A “robin blue” hue is often seen in the distal ICA, which signifies
a soft area for safe clamp placement.
Shunting ■ Be prepared in all cases for potential shunt placement. This should
be flushed and prepared on the back table prior to performing the
arteriotomy.
Conventional ■ Lavage the arterial lumen with heparinized saline to identify and
endarterectomy remove luminal debris.
Eversion endarterectomy ■ Use caution in patients with high bifurcation (difficulty visualizing
and securing distal endpoint), those who require a shunt, or those
with a small ICA. These procedures are best suited for patients
with redundant ICAs.
Interposition bypass ■ Use the anastomotic suture line to tack down distal residual plaque
as necessary to prevent antegrade dissection.
Ensuring technical ■ A completion imaging study, either an on-table angiogram or a
perfection carotid duplex study, can help to ensure technical perfection prior
to skin closure.
Closure ■ If a closed suction drain is placed, it should be removed on
postoperative day 1.
POSTOPERATIVE CARE
■
Patients should be placed on continuous monitoring to assess for blood pressure lability. Patients
generally are discharged on postoperative day 1 or 2.
■
A postoperative duplex should be obtained within 30 days of intervention to assess the
reconstruction, provide a new baseline for long-term surveillance, and monitor wound healing and
plaque incorporation. Serial ultrasounds should be obtained to identify and manage restenosis,
which most commonly occurs in the first 2 years following endarterectomy.
OUTCOMES
■
The North American Symptomatic Carotid Endarterectomy Trial (NASCET) demonstrated the 30-
day CEA stroke and death rate of 5.5% for symptomatic patients.1
■
The Asymptomatic Carotid Atherosclerosis Study (ACAS) demonstrated a combined 30-day CEA
stroke and death rate of 2.3%.2
■
More recently, the Carotid Revascularization Endarterectomy versus Stenting Trial (CREST)
demonstrated the 30-day stroke, death, or rate of myocardial infarction (MI) to be 5.4% in
symptomatic patients and 3.6% in asymptomatic patients, and the 30-day death and stroke rates
were found to be 3.2% in symptomatic patients and 1.4% in asymptomatic patients undergoing
CEA. In the periprocedural period, there is a lower rate of stroke with CEA versus stenting (2.3%
vs. 4.1%) but a higher rate of MI (2.3% vs. 1.1%). Mortality rates are similar.9
COMPLICATIONS
■
Cervical hematoma
■
Hemodynamic instability
■
Cerebral hyperperfusion syndrome manifested by severe headache
■
Cranial nerve palsy
■
Stroke/MI
■
Thrombosis (early)
■
Recurrent stenosis (late)
REFERENCES
1. North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in
symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445–453.
2. Walker MD, Marler JR, Goldstein M. Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the
Asymptomatic Carotid Atherosclerosis Study. JAMA. 1995;273:1421–1428.
3. 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. Circulation. 2011;124(4):489–532.
4. American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines, American Society of
Echocardiography, American Society of Nuclear Cardiology, et al. 2009 ACCF/AHA focused update on perioperative beta
blockade incorporated into the ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac
surgery. J Am Coll Cardiol. 2009;54:e13–e118.
5. Ricotta JJ, Aburahma A, Ascher E, et al. Updated Society for Vascular Surgery guidelines for management of extracranial carotid
disease. J Vasc Surg. 2011;54:e1–e31.
6. Samson RH, Showalter DP, Yunis JP. Routine carotid endarterectomy without a shunt, even in the presence of a contralateral
occlusion. Cardiovasc Surg. 1998;6:475–484.
7. Mcgirt MJ, Perler BA, Brooke BS, et al. 3-Hydroxy-3-methylglutaryl coenzyme A reductase inhibitors reduce the risk of
perioperative stroke and mortality after carotid endarterectomy. J Vasc Surg. 2005;42:829–835.
8. Dorafshar AH, Reil TD, Ahn SS, et al. Interposition grafts for difficult carotid artery reconstruction: a 17-year experience. Ann
Vasc Surg. 2008;22(1):63–69.
9. Mantese VA, Timaran CH, Chiu D, et al. The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST): stenting
versus carotid endarterectomy for carotid disease. Stroke. 2010;41(suppl 10):S31–S34.
Carotid Surgery: Bifurcation Stenting with Distal
Chapter 4 Protection
Zhen S. Huang Darren B. Schneider
DEFINITION
■
Carotid artery stenosis was first successfully treated via percutaneous balloon angioplasty in 1977
by Mathias and colleagues.1,2 This technique has evolved over time to include use of self-
expanding nitinol stents and distal embolic protection devices (EPD). Carotid angioplasty and
stenting (CAS) is indicated as an alternative to open carotid endarterectomy (CEA) in certain
clinical scenarios where the patient’s anatomy and/or physiology pose a greater risk for
complications with CEA. However, these specific clinical conditions are not absolute and must be
weighed against risks for endovascular intervention.
■
Distal EPD
■
According to the 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,
“EPD deployment during CAS can be beneficial to reduce the risk of stroke when the risk of
vascular injury is low.”3
■
A distal filter is placed in the internal carotid artery (ICA) distal to the lesion but below the skull
base, with the purpose of capturing debris to prevent distal embolization during CAS (FIG 1).
The target lesion must be crossed by the filter before deployment but this system allows for
cerebral protection with maintenance of blood flow to the brain during subsequent steps of the
procedure. The filter is mounted on the same wire used to perform CAS and after successful
CAS, the filter is retrieved along with any captured debris.
■
A thorough history should be obtained prior to intervention and should include a detailed
description of, if present, symptoms (quality, duration, etc.) that may be indicative of transient
ischemic attacks (TIA) or prior stroke, past medical/surgical history (e.g., prior cerebrovascular
disease/interventions), current medications (e.g., antiplatelet or anticoagulation medications), and
social history (e.g., tobacco use).
■
A comprehensive physical exam is mandatory and should include a complete vascular and
neurologic/stroke evaluation. Vascular exam should note the presence of palpable femoral and
distal lower extremity pulses and carotid bruits.

■
Initial carotid duplex ultrasound is obtained to evaluate the degree of stenosis and plaque
morphology. Studies have highlighted a higher potential for embolism during CAS with
hypoechoic lipid-containing plaque.4
■
Angiographic imaging of the aortic arch and carotid and cerebral arterial vasculature must be
obtained to aid in proper patient selection and procedural planning. This is accomplished through
computed tomographic arteriography (CTA) (FIG 2), magnetic resonance arteriography (MRA),
or catheter-based contrast arteriography.
■
Arch anatomy
■
Aortic arch morphology is variable and can change with advancing age. The arch anatomy can
be divided into three types, dictated by the position of the innominate artery origin relative
to two horizontal lines drawn across the apices of the outer and inner aortic arch curvatures
(FIG 3).
■
Type I—the innominate origin arises at or above the horizontal plane of the outer arch
curvature (FIG 3A)
■
Type II—the innominate origin arises in between the two horizontal planes of the outer and
inner arch curvatures (FIG 3B)
■
Type III—the innominate origin lies below the horizontal plane of the inner arch curvature
(FIG 3C)
■
The difficulty in gaining access to the carotid arteries increases from types I to III. There is an
increase in angle acuity of the great vessel origins off the arch with increasing arch types that
make wire/catheter guidance/exchange more difficult.
■
Bovine arch—congenital arch variations where the left common carotid artery (CCA) shares a
common origin with the innominate artery (more frequent) or the left CCA branches off the
innominate artery. In a pure bovine arch (extremely rare), the right subclavian, common
carotid—both right and left—and left subclavian all derive from one common arterial trunk
off the aortic arch.
■
Shaggy aorta—when extensive aortic wall irregularities exist, there is a high risk for
significant atheroembolism and thus, this may be a contraindication to CAS.
■
Eggshell aorta—with severe aortic wall calcification, there is increased risk of intimal
disruption and difficulty of wire/catheter manipulation/advancement.
■
Cerebral flow to both hemispheres is assessed to determine cerebral reserve.
■
Carotid vessel size, tortuosity, and calcification—carotid artery diameter should be assessed to
aid in determining device sizes. In addition, severe carotid circumferential calcification and
vessel tortuosity may negatively impact procedural success (e.g., difficulty with inserting stent,
placement of EPD in distal ICA) and may represent a contraindication to CAS.
■
Preoperative brain imaging with computed tomography (CT) or magnetic resonance imaging (MRI)
is needed for symptomatic patients to document prior infarcts and to rule out preexisting
hemorrhagic stroke prior to the initiation of the procedure.
SURGICAL MANAGEMENT
■
The indications for any surgical intervention for carotid disease depend on the patient’s clinical
status (i.e., symptomatic or asymptomatic) and the characteristics of the carotid lesion.
■
It has been widely accepted that appropriate candidates for CEA are symptomatic patients with
carotid stenosis of 70% to 99% on noninvasive imaging and an anticipated perioperative risk of
stroke or mortality of less than 6%. Benefit of intervention for symptomatic patients with lesser
degrees of stenosis (50% to 69%) has also been shown but not for symptomatic patients with less
than 50% carotid stenosis. CAS is an alternative to CEA for symptomatic patients meeting similar
criteria along with anatomic and/or physiologic factors unfavorable for CEA (Table 1).3,5
■
The recommendations/indications for CAS in asymptomatic patients are still issues for debate and
no consensus exists. CAS may be considered for patients with asymptomatic ICA stenosis between
70% and 99%, but there are insufficient data to recommend CAS for primary therapy in
asymptomatic patients. Therefore, these patients need to be addressed on a case-by-case basis
with consideration of patient comorbidities and risks of CAS.
■
The contraindications for CAS are predominantly related to aortic arch and carotid artery anatomic
factors (Table 2).
■
Patients are initiated on antiplatelet therapy with aspirin 325 mg per day and clopidogrel 75 mg per
day for 5 days prior to intervention. Alternatively, a clopidogrel loading dose of 300 mg can be
administered 4 to 6 hours prior to the intervention.
■
Antihypertensive medications can be held off the day of intervention to prevent contribution to the
possible periprocedural hypotension.
Positioning
■
The patient is placed in the supine position with adequate monitoring throughout the peri- and
postprocedural period. Minimal monitoring includes continuous electrocardiogram (EKG),
intraarterial blood pressure, and pulse oximetry. The patient’s neurologic status must be frequently
evaluated during the procedure via answering of simple questions and squeezing a plastic sound
toy (e.g., rubber duck squeaky toy) in the contralateral hand.
■
Intraarterial blood pressure monitoring is established usually via a radial arterial line.
■
In order to maintain patient cooperation/comfort and frequent neurologic monitoring, minimal or no
sedation is administered and only local anesthesia is infiltrated for the access site.
TECHNIQUES
PERCUTANEOUS RETROGRADE FEMORAL ARTERY ACCESS

■
Obtain retrograde access via the common femoral artery (CFA) using a percutaneous micropuncture
(21-gauge needle) system under ultrasound guidance. The CFA should be accessed immediately
proximal to the femoral bifurcation in an area with minimal disease. The right CFA is the most
convenient site for right-handed operators. The left CFA and brachial and radial arteries are
alternative access sites. Ultimately, the safest and simplest access site to the target lesion should
be employed.
■
The micropuncture sheath is then exchanged for a 5-Fr introducer sheath over the 0.035-in access
wire.
ARCH AORTOGRAPHY
■
A guidewire is advanced into the aortic arch followed by a pigtail catheter. The pigtail catheter is
positioned in the mid-ascending aorta and arch aortography is performed in a 45- to 60-degree left
anterior oblique projection in order to adequately visualize the origin of the great vessels (FIG 4).
SELECTIVE COMMON CAROTID CATHETERIZATION

■
Before further manipulation of wires/catheters in the arch and great vessel origins, the patient is
administered systemic heparin at 70 to 100 U/kg intravenously (IV) with a goal activated clotting
time of 250 to 300 seconds.
■
While maintaining the left anterior oblique (LAO) projection that allows for optimal visualization of
the great vessels origins, a road map image is used to assist in selective catheterization of the
CCA. The pigtail catheter is exchanged for the operator’s catheter of choice.
■
Multiple curved catheters are available (FIG 5), each with unique features that may be beneficial in
different anatomies. However, frequently, selective common carotid catheterization can be
accomplished with a combination of an angled or simple curved catheter and a floppy angled
Glidewire™.
■
However, a retroflexed or complex curved catheter (e.g., SIM or Vitek) may be necessary with a
difficult arch anatomy such as type III arch or bovine configuration (FIG 6).
■
After the Glidewire™ has accessed the common carotid (but taking extreme care not to advance past
the bifurcation), the selective catheter is advanced over the Glidewire™ into the common carotid.
Common carotid–selective angiograms are then performed typically in the anteroposterior, lateral,
and oblique projections (more views are performed as needed) (FIG 7). Contralateral carotid
arteriogram can be performed as well if necessary, but this usually is not performed during CAS of
a unilateral lesion.
■
Cerebral vessel angiography is then performed, typically in anteroposterior and lateral views (FIG
8). Additional views can be done if necessary.
PLACEMENT OF GUIDING SHEATH

■
After common carotid angiography is complete, it is recommended that the appropriate necessary
equipment to complete the procedure is selected prior to further selective cannulation of the
carotid vessels (e.g., access sheaths, wires, catheters, filter and filter retrieval system, pre- and
postdilatation balloons, stent).
■
In order to advance a sheath into the proximal common carotid, adequate exchange support is needed
with a stiff guidewire. To achieve this, the selective catheter is carefully advanced over the floppy
Glidewire™ into a branch of the external carotid artery (ECA). The floppy Glidewire™ is then
exchanged for a stiff guidewire (e.g., long Amplatz™ Superstiff wire with floppy tip). Caution
needs to be exercised to ensure the stiff wire tip does not inadvertently advance and potentially
perforate the ECA branch. The catheter is then removed leaving the stiff wire in place in the ECA
(FIG 9). If there is significant atherosclerotic stenosis involving the carotid bifurcation, or if the
ECA is severely stenotic/occluded that prevents safe ECA access, an Amplatz™ wire with a 1-cm
floppy tip may be left in the distal CCA.
■
Once the supportive wire is in place, the groin introducer sheath is exchanged for a 6-Fr 90-cm
sheath. The sheath is tracked over the stiff wire and placed into the distal CCA proximal to the
bifurcation. It is imperative that sheath advancement is performed on live fluoroscopy, especially
when negotiating the turn at the common carotid origin, to ensure the sheath is advancing
appropriately.
CROSSING THE LESION WITH DISTAL EMBOLIC PROTECTION

DEVICES
■
With the sheath in place and using a road map image, the ICA lesion is crossed with the 0.014-in
wire component of the distal EPD. The distal EPD should be deployed in a straight portion of the
distal ICA proximal to the petrous portion at skull base (FIG 10). It is important not to allow
inadvertent migration of the EPD further distally for risk of injury to the intracranial ICA.
PREDILATATION WITH ANGIOPLASTY BALLOON
■
After the distal EPD is in position, the carotid lesion is predilated with a 3- or 4-mm coronary
angioplasty balloon up to nominal pressure (FIG 11). A higher inflation pressure may be required
for heavily calcified lesions. Using a balloon length of 4 cm should help to minimize the risk of the
balloon slipping (“watermelon seeding”) during inflation. In addition, it is important to be extra
vigilant in monitoring the patient’s heart rate for possible bradycardia (or even asystole) during
lesion predilatation and atropine must be readily available for administration before predilatation.
STENTING AND POSTDILATATION

■
Following predilatation, a channel is created that will accommodate the advancement of the stent
system. A self-expanding stent compatible with the distal EPD system is advanced over the wire
and deployed under a road map. The distal and proximal stent landing zones must be at areas of
normal vessel wall and this will frequently necessitate stenting across the ECA origin with the
proximal landing zone in the distal CCA (FIG 13). After stent deployment, it is postdilated
(usually using a 5 to 6 mm × 2 cm balloon), treating only the stented portions of the ICA to
minimize injury to the native vessel wall (FIG 12) and over postdilatation is strictly avoided to
reduce risks of embolization. During postdilatation, the patient’s heart rate must be closely
monitored for any changes and atropine should still be readily available.
EMBOLIC PROTECTION DEVICE RETRIEVAL AND COMPLETION
ANGIOGRAM
■
Completion angiography is performed to assess stent placement and poststent carotid antegrade flow
before the distal EPD is removed (FIG 13). With normal flow through the stent and no filling
defects present, the filter is retrieved. Slow flow and/or filling defects at the filter can be
secondary to significant debris and this must be aspirated prior to retrieval. The EPD retrieval
system is advanced carefully past the stent without engaging/catching on the stent. With extensive
debris present in the filter, it is important not to fully recapture the filter in the retrieval catheter as
this can extrude debris from the filter and cause distal embolization. Distal ICA vasospasm can be
present as well and it is usually secondary to migration of EPD during the procedure. Typically,
this is managed conservatively but with significant ICA spasm, nitroglycerin (50 to 200 μg) can be
administered in small doses directly intraarterially in the ICA.
ACCESS HEMOSTASIS
■
The femoral access arterial puncture can be closed using standard techniques either with a closure
device or by direct manual compression. We prefer to use a closure device and do not routinely
reverse heparin anticoagulation with protamine. For brachial artery access, direct manual
compression is the preferred method for achieving hemostasis.
PEARLS AND PITFALLS

Selective common carotid ■ Tortuous aortic arch/great vessel anatomy may require additional
catherization manipulation with various retroflexed catheters in order to select
the common carotid. However, with increasing manipulation, there
is a greater risk of embolization/aortic injury. Therefore, aortic
arch/great vessel anatomy should be analyzed preoperatively and,
when indicated, suitable alternative plans should be prepared if
the initial method proves unsuccessful.
■ An extremely diseased aortic arch may be a relative
contraindication to CAS.
Placement of guiding sheath ■ When the ECA is occluded, a supportive guidewire cannot be
placed to allow tracking of the sheath and an alternative method is
needed. Alternatively, an Amplatz guidewire with a 1-cm floppy
tip in the distal CCA may provide sufficient support for sheath
placement. Shuttle systems that permit telescoping the sheath into
the CCA over a guidewire and catheter assembly are another
alternative.
Crossing the lesion with ■ Difficulty crossing the lesion can be addressed by changing the
EPD shape of the crossing wire tip or using a directional catheter.
Additionally, changing the patient’s head/neck position may make
a vessel less angulated.
■ Certain EPD such as the Nav-6 (Abbott Vascular, Abbott Park, IL)
and Spider (Covidien, Plymouth, MN) are introduced over a wire
that is introduced independently before the filter. Introduction of
the independent wire may facilitate subsequent introduction of the
filter across a tightly stenotic lesion or a lesion with an acute entry
angle.
■ A “buddy wire” (additional 0.014-in wire) can also be used to
provide extra support and facilitate crossing a difficult lesion.
■ If the crossing profile of the EPD is too large to cross the stenotic
lesion, the stenotic lesion can also be predilated with a 2.5-mm
balloon in order to create a channel large enough for EPD.
However, dilating the lesion without an EPD in place increases
the risk of distal embolization.
Distal ICA spasm ■ Usually caused by distal EPD and resolves after EPD and wire are
removed.
■ Small doses of nitroglycerin administered directly to carotid may
aid in resolution.
Occlusion of flow proximal ■ Distal ICA filter may be full of debris causing slow flow or ICA
to EPD after stent placement occlusion. The debris should be aspirated from the filter using an
aspiration catheter and repeat angiogram is performed after to
confirm return of flow prior to EPD retrieval.
■ If it is determined that occlusion is due to acute stent thrombosis
then immediate conversion to open exploration, stent removal, and
formal CEA may be necessary. Preparations for carotid stenting
should always include this possibility.
Distal embolization with ■ Neurorescue techniques are used to treat distal embolization or
neurologic symptoms and/or thrombosis, including the following:
intracranial arterial ■ Catheter-directed thrombolysis with tissue plasminogen activator
occlusion (tPA)
■ Mechanical thrombolysis with aspiration
■ Glycoprotein (GP) IIa/IIIb inhibitor administration
■ Direct removal with snare (intraarterial)
■ Direct balloon angioplasty to restore a lumen
Note: Intracranial neurorescue techniques should be performed by
physicians with appropriate experience and training.
POSTOPERATIVE CARE
■
Neurologic status is immediately evaluated after completion of the procedure and continuous
invasive blood pressure monitoring and pulse oximetry are maintained. Typically, CAS patients
are observed in a monitored step-down unit overnight.
■
Goal systolic blood pressures should be based on preoperative measurements. Vasopressor and/or
inotropic support may be required to compensate for hypotension and/or bradycardia likely due to
carotid sinus distension related to the procedure until the carotid sinus adapts to the presence of
the stent. Other causes of hypotension need to be excluded prior to attributing the cause to
angioplasty/stenting alone. Conversely, antihypertensives should be used as needed to prevent
hypertension and potential cerebral hyperperfusion.
■
The patient needs to remain on bed rest in the supine position for 4 to 6 hours after access site
hemostasis is achieved. The head of the bed can be inclined to a maximum 30 degrees to promote
patient comfort and respiratory function. Afterward, the patient can ambulate as tolerated.
■
Immediate head and neck imaging along with neurology consultation are mandatory if the patient
experiences a postoperative neurologic event.
■
Antiplatelet therapy with clopidogrel should be continued for at least 1 month post-CAS, whereas
aspirin is continued indefinitely.
OUTCOMES
■
Studies prior to year 2000 failed to define the role of CAS in treating carotid artery disease due to
numerous factors. More recent randomized controlled trials (RCTs) were performed in order to
elucidate CAS’ role in carotid disease, namely as a noninferior alternative to CEA.
■
The Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy
(SAPPHIRE) trial6 randomized symptomatic patients with 50% or greater carotid stenosis or
asymptomatic patients with 80% or greater stenosis with comorbidities that increased their risk of
surgery to receive either CEA or CAS. For the CAS patients, they all had self-expandable nitinol
stents (S.M.A.R.T. or PRECISE; Cordis, Miami Lakes, FL) placed with EPD (Angioguard or
Angioguard XP; Cordis, Miami Lakes, FL). The primary endpoint was composite incidence of
death, stroke, or myocardial infarction (MI) within 30 days postprocedure or death or ipsilateral
stroke between 31 days and 1 year. Only 334 patients were randomized—167 to CEA and 167 to
CAS (trial stopped early due to poor enrollment). No significant difference in the primary
composite endpoint rate was detected in the periprocedural period (30 days) for CAS compared to
CEA. However, 1-year primary composite endpoint rate was lower in CAS compared to CEA
(12.2% vs. 20.1%; P = .004) with a more pronounced difference in asymptomatic (9.9% in CAS
vs. 21.5% in CEA; P = .02) than in symptomatic patients (16.8% in CAS versus 16.5% in CEA; P
= .95). This difference vanished in long-term follow-up and at 3 years, the major secondary
endpoint (primary endpoint plus death or ipsilateral stroke 1 to 3 years) cumulative incidences
were 24.6% for CAS vs. 26.9% for CEA; P = .71.7 Thus, the SAPPHIRE authors concluded that
CAS with EPD was not inferior to CEA in patients with severe carotid artery stenosis and
increased surgical risk.
■
However, these results were not mirrored in two large European multicenter RCTs—Stent-
Supported Percutaneous Angioplasty of the Carotid Artery versus Endarterectomy (SPACE)8 and
Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-
3S)9 trials. Both of these studies failed to show noninferiority of CAS compared to CEA in their
respective study populations. In SPACE, the primary endpoint (rate of death or ipsilateral
ischemic stroke 30 days postprocedure) was 6.84% in CAS and 6.34% in CEA (absolute
difference 0.51%, 90% CI −1.89% to 2.91%; noninferiority P = .09). In EVA-3S, the results
demonstrated greater rates of stroke and death in the CAS group as compared to the CEA group:
30-day incidence of stroke or death was 9.6% in CAS (95% CI, 6.4 to 14.0) and 3.9% in CEA
(95% CI, 2.0 to 7.2); the relative risk of any stroke or death after CAS as compared with CEA was
2.5 (95% CI, 1.2 to 5.1). At 6 months, the incidence of any stroke or death was 11.7% after CAS
and 6.1% after CEA (P = .02). However, long-term data at 4 years from EVA-3S did not
demonstrate significant differences in the risk of any stroke or death in between both CAS and
CEA; the hazard ratio (HR) was 1.39 (0.96 to 2.00; P = .08).10 The authors interpreted these
results to “suggest that carotid stenting is as effective as carotid endarterectomy for middle-term
prevention of ipsilateral stroke, but the safety of carotid stenting needs to be improved before it
can be used as an alternative to carotid endarterectomy in patients with symptomatic carotid
stenosis.”
■
A more recent international multicenter RCT, the International Carotid Stenting Study (ICSS),
demonstrated that CEA was safer than CAS as treatment for patients with symptomatic carotid
stenosis of 50% or greater (enrolled 1,713 patients; CAS, n = 855; CEA, n = 858).11 The primary
composite endpoint, 120-day incidence of stroke, death, or MI was higher in CAS compared to
CEA (8.5% vs. 5.2%; HR, 1.69; 95% CI, 0.16 to 2.45; P = .006). The adverse events occurring
with the 30-day postprocedure period accounted for the majority observed at 120 days where the
cumulative incidence of stroke, death, and MI was 7.4% in CAS compared to 4.0% in CEA (P =
.003). The authors concluded that CEA should remain the treatment of choice for symptomatic
carotid stenosis patients that are suitable for surgery while awaiting the long-term follow-up data
of ICSS.
■
The Carotid Revascularization Endarterectomy versus Stenting Trial (CREST) is a U.S. trial that is
the most recent and largest RCT to compare the efficacy between CAS and CEA in standard-risk
patients.12 Two thousand and five hundred two patients with asymptomatic carotid stenosis of 70%
or greater (based on ultrasound criteria) or symptomatic carotid stenosis of 50% or greater (based
on angiographic North American Symptomatic Carotid Endarterectomy Trial criteria) were
randomized to either CAS (n = 1,262; RX Acculink stent; Carotid Stent System, Abbott Vascular,
Abbott Park, IL) and a distal EPD (RX Accunet Embolic Protection System, Abbott Vascular,
Abbott Park, IL) or CEA (n = 1,240). The primary composite endpoint was stroke, death, or MI
during the periprocedural period or any ipsilateral stroke within 4 years. During the
periprocedural period, the primary endpoint incidence was similar with CAS and CEA (5.2% and
4.5%, respectively; HR for stenting 1.18; 95% CI, 0.82 to 1.68; P = .38). However, the rates of
individual endpoints differed between CAS and CEA: greater risk of stroke in CAS (4.1% vs.
2.3%, respectively; P = .01), greater risk of MI in CEA (1.1% vs. 2.3%, respectively; P = .03), no
difference in death (0.7% vs. 0.3%, respectively; P = .18). The periprocedural risk of stroke or
death was higher after CAS for symptomatic patients (6.0% vs. 3.2%; P = .02). There was no
significant difference in the estimated 4-year rate of the primary endpoint between CAS and CEA
(7.2% vs. 6.8%, respectively; HR, 1.11; P = .51; 95% CI, 0.81 to 1.51). CREST also
demonstrated an interaction between age and treatment efficacy (P = .02) where CAS tended to
show greater efficacy at younger than 70 years of age and CEA at older than 70 years of age.
■
Overall, CAS as a noninferior or equivalent alternative treatment compared to CEA has not been
definitively established and further studies are needed.
COMPLICATIONS
■
Postoperative complications
■
Stroke—the incidence of stroke is higher with CAS than CEA.11 Risk factors include advanced
age, symptomatic carotid stenosis, and complex anatomy. Postoperative stroke needs to be
addressed immediately with full neurologic evaluation and potential intervention.
■
Hypotension—frequently observed post-CAS; however, it usually will resolve spontaneously.
Patients may require transient blood pressure support with vasopressors/volume.
■
Cerebral hyperperfusion syndrome—may occur within the first week post-CAS and is usually
associated with poorly managed underlying hypertension. It presents as a unilateral headache
and can progress to seizures, intracranial hemorrhage, and/or coma. Head CT is obtained and
focal cerebral edema may be observed. The treatment is aggressive blood pressure
management.
■
MI—cardiac complications, namely MI, may occur during the periprocedural period for CAS.
This is likely due to the typically high-risk patient population selected for CAS given that most
are poor candidates for CEA.
■
Access site complications—the most common access site complications that are inherent to
endovascular procedures are hematoma, pseudoaneurysm, retroperitoneal hematoma, and
arteriovenous fistula. To minimize the risk for these complications, we recommend direct
visualization of the access vessel under ultrasound and using a micropuncture access system. In
addition, proper use of vessel arteriotomy closure devices and/or manual vessel compression is
mandatory to reduce the risk for these complications.
■
Stent restenosis—restenosis will occur in any current stent placed in the body and can be
managed with reintervention as needed.
REFERENCES
1. Mathias K. A new catheter system for percutaneous transluminal angioplasty (PTA) of carotid artery stenoses. Fortschr Med.
1977;95(15):1007–1011.
2. Mathias K, Mittermayer C, Ensinger H, et al. Percutaneous catheter dilatation of carotid stenoses. Rofo. 1980;133(3):258–261.
3. 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. Circulation. 2011;124(4):489–532.
4. Biasi GM, Froio A, Diethrich EB, et al. Carotid plaque echolucency increases the risk of stroke in carotid stenting: the Imaging in
Carotid Angioplasty and Risk of Stroke (ICAROS) study. Circulation. 2004;110(6):756–762.
5. Ricotta JJ, Aburahma A, Ascher E, et al. Updated Society for Vascular Surgery guidelines for management of extracranial carotid
disease. J Vasc Surg. 2011;54(3):e1–e31.
6. 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.
7. 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.
8. 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. 2006;368(9543):1239–1247.
9. 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.
10. 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.
11. 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.
12. 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.
Carotid Surgery: Distal Exposure and Control
Chapter 5 Techniques and Complication Management
Cheong J. Lee
DEFINITION
■
The carotid artery typically bifurcates at the level of the C3-C4 cervical spine. High carotid
bifurcations and lesions that extend to the C1-C2 level pose technical challenges that may increase
perioperative risk of stroke and cranial nerve injury. Ideally, the need for high access in carotid
surgery should be anticipated preoperatively, with familiarity of the anatomy and exposure
necessary for distal carotid control.

■
As with any medical therapy, the clinician must first clearly define the goals of treatment and
thoroughly review the operative risk with the patient.
■
Optimal medical therapy must be instituted prior to intervention (e.g., antiplatelet agent, statin, beta-
blocker).
■
Patients with hostile neck anatomy, such as those with history of high-dose neck radiation or severe
systemic comorbidities contraindicating general or cervical block anesthesia, should be offered
carotid angioplasty and stenting (CAS) as an alternative procedure.
■
Patients with prior contralateral carotid revascularization procedures should have laryngeal,
hypoglossal, and glossopharyngeal nerve function documented prior to ipsilateral dissection and
exposure. When evidence of prior injury to CN IX, X, or XII is evident, CAS should be
considered as an alternative. If CAS is not feasible under these circumstances, the potential need
for tracheostomy to manage postoperative airway obstruction should be reviewed with the patient.
■
Although duplex scanning provides accurate and reproducible assessment of the presence and
severity of carotid stenosis, precise anatomic detail required for surgical planning is optimally
obtained from computed tomographic angiography (CTA) or magnetic resonance arteriography
(MRA). Localization of the carotid bifurcation in regard to cervical landmarks, as well as the
distal extent of internal carotid artery (ICA) disease, is best assessed by CTA or MRA (FIG 1).

■
Current indications for carotid endarterectomy were reviewed in Chapter 3.1–3
■
In recent years, CTA and MRA have assumed preeminent roles in carotid intervention planning.
Improved resolution has enabled highly accurate characterization of plaque morphology, which
may provide useful guidance regarding plaque vulnerability during operative manipulation.
■
MRA and CTA also provide essential information regarding potential collateral arterial flow
through the circle of Willis and the need for adjuvant maneuvers such as shunt placement during
carotid revascularization (FIG 2).
SURGICAL MANAGEMENT
Preoperative Planning for Distal Cervical Carotid Exposure
■
Knowledge of patient-specific cervical anatomy is essential to successful management of distal
carotid disease. When recognized as necessary, specifying nasotracheal, rather than orotracheal,
intubation for general endotracheal anesthesia is a simple and highly effective maneuver to
improve exposure. Nasotracheal intubation allows the mouth to stay closed during surgery,
providing more room between the ramus of the mandible and mastoid process for distal dissection.
■
Temporomandibular subluxation may further advantage carotid exposure cephalad to the C2
cervical spine. Subluxation of the ipsilateral mandibular condyle, performed via intraoral wiring,
facilitates exposure from infratemporal ICA to the skull base. Subluxation is distinguished from
dislocation, which is more injurious and can potentiate long-term temporomandibular joint pain
syndromes.
Positioning
■
The patient is positioned supine, with the head extended and rotated away from the operative site.
Shoulder rolls and shays are placed to stabilize the neck and optimize extension. The nasotracheal
tube is secured over the head (FIG 3).
■
Arms are tucked to the patient’s side to allow the operator and the assistant to maneuver and stand
comfortably. This position also facilitates C-arm positioning when needed.
■
The patient is placed in the “beach chair” position to limit venous hypertension (FIG 4).
TECHNIQUES
ANTERIOR APPROACH TO THE DISTAL INTERNAL CAROTID ARTERY

Incision
■
A vertical, rather than transverse, cervical incision is recommended for optimal distal ICA access
(FIG 5).
■
Standard exposure of the carotid artery in the sheath was previously described in Chapter 3.
Exposure of the Internal Carotid Artery Distal to the Bifurcation
■
Key structures that lie superior to the carotid bifurcation are the posterior belly of the digastric
muscle, the hypoglossal nerve, crossing veins from the sternocleidomastoid muscle to the internal
jugular vein, and muscular arterioles of the posterior branches of the external carotid artery (ECA)
(FIG 6).
■
The hypoglossal nerve is identified safely using a posterolateral to anteromedial dissection of the
ICA. Moving cephalad, the hypoglossal nerve is dissected free from the medial surface of the
digastric muscle. Crossing artery and veins of the SCM often tether this nerve closer to the
bifurcation. Meticulous identification and controlled division of these tethering vessels will enable
mobilization of the nerve. Tracing the course of the descending branch of the ansa cervicalis back
to the hypoglossal itself provides positive confirmation of the location and course of the nerve
(FIG 7).
■
The posterior digastric muscle belly may be retracted or divided as required for exposure,
following release of the adherent hypoglossal nerve.
■
Additional cephalad exposure at this juncture requires division of the occipital branch of the ECA.
This further releases the hypoglossal nerve. This maneuver also requires division of the styloid
musculature (styloglossus, stylopharyngeus).
■
Continued cephalad dissection exposes the glossopharyngeal nerve, seen as a single or double trunk
crossing the ICA anteriorly and coursing posterior to the external carotid. Care must be taken in
separating the hypoglossal and glossopharyngeal nerves, as small motor fibers exiting the vagus
nerve also course in this plane. Damage to these nerves or the glossopharyngeal can cause
swallowing dysfunction. Classically, injury to the glossopharyngeal nerve in this region may
impair the ability of the soft palate to rise sufficiently with swallowing to prevent nasopharyngeal
liquid reflux.
■
When these steps are safely completed, the ICA may be adequately exposed for reconstruction up to
the level of C2 (FIG 8). Further exposure to the level of C1 following this course requires
styloidectomy and/or preoperative mandibular subluxation.
■
Distal dissection may also be facilitated by mobilization of the parotid gland and facial nerve. This
is most safely accomplished with assistance from otolaryngologists or craniomaxillofacial
surgeon. To provide this method of exposure, the skin incision is carried cephalad anterior to the
ear (FIG 9). This enables mobilization of the parotid gland superiorly and medially.
■
The parotid fascia is entered and the branches of the facial nerve are dissected, identified, and
protected before dividing the posterior belly of the digastric muscle.
■
Care is again taken to identify the glossopharyngeal nerve and the motor fibers of the vagus nerve
(FIG 10).
■
Distal control of the ICA at high C1-C2 level may require specialized instrumentation. Small
detachable occluding clamps (such as the Heifetz or Yasargil clips) may provide improved
exposure compared to traditional “handled” vascular clamps in this region. When used, however,
care must be taken to avoid clamp dislodgement in this crowded and moving field, which when it
does happen usually does so at the maximally inconvenient time.
■
As an alternative to distal clamp control, short occluding intraluminal catheters can be used, such as
a #2 Fogarty embolectomy catheter with stopcock. Extreme care must be taken in positioning and
deploying embolectomy balloons in this area, however, as inflation within the petrous portion or
overinflation in any region may precipitate dissection, arterial rupture, or thrombosis. Only the
lowest amount of inflation required to prevent back-bleeding should be used. The carotid artery is
thin-walled at this level and easily traumatized by balloon inflation. Late complications also
include pseudoaneurysm or arteriovenous fistula formation. The inflated catheter should be
secured to prevent its migration. Stay sutures may be placed in the distal carotid to maintain access
should control be lost due to reflux of the balloon from the distal artery or balloon puncture during
suture closure of the anastomosis.
RETROJUGULAR APPROACH TO THE DISTAL INTERNAL CAROTID

ARTERY
Retrojugular Dissection
■
A third approach to the distal ICA is provided by retrojugular access. The internal jugular (IJ) vein
angles anteriorly as it ascends from the base of the neck to the base of the skull and overlies the
distal ICA as the artery approaches the transverse process of C1.
■
Using the posterior approach, dissecting behind the IJ vein, obviates the need for hypoglossal
exposure and relocation, as that nerve passes anteriorly over the ICA.
Identification of the Spinal Accessory Nerve
■
The retrojugular dissection uses the same incisions as other approaches to the distal internal carotid,
with the incision made vertically, anterior to the SCM muscle.
■
Using this approach, it is essential to identify the spinal accessory nerve where it exits 2 to 3 cm
below the edge of the mastoid process, anterior to the SCM. The SCM is fully mobilized to
facilitate this exposure.
■
Once the spinal accessory nerve is identified and isolated, the IJ vein is dissected along its posterior
border. The vagus nerve is identified and reflected anteriorly. With the vein and vagus nerve
mobilized anteriorly, the hypoglossal nerve remains anterior to the distal ICA (FIG 11).
Identification of the Superior Laryngeal Nerve

■
In the retrojugular space, the ICA can be dissected along its posterior lateral wall superiorly
whereupon the superior laryngeal nerve will be encountered exiting the vagus nerve and looping
around the distal ICA. Often, the superior cervical ganglion can be identified just lateral to this
looping point (FIG 12).
■
For added exposure, the nerve is carefully lifted from the ICA adventitia.
PEARLS AND PITFALLS

Indications ■ Make note of significant radiation or surgery to the neck, which
may inform the choice of procedure (surgery vs. stent).
■ Make certain the patient’s cranial nerve status is documented,
especially in the setting of prior neck operations.
Imaging ■ Although duplex imaging alone is sufficient to plan most routine
carotid surgery, cross-sectional imaging (CTA/MRA) provides
essential guidance for complex exposures and reconstructive
techniques.
■ The status of the circle of Willis should be defined in the course of
preoperative planning.
Technique ■ For lesions extending to the C1-C2 cervical spine, consider at a
minimum nasotracheal intubation.
■ In extreme situations, mandibular subluxation may provide critical
additional degrees of freedom.
■ Mandibular dislocation is not recommended and should not be
performed to assist carotid surgery.
■ Knowledge of cranial nerve anatomy is the most important
determinant of success.
■ Any neural tissue crossing anterior to the carotid bifurcation and
the ICA should not be divided.
■ Mobilization of diseased arterial segments, including the carotid
bifurcation, should be avoided or minimized prior to
heparinization.
■ Anterior distal ICA exposure is dependent on the extent to which
the hypoglossal nerve can be safely mobilized.
■ Posterior, retrojugular exposure requires early identification of the
spinal accessory nerve and anterior reflection of the vagus nerves
to visualize the superior laryngeal nerve encircling the distal
internal carotid.
■ Balloon occlusion may facilitate far distal carotid control, but
overadvancement and overinflation are real risks that must be
considered. Placement of stay sutures will facilitate future control
maneuvers should the catheter become dislodged.
POSTOPERATIVE CARE
■
Following carotid revascularization, the immediate postoperative care is focused on close
neurologic surveillance. Patients are recovered typically in an intensive care unit or monitored
setting to facilitate ready identification of evolving neurologic deficits.
■
Careful blood pressure monitoring and management is also essential. Following carotid
revascularization, patients need to avoid the extremes of blood pressure, which may elicit
hemodynamic stroke and intracerebral hemorrhage.
■
Immediate postoperative (<24 hours) neurologic deficits should be assumed to be thromboembolic
in nature, most commonly associated with a technical (surgical) error. Further imaging studies are
unlikely to alter decision making and should not delay immediate reoperation. Neurologic deficits
arising later in the postoperative period (>24 hours) may be due to intracranial hemorrhage; in
these cases, computed tomography (CT) or magnetic resonance (MR) imaging may assist the
decision-making process and should be considered when etiologic circumstances are less certain.
■
Bleeding complications following carotid surgery are rare but potentially serious or fatal. These
may occur during the first several hours after surgery or even later, particularly in patients
resuming anticoagulation therapy for existing conditions early in the postoperative period.
Recognition and expeditious control of the airway is of utmost importance as a wound hematoma
develops, as cord and airway edema rapidly worsen in response to reduced venous and lymphatic
drainage. Reopening a carotid incision prior to anesthetic induction may facilitate emergency
endotracheal intubation; however, this dramatic maneuver is best performed in a controlled
environment with resuscitation equipment available should complications ensue. Ideally,
preparations are made for wound decompression as endotracheal intubation is being attempted,
with the wound being opened as a last step maneuver prior to emergency cricothyroidotomy. Cord
edema in these circumstances may be profound, however, and visualization may not improve
sufficiently after hematoma evacuation to enable orotracheal or nasotracheal intubation. Therefore,
cricothyroidotomy may become necessary in extreme circumstances, and all carotid surgeons
should be facile in this maneuver as a matter of course.
OUTCOMES
■
Although carotid endarterectomy is a well-established technique continually refined over several
decades, good outcomes are not limited to regional centers of excellence. Data provided to the
American Board of Surgery regarding surgical case experience in the 12 months preceding
application for recertification in vascular surgery, carotid endarterectomy is recorded as one of
the most common procedures performed by contemporary vascular surgeons. A recent query of the
Nationwide Inpatient Sample (NIS) identified 259,080 carotid revascularization procedures
performed during 2003 and 2004. Although the study examined and compared outcomes of both
carotid endarterectomy and carotid artery stenting, endarterectomy outcomes alone demonstrated
an impressive overall stroke rate of 0.88% and operative mortality rate of 0.39%.4 Similarly, data
prospectively obtained from National Surgical Quality Improvement Program (NSQIP)
participation reviewed 13,622 carotid endarterectomies performed between 2000 and 2003 at 123
Veterans Affairs and 14 private sector academic medical centers demonstrated a combined stroke
and death rate of 3.4%.5
■
Data describing outcome of distal (base of skull) carotid revascularizations is based on more
limited, institution-specific case series. In these circumstances, outcomes are more difficult to
benchmark. One recent series reported that one of five patients requiring a distal ICA bypass for
aneurysm repair suffered a stroke; 60% suffered varying degrees of cranial nerve deficit.6 The
largest experience reported to date is that of Sessa et al.,7 who reported a 3% and 6% rate of
perioperative stroke and restenosis at 1 year, respectively. When distal carotid/skull base
exposure appears to be necessary to safely manage an occlusive lesion, consideration should again
be given to CAS as a lower risk alternative technique to open endarterectomy or interposition
grafting.
COMPLICATIONS
■
Stroke
■
Cranial nerve injury
■
Horner’s syndrome
■
Seroma
■
Infection
REFERENCES
1. North American Symptomatic Carotid Endarterectomy Trial. Methods, patient characteristics, and progress. Stroke. 1991;22:711–
720.
2. Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis
Study. JAMA. 1995;273:1421–1428.
3. Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery
Trial (ECST). Lancet. 1998;351:1379–1387.
4. McPhee JT, Hill JS, Ciocca RG, et al. Carotid endarterectomy was performed with lower stroke and death rates than carotid artery
stenting in the United States in 2003 and 2004. J Vasc Surg. 2007;46:1112–1118.
5. Stoner MC, Abbott WM, Wong DR, et al. Defining the high-risk patient for carotid endarterectomy: an analysis of the prospective
National Surgical Quality Improvement Program database. J Vasc Surg. 2006;43:285–295; discussion 295–296.
6. Eliason JL, Netterville JL, Guzman RJ, et al. Skull base resection with cervical-to-petrous carotid artery bypass to facilitate repair of
distal internal carotid artery lesions. Cardiovasc Surg. 2002;10:31–37.
7. Sessa CN, Morasch MD, Berguer R, et al. Carotid resection and replacement with autogenous arterial graft during operation for
neck malignancy. Ann Vasc Surg. 1998;12:229–235.
Chapter 6 Vertebral Transposition Techniques and Stenting
Mark D. Morasch
DEFINITION
■
Treatment for occlusive lesions involving the origin of the vertebral artery (V1 segment) is
undertaken to relieve posterior brain circulation ischemia, otherwise known as vertebrobasilar
insufficiency. Revascularization options include open surgical and endovascular techniques. The
most common operation is a proximal vertebral to common carotid transposition. Endoluminal
treatment includes balloon angioplasty and (typically) stenting.
DIFFERENTIAL DIAGNOSIS
■
Other medical conditions mimicking posterior circulation ischemia include postural hypotension,
cardiac arrhythmias, anemia, brain tumors, and benign vertiginous states. A thorough investigation
consists of ruling out (1) inner ear pathology, (2) cardiac arrhythmias, (3) internal carotid artery
stenosis/occlusion, and (4) complications of excessive blood pressure control (Table 1).
■
Evaluation of patients with posterior circulation ischemia requires defining the precise
circumstances that elicit symptoms. Vertigo, instability, and occasional loss of consciousness often
accompany positional changes and standing in older individuals due to reduced sympathetic
venous tone. This is particularly common in patients with diabetes. The presence of orthostatic
hypotension should be evaluated as a common alternative cause for vertebrobasilar symptoms.
Any decreases in basilar artery perfusion pressure may precipitate hemodynamic symptomatology,
with or without concomitant vertebral occlusive disease.
■
The next most common cause of brainstem ischemia is reduced cardiac output. When suspected,
evaluation includes 24-hour Holter monitoring and echocardiography. In patients with
vertebrobasilar insufficiency, palpitations may be noted with the onset of symptoms.
Transesophageal echocardiography may be necessary to rule out structure heart issues.
■
Inner ear pathology, including rare cerebellopontine angle tumors, produces symptoms suggestive of
vertebrobasilar insufficiency. Benign vertiginous states should also be considered. Physical
examination can alert the physician to the possibility of subclavian steal in patients with
differences in brachial blood pressure greater than 25 mmHg or with diminished left upper
extremity pulses. Reversed flow in the ipsilateral vertebral artery demonstrated on duplex
scanning is pathognomonic for subclavian steal physiology and subclavian steal syndrome in
patients with appropriate symptoms at rest or following exercise in the ipsilateral upper extremity.
■
Patients may relate symptoms of vertebrobasilar insufficiency to positional changes, including
turning or extending their head. These dynamic symptoms usually appear when turning the head to
one side. In this circumstance, symptoms may be elicited by extrinsic compression of the dominant
or sole vertebral artery (in the case of unilateral occlusion) by adjacent arthritic bone spurs.1

■
In general, ischemic mechanisms in vertebrobasilar insufficiency can be categorized as
hemodynamic or embolic. Symptoms of vertebrobasilar insufficiency include dizziness, vertigo,
drop attacks, diplopia, perioral numbness, alternating paresthesia, tinnitus, dysphasia, dysarthria,
and ataxia. When two or more of these symptoms are present, vertebrobasilar ischemia is more
likely to be the inciting cause. Unlike other regions of the brain, strokes in the posterior circulation
territory occur due to large artery occlusive diseases.
■
Patients with “hemodynamic” ischemia experience transient vertebrobasilar symptoms due to
inadequate vertebral artery inflow or collateral circulation. Symptoms are typically short lived,
repetitive, somewhat predictable, and rarely result in stroke. Postural hypotension may precipitate
serious traumatic injury, however, when patients lose their balance with standing.
■
Embolic events may also precipitate vertebrobasilar ischemia as well as cerebellar and brainstem
infarction. Microemboli from the heart, aortic arch, or any arteries leading directly to the basilar
artery may arise from atherosclerotic lesions, intimal defects, repetitive trauma, fibromuscular
dysplasia lesions, aneurysms, or dissections. Although much less common than hemodynamic
vertebrobasilar insufficiency, when present, microemboli are much more likely to cause fatal
events or debilitating infarcts.2–4
■
Timing of the onset of symptoms following positional changes may help differentiate vertebrobasilar
insufficiency from labyrinthine disorders. In the latter circumstance, rapid head movement invokes
immediate symptoms. In the case of vertebrobasilar insufficiency, however, a short delay usually
precedes the onset of symptoms, including nystagmus.

Duplex ultrasound, an otherwise excellent tool for the assessment of extracranial cerebrovascular
disease, has limitations in the diagnosis of vertebral artery pathology. Direct visualization of the
second portion is obscured by the transverse processes of C2–C6. As previously mentioned,
however, duplex imaging reliably identifies subclavian steal physiology, as well as detect proximal
velocity increases consistent with orificial vertebral or proximal subclavian stenosis.5
■
Magnetic resonance imaging (MRI) provides safe, noninvasive, and detailed evaluation of the aortic
arch and great vessels, the extracranial and intracranial arterial vasculature, as well as the
presence of mass lesions, fluid collections, or parenchymal defects in the posterior fossa.
Contrast-enhanced magnetic resonance angiography (MRA), with three-dimensional reconstruction
and maximum image intensity techniques, provides excellent image quality in high resolution (FIG
1). As in other applications, however, in low-flow circumstances, excessive signal dropout may
result in overestimation of lesion severity based on signal intensity alone.
■
In contrast to computed tomographic (CT) imaging, transaxial MRI readily diagnoses both acute and
chronic brain infarctions in the posterior fossa. Brainstem infarctions are typically small and as
such may be overlooked with noncontrast CT imaging. Brain MRI is performed in symptomatic
patients prior to vertebral artery intervention to identify infarctions when they are present and
provide baseline images for future comparison.
■
Evaluation of vertebral anatomy via catheter-based, contrast arteriography requires acquisition of
images in multiple projections to fully evaluate the entire extent of both vertebral arteries.
Evaluation begins with the aortic arch to determine the origin of the bilateral vertebral arteries.
Anomalous origin of the left vertebral artery, arising directly from the aorta proximal to the left
subclavian, is present in 6% of patients. Much less frequently, the right vertebral artery originates
from the innominate or right common carotid artery. This anomaly often accompanies an aberrant
right subclavian artery, which itself may precipitate symptoms of dysphagia lusoria.
■
Usually, right and left posterior oblique projections are sufficient to comprehensively evaluate the
V1 (first) vertebral artery segment from the origin to the transverse process of C6. In most patients,
the left artery is usually dominant, but a number of normal variants may be encountered, including
congenital atresia of either vertebral artery.
■
The vertebral artery origin may not be visualized adequately with either duplex ultrasonography or
MRA. Oblique projections are required during arteriography due to superimposition of the
subclavian artery over the vertebral origin. Additional projections, including craniocaudal tube
angulation, may also be required to optimize visualization. The presence of a poststenotic
dilatation in the first centimeter of the vertebral artery is a clue that should prompt further
projections to isolate the origin from the overlying subclavian artery.
■
Dynamic arteriography, incorporating provocative positioning, may be required to assess the
possibility of extrinsic vertebral artery compression. Finally, delayed imaging may demonstrate
reconstitution of patent distal extracranial vertebral arteries through cervical collaterals when the
origin initially appears occluded.
SURGICAL MANAGEMENT
■
Some degree of vertebral artery orificial stenosis is present in 20% to 40% of patients with other
manifestations of cerebrovascular disease.2 A number of operative approaches will satisfactorily
address V1 segment disease and orificial stenosis.6,7 Vertebral transposition, or repositioning of
the origin of the vertebral artery onto the adjacent common carotid artery is the most common.
Endoluminal dilatation, with or without stenting, is also appropriate in selected circumstances.
Vertebral to Common Carotid Transposition
■
General endotracheal anesthesia is preferred. Positioning supine, with the back of the table slightly
elevated toward a chair position with the head rotated away from the planned incision site
facilitates additional deep mediastinal exposure when required.
■
Proximal vertebral artery exposure is similar to that required for subclavian-to-carotid
transposition. One fingerbreadth above the clavicle, a transverse incision is created directly over
the two heads of the sternocleidomastoid muscle (SCM). Between the SCM heads, the omohyoid
muscle is identified and divided. Lateral retraction of the internal jugular vein and vagus nerve
exposes the carotid sheath medially. Maximal proximal carotid artery exposure, facilitated by
positioning of the primary operator at head of the patient, is necessary to ensure an optimal result
(FIG 2).
■
The sympathetic ganglia are identified running behind and parallel to the carotid artery. On the left
side, the thoracic duct is divided between ligatures to minimize lymphatic leaks. The proximal end
should be doubly ligated, avoiding transfixion sutures. Accessory lymph ducts—often seen on the
right side—should also be ligated and divided when identified. The entire dissection is confined
medial to the prescalene fat pad covering the scalenus anticus muscle and phrenic nerve. These
latter structures are left unexposed lateral to the field. The inferior thyroid artery, running
transversely across the field, is also ligated and divided.
■
The vertebral vein is next identified emerging from the angle formed by the longus colli and
scalenus anticus and overlying the vertebral artery and, at the bottom of the field, the subclavian
artery. Unlike its sister artery, the vertebral vein has branches. It is ligated in continuity and
divided. Below the vertebral vein lies the vertebral artery. It is important to identify and avoid
injury to the adjacent sympathetic chain. The vertebral artery is dissected superiorly to the tendon
of the longus colli and inferiorly to its origin in the subclavian artery. The vertebral artery is freed
from the sympathetic trunk resting on its anterior surface without damaging the trunk or the
ganglionic rami. Preserving the sympathetic trunks and the stellate or intermediate ganglia resting
on the artery usually requires freeing the vertebral artery from these structures, and after dividing
its origin, the latter is transposed anterior to the sympathetics.
■
Once the artery is fully exposed, an appropriate site for reimplantation in the common carotid artery
is selected. The patient is systemically anticoagulated with intravenous heparin. The distal portion
of the V1 segment of the vertebral artery is clamped below the edge of the longus colli with a
microclip placed vertically to indicate the orientation of the artery and to avoid axial twisting
during its transposition. The proximal vertebral artery is closed by transfixion with 5-0
polypropylene suture immediately above the stenosis at its origin. The artery is divided at this
level, and its proximal stump is further secured with a hemoclip. The artery is then brought to the
common carotid artery and its free end is spatulated for anastomosis.
■
The carotid artery is then cross-clamped. An elliptical 5- to 7-mm arteriotomy is created in the
posterolateral wall of the common carotid artery with an aortic punch. The anastomosis is
performed in open fashion with continuous 6-0 or 7-0 polypropylene suture while avoiding any
tension on the vertebral artery, which tears easily. Before completion of the anastomosis, any slack
in the suture is tightened appropriately with a nerve hook, standard flushing maneuvers are
performed, and the suture is tied to reestablish flow (FIG 3).
Vertebral Artery Angioplasty and Stent Placement

■
In the past decade, endovascular treatment of vertebral artery disease has gained increasing
acceptance. For endovascular intervention, patients are pretreated with dual antiplatelet therapy
(aspirin and clopidogrel). The procedure is usually performed with local anesthesia and conscious
sedation, enabling continuous neurologic monitoring of the patient. The patients are positioned
supine and prepped to allow percutaneous entry into the chosen access vessel. Most cases are
performed from a femoral approach (93%), although transbrachial (3%) and transradial (5%)
access has also been used as noted in one recent review.8 The stenotic lesions are crossed and
then dilated with 0.014- or 0.018-in guidewires and small coronary-diameter balloons. If a stent is
chosen, these are usually bare metal type, but drug elution has also been used. The same 0.014- or
0.018-in guidewires are used as platforms over which the stents are delivered and then deployed.
Postdeployment angioplasty may be necessary in selected cases. Procedures can be performed
with or without the assistance of embolic protection, although most vertebral arteries are too small
to accommodate most distal protection devices.
PEARLS AND PITFALLS
Placement of incision ■ It is important to place the incision medially enough to dissect
between the heads of the sternocleidomastoid. An approach lateral
to this structure will make the transposition challenging, if not
impossible, to complete.
Orientation ■ Enough of the V1 segment of the vertebral artery, up to near where
it disappears into the transverse process of C6, needs to be
mobilized. Also, plan ahead and see where on the carotid is best
to reimplant the vertebral before creating the carotid arteriotomy.
Closure ■ A drain is usually helpful, especially on the left side where the
thoracic duct crosses the exposure, just in case a tie comes off of a
large lymphatic. The drain allows for early diagnosis of this
complication.
POSTOPERATIVE CARE
■
Following surgical transposition, absent significant lymphatic drainage from the wound, the patient
may be safely discharged on the first or second postoperative day. Similarly, after endoluminal
therapy, patients are kept overnight to ensure neurologic stability.
OUTCOMES
■
After proximal vertebral–to–common carotid transposition, patency rates at 5 and 10 years equal or
exceed 95% and 91%, respectively. When selected appropriately, more than 80% of patients will
experience symptomatic relief following proximal surgical reconstruction.9
■
Appropriate reconstruction and subsequent reperfusion of the brainstem in patients experiencing
hemodynamic vertebrobasilar symptoms may also improve hypertension management.
■
Overall, retrospective reviews suggest that endoluminal vertebral artery intervention is reasonably
safe, although a selection bias exists. A 2005 Cochrane review identified 313 interventions for
vertebral artery stenosis, with just over half using stent placement as part of the treatment. The
technical success rate was 95%, and the 30-day stroke and death rate was 6.4%.10
■
Despite high technical success rates, vertebral artery angioplasty alone, especially when used for
the treatment of disease at the origin of the vessel, appears to have an unacceptably high rate of
restenosis. Adjuvant stent placement adds to the clinical durability but adds potential morbidity
such as malposition or potential fracture. In their series of 105 patients who underwent
endovascular stenting for symptomatic vertebral artery disease, Jenkins et al.11 achieved 100%
radiographic improvement (residual stenosis ≤30%). The authors reported immediate (30-day)
periprocedural risk of death of 1% and periprocedural complication rate of 4.8%. Complications
included transient ischemic attack, flow-limiting dissection, hematoma, and catheter-access-site
problems. At 1 year of follow-up, six patients had died and five had experienced a vertebrobasilar
stroke, and at approximately 2.5 years of follow-up, 70% of patients remained symptom free, but
13% of patients had restenosis requiring retreatment.11
■
A recent systematic review of the available literature noted a weighted mean technical success rate
of 97%. The authors estimated mean periprocedural stroke and death rate from combined
angioplasty and stenting to be around 1.1%. Transient ischemic events occurred in 1.5% of
patients. Recurrent symptoms occurred in 8% of patients within a reported range of follow-up of 6
to 54 months and greater than 50% restenosis developed in 23% of the subset of patients who
underwent follow-up imaging.8
COMPLICATIONS
■
Proximal vertebral to common carotid transposition has been reported to have a combined stroke
and death rate of 0.9%.9 Among patients undergoing this operation, in one report, there were no
deaths or strokes in those who underwent only a vertebral reconstruction. Berguer and coauthors
reported four instances of immediate postoperative thrombosis (1.4%). Three of the four patients
had vein grafts interposed between the vertebral artery and the common carotid because of a short
V1 segment. The grafts kinked and thrombosed. Other complications that are particular to proximal
reconstruction include vagus and recurrent laryngeal nerve palsy (2%), Horner’s syndrome (8.4%
to 28%), lymphocele (4%), and chylothorax (0.5%).
■
Periprocedural risks for angioplasty and stenting include access complications, distal embolization
and stroke, arterial rupture, stent malposition, and vessel thrombosis or dissection. Later,
restenosis and stent fracture are not uncommon (FIG 4).
REFERENCES
1. Bauer R. Mechanical compression of the vertebral arteries. In: Berguer R, Bauer R, eds. Vertebrobasilar Arterial Occlusive
Disease: Medical and Surgical Management. New York: Raven; 1984:45–71.
2. Caplan LR, Wityk RJ, Glass TA, et al. New England Medical Center Posterior Circulation registry. Ann Neurol. 2004;56:389–398.
3. Caplan L, Tettenborn B. Embolism in the posterior circulation. In: Berguer R, Caplan L, eds. Vertebrobasilar Arterial Disease. St.
Louis, MO: Quality Medical; 1992:52–65.
4. Pessin M. Posterior cerebral artery disease and occipital ischemia. In: Berguer R, Caplan L, eds. Vertebrobasilar Arterial
Disease. St. Louis, MO: Quality Medical; 1992:66–75.
5. Berguer R, Higgins R, Nelson R. Noninvasive diagnosis of reversal of vertebral-artery blood flow. N Engl J Med. 1980;302:1349–
1351.
6. Edwards WH, Mulherin JL Jr. The surgical approach to significant stenosis of vertebral and subclavian arteries.
Surgery.1980;87:20–28.
7. Roon AJ, Ehrenfeld WK, Cooke PB, et al. Vertebral artery reconstruction. Am J Surg. 1979;138:29–36.
8. Antoniou GA, Murray D, Georgiadis GS, et al. Percutaneous transluminal angioplasty and stenting in patients with proximal vertebral
artery stenosis. J Vasc Surg. 2012;55:1167–1177.
9. Berguer R, Flynn LM, Kline RA, et al. Surgical reconstruction of the extracranial vertebral artery: management and outcome. J
Vasc Surg. 2000;31:9–18.
10. Coward LJ, Featherstone RL, Brown MM. Percutaneous transluminal angioplasty and stenting for vertebral artery stenosis.
Cochrane Database Syst Rev. 2005;(2):CD000516.
11. Jenkins JS, Patel SN, White CJ, et al. Endovascular stenting for vertebral artery stenosis. J Am Coll Cardiol. 2010;55(6):538–542.
Neurogenic Thoracic Outlet Syndrome Exposure and
Chapter 7 Decompression: Supraclavicular
Robert W. Thompson Chandu Vemuri
DEFINITION
■
Thoracic outlet syndrome (TOS) is a group of conditions caused by compression of one of the
neurovascular structures that serve the upper extremity.1–3 Neurogenic thoracic outlet syndrome
(NTOS) is the most frequent of these, occurring in 85% to 90% of thoracic outlet patients. It is
caused by compression and irritation of the brachial plexus nerves within the supraclavicular
scalene triangle and/or underneath the pectoralis minor muscle tendon in the subcoracoid space
(FIG 1). NTOS tends to occur in patients between the ages of 15 and 40 years, typically
manifesting as neck and upper extremity pain, paresthesias, and functional limitations in the
ipsilateral arm. Although relatively uncommon, clinical recognition and appropriate treatment are
crucial to optimizing outcome in young active individuals with NTOS-related disability.4
■
The causes of NTOS include anatomic variations (anomalous scalene musculature, aberrant
fibrofascial bands, and/or cervical ribs) and previous neck or upper extremity injury, which
promotes scalene/pectoralis muscle spasm, fibrosis, and other pathologic changes.4 These
muscular alterations, in turn, lead to compression and irritation of the adjacent brachial plexus
nerves. The presence of a cervical rib is often cited as a risk factor for NTOS; however, few
NTOS patients (approximately 10%) have a definable cervical rib, and development of NTOS
symptoms are rare in cervical rib patients in the absence of predisposing injury.5
■
NTOS often occurs in individuals involved in occupational or recreational activities requiring
repetitive overhead activities with the arms and/or heavy lifting, occasionally aggravated by injury
(e.g., motor vehicle collisions or falls upon the outstretched arm). Other predisposing conditions
include low-grade repetitive strain injury (e.g., prolonged keyboard use), poor posture, and
dysfunctional shoulder girdle mechanics.
■
Surgical treatment for NTOS may be effectively accomplished by several different approaches,
including transaxillary 1st rib resection and anterior (supraclavicular) decompression. The
supraclavicular approach has long been a mainstay in the surgical treatment of NTOS, providing
excellent exposure for safe and definitive decompression of the relevant neurovascular structures
as well as the flexibility to manage the entire spectrum of circumstances that may be encountered
intraoperatively.6–10
■
NTOS-related symptoms may mimic or overlap those observed in other upper extremity neurologic
and musculoskeletal disorders, expanding the differential diagnosis (Table 1).11,12 Successful
intervention requires differentiation of NTOS from other cervical–brachial syndromes as well as
optimal patient and procedural selection.13
■
NTOS should be readily differentiated from venous TOS, which produces marked arm swelling,
cyanotic discoloration, and distention of subcutaneous veins around the shoulder and chest wall.
Venous TOS often presents clinically as axillary-subclavian vein “effort-related thrombosis”
(Paget-Schroetter syndrome). NTOS should also be distinguished from arterial TOS, which causes
either fixed subclavian artery obstruction or poststenotic aneurysm formation. The former may
precipitate arm or hand pain with exercise (“arm claudication”), the latter aneurysm thrombosis
and distal embolization, hand ischemia, rest pain, and/or digital ulceration and necrosis.
■
Some NTOS patients exhibit severe upper extremity pain and hypersensitivity, with digital swelling
and discoloration, suggesting the presence of sympathetic nerve overactivity. In such cases, the
coexistence of reflex sympathetic dystrophy (complex regional pain syndrome [CRPS]) should be
determined by assessing the symptomatic response to a temporary cervical sympathetic (stellate
ganglion) anesthetic block.

■
Symptoms attributable to brachial plexus nerve compression include pain, numbness, and tingling
(paresthesia) in the neck, shoulder, arm, and hand. The distribution of symptoms in the hand often
extends beyond that expected for either the median or ulnar nerves, involving all fingers. Patients
with NTOS attributable to compression at the pectoralis minor tendon often describe upper
anterior chest and axillary pain. The intensity of symptoms of NTOS can vary with the extent of
upper extremity activity and are usually reliably exacerbated with arm elevation and abduction.
■
Many NTOS patients experience relatively mild symptoms, with gradual progression in severity
punctuated by periodic exacerbations. Others experience steady, progressive worsening of
symptoms and related disability. Hand muscle weakness and atrophy (Gilliatt-Sumner hand) are
rare, typically following long-standing brachial plexus compression due to an associated cervical
rib or similar bony anomaly.
■
Physical examination typically identifies reproducible tenderness to palpation over the
supraclavicular scalene triangle and/or the infraclavicular subcoracoid space (FIG 2).
■
Most NTOS patients experience recurrent upper extremity symptoms in response to provocative
positional maneuvers, such as the upper limb tension test (ULTT) or the 3-minute elevated arm
stress test (EAST) (FIG 2). Positional dampening of the radial artery pulse at the wrist during arm
abduction and external rotation (Adson’s test) is nonspecific and inaccurate and is generally not
useful in establishing or excluding a diagnosis of NTOS.
■
Directed physical examination is performed to determine the presence of cervical spine
degenerative disease or peripheral nerve compression (carpal tunnel and cubital canal syndromes)
as potential alternative sources of NTOS-like symptoms as well as evidence of arterial or venous
compromise to the affected extremity. Signs of increased upper extremity sympathetic tone are also
sought, including digital swelling, discoloration, and skin hypersensitivity (allodynia).
■
Documentation of patient-reported symptoms and quantification of disability prior to treatment are
accomplished by completion of standardized outcomes measurement tools such as the Disabilities
of the Arm, Shoulder, and Hand (DASH) questionnaire and quality-of-life instruments.14 Repeated
use of these instruments at various intervals before and after treatment has provided increasing
insight into the relative value of alternative management strategies.15

■
Although imaging and other diagnostic studies may provide helpful ancillary information, there is no
definitive test to confirm or exclude the diagnosis of NTOS. Diagnosis remains quintessentially
clinical and dependent on experienced pattern recognition.
■
Plain anteroposterior chest radiographs will identify a cervical rib when present. No other currently
available imaging study adds significant value to the clinical diagnosis of NTOS (FIG 3).
■
Conventional electrophysiologic tests (electromyography and nerve conduction studies) are often
performed to exclude peripheral nerve compression disorders or cervical radiculopathy. These
tests are usually negative or nonspecific in NTOS and cannot be used to establish or exclude the
diagnosis.
■
Vascular laboratory studies (Duplex ultrasound) may detect alterations in upper extremity blood
flow attributable to subclavian artery compression during arm elevation. However, positional
subclavian artery compression may represent an incidental and unrelated vascular finding and
does not establish a diagnosis of neurogenic or arterial TOS. As they do not assess the presence or
severity of brachial plexopathy, vascular laboratory studies add little specificity beyond the
clinical diagnostic criteria.
■
Performance of image-guided anterior scalene and/or pectoralis minor muscle anesthetic blocks may
assist the clinical diagnosis of NTOS.16 A positive block, characterized as temporary relief or
improvement in the presenting symptoms, strongly supports the clinical diagnosis of NTOS. A
positive block may predict symptomatic relief from surgical decompression and is therefore highly
useful in selecting candidates for 1st rib resection. Unfortunately, however, failure of temporary
symptom resolution following muscle blockade does exclude the diagnosis of NTOS and should
not preclude consideration of surgical management in otherwise compelling clinical candidates.
■
Initial treatment for NTOS is based on physical therapy to relieve scalene/pectoralis minor muscle
spasm, improve posture, enhance functional limb mobility, strengthen associated shoulder girdle
musculature, and diminish repetitive strain exposure in the workplace. Incorrect approaches to
physical therapy can result in worsening of symptoms and failure of conservative management. In
many NTOS patients, significant symptomatic improvement may be experienced in response to
physical therapy, particularly in the first 4 to 6 weeks. Because NTOS is commonly chronic,
however, and subject to acute symptomatic “flare ups” (often related to overuse activities or new
injury), such patients should continue prescribed physical therapy exercises during long-term
follow-up. Patients that fail a conscientious and effective physical therapy, as well as alternative
conservative measures, are referred for consideration of surgical intervention.
SURGICAL MANAGEMENT
■
Supraclavicular decompression (scalenectomy, 1st rib resection, and brachial plexus neurolysis) is
recommended on the basis of (1) sound clinical diagnosis of NTOS, (2) substantial resulting
disability (interference with daily activities and/or work), and (3) an inadequate response to
standard physical therapy. Supraclavicular decompression may also provide relief from persistent
or recurrent NTOS symptoms following prior surgery, particularly when continued conservative
measures prove ineffective.
■
For patients with symptoms referable to the subcoracoid space, release of the pectoralis minor
tendon should be included in the supraclavicular thoracic outlet decompression procedure.
Pectoralis minor tenotomy may also be performed as a stand-alone procedure when nerve
compression symptoms are limited to this area.17,18
■
Decompression should be performed as a staged, sequential procedure in patients with bilateral
NTOS symptoms. The initial supraclavicular decompression, with or without pectoralis minor
tenotomy, is performed on most symptomatic or dominant extremity. If symptoms remain present or
progress, contralateral supraclavicular decompression may be performed within 6 to 12 weeks of
the initial procedure. Normal phrenic nerve function should be verified on the side of the previous
procedure, by chest fluoroscopic examination, before contralateral intervention.
■
The supraclavicular surgical site is marked in the preoperative holding area, including the
subcoracoid space when concomitant pectoralis minor tenotomy is planned. Prophylactic
antibiotics are administered within an hour of the planned procedure.
Positioning
■
After the induction of general endotracheal anesthesia, the patient is positioned supine with the head
of the operating table elevated 30 degrees. The neck is extended and turned to the opposite side; a
small inflatable pillow is placed behind the shoulders; and the neck, chest, and affected upper
extremity are prepped into the field. The arm is wrapped in stockinette to permit free range of
movement during the operation and then held comfortably across the abdomen (FIG 4). Lower
extremity sequential compression devices are used for thromboprophylaxis. Neuromuscular
blocking agents are not used following the initial induction of anesthesia.
TECHNIQUES
SUPRACLAVICULAR DECOMPRESSION
Incision and Mobilization of the Scalene Fat Pad
■
A transverse neck incision is made parallel to and just above the clavicle, beginning at the lateral
edge of the sternocleidomastoid muscle and extending to the anterior edge of the trapezius muscle.
The incision is carried through the subcutaneous layer, the platysma muscle is divided, and
subplatysmal flaps are developed to expose the scalene fat pad. The sternocleidomastoid muscle is
retracted medially but is not divided (FIG 5).
■
One of the keys to simplifying the supraclavicular exposure is proper mobilization and lateral
reflection of the scalene fat pad. This begins with detachment of the fat pad along the lateral edge
of the internal jugular vein and the superior edge of the clavicle, with ligation of small blood
vessels and lymphatic tissues. The thoracic duct, usually observed near the junction of the internal
jugular and subclavian veins on the left side (a prominent accessory thoracic duct may also exist
on the right side), may be ligated and divided. The omohyoid muscle is routinely divided (FIG 5).
■
The scalene fat pad is progressively elevated in a medial to lateral direction, by gentle fingertip
dissection over the surface of the anterior scalene muscle. The phrenic nerve is observed passing
in a lateral to medial direction as it descends along the muscle surface. Gentle manipulation of the
phrenic nerve produces a “dartle” (diaphragmatic startle) response.
■
Upon further lateral rotation of the scalene fat pad, the brachial plexus nerve roots (posterior and
lateral to the anterior scalene muscle) and the middle scalene muscle (behind the brachial plexus)
are brought into view. The lateral aspect of the 1st rib is palpated and visualized, and the long
thoracic nerve is identified as it emerges from the body of the middle scalene muscle to course
past the lateral part of the 1st rib. The scalene fat pad is then held in position with several silk
retraction sutures and the exposure is maintained with a Henley self-retaining retractor (using the
third arm to hold the edge of the sternocleidomastoid muscle). The resulting exposure represents
the first and most important of six “critical views” to be obtained during supraclavicular
decompression (Table 2) (FIG 6).
Anterior Scalenectomy
■
Attention is turned to the insertion of the anterior scalene muscle on the 1st rib. At the lower lateral
edge of the anterior scalene muscle, the subclavian artery and brachial plexus are carefully
mobilized until a fingertip can be easily passed behind the muscle just above the 1st rib, thereby
displacing the neurovascular structures posterolaterally. Blunt fingertip dissection is continued
behind the muscle to its medial edge, taking care to avoid the phrenic nerve. Once the insertion of
the anterior scalene muscle onto the 1st rib has been isolated under direct vision to protect the
phrenic nerve, the subclavian artery, and the brachial plexus, it is sharply divided from the top of
the bone with scissors (FIG 7).
■
The end of the divided anterior scalene muscle is elevated and its attachments to the underlying
extrapleural fascia are sharply divided (electrocautery is not used to avoid inadvertent nerve
injury). Muscle fibers extending from the posterior aspect of the muscle often pass around the
subclavian artery to form a tethering “sling” and should also be resected to fully release the artery.
Any scalene minimus muscle fibers found to be present (passing between the roots of the brachial
plexus) are divided as the anterior scalene muscle is mobilized. As the anterior scalene muscle is
lifted further, it is passed underneath and medial to the phrenic nerve and its posterior attachments
are divided with direct visualization and protection of the upper brachial plexus nerve roots.
Dissection of the muscle is carried superiorly to its origin on the C6 transverse process, which is
easily palpated in the upper aspect of the operative field (the apex of the “scalene triangle”). The
anterior scalene muscle is then divided with scissors from its origin on the transverse process
under direct vision and the entire muscle is removed, with a typical specimen weighing 5 to 10 g.
Any minor bleeding from the edge of the divided muscle origin is controlled with small
polypropylene sutures rather than electrocautery, given the proximity of the nerve roots (FIG 7).
■
Anomalous fibrofascial bands may be observed after anterior scalene muscle resection, typically
passing in front of the lower brachial plexus nerve roots. These structures are also resected as they
are encountered to ensure thorough decompression and full nerve root mobility.
Mobilization of the Brachial Plexus and Middle Scalenectomy
■
The brachial plexus nerve roots are next separated from the front edge of the middle scalene muscle.
Blunt fingertip dissection along the lateral aspect of the nerves is used to extend the exposure
deeper to the inner curve of the 1st rib and the extrapleural space, and a small malleable retractor
is placed between the brachial plexus nerves and the middle scalene muscle. With gentle medial
retraction of the brachial plexus, each nerve root from C5 to T1 is sequentially identified (FIG 8).
■
The transverse cervical artery and vein should be ligated and divided where they pass through the
brachial plexus and middle scalene muscle to avoid bleeding should these vessels be avulsed
during retraction.
■
A second malleable retractor is placed lateral to the middle scalene muscle and 1st rib, to displace
the long thoracic nerve posteriorly. The oblique attachment of the middle scalene muscle along the
top of the posterolateral 1st rib is exposed. This muscle insertion is carefully divided from the
surface of the bone with the electrocautery, using a periosteal elevator as the dissection proceeds
posteriorly, extending to a point on the 1st rib that is parallel with the underlying T1 nerve root.
The bulk of the middle scalene muscle anterior to the long thoracic nerve is then sharply excised,
with a typical specimen weight of 3 to 8 g (FIG 9). Minor bleeding from the cut edge of the middle
scalene muscle should be controlled with sutures rather than the electrocautery to avoid thermal
injury to the C8 nerve root or long thoracic nerve.
First Rib Resection

■
Once the scalenectomy has been completed, the intercostal muscle attaching to the lateral edge of the
1st rib is separated from the bone with the electrocautery. The 1st rib is fully exposed posteriorly,
where the T1 nerve root emerges from underneath the bone to join the C8 nerve root in forming the
lower trunk of the brachial plexus. A right-angle clamp is passed underneath the posterior neck of
the 1st rib and gently spread to detach additional intercostal tissues. A modified Stille-Giertz rib
cutter is inserted around the neck of the 1st rib. After verifying protection of the C8 and T1 nerve
roots, the bone is sharply divided. A Kerrison bone rongeur is used to smooth the posterior end of
the bone, to a level medial to the underlying T1 nerve root, and the end of the bone is sealed with
bone wax (FIG 9).
■
The free end of the divided posterior 1st rib is elevated, and blunt fingertip dissection is used to
separate the remaining extrapleural fascia and intercostal muscle attaching to the undersurface of
the rib, progressing anteriorly to the level of the scalene tubercle (the previous site of attachment
of the anterior scalene muscle). No effort is made to avoid opening the pleura during 1st rib
resection, as the opened pleural space will allow better drainage of postoperative fluids away
from the brachial plexus (which might otherwise promote perineural adhesions).
■
The soft tissues underneath the clavicle, including the subclavian vein, are elevated with a small
Richardson retractor. The posterior 1st rib is displaced inferiorly with fingertip pressure to open
the anterior costoclavicular space, and the subclavian artery and brachial plexus are displaced
laterally with a small malleable retractor. The Stille-Giertz rib cutter is placed around the anterior
1st rib, immediately medial to the scalene tubercle (FIG 10). The 1st rib is then divided under
direct vision, and the intact specimen is extracted from the operative field (FIG 11). The
remaining anterior end of the 1st rib is remodeled to a smooth surface with a bone rongeur, to a
level well underneath the clavicle. Oxidized cellulose fabric (Ethicon, Inc., Somerville, NJ) is
placed within the bed of the resected 1st rib as a topical hemostatic agent.
■
Cervical ribs arise within the plane of the middle scalene muscle, posterior to the brachial plexus
and subclavian artery and anterior to the long thoracic nerve. Incomplete cervical ribs typically
have a ligamentous extension to the 1st rib, whereas complete cervical ribs attach to the lateral 1st
rib in the form of a true joint. The posterior portion of a cervical rib is thereby readily encountered
during dissection of the middle scalene muscle and is divided in a manner similar to the posterior
1st rib. The anterior attachment of the cervical rib is then divided and the bone is removed prior to
1st rib resection. When there is a true joint between a complete cervical rib and the 1st rib, the
anterior portion of the cervical rib is left attached while the 1st rib resection is completed, and the
two are removed together as a single specimen (FIG 11).
Brachial Plexus Neurolysis
■
The last step of supraclavicular decompression is to fully mobilize each of the individual nerve
roots contributing to the brachial plexus. Each nerve root from C5 to T1 is meticulously dissected
free of any adherent perineural fibrous scar tissue that might impair mobility (external neurolysis).
Inspection of the most proximal aspect of the C8 and T1 nerve roots will often reveal a small
fibrofascial band overlying these nerves, which should be specifically sought out and resected.
This aspect of the operation is not considered complete until each nerve root has been completely
cleared throughout its course in the operative field (FIG 12).
Drain Placement and Closure
■
Upon the completion of supraclavicular decompression, the apex of the pleural membrane is opened
to promote postoperative drainage of fluid into the chest cavity, away from the brachial plexus. 19-
Fr closed suction drain is placed through a separate stab wound into the operative field, placed
posterior to the brachial plexus with its tip extending into the posterior pleural space. Two
multihole perfusion catheters are placed within the wound, positioned adjacent to the brachial
plexus and within the bed of the resected 1st rib, and connected to an osmotic pump for continuous
postoperative infusion of local anesthetic (0.5% bupivacaine for 3 days). A bioresorbable
polylactide film (Ethicon, Inc., Somerville, NJ) is placed around the brachial plexus to suppress
development of postoperative perineural fibrosis and held in place with several 5–0
polydioxanone sutures. The scalene fat pad is restored to its anatomic position overlying the
brachial plexus and held in place with several tacking sutures to the back of the
sternocleidomastoid muscle and to the periclavicular subcutaneous fascia. The platysma muscle
layer is reapproximated with interrupted sutures and the skin is closed with an absorbable
subcuticular stitch.
PECTORALIS MINOR TENOTOMY
Incision and Exposure
■
A short vertical incision is made in the deltopectoral groove, beginning at the level of the coracoid
process. The deltoid and pectoralis major muscles are gently separated and the plane of deeper
dissection is carried medial to the cephalic vein. The lateral edge of the pectoralis major muscle is
gently lifted with a small Deaver retractor, and the plane underneath the muscle is separated from
the underlying fascia by blunt fingertip dissection. The fascia over the pectoralis minor muscle is
exposed, where the muscle can be easily identified by palpation (FIG 13).
Division of the Pectoralis Minor Muscle Tendon

■
The pectoralis minor muscle tendon is identified where it extends from the anterior chest wall to the
coracoid process. The fascia along its medial border is opened and the muscle is encircled using
blunt fingertip dissection. The fascia along the lateral border of the pectoralis minor muscle is
opened to ensure its separation from the short head of the biceps muscle, which also inserts on the
coracoid process. Taking care to protect the underlying neurovascular bundle, the pectoralis minor
tendon is then elevated with umbilical tape or rubber tubing and its insertion on the coracoid
process is exposed with a small Richardson retractor. A finger is placed behind the muscle to
prevent thermal injury to the neurovascular structures and the insertion of the pectoralis minor
tendon is divided with the electrocautery. After the pectoralis minor muscle has been divided, the
lower edge will retract inferiorly to release any compression of the neurovascular bundle (FIG
14).
■
The inferior edge of the divided pectoralis minor muscle is oversewn with a running suture to ensure
hemostasis and to facilitate contraction of the muscle underneath the pectoralis major muscle. The
remaining clavipectoral fascia is also incised to the level of the clavicle, along with any other
anomalous fascial bands that might be present over the brachial plexus, such as Langer’s axillary
arch, but no further dissection of the brachial plexus nerves or the axillary vessels is performed.
The edge of the pectoralis major muscle is infiltrated with a long-acting local anesthetic and the
wound is irrigated, then closed in layers without a drain.
PEARLS AND PITFALLS

Indications ■ Operative treatment of NTOS should be based on a sound clinical
diagnosis, a substantial level of disability, and failure of
symptoms to improve with an adequate trial of conservative
management.
■ Imaging studies, electrophysiologic tests, and vascular laboratory
examinations add little in the evaluation of NTOS but may be
useful in excluding other conditions.
■ A positive anterior scalene muscle block supports the diagnosis of
NTOS and indicates a strong likelihood of responsiveness to
surgical treatment.
■ Assess the potential contribution of brachial plexus compression
at the level of the subcoracoid space and include pectoralis minor
tenotomy if present.
Mobilization of the scalene ■ Avoid division of the sternocleidomastoid muscle.
fat pad ■ Proper mobilization and lateral reflection of the scalene fat pad is
a key step in simplifying supraclavicular exposure for thoracic
outlet decompression. This permits the critical view to be
obtained in which all of the relevant structures can be visualized
in the same operative field (internal jugular vein, phrenic nerve,
anterior scalene muscle, brachial plexus, middle scalene muscle,
1st rib, and long thoracic nerve).
■ Ligate and divide the thoracic duct, if necessary, to prevent
postoperative lymph leak.
■ Visualize and protect the phrenic nerve.
Anterior scalenectomy ■ Divide all fibers passing from the posterior aspect of the anterior
scalene muscle to the subclavian artery and extrapleural fascia.
■ Divide any scalene minimus muscle encountered.
■ Pass the anterior scalene muscle underneath the phrenic nerve to
facilitate dissection of the muscle up to its superior origin on the
C6 transverse process.
Mobilization of the brachial ■ Visualize all five nerve roots of the brachial plexus.
plexus ■ Ligate and divide the transverse cervical vessels where they pass
through the brachial plexus and middle scalene muscle.
Middle scalenectomy ■ Visualize and protect the long thoracic nerve.
■ Control minor bleeding from the cut edge of the muscle with silk
sutures rather than electrocautery.
1st rib resection ■ Visualize the T1 and C8 nerve roots at the level of the posterior
1st rib, prior to division of the bone, to avoid nerve injury.
■ Remove a small segment of the divided posterior 1st rib to
facilitate fingertip dissection underneath the remaining lateral and
anterior portions of the bone.
■ Do not try to avoid opening the pleura.
■ Divide the anterior 1st rib at a level medial to the scalene
tubercle, underneath the clavicle and subclavian vein, while
protecting the subclavian artery and brachial plexus.
■ Resect any cervical rib present along with the 1st rib.
Brachial plexus neurolysis ■ Thoroughly remove fibrous scar tissues from around each nerve
root (C5 to T1) of the brachial plexus to avoid one of the causes of
persistent symptoms.
■ Resect any small fibrofascial bands overlying the proximal aspect
of the C8 and T1 nerve roots.
Drain placement and closure ■ Wrap the brachial plexus with a bioresorbable film to minimize
perineural fibrosis.
■ Place a closed suction drain behind the brachial plexus with its tip
extending into the pleural space.
■ Use continuous postoperative infusion of a local anesthetic to
diminish the need for opiate pain medications.
Pectoralis minor tenotomy ■ Include pectoralis minor tenotomy as part of the supraclavicular
decompression if there are concomitant symptoms of NTOS
referable to the subcoracoid space.
■ Divide the pectoralis minor tendon close to its insertion on the
coracoid process.
■ Oversew the divided edge of the pectoralis minor muscle for
hemostasis.
■ It is not necessary to place a separate drain in the subcoracoid
space.
POSTOPERATIVE CARE
■
An upright chest radiograph is performed in the recovery room and each morning for 3 days, and any
small air or pleural fluid collections are observed with the expectation of spontaneous resolution.
Postoperative analgesia is provided by continuous-infusion perineural local anesthesia
(discontinued on postoperative day 3) and patient-controlled intravenous opiates until adequate
pain control is achieved by oral medications alone. Oral narcotics, a muscle relaxant, and a
nonsteroidal antiinflammatory agent are routinely prescribed at hospital discharge and for at least
several weeks following surgery. Postoperative hospital stay is typically 3 to 4 days. The closed
suction drain is removed in the outpatient office when its output is less than 50 mL per day, usually
5 to 7 days after surgery.
■
Physical therapy is resumed the day after surgery to maintain range of motion and limit muscle
spasm. The patient is allowed to use the extremity as tolerated, with no use of a sling or other
restraint. Physical therapy is continued after hospital discharge, with advice to avoid excessive
reaching overhead or heavy lifting with the affected upper extremity and other activities that might
result in muscle strain, spasm, and significant pain in the sternocleidomastoid, trapezius, and other
neck muscles. Further rehabilitation is overseen by a physical therapist with expertise in the
management of NTOS, usually in conjunction with a physical therapist located near the patient,
emphasizing a gradual steady return to normal use of the upper extremity.
■
The majority of patients are permitted cautious light duty work activities by 4 to 6 weeks.
Restrictions on upper extremity activity are progressively lifted between 6 and 12 weeks, when
recovery from surgery is typically considered complete. Patients are seen in follow-up every 3
months in the first year to assess long-term results. Physical therapy and other aspects of care are
continued as long as necessary to achieve an optimal level of function.
OUTCOMES
■
In properly selected patients with disabling NTOS, approximately 80% to 85% can expect a
substantial improvement in symptoms and increased functional use of the upper extremity within
several months of supraclavicular decompression.1–3,19 This estimate is elevated to approximately
90% to 95% in those who exhibited a positive anterior scalene/pectoralis minor muscle block
prior to treatment. Factors that tend to diminish responsiveness to treatment include extremely
long-standing (>5 years) and debilitating symptoms, widespread pain syndromes, multiple
previous operations (cervical spine, shoulder, or peripheral nerves), depression, older age (>50
years), and preexisting use of opiate pain medications.
■
Patients with long-standing NTOS can often display residual symptoms that may not be completely
eliminated by thoracic outlet decompression. Although these symptoms may be tolerable and are
expected to gradually improve, the surgeon must provide continuing support and reassurance
during the prolonged period of recovery and rehabilitation.
■
Patients in the adolescent age-group (<21 years) tend to have even better outcomes than adults,
based on assessment of patient-reported survey instruments and postoperative use of opiate pain
medications.14 Patients that have been selected for isolated pectoralis minor tenotomy can exhibit
early outcomes similar to those of patients that have undergone combined supraclavicular
decompression and pectoralis minor tenotomy but require ongoing follow-up for recurrent
symptoms to determine if supraclavicular decompression may be warranted at a later time.17,18
■
Recurrent symptoms of NTOS that might warrant reoperation occur in 1% to 2% of patients, usually
within the first 2 years of treatment. Reoperations for NTOS are generally performed using the
supraclavicular approach, because this provides the most complete exposure of the anatomy with
the greatest margin of safety.20 Following lateral reflection of the scalene fat pad, the brachial
plexus nerve roots are carefully exposed and mobilized. Great care must be taken during this
dissection to avoid nerve and blood vessel injury, given the dense fibrous scar tissue that is
usually present within the operative field. Any structures that were retained at the initial operation
are then resected, including the scalene muscles, anomalous fibrofascial bands, and/or the 1st rib.
A complete brachial plexus neurolysis is performed and the nerves are protected with a
bioabsorbable film and soft tissue coverage with the scalene fat pad.
COMPLICATIONS
■
Persistent pain, numbness, and/or paresthesias
■
Postoperative bleeding, localized hematoma, or hemothorax
■
Wound infection (cellulitis or abscess)
■
Pleural effusion (serosanguineous)
■
Persistent lymph leak, chylothorax
■
Brachial plexus nerve dysfunction (temporary or sustained)
■
Phrenic nerve dysfunction (temporary or sustained)
■
Long thoracic nerve dysfunction (temporary or sustained)
■
Recurrent NTOS
REFERENCES
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2. Molina JE. New Techniques for Thoracic Outlet Syndromes. New York, NY: Springer; 2012.
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Rutherford’s Vascular Surgery. 7th ed. Philadelphia, PA: Elsevier; 2010:1878–1898.
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Vasc Surg. 2002;36(1):51–56.
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Pearce WH, et al, eds. Vascular Surgery: Therapeutic Strategies. Shelton, CT: People’s Medical Publishing House; 2010:129–
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14. Caputo FJ, Wittenberg AM, Vemuri C, et al. Supraclavicular decompression for neurogenic thoracic outlet syndrome in adolescent
and adult populations. J Vasc Surg. 2013;57(1):149–157.
15. Povlsen B, Belzberg A, Hansson T, et al. Treatment for thoracic outlet syndrome. Cochrane Database Syst Rev. 2010;
(1):CD007218.
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Vasc Surg. 1998;12(3):260–264.
17. Sanders RJ, Rao NM. The forgotten pectoralis minor syndrome: 100 operations for pectoralis minor syndrome alone or
accompanied by neurogenic thoracic outlet syndrome. Ann Vasc Surg. 2010;24:701–708.
18. Vemuri C, Wittenberg AM, Caputo FJ, et al. Early effectiveness of isolated pectoralis minor tenotomy in selected patients with
neurogenic thoracic outlet syndrome. J Vasc Surg. 2013;57(5):1345–1352.
19. Hempel GK, Shutze WP, Anderson JF, et al. 770 consecutive supraclavicular first rib resections for thoracic outlet syndrome. Ann
Vasc Surg. 1996;10(5):456–463.
20. Ambrad-Chalela E, Thomas GI, Johansen KH. Recurrent neurogenic thoracic outlet syndrome. Am J Surg. 2004;187(4):505–510.
Neurogenic Thoracic Outlet Syndrome Exposure and
Chapter 8 Decompression: Transaxillary
George J. Arnaoutakis Thomas Reifsnyder Julie

Ann Freischlag
DEFINITION
■
In 1821, Sir Astley Cooper recognized the constellation of neurovascular symptoms involving the
thoracic outlet. Ochsner called this the scalenus anticus syndrome in 1936 and described the
presence of muscle abnormalities secondary to repetitive trauma. Peet assigned this condition its
contemporaneous moniker thoracic outlet syndrome (TOS) in 1966.1
■
TOS is a condition defined as compression of one or more of the neurovascular structures contained
within the thoracic outlet.
■
The thoracic outlet is a narrowly defined anatomic region encompassing the space between the neck
and the shoulder, cephalad to the thoracic cavity, and beneath the clavicle. From the surgeon’s
point of view the thoracic outlet can be visualized as an anatomic triangle: the two sides being the
anterior and middle scalene muscles with the 1st rib serving as the base of the triangle. The
scalene muscles, which originate from the lower cervical spine, may hypertrophy with repetitive
neck motion or minor trauma. This hypertrophy is believed to contribute to compression of
thoracic outlet structures.
■
TOS is subdivided into three discrete entities.
■
Neurogenic
■
Venous
■
Arterial
■
Appropriate classification of the type of TOS is important in guiding perioperative management, as
well as surgical approach. This chapter focuses on transaxillary decompression and 1st rib
resection for neurogenic TOS.
■
Carpal tunnel syndrome
■
Ulnar nerve compression
■
Rotator cuff tendinitis
■
Pectoralis minor syndrome
■
Cervical spine strain
■
Cervical disc disease
■
Cervical arthritis
■
Brachial plexus injury
■
Fibromyositis

■
A careful history and physical examination enables proper classification of TOS.
■
The neurogenic form accounts for the majority of cases in modern series (>95%).2 Symptoms of
neurogenic TOS, which is more prevalent in women, include paresthesia; pain; and impaired
strength in the affected shoulder, arm, or hand along with occipital headaches and neck discomfort.
There is commonly an antecedent history of hyperextension neck injury or repetitive neck trauma.
Patients frequently manifest tenderness on palpation in the supraclavicular fossa over the anterior
scalene muscle. A careful vascular physical examination should confirm the presence of normal
circulation.
■
Three physical examination maneuvers support the diagnosis of neurogenic TOS.
■
Rotation of the neck and tilting of the head to the opposite side elicit pain in the affected arm.
■
The upper limb tension test in which the patient first abducts both arms to 90 degrees with the
elbows in a locked position, then dorsiflexes the wrists, and finally, tilts the head to the side.
Each subsequent step imparts greater traction on the brachial plexus, with the first two
positions causing discomfort on the ipsilateral side and the head-tilt position causing pain on
the contralateral side.
■
During the elevated arm stress test (EAST), the patient raises both arms directly above the
head and repeatedly opens and closes the fists. Characteristic upper extremity symptoms
arise within 60 seconds in patients with neurogenic TOS.
■
Approximately 4% of patients with TOS present with venous involvement. Venous TOS patients
typically present with acute onset of dull aching pain of the upper extremity associated with arm
edema and cyanosis. Paresthesias may be present but are due to hand swelling instead of thoracic
outlet nerve involvement. A history of strenuous and repetitive work or athletics involving the
affected extremity is common, and most patients are young. This specific condition is also known
as Paget-Schroetter syndrome or effort vein thrombosis, as the entrapped subclavian vein has
progressed to thrombosis. Some patients will present less acutely with nonthrombotic subclavian
vein occlusion or stenosis manifested by intermittent swelling with activity. Regardless, the
etiology of venous TOS is mechanical, and treatment is ultimately aimed at eliminating not only the
venous obstruction but also the muscular bands and ligaments that have entrapped and damaged the
vein.
■
Arterial TOS typically presents in one of three ways: (1) asymptomatic, (2) arm claudication, and
(3) critical ischemia of the hand. The majority of these patients have a cervical rib, which may or
may not be fused to the 1st rib and is most commonly posterior to the subclavian artery. The
etiology is chronic repetitive injury to the subclavian artery as it exits the thoracic outlet. This
injury may cause subclavian artery stenosis but more commonly leads to ectasia or a true
aneurysm.
■
In asymptomatic patients, a pulsatile mass or supraclavicular bruit can be detected on physical
examination.
■
Arm claudication is caused by areas of stenosis which may be static due to long-standing
repetitive injury or dynamic, occurring only with arm abduction or extension.
■
Critical ischemia is due to emboli of fibrinoplatelet aggregates that originate from an ulcerated
mural thrombus in the aneurysmal segment.
PREOPERATIVE EVALUATION AND OTHER DIAGNOSTIC STUDIES

■
In young patients (<40 years of age) with a classic presentation of neurogenic TOS, there is no need
for extensive preoperative testing.
■
Older patients and those with a history of neck trauma should undergo magnetic resonance imaging
(MRI) to rule out cervical disc pathology.
■
Preoperative physical therapy should be attempted for at least 8 weeks in patients with a diagnosis
of neurogenic TOS. The aims of therapy are to improve posture and achieve greater range of
motion. Patients with persistent symptoms of neurogenic TOS despite 8 weeks of physical therapy
merit surgical intervention. At least 60% of patients will improve with physical therapy and
lifestyle alterations.
■
A radiographically guided anterior scalene block with local anesthetic (lidocaine) injection may
provide a few hours of symptomatic relief. Patients with suspected neurogenic TOS often present
with a wide constellation of physical complaints, not all of which are directly attributable to the
disorder. A scalene block not only helps confirm the diagnosis but also simulates the expected
postoperative result, especially in older patients.3 This provides the patient and the surgeon
reassurance that surgical intervention will be of benefit and demonstrates which symptoms can be
reliably expected to improve.
■
As an alternative to surgical therapy, patients can then opt for a Botox (Allergan, Irvine, CA)
injection. The Botox takes an average of 2 weeks to work and may be repeated. This may provide
symptomatic relief for 2 to 3 months, allowing participation in physical therapy. However, not all
TOS patients respond to Botox. This practice is especially helpful in patients who have had
cervical spine fusions or shoulder operations as they can strengthen the muscles of their neck and
back, which may alleviate the TOS symptoms.
■
Plain film chest x-ray is recommended for all patients undergoing surgical intervention for TOS to
rule out a cervical rib.
■
Nerve conduction studies are typically normal in neurogenic TOS but may be useful in ruling out
nerve compression such as carpal tunnel or cubital compression syndrome.
■
Duplex ultrasonography is the initial diagnostic modality to confirm pathology in patients with
arterial TOS. Although useful to confirm axillosubclavian vein thrombosis in patients with
suspected venous TOS, venography often supplants it for both diagnostic and therapeutic reasons.
Lastly, venous TOS is frequently bilateral.
SURGICAL MANAGEMENT
Surgical Approach
■
Patients with a diagnosis of TOS who are appropriate surgical candidates should undergo surgical
decompression of the thoracic outlet.
■
The optimal approach should be individualized depending on the patient’s symptoms, anatomy, and
surgeon’s experience.
■
The transaxillary approach is preferred by many surgeons because of its relative ease, low-risk
profile, and documented improvement in patients’ quality of life.4,5 This approach effectively
decompresses the thoracic outlet and is generally reserved for patients with neurogenic or venous
TOS.
■
If vessel reconstruction is anticipated, a different approach should be considered as the transaxillary
approach limits vessel exposure.
Surgical Anatomy
■
The subclavian artery and the five nerve roots (C5–T1) to the brachial plexus are located within the
thoracic outlet. The artery courses anterior to the brachial plexus nerve roots and exits the
mediastinum in its course over the 1st rib behind the posterior border of the anterior scalene
muscle. The cervical spine nerve roots join to form the initial trunks of the brachial plexus within
the thoracic outlet and are located posterior to the subclavian artery. Subsequent merging and
branching of these trunks into divisions, cords, and terminal nerves occurs outside the thoracic
outlet.
■
Other significant nerves within the thoracic outlet are the phrenic and long thoracic nerves.
■
The phrenic nerve receives fibers from C3–C5 and courses in a descending oblique direction
from the lateral to the medial edge of the middle portion of the anterior scalene muscle. The
phrenic nerve approaches the mediastinum posterior to the subclavian vein.
■
The long thoracic nerve, composed of nerve fibers from C5–C7, passes through the center of the
middle scalene muscle and heads toward the chest wall to innervate the serratus anterior
muscle.
■
The subclavian vein technically does not course through the thoracic outlet. It passes over the 1st rib
anterior to the anterior scalene muscle. However, the middle segment of the vein remains
susceptible to compression between the anteromedial 1st rib, clavicle, and the subclavius muscle
(FIG 1). Hypertrophy of the subclavius muscle and tendon may occur in athletes and is often
implicated in venous TOS.
■
Several anatomic anomalies are relevant to the surgeon, as they predispose patients to the
development of TOS.
■
The most common is a cervical rib, and a preoperative chest radiograph is adequate for its
detection. When present, cervical ribs appear as extensions of the transverse process of C7.
Cervical ribs may be complete or partial, with the anterior end attaching to the 1st rib or
floating freely. Additionally, the anterior end may be fibrous and not calcified and thus not
completely visualized on chest radiograph. By rigidly confining the thoracic outlet, cervical ribs
render the neurovascular structures more prone to compression. Although present in the general
population with an incidence of 0.5% to 1%, they are found in 5% to 10% of all TOS patients.
■
A prominent C7 transverse process or bifid 1st rib is also associated with TOS.
Positioning
■
General endotracheal anesthesia is induced and sequential compression devices are applied.
■
The patient is then moved to the lateral decubitus position using a beanbag to facilitate positioning.
■
Care should be taken to pad the dependent axilla and support the head. The sterile field
incorporates the arm, axilla, and shoulder.
■
An adjustable Machleder arm support is affixed to the operating table with the vertical support bar
attached to the operating table at the level of the patient’s chin.
■
Generous padding around the patient’s arm prior to placement in the arm holder protects the
median and ulnar nerves from compression as they cross the elbow joint (FIG 2).
TECHNIQUES
INCISION
■
Prophylactic antibiotics are administered. A first-generation cephalosporin is preferred. In patients
with penicillin allergy, clindamycin or vancomycin is used.
■
After securing the arm in the retractor, the surgeon identifies the anterior border of the latissimus
dorsi muscle and the posterior surface of the pectoralis major muscle.
■
A transverse skin line incision should be made in the inferior axillary hairline extending between
these two muscle borders.
EXPOSURE
■
Electrocautery is used to divide the subcutaneous tissue until thin areolar tissue superficial to the
chest wall is encountered. A self-retaining Cerebellar or Weitlaner retractor is then inserted into
the wound. Upon encountering the chest wall—and if in the correct anatomic plane—gentle blunt
dissection with the surgeon’s fingers or a pair of Kittner or peanut dissectors easily separates the
soft tissues from the chest wall. This dissection is in a cephalad direction and the 2nd rib will
rapidly come into view.
■
The intercostobrachial nerve is located in the 2nd intercostal space. Although frequently difficult to
avoid, care should be taken not to impart excess traction as injury results in numbness or
dysesthesia of the medial aspect of the proximal arm.
■
Raising the Machleder arm support at this point allows for optimal access to the 1st rib and thoracic
outlet. The aid of fiberoptic-lighted Deaver retractors facilitates visualization during this portion
of the dissection. Alternatively, the surgeon should wear a headlight.
■
The 1st rib is identified near its insertion at the sternoclavicular joint and generally encountered
higher than anticipated. A Kittner or peanut dissector is then used to gently sweep away the loose
fibrous tissue overlying the 1st rib partially exposing the brachial plexus, subclavian artery and
vein, and scalene muscles. There is occasionally a small branch of the subclavian artery that must
be ligated and divided in order to fully expose the operative field.
■
The next step is to fully expose the rib. Depending on the patient’s anatomy, it generally is easiest to
first clear off the intercostal muscles laterally. A Cobb periosteal elevator works best, but any type
of long elevator may be used (FIG 3). The dissection proceeds in the anterior and posterior
directions until all the intercostal muscle attachments are divided from the rib. The elevator can
then be used to elevate the 1st rib, thus separating the rib from the underlying parietal pleura. This
mobilization should continue from behind the brachial plexus in the posterior direction to beyond
the subclavian vein in the anterior direction.
■
Attention is then directed to the superior border of the 1st rib, where the periosteal elevator is used
to bluntly detach the scalene medius fibers from the rib. The long thoracic nerve courses along the
lateral edge of the scalene medius muscle but is generally not visualized. Avoiding sharp
dissection and closely adhering to the surface of the rib during blunt dissection prevents injury to
the long thoracic nerve.
■
The anterior scalene muscle should now be clearly identified as it arises from the medial superior
aspect of the 1st rib (FIG 4). A right-angled clamp is passed behind the anterior scalene muscle
near its insertion on the scalene tubercle. Gently lifting the anterior scalene with the right-angled
clamp protects the subclavian artery as it courses posterior to the muscle (FIG 5). It is important to
free several centimeters of the muscle prior to dividing it with Metzenbaum scissors (FIG 6). This
maneuver facilitates resection of a portion of the anterior scalene muscle, which has been shown to
reduce recurrence rates when compared with division at its insertion point on the rib.
■
Lastly, the subclavius muscle will appear as a crescent-shaped ligamentous attachment to the 1st rib
adjacent to the subclavian vein. With care not to injure the subclavian vein, the subclavius muscle
is sharply divided with scissors.
RIB RESECTION
■
With the rib completely mobilized, a bone cutter is used to divide the 1st rib. Generally, it is
divided anteriorly and then posteriorly; however, the patient’s body habitus may make the reverse
order easier (FIG 7).
■
In its anterior extent, the rib is divided adjacent to the subclavian vein, and in the posterior
direction, it is divided just anterior to the brachial plexus; this ensures that the nerve roots are not
inadvertently injured. The rib is then removed.
■
A bone rongeur is used to remove residual rib and to smooth the cut ends until there is no residual
nerve impingement. A Roos retractor or similar instrument may be used to protect the nerves
during use of the rongeur (FIG 8).
■
It is important to ensure that no residual fibers from the anterior scalene muscle crosses beneath the
subclavian artery and inserts onto the thickened surface at the apex of the pleura, known as
Sibson’s fascia. Any such fibers should be identified and divided.
CLOSURE
■
The surgical field is next inspected for bleeding. Temporarily packing the wound reliably controls
minor bleeding. The wound is then reinspected, and hemostasis is completed with judicious use of
electrocautery.
■
The wound is then filled with saline. Several positive pressure ventilations are administered with
saline left in the wound to assess for an air leak indicative of a postoperative pneumothorax. If an
air leak is present, a small caliber (12 French [Fr]) chest tube is warranted prior to closure.
■
If the irrigation drains into the pleural space but there is no air leak, the pleura has been breached,
but a chest tube may not be necessary. In this situation, a 12- or 14-Fr red rubber catheter is placed
into the bed of the 1st rib and attached to gentle suction. The Machleder arm holder is lowered to
facilitate a tension-free closure. The subcutaneous fascia is then closed around the tube. While
suction is applied to the red rubber catheter, the anesthesia team provides a sustained Valsalva and
the fascial suture is tied as the suction tube is rapidly removed. This maneuver generally avoids a
clinically significant postoperative pneumothorax.
■
Closure is performed with absorbable 2-0 suture in the fascia and a 4-0 subcuticular skin closure.
PEARLS AND PITFALLS

Operative mantra ■ Look twice and cut once. Always double-check placement of the
bone cutters before dividing the 1st rib.
Incorrect diagnosis ■ A successful operation hinges on an accurate preoperative
diagnosis. A thorough history and physical and the anterior
scalene block help to identify patients likely to benefit from 1st rib
resection.
Brachial plexus injury ■ Proper positioning and careful retraction help prevent excessive
traction and injury to the brachial plexus.
Misidentification of the 1st ■ During initial exposure, the 2nd rib is often mistaken for the 1st
rib rib. The cephalad surface of the 1st rib is flat unlike the 2nd,
which is more concave.
Incomplete 1st rib resection ■ Incomplete 1st rib resection has been associated with recurrent
TOS. After cutting and removing the rib, take your time to trim
back the ends with the rongeur.
Hemostasis ■ To keep a clean operative field, pack a 4 × 4 gauze into the
wound, lower the arm retractor, and wait a couple of minutes.
This often aids in hemostasis.
POSTOPERATIVE CARE
■
A chest x-ray is performed in the recovery room.
■
Small, clinically asymptomatic pneumothoraces may be observed with a follow-up chest x-ray
the next morning.
■
Patients are typically discharged from the hospital when adequate oral analgesia has been achieved.
■
Activity is restricted by the amount of postoperative pain. Occasionally, a sling is required for
patient comfort, but it is preferable to have the arm as mobile as tolerated.
■
Physical therapy should be prescribed after 2 weeks in all patients undergoing transaxillary 1st rib
resection, regardless of the cause, to restore range of motion and strength.
OUTCOMES
■
Improvement after surgery for neurogenic TOS is somewhat subjective and based on the patient’s
perception of disability before and after decompression. Improvement in symptoms exceeds 90%.6
■
Over time, the durability of these results may decrease, reinforcing the need for close follow-up of
these patients beyond 2 years.7,8
■
Factors that predict surgical failure include major depression, chronic symptoms, work-related
injury, lack of response to anterior scalene muscle blocks, and a short segment of divided anterior
scalene muscle.9
COMPLICATIONS
■
Vascular injury
■
A national query identified injury to the subclavian vessels as the most common complication
following transaxillary rib resection for neurogenic TOS, occurring in 1% to 2% of cases.4
■
Patients experiencing a vascular injury have greater lengths of stay as well as increased hospital
charges.
■
It is difficult to obtain proximal control of these vessels from the transaxillary approach, and
therefore, the surgeon should exercise extreme caution when dissecting near these vessels.
■
Nerve injury
■
Major nerve injury has been traditionally regarded as the most common complication following
surgery for TOS. However, large contemporary series disprove this belief, with rates of
brachial plexus injury for patients undergoing transaxillary 1st rib resection approaching 0%.4,8
■
Temporary or permanent numbness of the upper medial arm due to excessive traction or division
of the intercostobrachial nerve occurs in up to 10%. Frequently, these symptoms will improve
over time.
■
Pneumothorax
■
This complication occurs in 2% to 10% of patients.8 Accordingly, an upright chest x-ray is
routinely performed in the recovery room.
■
Radiographically detected pneumothoraces only require a chest tube if symptomatic or enlarging.
■
Adhering closely to the inferior surface of the 1st rib during blunt dissection will help protect
against postoperative pneumothorax.
■
Recurrence
■
Symptoms of TOS recur in 10% to 20% of patients.10–12
■
Two intraoperative factors are known to reduce recurrence rates.
■
Resecting a significant portion (2 to 3 cm) of the anterior scalene muscle as opposed to simply
dividing it at its insertion point
■
Ensuring that the posterior edge of the 1st rib is resected sufficiently so as to leave as short a
rib stump as technically feasible
■
Patients with spontaneous recurrence compared to those that are reinjured have worse outcomes
when reoperation is performed.
REFERENCES
1. Roos DB. Transaxillary approach for first rib resection to relieve thoracic outlet syndrome. Ann Surg. 1966;163:354–358.
2. Sanders RJ, Hammond SL, Rao NM. Diagnosis of thoracic outlet syndrome. J Vasc Surg. 2007;46:601–604.
3. Lum YW, Brooke BS, Likes K, et al. Impact of anterior scalene lidocaine blocks on predicting surgical success in older patients
with neurogenic thoracic outlet syndrome. J Vasc Surg. 2012;55:1370–1375.
4. Chang DC, Lidor AO, Matsen SL, et al. Reported in-hospital complications following rib resections for neurogenic thoracic outlet
syndrome. Ann Vasc Surg. 2007;21:564–570.
5. Chang DC, Rotellini-Coltvet LA, Mukherjee D, et al. Surgical intervention for thoracic outlet syndrome improves patient’s quality of
life. J Vasc Surg. 2009;49:630–635; discussion 635–637.
6. Roos DB. The place for scalenectomy and first-rib resection in thoracic outlet syndrome. Surgery. 1982;92:1077–1085.
7. Rochlin DH, Gilson MM, Likes KC, et al. Quality-of-life scores in neurogenic thoracic outlet syndrome patients undergoing first rib
resection and scalenectomy. J Vasc Surg. 2013;57:436–443.
8. Altobelli GG, Kudo T, Haas BT, et al. Thoracic outlet syndrome: pattern of clinical success after operative decompression. J Vasc
Surg. 2005;42:122–128.
9. Axelrod DA, Proctor MC, Geisser ME, et al. Outcomes after surgery for thoracic outlet syndrome. J Vasc Surg. 2001;33:1220–
1225.
10. Mingoli A, Feldhaus RJ, Farina C, et al. Long-term outcome after transaxillary approach for thoracic outlet syndrome. Surgery.
1995;118:840–844.
11. Mingoli A, Sapienza P, di Marzo L, et al. Role of first rib stump length in recurrent neurogenic thoracic outlet syndrome. Am J Surg.
2005;190:156.
12. Sanders RJ, Haug CE, Pearce WH. Recurrent thoracic outlet syndrome. J Vasc Surg. 1990;12:390–398; discussion 398–400.
Chapter 9 Venous and Arterial Thoracic Outlet Syndrome
Jason T. Lee
DEFINITION
■
Venous thoracic outlet syndrome (vTOS), also known as effort thrombosis or Paget-von Schrotter
syndrome, involves repetitive subclavian venous compression that leads to endothelial injury and
intermittent stasis that ultimately contributes to acute thrombosis of the axillosubclavian venous
system. The external compression of the vein occurs between the clavicle and subclavius muscle
from above and by the 1st rib and the anterior scalene muscle insertion from below (FIG 1).
■
Arterial thoracic outlet syndrome (aTOS) is the least common presentation of thoracic outlet
syndrome and most often involves subclavian artery compression leading to extrinsic
compression, poststenotic dilatation, aneurysmal degeneration, and subsequent distal
embolization.1 Bony and muscular abnormalities are typically present in patients with aTOS and
can include a cervical rib, anomalous 1st rib, anterior or middle scalene muscle bands, or
hypertrophic callus from a healed clavicular injury or fracture (FIG 2).
■
Compared to neurogenic thoracic outlet syndrome (TOS), vTOS and aTOS are much more
straightforward in their diagnostic workup. vTOS patients with swelling must be distinguished
from secondary causes of axillosubclavian thrombosis, namely iatrogenic catheterization or
instrumentation of the venous system leading to thrombosis, which is obvious upon eliciting a
careful history. Also, a hypercoagulable state or malignancy can present as isolated upper
extremity venous thrombosis and there is some debate about the need for additional medical
workup in patients suspected of having vTOS.2
■
Because aTOS usually involves distal embolization to the hand from thrombus in a subclavian
aneurysm, a thorough workup for a cardiogenic source should be sought before assigning the
etiology to aTOS. Transesophageal echocardiography, with bubble enhancement to identify
paradoxical emboli, may be necessary to exclude cardiogenic emboli. Computed tomography
angiography (CT-A) of the arch and upper extremity vessels would also be reasonable to exclude
other arterial causes including axillary branch artery aneurysms, congenital abnormalities, or
traumatic injuries and dissections of the axillosubclavian arterial system, which can be seen in
high-performance athletes and individuals performing repetitive upper extremity motions.

■
Most patients with vTOS are young, healthy, and often athletically inclined who present with the
abrupt onset of unilateral arm swelling in their dominant arm after repetitive, strenuous use for
sport, work, or recreation. Athletes affected can include baseball pitchers, rowers, swimmers,
water polo players, weightlifters, volleyball players, surfers, football quarterbacks, or any others
relying on repetitive upper extremity effort. The swelling is noted in the shoulder, arm, and hand
and can be accompanied by aching, throbbing, or tightness that worsens with more activity.
Because most patients are otherwise young and healthy, an orthopedic cause such as strain, muscle
pull, or joint injury is often considered initially. Cyanosis of the affected extremity, visible chest
wall venous collaterals, or progressively worsening symptoms suggest a vascular etiology,
prompting referral to an interventionalist. On exam, the arm is swollen, tender to palpation, warm,
and often has visible superficial collaterals that track onto the anterior chest wall (FIG 3). Range
of motion of the affected extremity can be impeded due to patient discomfort.
■
aTOS patients will present with mild hand ischemia due to distal embolization, which manifests as
digital ischemia or splinter hemorrhage. The diagnosis is often delayed due to the fact that these
patients have no typical atherosclerotic risk factors and are mostly young and athletic. A pulsatile
mass or bruit may be present in the supraclavicular fossa or a bony prominence in that region may
hint toward a cervical rib or muscular abnormality. Symptoms often are gradual and unnoticed by
patients until occurring more frequently or when complete thrombosis occurs and the patient
presents with critical upper extremity ischemia.

■
Patients suspected of having vTOS should undergo duplex ultrasound of the affected area.
Axillosubclavian venous imaging can be challenging due to the clavicle’s location as well as many
of these patients being quite muscular. Color flow duplex, phasicity of flow with respiration, and
augmentation with compressive maneuvers can all aid in confirming the diagnosis of deep venous
thrombosis (DVT). An experienced vascular sonographer and interpreter can make the diagnosis
with high accuracy based on duplex alone. Cross-sectional imaging with magnetic resonance
imaging (MRI) or computed tomography (CT) venography is rarely needed or indicated in the
workup of vTOS. Catheter-based venography is the key confirmatory imaging study to document
the extent of vTOS and leads to the initial recommended therapeutic strategy of thrombolysis and
reduction of clot burden.
■
Patients presenting with digital ischemia suspicious for aTOS should undergo plain radiographic
imaging to assess for a cervical rib (FIG 4). Digital plethysmography of bilateral upper
extremities can be performed to visualize blood flow to each finger and can rule out Raynaud’s
type etiologies in the differential diagnosis. Wrist–brachial indices should be documented prior to
any further intervention to establish baseline flow characteristics. CT-A of the neck and upper
extremity in provocative positioning (arms at 180 degrees overhead) provides the most definitive
visualization of the affected region, confirming the presence of the cervical rib, delineating the
amount of thrombus in the subclavian aneurysm, and documenting the proximal and distal
vasculature for operative planning (FIG 5).
SURGICAL MANAGEMENT
■
vTOS patients diagnosed with acute axillosubclavian DVT should be anticoagulated with weight-
based dosing of unfractionated heparin or low-molecular-weight heparin. Depending on the
resource availability, admission for thrombolysis or urgent referral to a center capable of catheter-
directed interventions has been generally accepted as standard of care.3 There are patients that are
simply put on anticoagulation that get referred much later (more than 2 weeks) due to lack of
recognition of the TOS etiology of the DVT and this leads to a diminished success rate of
thrombolysis.4
■
Successful thrombolysis involves a combination of chemical and mechanical thrombectomy and is
often quite effective in decreasing clot burden and reducing long-term sequelae of upper extremity
DVT (FIG 6A,B). Technical details of thrombolysis are well described and can be performed
with minimal morbidity.5
■
Definitive therapy for vTOS after thrombolysis involves thoracic outlet decompression, consisting
of anterior and middle scalenectomy, resection of the subclavius tendon, 1st rib resection, and
venolysis or venous reconstruction. Timing of definitive surgery after thrombolysis is somewhat
controversial and is limited by anecdotal reports and various surgeon biases.6 Successful
outcomes can be achieved with definitive thoracic outlet decompression performed during the
same hospitalization as the thrombolysis7 and up to 3 months later with nonresolution of mild
venous obstructive symptoms,5 leading some to adopt a more selective approach for offering rib
resection. This lack of consensus provides some flexibility in offering definitive surgery as many
of these young patients are often student-athletes and cannot miss certain periods of the school
year. Management of anticoagulation during this time also impacts decisions about planning
surgery, as intolerance to blood thinners or difficulty with maintaining adequate anticoagulation
can affect the urgency of the required definitive decompression. If there is a delay in scheduling
definitive rib resection, a duplex immediately prior to surgery after successful thrombolysis is
important to document the status of the vein during the immediate pre-operative period.
■
In contradistinction to the numerous pathways for vTOS surgery planning aTOS in the presence of an
ipsilateral cervical rib and subclavian aneurysm presents a strong indication for definitive surgical
intervention. Preoperative planning consists mainly of ensuring adequate and healthy vasculature
proximal and distal to the diseased segment and determining a bypass route that is reasonable.
Extraanatomic bypass via a carotid–subclavian or carotid–axillary with interval ligation may be
necessary, depending on the size and length of the subclavian aneurysm and thrombus. Direct
repair of the subclavian aneurysm with interposition grafting can be accomplished only when there
is a short segment of disease that limits itself to the visualized region in the supraclavicular fossa.
The preoperative CT-A provides the best road map to help decide amongst these reconstructive
strategies. Endovascular techniques of the subclavian artery such as stent grafting in the setting of
aTOS are generally not recommended, given the age of the typical patient, the compression that
can occur from scarring even after cervical or 1st rib decompression, and the likely desire to
resume prior activities that often brought about these symptoms in the postoperative period.
Positioning
■
vTOS decompression will often involve an infraclavicular incision (some prefer only this incision;
some prefer a paraclavicular approach; still others prefer transaxillary), which is facilitated by
positioning the patient with a small bump between the shoulder blades and in a “head up” position
of 30 degrees. The affected arm is prepped out and placed in a stocking on the side of the patient
to allow full movement during the case. This affords the anterior visualization of the 1st rib and
particularly the subclavius tendon and costoclavicular ligament for safe and effective
decompression. The entire ipsilateral neck, shoulder, arm, and anterior chest wall are prepped
into the field as well as a region on the lateral chest wall should there be a small pneumothorax
postprocedure.
■
aTOS decompression with cervical rib is most often performed with a supraclavicular approach.
When arterial reconstruction is planned, preparations should be made for saphenous or femoral
vein harvesting.
TECHNIQUES
VENOUS THORACIC OUTLET SYNDROME

Infraclavicular Approach
■
A 5-cm transverse incision is made one fingerbreadth below the clavicle, starting along the edge of
the sternum travelling laterally, and is carried through the subcutaneous tissue and pectoralis fascia
to expose the upper fibers of the pectoralis muscles (FIG 7). Gentle spreading between muscle
fibers in this region exposes the anteromedial quadrant of the axillary fat pad and allows easy
palpation of the 1st rib. Appropriate retractors can be placed to fully expose the most anterior
portion of the 1st rib beneath a layer of axillary fat (FIG 8).
■
When the rib is visualized, cautery is used to separate the inferior-lying intercostal musculature from
the rib, with curved dissection heading superolaterally along the C curve of the rib (FIG 9). Lung
pleura are often visualized immediately beneath the rib and care should be taken to not injure lung
parenchyma. Superiorly, the subclavius tendon and costoclavicular ligament are taken down
sharply with cautery to free up the anterior portion of the 1st rib from the overhanging clavicle.
Following along the superior aspect of the 1st rib, the anterior scalene fibers are also sharply taken
down and further superior dissection takes place along the lateral edge of the 1st rib until palpation
of the subclavian artery is noted. This level is as far necessary to decompress the subclavian vein.
Often, moving the arm in a superior position facilitates more superior exposure of the 1st rib near
the artery.
■
When the rib is clear on its superior, lateral, and inferior edge, a rib cutter can be inserted
superiorly, taking care to visualize the jaws, and then the superior cut is made in the rib. The
inferior cut is done near the manubrial junction, commonly with a power saw. As the rib is pulled
away from the body, sharp cautery can be used to facilitate hemostasis of individual muscle fibers
(intercostals, anterior and middle scalene) holding the 1st rib in place.
Venous Reconstruction
■
With the anterior half to two-thirds of the rib removed from this infraclavicular approach, the vein is
often palpable in a bed of tissue and muscle fibers immediately below the clavicle. Venolysis
consists of freeing up these muscle fibers to expose the vein (FIG 10). More proximal exposure of
the vein can be accomplished via a transmanubrial extension of the infraclavicular incision to the
center of the sternum and vertically up to the sternal notch (FIG 11). This can be necessary to
obtain adequate vascular control for patching of chronically diseased venous segments. When a
strictured segment of vein is localized, saphenous vein or bovine pericardial or bovine pericardial
patching provides an excellent strategy for restoration of luminal diameter and can be performed
with adequate proximal and distal control of the vein under direct visualization (FIG 12).
Closure
■
Careful attention to the stump of rib remaining for hemostasis is performed, as well as the region of
vein after venolysis and/or reconstruction.
■
If the pleura or lung parenchyma has been injured, a small-caliber (12 Fr) pediatric chest tube can
be place in the anterior pleural space under direct visualization.
ARTERIAL THORACIC OUTLET SYNDROME

Supraclavicular Approach
■
A 7-cm incision is made one fingerbreadth above the clavicle, starting lateral to the palpable edge
of the sternal head of the sternocleidomastoid muscle and carried through the platysma. This
exposes the clavicular head of the sternocleidomastoid, which is transected with a cuff to sew
back together later, which now exposes the anterior scalene fat pad (FIG 13). The fat pad is
dissected along three borders, inferiorly, laterally, and medially, to allow it swing northward to
expose the anterior scalene muscle and the phrenic nerve (FIG 14). When operating on the left
side, extra care is taken to visualize the thoracic duct when present, which is suture ligated to
prevent postoperative chyle leaks if it becomes injured.
■
With the phrenic nerve slung and protected, transection of the anterior scalene muscle off the
superior edge of the 1st rib is done using bipolar scissors. Care is taken to stay on the bone during
this portion so as not to injure the underlying subclavian artery. After the inferior edge of the
anterior scalene is removed, a portion of muscle can be transected to allow room for further
visualization and subsequent dissection around the brachial plexus (FIG 15). The long thoracic
nerve is identified laterally, and the entire nerve structures are slung around a thick clear silastic
loop.
■
A cervical rib, when present, is often visualized at this time, with abnormal vasculature or
musculature surrounding it, and can be fused to the 1st rib (FIG 16). Care is taken to dissect nerves
and vessels away from the abnormal rib or its osseus portions that may not have appeared on
radiography.
■
The 1st rib is visualized by maneuvering the subclavian artery and the nerve bundle back and forth
while dissecting middle scalene fibers and intercostal musculature off the 1st rib (FIG 15). This
can be done sharply with bipolar scissors or by using a periosteal elevator. One should avoid the
use of cautery in this area as it is likely to transmit to the brachial plexus or phrenic nerve.
■
When the rib is clear from the region inferior to the subclavian artery and superior to the upper
aspect of the brachial plexus, a power saw can be used to transect the rib. If there is a fused
portion of cervical rib, it should be attempted to be removed as a single piece (FIG 17) to assure
that all bony abnormalities have been freed up to allow for adequate decompression.
Arterial Reconstruction
■
Subclavian aneurysm resection, when needed, consists of appropriate bypass principles and
replacement with an autogenous or prosthetic interposition graft or extraanatomic bypass of carotid
to distal subclavian or carotid to axillary graft. Typical sizes and types required for prosthetic
grafts include 6- or 8-mm ringed polytetrafluoroethylene (PTFE) or Dacron.
PEARLS AND PITFALLS
Indications ■ vTOS definitive therapy consists of prompt diagnosis, venography
and subsequent thrombolysis, and appropriate selection of patients
to undergo thoracic outlet decompression.
■ aTOS patients often present with hand ischemic symptoms that
will have some delay in management due to a wide differential.
Abnormal bony or muscular anatomy along with presence of
subclavian aneurysmal disease requires definitive repair including
arterial reconstruction.
Preoperative workup ■ Venous duplex, venography, and pharmacomechanical
thrombolysis provides the optimal reduction of clot burden to
restore functional venous patency in patients with vTOS. Timing
of rib resection and definitive thoracic outlet decompression are
somewhat variable and the approach should be individualized.
■ aTOS patients should undergo plain radiography to search for a
cervical rib and CT-A to determine the portions of diseased
subclavian artery that might need resection.
Patient setup ■ Prepping the affected arm in the vTOS patients affords the ability
to move the arm and, from the infraclavicular approach, gain
access to the majority of the rib that is responsible for venous
compression.
■ For cervical rib and arterial reconstructions, the supraclavicular
approach gives numerous options for reconstructive purposes as
well as the possibility of the carotid artery as an inflow source.
Infraclavicular approach ■ Visualization of the subclavius tendon and its fibers as well as the
costoclavicular ligament is paramount in decompressing the region
that compresses the subclavian vein in vTOS.
■ Liberal patching of the subclavian vein and extensive venolysis
provide the best long-term patency results after vTOS
decompression.
Supraclavicular approach ■ Carefully mobilizing the anterior scalene fat pad allows good
visualization of the anterior scalene muscle and phrenic nerve.
■ When performing left-sided supraclavicular TOS decompression,
one must be careful to identify and ligate the thoracic duct.
■ Slinging the subclavian artery and brachial plexus fibers allows
gentle traction back and forth to expeditiously dissect free the
entire 1st rib.
POSTOPERATIVE CARE
■
At the conclusion of the procedure, patients are extubated and an immediate chest x-ray is obtained
to ensure there is no pneumothorax. A small pneumothorax can be treated with oxygen and
incentive spirometry, but a 25% lung volume reduction requires a chest tube to suction for 24
hours.
■
Patients do not need a sling for their arms. They are given range-of-motion exercises immediately to
encourage strengthening and are given a taper of muscle relaxant and opioid narcotics for pain
control. Most patients are discharged the following day after surgery.
■
Anticoagulation for vTOS patients is usually resumed 3 to 4 days postoperatively at home, typically
consisting of Lovenox for a week, then they return for postoperative venography to see if further
balloon venoplasty is necessary.8
■
Anticoagulation for aTOS patients, especially if arterial reconstruction was performed, consists of
antiplatelet therapy with aspirin.
OUTCOMES
■
Patients treated for vTOS with lysis and subsequent thoracic outlet decompression have a very low
recurrence rate of thromboembolic disease. Morbidity and mortality is minimal, as these are often
young and healthy patients, but typically revolve around wound issues and bleeding given the need
for a short course of anticoagulation. Satisfactory quality of life scores and return to full function
are reported in the 80% to 90% range, and most patients can be counseled to expect a near full
return to sport.9
■
aTOS and the cervical rib patients often have the most dramatic recovery, as they are often the most
symptomatic to begin with. Although the literature is much sparser with regard to this entity,
results are uniformly positive with resolution of hand ischemic symptoms and lack of significant
disease recurrence.
COMPLICATIONS
■
Perioperative complications related to either form of thoracic outlet decompression revolve around
lung injury and wound issues. Pneumothoraxes are often self-limited and treated effectively with
chest tubes. Wound complications can include chyle leaks, seromas, and skin breakdown. Most of
these are managed expectantly. Brachial plexus injuries may also occur, most commonly as a
function of not recognizing important anatomic structures or not providing sufficient exposure to
eliminate collateral damage during rib transection and removal.
■
Timing of restarting anticoagulation in vTOS patients can lead to postoperative bleeding, which can
manifest as delayed hemothorax. The cause of this bleeding is often related to recent thrombolysis
and raw surfaces of muscle and cut bone, and this has led to the general recommendation of
holding off on restarting anticoagulation until 3 or 4 days postoperation.
REFERENCES
1. Lee JT. Clinical incidence and prevalence. In: Illig KA, Thompson RW, Freischlag J, et al , eds. Thoracic Outlet Syndrome.
London, United Kingdom: Springer-Verlag; 2013.
2. Cassada DC, Lipscomb AL, Stevens SL, et al. The importance of thrombophilia in the treatment of Paget-Schroetter syndrome.
Ann Vasc Surg. 2006;20:596–601.
3. Urschel HC, Razzuk MA. Paget-Schroetter syndrome: what is the best management? Ann Thorac Surg. 2000;69:1663–1669.
4. Johnston PC, Conte MS, Eichler CM, et al. Infraclavicular first rib resection for focused and effective treatment of venous thoracic
outlet syndrome. J Vasc Surg. 2010;52:525–526.
5. Lee JT, Karwowski JK, Harris EJ, et al. Long-term thrombotic recurrence after non-operative management of Paget-Schroetter
syndrome. J Vasc Surg. 2006;43:1236–1243.
6. Lee JT. Timing of first rib resection after thrombolysis. In: Illig KA, Thompson RW, Freischlag J, et al , eds. Thoracic Outlet
Syndrome. London, United Kingdom: Springer-Verlag; 2013.
7. Angle N, Gelabert HA, Farooq MM, et al. Safety and efficacy of early surgical decompression of the thoracic outlet for Paget-
Schroetter syndrome. Ann Vasc Surg. 2001;15:37–42.
8. Chang KZ, Likes K, Demos J, et al. Routine venography following transaxillary first rib resection and scalenectomy (FRRS) for
chronic subclavian vein thrombosis ensures excellent outcomes and vein patency. Vasc Endovasc Surg. 2012;46:15–20.
9. Chandra V, Little C, Lee JT. Thoracic outlet syndrome in high performance athletes [published online ahead of print May 14, 2014].
J Vasc Surg. doi:10.1016/j.jvs.2014.04.013.
Proximal to the Wrist: Upper Extremity
Chapter 10 Reconstruction/Revascularization
Mohamed A. Zayed Ronald L. Dalman
DEFINITION
■
The content discussed in the following text assumes the reader has familiarity with standard upper
extremity arterial anatomy and its most common variations. For additional information, the reader
may refer to excellent existing references.1,2
■
Various occlusive and/or aneurysmal disease processes in the upper extremity arterial system may
necessitate revascularization or reconstruction (Table 1).
■
Acute upper extremity ischemia is less common than in the lower extremity due to the rich
preexisting collateral circulation in both the upper arm and forearm. The majority (~50%) of acute
ischemic complications in the upper extremity occur in elderly females as a result of embolic
phenomenon rather than primary vessel thrombosis (which accounts for ~25% of acute ischemic
events).3 The differential diagnosis for embolic sources includes intracardiac sources, proximal
arterial atherosclerotic plaque, proximal arterial aneurysm thrombus, endocarditis, or paradoxical
embolus from venous circulation.
■
Chronic arterial occlusive disease is rarely symptomatic. Associated comorbid conditions include
diabetes, chronic atherosclerotic occlusive disease, subclavian or arteriovenous steal syndromes,
or failure of prior arterial repair or grafting.4,5
■
Venous occlusive disorders in the upper extremity are common and are usually associated with
iatrogenic injury, indwelling catheters, or thoracic outlet pathology. For further information
regarding venous thoracic outlet disorders. Distal to the thoracic outlet, venous occlusive
disorders are for the most part managed expectantly with anticoagulation therapy. Open surgical
and endovascular therapies are rarely used and, due to high recurrence and failure rates, are not
enthusiastically recommended. For further recommendations regarding upper extremity venous
disease management, please refer to additional references.6,7

■
Initial evaluation should include an assessment of associated comorbidities, including cardiac
pathologies (myocardial infarction, arrhythmia, heart failure, or prior coronary artery
revascularization), hypertension, hyperlipidemia, diabetes, hypercoagulability, smoking, prior
upper or lower extremity arterial intervention, or index extremity trauma.
■
Symptoms and signs of acute arterial ischemia include pain, paresthesia, pulselessness, paralysis,
and/or poikilothermia. A thorough vascular, sensory, and motor examination will help assess the
severity of arterial insufficiency. Although dated, the Rutherford classification system remains
useful for prognostic determinations.8 For classes 5 and 6 ischemia, urgent or emergent
intervention may be necessary to preserve limb function and viability. Prompt removal of embolic
debris in limbs with sufficient residual viability produces excellent long-term results.3
■
Chronic limb ischemia may also present with symptoms of rest pain, pain with extremity use,
paresthesia, pulselessness, poikilothermia, and/or ulcerations/wounds/gangrene of fingers or
fingertips. Subjects should be asked to describe what, if any, activities exacerbate these potential
symptoms (i.e., lifting or carrying material with affected arm/hand, arm raising, or repetitive
arm/hand movement). Patients with vocational or recreational activities that require regular or
frequent use of their upper extremities should describe convincing symptoms they experience in
relation to these activities. More commonly, chronic upper extremity arterial ischemia is
asymptomatic, particularly in older and less physically active individuals. In general,
revascularization is not necessarily indicated in these circumstances. Discrepancy in upper
extremity pulses, or brachial blood pressure differential of more than 15 mmHg, is a hallmark of
chronic upper extremity arterial insufficiency with or without accompanying symptoms.
■
Traumatic or iatrogenic injury accounts for 25% of patients presenting with acute upper extremity
arterial insufficiency. Consideration of the mechanism of injury (blunt, penetrating, hyperextension,
or avulsion) will help delineate the likely nature of the resulting arterial disruption (transection,
dissection, or thrombosis, with or without ongoing extravasation). Following completion of the
trauma primary survey, determination of extremity arterial continuity should be performed
following reduction of obvious ipsilateral upper extremity fractures and dislocations. In complex
injuries, including avulsions and crush injuries, baseline sensory and motor status should be
documented early to formulate the most appropriate course of therapy. When severe arterial injury
is associated with transection or avulsion of the brachial plexus and compound long bone
fractures, meaningful functional recovery, despite ultimately successful revascularization, may not
be possible.9
■
More commonly, upper extremity arterial injuries can be more subtle and are frequently missed on
primary or secondary surveys. The extensive collateral network present around the elbow often
masks the presence of brachial artery thrombosis following posterior elbow dislocation, or
dissection and thrombosis following brachial artery catheterization. When physical signs suggest
asymmetric or reduced upper extremity arterial perfusion, objective imaging should be obtained
promptly to direct therapy and maximize long-term function. Depending on hand perfusion and
viability, occasionally, immediate revascularization can be at least temporarily deferred to allow
for more urgent resuscitation and stabilization procedures to proceed. Similarly, non–flow-
limiting dissections may be monitored without immediate intervention, particularly when the
patient’s overall condition merits observational management.

■
Depending on clinical circumstances, revascularization may be undertaken on the basis of clinically
apparent injuries and limb ischemia. More commonly, physiologic assessment is indicated and
necessary to determine the most efficacious method of revascularization. Arteriography, typically
performed during or immediately prior to revascularization, remains an essential tool to guide
intervention and confirm procedural success. As a general observation, physiologic testing helps
determine when intervention is necessary, whereas arteriography provides the necessary anatomic
information to ensure procedural and functional success.
■
Computed tomography (CT) arteriography can potentially add useful information to surgical
planning for upper extremity revascularization. However, unlike in the abdomen and lower
extremities, significant insight into disease localization and severity in the upper extremities can
be gleaned from physical examination and nonionizing imaging modalities such as ultrasound. The
potential additional diagnostic benefit associated with CT angiography needs to be balanced with
the not insignificant radiation dosage delivered with this imaging modality, particularly in regard
to the longer life expectancy of younger patients. When vascular disease is known to be limited to
the extrathoracic upper extremity arterial system, CT angiography provides little additional, useful
information over diagnostic arteriography alone, especially when the latter can be paired with a
therapeutic intervention.
■
Noninvasive vascular testing for evaluation of the upper extremities includes segmental systolic
pressure measurements using a Doppler flow detector, digital plethysmography, and arterial
duplex scanning.
■
Serologic tests are the basis for the workup of patients with suspected vasculitic pathologies (e.g.,
Takayasu’s arteritis, giant cell arteritis, Buerger’s disease, and/or scleroderma). Customary tests
include baseline complete blood count, platelets, fibrinogen, C-reactive protein (CRP), and
erythrocyte sedimentation rate (ESR).10,11 In certain circumstances, color duplex evaluation may
also provide additional clues to aid in the diagnosis.12 Additional serial serologies and
rheumatologic consultation may be necessary depending on the severity and progression of the
suspected vasculitic disease process.
■
Young patients with acute primary arterial thrombosis, patients with recurrent arterial thrombosis,
or patients with a prior history of unprovoked deep venous thrombosis preceding an arterial event
should be considered for a hypercoagulability workup and hematology consultation. Initial testing
may include protein C function, free protein S, antithrombin III activity, anticardiolipin antibodies,
factor V Leiden mutation, prothrombin mutation, and homocysteine level.13
SURGICAL MANAGEMENT
■
Prior to attempted upper extremity arterial repair or revascularization, a clear understanding of the
extent and location of arterial pathology is essential. This knowledge guides the location of
arterial exposure or optimal method of arterial access, the identification of optimal inflow sources
and outflow targets, and the most effective and efficient methods of reconstruction. When
uncertainty persists, intraoperative arteriography provides essential and timely guidance.
■
As in all methods of peripheral arterial reconstruction, heparin is typically administered when an
interventional sheath is first placed, or arterial control is anticipated. Typically, 100 units/kg of
intravenous heparin is administered, with additional anticoagulation guided by the activated
clotting time monitored during the course of the procedure.
■
As discussed in Chapter 2, the preferred extrathoracic method of innominate or proximal left
subclavian artery surgical reconstruction is carotid subclavian bypass. Frequently, however,
endovascular options are available and preferable in patients who cannot tolerate the risks or
morbidity associated with open reconstruction. For example, in the setting of uncontrolled, life-
threatening hemorrhage from penetrating or crush injuries or limb avulsion, bleeding may be
controlled by insertion of covered, self-expanding stents across the area of injury in the subclavian
or axillary arteries. However, with few other exceptions (such as lesions associated with giant
cell or Takayasu’s arteritis), angioplasty and stenting of arterial lesions at or distal to the clavicle
is poorly tolerated and ill advised. Stents placed in this area are at high risk for fragmentation and
subsequent arterial thrombosis, pseudoaneurysm formation, or stent migration.
■
Surgical management of arterial pathology distal to the subclavian artery (surgical management of
arterial disease of the arch vessels and subclavian artery are discussed in Chapters 1, 2, and 9)
and proximal to the wrist (surgical management of arterial disease distal to the wrist is discussed
in Chapter 11) will depend on acuity, cause/type of pathology (penetrating trauma, blunt trauma,
occlusion, stenosis, or aneurysm), severity of patient symptoms, patient comorbidities, and
required durability of the planned repair.
■
Axillary artery exposure is guided by the nature of the planned reconstruction. The proximal artery
is most easily exposed via a transverse infraclavicular incision. Exposure of the second and third
portions requires deltopectoral or axillary approaches, respectively.1
■
Acute symptomatic embolic occlusion of the axillary or brachial arteries are best managed by open,
preferably image-guided, balloon catheter or direct thromboembolectomy.1,2 Essential elements
required for thromboembolectomy include (1) determination of the optimal treatment environment
(operating room [OR] with portable vs. fixed imaging), (2) arterial access (level of incision), (3)
acquisition of catheters and guidewires required to transverse the embolus and accumulated
luminal thrombus, (4) availability of balloon and over-the-wire embolectomy catheters, (5) need
for adjuncts such as aspiration catheters (Export™ catheter, Medtronic, Minneapolis, MN) and
thrombolytic agents (tissue plasminogen activator [tPA]), (6) options for managing postischemic
hyperemia and elevated compartment pressures, and (7) consideration of treatment alternatives
should preexisting atherosclerotic occlusive disease preclude or complicate catheter-directed
thromboembolectomy.
■
For symptomatic axillary or brachial artery thrombosis not amenable to direct or catheter-based,
image-guided thromboembolectomy, open surgical bypass or interposition grafting is the preferred
method of repair. When considering open bypass or interposition grafting distal to the clavicle,
key planning elements include (1) determination of optimal inflow and outflow, (2) conduit
(almost exclusively autogenous vein), and (3) assessment of distal compartment pressures and
potential need for fascial release. Commonly, more vasospasm is engendered by injury and
surgical manipulation in the upper extremity arteries as compared to those of the lower
extremities, and accommodations may need to be made to ensure graft and bypass patency in this
context.
■
Branch vessel injuries and aneurysms, particularly those arising from the axillary and brachial
arteries, are best treated with ligation and excision.14 Preoperative planning of these procedures
involves selection of an appropriate exposure through the muscles of the upper extremity that will
facilitate rapid recovery and minimize risk of disability in a usually young and active patient
cohort.
■
The relatively superficial location of the brachial artery in the antecubital fossa increases its
vulnerability to traumatic and iatrogenic injury.15 Most brachial injuries are associated with
penetrating trauma; however, blunt injuries also occur, particularly in the distal brachial artery,
following posterior elbow dislocations and supracondylar fractures (the latter more commonly in
children).16 In these situations, key elements for repair will include inspection of injured arterial
segment on preoperative imaging for possible intimal disruption, short segment thrombosis, or
thrombosis extending distally into the forearm.
■
An increasing number of cardiac catheterizations and coronary interventions are performed via
radial or brachial access.17 Cannulation site complications, including thrombosis or
pseudoaneurysm formation, often necessitate operative repair.17,18 For these patients, preoperative
planning will include identifying the extent of injury, options for graft conduit (smaller diameter
vein), and alternative management options including arterial ligation in extenuating circumstances.
■
The ulnar artery at the wrist is the dominant hand artery in the majority of patients. Achieving or
maintaining sufficient arterial outflow at the wrist is essential to the hemodynamic and clinical
success of forearm revascularization procedures. The status of the radial and ulnar arteries at the
wrist should be confirmed in the course of evaluating all patients for upper extremity
revascularization options.
Operating Room Setup
■
The majority of upper extremity revascularization procedures are suited for a hybrid operating
environment, or an OR equipped with a radiolucent, floating-point carbon fiber operating table
and fluoroscopy radiation source and image intensification system, preferably equipped with
digital subtraction angiography and last-image hold capabilities. When optimal x-ray penetration
and resolution is not available, or in circumstances when diagnostic angiography alone is
anticipated, less sophisticated portable imaging systems may suffice.
■
Elective and emergent upper extremity surgical revascularization procedures may be performed
with either regional or general anesthesia. Considerations include the overall status of the patient,
ability to tolerate the specific challenges associated with either anesthetic techniques, and the
abilities of the anesthesiologist responsible for anesthetic management.
■
For the majority of upper extremity procedures, the operative limb is typically extended at 90
degrees. For optimal surgical exposure, we prefer arm positioning systems that move freely with
the OR table rather than those with separate floor extensions. To avoid exacerbation of potential
brachial plexus injuries in appropriate clinical settings, care should be taken to avoid
hyperabduction and extension of the limb. The operative field should include, at a minimum, the
ipsilateral axilla, chest, and neck, with the head rotated and extended to the contralateral side. A
shoulder roll may be positioned under the ipsilateral shoulder to aid with neck and shoulder
extension (FIG 1A). Alternatively, for optimal deltopectoral exposure of the axillary artery, the
arm can be externally rotated and abducted at 30 degrees relative to the lateral chest.
■
In situations where venous interposition conduit may be needed, a lower extremity should also be
prepared into the surgical field to allow for greater or lesser saphenous vein harvest as indicated
by the estimated diameter of the target artery. In the setting of extensive traumatic injuries, vein
should be harvested from the least affected lower extremity.
TECHNIQUES
■
Systemic anticoagulation should be considered whenever major open or endovascular
revascularizations are undertaken. Exceptions include profound systemic coagulopathy or concern
related to concomitant risks such as occult intracranial hemorrhage. Sufficient intravenous
unfractionated heparin should be administered to achieve an activated clotting time of more than
250 seconds.
■
Open surgical revascularization and repair techniques are described in the sections in the following
text relative to upper extremity anatomic location.
■
The last section describes general endovascular techniques used for upper extremity interventions.
PROXIMAL AXILLARY ARTERY

First Step
■
Exposure of the proximal (first) portion of the axillary artery is best achieved through an incision
placed one fingerbreadth below the middle third of the clavicle (FIG 1B). Deep to the
subcutaneous tissue, the pectoral fascia is opened longitudinally. The pectoralis major muscle is
divided with a muscle-splitting incision. The underlying clavipectoral fascia is then sharply
incised to expose the proximal axillary sheath. Additional exposure is aided by lateral retraction
or division of the pectoralis minor muscle.
Second Step
■
Fine dissection should be used to expose and control the axillary artery deep to the clavipectoral
fascia. Careful dissection and retraction minimizes injury to the cords of the brachial plexus
surrounding the artery. The lateral pectoral nerve and proximal cephalic vein are also prone to
injury during dissection or traction from misplaced self-retaining retraction devices.
Third Step
■
The axillary vein lies anterior and caudal to the artery within the axillary sheath. Mobility of the
vein is achieved with gentle dissection, ligation of associated venous tributaries, and mild caudal
retraction with a circumferential vessel loop or small handheld retractor (FIG 1C).
■
In smaller patients, division of the thoracoacromial artery and vein may be required to facilitate
proximal axillary exposure. Once again, injury to the lateral pectoral nerve is avoided by gentle,
deliberate dissection.
Fourth Step
■
Once circumferential dissection and exposure of the proximal axillary artery is complete, the artery
is optimally controlled with silastic vessel loops (FIG 1C).
■
Familiar anatomic relationships may be less recognizable during redo or complex exposures, or in
the setting of traumatic injuries, ongoing extravasation, and hematoma formation. The risk of
associated brachial plexopathy is heightened in these situations. Extending exposure through the
deltopectoral groove may help delineate otherwise indistinct tissue planes. Repositioning the arm
throughout the range of available abduction may also reduce position-related anatomic distortion.
Fifth Step
■
For axillofemoral bypass grafting, the first or most proximal axillary segment is chosen for
anastomotic access to minimize the risk of traction and potential graft disruption from shoulder and
arm movement. Locating the anastomosis as proximate to the clavicle as possible optimizes long-
term performance and durability. Based on the patient’s body habitus and planned graft
configuration (uni- or bifemoral), an appropriately sized (6, 8, or 10 mm) externally supported
expanded polytetrafluoroethylene (ePTFE) is employed. For most patients, in most situations, an 8-
mm diameter, removable ring graft is optimal. The axillary arteriotomy is always created proximal
to the overlying pectoralis minor muscle, which is itself usually divided to further minimize undue
traction on the graft.
■
When considering direct ipsilateral axillo–axillo or axillobrachial bypass grafting, conduit choice
depends on surgical context. In contaminated fields (with open penetrating or avulsion injuries of
the axillary artery), vein is preferred and is sourced from the long or short saphenous or superficial
femoral veins in the (least involved) lower extremity, or contralateral arm vein. For elective
revascularization procedures, depending on the age of the patient, bypass length, target artery
diameter, and indications for reconstruction, ePTFE or knitted polyester prosthetic grafts may
provide acceptable alternatives. However, in nearly all situations requiring upper extremity
bypass at or distal to the clavicle, autogenous vein is optimal and highly preferred.
■
For ipsilateral revascularization, graft is tunneled parallel to the existing axillary artery beneath the
pectoralis major and minor muscles to the anterior axillary line.
■
For upper extremity revascularization procedures, tunneling is extended distally through
subcutaneous planes along the arm and forearm as necessary to reach the target artery. In the case
of axillofemoral bypass grafting, the ePTFE graft tunnel is created retrograde, extending from the
femoral incision superiorly to the exposed axillary artery, with care being taken to position the
graft anterior to the anterior superior iliac crest and advanced upward along the anterior axillary
line. The tunnel must not breach the abdominal fascia or thoracic cavity. With a tunneling device of
sufficient length, a counterincision is not usually necessary to reach the axillary artery. At the
inferior border of the pectoralis muscle, the tunnel transitions to a subfascial plane extending
below the pectoralis major muscle to reach the exposed axillary artery medial to its intersection
with the pectoralis minor muscle. Use of a purpose-specific tunneling device for this maneuver
will not only obviate the need for a counterincision but also minimize risks of kinking, twisting, or
graft compression.
■
The conduit should be beveled appropriately for end-to-side anastomoses at both ends. At the
axillary anastomosis, slightly more graft length redundancy is needed to prevent excessive traction
on the anastomosis and late graft or arterial injury. The use of stretch polytetrafluoroethylene
(PTFE) is also preferred for this reason.
Sixth Step
■
Traumatized, thrombosed, or aneurysmal proximal axillary artery segments may be transected or
resected as necessary, reconstituted by interposition grafting with venous or prosthetic conduit
(FIG 1D).
■
For interposition grafting, the damaged or diseased arterial segment is fully transected and removed.
The lumen within the proximal and distal arterial segments should be inspected for trauma,
dissection, or thrombus formation. In the case of the distal artery, flushing with heparinized saline
may help confirm patency and sufficient runoff. Retrograde flushing of diseased or damaged
brachial, axillary, or subclavian arteries is not recommended given the potential risk for vertebral
artery embolization of residual luminal detritus and subsequent central nervous system (CNS)
infarction or injury.
■
When uncertainty exists regarding the extent of axillary injury, further exposure may be necessary to
ensure success. In rare and extenuating circumstances, clavicular resection and replacement (or
removal) may be required for satisfactory arterial exposure. Similarly, when fragmented or
chronically infected, the clavicle should be removed as necessary to optimize long-term graft
patency and limb viability.
■
For upper extremity arterial reconstruction, once exposure is complete and the appropriate tunnel is
created, the appropriate conduit is selected for use and prepared for interposition grafting (FIG
1D). The conduit should be fashioned to an appropriate length to avoid potential kinking during
future arm motions. Proximal and distal anastomoses are performed end-to-end or end-to-side
depending on the respective diameters of the inflow and outflow segments.
Seventh Step
■
Catheter embolectomy should be performed as necessary, often using over-the-wire, image-guided
techniques, to remove luminal thrombus from inflow or outflow arterial segments as necessary.
Care should be taken with proximally directed embolectomy to avoid dislodging clot fragments
into the vertebral artery.
■
To minimize iatrogenic injury from embolectomy catheters, proximal embolectomy is best initiated
at the level of the axillary rather than brachial artery. Attempting antegrade embolectomy
proximally from an antecubital brachial access incision risks traumatic injury to the axillary or
brachial artery at the origin of the deep brachial artery, where the diameter of the brachial artery
decreases significantly, just distal to the axillary fossa.
■
Appropriately sized Fogarty thrombectomy catheters for upper extremity embolectomy include sizes
2 through 5 Fr, depending on the diameter of the artery being instrumented and the technique
(antegrade or retrograde) being employed.
MID-DISTAL AXILLARY ARTERY

First Step
■
The mid-distal axillary artery may be exposed via an axillary or deltopectoral incision. For distal
exposure, the incision is extended through the posterolateral border of the pectoralis major muscle
to allow for partial mobilization and medial retraction of that muscle (FIG 2A). In the superior
aspect of the surgical incision, the coracobrachialis muscle will be visualized at 90 degrees
relative to the medially retracted pectoralis major muscle. Within this angle, gentle blunt
dissection is applied to identify the axillary sheath running along the inferoposterior border of the
coracobrachialis muscle.
■
For deltopectoral exposure, dissection is performed along the anterior border of the deltoid muscle,
extending through the subcutaneous tissue in the deltopectoral groove (FIG 2B). With medial
retraction of the pectoralis major, the neurovascular bundle is then exposed in the underlying
clavipectoral fascia.
Second Step
■
Upon entry of the axillary sheath, the axillary artery is visualized directly under the median nerve. At
the lateral border of the pectoralis major muscle, the medial and lateral cords form the median
nerve form over the anterior surface of the axillary artery. The ulnar nerve and axillary artery are
visualized along the inferoposterior border of the mid-distal axillary artery in this exposure.
Identification of surrounding structures during axillary exposure minimizes risks of inadvertent
injury. Elevation and caudal retraction of the exposed axillary artery with vessel loops also
augments exposure and reduces risk of adjacent nerve injury during arterial clamping (FIG 2C).
Third Step
■
When further exposure of the second portion of the axillary is required, the pectoralis minor muscle
is divided near its insertion on the coracoid process. The pectoral nerves should be identified and
protected during this maneuver. Caudal retraction of the muscle allows for exposure of the
underlying neurovascular bundle (FIG 2D).
■
In the second portion, the axillary artery is surrounded on three sides by brachial plexus nerves,
leaving the anterior surface of the artery uncovered. For sufficient circumferential exposure of the
vessel, the thoracoacromial artery can be ligated and divided at its origin. However, during
mobilization of the axillary artery segment, care should be taken to not injure the lateral thoracic
artery and the lateral and medial cords as they join over the distal axillary artery to form the
median nerve.
Fourth Step
■
Similar to the steps outlined for reconstruction of injuries to the first or second portion, traumatized,
thrombosed, or aneurysmal segments in the second or third portions of the axillary artery may be
transected or bypassed, with interposition grafting or bypass as necessary.
■
Repair of axillary branch injuries and aneurysms requires sufficient segmental exposure of the
axillary artery itself, as well as the branch artery of concern. Subscapular, medial humeral
circumflex, or lateral humeral circumflex branch artery aneurysms can be exposed through the
axillary fossa and divided free from the axillary artery once ligated to prevent persistent distal
arterial embolization and hand ischemia in the setting of chronic overuse or athletic injuries.
Occasionally, aneurysmal degeneration of the branch compromises the integrity of the axillary
artery itself, and interposition grafting may be required for optimal reconstitution of distal limb
blood flow. Autogenous vein (or artery harvested from the distal internal iliac circulation in the
pelvis) is the optimal conduit choice for this application (FIG 3).
■
Axillary or branch artery injuries resulting in substantial distal and symptomatic upper extremity
arterial emboli and digital ischemia may benefit from a trial of intraarterial thrombolytic therapy,
administered preoperatively, to improve runoff, graft patency, hand perfusion, and functional
status.
BRACHIAL ARTERY
First Step
■
In the upper arm, the proximal brachial artery is optimally exposed via a 5- to 8-cm longitudinal
incision in the medial groove between the biceps and triceps muscles (FIG 4A).
■
As the subcutaneous tissue is dissected, care should be taken to visualize and avoid injury to the
basilic vein as it crosses near the brachial sheath in the distal upper arm. To aid in exposure, the
basilic vein can be retracted into the posterior wound, and vein branches crossing over the
brachial artery sheath can be ligated and divided. Significant plexus of sensory nerves are also
encountered in this dissection and should be protected from injury.
Second Step
■
By incising the deep fascia at the medial border of the biceps muscle, the neurovascular bundle may
be further exposed. The median nerve will be the first structure to be encountered in the brachial
sheath with this exposure. Wide mobilization of the nerve allows for its gentle retraction into the
anterior wound (FIG 4B).
■
Just deep to the median nerve, the brachial artery will be visualized along with two flanking
brachial veins. Interconnecting communications between these veins may be ligated to aid in
further exposure of the brachial artery.
Third Step
■
Exposure of the brachial artery in the mid-upper arm may require identification and control of the
deep brachial artery, which arises on the posteromedial surface of the brachial artery, just distal to
the lateral border of the teres major muscle in the distal axillary fossa. In the distal upper arm, the
superior and inferior ulnar collateral arteries may also require control during brachial artery
exposure.
Fourth Step
■
Alternatively, the brachial exposure can be gained through an oblique incision along the anticipated
course of the brachial artery in the distal upper arm proximal to the antecubital fossa.
■
Once again, care should be taken to avoid injury of the median nerve, which can be found
posteromedial relative to the brachial artery in this area (FIG 5). Elevation of the brachial artery
with vessel loops prior to clamping can decrease the chance of nerve injuries during this process.
Fifth Step
■
Pseudoaneurysm or transection of the brachial artery can be repaired following proximal and distal
brachial artery exposure and control. In the setting imminent rupture or exsanguination, proximal
control in this area may be obtained with a proximal sterile tourniquet. Following tourniquet
control, the injured brachial artery segment or pseudoaneurysm sac can be isolated and explored
with confidence. This technique is particularly useful in preventing catastrophic rupture and
contamination of the OR environment with blood-borne pathogens in the setting of iatrogenic or
self-inflicted mycotic aneurysms.
■
Puncture wounds may be amenable to primary suture repair or minimal resection of the injured
segment and primary reapproximation. Larger defects and partial transections may require patch
angioplasty for satisfactory repair (FIG 4C).
■
When uncertain as to whether a primary repair is indicated or even possible, the most reliable
course of action is interposition vein grafting, usually harvested from a long saphenous vein, with
care taken to account for differences in length based on movement at the elbow (e.g., avoid kinking
while limiting tension). Risk of kinking is also reduced by reconstructing other injured structures in
the antecubital fossa (e.g., biceps brachialis tendon) to limit graft motion during elbow flexion.
■
Distal forearm thrombectomy is best performed through a brachial incision created in the antecubital
fossa. Exposure of the distal brachial artery may be necessary to sequentially catheterize the
individual forearm arteries. Alternatively, proximal sheath access in the axillary fossa may
facilitate image-guided access of the forearm arteries and over-the-wire embolectomy.
■
In the antecubital fossa, distal thromboembolectomy may be performed with a 2- or 3-Fr Fogarty
catheter (FIG 5C). Further endovascular imaging and treatment (see in the following text) may be
required to optimally restore distal arterial perfusion.
■
Apropos the prior discussion regarding axillary exposure and embolectomy, attempting removal of
proximal emboli from antecubital brachial access (e.g., “retrograde” positioning of the
embolectomy catheter into the proximal brachial and axillary arteries) carries a significant risk of
catheter-related injury to the proximal brachial artery at the origin of the deep brachial artery,
where a significant diameter reduction occurs due to the bifurcation of superficial and deep
brachial arteries. For proximal embolectomy, the safer approach is to generally gain access in the
axillary rather than antecubital fossa.
■
Brachial occlusion associated with elbow or shoulder dislocation typically results from intimal
disruption or dissection beginning at the point of injury and extending distally. Accordingly, when
focal arterial injury is present in the setting of complete occlusion, the injured segment is optimally
repaired by resection and replacement rather than attempts at anticoagulation or embolectomy
alone.
RADIAL ARTERY
First Step
■
Direct open exposure of the radial artery can be performed at almost every level proximal to the
wrist. As with other arterial segments, exposure of the radial artery should be sufficient to allow
both proximal and distal arterial control.
■
The brachial artery typically bifurcates to give rise to the radial artery and ulnar/interosseus trunk at
the level of the radial tuberosity (FIG 5B). However, not infrequently, the radial artery originates
from the upper arm brachial artery or even the axillary artery (up to 15% incidence in cadaveric
studies).19 Several clinical circumstances highlight the significance of this anomaly, including the
need to base distal bypass or arteriovenous access procedures off the “brachial” artery in the
antecubital fossa. To ensure adequate arterial inflow, it is essential to identify which arterial
conduits are present and identified in the antecubital fossa. Preoperative CT angiography, catheter-
based contrast arteriography, or ultrasonography can provide essential information in this regard.
■
Alternative exposure options exist for the brachial bifurcation and proximal radial artery in the
antecubital fossa. A 4- to 5-cm transverse incision, two fingerbreadths distal to the antecubital
crease, provides optimal exposure for the distal brachial artery as well as the origins of the
forearm arteries (interosseus, radial, and ulnar). Alternatively, for more extensive brachial artery
exposure, an S-shaped incision is employed extending from the medial aspect of the biceps muscle
tendon, through the midpoint of the antecubital fossa, and toward the lateral aspect of the volar
forearm (FIG 5A).
■
Exposure of the mid- or distal radial artery can be performed through 4- to 5-cm longitudinal
incisions along the lateral aspect of the volar forearm (FIG 6A). A useful landmark for these
incisions is the imaginary line extending from the midpoint of the antecubital crease to the styloid
process of the radius, which often anatomically corresponds to the groove of the medial edge of the
brachioradialis muscle.
Second Step
■
Superficial, subcutaneous veins overlying the target arteries (medial antecubital vein in the
antecubital fossa and cephalic vein branches in the forearm) may be mobilized or ligated to aid
with the exposure process. Prior to ligation, care should be taken to consider the totality of
remaining forearm runoff veins, especially in the setting of blunt or avulsive traumatic injuries.
■
In the proximal forearm, the antebrachial fascia will need to be excised along the medial edge of the
brachioradialis muscle along the length of the incision. The radial artery can then be visualized
with lateral retraction of the brachioradialis muscle.
■
Similarly, in the midforearm, the radial artery can be visualized following excision of the overlying
antebrachial fascia and retracting apart the brachioradialis and pronator teres muscles (FIG 6A).
■
During exposure maneuvers, care should be taken to visualize and avoid injury to closely associated
radial artery structures. This includes the paired radial artery veins that accompany the radial
artery throughout its course in the forearm. The superficial radial nerve is also closely associated
with the lateral aspect of the radial artery in the midforearm and can be preserved with gentle
lateral retraction.
Third Step
■
Given the dominance of the ulnar circulation in most patients, isolated distal radial reconstruction
may be optional, depending on the totality of coexisting conditions and injuries. Superimposed
acute or chronic traumatic injury, renal failure, diabetes mellitus, or chronic embolization may
justify radial reconstruction, particularly in circumstances where hand viability is at significant
risk.
■
Radial artery transections or pseudoaneurysms, like all types of arterial reconstruction, are best
approached following adequate exposure and proximal/distal control. Detailed exploration and
arterial exposure follows shortly thereafter. Depending on extent of injury and integrity of the
arterial lumen at the site of injury, either primary repair or interposition grafting may be
considered (FIG 6B).
■
Acute embolic occlusions of the radial artery can be removed through retrograde embolectomy,
performed through a controlled proximal, transverse arteriotomy. Given the caliber of the forearm
arterial system, a 2-Fr Fogarty catheter is best suited for this purpose. As was the case more
proximally in the upper extremity arterial system, image-guided, over-the-wire embolectomy,
combined with judicious use of intraarterial thrombolytic agents such as tPA (see “Upper extremity
angiography and stenting” section in the following text), may be necessary to achieve satisfactory
runoff and hand and digital perfusion. Thus, arrangements should be made preoperatively to initiate
the embolectomy procedure in an operating environment that can support image-guided
intervention.
■
Both forearm arteries at the wrist may provide appropriate inflow for dialysis access procedures.
Considerations for arteriovenous access creation and maintenance are beyond the scope of this
chapter. Interested readers are referred to other references for options regarding dialysis access
creation.
ULNAR ARTERY
First Step
■
Similar to the radial artery, the ulnar artery may also be exposed along its course in the forearm, and
the extent of exposure will depend on the site and type of pathology as well as ability to obtain
adequate proximal and distal arterial control (FIG 6C).
■
The proximal ulnar artery can also be exposed at the brachial bifurcation in the antecubital fossa
through an S-shaped incision (see “Radial artery” earlier; FIG 5A,B).
■
Although more challenging, the proximal ulnar artery may also be exposed in the medial aspect of
the proximal forearm. Four fingerbreadths below the medial epicondyle, a 7- to 9-cm longitudinal
incision can be created along a line extending from the medial epicondyle to the pisiform bone.
Incising the deep fascia facilitates exposure of the ulnar artery through the space between the flexor
carpi ulnaris and flexor digitorum superficialis muscles (FIG 6C).
■
The distal ulnar artery, proximal to the wrist, is optimally exposed through a longitudinal incision
just lateral to the flexor carpi ulnaris muscle. The ulnar nerve lies medial to the artery at this level
and is prone to injury with this exposure. Care should be taken to identify and mobilize it safely.
The superficial palmar branch of the ulnar artery and nerve also crosses superficial to the
antecubital fascia at the wrist level, and care should be taken to prevent traction or compression
injuries to these structures during ulnar artery exposure.
Second Step
■
Thrombectomy of the ulnar artery proceeds in a fashion similar to that previously described for the
radial artery.
■
Ulnar artery traumatic transections may be repaired primarily or with an appropriately sized
interposition vein graft. Vein harvested from the dorsum of the foot frequently serves this purpose
well.
■
Ulnar artery arteriovenous dialysis accesses are rarely performed due to this vessel’s relative
difficulty in exposure compared to the radial artery, its close proximity to the ulnar nerve
throughout its length, and its relative dominance in maintaining adequate perfusion to the hand.
UPPER EXTREMITY ANGIOGRAPHY AND STENTING

First Step
■
Access depends largely on the area and type of anticipated arterial pathology. For innominate or
proximal subclavian artery disease or injury, retrograde transbrachial or transfemoral artery
approach may both suffice. For distal diagnostic or interventional procedures, retrograde radial or
antegrade access may be considered.
■
Standard Seldinger technique is used for percutaneous arterial access, using either ultrasonographic
or fluoroscopic guidance. Placement of a 4-Fr microsheath may help stabilize the initial
cannulation site and allow for preliminary diagnostic imaging.
Second Step
■
Intraarterial pharmacologic adjuncts may be administered through appropriately positioned arterial
infusion systems.
■
For arterial thrombosis, catheter-directed, limb-specific, intraarterial tPA is administered in doses
related to the extent of thrombus load, ranging from 0.25 to 2.0 mg per hour, following an initial
“seeding” dose of 4 mg across the region in question over 10 to 30 minutes. Combined
pharmacologic/mechanical thrombus disruption systems useful in other arterial and venous beds,
including the Trellis™ system (Covidien, Mansfield, MA), may be too large or unwieldy for the
upper extremity arterial vasculature. Newer low-profile systems, however, such as the
MicroLysUS™ infusion catheter (EKOS Corporation, Bothell, WA), may be more useful and
appropriate in this application. Care should always be taken to account for risk of particulate
embolus in the vertebral artery when planning embolectomy or thrombectomy procedures in the
upper extremity.
■
Similarly, the upper extremity arterial system is particularly prone to vasospasm during
catheterization. During diagnostic examinations, particularly in younger patients, care should be
taken to avoid catheterization distal to the antecubital fossa to minimize artifactual degradation of
the angiographic image due to vasospasm. Similarly, using warm flush solutions may minimize this
effect. When the radiographic appearance of vasospasm is encountered (“string sign” or “string of
beads” appearance), direct intraarterial infusion of papaverine (10 to 50 mg) or nitroglycerine (50
to 200 μg) may improve image resolution in hand or digital arteries. Papaverine will precipitate
out of solution when exposed to heparin and may not be optimal for all potential clinical
applications for this reason.
Third Step
■
If further endovascular diagnostic or interventional procedures are planned, wire access with a
0.018-in or 0.035-in guidewire to the arterial segment of interest must be achieved.
■
From a brachial artery approach, a short guide sheath and a guide catheter combination usually
allows for successful catheterization of adjacent proximal upper extremity arterial segments.
■
From a femoral artery approach, a long (90 cm) 6- or 7-Fr sheath is typically advanced over the
guidewire to facilitate stable catheterization of innominate or proximal left subclavian artery.
Long, curved 5-Fr catheters (i.e., angled, JB 2, headhunter, or vertebral catheter) may be used to
aid in successful cannulation and subsequent catheterization of the arch vessel of interest.
Confirmatory angiograms will help confirm successful cannulation and aid in identifying the
arterial segment of interest (FIG 7A).
■
Once stable catheterization of the target vessel is achieved, magnified angiograms may be obtained
in the appropriate obliquities to accurately assess the arterial segments of interest. Additional
runoff imaging may be necessary to evaluate the arterial outflow distal to the diseased segment.
The operator should inspect these angiograms to determine once again the candidacy for
endovascular treatment and obtain additional measurements to facilitate appropriate device
selection.
Fourth Step
■
Successful wire advancement across the lesion of interest is the next step in order to facilitate any
planned treatments with angioplasty or stenting.
■
With the guidance of a 4- or 5-Fr guide catheter, a 0.018-in or 0.035-in hydrophilic wire can be
advanced across a hemodynamically significant stenosis (e.g., innominate artery, proximal
subclavian artery, or upper arm brachial artery). During advancement, care should be taken to
remain intraluminal as much as possible to minimize the risk of dissection and reentry. Adequate
wire purchase should be acquired past the stenosis after crossing the lesion of interest to decrease
the chance of losing subsequent wire access across the lesion.
■
In situations where stenoses or occlusions preclude access from a “preferred” side, crossing the
lesion from the alternate side and advancing a wire from the opposite direction using a snare
technique may be required.
■
Simultaneous antegrade and retrograde, through and through (“body floss”) cannulation may
facilitate lifesaving management of traumatic subclavian artery injuries. In dire circumstances
where arterial continuity has been completely lost, and transluminal wire passage is not possible,
advancing snare and wire from opposite directions simultaneously, employing multiple-angled
view may allow for successful snaring in perivascular soft tissue and subsequent spanning of the
arterial tissue defect with a flexible covered stent (e.g., Viabahn™). This technique may generate
immediate and effective hemostasis while maintaining luminal patency and limb viability,
especially as an alternative to ligation or emergency embolization (FIG 7).
Fifth Step
■
Proximal subclavian artery and innominate stenoses are typically well managed by precise
placement of stiff, balloon-expandable stents or stent grafts. Compared to the axillary artery,
proximal to the costoclavicular junction, there is little or no movement in the proximal subclavian
artery. In the setting of a prior internal mammary-to-coronary artery revascularization, or a history
of vertebral–basilar insufficiency, precise stent placement is tantamount to procedural success. For
this reason, appropriately sized covered (e.g., Atrium iCAST) or bare metal (e.g., Omnilink,
Abbott, Redwood City, CA; Palmaz, Cordis Endovascular, Warren, NJ.) balloon-expandable
stents are generally preferred.
■
Appropriately size-matched, covered stents are also essential adjuncts for management of proximal
subclavian artery injuries or chronic pseudoaneurysms (FIG 7).
■
As noted earlier, however, stents of any kind should not be deployed in proximity to the junction of
the 1st rib and clavicle, as chronic traumatic damage from compression between these bony
structure will cause certain stent failure and further compromise limb viability.
PEARLS AND PITFALLS

Upper extremity nerve ■ Upper extremity arterial injuries frequently are associated with
injuries concomitant nerve injuries.20 Early recognition and diagnosis of
these associated injuries is paramount to long-term functional
restoration.
■ When nerve injury is identified or suspected, prompt repair in the
same setting is recommended. Plastic surgery consultation in these
circumstances is usually required.
Iatrogenic nerve injury ■ As a general rule of thumb, whenever possible, axillary exposure
during axillary artery proximal to the axilla should be acquired as proximal as possible,
exposure to limit the risk of nerve injury, as the cords of the brachial plexus
become more intimately related to the axillary artery as it
proceeds laterally from the clavicle. Also, the amount of axillary
artery displacement and traction as a result of arm movement is
minimized with far proximal anastomotic positioning.
■ Unless repair of the axillary artery requires a deltopectoral
exposure, the preferred choices for axillary artery exposure are
proximal or distal to the second portion of the axillary artery.
Arterial repair following ■ In the setting of arterial trauma, the extent of arterial injury should
segmental resection be precisely determined prior to attempts at reconstruction.
Failure to completely delineate the extent of injury will
complicate attempts at repair.
■ As a general rule of thumb, all involved arterial segment should be
resected and/or bypassed prior to attempts at reconstruction.
Although primary repair with native arterial preservation is often
appealing, long-term success typically requires interposition vein
grafting for anything more than the simplest of injuries.15,21
Inflow assessment ■ Prior to completion of an upper extremity arterial repair, the
operator must ensure that arterial inflow is adequate.
■ This can be confirmed on preoperative CTA if available, or
alternatively, with an intraoperative angiogram.
Outflow assessment ■ Adequate arterial outflow is paramount to maintain patency of
proximal repairs and help alleviate potential extremity ischemic
symptoms.
■ Some authors recommend routine outflow assessments following
upper extremity revascularization.22 However, if this strategy is
not regularly employed, intraoperative outflow assessment should
be performed in circumstances where the distal arm and/or wrist
vascular examination is abnormal following operative
revascularization.
■ Because the ulnar artery is the dominant vessel of the distal
forearm and hand, restoration of flow to this outflow vessel is
often necessary to avoid subsequent complications.
Compartment syndrome of ■ With prolonged acute ischemia (>4–6 hours), upper extremity
the upper extremity compartment release via fasciotomies is highly recommended.
■ Upper arm fasciotomies include two incisions into the brachium’s
two compartments.
■ Forearm fasciotomies are performed with three or more discrete
incisions to decompress the volar forearm, dorsal forearm, and
mobile wad.23
■ The hand may also require decompression via multiple
incisions.24 A carpal tunnel release may be necessary if median
and ulnar nerve dysfunction is evident. Consultation with hand or
plastic surgeons is recommended when considering the potential
benefit of hand fasciotomy to maximize compartmental release and
long-term functional and cosmetic recovery.
POSTOPERATIVE CARE
■
At the conclusion of arterial reconstructive procedures, reversal of heparin-induced coagulopathy
with protamine may or may not be indicated, depending on the status of the limb, the patient, and
the reconstructive procedure itself. Care should be taken to provide a test dose of protamine
before full reversal, if indicated, to minimize associated hypotension when antiprotamine
antibodies are present.
■
Motor and sensory examination as well as determination of upper extremity arterial status (including
a Doppler and pulse examination) should be performed immediately postoperatively to determine
the new baseline for subsequent serial examinations and to document improvement.
■
Patients are typically observed for an extended period (at least several hours) following upper
extremity arterial intervention to ensure procedural success and recovery from anesthesia. During
this period, the patient is observed for bleeding, hematomas, or change in serial vascular
examinations.
■
Patients treated for primary thrombosis or occlusion of an arterial segment are typically managed
with long-term, adjunctive systemic anticoagulation. The length of treatment period is debated and
is variable between practitioners but may be directed by severity of presenting symptoms,
frequency of prior occurrences, or history of a hypercoagulable condition.25
■
Patients who presented with a presumed embolic occlusion of an arterial segment should undergo a
medical workup for possible cardiac, proximal arterial atherosclerotic, endocarditis, paradoxical,
or tumor embolic sources.
■
Patients who underwent angioplasty or stenting of an arterial segment in the upper extremity are
typically initiated on a single-agent antiplatelet regimen with either aspirin or clopidogrel.
■
Patients who had a concomitant nerve injury or required fasciotomy compartment release should be
engaged in rehabilitation activities promptly to aid in restoration of extremity function.23
■
Postoperative surveillance of patients with upper extremity arterial interventions is necessary.
Duplex evaluation of the repaired arterial segment 1 to 3 months following intervention is usually
recommended followed by serial duplex evaluations every 6 months for at least 1 to 2 years.
Patients with no evidence of repair site compromise may then be imaged on a yearly basis. If there
is evidence of arterial segment compromise (stenosis, decreased flow, or occlusion), primary
assisted patency and secondary patency may be enhanced with reintervention.
OUTCOMES
■
Upper extremity revascularization with open arterial bypass has a reported average primary patency
of 82% to 87% and excellent limb salvage rates.26
■
Some series suggest arterial graft patency is lowest in female smokers with long bypass segments
that cross multiple joints.27
■
Because acute embolic episodes more commonly occur in elderly patients, the perioperative
mortality and morbidity in this patient cohort is higher compared to age-matched background
populations.28
■
Catheter-based revascularization of the proximal subclavian artery and innominate artery have a
high reported technical success rate (>98%), with excellent primary rates and low associated
procedure morbidity.29
■
Percutaneous treatment of upper extremity traumatic arterial injuries of subclavian artery are
associated with decreased operative time and intraoperative blood loss while maintaining
equivalent patency rates to standard open repairs.30,31
■
Axillary artery branch vessel repair outcomes are met with high success rates of symptom resolution
and lack of recurrence if distal emboli are lysed and proximal branch vessel embolic source is
completely isolated from the circulation.14
COMPLICATIONS
■
Intraoperative arterial vasospasm or occlusion
■
Missed concomitant venous or nerve injuries during traumatic arterial injuries
■
Iatrogenic brachial plexus, median, or ulnar nerve injuries from intraoperative electrocautery,
traction, or accidental transection
■
Iatrogenic injury to the brachial artery when attempting retrograde catheter embolization, especially
when failing to take into account the significant taper present in the proximal brachial artery
■
Arterial bypass graft stenosis or thrombosis
■
Repair site bleeding
■
Wound or graft site infection
■
Digital or vertebral artery embolization, complicating thromboembolectomy
■
Postrevascularization compartment syndrome in the arm or hand
■
Stent failure when deployed in proximity to the clavicle/1st rib
REFERENCES
1. Valentine RJ, Wind GG. Axillary artery. In: Valentine RJ, Wind GG, eds. Anatomic Exposures in Vascular Surgery. Philadelphia,
PA: Lippincott Williams & Wilkins; 2003:155–175.
2. Valentine RJ, Wind GG. Brachial artery. In: Valentine RJ, Wind GG, eds. Anatomic Exposures in Vascular Surgery. Philadelphia,
PA: Lippincott Williams & Wilkins; 2003:177–188.
3. Stonebridge PA, Clason AE, Duncan AJ, et al. Acute ischaemia of the upper limb compared with acute lower limb ischaemia; a 5-
year review. Br J Surg. 1989;76:515–516.
4. Ahn SS, Kudo T. Thoracic outlet syndrome and vascular disease of the upper extremity. In: Moore WS, ed. Vascular and
Endovascular Surgery: A Comprehensive Review. Philadelphia, PA: Saunders Elsevier; 2006:675–693.
5. Yeager RA, Moneta GL, Edwards JM, et al. Relationship of hemodialysis access to finger gangrene in patients with end-stage renal
disease. J Vasc Surg. 2002;36:245–249.
6. Engelberger RP, Kucher N. Management of deep vein thrombosis of the upper extremity. Circulation. 2012;126:768–773.
7. Kucher N. Clinical practice. Deep-vein thrombosis of the upper extremities. N Engl J Med. 2011;364:861–869.
8. 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.
9. Slauterbeck JR, Bitton C, Moneim MS, et al. Mangled extremity severity score: an accurate guide to treatment of the severely
injured upper extremity. J Orthop Trauma. 1994;8:282–285.
10. Maksimowicz-McKinnon K, Hoffman GS. Large vessel vasculitis. Clin Exp Rheumatol. 2007;25:S58–S59.
11. Lazarides MK, Georgiadis GS, Papas TT, et al. Diagnostic criteria and treatment of Buerger’s disease: a review. Int J Low Extrem
Wounds. 2006;5:89–95.
12. Schmidt WA, Wernicke D, Kiefer E, et al. Colour duplex sonography of finger arteries in vasculitis and in systemic sclerosis. Ann
Rheum Dis. 2006;65:265–267.
13. Macik BG, Ortel TL. Clinical and laboratory evaluation of the hypercoagulable states. Clin Chest Med. 1995;16:375–387.
14. Dalman RL, Olcott C. Upper extremity revascularization proximal to the wrist. Ann Vasc Surg. 1997;11:643–650.
15. Degiannis E, Levy RD, Sliwa K, et al. Penetrating injuries of the brachial artery. Injury. 1995;26:249–252.
16. Slowik GM, Fitzimmons M, Rayhack JM. Closed elbow dislocation and brachial artery damage. J Orthop Trauma. 1993;7:558–561.
17. Tonnessen BH. Iatrogenic injury from vascular access and endovascular procedures. Perspect Vasc Surg Endovasc Ther.
2011;23:128–135.
18. Machleder HI, Sweeney JP, Barker WF. Pulseless arm after brachial-artery catheterisation. Lancet. 1972;1:407–409.
19. Rodriguez-Niedenfuhr M, Vazquez T, Nearn L, et al. Variations of the arterial pattern in the upper limb revisited: a morphological
and statistical study, with a review of the literature. J Anat. 2001;199:547–566.
20. Shaw AD, Milne AA, Christie J, et al. Vascular trauma of the upper limb and associated nerve injuries. Injury. 1995;26:515–518.
21. Fitridge RA, Raptis S, Miller JH, et al. Upper extremity arterial injuries: experience at the Royal Adelaide Hospital, 1969 to 1991. J
Vasc Surg. 1994;20:941–946.
22. Zaraca F, Ponzoni A, Sbraga P, et al. Does routine completion angiogram during embolectomy for acute upper-limb ischemia
improve outcomes? Ann Vasc Surg. 2012;26:1064–1070.
23. Gelberman RH, Garfin SR, Hergenroeder PT, et al. Compartment syndromes of the forearm: diagnosis and treatment. Clin Orthop
Relat Res. 1981;(161):252–261.
24. Ko JH, Hanel DP. Technique of fasciotomy: hand. Tech in Orthop. 2012;27:38–42.
25. Guyatt GH, Akl EA, Crowther M, et al. Executive summary: antithrombotic therapy and prevention of thrombosis, 9th ed: American
College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141:7S–47S.
26. Hughes K, Cubangbang M, Blackman K, et al. Upper extremity bypass for chronic ischemia—a national surgical quality
improvement program study database study. Vasc Endovascular Surg. 2013;47:192–194.
27. Hughes K, Hamdan A, Schermerhorn M, et al. Bypass for chronic ischemia of the upper extremity: results in 20 patients. J Vasc
Surg. 2007;46:303–307.
28. Licht PB, Balezantis T, Wolff B, et al. Long-term outcome following thromboembolectomy in the upper extremity. Eur J Vasc
Endovasc Surg. 2004;28:508–512.
29. Patel SN, White CJ, Collins TJ, et al. Catheter-based treatment of the subclavian and innominate arteries. Catheter Cardiovasc
Interv. 2008;71:963–968.
30. Carrafiello G, Lagana D, Mangini M, et al. Percutaneous treatment of traumatic upper-extremity arterial injuries: a single-center
experience. J Vasc Interv Radiol. 2011;22:34–39.
31. Xenos ES, Freeman M, Stevens S, et al. Covered stents for injuries of subclavian and axillary arteries. J Vasc Surg. 2003;38:451–
454.
Distal to the Wrist: Upper Extremity
Chapter 11 Revascularization and Reconstruction
Michael G. Galvez James Chang
DEFINITION
■
Arterial reconstruction and revascularization distal to the wrist requires reconstituting the complex
vascular supply to the hand. This includes the ulnar and radial arteries, superficial and deep
palmar arches, and common and proper digital arteries. This reconstitution is performed with
either end-to-end primary vascular repair, interposition vascular graft bypass with proximal and
distal anastomoses, or addressing the digital arteries individually. Additionally, fasciotomy for
compartment syndrome following trauma or reperfusion injury may be a necessary adjunct.
DIFFERENTIAL DIAGNOSIS/PRECIPITATING CAUSES OF HAND

ISCHEMIA
■
Arterial injury
■
Traumatic (laceration, high energy or crush injury, etc.) or iatrogenic injury (including inadvertent
or intentional cannulation for vascular access).
■
Proximal embolization
■
Intraluminal thrombosis
■
Hypothenar hammer syndrome occurs when the base of the hypothenar eminence sustains repeated
blunt trauma resulting in chronic injury to the distal ulnar artery and the superficial palmar arch.
In this scenario, compression occurs between the roof of Guyon’s canal and the hook of the
hamate bone, resulting in aneurysmal degeneration of the ulnar artery, luminal thrombus
accumulation, and digital embolization (typically the ring and small finger). This typically
occurs on the dominant hand of individuals participating in vocational or avocational activities
involving repeated palmar impact (e.g., pipe fitters and mountain bike riders).
■
Spontaneous radial artery thrombosis may be associated with Buerger’s disease and is not as
common as ulnar artery thrombosis.
■
Chronic digital ischemia secondary to vasospastic and rheumatologic disease:
■
Primary Raynaud’s syndrome refers to cold-induced vasospasm present in the absence of
concomitant disease. The etiology of this condition remains uncertain but is likely due to an
exaggerated adrenergic receptor–mediated response to cold exposure.
■
Secondary Raynaud’s syndrome refers to digital vasospasm which occurs in the setting of known
autoimmune collagen vascular diseases and related rheumatologic disorders (such as
rheumatoid arthritis). In this circumstance, a normal vasospastic response to cold or
environmental stimuli is superimposed on chronic digital artery occlusive disease.
Differentiation from primary Raynaud’s syndrome is most commonly made based on digital
ulceration and tissue loss, conditions which uniformly develop in secondary Raynaud’s
syndrome.
■
CREST syndrome encompasses the most common phenotypic presentation of systemic
scleroderma/sclerosis: calcinosis, Raynaud’s phenomenon, esophageal stenosis, sclerodactyly,
and associated telangiectasias.
■
Buerger’s disease, or thromboangiitis obliterans, represents a progressive, recurring necrotizing
arteritis of small and medium vessels closely linked to tobacco exposure.
■
Compartment syndrome occurs in response to increased pressure within a fixed osteofascial
anatomic space, leading to decreased arterial perfusion, irreversible myonecrosis, neuropathy, and
potential limb loss. In the hand, compartment syndrome most commonly develops following crush
injuries; however, intravenous infiltration, external compression, and other mechanisms may also
induce increased compartment pressure.

■
Determine the hand dominance of the patient and relevant history of trauma, tobacco use, medical
history (coagulopathic disorders), and occupational exposures. Additionally, the presence of
palpable masses, pain, sensory changes, or color changes should be evaluated.
■
An Allen’s test may provide additional information regarding the relative contribution of the ulnar
and radial arteries to hand perfusion. This test is performed by manual compression of both the
radial and ulnar arteries, with elevation and successive opening and closing performed to drain
venous blood from the hand. The time differential to reperfusion, following respective arterial
release, provides qualitative insight into relative radial or ulnar dominance. In most cases,
however, the ulnar artery is dominant, and modern quantitative arterial perfusion assessment by
duplex imaging and digital plethysmography has largely supplanted subjective physical exam
findings in the assessment of adequacy of arterial inflow.
■
Patients with hypothenar hammer syndrome can have complaints of pain and tenderness of the
hypothenar mass, with cold sensitivity and numbness of the ring and small finger secondary to
digital embolization and direct ulnar nerve compression. A pulsatile mass may, on occasion, be
appreciable in the palm. Discoloration of the lateral three fingers of the hand may also be present
as a result of chronic digital embolization.
■
Patients with spontaneous radial artery thrombosis present with pain, numbness, and discoloration
of the tips of the radial-sided digits. The area of occlusion is commonly beneath the first and third
extensor compartments and can be related to compression of the radial artery by the extensor
pollicis longus.1
■
Patients with Raynaud’s syndrome report ischemic symptoms and digital discoloration on exposure
to cold. Cold-induced vasospasm may be elicited by cold emersion testing in an ice bath. A
positive test is elicited by the elimination of plethysmographic pulsatile phasicity on exposure to
cold, in addition to the onset of symptoms. Most patients, however, cannot tolerate this
provocative test, and the clinical use of eliciting vasospastic symptoms, particularly in the
presence of existing digital ulceration, is uncertain.
■
Compartment syndrome is a clinical diagnosis. Cardinal signs include persistent and progressive
pain unrelieved with immobilization/elevation, tightness of skin, pain with passive extension, and
decreased sensation. Reduced skin temperature, pallor, and pulselessness are often late findings.
■
The intrinsic compartments are tested for pain with passive adduction and abduction of the
fingers. The thenar compartment is tested by adduction of the thumb. The adductor of the thumb
is tested by passive palmar abduction. The hypothenar compartment is tested by adduction of the
small finger.
■
Normal intracompartment pressures are less than 10 mmHg; between 10 and 20 mmHg is
considered high but not enough to cause muscle necrosis. An acute compartment syndrome is
assumed if the measured interstitial tissue pressures are within 30 mmHg of the mean arterial
pressure or 20 mmHg of the diastolic blood pressure.2 Hand pressures are typically difficult to
assess on the basis of direct measurement, given the extensive septation of the fascial
compartments, underscoring the importance of clinical diagnosis. When in doubt, it is prudent to
proceed with operative fasciotomy.
IMAGING AND OTHER DIAGNOSTICSTUDIES
■
As previously mentioned, noninvasive vascular imaging and physiologic assessment are essential to
establishing the diagnosis of hand and digital ischemia as well as providing a physiologic
corollary to subsequent arterial imaging studies obtained to outline the relevant anatomy.
Noninvasive testing informs and should always precede anatomic imaging studies regardless of
modality.
■
Imaging provides essential identification of normal and variant arterial anatomy, recognition of the
location and extent of obstructive and aneurysmal disease, and operative planning.
■
The vascular anatomy of the hand includes the ulnar artery, radial artery, and sometimes a persistent
median artery (5% of the population). The ulnar and radial arteries anastomose to form the
superficial and deep palmar arches, with the ulnar artery being the main contributor to the
superficial arch and the radial artery the main contributor to the deep palmar arch (FIG 1). There
is significant variation in the vascular patterns of the superficial and deep palmar arches.
■
The superficial palmar arch is completed by either the branches of the deep palmar arch, radial
artery, or median artery in about 80% of patients. The deep palmar arch is completed by the
superior branch of the ulnar artery, the inferior branch of the ulnar artery, or both in about 97% of
patients.
■
The main branches from the superficial palmar arch are the three common digital arteries, which go
to the index-middle, middle-ring, and ring-small finger webspaces, as well as the proper digital
artery to the ulnar aspect of the small finger. Each digit has a dual blood supply from the radial and
ulnar proper digital vessels.
■
The thumb has blood supply from the princeps pollicis artery, which variably arises from the radial
artery, the deep palmar, or superficial palmar arch.
■
Catheter-directed, contrast-enhanced, digital subtraction hand arteriography provides highly
detailed anatomic information and represents the gold standard in vascular imaging (FIG 2).
However, there are risks from this invasive procedure, which include contrast allergic reaction,
vasospasm, contrast-induced nephropathy, thromboembolic events including digital embolization
and stroke, and drug reactions precipitated by intraarterial injection of vasoactive agents including
Priscoline and nitroglycerin. Hence, catheter-based arteriography is best suited to operative
planning in patients already determined to need reconstructive surgery.
■
Magnetic resonance arteriography (MRA) is another option for imaging that is noninvasive,
eliminating risks of radiation, contrast reaction, and vasospasm. However, the resolution of MRA
is not sufficient for detailed surgical planning.
■
Computed tomographic arteriography (CTA) is also noninvasive, although contrast and (significant)
radiation exposure are required for image acquisition. Similar to MRA imaging, the resolution of
CTA is typically not sufficient to support detailed surgical planning.
■
Measuring compartment pressures of the hand can be performed with the Stryker Intra-
Compartmental Pressure Monitor (Kalamazoo, Michigan), which involves placing the device
needle perpendicular to the skin and evaluating individual compartments including sites of
maximum swelling of the thenar, hypothenar, and interosseous compartments. The compartment
being measured should be at the level of the heart. In an intensive care unit setting, using an arterial
pressure line connected to a strain gauge, zeroed at the level of needle entry into the hand, can also
provide rapid and accurate compartmental measurements. A 20-gauge needle is inserted into the
compartment and flushed, with measurement acquired after the flush bolus has disseminated in the
compartment and the pressure spike from the flush returns to baseline.
SURGICAL MANAGEMENT
■
The overall goal is to restore distal blood flow to baseline/maximal levels, given anatomic
constraints, available arterial conduit, central arterial perfusion pressure and cardiac output, and
end-organ (hand) viability.
■
Treatment of thromboembolic disease can include medical management and catheter-based chemical
and mechanical thrombolysis, angioplasty, and stenting to maximize arteriolar outflow and arterial
inflow, respectively. Upper extremity revascularization techniques are discussed in Chapter 10.
■
End-to-end primary vascular repair can be performed if arteries are tension free after mobilization,
and the zone of injury is accurately identified to be uninvolved in the site of anastomosis. If there
is any difficulty in approximating the vessels ends, then vascular grafts are preferred.
■
In ulnar or radial artery thrombosis, reconstruction is preferred over ligation. Proximal
reconstructions are attempted even in the setting of more distal occlusions, based on the rationale
of augmenting collateral flow via direct or indirect means.3
■
Determining venous or arterial graft harvest site is important for preoperative planning. Dorsal hand
or foot veins provide the most appropriate size match for intrinsic arteries of the hand (and feet).
Donor sites for arterial graft conduits include the deep inferior epigastric artery, subscapular
artery, thoracodorsal artery, or descending branch of the lateral femoral circumflex artery.
Typically, arterial grafts patency rates are superior to those obtained with venous grafts.4
■
For chronic ischemia, medical management including pharmacologic treatment with vasodilators,
topical nitroglycerin, calcium channel blockers, or botulinum toxin should be attempted first, prior
to surgical management.5 Evidence of gangrene, osteomyelitis, and so forth of the involved digit
may require debridement or digital amputation.
■
Periarterial sympathectomy in the hand, which involves stripping the adventitial layers from affected
arteries, removes sympathetic nerve input to the media and has proven effective in promoting
distal finger lesion healing in scleroderma patients. In scleroderma specifically, the thickened
adventitia apparently contributes to decreased digital arterial flow.6,7
Positioning
■
Hand surgery is usually performed with the patient in the supine position. The operated hand is
placed on a hand surgery table, which is stabilized by two legs. Reconstructive surgery may be
performed under tourniquet, depending on systemic comorbidities and the adequacy of arterial
inflow. For tourniquet control, the upper arm is well padded with Webril (cotton) wrapped
circumferentially, and then an 18-in (or appropriately sized) pneumatic tourniquet is secured
around the upper arm (FIG 3). Alternatively, depending on inflow status, the tourniquet may be
placed at the forearm or wrist. Finally, an impervious barrier (3M Steri-Drape 1000) is placed
circumferentially just distal to the tourniquet to prevent see page of the sterile prep solution. The
arm/hand are then sterilely prepped and draped.
■
Intraoperatively, the arm is exsanguinated with an elastic bandage (Esmarch bandage) wrap and
elevation immediately prior to tourniquet inflation. In adults, the tourniquet is typically inflated to
250 mmHg; in children, it is set 100 mmHg above the systolic pressure. The tourniquet inflation
should last no more than 2 hours and must be deflated for a 20-minute interval to allow reperfusion
prior to reinflation, if needed. Consideration should be made to establishing systemic
anticoagulation prior to tourniquet inflation when indicated.
■
Appropriate concurrent sterile prep should be performed on graft harvest sites as necessary.
■
Microsurgery prep includes ensuring that the operating scope is working properly and sterilely
draped. Positioning is extremely important to reduce surgeon fatigue, which includes ensuring
good table height, working height (with appropriate padding support of the wrists with stacks of
surgical towels), and sitting position. Microsurgery instruments should be available as necessary,
depending on the level of revascularization considered. 9-0 and 10-0 sutures are employed for
more distal reconstructive procedures and digital reimplantation. For proximal radial and ulnar
reconstruction procedures, at or immediately adjacent to the wrist, 2.5× to 3.5× surgical loupe
magnification will provide adequate anatomic resolution and suture placement for operators with
normal visual acuity.
TECHNIQUES
ULNAR ARTERY RECONSTRUCTION

Placement of Incision
■
Identify the ulnar artery aneurysm (FIG 4A), and incise the skin longitudinally over the ulnar artery
as it crosses Guyon’s canal. Extension across the midpalmar crease may be necessary to expose
the distal ulnar artery as it curves radially to become the superficial palmar arch.
■
The volar carpal ligament, the roof of Guyon’s canal, is a continuation of the deep palmar fascia and
fibers of the flexor carpi ulnaris and must be carefully incised for access to the ulnar artery and
nerve.
■
The ulnar nerve, particularly the motor branch, must be carefully protected.
Resection of Ulnar Aneurysm
■
Once the deep palmar fascia is incised, the aneurysm is generally recognizable (FIG 4B AND FIG
5A). The aneurysm itself may be thrombosed or tortuous or elongated as a result of chronic
posttraumatic remodeling. Microvascular clamps are placed on the ulnar artery proximal and distal
to the aneurysm.
■
Preserve the common digital arteries and other large branches distal to the thrombosed segment.
Place microvascular clamps and vessel loops as needed on vessels that will require
revascularization.
■
Resect the affected artery and trim the ends sharply.
■
The adventitia is excised as needed, and the intima inspected at the proximal and distal end of the
anastomoses to ensure that the entire disease segment is removed. Failure to remove the entirety of
diseased artery may precipitate early graft thrombosis and recurrent digital embolization.
Vein Graft Interposition
■
Occasionally, sufficient redundancy is present in the ulnar artery to allow direct primary repair
(FIG 4C); in most cases, interposition vein grafting (FIG 4D) is required to complete the
reconstruction without tension.
■
When the superficial palmar arch and adjacent common digital arteries are involved, then a more
complex “palmar arch” reconstruction may be necessary to restore perfusion to the dependant
digits (FIG 5B), with end-to-side anastomoses of the common digital arteries into the distal extent
of the vein graft.
■
Vein harvest is typically chosen from the hand and foot veins. Length of vein harvest should be
several centimeters longer to allow for trimming.
■
Marking the superficial surface of the vein helps avoid twisting or kinking of the vein graft. Marking
one end (typically distal) provides a reminder to reverse the graft prior to implantation. If needed,
ends with valves are excised. Arterial graft may also be used when available and of suitable
diameter and length.
■
Longer grafts may also be used (FIG 4D) when more proximal arterial inflow is required.
■
Microvascular anastomosis of vessel graft.
■
Anastomosis completion may require microsurgical technique, given that common digital arteries
may be 1 to 2 mm in diameter.
■
Both ends of the vessels are held in place by an appropriately tensioned microvascular double-
armed clamp.
■
After irrigation with heparinized saline, interrupted sutures are placed circumferentially using a
triangulation technique.
■
The proximal anastomosis is performed first, then flushed with heparin and clamped to allow the
vein graft to extend to length before preparing and completing the distal anastomos(e)s.
SNUFFBOX RADIAL ARTERY RECONSTRUCTION

■
At the level of wrist, the radial artery turns dorsally underneath the first extensor compartment
(containing the abductor pollicis longus and extensor pollicis brevis), then runs between the first
and third extensor compartments (extensor pollicis longus) in the area known as the “anatomic
snuffbox.” The diseased segment and distal targets should be confirmed by reference to the
specific preoperative imaging studies (FIG 6A,B). A skin incision is made on the dorsum of the
hand directly over the anatomic snuffbox parallel to the second metacarpal (FIG 7A).
■
The superficial radial nerve is identified and preserved.
Resection/Bypass of Diseased Segment
■
This dissection is continued distally between the heads of the first dorsal interosseous muscle,
allowing further mobilization of the distal radial artery and visualization of the origin of the deep
palmar arch.
■
Microvascular clamps are placed proximal and distal to the thrombosed segment of the radial artery.
■
All branches from the thrombosed segment should be ligated and removed en bloc (FIG 7B).
Vein Graft Interposition
■
The vein graft should be reversed and placed superficial to the extensor pollicis longus and extensor
pollicis brevis (making the graft immediately beneath the skin) and then sutured end-to-end to the
radial artery proximally and end-to-end to the deep arch distally (FIG 7C). See the “Ulnar Artery
Reconstruction” section for further description on vein harvest and microvascular anastomosis
technique.
HAND FASCIOTOMY
Placement of Incisions
■
The 10 compartments of the hand include the thenar, hypothenar, adductor, and 4 dorsal and 3 volar
interossei compartments. Four incisions are required to release all 10 compartments.
■
The dorsal and volar interosseous compartments are decompressed with two dorsal incisions over
the index finger and ring finger metacarpal (FIG 8A). These incisions are carried down to either
side of the metacarpal to release the dorsal interossei. Dissection along the ulnar and radial
aspects of the index metacarpal must be sufficiently deep (FIG 8C) to release the first dorsal
palmar interosseous and the adductor compartments. Similarly, to release the remaining palmar
interossei, deep dissection is required along the ulnar and radial aspects of the ring metacarpal.
Meticulous release along the length of the metacarpal is essential to ensure adequate
decompression.
■
The thenar compartment is bound by thenar fascia and contains the abductor pollicis brevis, flexor
pollicis brevis, and the opponens pollicis. This compartment is decompressed with a longitudinal
incision along the radial/volar (FIG 8A) aspect of the thumb metacarpal.
■
The hypothenar compartment is bound by the hypothenar fascia and contains the abductor digiti
minimi, flexor digiti minimi, and opponens digiti minimi. This compartment is decompressed with
a longitudinal incision along the ulnar/volar (FIG 8B) aspect of the small metacarpal.
■
The finger can also have compartment syndrome if there is excessive swelling and depending on
clinical assessment. Here, the fascial compartments are bound by Cleland’s and Grayson’s
ligaments. The finger fasciotomy is performed by making midaxial incisions along the ulnar aspect
of the index, ring, and long fingers and on the radial aspects of the thumb and small finger. Once
incisions are made, blunt dissection is continued through Cleland’s ligament (firm fascia bands that
run from side of the phalanges to the skin and are dorsal to the neurovascular bundle), retracting
the neurovascular bundles in a volar direction and remaining volar to the flexor tendon sheath.
Carpal Tunnel Release
■
If any compartment pressure is elevated in the hand, then all compartments should be released
including the carpal tunnel.
■
A longitudinal palmar incision is made just distal to the volar wrist crease and extending distally for
3 to 4 cm in the proximal palm along the course of the radial aspect of the ring finger.
■
The palmaris fascia is divided longitudinally to expose the underlying transverse carpal ligament,
which is then incised under direct visualization.
■
The incision is extended at least 2 cm into the forearm to ensure release of the deep antebrachial
fascia.
■
The carpal tunnel release incision is closed primarily with interrupted nylon sutures.
Wound Care
■
Fasciotomy wounds are left open for a minimum of 48 hours or until swelling has resolved.
■
Secondary closure with wet-to-dry dressings may occur over open incisions.
■
Eventually, these wounds may need split-thickness skin grafting.
■
The hand should be splinted in a safe position (70 to 90 degrees of metacarpophalangeal [MCP]
flexion and proximal interphalangeal [PIP] joints straight).
PEARLS AND PITFALLS
■ Although a thrombosed ulnar artery can be ligated, reconstruction of the ulnar artery can
reconstitute normal flow and should be attempted.
■ Hand vascular repair and grafting requires meticulous microvascular technique.
■ The dorsal sides of the hand and foot have veins of similar size that are ideal for vein graft
reconstruction.
■ Periarterial sympathectomy is particularly effective in scleroderma because the vessels are
encased in adventitial scarring.
■ Early diagnosis and treatment for hand compartment syndrome is critical: When in doubt, release
all compartments.
POSTOPERATIVE CARE
■
Postoperative monitoring of the hand after vascular reconstruction is similar to finger replantations
and can be performed with pencil Doppler monitoring or with pulse oximetry (FIG 9).
■
Aspirin 81 mg is given for 6 weeks postoperatively after vessel reconstruction.
■
For periarterial sympathectomy, immediate digital range of motion is encouraged, and cold
temperature and vasoconstrictive drugs or substances (smoking, caffeine, etc.) are avoided for at
least 6 weeks.
■
For compartment syndrome, aggressive strengthening and range of motion should be started once
wounds have stabilized.
OUTCOMES
■
Radial artery reconstruction patency in a study of 13 patients found that all vein grafts were patent
after mean follow-up of 22 months, with a significant decrease in pain; however, no difference in
numbness was seen.3 In another study of 145 patients, an overall patency of vein grafts of 85%
over an average follow-up period of 34 months was found as well as 100% with arterial grafts.4
■
Long-term recovery after compartment syndrome release depends on the extent of injury and
requires long-term hand therapy for recovery of hand function. Compartment release of the hand
can result in normal function; however, contractures can develop, which may need eventual
reoperation for contracture release.
COMPLICATIONS
■
Infection
■
Dehiscence of incisions and other wound healing complications
■
Failure of revascularization
■
Distal emboli
■
Thrombosis at anastomosis
■
Long-term patency
■
Stiffness of the fingers
■
Continued ischemia, pain, and ulcerations
REFERENCES
1. Pomahac B, Hagan R, Blazar P, et al. Spontaneous thrombosis of the radial artery at the wrist level. Plast Reconstr Surg.
2004;114(4):943–946.
2. Leversedge FJ, Moore TJ, Peterson BC, et al. Compartment syndrome of the upper extremity. J Hand Surg Am. 2011;36(3):544–
559.
3. Ruch DS, Aldridge M, Holden M, et al. Arterial reconstruction for radial artery occlusion. J Hand Surg Am. 2000;25(2):282–290.
4. Masden DL, Seruya M, Higgins JP. A systematic review of the outcomes of distal upper extremity bypass surgery with arterial and
venous conduits. J Hand Surg Am. 2012;37(11):2362–2367.
5. Porter SB, Murray PM. Raynaud phenomenon. J Hand Surg Am. 2013;38(2):375–377. doi:10.1016/j.jhsa.2012.08.035.
6. Hartzell TL, Makhni EC, Sampson C. Long-term results of periarterial sympathectomy. J Hand Surg Am. 2009;34(8):1454–1460.
7. Bogoch ER, Gross DK. Surgery of the hand in patients with systemic sclerosis: outcomes and considerations. J Rheumatol.
2005;32(4):642–648.
Exposure and Open Surgical Reconstruction in the
Chapter 12 Chest: The Thoracoabdominal Aorta
Germano Melissano Efrem Civilini Enrico

Rinaldi Roberto Chiesa
DEFINITION
■
A thoracoabdominal aortic aneurysm (TAAA) involves the aorta at the diaphragmatic crura and
extends variable distances proximally and/or distally from this point (FIG 1).1 TAAAs can be
classified in terms of their causes, the two most common being medial degeneration and
dissection.
■
Open treatment of TAAAs consists of graft replacement with reattachment of the main aortic
branches: The inclusion technique was introduced by S. E. Crawford in the 70s and refined by
subsequent surgeons in the following decades. TAAA repair, especially in extensive aortic
disease, is associated with greater operative risk than repair of other aortic segments. The main
sources of morbidity are spinal cord (SC) ischemia and renal as well as respiratory and cardiac
complications.
■
Experienced surgical centers now report lower mortality and morbidity rates for TAAA repair,2
largely due to multimodal approaches to reduce surgical trauma and maximize organ protection.3

■
To plan the best possible treatment strategy for each patient, our preferred modality is computed
tomographic arteriography (CTA). The acquisition of computed tomography (CT) data in
particular has benefited from spectacular progress, including multirow detectors, higher rotation
and translation speeds with reduced scan times (single breath-hold), cardiac cycle
synchronization, and better postprocessing capabilities.
■
Digital Imaging and Communications in Medicine (DICOM) slices of adequate thickness (≤1 mm)
should be postprocessed on a digital workstation using a multiplanar reformatting (MPR) tool to
visualize a scan which angulation matches that of the aorta or the vessel under investigation.
Postprocessing may be performed on a dedicated workstation (AquariusNet®, TeraRecon, Inc) or
desktop computer with open source software (OsiriX and others) in a user-friendly and
time/resources-efficient way (FIG 2).
■
Beyond analysis of aortic diameter and the extent of pathologic involvement, reformatted images are
particularly useful for evaluating the presence, extension, and characteristics of dissection and
thrombus, particularly at proposed sites of clamp placement and the infradiaphragmatic aorta when
direct aneurysm cannulation is considered for distal aortic perfusion. The exact location and
geometry of aortic branches is obtained to reveal possible anatomic variations or anomalies,
which are particularly common at the level of the renal arteries and arch vessels. Vessel patency is
also routinely evaluated; in particular, obstruction of the superior and inferior mesenteric artery
and the hypogastric arteries and dominance of one vertebral artery are assessed.
■
Three-dimensional rendering tools such as maximum intensity projection (MIP), volume rendering,
surface rendering, and so forth produce realistic imaging of the anatomic structures that may
expand anatomic understanding, including, for instance, the most appropriate intercostal space to
perform thoracotomy (FIG 3).
■
Perioperative SC ischemia may precipitate paraparesis or paraplegia. Prior knowledge of the SC
arterial supply informs both procedural planning and risk stratification. Recent advances in
imaging techniques, especially noninvasive techniques, increased the likelihood that patient-
specific risk criteria may soon be recognized and be widely available4 (FIG 4).
SURGICAL MANAGEMENT
Preoperative Workup and Patient Optimization
■
Preoperative transthoracic echocardiography is a satisfactory noninvasive screening method to
evaluate both valvular and biventricular function. Stress testing identifies patients who require
coronary catheterization and possible intervention.5 Electrocardiographically (EKG) gated CT has
recently emerged as a less invasive method of visualizing coronary anatomy. For severe,
symptomatic coronary disease requiring percutaneous transluminal angioplasty prior to aneurysm
repair, use of drug-eluting stents requiring prolonged double antiplatelet therapy should be
avoided to reduce subsequent perioperative bleeding.
■
The use of estimated glomerular filtration rate (eGFR), rather than serum creatinine levels alone, is
recommended to assess renal function.6 Based on the eGFR metric, chronic kidney disease has
been shown to be a strong predictor of death following open or endovascular thoracic aneurysm
repair, even in patients without other clinical evidence of preoperative renal disease.7
Pulmonary function evaluation with arterial blood gases and spirometry is used to evaluate the
respiratory reserve of all patients undergoing open surgery of the descending aorta. In patients
with a forced expiratory volume in 1 second (FEV1) of less than 1 L and a partial pressure of
carbon dioxide (PCO2) greater than 45 mmHg, operative risk may be improved by cessation of
cigarette smoking, treatment of chronic bronchitis (if present), weight loss, and participation in a
supervised exercise program for a period of up to 6 months prior to surgery. However, in patients
with aneurysm-related symptoms, this type of respiratory rehabilitation may not be practical or
possible.
Positioning
■
After inserting a cerebrospinal fluid drainage (CSFD)8 catheter into the subarachnoid space
between L2 and L3 or L3 and L4 (FIG 5), the patient is turned to a right lateral decubitus position,
with the shoulders at 60 degrees and the hips flexed back to 30 degrees.
■
Preparation should allow for access to the entire left thorax, abdomen, and both inguinal regions.
Patient position is maintained with a moldable beanbag attached to a suction line for vacuum
creation. A circulating water mattress is placed between the beanbag and the patient in order to
modify body temperature as necessary (FIG 6).
TECHNIQUES
THORACO-PHRENO-LAPAROTOMY
■
The thoracic incision varies in length and level, depending on exposure requirements. Usually, the
5th, 6th, or 7th intercostal space is employed according to the aneurysm anatomy. The posterior
section of the ribs is gently spread to reduce thoracic wall trauma and fractures; anterolaterally, the
incision curves gently as it crosses the costal margin to minimize subsequent tissue necrosis. The
pleural space is entered after single right lung ventilation is initiated. Monopulmonary ventilation
is maintained throughout thoracic aorta replacement (FIG 7).
■
Paralysis of the left hemidiaphragm contributes significantly to postoperative respiratory failure;
therefore, a limited circumferential rather than radial section of the diaphragm is routinely
performed, sparing the phrenic center. Under favorable anatomic conditions, this approach reduces
respiratory weaning time9 (FIG 8).
■
Special care must be taken when isolating the proximal aneurysm neck. The insertion of a large
caliber esophageal probe makes it easier to distinguish the esophagus at this level. The vagus
nerve and the origin of the recurrent laryngeal nerve must also be identified because they can also
be damaged during isolation and clamping maneuvers (FIG 9). Identification and clipping of some
“high” intercostal arteries can sometimes facilitate the preparation for the proximal anastomosis,
thus reducing aortic bleeding.
■
The upper abdominal aortic segment is exposed via a transperitoneal approach; after entering the
peritoneum, medial visceral rotation is performed to retract the left colon, spleen, and left kidney
anteriorly and to the right (FIG 10). Use of a transperitoneal approach allows direct assessment of
the abdominal organs at the end of procedure. Extra care must be taken to avoid damage to the
spleen, which is particularly prone to bleeding after capsular injuries regardless of size.
DISTAL AORTIC PERFUSION

■
Cross-clamping of the descending thoracic aorta produces immediate and significant increases in
left ventricular afterload, myocardial oxygen consumption, and visceral and renal ischemia.
Techniques incorporating distal aortic perfusion with left heart bypass (LHBP) have significantly
improved outcomes in thoracic aortic surgery.10 In preparation for LHBP and aortic cross-
clamping, low-dose intravenous heparin is administered. If cessation of pump support is
anticipated during the case, additional heparin should be administered at that time to provide full
anticoagulation.
■
The upper left pulmonary vein is usually cannulated for inflow of oxygenated blood, which is routed
through a centrifugal pump (Bio-Medicus®) into the left femoral artery (FIG 11). A “Y” connector
included in the circuit provides two occlusion/perfusion catheters (9 Fr) for selective visceral
perfusion when necessary.
AORTIC REPAIR
■
Once the neck of the TAAA is isolated and controlled between clamps, the descending thoracic
aorta is transected and separated from the esophagus (FIG 12). The graft is sutured proximally to
the descending thoracic aorta using 2-0 polypropylene suture in a running fashion. The anastomosis
is reinforced with Teflon felt (individual pledgets or single strip) (FIG 13). An additional aortic
clamp is applied onto the abdominal aorta above the celiac axis before the proximal aortic clamp
is removed (sequential cross-clamping).
■
Intercostal artery reimplantation into the aortic graft plays a critical role in SC protection. Patent
intercostal arteries from T7 to L2 are temporarily occluded to prevent back-bleeding/maximize
cord perfusion pressure11 then selectively reattached to the graft by means of aortic patch or graft
interposition (FIG 14). When ready, the distal clamp is moved below the renal arteries, and the
aneurysm is opened across the diaphragm. The centrifugal pump maintains visceral perfusion (400
mL per minute) following insertion of the 9-Fr irrigation-perfusion catheters (LeMaitre Vascular)
into the celiac trunk and the superior mesenteric artery. Cold perfusion of Custodiol12 (histidine-
tryptophane-ketoglutarate) is directed into the renal arteries (FIG 15). For visceral artery
reimplantation, a fenestration is created in the graft and the visceral vessels are reattached as a
single patch. Usually, the left renal artery is reconnected with an 8-mm polyester interposition
graft. If visceral artery orificial stenosis is encountered, before placing the irrigation perfusion
catheter, the stenosis may be resolved by direct placement of an appropriate-sized balloon-
expandable stent within the artery13 (FIGS 16 and 17). If creation of the visceral patch requires
retaining a large segment of native aorta, we prefer to place a multibranched graft instead. This
prosthesis, although somewhat more time consuming, significantly reduces the risk of recurrent
aortic patch aneurysm (FIG 18). Finally, the distal end-to-end anastomosis with the distal aorta is
performed, the graft flushed, and clamps removed (FIG 19).
CLOSURE
■
The entire aortic repair (FIG 20) is inspected. All exposed aortic branch pulses are palpated after
derotation and replacement of the abdominal viscera. Any bleeding or kinking of the aortic
branches is addressed at this juncture. The atrial and femoral cannulae are removed; the purse-
string sutures are tied and reinforced. Anticoagulation is reversed with protamine. The crus of the
diaphragm is reapproximated to restore the aortic hiatus (FIG 21) and the left hemidiaphragm
loosely sutured with a running polypropylene suture. The left lung is temporarily inflated to check
for air leakage.
■
A closed-suction abdominal drain is placed next to the aortic graft in the left retroperitoneal space,
and two chest tubes are placed in the posteroapical and basal pleural space. Absorbable pericostal
sutures are placed to approximate the ribs (FIG 22), and two steel wires are used to stabilize the
costal margin. The lung is inflated, and the correct expansion of all the segments is carefully
checked; the pericostal and diaphragmatic sutures are tightened and ligated. The steel wires are
twisted and buried in the cartilaginous costal margin. The abdominal fascia is closed with a
running suture. The abdominal and thoracic drains are connected to suction. The serratus and
latissimus dorsi muscles are approximated with separate absorbable sutures. Subdermal layer is
sutured, and the skin is closed with staples (FIG 23).
PEARLS AND PITFALLS

Indications ■ Aortic diameter and aneurysm morphology
■ Signs and symptoms of acute aortic syndrome
Preoperative planning ■ Level of intercostal incision
■ Graft selection
■ Identification of accessory renal arteries and other visceral
anomalies (e.g., horseshoe kidney)
■ Potential need for multibranch graft vs. Carrel patch
Surgical access ■ Avoid skin flap necrosis.
■ Rib section
■ Limited phrenotomy (circumferential diaphragmatic incision)
■ Transperitoneal approach
■ Careful and limited lung manipulation
■ Nonocclusive femoral cannulation
Technical adjuncts for organ ■ Spinal cord drainage
protection ■ Left heart bypass
■ Sequential aortic clamping
■ Critical intercostal artery reattachment
■ Visceral perfusion from left heart bypass cannulas
■ Renal perfusion with cold Custodiol® or similar solution
■ Direct stenting of renal and visceral orificial lesions as needed
POSTOPERATIVE CARE
■
The main focus of immediate postoperative management is the early detection of neurologic or
cardiovascular complication as prompt intervention may prevent substantial long-term morbidity.
As soon as baseline blood pressure and body temperature are restored, sedation is lightened
regardless of ventilatory status. When SC or cerebral neurologic injury is suspected, CT imaging
is performed immediately to address the possibility of intracranial or intradural SC hematoma. In
case of paraparesis or paraplegia, mean arterial pressure is chemically maintained above 80
mmHg, CSFD is drained in order to lower the cerebrospinal fluid pressure below 10 mmHg, and
methylprednisolone (1 g bolus followed by 4 g per 24 hours continuous infusion) and 18%
mannitol (5 mg/kg, four times a day) are administrated.
■
If malperfusion develops in the lower limbs, renal or visceral circulation, efforts should be made to
restore normal circulation immediately. For a precise visualization of visceral organ perfusion,
emergency arteriography (catheter-based or CT) is required.
■
Blood pressure fluctuations, including recalcitrant hypertension, is common in the early
postoperative period, especially in the chronically hypertensive patient; prompt attention should
be paid to regulating the mean arterial pressure in a physiologic range. Immediate intervention may
be required to reduce the risk of anastomotic bleeding, especially in the setting of dissection.
■
In uncomplicated cases, drainage tubes are removed at 36 to 48 hours postoperatively, whereas the
intrathecal CSFD catheter is removed usually after 72 hours. A prolonged requirement for
ventilatory support is not unusual, especially after emergency operations, in patients with
significant blood loss and after longer periods of circulatory arrest (if necessary for concurrent
arch or ascending aortic reconstruction). In case of severe chronic kidney disease, transient
temporary renal replacement therapy may also be necessary in the early postoperative period.
COMPLICATIONS
■
Bleeding
■
Multiorgan failure
■
Dialysis
■
Paraplegia
■
Stroke
■
Death
■
Aneurysm recurrence
REFERENCES
1. Johnston KW, Rutherford RB, Tilson MD, et al. Suggested standards for reporting on arterial aneurysms. Subcommittee on
Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and North
American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg. 1991;13:452–458.
2. Coselli JS, Bozinovski J, LeMaire SA. Open surgical repair of 2286 thoracoabdominal aortic aneurysms. Ann Thorac Surg.
2007;83:S862–S864.
3. MacArthur RG, Carter SA, Coselli JS, et al. Organ protection during thoracoabdominal aortic surgery: rationale for a multimodality
approach. Semin Cardiothorac Vasc Anesth. 2005;9:143–149.
4. Melissano G, Civilini E, Bertoglio L, et al. Angio-CT imaging of the spinal cord vascularisation: a pictorial essay. Eur J Vasc
Endovasc Surg. 2010;39:436–440.
5. Kieffer E, Chiche L, Baron JF, et al. Coronary and carotid artery disease in patients with degenerative aneurysm of the descending
thoracic or thoracoabdominal aorta: prevalence and impact on operative mortality. Ann Vasc Surg. 2002;16:679–684.
6. 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.
7. Mills JL Sr, Duong ST, Leon LR Jr, et al. Comparison of the effects of open and endovascular aortic aneurysm repair on long-term
renal function using chronic kidney disease staging based on glomerular filtration rate. J Vasc Surg. 2008;47:1141–1149.
8. Cina CS, Abouzahr L, Arena GO, et al. Cerebrospinal fluid drainage to prevent paraplegia during thoracic and thoracoabdominal
aortic aneurysm surgery: a systematic review and meta-analysis. J Vasc Surg. 2004;40:36–44.
9. Engle J, Safi HJ, Miller CC III, et al. The impact of diaphragm management on prolonged ventilator support after thoracoabdominal
aortic repair. J Vasc Surg. 1999;29(1):150–156.
10. Coselli JS. The use of left heart bypass in the repair of thoracoabdominal aortic aneurysms: current techniques and results. Semin
Thorac Cardiovasc Surg. 2003;15:326–332.
11. Etz CD, Homann TM, Plestis KA, et al. Spinal cord perfusion after extensive segmental artery sacrifice: can paraplegia be
prevented? Eur J Cardiothorac Surg. 2007;31(4):643–648.
12. Schmitto JD, Fatehpur S, Tezval H, et al. Hypothermic renal protection using cold histidine-tryptophan-ketoglutarate solution
perfusion in suprarenal aortic surgery. Ann Vasc Surg. 2008;22(4):520–524.
13. LeMaire SA, Jamison AL, Carter SA, et al. Deployment of balloon expandable stents during open repair of thoracoabdominal aortic
aneurysms: a new strategy for managing renal and mesenteric artery lesions. Eur J Cardiothorac Surg. 2004;26:599–607.
Thoracic Aortic Stent Graft Repair for Aneurysm,
Chapter 13 Dissection, and Traumatic Transection
Brant W. Ullery Jason T. Lee
DEFINITION
■
In 1994, Dake and colleagues,1 at Stanford University, were the first to report the use of custom-
designed thoracic aortic stent grafts for the treatment of descending thoracic aortic aneurysms in
patients deemed high risk for conventional open surgery. Each of these devices was deployed
through peripheral arterial access, successfully excluding the aneurysm from systemic
pressurization. This groundbreaking minimally invasive technique thereby avoided many of the
physiologic insults associated with open surgery, including the need for thoracotomy, aortic cross-
clamping, reperfusion injury, and acute hemodynamic changes.
■
Results from the first multicenter U.S. Food and Drug Administration–sponsored trial for thoracic
aortic stent grafts demonstrated significantly less perioperative mortality, respiratory failure, renal
insufficiency, and spinal cord ischemia in patients after thoracic endovascular aortic repair
(TEVAR) compared to a matched cohort of patients undergoing open descending thoracic aortic
aneurysm repair.2
■
After two decades of surgeon experience and endovascular technologic advancement, TEVAR has
evolved to serve as a primary treatment strategy for an increasingly diverse group of acute and
chronic aortic pathologies including thoracic aortic aneurysms, dissections, and traumatic
transections.
■
Depending on the type and extent of pathology, TEVAR may include the use of fenestrated or
branched stent grafts, advanced snorkel/chimney/periscope techniques, or the need for hybrid
debranching procedures. The decision to treat thoracic aortic pathology with stent grafts is based
on individual patient comorbidity burden, detailed analysis of thoracic aortic anatomy, and
physician experience.
■
Acute thoracic aortic pathologies often present with chest pain and therefore must be considered in
the workup for acute coronary syndrome. The ubiquitous use of computed tomography (CT)
scanning for pain, shortness of breath, trauma, and to “rule out” many pathologies has led to an
increase in the recognition of thoracic aortic pathology potentially benefitting from TEVAR
technology.

■
Thoracic aortic aneurysms (TAAs) are defined as localized or diffuse dilation of 50% or more
relative to the diameter of the adjacent normal-sized aorta. Common risk factors for aneurysmal
degeneration include smoking, hypertension, chronic obstructive pulmonary disease,
atherosclerosis, and connective tissue diseases. Indications for repair of descending TAAs are
similar to those for conventional open repair: maximum aortic diameter greater than 6 cm, rapid
aneurysmal growth (>5 mm of growth over 6 months), or symptoms such as persistent chest or
back pain, rupture, or dissection. In most patients with TAA, the aneurysms were diagnosed
following routine imaging ordered for other reasons and are therefore most commonly
asymptomatic.
■
Aortic dissection occurs when an intimal tear in the aorta causes blood to flow between the layers
of the wall of the aorta and most often presents as tearing chest pain that radiates to the back.
Potential etiologic factors leading to aortic dissection include poorly controlled hypertension,
connective tissue disorders, trauma, or vasculitis. Medical management of uncomplicated type B
thoracic aortic dissection serves as the current standard of care. These practice guidelines stem
from the results of the INvestigation of STEnt grafts in patients with type B Aortic Dissection
(INSTEAD) trial, the first prospective, multicenter randomized trial comparing optimal medical
therapy (e.g., blood pressure control) to TEVAR for uncomplicated type B dissection.3 This trial
demonstrated no significant improvement in 2–year survival or adverse event rates with TEVAR
despite favorable aortic remodeling, although recently reported 5-year data suggest improved
long-term survival in patients undergoing TEVAR. In contrast, for patients with complicated type
B dissections involving rupture, malperfusion (e.g., visceral or limb ischemia), or refractory back
pain despite optimal medical management, TEVAR is indicated. The goal of TEVAR in this setting
is to cover, or exclude, the primary entry tear and reexpand the true lumen while promoting
thrombosis of the false lumen.
■
Traumatic aortic transection results from a high-velocity or deceleration injury to the aorta. The
tethering of the aorta by the ligamentum arteriosum makes this site most susceptible to shearing
forces during sudden deceleration. A high index of suspicion is necessary to help make the
diagnosis. Trauma workups most often involve whole-body CT scanning, which allows rapid
triage for possible treatment. CT-A commonly demonstrates an irregular outpouching beyond the
takeoff of the left subclavian artery at the aortic isthmus, which corresponds to the presence of an
aortic pseudoaneurysm caused by the traumatic event. Extent of blunt traumatic aortic injury and
the corresponding physiologic insult may range from clinically occult intimal injury to life-
threatening complete transection and rupture (FIG 1).4 Early diagnosis and endovascular treatment
is generally recommended for those presenting with a traumatic aortic transection, particularly
when there is a contour abnormality visualized on cross-sectional imaging.

■
Transesophageal echocardiography (TEE) may serve as a useful imaging tool, particularly in the
setting of acute thoracic aortic pathology. TEE can confirm the presence of aortic dissection,
distinguish between types A and B dissections, identify involvement of supra-aortic vessels, and
assess for contained rupture.
■
High-resolution computed tomography angiography (CT-A) with three-dimensional reconstructive
software allows for the most complete anatomic analysis, including details regarding aneurysm
morphology, diameter, dissection flap characterization, thrombus burden, calcification, angulation,
and branch vessel orientation.
■
Familiarity and routine usage of three-dimensional workstations and the ability to customize
measurements provide an accurate road map to guide endovascular strategy, device selection, and
stent graft sizing.
SURGICAL MANAGEMENT
■
Patients scheduled for elective TEVAR undergo routine preoperative cardiac evaluation. Based on
cardiovascular risk profile, symptomatology, and presence of electrocardiogram abnormalities,
selected patients undergo further evaluation in the form of an exercise stress test, dobutamine
stress echocardiography, or Persantine thallium stress testing. Coronary angiography is pursued in
cases involving extensive or symptomatic coronary artery disease.
■
Aortic transections or symptomatic dissections and aneurysms should have early and aggressive
blood pressure control using intravenous beta-blocker or calcium channel blocker medications.
After obtaining a reliable clinical examination, refractory chest, back, or abdominal pain should
be treated with narcotic analgesics.
■
Renal protective strategies should be employed preoperatively to minimize the risk of contrast-
induced nephropathy. Intravenous hydration is initiated preoperatively and, in the setting of
baseline renal insufficiency, may warrant early hospital preadmission and concomitant
administration of Mucomyst and bicarbonate infusion.
■
Suspected blunt aortic injury should prompt a referral to a level I trauma center in order to facilitate
early evaluation by a vascular specialist and other pertinent members of a multidisciplinary trauma
team.
■
General anesthesia is routinely performed in TEVAR cases. Prophylactic lumbar cerebrospinal
fluid (CSF) drainage is considered in every case based on the relative risk of spinal cord
ischemia, hemodynamic status, and acuity of clinical presentation. Arterial monitoring is
performed via a right radial artery approach. Peripheral intravenous lines are typically adequate;
however, more intensive central venous monitoring may be required in cases involving unstable
traumatic transections, patients with significant baseline cardiovascular comorbidities, or any case
involving hemodynamic instability.
■
Preoperative imaging should be heavily scrutinized for the adequacy of iliofemoral access anatomy.
An iliac conduit may be required in cases involving small-caliber, tortuous, or heavily calcified
access vessels. Anticipated use of a conduit should prompt consideration of an autotransfusion or
cell saver machine to be available during the procedure.
■
Numerous variables have been identified as risk factors for the development of spinal cord ischemia
after TEVAR. Given that hypoperfusion represents the primary etiology of spinal cord injury
following TEVAR, commonly cited risk factors involve those relating to the extent of impairment
or exclusion of the collateral perfusion to the spinal cord. The European Collaborators on
Stent/Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) investigators reported results
from the largest multicenter registry to date (N = 606).5 In the EUROSTAR registry, the incidence
of spinal cord ischemia was 2.5% and independent risk factors included left subclavian artery
coverage without revascularization (odds ratio [OR], 3.9; p = .037), concomitant open abdominal
aortic surgery (OR, 5.5; p = .037), and the use of three or more stent grafts (OR, 3.5; p = .043).
■
Based on the principle that spinal cord perfusion pressure is approximated by the difference
between the mean arterial pressure (MAP) and CSF pressure, placement of a prophylactic lumbar
drain has the potential to increase spinal cord perfusion pressure by decreasing CSF pressure and
may be beneficial in select patients at high risk for spinal cord ischemia. Percutaneous drainage of
CSF is performed by inserting a silastic catheter 10 to 15 cm into the subarachnoid space through a
14-gauge Tuohy needle at the L3–L4 vertebral interspace. The open end of the catheter is attached
to a sterile closed circuit reservoir and the lumbar CSF pressure is measured with a pressure
transducer zero-referenced to the midline of the brain. Lumbar CSF can be drained continuously or
intermittently in the operating room to achieve target CSF pressures of 10 to 12 mmHg.
Postoperatively, intermittent or continuous CSF drainage can be continued in the intensive care
unit for CSF pressures exceeding 10 mmHg or at the first sign of lower extremity weakness. In the
absence of neurologic deficits, the lumbar CSF drainage catheter can be clamped 24 hours
postprocedure followed by continued monitoring of CSF pressure together with serial neurologic
assessments. The CSF drain can then be removed at 48 hours after operation. Although
prophylactic or therapeutic lumbar CSF drainage has an established record of safety,
complications have been reported to occur in approximately 1% of patients, which may include
neuraxial hematoma, subdural hematoma, catheter fracture, meningitis, intracranial hypotension,
chronic CSF leak, and spinal headache.
Selection and Sizing of Thoracic Stent Graft
Landing zones
■
Proximal and distal landing zones must be of sufficient length (usually at least 2 cm) to enable safe
and accurate deployment bracketing the area of thoracic aortic pathology, which often includes the
subclavian artery proximally or the celiac artery distally.
■
Intentional coverage of the left subclavian artery is sometimes required due to a very proximal
extent of aortic pathology, especially transections. Left subclavian artery revascularization may be
required in select cases. The celiac artery rarely requires intentional coverage.
■
Significant tortuosity, circumferential mural thrombus, and extensive calcification can compromise
the proximal or distal landing zone, thereby predisposing to inadequate fixation and subsequent
development of endoleak or migration. Site of proximal and distal landing zones should be
selected in order to minimize the impact of these anatomic features, even if it requires extending
the length of aortic coverage.
■
A variety of anatomic measurements are taken from preoperative CT-A imaging to assist in the
sizing and selection of the thoracic stent graft (FIG 2). Interventionalists should be proficient in
accurate sizing and measuring of key thoracic aortic locations that influence device selection and
ultimately determine patient outcomes.
Sizing of stent grafts

■
The degree of stent graft oversizing can vary based on the indication for intervention. Stent grafts are
generally oversized by 10% to 20% based on the aortic diameter at the proximal and distal
fixation sites for aneurysmal disease. Insufficient oversizing for the treatment of TAAs may
predispose to inadequate exclusion and the potential for endoleak or migration. Aggressive
oversizing, on the other hand, increases the risk for stent graft collapse, graft thrombosis, access
arterial injury, and potential for peri- or postprocedural iatrogenic retrograde type A dissection.
■
Chronic type B dissections are frequently characterized by a thick, nonmobile dissection flap, or
septum, that separates true and false lumens into concave or convex discs of flow lumen. Such
dissection flaps have limited compliance; therefore, minimal or no oversizing may be required in
order to achieve a suitable proximal or distal seal.
■
Aortic transections frequently occur in young trauma patients with normal or minimally diseased
aortas. As such, minimal oversizing is needed to achieve an adequate seal and only recently did
device manufacturers create devices meant for smaller diameter aortas. Note also that under-
rescucitated patients on admission will have smaller aortic diameters on their CT-A.
■
Currently available stent grafts range in diameter from 22 to 46 mm. Given the traditional 10% to
20% rule of device oversizing, these devices are designed to safely treat aortas with landing zones
ranging from 19 to 43 mm in diameter.
Access vessel anatomy
■
Current thoracic aortic stent grafts require large-caliber delivery systems, ranging from 18 to 26 Fr
in outer diameter. Small, tortuous, and heavily calcified iliofemoral arteries may prohibit sheath
advancement and predispose to access site–related complications, including groin hematoma,
dissection, or rupture.
■
Careful evaluation of access vessel anatomy on preoperative imaging should be performed in order
to assess the caliber, tortuosity, thrombus burden, and extent of calcification of the iliofemoral
arteries. Such anatomic information will serve as the basis for deciding laterality of femoral
access as well as to determine the need for an iliac conduit.
■
Serial dilation may be attempted for patients with small iliofemoral vessels. Iliac atherosclerotic
lesions may be pretreated with balloon angioplasty and/or stent grafting in order to facilitate
sheath advancement and introduction of the thoracic stent graft components.
■
Iliac conduits serve as a safe and reliable technique to circumvent issues related to suboptimal
access vessel anatomy. From either flank incision, a retroperitoneal exposure provides
visualization of the common iliac artery or distal abdominal aorta. A 10- or 12-mm Dacron graft is
commonly used as the conduit of choice. The conduit can be modified by creating a patch at the
distal end in order to further facilitate the delivery of large-caliber sheath and enable additional
degrees of torqueability (FIG 3). This modification involves creating a patch by cutting the
Dacron graft along its long access, thereby enlarging the transition zone from the graft to artery.
TECHNIQUES
EARLY PROCEDURAL CONSIDERATIONS

Positioning
■
The C-arm is typically configured in the “head” position. The left arm may be abducted to 75 to 90
degrees and circumferentially prepped into the field if an embolization or snorkel/chimney
procedure involving the left subclavian artery is anticipated. The chest, abdomen, and bilateral
groins should be prepped. As frequently only one groin access is required for the performance of a
routine TEVAR, laterality of the operator position may vary based on surgeon preference or
anticipated access site location.
Establishing Vascular Access
■
The ipsilateral femoral artery is accessed either percutaneously or from an open exposure.
Secondary access may be obtained from the contralateral femoral artery or brachial artery as
needed for a 5-Fr sheath and flush catheter. Surgical exposure is obtained from a small oblique
incision at the level of the inguinal ligament. The common femoral artery is exposed, with
proximal control obtained at the level of the external iliac artery and distal control at the level of
the femoral bifurcation or proximal superficial femoral and profunda femoral arteries. Heavy
calcification may require preemptive endarterectomy and patch angioplasty in order to facilitate
safe sheath placement.
■
The femoral artery is punctured using a standard micropuncture set, and if arterial access is obtained
percutaneously, a sheathogram is performed to confirm adequate puncture site location (mid–
common femoral artery). A standard length Bentson wire is inserted into the aorta through
micropuncture sheath and exchange for a 7-Fr sheath is then performed using Seldinger technique.
Wire exchange is then done for a 260-cm stiff Lunderquist wire. The Lunderquist wire should have
a flexible, curved proximal end that should be advanced under fluoroscopy across the aortic arch
to abut the aortic value. The location of the distal end of the Lunderquist wire should be marked on
the operating table and this wire position should be maintained throughout the procedure.
■
Over the stiff Lunderquist wire platform, the 7-Fr sheath is removed and serial dilators are
advanced to gradually enlarge the subcutaneous tract and arteriotomy site in order to accommodate
either the stent graft device itself or a larger 18- to 26-Fr introducer sheath required for device
delivery.
■
After placement of the larger sheath, systemic heparin is administered at a dose of 100 units/kg (goal
activated clotting time of >250 seconds). Concomitant traumatic injuries, particularly intracranial
hemorrhage, may alter the dose or decision to administer heparin.
INITIAL AORTOGRAM
■
A 5-Fr 100-cm Omniflush or pigtail catheter is inserted into aorta and advanced to the level of the
aortic arch. This catheter may be advanced via a contralateral 5-Fr sheath or it may be inserted
into an additional ipsilateral 5-Fr sheath placed distal to the arteriotomy for the main body
delivery sheath.
■
If satisfied with stent graft sizing based on available preoperative imaging, the thoracic aortic stent
graft may be advanced over the Lunderquist wire and be positioned in the proximal to midportion
of the thoracic aorta prior to initial aortogram.
■
Optimal angiographic imaging of the aortic arch is obtained by placing the fluoroscopic C-arm in a
left anterior oblique orientation, often 35 to 65 degrees, and can be optimized by referencing the
preoperative CT-A. The location of the supra-aortic vessels, particularly the left subclavian artery,
should be noted and marked on viewing monitors (FIG 4A).
■
Intravascular ultrasound (IVUS) may be used an adjunct in cases involving dissection to assist in the
identification of true and false lumens, as well as to gain additional information on aortic diameter,
branch vessel location, and morphology of proximal and distal landing zones. IVUS also aids in
limiting intravenous contrast exposure in those patients with baseline impaired renal function.
■
If necessary to guide distal extent of stent graft placement, the celiac artery is best imaged from a full
lateral projection. Additional structures to note are large, patent intercostal arteries at the level of
the aortic hiatus. Efforts should be made to avoid covering these if at all possible during the course
of the repair.
Device Deployment
■
Precise proximal positioning of the stent graft is facilitated by either marking the location of the left
subclavian artery on the viewing screen and/or using the road-mapping feature. The distal
radiopaque line of the endotracheal tube seen on fluoroscopy at about 45 degrees left anterior
oblique can sometimes correlate to the position of the left common carotid artery, thereby serving
as a convenient landmark in cases requiring left subclavian artery coverage.
■
Immediately prior to stent graft deployment, systemic arterial blood pressure is reduced below 100
mmHg to reduce risk of caudal migration.
■
The stent grafts are generally deployed in a proximal-to-distal sequence. However, a distal-to-
proximal sequence may be preferred in cases involving precise deployment near the celiac artery
or in aortas with significant diameter taper and a larger proximal landing zone compared to the
distal landing zone (where devices of different diameter may need to be stacked up on each other).
■
Deployed endografts will naturally extend toward the outer curvature of the aorta and precision
deployment is facilitated by gently providing forward traction on the wire toward the outer curve
during deployment. This maneuver also facilitates straightening out of the transverse arch, which
can be helpful in minimizing the “bird-beaking” effect at the proximal graft margin, where the
device may not fully oppose to the “inner” aortic wall. Bird beaking, when present, can predispose
to proximal type I endoleaks, endograft collapse, and potential aortic occlusion.
■
Additional graft components are added, when necessary, by exchanging the first device over the
Lunderquist wire. A minimum overlap of 5 cm between pieces is recommended to ensure adequate
apposition and minimize risk of junctional (type III) endoleak.
Balloon Molding
■
Balloon molding is often required in cases involving TAAs. Under fluoroscopic guidance, a
noncompliant molding balloon (Coda [Cook Medical, Bloomington, IN, USA] or Tri-Lobe [W. L.
Gore, Flagstaff, AZ, USA]) is advanced up to the proximal edge of the stent graft and balloon
molding is performed in a proximal-to-distal sequence. Balloon molding should be performed at
the proximal and distal fixation sites, as well as at areas of stent graft overlap in those cases
requiring multiple stent grafts.
■
Aggressive ballooning can cause component fracture and aortic injury, and care must be taken during
inflation with constant visualization and knowledge of the tension applied to the balloon.
■
Balloon molding is not typically required in cases involving aortic dissection or transection,
particularly in cases where no obvious endoleak is visualized. Balloon molding may increase risk
for iatrogenic retrograde type A conversion if performed in a region of friable or fragile aorta and
is generally not recommended during dissection cases.
COMPLETION AORTOGRAM
■
After stent graft deployment, the pigtail catheter is withdrawn along the outside of the deployed
device(s) over a wire to below the level of the stent graft. The catheter is then readvanced over a
wire within the stent graft lumen and positioned at the level of the aortic arch.
■
Additional aortograms may be performed at this time as necessary in order to ensure adequate stent
graft position and patency of the supra-aortic and celiac arteries and to assess for the presence of
endoleaks.
REMOVAL OF SHEATH AND ARTERIOTOMY CLOSURE

■
In cases involving percutaneous access, the two previously placed Perclose ProGlide devices are
used to close the arteriotomy site(s) (see Chapter 23 for details). If open surgical exposure was
obtained, proximal and distal vascular control is obtained in the respective groin. All wires and
sheaths are removed. The arteriotomy is closed transversely using a polypropylene suture in either
a running continuous or interrupted fashion. Antegrade and retrograde flushing maneuvers should
be performed prior to completion of the arteriotomy closure.
LEFT SUBCLAVIAN ARTERY REVASCULARIZATION

■
Endovascular procedures that require coverage of the left subclavian artery have the potential to
increase the risk of spinal cord injury by compromising blood flow to the ipsilateral vertebral
artery, an important collateral pathway for arterial flow to the anterior spinal artery. Subclavian
artery revascularization therefore serves as an additional strategy to decrease the risk of spinal
cord ischemia in select patients deemed high risk.
■
Techniques to revascularize the left subclavian artery include transposition of the subclavian onto
the left carotid artery or left carotid–subclavian bypass grafting with subsequent embolization of
the left subclavian artery proximal to the bypass graft (FIG 5). These revascularization procedures
may be performed as part of a staged repair or at the time of TEVAR.
■
The existing clinical evidence to support the efficacy of routine left subclavian artery
revascularization remains controversial; there are advocates for routine revascularization,
selective revascularization, or no revascularization. A meta-analysis of published studies showed
a trend toward increased risk of spinal cord ischemia when the left subclavian artery was covered,
suggesting a potential benefit for left subclavian artery revascularization, but the finding was not
statistically significant.4–6
SPECIAL CONSIDERATIONS BASED ON AORTIC PATHOLOGY

Aortic Dissection
■
The primary goal of TEVAR for the treatment of dissection is coverage of the proximal entry tear
(FIG 6A,B). Stent graft sizing is based on the diameter of the adjacent nondissected thoracic aorta.
Minimal or no oversizing of the stent graft is recommended.
■
In acute type B dissections, the septum is relatively mobile and compliant. Therefore, the diameter
of the small true lumen in the dissected portion often returns to normal diameter following
successful exclusion of the proximal entry tear.
■
Chronic dissections have thicker, less compliant septa, which may limit expansion of the true lumen
despite adequate entry tear coverage. Often, these patients have chronic false lumen aneurysmal
dilation, and entry tear and fenestration covering serve simply to decrease false lumen
pressurization and promote thrombosis.
■
IVUS serves as a useful adjunct in dissection cases, both in terms of initial identification of true and
false lumen, as well as assisting in precise positioning of the device.
Aortic Transection
■
Traumatic aortic injuries are typically located along the inner curve of the proximal descending
thoracic aorta (FIG 7). Given the proximal location, left subclavian artery coverage is sometimes
needed.4
■
In the absence of concomitant hemorrhage or brain injury, routine heparin is recommended.
■
Trauma patients are frequently hypovolemic and, as a result, may have an underdistended aorta on
preoperative cross-sectional imaging. Initial cross-sectional imaging can underestimate true aortic
morphology at the region of the subclavian by as much as 10% to 20%. In such settings, IVUS may
assist in more accurate stent graft sizing performed in vivo.7
PEARLS AND PITFALLS

Indications ■ TEVAR follows general recommendations for elective repair of
descending thoracic and thoracoabdominal aortic aneurysms and
should be offered to good anatomic risk patients with aneurysms
>6 cm.
■ Patient selection should take into account the need for regular
interval clinical and radiologic follow-up in order to monitor for
stent graft–related complications and endoleaks.
Preoperative workup ■ High-quality imaging and ability to configure three-dimensional
reconstructive software are essential for successful preoperative
planning and device selection.
■ Pre- and perioperative hydration is a central part in the protection
from contrast-induced nephropathy.
■ Patients should be stratified according to baseline risk of spinal
cord ischemia. A prophylactic lumbar drain should be considered
in those at high risk.
Patient setup ■ A hybrid endovascular suite provides optimal opportunity for
accurate imaging and capability to perform necessary open
surgical exposure or repair of access-related complications.
■ Anticipated adjunct procedures, including left subclavian artery
embolization or revascularization, may require prepping the left
neck and/or arm into the surgical field.
Thoracic aneurysms ■ Oversizing of stent grafts by 10% to 20% and balloon molding is
generally recommended in order to maximize proximal and distal
fixation.
■ Proximal and distal landing zones should be relatively free of
stenosis, calcification, and thrombus to maximize durability of this
minimally invasive technology.
Type B dissection ■ Accurate identification of true and false lumen is essential prior to
deployment of the stent graft. IVUS may be a useful adjunct in this
setting to confirm true or false lumen position.
■ Aggressive oversizing of stent grafts is not recommended in
patients with aortic dissection. Balloon molding is generally
reserved only for those with type I or III endoleak on completion
angiography and not against the region where there is a mobile
septum.
Traumatic transection ■ Routine heparin is recommended unless contraindicated by
concomitant intracranial or solid organ injury.
■ Similar to dissections, aggressive oversizing and balloon molding
is not routinely performed during the treatment of transections.
POSTOPERATIVE CARE
■
Patients are typically extubated immediately following the procedure unless prohibited by
concomitant physiologic insults (e.g., hemodynamic instability, trauma patient).
■
Intensive care unit monitoring is required for patients who require a lumbar drain for 24 to 48 hours.
Immediate and frequent neurologic assessments are critical in the early perioperative period to
assess for spinal cord ischemia. Raising MAP goals are an additional way to minimize risk of
cord ischemia.
■
Durability of TEVAR is reliant on routine imaging to evaluate for stent graft–specific complications
postoperation. Follow-up chest CT-A and plain x-rays are typically obtained at 1, 6, and 12
months and at intervals thereafter. Consideration should be made between balancing risks for
cumulative lifetime iodinated contrast and radiation exposure versus the necessity for serial graft
monitoring. In stable patients, chest x-rays may suffice to confirm device position, with CT
scanning reserved for those with migration suggested by CT or evidence of progressive aortic
enlargement or onset of recurrent symptoms such as chest pain.
OUTCOMES
■
The largest published series, which has reported 1-year follow-up, included 443 patients treated
with TEVAR for a variety of indications, both emergent and elective, as follows: TAA (n = 249),
thoracic aortic dissection (n = 131), traumatic aortic injury (n = 50), and false anastomotic
aneurysm (n = 13).8 Technical success was achieved in nearly 90% of patients, with an all-cause
mortality among patients treated for aortic aneurysm and aortic dissection of 20% and 10%,
respectively.
■
No randomized trials comparing TEVAR to open surgery have been published to date. However,
multiple nonrandomized comparisons suggest equivalent or better outcomes with TEVAR. In a
single-center, retrospective study of over 700 patients who underwent either TEVAR or open
surgery, mortality was not significantly different at 30-day (5.7% vs. 8.3%, respectively) or 1-year
(15.6% vs. 15.9%, respectively) follow-up.9 Two smaller studies demonstrated a reduction in 30-
day perioperative mortality with TEVAR compared with open surgery (1.9% vs. 5.7%).10,11
COMPLICATIONS
■
Stroke continues to be a common complication following TEVAR and is associated with significant
in-hospital mortality. Recent clinical series have reported an incidence of stroke after TEVAR to
range from 2% to 8%.12,13 The underlying mechanisms contributing to acute ischemic stroke after
TEVAR and the temporal relationship of stroke to the procedure are not completely understood.
However, the constellation of preoperative risk factors, neurologic examinations, and patterns of
brain infarction observed in these patients has led most investigators to conclude that cerebral
embolization and ischemic events are the primary mechanisms for perioperative stroke in
TEVAR.5,13,14 Embolic events are related to instrumentation of the aortic arch in patients with
severe atheromatous disease, whereas ischemia is a result of the planned or inadvertent
endovascular coverage of supra-aortic vessels.
■
Spinal cord ischemia and subsequent acute or delayed paraplegia represents the most devastating
complication of TEVAR. The pathogenesis of spinal cord injury after TEVAR is likely
multifactorial but still poorly understood. The deployment of thoracic stent grafts results in rapid
complete exclusion of varying lengths of segmental collateral vessels without the ability to
surgically reimplant or revascularize the intercostal arteries. Stent deployment and catheter
manipulation can predispose patients to dislodgement of thrombotic or atheromatous debris from
the aortic wall into segmental vessels, with subsequent distal embolization and occlusion of
arteries supplying the spinal cord. Moreover, endovascular coverage of the left subclavian artery
may compromise spinal cord perfusion in patients with a dominant left vertebral artery, solitary
vertebral artery, carotid artery disease, or an incomplete circle of Willis. Access site injuries to
the iliofemoral vessels may further increase the risk of spinal cord ischemia by compromising
collateral flow to the anterior spinal artery through the hypogastric and pelvic vascular plexus.
Lastly, pharmacologic measures aimed at decreasing arterial blood pressure to enhance accuracy
of device deployment in cases involving difficult aortic anatomy may lead to hypotension similar
to that observed in open surgery.
■
Due to the large sheath sizes required for the delivery of thoracic stent grafts, small-diameter,
tortuous, or heavily calcified access vessels can predispose to iliofemoral arterial injury.
Postoperative CT-A often documents arterial dissections and injury that can be followed with
noninvasive duplex and managed expectantly until patients have claudication-like symptoms.
■
Endoleaks are a relatively common finding after TEVAR, affecting nearly 15% of patients in the
early or late postoperative periods. Type I or III endoleaks typically require additional stent
placement or balloon molding in order to improve proximal, distal, or junctional fixation. Most
type II endoleaks observed on completion angiogram or early follow-up cross-sectional imaging
will resolve spontaneously. Persistent type II endoleaks, especially those with aneurysm sac
expansion or failure to adequately seal a proximal entry tear or transection, warrant additional
intervention. Retrograde flow from intercostal or left subclavian arteries can be treated using coil
embolization or vascular plug placement.
REFERENCES
1. Dake MD, Miller DC, Semba CP, et al. Transluminal placement of endovascular stent-grafts for the treatment of descending
thoracic aortic aneurysms. N Engl J Med. 1994;331:1729–1734.
2. Bavaria JE, Appoo JJ, Makaroun MS, et al. Endovascular stent grafting versus open surgical repair of descending thoracic aortic
aneurysms in low-risk patients: a multicenter comparative trial. J Thorac Cardiovasc Surg. 2007;133:369–377.
3. 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.
4. Lee WA, Matsumura JS, Mitchell RS, et al. Endovascular repair of traumatic aortic injury: clinical practice guidelines of the Society
for Vascular Surgery. J Vasc Surg. 2011;53:187–192.
5. Buth J, Harris PL, Hobo R, et al. Neurologic complications associated with endovascular repair of thoracic aortic pathology:
incidence and risk factors. A study from the European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair
(EUROSTAR) registry. J Vasc Surg. 2007;46:1103–1110.
6. Rizvi AZ, Murad MH, Fairman RM, et al. The effect of left subclavian artery coverage on morbidity and mortality in patients
undergoing endovascular thoracic aortic interventions: a systematic review and meta-analysis. J Vasc Surg. 2009;50:1159–1169.
7. Pearce BJ, Jordan W. Using IVUS during EVAR and TEVAR: improving patient outcomes. Semin Vasc Surg. 2009;22:172–180.
8. Leurs LJ, Bell R, Degrieck Y, et al. Endovascular treatment of thoracic aortic diseases: combined experience from the
EUROSTAR and United Kingdom Thoracic Endograft registries. J Vasc Surg. 2004;40:670–679.
9. Greenberg RK, Lu Q, Roselli EE, et al. Contemporary analysis of descending thoracic and thoracoabdominal aneurysm repair: a
comparison of endovascular and open techniques. Circulation. 2008;118:808–817.
10. 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(2):247–257.
11. Bavaria JE, Appoo JJ, Makaroun MS, et al. Endovascular stent grafting versus open surgical repair of descending thoracic aortic
aneurysms in low-risk patients: a multicenter comparative trial. J Thorac Cardiovasc Surg. 2007;133:369–377.
12. Feezor RJ, Martin TD, Hess PJ, et al. Risk factors for perioperative stroke during thoracic endovascular aortic repairs (TEVAR). J
Endovasc Ther. 2007;14:568–573.
13. Gutsche JT, Cheung AT, McGarvey ML, et al. Risk factors for perioperative stroke after thoracic endovascular aortic repair. Ann
Thorac Surg. 2007;84:1195–1200.
14. Fattori R, Nienaber CA, Rousseau H, et al. Results of endovascular repair of the thoracic aorta with the Talent Thoracic stent graft:
the Talent Thoracic Retrospective Registry. J Thorac Cardiovasc Surg. 2006;132:332–339.
Exposure and Open Surgical Management at the
Chapter 14 Diaphragm
Peter H. U. Lee Ramin E. Beygui
DEFINITION
■
Thoracoabdominal aneurysms and complicated descending aortic dissections are the two most
likely reasons for requiring surgical exposure of the diaphragm in vascular surgery. The need to
expose the aorta both above and below the diaphragm requires an extended incision spanning the
left thorax to the abdomen, the length and exact location of which depends on the location of the
targeted aortic pathology. Often, the diaphragm must be divided, necessitating an awareness of the
regional anatomy as well as various surgical management considerations.
■
Thoracoabdominal aneurysm: The Crawford classification categorizes thoracoabdominal aneurysms
according to the extent of the aneurysm and is the most widely used1 (FIG 1). The classification is
as follows: type I, from the left subclavian artery to just above the renal arteries; type II, from the
left subclavian artery to the infrarenal aorta; type III, from the mid-descending thoracic aorta to
below the renal arteries; type IV, from the diaphragmatic aorta to the iliac bifurcation; and type V
(modified classification by Safi et al.2): from the mid-descending thoracic aorta.
■
Descending (type B) aortic dissection: Two classifications systems are commonly used to describe
the extent of aortic dissections (FIG 2). Stanford type A dissections involve the ascending aorta
with or without involving the descending aorta, whereas type B dissections only involve the
descending aorta beyond the left subclavian artery. The DeBakey classification includes type I,
which involves both the ascending and descending aortas; type II, which involves only the
ascending aorta; and type III, which involves only the descending aorta.

■
Most patients who are referred for surgery for a thoracoabdominal aneurysm present with no
symptoms. However, when they do have signs and/or symptoms, they may present with pain in the
chest, abdomen, or lower back; a mass in the abdomen, which may be pulsatile, or rigid abdomen;
and evidence of atheroembolism distally. The aforementioned symptoms, with signs of
hypovolemic shock, may indicate a ruptured aneurysm.
■
Uncomplicated descending aortic dissections are generally managed medically. However, if the
dissection is complicated, such as when it is associated with significant symptoms or leads to
visceral or distal malperfusion, rapid surgical intervention is warranted.
■
A more complete discussion regarding indications for intervention in aortic dissections and
thoracoabdominal aortic aneurysm can be found in a number of relevant reference textbooks.

■
Imaging is used to determine the proximal and distal extent of repair required. It impacts the type of
exposure required (i.e., thoracotomy vs. laparotomy vs. thoracoabdominal incision) as well as the
level of incision.
■
If the exposure is for the repair of thoracoabdominal aortic pathology, all patients require adequate
preoperative imaging, ideally consisting of a computed tomography aortography (CTA) with or
without 3-D reconstruction. Magnetic resonance aortography (MRA) may also provide the
necessary information, but this generally requires more time, is more expensive, and requires more
extensive postprocessing. However, MRA is the study of choice when CTA is contraindicated or
unsafe, such as in patients with a contrast allergy or renal insufficiency. Catheter-based invasive
aortography has generally been supplanted by CTA and MRA as the primary preoperative imaging
modality of choice, as it is more cumbersome and does not provide a complete assessment of the
aneurysm, including thrombus volume and adjacent anatomic structures.
■
If the surgery is elective, as in the case of an incidentally found aneurysm, extensive preoperative
evaluations are necessary to minimize postoperative morbidity and mortality.
■
Thorough evaluations of the cardiac, pulmonary, and renal systems are necessary, especially
because these systems are most commonly affected when there are complications. Depending on
the risk factors and prior history, further testing may be required and patients should be referred to
appropriate specialists for proper evaluation. A good neurologic evaluation is also warranted,
particularly if the patient has a prior history or symptoms suggestive of a lower extremity
weakness or spinal injury.
SURGICAL MANAGEMENT
■
Determine the possible need for adjuncts such as cardiopulmonary bypass and neurophysiologic
monitoring. In some instances, pulmonary artery catheters may be warranted for monitoring
cardiovascular hemodynamics.
■
Assess the need for spinal cord protection, including the use of lumbar drainage of cerebrospinal
fluid (CSF), distal aortic perfusion, epidural cooling, and distal aortic perfusion.
■
Given the expected amount of blood loss, a Cell Saver and rapid infuser should be available.
■
Double lumen endotracheal tube should be used for single-lung ventilation of the right lung.
Bronchial blockers are not reliable adjuncts for this purpose.
Positioning
■
Initially, place the patient supine on a deflated beanbag (FIG 3). Roll the left chest upward and
toward the right and place a shoulder roll under the right axilla and a bump under the left scapula
while also gently pulling and securing the right arm over to the right side. Ideally, the upper back
should be rotated about 60 degrees to the table with the pelvis remaining flat, such that the trunk is
twisted to the right. Position the patient with the break located halfway between the left costal
margin and the left iliac crest. Jackknife the table and then inflate the beanbag. Be sure to support
and secure the arms (“airplane” splint for the left arm) and pad all pressure points on the body and
extremities.
■
Prep the left chest with the following boundaries: the axilla superiorly, the spine posteriorly, and the
sternum and abdomen beyond the right of midline anteriorly. Keep the groins in the field for
surgical access to the femoral vessels for possible cannulation if necessary.
TECHNIQUES
PLANNING THE INCISION

■
This chapter deals with distal thoracic aortic pathology requiring exposure of the diaphragm where
a simple thoracotomy incision would not be adequate. Such more limited pathologies are
described elsewhere.
■
The proximal extent of the pathology and the anticipated location of the proximal clamp determine
the level of the thoracic portion of the incision.
■
If the proximal clamp is to be placed between the aortic arch and just beyond the left subclavian
artery, the chest is entered through the 4th or 5th intercostal spaces (e.g., Crawford types III and
V aneurysms).
■
If the proximal clamp is to be placed just above or at the diaphragm, the 8th or 9th interspace
should be entered (e.g., Crawford type IV aneurysms).
■
Consider the possible use of parallel or “double” thoracotomy incisions if exposure of both the
proximal and distal extent of the thoracic aorta is needed. In this case, the skin incision is placed
between the levels of the two interspaces anticipated to be entered.
■
The length and location of abdominal incision is determined by distal extent of the aortic pathology.
■
A modified thoracoabdominal incision that does not extend to midline is adequate if limited
exposure of the abdominal aorta to the level of the celiac artery is required.
■
Extend the incision to the midline for exposure of the visceral aorta.
■
The incision should be extended down the abdominal midline for more extensive exposure of the
infrarenal abdominal aorta (types II, III, and IV) to the aortic bifurcation or common iliac
arteries (FIG 4).
THE INITIAL INCISION AND EXPOSURE

■
Mark where the incision is to be made including finding the appropriate interspace and the extent of
the abdominal incision as described earlier.
■
Start with the thoracic incision over the appropriate interspace and then extend it across the costal
margin. Depending on the degree of the abdominal exposure required, extend this incision
obliquely to the midline of the abdomen. The midline incision can then be extended to the level of
the symphysis pubis, if necessary.
■
The abdominal incision is carried through the subcutaneous tissues, the external abdominal oblique
aponeurosis, and the anterior rectus sheath.
■
Split the external abdominal oblique muscle in the direction of its fibers.
■
Divide the underlying internal oblique and transversus abdominus muscles between the costal
margin and lateral edge of the rectus sheath.
■
Divide left rectus muscle.
■
The thoracic incision should provide adequate exposure posteriorly and should be extended to the
erector spinae fascia.
■
Expose the intercostal muscles by incising through the subcutaneous tissues and the external oblique
fascia.
ABDOMINAL EXPOSURE
■
Develop the abdominal portion of the incision before entry into the left pleural cavity
■
The aorta may be exposed by an extraperitoneal or transperitoneal approach.
■
Extraperitoneal: This approach is ideal for repairing thoracoabdominal aneurysms, especially
those involving the upper abdominal aorta (FIG 5).
■
Develop the plane between the transversalis fascia and the parietal peritoneum.
■
Separate the peritoneum from the lateral and posterior abdominal walls as well as from the
diaphragm superiorly.
■
Transperitoneal: This approach provides better exposure for visceral artery revascularization when
required, especially when bypass is required to the right renal artery.
■
Additional details of these approaches can be found elsewhere and are beyond the scope of this
chapter.
THORACIC EXPOSURE
■
Develop a plane superficial to the ribs and intercostal muscles.
■
Hold ventilation to the left lung and allow it to collapse.
■
Enter the left chest by opening the intercostal space along the superior edge of the lower rib, making
sure not to injure the lungs.
■
To maximize the exposure, it may be necessary to perform a subperiosteal resection of the rib above
or below the interspace entered, depending on the target location.
■
Additional exposure can be obtained from “notching” an adjacent rib. This is accomplished by
excising a 2-cm segment of the rib posteriorly
■
If two interspaces are being entered, develop an adequate plane anterior to the ribs. The skin and
overlying muscles can be retracted to accommodate both thoracic interspace exposures.
■
Use a self-retaining retractor to maintain exposure.
■
Be aware that there can be extensive adhesions within the pleura that may predispose to lung injury.
Usually, these adhesions can be mobilized bluntly if thin but may need bovie cautery or scissors if
more substantial.
EXPOSURE AND DIVISION OF THE DIAPHRAGM

■
Release any adhesions that may be present, mobilize the lung by dividing the inferior pulmonary
ligament, and retract the lung cephalad to expose the diaphragm.
■
Next, join the left thoracic cavity and the retroperitoneum or abdomen by dividing the diaphragm.
■
The diaphragm can be incised partially or completely (FIG 6).
■
Partial incision: Incise the muscular portion of the diaphragm and preserve the central tendinous
portion. This approach minimizes respiratory complications.
■
Complete division: This approach provides the best exposure of the aorta. This extends the
incision from the divided costal margin to the aortic hiatus. Division can be accomplished either
radially or circumferentially. Be sure to leave approximately 2 to 3 cm of diaphragm from the
internal costal margin to aid in the later closure of diaphragm. The circumferential approach
also theoretically minimizes disruption of the phrenic nerve and is generally preferred.
CLOSURE
■
After completion of the core surgical procedure, close the diaphragm.
■
Take patient out of flexed position and close the diaphragm with heavy running suture.
■
Place chest tubes.
■
Reapproximate the interspace with multiple simple or figure-of-eight heavy (no. 1) nonabsorbable
suture.
■
Close the incision in layers, including the muscle with running Vicryl as well as the deep dermal
layer. Close the skin with subcuticular sutures or staples.
PEARLS AND PITFALLS

Indications ■ Preoperative CTA or MRA is mandatory to determine the
suitability of the aortic pathology for surgical repair.
Placement of incision ■ The placement of the incision should be carefully considered
preoperatively based on imaging and the extent of the pathology. A
single thoractomy incision can be placed even if two intercostal
spaces need to be entered. To minimize morbidity, begin with a
smaller incision because it can always be extended when
necessary.
Injury to phrenic ■ A circumferential division of the diaphragm can provide the best
exposure while also minimizing the risk of injury to the phrenic
nerve.
Closure ■ When carrying out a circumfrential division of the diaphragm,
leave 2 to 3 cm of diaphragm from the internal costal margin for
the repair of the diaphragm when closing.
POSTOPERATIVE CARE
■
Monitor in the surgical intensive care unit as necessary for the extent of the aortic reconstruction
required.
■
Remove chest tubes when drainage is adequately low.
■
Continuous spinal cord protection and neurologic monitoring immediately postoperatively; continue
CSF drainage for ~3 days.
■
Follow-up imaging with CTA to establish a baseline
■
Standard postoperative incision and wound care
OUTCOMES
■
It is proposed that pulmonary dysfunction associated with thoracoabdominal aortic surgery is to a
large part associated with diaphragmatic dysfunction. Stickley and Giglia3 recommend a new
technique using a gastrointestinal stapler to divide the diaphragm. This technique is proposed to be
“rapid, hemostatic, and aids with reapproximation at the completion of the case” and that “this
method of diaphragm division is quicker and less traumatic and has the potential to decrease the
incidence of postoperative pulmonary dysfunction.”
■
Huynh et al.4 conclude that renal failure, spinal cord deficit, and pulmonary complication were the
major determinants of length of stay (LOS) in patients for thoracoabdominal aortic aneurysm
(TAAA) repair. Their study has shown that the preservation of diaphragmatic function and the use
of the adjunct distal aortic perfusion and CSF drainage may reduce hospital LOS.
COMPLICATIONS
■
Bleeding; take back
■
Phrenic nerve palsy or paralysis
■
Diaphragmatic hernia
■
Pulmonary complications, respiratory failure
■
Wound complications
■
Paralysis; spinal cord ischemic injury, associated with thoracoabdominal aortic surgery
■
Stroke/transient ischemic attack (TIA), associated with thoracoabdominal aortic surgery
■
Multiorgan failure, associated with thoracoabdominal aortic surgery
■
Death, associated with thoracoabdominal aortic surgery
REFERENCES
1. Crawford ES, Crawford JL, Safi HJ, et al. Thoracoabdominal aortic aneurysms: preoperative and intraoperative factors determining
immediate and long-term results of operations in 605 patients. J Vasc Surg. 1986;3(3):389–404.
2. Safi HJ, Winnerkvist A, Miller CC III, et al. Effect of extended cross-clamp time during thoracoabdominal aortic aneurysm repair.
Ann Thorac Surg. 1998;66(4):1204–1209.
3. Stickley SM, Giglia JS. Novel use of a gastrointestinal stapler for diaphragm division during thoracoabdominal aortic exposure. Ann
Vasc Surg. 2013;27(5):689–691. doi:10.1016/j.avsg.2012.11.005.
4. Huynh TT, Miller CC III, Estrera AL, et al. Determinants of hospital length of stay after thoracoabdominal aortic aneurysm repair.
J Vasc Surg. 2002;35(4):648–653.
Chapter 15 Retroperitoneal Aortic Exposure
Matthew Mell

General Considerations
■
Retroperitoneal aortic exposure may be desirable for a variety of vascular conditions, including
abdominal aortic aneurysms, aortoiliac occlusive disease, and mesenteric or left renal artery
occlusive disease.
■
Retroperitoneal exposure may be preferred for patients with a hostile abdomen from previous
intraabdominal infection, surgery, or radiation.
■
Compared with transabdominal aortic exposure, retroperitoneal exposure may be associated with
shorter postoperative ileus, decreased pulmonary complications, decreased pain, and lower
incidence of late complications including small bowel obstruction or aortoenteric fistulae.1
■
Retroperitoneal aortic exposure can be converted, when necessary, to thoracoabdominal exposure
with excellent visualization of the superior mesenteric artery (SMA), left renal artery, celiac axis,
and descending thoracic aorta.2
■
Examination of intraabdominal contents is possible through a retroperitoneal approach by simply
opening a peritoneal window as necessary.
Preoperative Imaging
■
Prior to aortic reconstruction, detailed anatomic imaging derived from modern, multirow detector
computed tomographic arteriography (CTA) will greatly facilitate surgical planning. Image
acquisition should extend from the normal proximal aorta to the common femoral artery
bifurcations bilaterally. Runoff imaging may also aid decision making depending on clinical
circumstances.
■
Data derived from submillimeter imaging slices may be readily reformatted into multiplanar and 3-
D reconstructions, with excellent resolution of the peripheral mesenteric and renal vasculature.
■
Noncontrast images should also be obtained to help assess the degree of mural calcification present
in diseased proximal aorta. Recognition of extensive mural calcification may modify the location
chosen for clamp placement, or prohibit safe clamping entirely in diseased segments.
■
CTA may require larger contrast dose than that required for catheter-based contrast aortography.
Contrast volumes required for CTA may be reduced significantly by modifying the field of view or
imaging parameters required for the procedure. Consultation with the responsible radiologist will
ensure optimal imaging of the necessary arterial anatomy with minimal contrast and radiation
exposure.
■
Contrast-based aortography, either CT or catheter-based, may be contraindicated for patients with
reduced creatinine clearance or an anaphylactic reaction to contrast. Milder allergic responses
(hives, rash) may be successfully tempered by premedication with steroids and antihistamines,
depending on the relative indication for contrast administration and the patient’s overall medical
condition. Adverse effects of intravenous or intraarterial contrast administration on creatinine
clearance may be partially ameliorated by preprocedural oral or intravenous hydration and
administration of N-acetylcysteine (Mucomyst). Although sometimes considered a reasonable
alternative under these circumstances, gadolinium-based contrast administration for magnetic
resonance arteriographic indications is also contraindicated in patients with a creatinine clearance
less than 60 mL per minute. When contrast administration is absolutely out of the question, CT
images acquired without contrast may provide adequate anatomic imaging to proceed with surgery,
with the caveat that anomalies such as a retroaortic left renal vein may be present and
unrecognized until exposed at surgery.
SURGICAL MANAGEMENT
Instrumentation
■
In addition to standard vascular instrumentation, additional equipment may aid in exposure of the
aorta and its visceral branches from the retroperitoneal approach:
■
Beanbag and airplane for positioning
■
A fully articulated operative table, capable of flex and reflex at the level of the umbilicus
■
Self-retaining, table-mounted retractor (e.g., Bookwalter, Omni, or other)
■
Finochietto chest retractor
■
Nos. 3, 4, and 5 Fogarty occlusion balloons
■
Cold renal perfusion
■
Arterial cannulas for renal perfusion
Positioning
■
The patient is placed supine on a beanbag and all lines and tubes are placed. For exposure of the
infrarenal aorta and iliac arteries, the left shoulder is lifted and protected with the beanbag and
padding. The left arm can be abducted or rotated to the patient’s right with a padded airplane
retractor for support. The table break and the kidney bar are used to open up the retroperitoneal
space between the 12th rib and the iliac crest as the incision is developed. For this reason, it is
essential that the patient be positioned with the umbilicus on the table break. An oblique incision
is made from below the umbilicus to the tip of the 11th rib. With this location, the incision can be
extended into the 10th intercostal space and the chest entered if additional proximal exposure is
required (FIG 1). When additional iliac artery or pelvic exposure is anticipated, the incision
should be initiated distal to the umbilicus. Either way, in patients with considerable abdominal
girth and redundant pannus, landmarks should be confirmed to ensure that the incision is not placed
too far distally on the abdomen, as juxtarenal aortic control can be extremely difficult when the
incision is placed too far distally on the abdomen.
■
For thoracoabdominal exposure, the patient is placed in the right lateral decubitus position using a
beanbag and axillary role for support. The left arm is protected with adequate padding and an
airplane-type retractor. It is important to secure the left arm such that the scapula rolls anteriorly,
providing exposure of the posterior lateral chest. The incision will be made overlying the 8th
intercostal space and extended toward the umbilicus.
TECHNIQUES
■
The incision is carried through the external oblique, internal oblique, and transversus abdominis
muscles. The retroperitoneal space is then entered laterally near the tip of the 11th rib by
identifying the characteristic yellow preperitoneal fat. The retroperitoneal space is then developed
from lateral to medial using a sponge stick or hands for blunt dissection. Anteriorly, the peritoneum
tends to be more adherent at the level of the rectus sheath; care should be taken to avoid entering
the peritoneal cavity in this area. The psoas fascia is encountered as the dissection is developed
posteriorly in the course of this dissection, which leads directly to the left iliac vessels and ureter.
Dissection is continued proximally anterior to the ureter; the ureter is either left in situ to limit
injury or gently retracted medially with silastic slings as the retroperitoneal space is developed.
■
Superiorly, the kidney is identified as the dissection is continued anterior to Gerota’s fascia—a
potential space exists between descending colon and Gerota’s fascia in the retroperitoneum, which
is progressively developed in a cephalad direction from the psoas muscle, adjacent to the aorta.
Once the renal vein is visualized in this space, the superior margin of the dissection is complete. If
suprarenal aortic control and exposure is required, this same dissection plane should be developed
posterior to the kidney, elevating the kidney and ureters along with the peritoneal contents and
retracting all to the right to expose the subdiaphragmatic visceral aorta.
■
Self-retaining retractor systems are best deployed either after the psoas muscle is identified or
following exposure of the renal vein or elevation of the left kidney. Deploying the retractor system
earlier will interfere with the dissection necessary to access the appropriate retrocolic space.
Following placement of the initial padded retractor blade along the medial margin of the wound,
circumferential retraction is secured by placement of additional blades, typically opposite each
other to prevent undue tension on the retraction system, with sequential replacement with deeper
blades and additional retraction until the entire periaortic retroperitoneum is exposed.
■
The aorta and iliac arteries are then dissected free of surrounding tissue. Circumferential aortic
control is an essential safety element of all aortic procedures, and care should be taken to gently
and patiently create a space between the inferior vena cava (IVC), aorta, and vertebral bodies
posteriorly to pass an umbilical tape around the aorta with a right-angle clamp. Circumferential
control of the common iliac arteries, on the other hand, is not necessary in all circumstances.
Sufficient medial and lateral dissection to allow for placement of a Wylie hypogastric clamp
around the common iliac artery will usually suffice. Avoidance of attempts at circumferential iliac
control will reduce the risk of right iliac vein injury. When circumferential control is required,
patience is necessary to gradually separate the right common iliac artery from the distal IVC and
left common iliac vein. When a venous injury is encountered during this maneuver, division of the
common iliac artery may be necessary to gain adequate exposure for control. Alternatively, an
occlusion balloon may be introduced from the right common femoral or external iliac veins will
tamponade the venous bleeding until sufficient exposure is gained to repair the wound. Finally, a
covered self-expanding endograft may also be deployed over a wire to gain control. Again,
readjustment of the retractor system with each consecutive stage of exposure will optimize
operative efficiency. Frequently, to optimize distal exposure, the proximal retractor blades need to
be temporarily relaxed and vice versa.
■
This exposure provides adequate exposure to the infrarenal aorta (and inferior mesenteric artery if
reimplantation is anticipated), right and left common and left external iliac arteries. The right
external iliac artery is not well visualized from this approach, although tunneling to the right
femoral artery is readily achieved for aortofemoral bypass grafting when necessary. Care should
be taken to develop the tunnel immediately anterior to the iliac arteries to avoid injury to the right
ureter or trapping the ureter between the graft limb and adjacent artery. When right external iliac
artery exposure is required during a left retroperitoneal exposure, a counterincision may also be
placed in the right lower quadrant, although patient positioning and retractor system placement may
limit the potential use of this maneuver.
■
For procedures requiring more proximal, visceral aortic exposure, the latissimus dorsi is identified
and dissected from surrounding superficial and deep tissues and retracted laterally. The 8th
intercostal space is opened posteriorly to the paraspinal muscles and anteriorly to the costal
margin, which is divided. As the retroperitoneal space is developed, the peritoneum is bluntly
separated from the inferior surface of the diaphragm. The diaphragm is divided in a
circumferential manner 1 to 2 cm from its attachments to the chest wall to avoid injury to the
phrenic nerve (FIG 2). The median arcuate ligament is identified and divided. Proximal aortic
control can now be obtained under direct vision, again following strategic placement of self-
retaining retractor blades, taking care to identify and avoid injury to the esophagus.
■
Dissection of the plane posterior the Gerota’s fascia allows for exposure of the left renal artery,
which is an important landmark in further dissection of the visceral aorta. Once the origin of the
left renal artery is identified and the median arcuate ligament has been divided, the visceral aorta
and origins of the celiac axis and SMA can be isolated with sharp dissection. With the left kidney
rotated anteriorly, the SMA can be exposed over a distance of approximately 5 cm (FIG 3).
Additional exposure can be obtained by rotating the kidney posterior to expose the SMA as it
courses behind the pancreas (FIG 4).
■
Following vascular repair, the retroperitoneal space should be inspected for hemostasis. The ureter
should be inspected, and any suspected injury or leak can be investigated with intravenous
methylene blue. If needed, the peritoneum can be opened for inspection of abdominal contents.
■
Removing the table break or lowering the kidney bar if used will aid in approximating tissue layers
without tension.
■
If divided, the diaphragm can be reapproximated with a continuous running absorbable suture. The
suture can be secured at the anterior costal margin and will help approximate these structures as
well.
■
If the thorax was entered, a large-bore chest tube is placed dependently and secured with U stitches.
■
A large Blake or Jackson-Pratt drain can be placed in the retroperitoneal space to avoid early
postoperative fluid collections.
■
The muscular layers are closed with continuous absorbable sutures and the subcutaneous tissue and
skin closed with standard techniques.
PEARLS AND PITFALLS

■ Choosing the most appropriate procedure for any given patient with mesenteric or renal artery
occlusive disease is dependent on a multitude of factors, especially with the widespread
availability of percutaneous interventions. Open surgical procedures continue to remain an
excellent alternative for patients with multivessel disease, with coexisting aortoiliac occlusive
or aneurysmal disease, and with disease too extensive to be adequately treated with wire-based
techniques. When selecting from the variety of open procedures, patient comorbidity, body
habitus and its impact on adequate exposure, quality of the inflow and outflow vessels, and
ability to safely clamp vessels should all be taken into consideration. Having a working
knowledge of all alternatives is important, as occasionally, intraoperative findings dictate a
deviation from the preoperative plan.
■ Intraoperative management is similar to that for other abdominal vascular procedures. When the
dissection is complete, patients are given heparin at a dose of 100 units/kg prior to clamping
vessels, achieving a target activated clotting time (ACT) of 200 to 250 seconds. For cases where
renal perfusion is interrupted, 0.25 to 0.5 g/kg of mannitol is given prior to cross-clamping. As
soon as possible, the kidney is perfused with 300 to 400 mL of saline cooled to 4°C. This may be
done at the renal artery ostium immediately after a renal endarterectomy, or directly into the renal
artery at the level of the distal anastomosis. Renal artery cannulas, which come in a variety of
sizes, are used for perfusion. Using a size that most closely matches the diameter of the renal
vessel assures that the perfusate will go into the kidney and not spill onto the operative field.
■ When revascularization is complete, heparin is reversed with protamine while checking for
hemostasis. The patency of revascularization may be checked with intraoperative duplex
imaging. Confirmation of an adequate endpoint is especially important when endarterectomy has
been performed, as intimal flaps may present as a delayed vessel occlusion and end-organ loss.
POSTOPERATIVE CARE
■
In addition to the standard postoperative strategies for patients undergoing aortic surgery, including
serial hematocrit and hemoglobin, electrolytes, creatinine, and lactic acid, it is important to
monitor renal and intestinal function. Patients undergoing renal revascularization commonly have
an obligatory diuresis for the first 12 hours after surgery. This phenomenon may be due to residual
effects of operative mannitol as well as a response to transient renal ischemia. During this time,
urine output is not reflective of the patient’s overall volume status, and crystalloid should be given
at rates sufficient to maintain central filling pressures. Also, serum creatinine should be serially
measured. It is common for the serum creatinine to increase slightly in the first 1 or 2
postoperative days, but increases of more than 20% or 30% warrant further investigation,
especially if associated with oliguria. Sudden changes in renal function that are unexplained or
unresponsive to corrective measures warrant duplex imaging to determine renal perfusion.
■
Patients after mesenteric revascularization often develop hyperactive peristalsis, sometimes while
the incision is still open. Under these circumstances, serial examination for bowel sounds in the
first 24 hours can provide clues to the continued patency of the revascularization. Serial lactate
levels are also checked. Although immediate postoperative lactate levels are elevated, they should
return to normal as the patient is warmed and resuscitated. Coagulation parameters may also be
elevated initially in response to blood loss and transient hepatic ischemia. These parameters
should be monitored and corrected for active bleeding; normal values are usually present by the
first postoperative day.
COMPLICATIONS
General Considerations
■
As with all aortic surgery, potential complications after visceral artery revascularization include
myocardial infarction, respiratory failure, and postoperative bleeding. Additionally, renal failure
is always a potential complication during visceral revascularization, although its incidence is
low.3–5 Potential causes of renal failure include generalized hypoperfusion from cardiac
dysfunction or hypovolemia, prolonged intraoperative ischemia, or thrombosis of the repair.
Progressive or unexpected renal failure should initiate a prompt workup including duplex imaging
of the kidneys to identify potentially treatable causes. Thrombosis with absence of flow to the
kidney is generally irreversible unless identified immediately.
■
Intestinal ischemia is the major concern after mesenteric revascularization. Signs and symptoms may
include severe abdominal pain, continued acidosis, and hematochezia. Ischemia may be secondary
to vessel or graft thrombosis or may result from distal embolization during or following the repair.
Patients with evidence of peritonitis should be promptly reexplored, and those treated initially for
acute mesenteric ischemia should have a planned second look at 12 to 24 hours if there was any
question of intestinal viability at the time of the original operation. Arterial duplex may confirm
the viability of the repair but cannot rule out embolization as a cause for postoperative intestinal
ischemia. At exploration, nonviable intestine can be resected, and issues with the
revascularization can be addressed.
Graft or Vessel Twisting or Kinking

■
When performing a bypass to the SMA, it is important to retract the mesentery in a caudal direction
to adequately assess graft length. Inadequate positioning will result in excessive graft length and
potential kinking and thrombosis once the peritoneal contents are reduced to the abdomen and the
incision is closed. Additionally, for retrograde bypass, the graft should be placed with enough
slack to allow the distal endpoint to be in-line with the SMA with caudal retraction of the
intestines. This positioning will prevent both kinking of the graft and tenting and narrowing of the
anastomosis. Bypass to the renal arteries should similarly be constructed with appropriate graft
length as it will lay in the retroperitoneum after retraction is released. For cases of arterial
reimplantation, it is important to maintain orientation of the target vessel to prevent twisting during
construction of the anastomosis. Additionally, the anastomotic site should be chosen in a similar
coronal plane to prevent kinking once the end organs assume their natural position.
Injury during Endarterectomy
■
Identifying the appropriate endarterectomy plane is usually straightforward in the aorta, renal
arteries, and SMA. The celiac artery can be challenging, as it may be thin-walled, and plaque
removal may injure the arterial wall. Limited injuries can be repaired with interrupted 4-0 or 5-0
Prolene sutures supported with Teflon pledgets, but larger injuries or those with severely
attenuated vessel walls may not be successfully repaired with this technique. If the integrity of the
artery is in doubt, it may be safer to transect it and perform a bypass from the aorta to the
transected celiac artery using an 8-mm or 10-mm graft. The celiac artery stump can be oversewn
with pledgeted 3-0 Prolene suture placed into healthy aorta. Unacceptable endpoints after renal
endarterectomy are best treated with conversion to a bypass.
Inadequate Distal Endarterectomy Endpoint
■
Plaque extending to the infrapancreatic SMA may be difficult to entirely remove with standard
thoracoabdominal exposure. Intraoperative duplex can confirm an adequate endpoint, and if there
is any uncertainty, the abdominal cavity can be entered and the SMA exposed by dividing the
ligament of Treitz. This maneuver will provide exposure of the SMA as it emerges from behind the
pancreas, usually at a place distal to the diseased segment. Inspection by palpation or with duplex
ultrasound can evaluate the repair. Incomplete endarterectomy or intimal flaps can be managed
through an arteriotomy at this location. A reasonably sized SMA can be transected and the retained
plaque removed; reapproximation with interrupted sutures will secure the intima distal to the
endarterectomy. Exposing the endpoint in a smaller vessel is most safely performed with a lateral
arteriotomy and subsequent patch angioplasty closure to prevent narrowing.
■
Problematic endarterectomy endpoints in the celiac artery or renal arteries may be best managed
with placement of a bypass graft. Conversion to bypass will require enough exposure of the target
vessel to allow for revascularization distal to the diseased segment. Either end-to-end or end-to-
side reconstruction is acceptable and should be performed, making certain that the intima is
secured with the suture line.
REFERENCES
1. Leather RP, Shah DM, Kaufman JL, et al. Comparative analysis of retroperitoneal and transperitoneal aortic replacement for
aneurysm. Surg Gynecol Obstet. 989;168(5):387–393.
2. Mell MW, Acher CW, Hoch JR, et al. Outcomes after endarterectomy for chronic mesenteric ischemia. J Vasc Surg.
2008;48(5):1132–1138.
3. Kasirajan K, O’Hara PJ, Gray BH, et al. Chronic mesenteric ischemia: open surgery versus percutaneous angioplasty and stenting.
J Vasc Surg. 2001;33(1):63–71.
4. Rapp JH, Reilly LM, Qvarfordt PG, et al. Durability of endarterectomy and antegrade grafts in the treatment of chronic visceral
ischemia. J Vasc Surg. 1986;3(5):799–806.
5. Weibull H, Bergqvist D, Bergentz SE, et al. Percutaneous transluminal renal angioplasty versus surgical reconstruction of
atherosclerotic renal artery stenosis: a prospective randomized study. J Vasc Surg. 1993;18(5):841–850; discussion 850–842.
Hybrid Revascularization Strategies for
Chapter 16 Visceral/Renal Arteries
Benjamin W. Starnes
DEFINITION
■
The term “hybrid” in vascular surgery traditionally refers to the use of both traditional open surgical
and endovascular techniques for remedy of the vascular condition (FIG 1).
■
Two hybrid approaches are described in this chapter.
■
Complete visceral debranching and endovascular tube graft repair
■
Partial visceral debranching and physician-modified fenestrated endovascular repair
■
Paravisceral aortic aneurysms may develop due to the following conditions:
■
Degenerative aneurysm
■
Aortic dissection
■
Mycotic aneurysm
■
Paraanastomotic juxtarenal aneurysm
■
Connective tissue disorders (Marfan’s syndrome)
■
Behçet syndrome

■
The majority of patients are asymptomatic and the diagnosis is made with imaging done for other
reasons. Some patients will complain of mild to moderate abdominal and low back pain. Severe
and unrelenting pain should raise the index of suspicion for a mycotic process which, if confirmed,
would make hybrid approaches prohibitive.

■
Contrast-enhanced, axial thin-slice computed tomography arteriography (CTA) is the current
standard for imaging paravisceral aneurysms. Detailed information can be gathered regarding the
precise origin of the celiac, superior mesenteric artery (SMA), and renal arteries (FIG 2).
■
Other important findings on CTA should be as follows:
■
Size and quality of access vessels for delivery of endovascular devices (>7 mm)
■
Location of left renal vein
■
Aberrant anatomy (e.g., replaced right hepatic artery)
■
Quality of gastroduodenal artery for possible celiac artery ligation or sacrifice
■
Renal cortical thickness
SURGICAL MANAGEMENT
■
Indications for repair include aortic aneurysms of more than 5.5 cm, symptoms, or evidence of rapid
expansion (>0.5 cm per 6 months).
■
As formal open repair would often include a bicavitary incision (chest and abdomen, as in a formal
thoracoabdominal repair), the standard preoperative assessment should focus on the patient’s
fitness to undergo major vascular surgery. This includes assessment of heart, lung, and kidney
function and reserve.
Positioning
■
Proper and precise positioning should be as follows (FIG 3):
■
Patient supine on standard operating room table or imaging table
■
Hair properly clipped over entire abdomen and both groins
■
Both arms tucked (option to have right arm at 90 degrees if planning brachial access)
■
Foley under one leg and padded
TECHNIQUES
COMPLETE VISCERAL DEBRANCHING AND ENDOVASCULAR TUBE

GRAFT REPAIR—STAGE 1
First Step—Exposure
■
Standard midline laparotomy and positioning of retractor system
■
Upon entry into the abdomen, the falciform ligament is divided between clamps and ligated. The
triangular ligaments above the liver are divided to facilitate adequate exposure/retraction while
minimizing risk of hepatic capsular injury, anticipating systemic anticoagulation later in the
procedure.
■
A nasogastric tube is positioned in the stomach to provide temporary decompression. The common
hepatic artery is identified following division of the gastrohepatic ligament and traced back to
origin of celiac artery. Once identified, the target artery is encircled with a silastic vessel loop.
Space is created along the left side of the aorta with blunt/finger dissection, beginning at the level
of the celiac artery, to create the retrograde bypass tunnel posterior to the pancreas (FIG 4).
■
The colon and omentum are lifted in a cephalad direction, the small bowel swept to the patient’s
right and packed in moist towels. Self-retaining retractors (Omni or Bookwalter) should be
positioned at this juncture to maintain exposure, with care taken to appropriately pad the retractor
blades as necessary.
■
The third and fourth portions of the duodenum are mobilized to the right following division of the
ligament of Treitz, exposing the anterior surface of the aorta. The inferior mesenteric vein is
ligated and divided as well and the dissection continued along the proximal aorta until the left
renal vein is clearly identified (FIG 5).
■
Widely mobilize the left renal vein sharply and encircle with a moist umbilical tape. The self-
retaining renal vein retractor blade is used to retract the left renal vein cephalad as necessary to
facilitate further exposure.
■
The origin of the renal arteries is identified by careful posterolateral dissection around the aorta,
just cephalad of the overlying renal vein. Exposure on the right is complicated somewhat by the
overlying inferior vena cava/left renal vein confluence. At least 2 cm of renal artery should be
exposed bilaterally. Encircle the renal arteries with silastic vessel loops. On the left, finger dissect
bluntly along the aorta in a cephalad fashion to complete the retropancreatic tunnel for the celiac
limb of the bypass graft.
■
The SMA is identified next by palpation within the base of the small bowel mesentery, directly
anterior to the pancreas. Doppler ultrasonography may assist identification when the pulse is faint.
Once identified, a 3-cm segment of SMA is isolated as proximal as possible to the root of the
mesentery. Beginning with the middle colic artery, multiple mesenteric arteries quickly branch
from the SMA as it emerges from the pancreas, underscoring the need for proximal identification
and isolation. The SMA is controlled with vessel loops.
■
The next step is to prepare the donor artery for hybrid bypass. The specific artery—most commonly
the common or external iliac arteries—should be selected from the preoperative imaging study.
The retroperitoneum is opened directly over the selected donor artery, which is exposed while
protecting the adjacent ureter. Alternatively, donor artery exposure may be achieved via medial-
visceral rotation, developing the entire retroperitoneal plane on the left. The latter approach
provides the added benefit of exclusion of the graft from the viscera and abdominal contents once
the viscera are returned to their original position. This maneuver adds significantly more time to
the case, however, and contributes to increased blood loss. Graft coverage can also be obtained
without developing the entire retroperitoneal plane, either via direct tunneling along the preferred
course of the graft or creation of an omental tongue affixed directly to the graft.
Second Step—Anticoagulation
■
Systemic anticoagulation is achieved with a bolus injection of unfractionated heparin, 50 units/kg.
Monitoring activated clotting time is a useful method of maintaining adequate anticoagulation
during the procedure.
Third Step—Multivisceral Bypass
■
Trifurcated grafts exist for the purpose of facilitating multivessel hybrid revascularization, but the
use of these are limited by the tendency of the middle limb to occlude when “squeezed” between
the outside limbs during graft routing and abdominal closure. In most circumstances, a standard 12
× 7 bifurcated, collagen-impregnated knitted polyester graft provides excellent conduits for
bilateral renal revascularization, with a separate 8-mm limb connected to the celiac and SMA.
Examples of bypass graft configurations are shown in FIGS 6 and 7.
■
The proximal (iliac/inflow) anastomosis is completed first with running 4–0 or 5-0 polypropylene
suture.
■
The next anastomosis to be completed should be one anticipated to be the technically most difficult,
given exposure and graft routing issues. Most commonly, this is the right renal artery. This is
divided following placement of a large clip at the origin. The appropriate graft limb is pulled to
length and anastomosed end-to-end with 5-0 polypropylene suture. The limb and artery are flushed
just prior to completion of the graft, after which the clamps are released to reperfuse the kidney.
Following this sequence, warm renal ischemia time is generally less than 12 minutes. The stump of
the right renal artery is then suture ligated; avoid clip dislodgement. Note: Excessive traction on
the confluence of the left renal vein and vena cava may cause caval injury and massive hemorrhage
during preparation and completion of the right renal artery anastomosis. Retractor positioning
needs to account for potential venous injury during exposure and significantly relaxed following
completion of the anastomosis.
■
The left renal anastomosis is completed in nearly identical fashion, minus many of the exposure
limitations present on the right.
■
The SMA graft is carefully sized to length so that it follows a “C”-shaped configuration without
kinking. Inflow can be obtained either from the many bodies of the graft or either of the completed
renal limbs. The SMA-graft anastomosis is completed end-to-side with interrupted or running 5-0
polypropylene suture. The end-to-side arteriotomy length is 1.5 to 2 times the width of the bypass
graft (12 to 16 mm). Alternatively, end-to-end anastomotic configuration may reduce the likelihood
of graft kinking depending on final configuration. Following completion of the anastomosis, the
proximal SMA is ligated with a large clip or circumference suture. Again, ischemia time should be
under 10 to 12 minutes.
■
Typically, following SMA and renal graft completion, repositioning of the retraction system is
necessary to reobtain and optimize celiac artery exposure. Prior to reexposing the celiac, a
vascular clamp is repassed through the retropancreatic tunnel left of the aorta. This position is then
maintained until the transverse colon and mesocolon are reduced to their usual location. This
reexposes the “looped” celiac and common hepatic arteries previously isolated in the lesser sac.
The clamp tip exiting the retrohepatic tunnel is identified, and a moist umbilical tape is pulled
through the tunnel. Following this, the celiac limb is tied to the umbilical tape, which is then pulled
cephalad behind the pancreas and into position for either end-to-end or end-to-side anastomosis.
Care again needs to be taken to optimize limb routing and length to minimize risk for kinking.
■
After coverage of remaining exposed graft limbs with omentum or parietal peritoneum as
appropriate, standard abdominal closure is performed.
COMPLETE VISCERAL DEBRANCHING AND ENDOVASCULAR TUBE

GRAFT REPAIR—STAGE 2
First Step—Percutaneous Access
■
Following the “debranching” procedure described in stage 1, endovascular aneurysm repair
(EVAR) may be performed either at the same setting or within several weeks of the initial
procedure. The risk of potential aneurysm rupture associated with a staged approach needs to be
balanced with the additional operative risk inherent in the longer anesthetic time required to
complete both stages in one sitting. For the EVAR procedure itself, standard percutaneous access
to an appropriately sized access vessel is obtained using Seldinger technique and a wire advanced
into the aorta under fluoroscopic guidance. In our practice, this is most commonly obtained
percutaneously, using ultrasound guidance and preplacement of polypropylene suture prior to
dilation of the access sites (also known as the “preclose” Perclose® technique (Abbott Vascular
Inc, Redwood City, CA).1 An 11-Fr standard sheath is placed into the common femoral artery and
flushed with heparinized saline. Wire advancement from the femoral artery to the aortic arch must
be visualized radiographically throughout its course, as the wire may preferentially enter the
debranching graft and cause end-organ injury or hemorrhage without real-time position monitoring
and guidance.
Second Step—Stiff Wire Exchange
■
After wire advancement to the transverse aortic arch, standard wire exchange technique is used to
position a 0.035-in stiff (e.g., Lunderquist®, Cook Medical, Bloomington, IN) wire through the
abdominal and thoracic aorta. Optimal final wire positioning is at/just distal to the left subclavian
artery orifice.
Third Step—Intravascular Ultrasound
■
An 8.2-Fr Visions® catheter (Volcano Therapeutics, Irvine, CA) is used to confirm appropriate
proximal and distal landing zones for endovascular graft placement. The optimal graft size and
configuration is determined by analysis of CTA images reformatted and visualized on a dedicated
3-D image workstation (AquariusNet®, TeraRecon, Inc, San Mateo, CA). Graft diameter should
be oversized by 10% to 15% for this application.
■
During advancement of the device, the origin of the debranching graft can also be visualized either
through fluoroscopic confirmation of a metallic clip placed during the debranching procedure or
under intravascular ultrasound (IVUS) real-time guidance. Using IVUS, the position of the IVUS
catheter is marked on the fluoroscopic monitor when the catheter itself recognizes the orifice of the
debranched graft. Alternatively, a contrast power injection can be performed through an
appropriately positioned arteriographic catheter with 30 mL of contrast injected at 15 mL per
second to confirm the proximal and distal landing zones.
Fourth Step—Endograft Deployment
■
The endovascular graft is deployed following device-specific instructions for use (IFU), covering
the native origins of the visceral vessels and excluding the aortic aneurysm. The femoral
arteriotomy is then closed.
PARTIAL VISCERAL DEBRANCHING AND PHYSICIAN-MODIFIED

ENDOVASCULAR REPAIR—STAGE 1
First Step—Exposure
■
Standard midline laparotomy and positioning of retractor system.
■
Upon entry into the abdomen, the falciform ligament is divided between clamps and ligated. The
triangular ligaments above the liver are divided to facilitate adequate exposure/retraction while
minimizing risk of hepatic capsular injury, anticipating systemic anticoagulation later in the
procedure.
■
A nasogastric tube is positioned in the stomach to provide temporary decompression. The common
hepatic artery is identified following division of the gastrohepatic ligament and traced back to
origin of celiac artery. Once identified, the target artery is encircled with a silastic vessel loop.
Space is created along the left side of the aorta with blunt/finger dissection, beginning at the level
of the celiac artery, to create the retrograde bypass tunnel posterior to the pancreas.
■
The colon and omentum are lifted in a cephalad direction, the small bowel swept to the patient’s
right and packed in moist towels. Self-retaining retractors (Omni or Bookwalter) should be
positioned at this juncture to maintain exposure, with care taken to appropriately pad the retractor
blades as necessary.
■
The third and fourth portions of the duodenum are mobilized to the right following division of the
ligament of Treitz, exposing the anterior surface of the aorta. The inferior mesenteric vein is
ligated and divided as well and the dissection continued along the proximal aorta until the left
renal vein is clearly identified.
■
Widely mobilize the left renal vein sharply and encircle with a moist umbilical tape. The self-
retaining renal vein retractor blade is used to retract the left renal vein cephalad as necessary to
facilitate further exposure.
■
The origin of the renal arteries is identified by careful posterolateral dissection around the aorta,
just cephalad of the overlying renal vein. Exposure on the right is complicated somewhat by the
overlying inferior vena cava/left renal vein confluence. At least 2 cm of renal artery should be
exposed bilaterally. Encircle the renal arteries with silastic vessel loops. On the left, finger dissect
bluntly along the aorta in a cephalad fashion to complete the retropancreatic tunnel for the celiac
limb of the bypass graft.
■
The SMA is identified next by palpation within the base of the small bowel mesentery, directly
anterior to the pancreas. Doppler ultrasonography may assist identification when the pulse is faint.
Once identified, a 3-cm segment of SMA is isolated as proximal as possible to the root of the
mesentery. Beginning with the middle colic artery, multiple mesenteric arteries quickly branch
from the SMA as it emerges from the pancreas, underscoring the need for proximal identification
and isolation. The SMA is controlled with vessel loops.
■
The next step is to prepare the donor artery for hybrid bypass. The specific artery—most commonly
the common or external iliac arteries—should be selected from the preoperative imaging study.
The retroperitoneum is opened directly over the selected donor artery, which is exposed while
protecting the adjacent ureter. Alternatively, donor artery exposure may be achieved via medial-
visceral rotation, developing the entire retroperitoneal plane on the left. The latter approach
provides the added benefit of exclusion of the graft from the viscera and abdominal contents once
the viscera are returned to their original position. This maneuver adds significantly more time to
the case, however, and contributes to increased blood loss. Graft coverage can also be obtained
without developing the entire retroperitoneal plane, either via direct tunneling along the preferred
course of the graft or creation of an omental tongue affixed directly to the graft.
Second Step—Anticoagulation
■
Systemic anticoagulation is achieved with a bolus injection of unfractionated heparin, 50 units/kg.
Monitoring activated clotting time is a useful method of maintaining adequate anticoagulation
during the procedure.
Third Step—Multivisceral Bypass
■
Trifurcated grafts exist for the purpose of facilitating multivessel hybrid revascularization, but the
use of these are limited by the tendency of the middle limb to occlude when squeezed between the
outside limbs during graft routing and abdominal closure. In most circumstances, a standard 12 × 7
bifurcated, collagen-impregnated knitted polyester graft provides excellent conduits for bilateral
renal revascularization, with a separate 8-mm limb connected to the celiac and SMA. Examples of
bypass graft configurations are shown in FIGS 6 and 7.
■
The proximal (iliac/inflow) anastomosis is completed first with running 4-0 or 5-0 polypropylene
suture.
■
The next anastomosis to be completed should be one anticipated to be the technically most difficult,
given exposure and graft routing issues. Most commonly, this is the right renal artery. This is
divided following placement of a large clip at the origin. The appropriate graft limb is pulled to
length and anastomosed end-to-end with 5-0 polypropylene suture. The limb and artery are flushed
just prior to completion of the graft, after which the clamps are released to reperfuse the kidney.
Following this sequence, warm renal ischemia time is generally less than 12 minutes. The stump of
the right renal artery is then suture ligated; avoid clip dislodgement. Note: Excessive traction on
the confluence of the left renal vein and vena cava may cause caval injury and massive hemorrhage
during preparation and completion of the right renal artery anastomosis. Retractor positioning
needs to account for potential venous injury during exposure and significantly relaxed following
completion of the anastomosis.
■
The renal anastomosis is completed in nearly identical fashion, minus many of the exposure
limitations present on the right.
PARTIAL VISCERAL DEBRANCHING AND PHYSICIAN-MODIFIED

ENDOVASCULAR REPAIR—STAGE 22
First Step—Creation of a Fenestrated Graft for the Celiac and Superior Mesenteric Artery
■
The appropriate endovascular device is chosen according to standard IFU sizing guidelines,
typically incorporating 10% to 15% oversizing. The sterile graft is unsheathed on a dedicated
sterile table in the operating room and marked with the relative locations (length from proximal
end and clockface measurements) of the celiac and SMA fenestrations as previously determined
via TeraRecon® workstation analysis. Minor adjustments are allowed to minimize strut overlap of
planned fenestration locations. Fenestrations in the polyester endograft fabric are created with a
disposable ophthalmic cautery to minimize fraying. The fenestrations are outlined and reinforced
with 15-mm gold Amplatz Gooseneck® snares (ev3 Endovascular, Inc, Plymouth, MN). These are
hand sewn into place using 4-0 Prolene suture in a double row circumferentially (FIG 8).
Diameter-reducing ties were then used to constrain the device along its posterior border (opposite
the SMA and or celiac fenestration at 6 o’clock) by rerouting the existing proximal trigger wire
through and through the graft material at the midportion of each of the top two Z stents. The
constraining ties are then tied down into place over the trigger wire. The entire graft is then wetted
with heparinized saline and then reloaded into the existing sheath.
Second Step—Percutaneous Access

■
Standard percutaneous access to an appropriately sized access vessel is obtained using Seldinger
technique. The initial guidewire is advanced into the aorta under fluoroscopic guidance. In our
practice, this is most commonly obtained percutaneously, using ultrasound guidance and
preplacement of polypropylene suture prior to dilation of the access sites (also known as the
“preclose” Perclose® technique (Abbott Vascular Inc, Redwood City, CA).1 An 11-Fr standard
sheath is placed into the common femoral artery and flushed with heparinized saline. Wire
advancement from the femoral artery to the aortic arch must be visualized radiographically
throughout its course, as the wire may preferentially enter the debranching graft and cause end-
organ renal injury, rupture of Gerota’s fascia, and retroperitoneal hemorrhage without real-time
position monitoring and guidance.
Third Step—Stiff Wire Exchange
■
A standard 4- or 5-Fr catheter is used to perform a wire exchange to a stiff 0.035-in Lunderquist®
wire (Cook Medical, Bloomington, IN). The wire is positioned so that its tip is just distal to the
left subclavian artery.
Fourth Step—Marking of the Target Vessels and Graft Deployment
■
A contrast power injection can be performed with 10 mL of contrast injected at 25 mL per second to
mark the precise origins of the celiac and SMA (FIG 9). The modified graft is positioned over the
target vessels, oriented, and deployed.
Fifth Step—Cannulation of the Target Vessels

■
An 18-Fr sheath is advanced from the contralateral groin and into the distal graft over a stiff wire.
Two 7-Fr Raabe® sheaths (Cook Medical, Bloomington, IN) are advanced together through the
18-Fr sheath. Working through these sheaths, the SMA and celiac vessels are selected through the
fenestrations using standard catheter and guidewire techniques, with the sheaths ultimately
advanced into the target vessels over stiff wires.
■
After sheath advancement and confirmation of target vessel acquisition, the main body is distended
flush with the surrounding aorta with a moulding balloon (e.g., Coda®, Cook Medical,
Bloomington, IN). This inflation represents the final opportunity to distend the endograft in the
region of the visceral stents. Lateral positioning of the image intensifier guides stent placement into
the SMA and celiac arteries (typically 8- to 9-mm stents; FIG 10). FIG 11 shows follow-up
computed tomography (CT) imaging of a patient 1 year after successful treatment with this
technique.
Sixth Step—Access Site Closure

■
The access sites are closed with the previously placed sutures.
PEARLS AND PITFALLS

Choice of operating room ■ Use standard OR tables for open surgical procedures and imaging
(OR) table tables for image-guided or hybrid procedures. Advanced planning
is essential to optimize outcome. Never sacrifice exposure!
Exposure of common iliac ■ Identify and protect the ureter.
artery
Placement of wires after ■ Pass guidewires under continuous fluoroscopic guidance
debranching procedure following debranching. An advancing aortic wire may
preferentially enter and traverse the debranching graft, causing
end-organ injury, disorientation, and possible endograft
maldeployment if not recognized.
Timing of stent graft balloon ■ Always seat the endograft with balloon inflation prior to
moulding during fenestrated placement of visceral bridging stents. Instrumentation or distention
EVAR of the fenestrated endograft following branch vessel stenting may
compromise stent positioning, integrity, and patency.
POSTOPERATIVE CARE
■
Open aortic debranching procedures are not benign; almost all patients will require intensive care
postprocedure. Spinal drainage is used selectively for aortic coverage extending more than 10 cm
cephalad to the celiac artery. Postoperative anuria or persistent acidosis/rising lactate require
immediate investigation to prove branch vessel patency.
OUTCOMES
■
Contemporary hybrid debranching procedures for complex abdominal aortic aneurysmal disease are
associated with a 13% operative mortality rate, 2% permanent paraplegia rate, and 1% stroke
rate.3
■
Hybrid approaches offer the advantage of versatility, avoidance of extensive operative exposures,
and potentially offer a broader range of therapies to a patient population that would not otherwise
be considered for aortic surgical repair.
COMPLICATIONS
■
Access-related complications
■
Hemorrhage requiring transfusion
■
Paraplegia
■
Stroke
■
Renal failure
■
Death
REFERENCES
1. Starnes BW, Andersen CA, Ronsivalle JA, et al. Totally percutaneous aortic aneurysm repair: experience and prudence. J Vasc
Surg. 2006;43(2):270–276.
2. Starnes BW, Quiroga E. Hybrid-fenestrated aortic aneurysm repair: a novel technique for treating patients with para-anastomotic
juxtarenal aneurysms. Ann Vasc Surg. 2010;24(8):1150–1153.
3. Starnes BW, Tran NT, McDonald JM. Hybrid approaches to repair of complex aortic aneurysmal disease. Surg Clin North Am.
2007;87(5):1087–1098, ix.
Snorkel/Chimney and Periscope Visceral
Revascularization during Complex Endovascular
Chapter 17 Aneurysm Repair
Jason T. Lee Ronald L. Dalman
DEFINITION
■
Although routine endovascular aneurysm repair (EVAR) has gained widespread acceptance as the
procedure of choice for patients with suitable aortic neck anatomy, the optimal approach to the
juxtarenal aortic aneurysm (JAA), often with challenging anatomy at the visceral neck, remains
controversial.1 Although open repair is an effective and durable option for patients with JAA,
particularly in centers of excellence for low physiologic risk patients,2 endovascular techniques
including fenestrated and branched EVAR (FBE) have emerged as effective, potentially less
invasive alternatives.3
■
In the United States, however, lack of widespread availability of FBE has allowed other techniques
to emerge, and in this chapter, we describe the increasingly popular “snorkel” or “chimney”
technique, defined as a parallel stent graft adjacent to the endograft main body to maintain
perfusion to renal and visceral branches during EVAR and placed from a cranial direction, and the
“periscope” technique, where the parallel stent graft is placed from the caudal direction.
■
First described by Greenberg and associates,4 the snorkel strategy can be employed either as a
bailout from accidental coverage of vital side branches during deployments requiring close
approximation of the main body to the branch artery in question, or the intentional cranial
relocation of the EVAR seal zone for JAAs.5–8
■
The challenge for the vascular specialist in treating JAAs revolves around an increasing number of
choices for intervention, including traditional suprarenal repair, hybrid type debranching
procedures, fenestrated and branched devices in clinical trials or certain centers, and
snorkel/chimney/periscope techniques. The choice is most often based on patient physiologic
parameters, physician experience with the multitude of techniques, and a very individualized
approach to complex aortic anatomy.

■
Most patients present electively and essentially without symptoms for consideration of repair of
their JAA, as it is most often discovered during radiographic workup for vague abdominal
discomfort, back pain, or as part of a screening program. A pulsatile, nontender abdominal mass
can be elicited on careful abdominal exam. Any signs of persistent abdominal or back pain or
hemodynamic instability or compromise should suggest the possibility of an acute aortic pathology
and prompt more urgent workup and treatment. Careful attention during the history and physical
examination to cardiac and renal comorbidities aids in risk-stratifying the patient for potential
repair of their JAA. Because most patients are asymptomatic and aneurysms are repaired to
prevent future rupture, some reasonable quality of life must be present for the patient to enjoy the
survival advantage.

■
High-quality computed tomography angiography (CT-A) on a modern 64-slice scanner able to
produce at least 2-mm–thin cuts is a requirement for treatment with snorkel techniques. These
imaging algorithms allow the creation of virtual models of the aneurysm for the surgeon to better
appreciate the relationship of branches and potential areas of technical challenge (FIG 1). Patients
with compromised kidney function who cannot undertake iodinated contrast are poor candidates
for snorkel procedures, as noncontrast scans fail to elucidate thrombus volume, branch artery
patency, and luminal diameter in the preoperative planning that is paramount to success.
■
Access to a three-dimensional (3-D) workstation/program and familiarity with reconstruction
software by the implanting surgeon for manipulation of the images and creating centerline
pathways should be mandatory to most accurately plan device orientation, selection, and sizing
(FIG 2).
■
Because the snorkel technique usually involves access of the brachial artery for delivery of the
parallel visceral stent grafts, visualization of the arch and proximal subclavian is most
conveniently obtained by including the chest in the standard CT-A of the abdomen and pelvis. The
presence of a challenging type III arch, where the subclavian inserts below the inner curve of the
aortic arch, makes the procedure more challenging and many times prohibitive due to concerns
about arch manipulation, cerebral emboli, and deliverability of stent grafts (FIG 3). If the patient
has already undergone an adequate CT-A abdomen and pelvis and one wishes to avoid the
additional contrast load of repeating the study, a noncontrast chest computed tomography (CT) can
be performed to visualize the arch but then should be combined with arterial duplex and
waveforms of the upper extremities to ensure patency of the axillosubclavian arterial system.
■
For patients with chronic kidney disease, high-grade renal stenosis, atretic kidneys, or multiple
visceral and renal vessels involved in the endovascular plan for snorkeling, nuclear medicine split
renal function tests can help determine if it is reasonable to sacrifice one of the renal arteries. This
can be done in order to simplify the snorkel strategy and keep the number of cranially oriented
stent grafts to two, which may have an influence on overall morbidity and mortality from the
procedure.1,7,8
SURGICAL MANAGEMENT
■
All patients considered for snorkel/chimney or periscope techniques should have undergone an
extensive informed consent discussion related to off-label use of endograft components for
treatment of their complex aneurysm. Alternatives often discussed include open surgery with
suprarenal clamping, hybrid debranching, referral to a center with access to fenestrated or
branched devices, or no surgery at all. Once the decision is made to proceed with the snorkel
strategy, we prefer a two-surgeon approach with one performing the femoral access portion and
one the brachial access portion. Both surgeons should have reviewed on the 3-D workstation the
anatomy, the endovascular plan, and the sequence for deployment.
■
Access to a hybrid endovascular suite is highly recommended, although not mandatory, for
successful completion of these procedures. Fixed imaging provides improved accuracy,
reliability, and reproducibility of the anatomy throughout the sequence of the snorkel procedure.
Knowledgeable operating room and cath-angio staff should be assigned to these cases and
available endografts and wires/catheters as well as backups should all be arranged ahead of time
to provide the safest working environment for the patient as well as the operative team.
■
Choosing the main body endograft, its configuration, and size has been described by numerous
authors who all report excellent results overall with a wide variety of devices and formulas.9 In
general, we often “oversized” to about 25% to 30% instead of the typical 15% to 20% for
standard EVAR to account for the additional fabric infolding to accommodate the snorkel stent(s).
■
Given the amount of dye often used as well as renal artery manipulation during the most complex of
snorkel cases, we prefer to admit the patient the evening before or several hours prior to surgery
for additional intravenous hydration when possible.
■
General anesthesia is preferred, with consideration for preoperative lumbar drainage based on risk
of spinal cord ischemia. Arterial monitoring, when necessary, is achieved via the right arm.
Adequate venous access can consist of either large-bore peripheral intravenous lines (IVs) or a
central line. There is usually not a need for autotransfusion or cell saver setups unless an iliac or
axillary conduit is planned where there is more potential for early blood loss during the
procedure.
Positioning
■
The hybrid room can be set up as either “head” position (FIG 4) or “right side, table rotated”
depending on the type of imaging equipment. With the right arm tucked, the left arm is prepped
circumferentially and placed on an armboard at about 75 to 90 degrees while the chest and
abdomen down to the groins are prepped. Surgeon A, who will stand at the patient’s right hip, has
control of the C-arm and imaging functions and is in charge of obtaining femoral access and
delivery of devices from the groins. Surgeon B stands above the outstretched left arm, with an
additional sterile table extending off the left hand to allow for wires and catheters to remain sterile
and available for arm access during the procedure. The monitor is placed at a slight angle toward
the foot of the bed to allow both surgeons to visualize, or a slave monitor can be employed.
TECHNIQUES
SNORKEL/CHIMNEY ENDOVASCULAR ANEURYSM REPAIR

Arm Access
■
A 5-cm transverse incision slightly below the left axilla over the palpable brachial pulse affords
several centimeters of longitudinal exposure of the high brachial artery (FIG 5A). Staying
proximal to the deep brachial artery takeoff allows a large enough caliber of brachial artery for
typical delivery of two 7-Fr sheaths for a double renal snorkel procedure. At least 7 to 8 cm of
healthy brachial artery should be dissected free and slung with vessel loops to allow accurate
puncture of the vessel. The two punctures should be placed at least 2 cm apart, and not next to each
other, to facilitate later simpler, individual primary closure.
■
For cases when larger delivery sheaths may need to be inserted or in cases where potentially up to
three or four snorkel stents need delivery, then an infraclavicular incision and exposure of the
axillary artery for possible 10-mm Dacron conduit placement is recommended (FIG 5B). When
this is planned, a 20-Fr or 22-Fr sheath can be inserted to get around the arch and then three 6-Fr
or 7-Fr sheaths can be used to cannulate the visceral vessels.
■
For the simplest of all snorkel cases, when just one renal artery needs stenting, a lower brachial
incision can be made to allow insertion of a single 7-Fr sheath (FIG 5C).
Renal/Visceral Cannulation and Sheath Advancement
■
A 5-Fr micropuncture access is obtained under direct visualization into the brachial artery. A
Bentson wire is advanced, under fluoroscopic guidance, most often into the ascending aorta. The
use of an Omniflush catheter and glidewire (either a 260-cm Rosen or Amplatz [Cook Medical,
Bloomington, IN]) combination, to direct the wire toward the visceral aorta, allows a wire
exchange for a stiffer platform. Over this stiffer platform, two 7-Fr 90-cm Pinnacle Destination
sheaths (Terumo Medical, Somerset, NJ) are positioned near the visceral target branches to
facilitate cannulation attempts (FIG 6A).
■
Through the 7-Fr sheaths, the targeted renal and visceral branches are cannulated using 260-cm–
length hydrophilic guidewires and a 125-cm JB1 catheter (Cook Medical, Bloomington, IN). An
angiographic run can be performed from a flush catheter advanced from femoral access to aid in
renal cannulation (FIG 6B). Thorough knowledge of the preoperative anatomy, derived from
reformatting from the 3-D workstation facilitates this portion of the procedure, guiding optimal
angulation of the C-arm.
■
Once cannulated, the sheaths are advanced coaxially into the target artery orifice. When necessary,
or in cases where there is a slight turn to the horizontal rather than downward angled, the soft
hydrophilic guidewire needs to be exchanged for a 260-cm J-tip Rosen wire (Cook Medical,
Bloomington, IN) or Amplatz Superstiff (1-cm tip) to facilitate sheath advancement into the target
renal artery. Confirmation angiography, through the sheath, is performed to ensure patency of the
renal arteries, cannulation of the main renal artery, and avoidance of accidental side branch
cannulation.
Positioning of Main Body Endograft and Snorkel Stent Grafts
■
Standard femoral access for EVAR is employed for snorkel technique. This is well described in
other chapters. Briefly, a small transverse incision, below the inguinal ligament, can be used to
expose the common femoral artery to the bifurcation for delivery of endograft components. The
percutaneous approach involves the “preclose” technique and employs two Perclose ProGlide
devices (Abbott Vascular, Santa Clara, CA) oriented at 10 o’clock and 2 o’clock positions.10
■
The main body endograft can then be delivered up the chosen femoral side to the paravisceral aorta
at the same time as the iCAST (Atrium Medical, Hudson, NJ) or Viabahn (Gore Medical,
Flagstaff, AZ) stents are advanced through the snorkel sheaths out to the target renal arteries (FIG
7A). The typical length of the iCAST is 59 mm, with the diameter sized appropriately to seal in the
target renal artery, most often 5, 6, or 7 mm. For Viabahn stents, similar diameters are used in 50-
or 100-mm lengths as appropriate. To prevent theoretical compression of the Viabahn stent by the
main body of the endograft, the Viabahn can be reinforced from the inside with a bare-metal,
balloon-expandable stent along the areas of overlap with the main body. The positioning of the
snorkel stent requires that at least 10 mm of fixation into the renal artery be present and that the
proximal extent of the graft is above the fabric of the main body endograft.
■
In a lateral projection angiography, the superior mesenteric artery (SMA) is visualized (when
performing the typical double renal snorkel) and the main body fabric edge placed immediately
below the origin of the SMA (FIG 7B).
■
At this point, final small adjustments can be made as well as further angiography to ensure that the
snorkel stents are in good position. To avoid the issue of the iCAST stent being unstable off its
balloon, we often leave the 7-Fr sheaths in place to protect them until final deployment.
Sequence of Stent Graft Deployment and Balloon Molding
■
The main body endograft is deployed at the target location with its fabric edge being immediately
below the SMA edge (FIG 8A). Depending on the endograft system used, deployment proceeds
down to the contralateral gate opening. From the contralateral femoral access, cannulation of the
gate is confirmed and a noncompliant molding balloon (32- or 40-mm Coda balloon; Cook
Medical, Bloomington, IN) is placed up to the level of the renal vessels.
■
The 7-Fr sheaths are slowly withdrawn from the brachial approach so the tip is just proximal to the
edge of the renal snorkel stents and deployment of the iCAST occurs, most often simultaneously
and to a nominal pressure of eight atmospheres (FIG 8B). At the same time that the iCAST stents
are being deployed by balloon inflation, slower inflation of the Coda occurs to slowly mold the
main body fabric around the snorkel stents to minimize gutter formation.
■
Only when the renal snorkel stents are maximally inflated can the Coda balloon go up to full main
body endograft diameter (FIG 8C). This step cannot be overemphasized, as deflation of the
snorkel stents while the Coda is inflated is likely to crush the balloon-expandable covered stents.
■
With the renal snorkel stents still maximally inflated, the Coda balloon can finally be let down after
a few seconds of balloon molding to complete the sequence (FIG 8D). After the proximal molding
balloon is completely deflated, the renal snorkel balloons are deflated to allow perfusion of the
kidneys.
Completion of Distal Components
■
Prior to losing wire access to the renal vessels, a proximal aortogram is performed to look for a
large type I endoleak or poor perfusion of either targeted kidney. If this is satisfactory, the distal
components of the endograft can be advanced and deployed in the usual fashion.
■
Repair of the access sites, particularly the brachial site, requires careful interrupted 6-0 or 7-0
Prolene sutures, and adequate hand and foot perfusion is verified prior to completion of the case.
■
Postoperative CTA demonstrates the typical appearance of the snorkel stents adjacent to the main
body endograft with minimal gutters (FIG 9A), and the 3-D reconstruction shows excellent
alignment and configuration of the snorkel EVAR components (FIG 9B).
PERISCOPE ENDOVASCULAR ANEURYSM REPAIR/THORACIC

ENDOVASCULAR AORTIC REPAIR
Femoral Access for Introduction of Main Body Endograft
■
Periscope EVAR/thoracic endovascular aortic repair (TEVAR) builds on the concept above of
parallel endografts but places the visceral stents from a femoral approach, requiring blood flow to
go through the main body stent graft, then turn around and return cranially to the visceral or renal
vessel.11
■
The femoral access for periscope, in contradistinction to snorkel/chimney strategies, often involves
the use of larger caliber thoracic or fenestrated main body components (often 22 Fr to 26 Fr),
leading to a slightly higher usage of open or endovascular iliac conduits.
■
One useful modification to an iliac conduit that can be helpful in delivering and torquing large-
caliber main body components or sheaths during periscope EVAR/TEVAR involves creating a
patch at the distal end (FIG 10). This patch region is created by cutting a 10- or 12-mm Dacron
graft along its long access, creating a sewing patch that enlarges the transition from graft to vessel,
and not limiting the flexibility of the branch to the initial angle it is sewn into.
Contralateral Access and Cannulation of Target Visceral Branch(es)
■
After the femoral access side has been chosen and prepared for main body endograft delivery, the
contralateral femoral site is used to cannulate the planned visceral or renal branches from the
bottom. In the periscope configuration, the parallel stent graft is often required to make a U-turn, so
the more flexible covered stent, the self-expanding Viabahn (Gore Medical, Flagstaff, AZ), is
preferred. This requires larger sheath access (up to 12 Fr) than the iCAST described earlier;
however, for a double periscope configuration, a larger 20-Fr or 22-Fr sheath is usually necessary
to perform multiple punctures into (FIG 11).
■
The typical periscope EVAR/TEVAR involves the need for a distal landing zone (FIG 12). In this
particular case, the celiac and one renal artery were already occluded, so the periscope technique
was used to revascularize the SMA and remaining renal artery, with an 11-mm Viabahn in the
SMA requiring a 12-Fr sheath (blue arrow) and an 8-mm Viabahn as the renal periscope requiring
an 8-Fr sheath (orange arrow) (FIG 13).
Sheath Advancement and Periscope Stent Graft Positioning
■
Similar to the snorkel/chimney EVAR procedure earlier, the general principles of advancing the
sheath into the target visceral vessel are repeated, but in periscope EVAR/TEVAR, all is
performed from the femoral approach. The SMA and renal periscopes are positioned several
centimeters into the target vessel origin, with the distal end (blue arrow) below the bottom end of
the main body stent graft (white arrow) (FIG 14).
Sequence of Deployment and Balloon Molding
■
The main body endograft is deployed with the periscope sheaths still in position (FIG 15A). The
sheaths are then slowly withdrawn to allow the periscope stent grafts (Viabahns) to deploy against
the main body endograft (FIG 15B). Because there is often some compression of the self-
expanding periscope stents, an additional balloon-expandable bare stent is placed along where
there is contact with the main body endograft and a similar sequence as earlier of balloon molding
is performed to minimize gutter formation (FIG 16).
■
The remainder of the proximal aspect of the aneurysm is visualized and appropriately stent grafted
with proximal extensions and ballooned (FIG 17), and postoperative CT-A confirms aneurysm
exclusion with wide patency of the periscope stent grafts and normal target vessel perfusion (FIG
18).
PEARLS AND PITFALLS
Indications ■ Follow general recommendations for elective repair of abdominal
aortic aneurysms (AAAs) and consider raising criteria when
applying complex snorkel/chimney/periscope procedures to these
often compromised patients.
■ Most of these procedures use approved devices in an off-label
manner so informed consent to discuss all available options is
important.
Preoperative workup ■ High-quality imaging and the ability to manipulate images on a 3-
D workstation are mandatory for successful preoperative planning
and device choices.
■ Adequate preoperative and perioperative hydration is important,
given the amount of renal artery manipulation that occurs during
these cases.
Patient setup ■ The advanced imaging afforded by a dedicated hybrid
endovascular suite allows improved visualization during these
very technically demanding procedures.
■ A well-trained staff and two-surgeon approach are important to
ensure safe delivery of endograft components from both the
femoral and brachial positions.
Arm access ■ Two 7-Fr sheaths can be placed in the high brachial position from
a transverse incision, and the puncture sites need to be at least 2 to
3 cm away from each other to allow safe and independent
arteriotomy closure.
Renal cannulations ■ A coaxial system with sheath and covered stent into the target
renal or visceral vessel from the brachial approach optimizes safe
and accurate deployment of snorkel stents.
■ Careful wire manipulation in distal renal and using less stiff wires
with J-tips, if possible, minimizes likelihood of renal parenchymal
injury and theoretical possibility of renal microemboli.
Balloon molding sequence ■ Careful attention to sequence of snorkel/chimney/periscope
balloon sequence minimizes gutter formation, promotes good neck
apposition, and prevents compression of vital visceral and renal
branches.
POSTOPERATIVE CARE
■
At the conclusion of the procedure, patients are usually extubated, observed for 2 to 3 days in a
monitored setting (in the intensive care unit overnight if lumbar drain present), and discharged
home when ambulating, tolerating a normal diet, and with stable renal function. Clopidogrel and
aspirin are given if the patients are not already taking these medications for at least 6 weeks
postoperatively.
OUTCOMES
■
Multiple reviews of the worldwide experience with snorkel/chimney and periscope techniques
continue to find it to be technically successful with target revascularization rates in the 95% to
100%, mortality in the 2% to 5% range, morbidity up to 10%, and midterm renal and branch
patency rates of 92% to 96%.12,13
■
Rupture-free survival after snorkel/chimney or periscope EVAR is excellent in the small amount of
literature published on this new approach but will be important to observe in the mid- and long-
term to ensure that this technique is durable as a strategy for endovascular repair of complex
aneurysms.
COMPLICATIONS
■
Perioperative complications related to complex EVAR in general include cardiac ischemia,
arrhythmias or exacerbation of heart failure, groin wound seroma and infection, early thrombosis
of endograft components, and bleeding issues related to access site. Reported rates of these issues
are not particularly different than the wealth of literature for routine EVAR.
■
Particular to snorkel/chimney techniques involve the use of the arm access, which has the potential
of leading to arm ischemia, nerve injury/irritation of the brachial plexus, and axillary seromas.
■
Wire and catheter manipulation and poor wire hygiene can lead to inadvertent renal parenchymal
injury that can lead to hematomas and excessive bleeding requiring transfusion. The rate of renal
function decline is certainly more than in standard EVAR, although we do not believe it to be
worse than open suprarenal surgery, fenestrated, or branched devices.
■
Right arm access for multiple snorkel/chimney stents has been reported to lead to higher rates of
cerebrovascular complications.1,8 This is likely due to moderate amounts of time that sheaths are
across the aortic arch and the possibility of thrombus formation that can lead to cerebral emboli.
■
Gutter leaks are a unique consequence of the parallel stent graft strategy and are poorly understood.
Some general guidelines involve placing as long of stents as possible in parallel configuration to
force gutter leaks to thrombose, and careful long-term imaging follow-up to ensure that the
aneurysm is excluded.
REFERENCES
1. Lee JT, Greenberg JI, Dalman RL. Early experience with the snorkel technique for juxtarenal aneurysms. J Vasc Surg.
2012;55:935–946.
2. Knott AW, Klara M, Duncan AA, et al. Open repair of juxtarenal aortic aneurysms (JAA) remains a safe option in the era of
fenestrated endografts. J Vasc Surg. 2008;47:695–701.
3. Greenberg RK, Sternbergh WC III, Makaroun M, et al. Intermediate results of a United States multicenter trial of fenestrated
endograft repair for juxtarenal abdominal aortic aneurysms. J Vasc Surg. 2009;50:730–737.
4. Greenberg RK, Clair D, Srivastava S, et al. Should patients with challenging anatomy be offered endovascular aneurysm repair? J
Vasc Surg. 2003;38:990–996.
5. Ohrlander T, Sonesson B, Ivancev K, et al. The chimney graft: a technique for preserving or rescuing aortic branch vessels in stent-
graft sealing zones. J Endovasc Ther. 2008;15:427–432.
6. Donas KP, Torsello G, Austermann M, et al. Use of abdominal chimney grafts is feasible and safe: short-term results. J Endovasc
Ther. 2010;17:589–593.
7. Bruen KJ, Feezor RJ, Daniels MJ, et al. Endovascular chimney technique versus open repair of juxtarenal and suprarenal
aneurysms. J Vasc Surg. 2011;53:895–905.
8. Coscas R, Kobeiter H, Desgranges P, et al. Technical aspects, current indications, and results of chimney graft for juxtarenal aortic
aneurysms. J Vasc Surg. 2011;53:1520–1527.
9. Moulakakis KG, Mylonas SN, Avgerinos E, et al. The chimney graft technique for preserving visceral vessels during endovascular
treatment of aortic pathologies. J Vasc Surg. 2012;55:1497–1503.
10. Al-Khatib WK, Dua MM, Zayed MA, et al. Percutaneous EVAR in females leads to fewer wound complications. Ann Vasc Surg.
2012;26:476–482.
11. Rancic Z, Pfammatter T, Lachat M, et al. Periscope graft to extend distal landing zone in ruptured thoracoabdominal aneurysms
with short distal necks. J Vasc Surg. 2010;51:1293–1296.
12. Katsargyris A, Oikonomou K, Klonaris C, et al. Comparison of outcomes with open, fenestrated, and chimney graft repair of
juxtarenal aneurysms: are we ready for a paradigm shift? J Endovasc Ther. 2013;20:159–169.
13. Donas KP, Pecoraro F, Bisdas T, et al. CT angiography at 24 months demonstrates durability of EVAR with the use of chimney
grafts for pararenal aortic pathologies. J Endovasc Ther. 2013;20:1–6.
Branched and Fenestrated Endovascular Stent Graft
Chapter 18 Techniques
Gustavo S. Oderich Karina S. Kanamori
■
Anatomic constraints for endovascular management of abdominal aortic aneurysms include the
presence of short or angulated surgical necks and aneurysmal degeneration of the origins of the
visceral arteries. Fenestrated and branched endografts were introduced to enable minimally
invasive repair of complex juxta- and suprarenal aortic aneurysms.1 These devices incorporate
reinforced fenestrations or directional branches, permitting incorporation of visceral artery origins
into the proximal endograft seal zone without compromising end-organ perfusion or aneurysm
exclusion.2 This chapter summarizes the technical features of endovascular aneurysm repair using
fenestrated and branched stent grafts for pararenal and thoracoabdominal aortic aneurysms.
DEFINITION
■
The term fenestrated repair refers to deployment of an endograft featuring custom orifices created
and reinforced at precise locations around the aortic perimeter to enable branch artery access,
cannulation, and placement of a bridging stent graft in the course of aneurysm exclusion.
Fenestration sites are created from patient-specific cross-sectional image data to enable exclusion
of aneurysms with short or angled infrarenal necks. In most circumstances, the target arteries (e.g.,
renal or mesenteric) must arise from normal aorta to enable fenestrated repair. As a rule,
fenestrations must be able to deploy flush with the aortic wall to ensure adequate aneurysm
exclusion. “Alignment” stents (covered or uncovered, depending on individual patient
circumstance) are deployed as needed to prevent target artery malperfusion as a consequence of
misalignment between the fenestration and target artery orifice.
■
Branched repair refers to endovascular aneurysm exclusion employing covered stents to directly
connect the main lumen of the endograft to the target visceral artery. These devices enable repair
of aneurysms involving or extending proximal to the origins of the renal or visceral vessels (e.g.,
type IV thoracoabdominal aortic aneurysms [TAAAs]). Of necessity, some distance must be
present between the main body of the endograft at full deployment and the aortic wall at the target
visceral artery orifice. Branched stent grafts are currently available in two distinct configurations:
■
Fenestrated branches arise from reinforced fenestrations bridged by balloon-expandable
covered stents.
■
Directional or cuffed branch devices feature appended fabric cuffs, precisely located to enable
straight, helical, down- or up-going guidewire egress, target vessel cannulation, and deployment
of bridging covered stents. Self-expanding flexible nitinol stents are usually employed for this
purpose.
■
Most aneurysms are degenerative (previously characterized as “atherosclerotic,” based on a
similar, although not identical, causal risk factor profile).
■
Other relevant etiologies include infection (e.g., mycotic aneurysms), inflammation (e.g.,
inflammatory aneurysm or aortitis), development of penetrating ulcers or asymmetric saccular
enlargement, and related aortic pathologies (dissection or intramural hematoma).

■
Most patients’ aneurysms do not prompt symptoms prior to catastrophic rupture and are diagnosed
incidentally or during screening. Indications for repair are size greater than 5.5 cm for males and
greater than 5 cm for females or enlargement greater than 5 mm in 6 months.3
■
In approximately 5% to 10% of patients, aneurysms induce periaortic inflammation and resultant
retroperitoneal fibrosis involving adjacent structures, including the duodenal and ureters.4 These
patients may present with abdominal or back pain, fatigue, malaise, or low-grade fever even at
relatively small diameters. Commonly, these aneurysms also enlarge at accelerated and
unpredictable rates. Other uncommon presentations of abdominal aortic aneurysm disease include
the presence of distal embolization with “blue toe syndrome,” congestive heart failure from
aortocaval fistulae, or gastrointestinal bleeding from primary aortoenteric fistulae.
■
A comprehensive history should be obtained to fully appreciate the potential natural history of each
patient’s disease, including a comprehensive assessment of cardiovascular risk factors, current
smoking habits, and a family history of aneurysmal disease or connective tissue disorders.
■
Evaluation of perioperative clinical risk emphasizes cardiac, pulmonary, and renal functional status
and reserve, including baseline laboratory testing, noninvasive cardiac stress testing, pulmonary
function assessment, and carotid duplex ultrasonography when indicated.
DIAGNOSTIC IMAGING
■
Preprocedural aortic imaging studies provide fundamental and necessary guidance for endovascular
repair strategies of all types. Aneurysm morphology is best analyzed through acquisition of high-
resolution computed tomography angiography (CTA) datasets.5 CTA with submillimeter slice
acquisition is recommended for optimal acquisition, allowing three-dimensional reformatting
techniques, maximum intensity projections, and volume rendering.
■
Stent grafts are currently custom-made to conform to patient anatomy, based on estimates of
longitudinal distance, axial clock position, arc lengths, and angles derived from centerline of flow
measurements.
■
Anatomic limitations to be considered include difficult iliac access, excessive aortic tortuosity,
visceral artery occlusive disease, and anatomic variants including multiple accessory renal
arteries or early renal branch bifurcation.
STENT GRAFT DESIGN

■
Device planning starts with selection of the proximal landing zone based on “healthy” aorta. The
proximal landing zone should include at least a 2-cm length of “normal,” noncalcified, parallel
aortic wall. The outer-to-outer aortic diameter should be more than 18 mm and less than 32 mm for
pararenal aneurysms and more than 18 mm and less than 38 mm for TAAAs.6 Landing zone
diameter should be no larger than the diameter of the next most proximal aortic segment.
■
Fenestrated stent grafts are currently manufactured with three fenestration options: small and large
circles and more proximal scallops (FIG 1A). Small fenestrations are 6 × 6 mm or 6 × 8 mm,
created without crossing struts and reinforced by circumferential nitinol rings. Large
fenestrations’ diameters are 8, 10, or 12 mm and may incorporate stent struts crossing the edge or
middle of the circular defect, limiting space available for alignment stents. Scallops are contoured
indentations along the upper edge of the main body endograft fabric, 10 mm wide and ranging in
height from 6 to 12 mm, depending on individual patient anatomy.5
■
Device designs vary with aneurysm extent. For pararenal aneurysms, 70% of patients are adequately
treated with two small fenestrations for the renal arteries and a scallop for the superior mesenteric
artery (SMA).5 Suprarenal and type IV TAAAs typically require four fenestrations (no scallops).
Extensive TAAAs (types I to III) need directional branches, particularly if the aortic diameter is
relatively large or aneurysmal at the level of the visceral arteries. The combination of directional
branches for celiac and SMA management with fenestrations for the renal arteries is increasingly
popular.
SURGICAL MANAGEMENT
Ancillary Tools
■
These procedures require advanced endovascular skills and a comprehensive inventory of
applicable catheters, balloons, and stents (Table 1). Dedicated training in fenestrated and
branched techniques is highly recommended for physicians already experienced in endovascular
disease management and ancillary procedures including renal and visceral artery disease
management.
Perioperative Measures
■
Patients with difficult aneurysm anatomy, chronic kidney disease, or advanced age are preadmitted
for bowel preparation and intravenous hydration with bicarbonate infusion. Oral acetylcysteine is
administered to minimize risk of periprocedural renal dysfunction following administration of
iodinated contrast.
■
Hybrid, fixed imaging platforms are essential for optimal results of these complex procedures. Most
are performed using general endotracheal anesthesia; local or regional anesthesia may be
sufficient in select cases.
■
Intraoperative blood salvage systems (“cell saver”) are recommended for difficult cases and all
TAAAs. The creation of large, impermeable pockets within dependent portions of the surgical
drapes will facilitate pooling and collection via the cell saver.
■
The use of iodinated contrast is minimized by avoidance of power injector digital substraction
angiography (DSA) runs during device implantation and side stent placement. Whenever possible,
hand injections of dilute contrast (70% saline) are used to locate the side branches. Completion
aortography is obtained only after all stents are positioned and postdilated, again using diluted
contrast (50%).
■
To minimize contrast, precatheterization of targeted visceral arteries or use of onlay computed
tomography (CT) images, when available, is recommended. In experienced hands,
precatheterization adds little to the overall procedure time.
Positioning
■
Patients are positioned supine with the imaging unit oriented from the head of the table. Both arms
are tucked for repair of pararenal aneurysms requiring up to three fenestrations.
■
Brachial artery access is used in patients treated by directional branches or those who need four
fenestrations. The left arm is abducted and prepped in the surgical field up to the axilla. A working
sterile side table is oriented in the same axis of the abducted arm for optimal support of necessary
wires and catheters.
■
Electrocardiogram (EKG) leads, urinary catheter, and other monitoring cables and lines should be
taped or secured so that they are not in the path of the x-ray beam of the fluoroscopic unit and do
not impede movement of the C-arm gantry.
Arterial Access
■
Access is established in the femoral arteries. Patients with small, calcified, or stenotic iliac arteries
may require creation of an iliac conduit for safe device delivery.
■
Total percutaneous femoral access is the preferred approach in patients with noncalcified arteries
or mild posterior plaque. The standard “preclose” technique enables complete hemostasis in more
than 95% of patients irrespective of sheath diameter.7 When femoral arteries are small, calcified,
or bifurcate close to the inguinal ligament, standard surgical exposure and access is obtained.
Proximal and distal control is obtained using vessel loops.
■
The left brachial artery is surgically exposed via small longitudinal incision in the upper arm, just
proximal to the origin of the deep brachial artery.
■
Intravenous heparin (80 to 100 units/kg) is administered immediately after femoral and brachial
access is established. An activated clotting time longer than 250 seconds is maintained throughout
the procedure with frequent rechecks every 30 minutes. Prior to deployment of the stent graft,
diuresis is induced with intravenous mannitol and/or furosemide.
TECHNIQUES
ENDOVASCULAR REPAIR USING FENESTRATED STENT GRAFTS
■
Fenestrated–branched repair is currently performed using the Cook Zenith® stent graft lineage.
Newer designs by Endologix (Ventana), Terumo (Anaconda), and Cook Medical (p-Branch) are
under clinical investigation.
■
The Cook Zenith® fenestrated stent graft consists of a proximal fenestrated tubular component, a
distal bifurcated universal component, and a contralateral iliac limb extension (FIG 1A). The
fenestrated tubular component is custom-made to fit the patient’s anatomy. Four to 6 weeks are
required for manufacturing and delivery in the United States.
■
Bilateral percutaneous femoral access is established under ultrasound guidance; each femoral
puncture is preclosed using two Perclose devices. Bilateral 8-Fr sheaths are introduced to the
external iliac arteries over Benson guidewires (Cook Medical, Bloomington, IN). The guidewires
are exchanged to 0.035-in soft glidewires and Kumpe catheters, which are advanced to the
ascending aorta and exchanged for stiff 0.035-in Lunderquist guidewires (Cook Medical,
Bloomington, IN).
■
Choice of access site is dependent on tortuosity and vessel diameter. Provided there are no issues
with both iliac arteries, the branches are performed via the right femoral approach, whereas the
fenestrated and bifurcated devices are introduced via the left femoral approach. A 20-Fr (two
fenestrations) or 22-Fr (three fenestrations) Check-Flo sheath (Cook Medical, Bloomington, IN) is
introduced via the right femoral approach (FIG 2A). The valve of the Check-Flo sheath has four
leaflets, which are accessed by two short 7-Fr sheaths at 2 o’clock and 7 o’clock positions.
■
Precatheterization of the renal arteries is performed using 0.035-in soft glidewires and 5-Fr Kumpe
or C1 catheters (Cook Medical, Bloomington, IN), which are supported by 7-Fr left internal
mammary artery (LIMA) guide catheters (FIG 2B). Alternatively, onlay fusion CTA is
recommended to minimize contrast use.
■
Once the target vessels are catheterized, the fenestrated stent graft is oriented extracorporeally,
introduced via the left femoral approach, and deployed with optimal apposition between the
fenestrations and the target catheters.
■
Proper device orientation, using the anterior and posterior markers, is essential. It is useful to
deploy the first two or three stents and then rotate the imaging unit laterally, confirming alignment
between the catheter and its respective fenestration. The device should be deployed slightly higher
than what is anticipated, with the catheter matching the lowest of the four radiopaque markers in
the fenestration. The diameter-reducing wire on the fenestrated component allows for some
rotational and cranial–caudal movement to optimize alignment following initial deployment.
■
After deployment of the fenestrated component, each catheter is removed from its target artery and
used to sequentially regain target vessel access through the respective fenestration. (FIG 2C). In
most cases, when alignment is carefully confirmed prior to attempted cannulation, the target vessel
is accessed without difficulty.
■
After the target vessel is catheterized, soft glidewire is removed and hand injection is used to
confirm location. The glidewire is exchanged for a 0.035-in Rosen guidewire (Cook Medical,
Bloomington, IN). The Rosen guidewire has a floppy J tip, reducing the risk of branch renal artery
perforations. When additional support is required, the Amplatz guidewire (Cook Medical,
Bloomington, IN) with 1-cm soft tip can be used.
■
After the Rosen or stiff guidewire of choice is positioned, a 7-Fr Ansel sheath with flexible dilator
is advanced. If there is difficulty to advance the sheath, an undersized balloon may be used as a
dilator to facilitate advancement.
■
Once the sheath is in position, an alignment stent is positioned under protection of the sheath with the
tip of the stent just beyond the tip of the sheath (FIG 2D).
■
For repairs requiring two or three vessel fenestrations, the target vessels are accessed sequentially
using femoral approach. For those requiring four fenestrations, the celiac axis is accessed via
brachial approach using a preloaded catheter, which is placed through the celiac fenestration and
exits the stent graft via an access scallop at the top of the device.
■
The diameter-reducing tie on the fenestrated segment is removed after all the target arteries are
accessed and secured by 7-Fr hydrophilic sheaths.
■
The top cap of the device is advanced forward to deploy the uncovered fixation stent (FIG 3A). The
top cap is retrieved prior to deployment of the alignment stents.
■
After the top cap and dilator are removed, the proximal landing zone is gently dilated using a
compliable balloon such as the Coda balloon (Cook Medical, Bloomington IN, FIG 3B). It is
critical that the balloon dilatation is performed prior to placement of alignment stents, or
alternatively, each stent has to be protected by separate balloons.
■
The alignment stents are sequentially deployed following removal of the diameter-reducing tie,
retrieval of the top cap, and balloon dilatation of the neck. The sequence of stent deployment is
renal arteries followed by SMA and celiac axis. Prior to each stent deployment, the position of
the stent is confirmed by hand injection. The stent is deployed 3 to 5 mm into the aorta (FIG 3C)
and flared using a 10-mm × 2-cm balloon (FIG 3D). A completion angiography of each branch is
performed using hand injection after direct injection of 100 to 200 μg of nitroglycerin to minimize
spasm.
■
Following placement of the alignment stents, a distal bifurcated stent graft is oriented, advanced, and
deployed with preservation of the ipsilateral internal iliac artery. The dilator of the bifurcated
device may encroach the contralateral renal stent or the SMA stent. In these cases, it is useful to
leave a 10-mm balloon ready to be inflated in the renal stent to prevent damage (FIG 4A, inset).
The minimum overlap between the bifurcated and the fenestrated component is two full-length
stents (17 mm each), but ideally, more than three full stents is recommended to minimize risk of
component separation (FIG 4B).8 After deployment of the bifurcated device, the dilator is
removed with care to avoid damage or dislodgement of the renal stents.
■
The contralateral gate is catheterized using a soft glidewire and 5-Fr catheter (FIG 4B). Access is
confirmed by 360-degree catheter rotation. The glidewire is exchanged for a 0.035-in Lunderquist
guidewire. Limited iliac angiography using contralateral oblique views with hand injection. The
contralateral limb extension is deployed with preservation of the internal iliac artery (FIG 4C).
■
A completion angiography of the aorta and iliac arteries is obtained using power injection to
demonstrate patency of the visceral arteries, main body, iliac limbs, and iliac arteries.
ENDOVASCULAR REPAIR USING MULTIPLE DIRECTIONAL

BRANCHES (MULTIBRANCH T-BRANCH STENT GRAFT)
■
Directional branches created with presewn cuffs are currently available from Cook Zenith® stent
graft lineage on an investigational-use basis (FIG 1B). A four-vessel multibranch stent graft design
(T branch) is also being investigated for treatment of TAAAs.9
■
The extent of repair varies depending on the proximal extension of aneurysm within the thoracic
aorta. The procedure is performed using bilateral femoral and left brachial approach. In general,
the repair starts with deployment of a proximal thoracic TX2 stent graft (Cook Medical,
Bloomington, IN) followed by deployment of the T-branch stent graft (Cook Medical, Brisbane,
Australia) and distal bifurcated component and contralateral limb extension. The self-expandable
stents are placed into the four branches following deployment of all aortic components. The
critical steps are reviewed as follows:
■
Bilateral femoral and left brachial arterial access is obtained (FIG 5A). A proximal thoracic
stent graft is deployed if needed depending on aneurysm extent.
■
Precatheterization of the renal arteries is not required, but it is critical that the distal edge of the
directional branch is deployed above its intended target vessel. To guide deployment of the T-
branch component, the SMA is precatheterized via the brachial approach (FIG 5B).
■
The T-branch stent graft is oriented extracorporeally, introduced via the femoral approach, and
deployed with the directional branches located proximal to its intended target vessel (FIG 5C).
■
Deployment of the distal universal bifurcated stent graft and contralateral iliac extension are
identical to what was described in the fenestrated technique (FIG 5D).
■
The femoral arteries are closed at this point, restoring flow into the lower extremities. It is useful
to maintain access into one of the femoral arteries with a 5-Fr sheath (FIG 5E, inset). This
maneuver allows passage of a 0.014-in guidewire from the left brachial artery to femoral artery.
The guidewire is clamped in both ends, which locks the 12-Fr sheath in place and provides
support for deployment of the side branches.
■
The 12-Fr Ansel I sheath (Cook Medical, Bloomington, IN) is advanced via the left brachial
approach and positioned inside the T-branch component in the descending thoracic aorta (FIG
5E). At this point, a 0.014-in guidewire is advanced through and through from the left brachial
to femoral artery, preventing movement of the 12-Fr sheath in the aortic arch.
■
Each side branch is individually catheterized in a sequential fashion, starting with the renal
arteries (FIG 5F) followed by the SMA and celiac axis. A 5-Fr main pulmonary artery (MPA)
or Kumpe catheter (Cook Medical, Bloomington, IN) is used to access the directional branch
and target vessel. Once the vessel is catheterized, the soft glidewire is exchanged for a stiff
guidewire (Rosen or short-tip Amplatzer, Cook Medical, Bloomington, IN), which is positioned
in the target vessel.
■
A 9-Fr 80-cm flexor sheath (Cook Medical, Bloomington, IN) is advanced coaxially within the
12-Fr sheath into the target vessel.
■
Each target vessel is stented with a self-expandable stent graft (FIG 5F). The stent graft should be
oversized by 1 to 2 mm and should provide at least 2 cm of distal landing zone in the target
vessel, extending 3 to 5 mm into the aortic lumen of the T-branch device.
■
To prevent kinks in the transition of the stent graft to the target artery, each self-expandable stent
graft is reinforced by a second self-expandable uncovered stent, which is deployed 1 cm beyond
the distal edge of the stent graft (FIG 5G). Selective completion angiography is obtained for
each sequential branch.
■
A completion angiography of the arch and thoracoabdominal aorta is obtained after all matting
stent grafts are deployed (FIG 5H).
ENDOVASCULAR REPAIR USING TWO DIRECTIONAL BRANCHES AND

TWO FENESTRATIONS (TWO BRANCH–TWO FENESTRATED STENT
GRAFT)
■
A design with directional branches for the celiac and SMA and fenestrations for the renal arteries
has been widely used at the Cleveland Clinic.10 More recently, a newer design with two straight
down-going branches and two fenestrations has been used (FIG 1C). The advantage of the latter is
the ability to provide short, transversely oriented branches for the renal arteries.
■
The same principles already described for fenestrated stent grafts are applied with respect to device
design, planning, and arterial access.
■
Bilateral femoral access and left brachial artery access is needed (FIG 6A). The right femoral
access is used for precatheterization of the renal arteries. The left brachial access is used for the
celiac axis and SMA (FIG 6B).
■
A proximal thoracic TX2 stent graft (Cook Medical, Bloomington, IN) is deployed first, depending
on proximal extension of the aneurysm (FIG 6A).
■
After the renal arteries and SMA are precatheterized, the fenestrated–branched stent graft is oriented
extracorporeally, introduced via the femoral approach and deployed with perfect apposition
between the renal fenestrations and the target renal arteries (FIG 6B).
■
The celiac and SMA branch are accessed using preloaded catheters and glidewires, which are
snared via the left brachial approach (FIG 6B).
■
Each catheter is sequentially removed from the renal arteries and used to regain access into the
fenestrated component, renal fenestration, and target renal artery (FIG 6C). Hydrophilic sheaths
and alignment renal stents are advanced as previously described.
■
The preloaded catheters in the SMA and celiac branch allow advancement of a 0.035-in soft
glidewire, which is snared via the left brachial approach (FIG 6B). A sheath and catheter are
advanced into the celiac branch. Following access into the celiac axis, a 0.035-in Amplatz
guidewire is placed.
■
The SMA is accessed using similar steps, and after access is established with Amplatz guidewire, a
9-Fr sheath is advanced to allow positioning of a self-expandable stent graft.
■
Once all four vessels are catheterized and sheaths are positioned into the renal arteries and SMA,
the diameter-reducing tie is removed, allowing complete expansion of the fenestrated–branched
component (FIG 6D).
■
Sequential target artery stenting is performed using balloon-expandable covered stents for the renal
fenestrated branches (FIG 6E, inset) and self-expandable stent grafts for the SMA and celiac axis
(FIG 6E, inset). Selective branch angiography is performed after each branch stent is placed.
■
Deployment of distal bifurcated component and contralateral iliac limb extension is identical to
what has been described for fenestrated stent grafts (FIG 6F).
PEARLS AND PITFALLS

Preoperative evaluation ■ Complete history and physical examination with emphasis on
cardiovascular risk factors, family history of aneurysm disease,
and connective tissue disorders
■ Preoperative medical evaluation focused on cardiac, pulmonary,
and renal performance
■ Aortic imaging with computed tomography angiography allows
detailed analysis of aneurysm morphology for stent graft design
and procedure planning.
Arterial access ■ Iliac conduits are recommended in patients with small, diseased,
or excessively tortuous iliac arteries.
■ Pelvic perfusion with maintenance of internal iliac artery flow
decreases risk of spinal cord injury.
Stent graft implantation ■ Precise stent graft design and implantation are critical aspects of
the procedure.
■ Minimize use of iodinated contrast by avoiding contrast
aortography during device implantation.
■ Precatheterization and/or onlay CT allows precise device
implantation with minimal need of angiography.
■ Fenestrations are typically accessed via the femoral approach and
stented using balloon-expandable covered stents.
■ Directional branches are accessed via the brachial approach and
stented using self-expandable stent grafts.
Misaligned fenestrations ■ Excessive tortuosity in the iliac or visceral segment may cause
misalignment of fenestrations and difficult target vessel
catheterization.
■ Rotation of the device, which is constrained by a diameter-
reducing tie, and use of balloon displacement or curved catheters
allow successful catheterization in most cases.
Branch perforation or ■ Small, diseased, and tortuous visceral arteries are prone to
dissection perforation or dissection, particularly if an Amplatz guidewire is
needed to provide more support.
■ Careful attention to detail and minimizing guidewire manipulation
with close attention to the tip of the guidewire help prevent this
complication.
Stent kinks ■ Branch tortuosity may lead to kinks within the side stents.
■ This should be immediately recognized and treated by placement
of a second self-expandable stent to prevent branch occlusion.
POSTOPERATIVE CARE
■
Length of stay averages 2 to 3 days for endovascular repair of pararenal aneurysms and 4 to 5 days
for TAAAs.
■
Cerebrospinal fluid drainage is discontinued on postoperative day 2, after a 6-hour clamp trial and
documentation of normal coagulation profile.
■
Oral diet is resumed the day after the operation for uncomplicated cases requiring two to three
fenestrations, but it is typically withheld for 1 or 2 days for difficult cases or those requiring four
fenestrations or branches.
■
A CTA and baseline duplex ultrasound of the visceral branches is obtained prior to dismissal.
Follow-up includes clinical examination and imaging (CTA and ultrasound) in 6 to 8 weeks, every
6 months during the first year, and yearly 1 year, and early thereafter.
■
Patients are started on aspirin indefinitely. Clopidogrel is not recommended unless there is a
specific concern with one of the side branches because of small size (<4 mm), occlusive disease,
or dissection. Clopidogrel should be avoided early after extensive TAAA repair because of risk
of delayed spinal cord injury and paraplegia, which may necessitate replacement of the spinal
drain.
OUTCOMES
■
Fenestrated and branched stent grafts have been widely applied to treat pararenal and TAAAs.
Early mortality rate is dependent on the extent of repair. For pararenal aneurysms, mortality ranges
from 0% to 3% in single-center reports11,12 and averages 1.8% in a systematic review.13 TAAAs
are associated with early mortality of 0% to 9% in single-center reports.14,15
■
Technical success is high for endovascular repair using fenestrated stent grafts (91% to 100%)16,17
and branched stent grafts (93% to 100%).11,18
■
Endoleaks from the attachment sites (type I and type III) are uncommon with fenestrated and
branched stent grafts. Type II endoleak is the most common type of endoleak and occurs in 0% to
20% of the patients.19,20
■
Branch vessel patency is excellent with fenestrated branches, averaging 90% to 100%.15,21 In a
recent report by Mastracci and associates,22 freedom from any branch-related complication
(occlusion, kink, reintervention) was 84% at 5 years.
COMPLICATIONS
Intraprocedural Complications
■
Fenestration misalignment
Neck angulation, tortuosity, and errors of design or implantation can lead to misalignment between
the fenestration and the target vessel. Several maneuvers can be used to overcome misalignment
between the fenestration and the vessel. Initially, the catheter and guidewire are rotated to “probe”
the aortic wall in search for the vessel. To maintain access into the fenestration, a 7-Fr Ansel
sheath is advanced into the fenestration and secured by a 0.018-in guidewire, whereas a 5-Fr
“buddy” catheter (e.g., Van Schie [VS] 3) is used to locate the renal artery. In patients with down-
going or stenosed renal arteries, it may be difficult to advance the catheter over a soft glidewire.
The catheter and glidewire may bounce up into the top cap, providing support for the catheter to be
advanced deep into the renal artery.
■
Diameter-reducing ties are located posteriorly, which may result in the fenestrations being pulled
slightly more posterior than its intended location. A useful maneuver is to gently rotate each
fenestration, usually anteriorly. Other maneuvers are rarely needed but included use of curved
catheters (e.g., VS1 or SOS) for down-going vessels or vessels that are originating from the lower
part of the fenestration, microcatheters, and balloon displacement of the main stent graft. The latter
is rarely needed but may provide more room for catheter manipulations.
■
Branch perforation or dissection
Branch vessel perforation and/or dissection can be prevented by meticulous technique,
visualization of the tip of the wire, and avoiding wire manipulations. The guidewire should not be
positioned in small terminal branches, which are prone to perforate or dissect. It should be
visualized and stabilized during exchanges manipulations, avoiding forward or retrograde
movement. If perforation occurs, it should be immediately recognized and treated using a
microcatheter and coil embolization. Dissections within the main renal artery can be treated by
placement of a self-expandable stent.
■
Endoleaks
Type II and type IV endoleaks may occur and should be left untreated. Type I and type III
endoleaks (<3%) are infrequent with proper selection of a healthy landing zone and adequate
planning.23 In the U.S. fenestrated trial, there were no type I or III endoleaks.5 In the event of a type
Ia endoleak, the proximal neck may be redilated, but all the alignment stents need to be protected
by separate balloons. Type III endoleaks may result from inadequate flare, lack of apposition, use
of bare metal stent, or inadequate length into the aorta.
■
Stent kinks or narrowing
Kinks are highly preventable and can be anticipated from careful review of vessel anatomy by
CTA. These remain a cause of reintervention or branch vessel loss if not recognized. Short stents
(<2 cm) tend to avoid bends and the mid- or distal portion of the renal artery, which has greater
respiratory motion. The right renal may have a posterior orientation from its course behind the
inferior vena cava. If a kink is anticipated by CTA or is evident by completion angiography, a self-
expandable stent should be placed. Kinks or narrowing may also result from inadequate flare, strut
compression, and ostial disease. In these cases, angioplasty or stenting with a second balloon-
expandable stent may be recommended.
Postoperative Complications
■
Spinal cord injury
■
Stroke
■
Cardiac events (myocardial infarction, arrhythmias, congestive heart failure)
■
Pulmonary complications (pneumonia, prolonged ventilation, tracheostomy)
■
Gastrointestinal complications (ileus, pancreatitis, cholecystitis)
■
Systemic inflammatory response (fever, leukocytosis, thrombocytopenia)
■
Renal function deterioration
■
Access-related problems (bleeding, thrombosis, pseudoaneurysm)
REFERENCES
1. Park JH, Chung JW, Choo IW, et al. Fenestrated stent-grafts for preserving visceral arterial branches in the treatment of abdominal
aortic aneurysms: preliminary experience. J Vasc Interv Radiol. 1996;7(6):819–823.
2. Nordon IM, Hinchliffe RJ, Holt PJ, et al. Modern treatment of juxtarenal abdominal aortic aneurysms with fenestrated endografting
and open repair—a systematic review. Eur J Vasc Endovasc Surg. 2009;38(1):35–41.
3. Brewster DC, Cronenwett JL, Hallett JW Jr, et al. Guidelines for the treatment of abdominal aortic aneurysms. Report of a
subcommittee of the Joint Council of the American Association for Vascular Surgery and Society for Vascular Surgery. J Vasc
Surg. 2003;37(5):1106–1117.
4. Hellmann DB, Grand DJ, Freischlag JA. Inflammatory abdominal aortic aneurysm. JAMA. 2007;297(4):395–400.
5. Greenberg RK, Sternbergh WC III, Makaroun M, et al. Intermediate results of a United States multicenter trial of fenestrated
endograft repair for juxtarenal abdominal aortic aneurysms. J Vasc Surg. 2009;50(4):730–737.e1.
6. Mendes BC, Oderich GS, Correa MP, et al. Endovascular repair of complex aortic pathology. Curr Surg Rep. 2013;1(2):67–77.
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. Dowdall JF, Greenberg RK, West K, et al. Separation of components in fenestrated and branched endovascular grafting—branch
protection or a potentially new mode of failure? Eur J Vasc Endovasc Surg. 2008;36(1):2–9.
9. Sweet MP, Hiramoto JS, Park KH, et al. A standardized multi-branched thoracoabdominal stent-graft for endovascular aneurysm
repair. J Endovasc Ther. 2009;16(3):359–364.
10. Greenberg RK, Qureshi M. Fenestrated and branched devices in the pipeline. J Vasc Surg. 2010;52(suppl 4):15S–21S.
11. Beck AW, Bos WT, Vourliotakis G, et al. Fenestrated and branched endograft repair of juxtarenal aneurysms after previous open
aortic reconstruction. J Vasc Surg. 2009;49(6):1387–1394.
12. Greenberg RK, Haulon S, O’Neill S, et al. Primary endovascular repair of juxtarenal aneurysms with fenestrated endovascular
grafting. Eur J Vasc Endovasc Surg. 2004;27(5):484–491.
13. Health Quality Ontario. Fenestrated endovascular grafts for the repair of juxtarenal aortic aneurysms: an evidence-based analysis.
Ont Health Technol Assess Ser. 2009;9(4):1–51.
14. Gilling-Smith GL, McWilliams RG, Scurr JR, et al. Wholly endovascular repair of thoracoabdominal aneurysm. Br J Surg.
2008;95(6):703–708.
15. Haulon S, D’Elia P, O’Brien N, et al. Endovascular repair of thoracoabdominal aortic aneurysms. Eur J Vasc Endovasc Surg.
2010;39(2):171–178.
16. O’Neill S, Greenberg RK, Haddad F, et al. A prospective analysis of fenestrated endovascular grafting: intermediate-term
outcomes. Eur J Vasc Endovasc Surg. 2006;32(2):115–123.
17. Semmens JB, Lawrence-Brown MM, Hartley DE, et al. Outcomes of fenestrated endografts in the treatment of abdominal aortic
aneurysm in Western Australia (1997–2004). J Endovasc Ther. 2006;13(3):320–329.
18. Roselli EE, Greenberg RK, Pfaff K, et al. Endovascular treatment of thoracoabdominal aortic aneurysms. J Thorac Cardiovasc
Surg. 2007;133(6):1474–1482.
19. Scurr JR, Brennan JA, Gilling-Smith GL, et al. Fenestrated endovascular repair for juxtarenal aortic aneurysm. Br J Surg.
2008;95(3):326–332.
20. Bicknell CD, Cheshire NJ, Riga CV, et al. Treatment of complex aneurysmal disease with fenestrated and branched stent grafts.
Eur J Vasc Endovasc Surg. 2009;37(2):175–181.
21. Verhoeven EL, Tielliu IF, Bos WT, et al. Present and future of branched stent grafts in thoraco-abdominal aortic aneurysm repair: a
single-centre experience. Eur J Vasc Endovasc Surg. 2009;38(2):155–161.
22. Mastracci TM, Greenberg RK, Eagleton MJ, et al. Durability of branches in branched and fenestrated endografts. J Vasc Surg.
2013;57(4):926–933; discussion 933.
23. Dijkstra ML, Eagleton MJ, Greenberg RK, et al. Intraoperative C-arm cone-beam computed tomography in fenestrated/branched
aortic endografting. J Vasc Surg. 2011;53(3):583–590.
Stenting, Endografting, and Embolization Techniques:
Celiac, Mesenteric, Splenic, Hepatic, and Renal
Chapter 19 Artery Disease Management
Mohamed A. Zayed Ronald L. Dalman
DEFINITION
■
The content discussed in the following text presupposes familiarity with basic wire and catheter-
based endovascular techniques. For a summary of such techniques, the reader may refer to
excellent existing references.1
■
Various occlusive and/or aneurysmal disease processes in renal and visceral arteries may
necessitate endovascular interventions (Table 1).
■
Progressive renal artery stenosis (RAS) or occlusion may predispose to renovascular hypertension
(RVH; most common form of secondary hypertension) and ischemic nephropathy.2 Aortic
atherosclerosis at the ostia or proximal renal artery accounts for two-thirds of cases.3
Fibromuscular dysplasia (FMD) also causes progressive serial stenoses throughout the renal
arteries and may also predispose to RVH. FMD occurs most commonly in younger female
patients.4
■
Acute mesenteric ischemia (AMI) and chronic mesenteric ischemia (CMI) are life threatening but
fortunately rare (1 in 1,000 and 1 in 100,000 hospital admissions, respectively) conditions.5,6 The
infrequent nature of symptomatic mesenteric ischemia may be due to the rich collateral supply
derived from the celiac, superior, and inferior mesenteric arteries. CMI most commonly develops
following progressive atherosclerotic occlusion of two or more mesenteric arteries, with the
superior mesenteric artery (SMA) being the most critical of the three. Arterial embolization,
leading to acute occlusion of the celiac artery or SMA, more commonly is associated with AMI.6
In rare circumstances, in critically ill patients, impaired intestinal perfusion due to arterial
vasospasm may occur in the absence of thromboembolic occlusion.
■
Extra- and intraparenchymal renal artery branch aneurysms occur with a reported autopsy incidence
between 0.01% and 0.7% and may arise from various disease etiologies.7 Overall, the risk of
acute clinical evolution (rupture or thrombosis) is low but may be increased during pregnancy,
with high resultant maternal and fetal mortality. The risk of progression/rupture, as is the case in
most visceral artery aneurysms, is presumed to decline significantly following menopause.
■
Aneurysms of the celiac artery, SMA, and their branches are also infrequent and associated with
varying etiologic entities. Splenic artery aneurysms are the most common (60%), followed by
aneurysms in the hepatic (20%), superior mesenteric, and celiac arteries, in that order.8,9
Syndromes such as polyarteritis nodosa or Kawasaki’s disease may be associated with aneurysms
in various segments of the mesenteric arterial circulation. Guidelines for intervention vary,
depending on aneurysm location, rate of enlargement, symptom status, and demographic
considerations: age, gender, and menstruation status.

■
RVH, with or without concurrent evidence of ischemic nephropathy, is seen in less than 50% of
individuals manifesting severe RAS.2,3 Hypertension in children, new onset hypertension in
individuals younger than 30 or older than 55 years old, or accelerated hypertension should prompt
suspicion for the presence of RAS. Older patients with RVH/RAS typically manifest other
stigmata of systemic vascular disease, including coronary and cerebrovascular disease, in addition
to peripheral vascular disease. In patients with severe bilateral RAS, renal failure may be
exacerbated with recent initiation of an angiotensin-converting enzyme (ACE) inhibitor.10 Acute
exacerbations of poorly controlled RVH may manifest with “hypertensive crisis,” flash pulmonary
edema, or neurologic symptoms ranging from headache to seizure and stroke. Physical examination
may reveal severe elevation of both systolic and diastolic blood pressures, abdominal bruits, and
other manifestations of peripheral arterial occlusive disease.
■
Patients with CMI are typically elderly and have a prior history of symptomatic vascular disease.
Like RAS/RVH patients, CMI rarely is present without other signs and symptoms of advanced
vascular disease, including aortic and mesenteric branch arterial calcification on plain x-ray films
of the abdomen. Symptoms produced by CMI are frequently nonspecific and intermittent, leading
to delayed diagnosis and disease progression. Classical symptoms usually include postprandial
dull/crampy midepigastric abdominal pain, progressive weight loss, and “food fear” with
decreased caloric intake.11 Findings on physical examination are usually noncontributory, save
those related to advanced peripheral vascular disease (e.g., absent pedal pulses); patients
frequently are malnourished and cachectic. Abdominal auscultation frequently reveals hyperactive
bowel sounds, and a bruit may sometimes be auscultated.
■
AMI presents more dramatically, with sudden onset of abdominal pain, often in patients suffering
acute embolic occlusion of the SMA. Although pain may seem out of proportion to objective
physical examination findings initially, progressive tenderness to palpation and ultimately
peritoneal signs develop in parallel with diminishing bowel viability. Clinical status also rapidly
deteriorates, with progressive metabolic acidosis, shock, and multisystem organ failure.6
■
Patients with renal artery aneurysms (RAAs) may provide a history of trauma, arterial dissection,
syndromic vascular conditions, connective tissue disorders, or RAS. The majority of RAAs are
asymptomatic at the time of diagnosis, identified as incidental findings on cross-sectional imaging
studies ordered for unrelated indications. Specific associated historical and physical findings are
rare but may include acute onset hypertension, abdominal distension, flank pain, hematuria,
syncope, and shock. Occasionally, an abdominal pulsatile mass is present on physical
examination.7 Although not always fatal, RAA rupture, particularly those in segmental branches,
frequently predisposes to renal infarction and resultant decrease in glomerular filtration capacity.
■
Patients with aneurysms of the celiac and SMAs and derived branches may manifest with a history
of arterial dissection, trauma, pancreatitis, or other local inflammatory processes or infections.
One-third of patients may also have aneurysmal disease in other segments of their arterial
anatomy.8 As is the case with RAAs, patients rarely present with symptoms other than rupture,
which itself is also rare. Free rupture may result in hemoperitoneum, hematobilia, or life-
threatening gastrointestinal hemorrhage. The risk of rupture is highest with hepatic (20% to 44% of
mesenteric arterial aneurysm ruptures) and splenic artery aneurysms, the latter notoriously at risk
during the third trimester of pregnancy.12,13 Presence of a splenic artery aneurysm recognized
during pregnancy should prompt consideration of immediate repair, regardless of the status of the
pregnancy.14

■
Renal artery disease assessment usually begins with duplex ultrasonography, which has a reported
sensitivity of 86% to 93%, specificity of 98%, and overall accuracy of 96%.15 Duplex criteria
used to diagnose more than 60% RAS include an arterial peak systolic velocity of more than 180
to 200 cm per second, a ratio of renal artery to aortic peak systolic velocity of more than 3.5, or
acceleration time between onset and peak of systole of more than 100 m per second. Kidney length
and resistive indexes derived from parenchymal insonation may also provide important insight into
the presence, nature, and severity of end-organ disease.
■
Similarly, duplex ultrasound provides a useful, noninvasive method of assessing for the presence of
chronic mesenteric occlusive disease.16 In the celiac artery, peak systolic velocities of more than
200 cm per second provides a sensitivity and accuracy for detecting a greater than 70% stenosis of
87% and 82%, respectively. In the SMA, peak systolic velocities of more than 275 cm per second
provides a sensitivity and accuracy for detecting a greater than 70% stenosis of 92% and 96%,
respectively.
■
Computed tomography angiography (CTA) is the current gold standard for confirming the presence,
severity, and extent of occlusive mesenteric vascular disease. CTA-derived images also provide
insights into the potential underlying mechanism of occlusion, including FMD, associated
dissection, evidence of inflammation/infection, or thromboembolic occlusion. Moreover, three-
dimensional reconstructions generated from CTA datasets also provide valuable guidance for
preprocedural planning. In emergent circumstances, such as those associated with suspected AMI,
CTA usually represents the “go-to” diagnostic test.
■
For patients with contrast allergies or other contraindications to computed tomography (CT)
scanning, magnetic resonance angiography (MRA) may provide a suitable alternative, particularly
for initial diagnosis and screening purposes. Overall resolution of MRA is not equal to that of
CTA and in some circumstances may not provide sufficient detail for the precise surgical or
interventional planning.
SURGICAL MANAGEMENT
Patient Selection
■
Appropriate patient selection for endovascular intervention is paramount and dependent on
therapeutic indication, anatomy, patient comorbidities, and acuity of the disease process. In the
following text, we discuss considerations for patients with renal/mesenteric arterial occlusive
disease, followed by considerations for patients with renal/mesenteric arterial aneurysmal
disease.
■
For RAS, the indication for endovascular intervention is contingent on severity of stenosis, the
presence and severity of presumed resulting hypertension, and extent of residual glomerular
filtration capacity. For RAS, there is no accepted indication currently for “prophylactic”
intervention. Endovascular intervention is considered only in patients with severe hypertension,
who have failed medical management with at least three concurrent antihypertensive medications
or have demonstrated progressive loss of renal function due to ischemic nephropathy in the setting
of more than 60% RAS. The future role for endovascular intervention in treating RVH has been
called into question by level I data demonstrating only modest reductions in blood pressure
following renal artery stenting.17
■
Patients with critical stenosis or occlusion of at least two mesenteric arteries, in the setting of signs
and symptoms consistent with CMI, are also potential candidates for endovascular management.
Patients with atypical symptoms who may meet anatomic criteria for mesenteric occlusive disease
often experience disappointing results following endovascular intervention.
■
Given the compromises inherent in management of AMI, often in the setting of uncertain bowel
viability, hybrid open and endovascular approaches may represent the safest and most expeditious
option. Particularly in regard to “acute-on-chronic” occlusion of the proximal SMA, with a patent
distal segment preserved by collateral flow, surgical exposure at celiotomy enables distal SMA
cannulation and sheath placement. Standard angiographic techniques are then employed to cross
the occlusive proximal lesion in a retrograde fashion, with subsequent angioplasty and stenting
performed to restore pulsatile antegrade flow.18 We have employed this technique reliably under a
variety of challenging clinical conditions with consistently good results.
■
In patients with disease in multiple mesenteric arterial segments and symptoms concerning for
mesenteric ischemia, SMA revascularization, either via endovascular or open surgical
approaches, represents the most reliable and effective method for resolving critical mid- and
distal gut ischemia. Decompressive laparotomy should always be considered as an essential
adjunct in these circumstances, regardless of revascularization method used, to facilitate selective
resection of nonviable bowel if needed and limit the noxious effects of abdominal compartment
syndrome in these already compromised patients.
■
In comparison, the safety and use of primary inferior mesenteric artery (IMA) endovascular
intervention remains controversial in patients with disease in multiple mesenteric arteries. Recent
series report relatively frequent procedure-related complications and poor outcomes following
attempted IMA intervention.19 These results may in part be due to the progressive nature of
occlusive vascular disease in the most distal aortic segment at the level of the IMA and resulting
difficulty in resolving significant ostial stenoses with even high-pressure angioplasty techniques.
■
The criteria for elective repair of asymptomatic RAAs is controversial. Recommendations vary for
intervention based on aneurysm diameter, also taking into account the size of the parent artery,
extent of mural calcification, and rate of enlargement, if available. Consensus exists regarding
treatment for all aneurysms larger than 3 cm in diameter.20,21 Similarly, patients with intact but
symptomatic true aneurysms, recent-onset false (pseudo-) aneurysms, and aneurysms resulting from
associated FMD are also typically repaired promptly, given their presumed higher risk of rupture.
RAAs in women of childbearing age with plans for future pregnancies are usually repaired, when
recognized, at almost any size. Less agreement is present for RAAs larger than 2 cm but smaller
than 3 cm in diameter, with treatment recommendations often customized based on individual
circumstances.
■
There are no set size criteria for visceral artery aneurysm repair. Although larger aneurysms are
thought to have an increased potential risk of rupture, small visceral artery aneurysms are also
known to rupture and manifest with life-threatening hemorrhage. Therefore, most visceral
aneurysms larger than 2 cm should be repaired when identified. This recommendation does not
necessarily apply to poststenotic arterial dilations (not true aneurysms) and distal SMA
aneurysms. The latter are generally best managed by embolization and/or resection of the
dependent loops of adjacent small intestine. In most circumstances, ruptured visceral artery
aneurysms are best managed by open or hybrid approaches, allowing for assessment of bowel or
end-organ ischemia in conjunction with restoration of arterial flow.
■
Prior to attempted repair or exclusion, aneurysm location and access issues should be precisely
determined via cross-sectional imaging studies. Luminal plaque, thrombus burden, associated
aneurysms, and preexisting dissections should also be noted. Finally, target vessel diameter should
be determined at several intervals before, within, and after the lesion of interest to optimize coil,
stent, and graft selection.
■
The preferred method of critical renal artery ostial lesion management is by balloon-expandable
stent placement. In rare circumstance, angioplasty predilation may be required to advance the
appropriate stent through the renal ostia and across the stenotic lesion. Renal artery stents range
from 10 to 30 mm in length and 4 to 7 mm in diameter. Transfemoral approaches to the renal artery
are generally preferred due to the shorter distance to target, smaller imaging fields, and abundant
availability of purpose-specific instrumentation. However, cephalad angulation of the renal artery
origins relative to the aorta, the presence of extensive infrarenal aortoiliofemoral arterial
occlusive disease, or significant iliac artery tortuosity may favor consideration of the left brachial
artery and descending thoracic aorta as the preferred route of access.
■
For the treatment of mid- to distal RAS in the setting of FMD, angioplasty alone is generally the
preferred treatment modality. Either transfemoral or transbrachial approaches may be considered,
depending on the considerations noted earlier. Care must be taken to minimize procedural trauma
with precise determination of target artery diameter and selection of appropriately sized
instruments (sheaths, balloons, and stents). Poor planning or ill-considered procedural technique
may precipitate arterial dissection, thrombosis, and renal infarction.
■
Depending on the degree of lesional calcification, the extent of associated juxtaostial aortic
occlusive disease, lesion length and associated target vessel tortuosity, balloon- or self-expanding
stent grafts may be chosen for luminal reconstitution and may provide improved long-term patency
in the proximal SMA.22 Cannulation of either the celiac or SMA may be achieved from both
femoral and brachial approaches. However, in emergent or extenuating circumstances, left
brachial access often proves more expeditious and effective. This is particularly true in the setting
of high-grade ostial stenosis or occlusion, where brachial access and antegrade aortic sheath
placement may provide improved guidewire, sheath, and crossing catheter pushability and
trackability.
■
Successful wire cannulation of ostial SMA and celiac lesions may require “telescoping” techniques
with different sheath and wire combinations (see in the following text). This is also true of
attempts to deploy devices in the mid- and distal splenic artery, where a triaxial catheter and
sheath combination extending into the target lesion is frequently most effective. Given the short and
often tortuous nature of the celiac artery, stable sheath placement is challenging, often representing
the most difficult aspect of the procedure.
■
Similar principles are used when treating aneurysms of renal and visceral arteries, including precise
catheter positioning and stable sheath support. Aneurysm size, location, neck anatomy, and extent
of tortuosity of feeding target vessels impact the strategy of repair. For example, for large
retropancreatic splenic artery aneurysms, coil embolization of the aneurysm sac (preferably with
large-end-first or nesting coils) prior to covered stent placement across the ostium of the aneurysm
is necessary to ensure long-term procedural success. For precise embolization of shallow or
wide-necked aneurysms, adjuncts such as distal balloon occlusion with deployment of detachable
coils may be necessary. For more accessible aneurysms with a wide-based aneurysm neck, bare
metal stenting may be performed across the ostium of the aneurysm first, followed by placement of
coils through the open interstices of the stent to keep the coils localized to the area of interest.
Branch artery aneurysms usually occur at bifurcation points and are accompanied by small, well-
defined necks and are ideally suited for embolization with microcoils (0.018-in catheter
compatible) delivered through a triaxial delivery system.
■
The preferred size/shape of embolization devices or covered stents may be either accurately
estimated from a preprocedural CT arteriogram or determined at the time of angiographic imaging
and sheath placement. Based on these measurements, coil and plug diameters may be oversized by
20% of the target vessel diameter. The length of coils selected is derived from the anticipated
arterial lumen surface area that requires embolization. Similarly, the length of vascular plugs
selected depends on the target artery to be embolized and the estimated luminal flow. For example,
higher flow arteries, such as those proximal to arteriovenous fistulae, usually need more extensive
coverage to ensure definitive occlusion. Both self-expanding and balloon-expandable stent grafts
are available. The former are also typically oversized by 20%, and the latter are usually sized 1
mm greater than the target artery diameter. Attention should be given to the sheath selection to
ensure adequate diameter and length. The device-specific instructions for use (IFU) should be
consulted in all circumstances prior to use of occlusion devices, or more generally, any
endovascular device with the potential risk for significant vascular injury.
■
Depending on their specific location, some visceral artery aneurysms may be embolized without
specific end-organ ischemic injury. However, embolization of distal aneurysms, such as those
located within the splenic hilum, may result in splenic infarction, further bleeding, or abscess
formation. Therefore, splenectomy remains a viable alternative method of splenic artery aneurysm
management for many patients. Appropriate vaccinations should be administered with sufficient
lead time to allow for an appropriate immunization response prior to elective splenic artery
embolization procedures or planned splenectomy.

■
Procedures may be performed in an angiography suite, or in an operating room, equipped with a
floating-point carbon fiber, radiolucent operating table; fluoroscopy platform; and monitor-
viewing bank. However, for precise visceral artery interventions requiring steep oblique/lateral
imaging and higher fluoroscopic kilovolt (kV), portable systems in the operating room setting may
not provide sufficient image clarity and resolution. Under these circumstances, use of a fixed-
imaging system, either in an angiography suite or hybrid operating room, will maximize the
likelihood of success.
■
For the majority of elective renal and visceral artery interventions, conscious sedation with a
combination of short-acting analgesic and sedative agents will provide adequate patient comfort,
immobility, and optimal imaging parameters. Standard patient safety measures for conscious
sedation, including supplemental oxygen, standard monitoring, and availability of resuscitation
equipment should be employed in compliance with local hospital policy. However, general
anesthesia is clearly indicated to facilitate treatment of AMI, urgent/emergent management of
aneurysm rupture, and/or hemorrhage potentially requiring bowel resection or open conversion.
■
For the most part, all renal and visceral artery endovascular interventions can be performed with the
patient in the supine position. The left arm may be positioned out at 90 degrees to allow for
transbrachial interventions. If a transfemoral intervention is planned, the patient’s arms may be
extended over the head to aid with image clarity; however, most patients can only tolerate this for
certain time periods prior to fatigue. Placing the patient in a 30-degree rotation to the right, on
bolsters placed behind the left flank, at the time of the procedure, will facilitate “true lateral”
position to localize and cannulate the origin of the SMA without requiring the image intensifier and
radiation source to be in full horizontal position and limiting operator access to the patient as a
result.
■
In addition to a full array of complementary wires, catheters, and sheaths, premounted balloon-
expandable stents and stent grafts should be available, including in low-profile platforms (0.014 in
or 0.018 in). Appropriate sizes of coils and plugs should also be identified and readily available.
TECHNIQUES
RENAL ARTERY ANGIOPLASTY AND STENTING

First Step
■
For arterial access, a retrograde transfemoral approach is usually selected; however, antegrade
transbrachial access may improve accessibility and sheath stability in the presence of significant
abdominal/pelvic girth, significantly down-sloping renal arteries, or tortuosity/obstruction of the
distal aorta or iliac arteries.
■
Arterial access is usually obtained percutaneously using standard Seldinger technique. Bedside
ultrasound may facilitate precise placement. Once an interventional sheath access is placed,
intravenous unfractionated heparin is administered to maintain an activated clotting time (ACT) of
more than 200 seconds.
Second Step
■
Wire access to the pararenal aorta may be achieved with 0.035-in guidewire. A 4- or 5-French (Fr)
flush catheter is advanced over the guidewire to approximately the level of the 1st lumbar
vertebral body.
■
If renal function permits, a complete aortoiliac arteriogram in anterior–posterior image intensifier
orientation should be performed to assess both the renal arteries and renal accessory arteries. A
power injector should be used for the road map aortogram, using a high injection rate (e.g., 15 to
20 mL per second) and low volume (e.g., 10 to 15 mL). Breath-holding instructions should be
given to the patient or the assisting anesthesiologist to allow for aortogram acquisition during end
expiration. Glucagon (0.25 to 2 mg intravenous; approximately 10 minutes preprocedure) can also
be administered to diminish intestinal motility and enhance arterial visualization.
■
A magnified angiogram can be repeated of areas of interest and intended treatment. For better
visualization of the renal artery, the image intensifier should be oriented with a few degrees in
cranial and lateral obliquity ipsilateral to the renal artery of interest.
■
Intraoperative angiographic measurements are obtained to confirm device selection. A marked flush
catheter or radiopaque ruler may facilitate accurate angiographic measurements.
Third Step
■
A stiff 0.035-in guidewire (i.e., Amplatz, Rosen) is placed in the pararenal aorta to facilitate
advancement of a 45-cm 8-Fr renal dilation guide catheter (RDC), or 6-Fr RDC sheath (i.e.,
Terumo Pinnacle™ destination or Cook Ansel™ Flexor™). The sheath dilator tip should not be
advanced into the target vessel to avoid compromise of the residual vessel lumen.
■
Wire cannulation of the renal artery is the essential first step. Depending on the angle of entry at the
orifice, a number of different catheter tip shapes may facilitate successful renal cannulation (Sos 1
or 2, Cobra, Vanchi, etc.). Once cannulated, the sheath tip is advanced immediately adjacent to, but
not across, the renal artery orifice (FIG 1). A 0.014-in or 0.018-in stiff guidewire with a floppy or
hydrophilic tip is then employed to probe across areas of severe stenosis, through a reverse curve
or angled catheter, depending on the optimal angle for access. Alternatively, a 0.035-in guidewire,
with improved handling and radiopacity, may provide suitable trackability for less critical
stenoses.
■
Once access is achieved, the wire should be advanced to a secondary branch to optimize positional
stability. Care should be taken to maintain wire tip visualization in the field of view, particularly
when using hydrophilic guidewires, as they can easily perforate parenchymal arterioles when
advanced too far into the segmental renal circulation. Parenchymal perforation may precipitate
intra- or extracapsular hematoma formation, renal hemorrhage, and circulatory collapse unless
immediately recognized and corrected.
Fourth Step
■
Prior to renal artery stenting, predilation may be necessary to provide sufficient luminal space for
delivery of the crimped stent/delivery catheter (FIG 1). A 2- to 4-mm low-profile, semicompliant,
or coronary balloon compatible with a 0.014-in or 0.018-in system can be used for this purpose.
Care needs to be taken to maintain wire position during subsequent stent exchange; loss of wire
position here can preclude stent delivery or precipitate luminal thrombosis if aortic and/or
orificial atheroma is displaced by predilation.
■
Using a low-profile 0.014-in or 0.018-in system (rapid exchange or over-the-wire [OTW]), a
balloon-expandable stent (e.g., Cordis Palmaz Blue, Boston Scientific Express SD, Cook Formula)
is delivered across the lesion (FIG 1). The low-profile nature of these devices enables facile
placement, as well as contrast delivery across the lesion to confirm appropriate position. Rapid
exchange or monorail systems allow for shorter wire length, aiding procedural efficiency vis-à-vis
catheter/wire/device exchanges. In contrast, OTW devices provide improved pushability and
trackability across constricting lesions.
■
For mid- or distal RAS, the shortest balloon-expandable stent length providing complete coverage
should be selected. For mid- or distal RAAs, appropriate length self-expanding or balloon-
expandable stent grafts should be selected to provide adequate pre- and postaneurysm renal artery
sealing zones (FIG 2).
■
Following stent placement under fluoroscopic guidance, the balloon should be deflated fully prior to
its withdrawal to avoid movement or dislodging of the stent. Areas with substantial tortuosity may
precipitate arterial kinking at the transition point between stented and nonstented segments.
Excessive oversizing, or overinflation of stents mounted on semicompliant balloons, may promote
renal artery injury, dissection, or thrombosis. Temptation to optimize the postprocedural
angiographic image, potentially at the expense of vessel integrity or anticipated long-term patency,
should also be avoided.
■
For ostial renal artery lesions, the balloon-expandable stent should be positioned so that the aortic
end is deployed approximately 1 mm into the aortic flow stream. The aortic edge of the stent can
be “flared” outward with a repeat angioplasty using the distal edge of the same balloon (FIG 1).
Fifth Step
■
After successful deployment, the sheath should only be withdrawn after the completion imaging
encompassing the entire ipsilateral kidney is performed to confirm uniform perfusion and absence
of parenchymal and/or capsular injury.
■
Following withdrawal of the sheath from the renal orifice, while maintaining wire access,
completion paraorificial aortography is performed to confirm stent positioning and target lumen
diameter. Residual stenosis, kinking, or dissection should be confirmed to be absent prior to
withdrawal of the wire.
VISCERAL ARTERY ANGIOPLASTY AND STENTING

First Step
■
As previously noted, access considerations need to account for individual patient anatomy, operator
experience and skill, available devices, potential complications, goals of treatment, and
anticipated time of the procedure. Most internationalists prefer the transfemoral approach for
visceral vascular access. However, proximal left brachial artery exposure and puncture often
facilitates access to significantly down-sloping or tortuous mesenteric arteries.
■
A 4- or 5-Fr sheath is placed in the arterial access site to facilitate advancement of a 4- or 5-Fr
marked flush catheter to the paravisceral aorta.
■
Intravenous unfractionated heparin is administered after sheath placement to achieve an ACT of
more than 200 seconds.
Second Step
■
After a standard aortogram, a magnified paravisceral aortogram can be performed with the image
intensifier placed in a steep oblique or true lateral position to optimize localization and
cannulation of the celiac artery and SMA origins.
■
Care should also be taken here to visualize the major branches of the celiac artery and/or SMA.
Attempts should be made to visualize the first significant branch of the SMA, usually the middle
colic artery, to avoid inadvertent coverage and/or compromise of colonic arterial perfusion as a
consequence of planned procedures.
■
Visceral lesions of interest can be further characterized at this time by optimizing image intensifier
obliquity. Accurate measurements are facilitated by marked flush catheter or radiopaque ruler
placement.
Third Step
■
After withdrawal of the flush catheter, a stiff guidewire and a long (90 cm), braided 6-Fr sheath
(i.e., Terumo Pinnacle™ destination, Cook Ansel™ Flexor™) is advanced to the paravisceral
aorta. Various angled sheath tips (i.e., straight, angled hockey tip, curved) can be used depending
on the degree of visceral artery angulation, aortic diameter, and access approach (femoral or
brachial).
■
Along with selected sheath, various guide catheter types (i.e., angled, vertebral, cobra, RDC, or
reverse curved SIM or Sos catheters) can be used to facilitate visceral artery cannulation.
Fourth Step
■
An exchange-length, stiff 0.014-in or 0.018-in guidewire, with a floppy tip, is advanced through the
preselected catheter and sheath combination. However, wire cannulation of a diseased visceral
arteries orifice may be challenging. From the brachial approach, successful cannulation may be
facilitated with sheath placement distal to the artery of interest, followed by gradual withdrawal of
the sheath with the selected angled catheter inside the sheath protruding slightly outward. When the
catheter “clicks” into place, an exploratory hydrophilic guidewire is then gently advanced to
obtain luminal access. Once the lumen is cannulated, the guidewire is then advanced to a
secondary visceral branch to facilitate catheter and sheath advancement, as indicated (FIG 3).
Another cannulation strategy is to withdraw wire and catheter combinations from a stable sheath
position across the anticipated vessel orifice area at various “clock” positions.
■
For a “no-touch” technique, a shaped catheter or sheath tip is positioned luminally in direct
proximity to the orifice of interest. A 0.014-in or 0.018-in hydrophilic guidewire is then used to
localize and facilitate cannulation. To improve trackability and pushability of the system, a
stabilizing “buddy” stiff guidewire may also be advanced, when necessary, to “pin” the
cannulation sheath to the opposite wall.
■
When single-wire cannulation proves inadequate to support catheter and sheath advancement in to
the target vessel, placement of a second, or even third 0.014-in or 0.018-in wire, across the area of
stenosis may facilitate successful catheter/sheath advancement.
Fifth Step
■
An appropriately sized self-expanding or balloon-expandable stent graft is preferred for the
treatment of visceral artery stenoses. Predilation of the tract may be necessary with a small, low-
profile balloon to facilitate advancement of the balloon-expandable stent (FIG 3).
■
The aortic end of a balloon-expandable stent used for the treatment of ostial or proximal visceral
artery lesions should be positioned 1 mm into aortic flow lumen, and the stent edge should be
flared out with the edge of an angioplasty balloon.
■
Accuracy of deployment of self-expanding stent grafts can be improved with partial deployment of
the stent while maintaining the cannulation sheath in the orifice of the visceral artery. Once the
distal portion of the stent graft is accurately deployed, the remainder of the proximal stent graft can
be unsheathed to allow for full deployment. An appropriately sized compliant balloon may then be
subsequently used to fully mold the self-expanding stent graft to profile and/or slightly flare the
aortic edge.
■
For friable lesions, or lesions that may include fresh thrombus, consideration should be given to
advancing and deploying balloons and stents over a filter wire (0.014-in eV3 SpiderFX embolic
protection system). Although placement of a distal filter may not preclude all embolic sequelae, it
may reduce the severity or significance of associated potential complications. This option may be
particularly valuable in SMA interventions.
HYBRID REPAIR OF PROXIMAL MESENTERIC ARTERY

STENOSIS/OCCLUSION
First Step
■
In the setting of acute or acute-on-chronic mesenteric ischemia, where exploratory laparotomy is
otherwise indicated to assess bowel viability, a hybrid retrograde catheterization approach is
generally preferred. At laparotomy, surgical exposure of the superior mesenteric or celiac artery is
obtained. To expose the celiac artery, the left triangular ligament is incised, the left hepatic lobe is
retracted to the right, and the gastroesophageal junction is retracted to the left. Further caudal
dissection along the surface of the aorta may be used to expose the SMA origin.
■
For purposes of both embolectomy and hybrid retrograde catheterization, exposure of the proximal
section/midsection of the SMA is preferentially obtained at the superior root of the small bowel
mesentery (FIG 4). This location generally provides access 4 or more centimeters distal to the
SMA orifice, which allows stable sheath positioning to facilitate retrograde cannulation and
stenting. Distal to the lower margin of the pancreas, the length of the SMA is limited by early
branching of the ileocolic artery and intestinal cascade, so relatively proximal positioning should
be achieved to minimize excessive dilation/trauma to the vessel by the sheath.18
Second Step
■
When embolic occlusion is present, embolectomy is performed gently through an anterior
arteriotomy. The tapering nature of the SMA in this area requires gentle catheter withdrawal with
gradual balloon deflation in order to avoid iatrogenic arterial damage, dissection, or thrombosis.
■
Retrograde cannulation of an exposed distal segment of the target vessel provides optimal access for
definitive endovascular intervention. In emergent conditions with compromised intestine, this
approach is preferential to open revascularization strategies, which may require prosthetic graft
placement following prolonged, extensive dissection of the mesentery and aortic root.
■
Retrograde mesenteric cannulation is facilitated by placement of a longitudinal arteriotomy in the
exposed distal segment of the target vessel. To reduce the risk of injury to the exposed artery
during cannulation, the arteriotomy site is closed with a prosthetic or autogenous patch. The patch
itself is then cannulated to facilitate sheath placement, angiogram, stent placement as well as
expedited puncture site closure at the end of the procedure (FIG 4).
■
Relatively long sheaths (20 cm or more) should be used during retrograde cannulation to ensure that
the operator’s hands are clear from the fluoroscopy field and minimize operator radiation exposure
during catheterization maneuvers.18
RENAL OR VISCERAL ARTERY EMBOLIZATION
First Step
■
Arterial access can be secured via either a left brachial artery or transfemoral approach, depending
on the intended target vessel and its angulation relative to the aorta.
■
For standard coil embolization, a 5- or 6-Fr sheath access will be adequate. However, if an
occlusion device will be used, a larger sheath size may be required depending on device
specifications.
■
Systemic anticoagulation with intravenous unfractionated heparin is also commonly used during
these procedures.
Second Step
■
Angiographic characterization may require angiograms in multiple different obliquities to fully
appreciate size, extent, and angulation of the lesion of interest, particularly those affecting
secondary visceral branches. In the angiographic parlance, regarding the extent, severity, and
profile of a luminal obstruction, “one view is no view.”
■
One should note the extent of vascular collateralization associated with the vascular segment that
will be embolized.
Third Step
■
A telescoping cannulation technique is usually used to enhance the positioning and stability of the
embolization system. To perform this, a sheath is advanced as close to the target lesion as
possible. A catheter is then extended from beyond the tip of the sheath and used to protrude into
target lesion (FIG 5).
■
Embolization of remote target lesions may require higher orders of telescoping. Placing a sheath into
another larger sheath, or a 0.018-in microcatheter (i.e., Codman Prowler™, Cook CXI™, BSCI
Renegade™) into a standard 0.035-in guide catheter, can help access more challenging lesions
(FIG 5). Alternating wire and microcatheter advancements may facilitate cannulation of smaller
and more tortuous arteries (such as the superior and inferior gastroduodenal arteries [FIG 6]) and
distal/hilar splenic artery.
■
If possible, the cannulation catheter/microcatheter should be advanced into the lesion slightly further
than the intended embolization site, because the system can draw back during deployment of coils
or plugs.
Fourth Step
■
Once the cannulation catheter is positioned in the target lesion, 0.018-in or 0.035-in coils are
delivered sequentially into the target area through their respective catheters. For detached coils,
the metal tube housing the coil is attached to the back end of the cannulation catheter, and the stiff
end of a guidewire is used to push the coil out of its housing unit and into the catheter shaft. The
floppy tip of the guidewire is then replaced into the catheter to push the coil along the entire shaft
of the catheter and into the lesion (FIG 5). The stiff end of the guidewire should not be used to
push the coil into the lesion because it can change the cannulating catheter tip shape and lead to
instability in the cannulation system and maldeployment.
■
Alternatively, small aneurysm may be occluded with detachable or nondetachable microcoils or
ethylene vinyl alcohol copolymer. IFU are variable and should be referred to for recommended
deployment techniques.
■
When coil deployment can be accurately localized, and precise coil positioning is critical to the
success of the procedure, large-to-small tapered coils should be used. When arterial blood flow is
needed/required to carry part of the coil into the preferred deployment location, small-to-large
tapered coils are preferred in this situation. Newer “nesting” coils will reform immediately into
larger, obstructing profiles. Older tubular coils need to be advanced as they are being deployed to
avoid simply lining the target artery without sufficient luminal obstruction. Attention to
understanding what coils are in inventory, and how respective coil choices are optimally
deployed, is essential for procedural success.
■
For larger aneurysms or planned occlusion of an entire vessel lumen, a vascular plug (i.e., AGA
Medical Amplatzer™ I or II vascular plug) may be preferable and a more effective means for
target embolization. However, plug placement usually requires stable sheath target artery
cannulation. Amplatzer™ I and II vascular plugs are produced in diameters ranging between 4 and
22 mm and lengths ranging between 6 and 18 mm. Recommended device IFU should be consulted
to ensure proper device selection and deployment. When sheath access cannot be withdrawn to
enable plug deployment, catheter-delivered coils should be deployed instead.
■
Once a coil or plug is delivered into a lesion, its position may be modified slightly by catheter tip
advancement. This maneuver, when performed properly, maximizes the obstructive surface area
and resulting coil thrombogenicity.
■
When multiple coils or plugs are used, deployment should also be strategized and deliberate. For
example, the first coil should be placed in the deepest part of the lesion (base of an aneurysm),
whereas the last coil should be placed in the entry point of the lesion (neck of an aneurysm).
■
For acutely bleeding vessels (such as the gastroduodenal arteries in the setting of duodenal
ulcerations), a “back-door”–“front-door” approach ensures hemostasis. This involves occluding
the culprit vessel pre and post the area of bleeding (FIG 6). Coiling only one side of the bleeding
artery may prevent further access attempts while not providing sufficient vessel occlusion and
hemostasis. Small bleeding pelvic arteries may similarly be embolized using a Gelfoam slurry
slush preparation.23 Recommended IFU should be consulted to ensure proper preparation and
administration of these slurries.
Fifth Step
■
It is customary to perform postembolization arteriography to confirm final coil/plug positioning.
Residual flow will still be evident in the recently embolized vessel segment, because the patient
generally remains heparinized during this period of the procedure. If uncertainty persists as to the
adequacy of embolization, arteriography may be repeated following reversal of anticoagulation,
taking into account increased risks of thrombosis/embolization around the delivery sheaths and
catheters proximal to the targeted lesion.
PEARLS AND PITFALLS
Indications ■ Preoperative imaging (duplex and CTA) should be reviewed in
detail to ensure patient suitability and help plan out appropriate
intervention.
■ Combining information gathered from duplex and CTA is
beneficial, especially in situations when the stenosis is
overestimated due to heavy luminal calcification.
Vessel cannulation ■ One should note the angulation of the target vessel relative to the
aorta. Because this angle may vary with respiration, angiograms
should be obtained while the patient is apneic (if intubated) or at
end expiration.
■ Generally, renal arteries and up-sloping visceral vessels may be
easier to cannulate from a transfemoral artery approach. Down-
sloping renal and visceral vessels may be easier to cannulate from
a proximal left brachial artery puncture.
■ Using an angulated, flexible, low-profile sheath system also aids
in the cannulation process.
Angioplasty balloon ■ Care should be taken in selecting appropriate size and types of
selection balloons.
■ Generally, only low-profile compliant balloons should be used for
angioplasty interventions in the renal and visceral arteries. In rare
circumstances, a noncompliant balloon may be used to help mold a
stent graft to full profile.
■ Diameter of angioplasty balloon should be estimated relative to
adjacent normal vessel lumen. Oversizing is generally not
necessary, and a smaller diameter balloon may be preferred when
performing angioplasty across highly calcified lesions.
Stent selection ■ Care should also be taken in selecting appropriately sized stents
for desired interventions.
■ Stent diameter should be estimated relative to normal vessel lumen
diameter adjacent to target lesion to be treated and is generally
oversized by approximately 1 mm.
■ Stent length should be estimated relative to the length of the target
lesion while providing enough coverage into the adjacent normal
vessel lumen (area of needed coverage is variable depending on
type of lesion and intervention).
■ Oversized stents are prone to kinking and may risk damaging the
target vessel. Undersized stents may lead to maldeployment,
migration, and ineffective seal with adjacent vessel lumen.
■ Sometimes, the angioplasty balloon of a balloon-expandable stent
gets stuck in the stent during its removal. In this situation, pulling
the balloon risks misplacing or dislodging the stent from its
desired location. Instead, the operator should ensure complete
deflation of the balloon and attempt slowly advancing the balloon
while rotating its catheter.
Coil/plug selection ■ Size of coils and plugs should be selected relative to lesion
dimensions. Undersized coils and plugs risk migration to
unintended vascular beds.
■ Stability of the embolization delivery system should be selected
relative to the size of the embolization device. Larger
embolization devices may cause instability in low-profile delivery
systems.
Renal/visceral artery ■ Sheath and large catheter cannulation of renal and visceral arteries
dissection should be avoided to prevent damage or dissection.
■ If a dissection occurs, angiographic evaluation is required to
determine whether it is flow limiting. All flow-limiting
dissections should be stented with an appropriately sized balloon-
expandable stent.
Renal/visceral arterial ■ Arterial spasms may be induced with vessel cannulation,
spasm angioplasty, or stenting. Younger patients are typically more prone
for this. Arterial vasodilators, such as nitroglycerin or papaverine,
may be infused into the vessel lumen by way of cannulation sheath
or catheter to help relieve this.
■ The operator should be aware that papaverine may precipitate out
of solution if mixed with heparin.
Renal capsular perforation ■ This may be caused by inadvertent advancement of cannulating
or hematoma wire into the renal parenchyma. To avoid this complication,
always keep the end of the wire in sight during sheath and device
advancements over the wire. Also, avoiding the use of straight or
angled-tip stiff glidewires in this circumstance can decrease the
risk of this complication.
■ Symptoms of renal capsular hematoma or perforation include
abdominal pain and nausea, accompanied by a vasovagal
response, which frequently requires aggressive resuscitation and
stabilization maneuvers by the interventional team.
■ If this complication is encountered, maintain wire access (do not
remove the offending wire) to facilitate a catheter exchange to
provide access to coil placement and occlusion of the perforation
site. Loss of wire access can further complicate this situation;
however, as long as sheath access remains in the renal artery, the
relevant segmental branches can be reaccessed for coil delivery.
Removal of ■ All attempts should be made to safely reposition

malpositioned/misplaced malpositioned/misplaced stents, endografts, coils, or plugs. This
devices may involve secondary cannulations, larger sheath placement, and
balloon angioplasty with gentle directional force.
■ If endovascular retrieval or repositioning is unsuccessful,
angiographic flow across malpositioned/misplaced devices
should be evaluated. If arterial flow is clearly obstructed to
unintended vital structures or may become a significant nidus for
thrombosis or hemodynamic stenosis, open surgical removal may
be indicated or attempted repositioning of devices in areas of less
critical hemodynamic significance (e.g., iliac arterial system).
POSTOPERATIVE CARE
■
At the conclusion of the procedure, hemostasis is achieved with manual compression or, in cases
requiring larger than 6-Fr sheath size, closure devices. Heparin reversal with protamine
administration is also helpful unless anticoagulation is to be continued following the procedure.
■
As is the case with all patients undergoing peripheral arterial intervention in our practice, patients
are observed for a 6- to 24-hour period following device placement. During this period, access
site hemostasis and ipsilateral pedal perfusion status is monitored periodically, along with
hydration status/urine output and signs of unintended end-organ malperfusion.
■
Patients treated with renal/visceral artery angioplasty or stenting receive exaggerated antiplatelet
therapy in the immediate perioperative period. In our practice, we load patients with 300 mg of
Plavix™ following the procedure, therapy continuing at 75 mg daily for 6 additional weeks.
■
Postoperative surveillance of patients with renal/visceral artery interventions is necessary. Duplex
evaluation of renal/visceral artery stents 1 to 3 months following intervention is usually
recommended, followed by repeat duplex evaluation every 6 months for at least 1 to 2 years.
Afterward, stents with no evidence of in-stent restenosis or de novo disease progression may be
imaged at yearly intervals. Evidence of restenosis, either by end-organ dysfunction or surveillance
imaging studies, should prompt reevaluation and reintervention as necessary to maintain luminal
patency and long-term success.
OUTCOMES
■
Endovascular treatment of RAS has a reported technical success rate of 88% to 100%. Treatment
effects on hypertension alone are quantitatively modest and inconsistent between studies.24,25
Improvement in renal function is reported in approximately 25% of patients.
■
Treatment of mesenteric occlusive disease has a reported technical success rate of 96%.
Postoperative symptom improvement/resolution is reported in approximately 88% of treated
patients. Primary patency is estimated at 65% to 92%, with primary assisted patency at 92% to
100%, and secondary patency at 99%.26,27
■
Embolization and stent graft techniques for repair of renal and visceral artery aneurysms are limited
to variably sized retrospective series but with acceptable technical success rates in appropriately
selected patients.
COMPLICATIONS
■
For renal artery interventions, complications most commonly arise from access site complications,
contrast-induced nephropathy, or atheroembolization. Renal artery restenosis is reported between
5% and 66%, depending on duration of follow-up and criteria used for continued surveillance.
The perioperative 30-day mortality is estimated at 0% to 5% and survival at 3 years is estimated
at 74%.28 Other less frequent complications include iatrogenic renal parenchymal perforation,
capsular hematoma, arterial dissection, thrombosis, or distal plaque embolization into branch or
accessory arteries.
■
For mesenteric artery interventions, restenosis or occlusion of treated visceral vessels is
documented in 10% to 27% of patients,29 emphasizing the need for continued postprocedural
surveillance. Less common complications include mesenteric artery perforation, dissection, or
distal parenchymal embolization due to wire/catheter manipulation of areas with fresh thrombus or
friable plaque. While treating branch artery aneurysms of the spleen, occasionally, portions of the
splenic parenchyma may be lost due to coiling and branch occlusion, with attendant symptoms
consistent with segmental splenic infarction.
REFERENCES
1. Schneider PA. Endovascular Skills, Guidewire and Catheter Skills for Endovascular Surgery. 3rd ed. New York, NY:
Informa Healthcare; 2009.
2. Garovic VD, Textor SC. Renovascular hypertension and ischemic nephropathy. Circulation. 2005;112:1362–1374.
3. Hansen KJ, Edwards MS, Craven TE, et al. Prevalence of renovascular disease in the elderly: a population-based study. J Vasc
Surg. 2002;36:443–451.
4. Beregi JP, Louvegny S, Gautier C, et al. Fibromuscular dysplasia of the renal arteries: comparison of helical CT angiography and
arteriography. AJR Am J Roentgenol. 1999;172:27–34.
5. McMillan WD, McCarthy WJ, Bresticker MR, et al. Mesenteric artery bypass: objective patency determination. J Vasc Surg.
1995;21:729–740.
6. Stoney RJ, Cunningham CG. Acute mesenteric ischemia. Surgery. 1993;114:489–490.
7. Tham G, Ekelund L, Herrlin K, et al. Renal artery aneurysms. Natural history and prognosis. Ann Surg. 1983;197:348–352.
8. Messina LM, Shanley CJ. Visceral artery aneurysms. Surg Clin North Am. 1997;77:425–442.
9. Tessier DJ, Abbas MA, Fowl RJ, et al. Management of rare mesenteric arterial branch aneurysms. Ann Vasc Surg. 2002;16:586–
590.
10. Hobbs SD, Thomas ME, Bradbury AW. Manipulation of the renin angiotensin system in peripheral arterial disease. Eur J Vasc
Endovasc Surg. 2004;28:573–582.
11. Chang JB, Stein TA. Mesenteric ischemia: acute and chronic. Ann Vasc Surg. 2003;17:323–328.
12. Carr SC, Mahvi DM, Hoch JR, et al. Visceral artery aneurysm rupture. J Vasc Surg. 2001;33:806–811.
13. Dave SP, Reis ED, Hossain A, et al. Splenic artery aneurysm in the 1990s. Ann Vasc Surg. 2000;14:223–229.
14. Selo-Ojeme DO, Welch CC. Review: spontaneous rupture of splenic artery aneurysm in pregnancy. Eur J Obstet Gynecol Reprod
Biol. 2003;109:124–127.
15. House MK, Dowling RJ, King P, et al. Using Doppler sonography to reveal renal artery stenosis: an evaluation of optimal imaging
parameters. AJR Am J Roentgenol. 1999;173:761–765.
16. Moneta GL, Lee RW, Yeager RA, et al. Mesenteric duplex scanning: a blinded prospective study. J Vasc Surg. 1993;17:79–84.
17. Wheatley K, Ives N, Gray R, et al. Revascularization versus medical therapy for renal-artery stenosis. N Engl J Med.
2009;361:1953–1962.
18. 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.
19. Oderich GS. Current concepts in the management of chronic mesenteric ischemia. Curr Treat Options Cardiovasc Med.
2010;12:117–130.
20. Pfeiffer T, Reiher L, Grabitz K, et al. Reconstruction for renal artery aneurysm: operative techniques and long-term results. J Vasc
Surg. 2003;37:293–300.
21. Panayiotopoulos YP, Assadourian R, Taylor PR. Aneurysms of the visceral and renal arteries. Ann R Coll Surg Engl.
1996;78:412–419.
22. Tallarita T, Oderich GS, Macedo TA, et al. Reinterventions for stent restenosis in patients treated for atherosclerotic mesenteric
artery disease. J Vasc Surg. 2011;54:1422–1429.
23. Bauer JR, Ray CE. Transcatheter arterial embolization in the trauma patient: a review. Semin Intervent Radiol. 2004;21:11–22.
24. Corriere MA, Pearce JD, Edwards MS, et al. Endovascular management of atherosclerotic renovascular disease: early results
following primary intervention. J Vasc Surg. 2008;48:580–587.
25. Tuttle KR, Chouinard RF, Webber JT, et al. Treatment of atherosclerotic ostial renal artery stenosis with the intravascular stent. Am
J Kidney Dis. 1998;32:611–622.
26. Sharafuddin MJ, Olson CH, Sun S, et al. Endovascular treatment of celiac and mesenteric arteries stenoses: applications and results.
J Vasc Surg. 2003;38:692–698.
27. Sivamurthy N, Rhodes JM, Lee D, et al. Endovascular versus open mesenteric revascularization: immediate benefits do not equate
with short-term functional outcomes. J Am Coll Surg. 2006; 202:859–867.
28. Yutan E, Glickerman DJ, Caps MT, et al. Percutaneous transluminal revascularization for renal artery stenosis: Veterans Affairs
Puget Sound Health Care System experience. J Vasc Surg. 2001;34:685–693.
29. Brown DJ, Schermerhorn ML, Powell RJ, et al. Mesenteric stenting for chronic mesenteric ischemia. J Vasc Surg. 2005;42:268–
274.
Visceral Reconstruction to Facilitate Cancer
Management: Celiac, Mesenteric, Splenic, Hepatic
Chapter 20 and Renal Artery Disease Management
Mohamed A. Zayed E. John Harris Jr.
DEFINITION
■
This chapter assumes basic knowledge of surgical oncology principles and the management of
patients with intraabdominal tumor pathology. For further review of these topics, please refer to
relevant background sources.1,2
■
Advanced primary and recurrent abdominal malignant tumors may frequently involve adjacent
arterial and venous structures. Surgical management may require curative en bloc tumor resection,
with the goal of achieving negative macroscopic and microscopic margins. Adjunct vascular
reconstruction may be necessary to achieve complete tumor removal.
■
A wide variety of malignancies may develop in the peritoneal space and retroperitoneum. A
representative range of pathologies involving intraabdominal arterial and venous structures is
summarized in Table 1.
■
Primary vascular tumors are exceedingly rare, frequently mimic other oncologic disease processes,
and may evolve slowly—leading to delay in diagnosis and treatment. Although most commonly
arising from large vessels such as the aorta and vena cava, primary vascular tumors may also
originate from distal branches of the iliac, mesenteric, and renal arteries. Classification systems
(Wright/Salm classification) have broadly categorized primary vascular tumors as intimal
(majority, 70%) and mural.3

■
Patients with complex intraabdominal oncologic pathology are best managed by a multidisciplinary
care team at a tertiary care center. If tumor extension to adjacent vascular structures is suspected,
surgical planning should include evaluation of potential revascularization options by a vascular
surgeon.
■
The initial assessment should include a thorough evaluation of the patient’s presenting symptoms.
This may include focal or regional abdominal pain resulting in tumor parenchyma pressing against
adjacent structures. Patients may also present with gastrointestinal symptoms such as early satiety,
nausea, and vomiting. Erosive gastrointestinal lesions may manifest with hematochezia, melena, or
hematemesis. Constitutional flu-like symptoms, fevers, malaise, fatigue, night sweats, and muscle
aches may also rarely present in patients with certain patients with rapidly expanding tumors.
■
Depending on the primary site and tissue of origin, tumor-associated physical findings may not be
obvious until relatively late in the disease process. Abdominal distension can result from
increasing tumor volume or from serous ascites due to portal venous compression. Tumor mass
effect or infiltration of the inferior vena cava (IVC) or iliac venous system may lead to unilateral
or bilateral lower extremity edema, dilated abdominal wall veins, evidence of deep venous
thrombosis (DVT), biliary symptoms, and renal insufficiency. Accordingly, physical examination
should not only include a thorough abdominal exam with palpation of all nodal basins but also a
complete vascular exam with evaluation of limb pulses, Doppler signals, and assessment of
extent/grade of limb edema.
■
Patient with primary vascular tumors, particularly ones with intimal expansion and growth, can
present with evidence of venous or arterial embolization. Manifestations of recurrent venous
pulmonary emboli include shortness of breath, respiratory distress, and hemodynamic changes
including tachycardia and right heart failure. Depending on the volume of arterial emboli,
symptoms can range from lower extremity pain to digital discoloration.

■
Tumor staging and classification systems are beyond the scope of this chapter. Please refer to other
excellent references for tumor-specific staging modalities and requirements.2,4
■
Patients deemed candidates for surgical resection by a multidisciplinary team should receive a high-
resolution, thin-slice (at least 1 mm), multidetector computed tomography (MDCT) scan with
intravenous contrast injection to allow for imaging during arterial and venous phases. Image
acquisition should allow for multiplanar sagittal, coronal, and three-dimensional reconstructions.
This type of detailed imaging provides valuable information regarding tumor margins, suspected
histologic subtype, and grade and can also help determine the morphology, patency, and extent of
involvement of adjacent vascular structures.
■
In situations where mesenteric venous thrombosis is visualized on MDCT, specific postprocessing
protocols may be further implemented to improve clarity regarding the extent of thrombus burden
and associated and/or resultant venous congestion.
■
Adjunct imaging studies may also include magnetic resonance imaging (MRI), ultrasonography, and
rarely, angiography/venography. Particularly, in patients with concern for osseous or neurogenic
tumor involvement, MRI may be particularly useful in defining tissue planes and tumor
parenchyma boundaries. MRI also has a nearly 100% sensitivity for detecting intracaval tumor
thrombus.
■
Autogenous vascular conduit may be necessary for adequate revascularization, particularly
following bowel resection and reconstruction. When anticipated, preoperative venous duplex
scanning of the lower extremities will help document the presence and usage of superficial
femoral vein as potential graft conduit. The presence of deep venous obstruction, either acute or
chronic, may preclude venous harvest from that particular extremity. Similarly, the bilateral lower
extremity greater saphenous veins should be evaluated for patency, diameter, and adequate length.
■
Occasionally, preoperative or intraoperative transesophageal echocardiography may be needed to
confirm the proximal extent of intracaval tumor thrombus visualized using other cross-sectional
imaging modalities and determine whether the tumor thrombus is encroaching into the right atrium.5
SURGICAL MANAGEMENT
Patient Selection
■
Whenever possible, the goal of surgical extirpation of abdominal solid organ tumors should be
oncologic cure. This assumption presupposes tumor localization to a distinct anatomic region that
will allow for resection with negative macroscopic and microscopic margins. Thus, the goals of
the procedure should be clearly defined by sufficient preoperative high-quality anatomic cross-
sectional imaging, multidisciplinary consultation, and discussions with the patient regarding the
operative risks, benefits, expectant outcomes, and overall prognosis.2,6
■
Abdominal solid organ tumors are traditionally considered unresectable when they involve the
arterial or venous vasculature, are diffusely metastatic throughout the peritoneum or at remote
sites, or involve the root of the mesentery or spinal cord to a significant extent. Patients with
extensive tumor burden precluding resection may still be offered incomplete removal or debulking
operations to potentially prolong survival and improve symptom palliation.6
■
Equally as important as the anatomic considerations, preoperative patient functional status is a
significant determinant of surgical eligibility. Performance assessments, such as outlined by the
Karnofsky or Eastern Cooperative Oncology Group (ECOG) score, help predict patient-specific
postoperative quality of life.2,7 At our institution, patients who are bedridden at the time of initial
assessment, severely disabled, or unable to independently perform activities of self-care are often
not offered curative resection.
■
Candidacy for intraabdominal vascular reconstruction is also contingent on the extent of potential or
preexisting vascular compromise. As such, we have typically attempted arterial reconstruction
when tumors involve critical arterial structures such as the aorta, celiac artery and its branches,
proximal superior mesenteric artery (SMA), common/external iliac artery, and the internal iliac
artery in the setting of an embolized, occluded, or resected contralateral internal iliac artery.
Similarly, venous reconstruction is also anticipated when tumors margins appear to include the
vena cava, portal, superior mesenteric, common, and external iliac veins.
■
Items to consider in preoperative multidisciplinary review include the extent of planned gross
surgical resection margins, the need for preoperative arterial or venous embolization, the need for
other prophylactic procedures such as placement of ureteral stents or nephrostomy tubes, and the
likelihood for intestinal resection and/or reconstruction.
■
Ureteral stent placement should be considered in all patients who demonstrate evidence of ureteral
obstruction, renal hydronephrosis, or urinary obstructive signs or symptoms from either tumor
mass effect or invasion of urologic structures. Moreover, ureteral stents should also be considered
in patients with pelvic tumors where there is potential concern of ureteral injury during resection
of the tumor or during vascular reconstruction.
■
A thorough review of detailed preoperative imaging will greatly facilitate proper conduit selection
and preparation and, ultimately, a successful outcome. Particular attention should be directed to
the length of vascular segment involved by adjacent tumor, the branch points and bifurcations
present along this length, and which segments, if any, are circumferentially encased by tumor
parenchyma.
■
Attention should be paid as to whether planned resection will include vessels which are already
occluded with adequate collateral circulation already in place, or whether adjacent or
contralateral vascular structures are capable of supplying adequate inflow and outflow. Vascular
segments to be reconstructed should be patent and preserved to the greatest extent possible during
the planned tumor resection.
■
Endovascular embolization is the preferred method of preoperative vascular occlusion prior to open
surgical resection. This strategy is commonly used for preoperative splenic artery/vein
embolization prior to planned surgical splenectomy, internal iliac artery embolization prior to
planned pelvic tumor resection, and renal artery/vein embolization prior to planned nephrectomy
with or without the need for further exposure of the retrohepatic IVC. For this purpose, the
preferred size of coils/plugs is estimated based on the diameter and length measurements of the
target vessel on preoperative cross-sectional imaging and is typically oversized by up to 20% of
the target vessel diameter. For additional details regarding visceral embolization techniques, refer
to Chapter 19 (Stenting, Endografting, and Embolization Techniques: Celiac, Mesenteric, Splenic,
Hepatic, and Renal Artery Disease Management). For additional details regarding internal iliac
artery embolization techniques, refer to Chapter 24 (Advanced Aneurysm Management
Techniques: Management of Internal Iliac Aneurysm Disease).
■
Aortoiliac arterial involvement often requires resection followed by reconstruction with patch
angioplasty, interposition, or extraanatomic bypass. Type of reconstruction and conduit type
(autogenous venous allograft, cryopreserved homograft, or synthetic conduit) is contingent on the
type of tumor, extent of vascular segment involvement, and degree to which intestinal
reconstruction is also anticipated. In the latter case, when contamination by succus entericus is
likely, autogenous femoral vein conduits for iliac artery reconstructions and IVC or spliced
femoral vein conduits for aortic reconstructions are preferred. Alternatively, when not available,
rifampin-soaked, gel-sealed knitted Dacron conduit may serve as a potential substitute with
acceptable results.8
■
Reconstruction of the celiac trunk, common hepatic artery, SMA, portal vein, and superior
mesenteric vein (SMV) are similarly contingent on the extent of involvement of these structures
with tumor pathology. Unless the artery in question is circumferentially involved, it is our
preference to resect only the portion of vessel wall directly involved with tumor while preserving
the remaining vessel architecture with patch repair. Autogenous venous conduit (using superficial
femoral vein or greater saphenous vein or femoral vein) is preferred for vessel segments requiring
interposition grafting.
■
The mainstay of treatment of primary and secondary tumors of the IVC is surgical resection and
reconstruction. The extent of reconstruction is contingent on the type of tumor, extent of caval
involvement, and the anatomic segments involved. Adequate retrohepatic caval exposure is
challenging and may require total vascular isolation of the liver to minimize blood loss during this
maneuver. In circumstances where the IVC is chronically occluded with tolerable lower extremity
edema and adequate renal function, ligation and resection without reconstruction should be
considered. On the other hand, patients with recent occlusion of the IVC, few venous collaterals,
notable lower extremity symptoms, or renal insufficiency should be considered for either
interposition grafting or patch venoplasty.
■
Preoperative endovascular embolization procedures should be performed in an angiography suite or
hybrid operating room, equipped with a fixed-imaging apparatus, floating-point carbon fiber
operating table, fluoroscopy platform, and monitor-viewing bank. A full complement of
compatible guidewires, catheters, sheaths, coils, and plugs should also be available.
■
Open tumor operative resection procedures are best performed in an operating room setting with
adequate space to facilitate the maneuvering of multiple surgical subspecialty teams and their
necessary operative trays/equipment.
■
Most intraabdominal operative tumor resection and reconstruction procedures may be performed
with the patient in the supine position. In the surgical field, the patient’s lower extremities should
be prepared for vein harvest if potentially necessary.
■
In patients who require retrohepatic IVC exposure and reconstruction, the left lateral decubitus
position should be employed to facilitate right thoracoabdominal exposure through the 8th or 9th
rib interspace.
■
Placement of ureteral stents will require initial positioning of the patient in lithotomy position and
then subsequent repositioning of the patient to facilitate further planned surgical intervention.
TECHNIQUES
AORTIC RECONSTRUCTION
■
For a discussion of the technical exposure of the paravisceral, pararenal, and infrarenal aorta,
please refer to Chapters 14 (Exposure and Open Surgical Management at the Diaphragm), 15
(Retroperitoneal Aortic Exposure), and 22 (Advanced Aneurysm Management Techniques: Open
Surgical Anatomy Repair).
First Step
■
The surgical exposure of an intraabdominal tumor either directly adjacent or involving the aorta
should aim to not only provide adequate exposure of tumor resection but also facilitate adequate
proximal and distal arterial control. A traditional midline abdominal incision, extending from the
xiphoid process to the pubis, can facilitate this in the majority of patients.
■
In patients with wide costal margins or an anticipated need for wide parahepatic or parasplenic
exposure, a bilateral subcostal incision (also known as Michigan smile) may also be useful.
■
For large abdominal tumors, renal tumors, or tumors with cephalad intraabdominal extension to the
level of the diaphragm, a lateral decubitus thoracoabdominal approach to facilitate both adequate
tumor exposure as well as vascular proximal control and reconstruction is advised.
Second Step
■
Proximal aortic control can often be obtained directly above the anticipated cephalad margin of the
tumor. In this circumstance, via either retroperitoneal or transperitoneal approaches, the medial
and lateral aortic margins are cleared for a distance of 2 to 3 cm proximal to the tumor margin. The
exposed segment is inspected for lumbar vessel branches, which may be externally ligated as
necessary to aid in exposure and control. A large, slightly curved vascular aortic clamp (e.g.,
DeBakey aortic occlusion clamp) is best suited to obtain proximal aortic control.
■
Supraceliac or suprarenal aortic exposure may be necessary for optimal control (FIG 1).
■
For control of the supraceliac aorta, the peritoneal cavity is entered below the level of the xiphoid
process. With cephalad retraction of the left lobe of the liver, the left triangular ligament of the
liver is divided and the lesser sac is entered via a longitudinal incision in the gastrohepatic
ligament. Care should be taken here to avoid injury to the esophagus (identified by aid of
orogastric/nasogastric tube placement) or a replaced left hepatic artery. For additional exposure,
the median arcuate ligament and the right crus may be divided (FIG 1).
■
Suprarenal aortic control is obtained following circumferential dissection and mobilization of the
left renal vein off the ventral surface of the aorta. Left renal vein inferior lumbar branches should
be ligated to facilitate mobilization. In rare circumstances, the left renal vein may need to be
ligated during this maneuver. When this is anticipated, existing collateral veins such as the left
gonadal, adrenal, or lumbar should be intentionally preserved prior to division of the left renal
vein.
■
Infrarenal aortic exposure can be achieved either via transperitoneal or retroperitoneal approaches.
If the tumor has pelvic extensions or if exposure/control of the right iliac system is anticipated, a
transperitoneal approach may be preferable.
Third Step
■
Depending on the extent of aortic tumor involvement, durable repair may be achieved using either
patch angioplasty or interposition grafting.
■
Patch repair is commonly performed with a woven Dacron, bovine pericardium, or autogenous
femoral vein. The patch is fashioned in a manner to facilitate a wide repair without narrowing the
residual the aortic lumen. The anastomosis is usually performed with 4-0 Prolene sutures, in a
running fashion, with one suture starting from each end of the patch repair. Depending on the age of
the patient, presence and extent of retroperitoneal soilage by intestinal contents, and amount of
retroperitoneal inflammation present, polyester pledgets may be required to minimize suture-
related aortic injury and needle hole bleeding (FIG 2).
■
Alternatively, when more extensive aortic segments are involved or the tumor cannot be safely
mobilized circumferentially around the aorta, interposition grafting may be more appropriate. After
resection, the residual aorta should be inspected for any intimal defects, tumor infiltration, or
intraluminal thrombus. Once clean endpoints are determined, the interposition graft of choice can
be brought to the field. Conduit choices include autogenous vena cava or spliced femoral veins,
cryopreserved homogenous arterial conduit, or knitted or woven polyester and expanded
polytetrafluoroethylene (ePTFE). Once selected, the proximal end is fashioned in such as way as
to minimize diameter differences between the aorta and graft. The anastomosis is usually
performed with a running 3-0 or 4-0 polypropylene suture. Once completed, the proximal clamp is
temporarily released to allow the conduit to be routed in such a way to avoid redundancy, kinking,
or twisting. After reclamping of the graft (to avoid repeated aortic clamping), the distal
anastomosis is completed in a similar fashion after sufficient proximal and distal flushing
maneuvers (FIG 3).
■
Autogenous tissue repairs of the aorta are preferred in circumstances where intestinal continuity has
been interrupted. However, if autogenous tissue is not available or not adequate for use, gel-
impregnated woven polyester graft material immersed in rifampin solution is the prosthetic conduit
of choice. To achieve adequate coverage, the graft is immersed in 50 mL of normal saline
containing 600 mg of rifampin for at least 30 minutes.
■
If the paravisceral or pararenal aorta reconstruction is required, visceral and renal vessels can be
reimplanted to the interposition aortic graft. Alternatively, a premanufactured or surgeon-modified
branched aortic graft can be used to facilitate end-to-end anastomoses to the visceral or renal
vessels following aortic interposition graft repair, with side limbs typically 6 to 8 mm in diameter
(FIG 3).
SUPERIOR MESENTERIC ARTERY RECONSTRUCTION

First Step
■
Exposure of the SMA, in situations where it is involved with the tumor, may be performed jointly
with the surgical oncology team. Particularly in situations where the SMA is extensively involved,
sufficient vascular control should obtained prior to significant debulking or resection maneuvers.
■
To expose the SMA at the base of the mesentery, the transverse colon and omentum are elevated
while packing the small bowel to the right. The peritoneum is then incised at the base of the
transverse mesocolon, taking care to identify and preserve the middle colic and jejunal arterial
branches. Judicious cephalad retraction of the inferior border of the pancreas may also improve
exposure (FIG 4).
■
Alternatively, proximal SMA exposure may be gained laterally, following division of the ligament
of Treitz and mobilization of the fourth portion of the duodenum. Visualization of the underlying
SMA can be further enhanced with gentle retraction of the inferior border of the pancreas to the
level of the left renal vein (FIG 4).
■
The splanchnic nerves must be sharply excised to effectively elevate the SMA off the anterior aortic
wall.
Second Step
■
Reconstruction approach is dictated by the extent of tumor ingrowth. SMA involvement may be
tangential or require segmental resection to achieve appropriate tumor margins.
■
Partial SMA involvement may only require resection and reconstruction of one of the SMA walls.
With arterial control established, the tumor tissue and involved SMA can be sharply resected en
bloc. Following inspection to ensure a disease-free patent lumen, the arteriotomy is repaired with
a patch angioplasty technique. Autogenous vein is the preferred patch material when available,
especially following interruption of intestinal continuity. When alimentary tract continuity is not
disrupted, bovine pericardial tissue, polytetrafluoroethylene (PTFE), or polyester patch may be
used for repair. 6-0 polypropylene monofilament suture is a good choice for arteriotomy closure
and repair.
Third Step
■
More extensive tumor involvement with the SMA may require segmental resection and interposition
grafting. Variables to consider include the length of the defect, whether the SMA origin is also
involved, and conduit material available for repair.
■
For short segment replacement, reversed greater saphenous vein is the preferred conduit for SMA
grafting. Appropriately sized saphenous vein is usually harvested from the thigh, distended, and
prepared for interposition. The tumor tissue is resected en bloc with the involved segment of SMA.
Following confirmation of adequate margins, sequential end-to-end proximal anastomosis is
performed. The graft is then brought to length while avoiding any twisting or kinking of the graft.
The distal end-to-end anastomosis is then similarly performed. Spatulation of both the arterial
endpoints and saphenous conduit may or may not be helpful, depending on size discrepancy.
■
For long segment resections or resections involving the origin of the SMA, a long retrograde
“question mark” graft, so named for its appearance on contrast arteriography following the
procedure, is used to route arterial blood from the right iliac artery around the base of the
mesentery to the distal SMA. Alternatively, an antegrade bypass from the supraceliac aorta may be
tunneled posterior to the pancreas and brought out coaxially along the course of the distal SMA.
Finally, when the SMA origin is involved but sufficient distal SMA is present to allow
mobilization, the SMA may be reimplanted on the distal aorta if a disease-free segment can be
identified by palpation or from assessment of preoperative imaging studies. For bypass options
under these circumstances, cryopreserved arterial homograft or 6-mm polyester or externally
supported PTFE are typically preferred conduits. Care is once again taken to avoid conduit
twisting or kinking during placement or tunneling.
■
Although a potential option, direct bypass from the region of the origin of the SMA to the distal
mesenteric artery is problematic in that fashioning the bypass requires elevation of the mesentery,
with the distal anastomosis positioned on the posterior aspect of the distal mesenteric artery.
Although the graft may function well with the mesentery elevated, reduction of the intestines into
the abdomen invariably causes graft conduit, autogenous or prosthetic, to kink and potentially
thrombose. In this circumstance, it is almost impossible to fashion an interposition graft of
appropriate length, so approaches such as retrograde grafting or reimplantation should be
considered as preferred alternatives.
SUPERIOR MESENTERIC VEIN OR PORTAL VEIN RECONSTRUCTION

First Step
■
Exposure of the portal vein is facilitated via entry of the peritoneal cavity and interruption of the
umbilical vein and falciform ligament. The porta hepatis can be better visualized with cephalad
retraction of the right lobe of the liver, downward retraction of the colonic hepatic flexure, and
medial mobilization of the first and second portions of the duodenum. The portal vein is then easily
identified in the right posterior border of the hepatoduodenal ligament. This exposure can be
extended from the hilum of the liver to the head of the pancreas inferiorly. Inferiorly, care should
be taken to identify and preserve the coronary vein and splenic vein (FIG 5).
■
In most instances, the neck of the pancreas is divided as part of the tumor exposure and resection,
which improves caudal exposure of the portal vein, splenic vein, and SMV.
■
Exposure of the SMV can be achieved via exposure distal to the splenic vein confluence or via
similar techniques used to expose the SMA. At the base of the transverse mesocolon, the SMV can
be found lying to the right of the SMA near the midline. Multiple dense lymphatics overlying the
vein often require careful dissection and meticulous control. Care should also be taken to identify
and preserve the middle colic vein proximally and ventral venous tributaries distally (FIG 5).
Second Step
■
The extent of tumor involvement with the SMV and portal vein is variable. Reconstruction is often
required to preserve mesenteric outflow.
■
Following establishment of vascular control, en bloc resection of the tumor and associated venous
structures can be performed. Partial involvement is best managed via patch venoplasty.
Preservation of an intact back wall of the splenic SMV confluence is often beneficial in
maintaining the structural integrity of the bifurcation. SMV and portal vein patch venoplasty repairs
can be performed using autogenous saphenous vein or bovine pericardium. A 6-0 polypropylene
suture repair is used to close the vein, running or interrupted (FIG 5).
■
Tumor involvement requiring complete resection of the portal vein or SMV will require
interposition graft reconstruction. Interposition grafting with autogenous superficial femoral vein
or cryopreserved venous homograft is preferred when intestinal resection and reconstruction is
anticipated. Alternatively, 6- or 8-mm ringed PTFE when venous conduit is unavailable or
inadequate. The distal end-to-end anastomosis is completed first, followed by the proximal end,
with either interrupted or triangulated running sutures to prevent purse-stringing and anastomotic
narrowing (FIG 5).
INFERIOR VENA CAVA RECONSTRUCTION

First Step
■
Infrahepatic IVC exposure can be facilitated either through right retroperitoneal or transperitoneal
exposure. Exposure is typically dictated by the extent of other planned intraabdominal procedures
and anticipated tumor resection margins.
■
For right retroperitoneal exposure, the flank is elevated to 15 to 20 degrees with the patient
positioned in the supine position. A transverse incision can then be made extending from the rectus
abdominis to the tip of the 11th or 12th rib. The external oblique, internal oblique, transversus
abdominis muscles, and transversalis fascia are divided to create the retroperitoneal plane via
blunt dissection. With judiciously placed self-retaining retractors, a 6-cm segment of the right
lateral aspect of the pararenal and infrarenal vena cava may be easily exposed (FIG 6).
■
For a transperitoneal exposure, either a midline laparotomy or bilateral subcostal incision will
facilitate adequate exposure. Once the peritoneal space is entered, the small bowel is retracted to
the left and the lateral peritoneal attachments of the right colon are divided. This facilitates medial
mobilization of the right colon and mesentery and provides access to the retroperitoneal
attachments of the second and third portions of the duodenum. Once these attachments are divided,
the underlying vena cava can then be adequately exposed from the suprarenal level to the common
iliac veins. Ligation and division of the ventral pararenal lymphatics, right lateral lumbar veins,
and anterior crossing left gonadal vein will aid in caval mobilization during proximal and distal
circumferential dissection. Vascular tapes may be placed around the proximal and distal exposed
segments of the vena cava to facilitate vascular control. Care should be taken to not avulse medial
lumbar veins with over aggressive mobilization of the vena cava during these maneuvers (FIG 6).
■
For extended retrohepatic IVC exposure, a right thoracoabdominal incision may be performed with
the patient positioned in a left lateral decubitus position. Once the peritoneal cavity is entered, the
right triangular ligament and lateral and posterior peritoneal attachments to the right hepatic lobe
can be divided. Medial retraction of the right hepatic lobe can then be performed to facilitate
visualization of the lateral surface of the retrohepatic IVC (FIG 6). Hepatic compression here,
especially following placement of self-retaining retractors, can increase hepatic congestion and
ischemia and should be minimized to the greatest extent possible. In situations where caval
visualization is not adequate despite optimal hepatic retraction, proximal extension or even
division of the sternum may be necessary to facilitate safe exposure. Once adequate exposure is
achieved, circumferential control can be achieved following ligation and division of small hepatic
venous branches that course between the caudate lobe of the liver and the IVC in this region.
■
The suprahepatic IVC can be exposed following ligation and division of the round ligament and
wide division of the falciform and coronary ligaments. Caudal retraction of the bare dome of the
liver facilitates visualization of the suprahepatic vena cava and at least two of the three main
hepatic veins. Careful dissection of the areolar tissue surrounding these veins allows for
circumferential exposure of each of these veins as well as this segment of the vena cava.
Second Step
■
Once the vena cava is controlled both proximally and distally, the tumor mass can be dissected off
other pertinent structures to facilitate en bloc resection. Systemic anticoagulation is accomplished
with unfractionated heparin sulfate (100 units/kg intravenous infusion) and reversed with
protamine sulfate, 1 mg/100 units of heparin, when vascular reconstruction or retraction is
complete.
■
Prior to removal of the tumor mass, the patient is placed in Trendelenburg position and vascular
clamps positioned proximal and distal to the anticipated margins of resection. If the involved
segment of the IVC is limited to only a few centimeters or one side wall, a long Satinsky side-
biting vascular clamp may be used for partial caval occlusion (FIG 6).
■
Acute occlusion of the suprarenal or retrohepatic IVC may induce profound hypotension due to
significant preload reduction. In these circumstances, preemptive aggressive fluid resuscitation,
gradual clamping of the vena cava, or partial occlusion may be better tolerated. Alternatively,
venovenous bypass or atriocaval shunt placement may be necessary. Please refer to prior
references for further details regarding preparation and placement of atriocaval shunts.9,10
■
Specific isolation of the retrohepatic vena cava requires control of both the hepatic inflow and
outflow. Inflow control is achieved with cross-clamping of the infrahepatic vena cava as well as
with a Pringle maneuver (clamping of the hepatic artery and portal vein). Outflow control is
achieved with suprahepatic or infradiaphragmatic clamping of the IVC.
Third Step
■
The strategy for reconstruction is dictated by the extent of the IVC defect and the concomitant need
for other vascular reconstructions. Typically, the vena cava is repaired, when necessary, following
arterial reconstructions to decrease end-organ ischemia. The duration of caval occlusion should be
limited to less than 30 minutes to minimize venous congestion and resultant ischemia.
■
For small caval defects, primary repair may suffice when the lumen diameter is reduced by less than
50%. Otherwise, autogenous internal jugular vein or bovine pericardial patch repair may be
incorporated into the repair. Lower extremity vein harvest is not preferred for caval reconstruction
due to increased risk for distal thrombotic complications.
■
For replacement of the IVC, when necessary, interposition graft using externally supported ePTFE is
the preferred conduit. Following resection of the involved segment, the transected ends of the vena
cava are inspected for any residual disease within the lumen. Controlled sequential flushing of the
transected ends also ensures patency. The graft diameter is chosen to be deliberately smaller than
the caval segment being replaced to promote higher velocities within the graft segment following
reconstruction. The proximal anastomosis is completed first using either a running 4-0 or 5-0
Prolene suture. The distal anastomosis is then similarly performed with the patient in
Trendelenburg position. Prior to completion of the distal anastomosis, proximal and distal clamps
are sequentially removed, a Valsalva maneuver is induced by the anesthesiologist, and the graft is
filled with heparinized saline while flushing is performed to minimize retained air and the risk for
air embolization.
■
External support rings are maintained to the greatest extent possible to avoid compression of the
graft, including at midgraft segments where end-to-side anastomoses are necessary for renal vein
or common iliac vein reimplantation. For repair of the confluence of the common iliac veins, we
have successfully modified this procedure by incorporating a short segment of nonsupported
bifurcated ePTFE graft into the repair. Externally supported ePTFE grafts are then sutured to the
nonringed segment with ePTFE suture. The suture lines are then covered with BioGlue or sterile
Dermabond to prevent suture line bleeding and the graft is then placed in situ (FIG 7).
PEARLS AND PITFALLS
Preoperative workup ■ It is imperative that a comprehensive plan for resection and
vascular reconstruction be developed and agreed upon by all
participating surgical specialties well in advance of the
procedure.
■ Adequate preoperative evaluation will facilitate discussion of
planned vascular reconstructions as well as the risks and
anticipated outcomes of the procedure.
Intraoperative ■ The presence of adequate systemic anticoagulation prior to
anticoagulation vascular occlusion is essential to the optimal outcome of the
procedure. Anticoagulation may be delayed to minimize tumor bed
bleeding during resection but should be established well in
advance of planned vascular reconstruction.
■ An activated clotting time (ACT) of greater than 250 seconds is
recommended during vascular repairs to avoid thrombotic
complications. Reversal of anticoagulation following completion
of arterial repairs is also standard practice.
Arterial repairs ■ If the aorta is known to be involved with tumor, it is imperative
that proximal control be established well proximal to the
anticipated margin of resection.
■ To optimize outcome, the presence and extent of underlying
vascular arterial disease should be fully appreciated. For
example, complete aortoiliac or aortofemoral reconstruction may
be necessary when significant atherosclerotic disease is present in
the distal aorta (as an alternative to segmental patching or
replacement). Similarly, endarterectomy of residual SMA or
celiac artery diseased lumens may be necessary to optimize
patency of patch or interposition graft repairs.
■ Attempts should be made to preserve as many SMA and celiac
artery branches as possible during vascular reconstruction to
maintain adequate bowel perfusion. This is particularly important
if concomitant bowel resection is anticipated.
Venous repairs ■ In the setting of complete compression or occlusion of the IVC, the
indications for reconstruction following resection may be less
compelling. Reconstruction of chronically occluded iliac veins is
generally not indicated under any circumstances during oncologic
resections—particularly when patients are free preoperatively of
significant lower extremity edema.
■ Air embolus is a significant potential complication of extensive
venous reconstruction. The risk of air embolization may be
minimized when repairs are performed with the patient in
Trendelenburg position and with timely Valsalva induction by the
anesthesiologist during retrograde flushing maneuvers prior to
completion. If a large air embolus is suspected, blood can be
aspirated directly from the vena cava or right atrium while the
patient is maintained in Trendelenburg and left lateral decubitus
position.
Renal vascular repairs ■ Right renal vein reconstruction and/or reimplantation to the vena
cava is necessary because there is no adequate collateral venous
outflow from the right kidney. During right renal vein
reimplantation, the right renal artery should also be controlled and
clamped to avoid venous congestion injury to the kidney.
■ Left renal vein can be sacrificed and ligated if the left adrenal and
gonadal veins are intact. However, if left kidney venous outflow
collaterals were ligated during exposure and reconstruction, the
left renal vein should be preserved or reconstructed whenever
possible.
Postoperative bleeding ■ In the immediate postoperative period, sudden or acute anemia,
abdominal pain, abdominal distension, or hemodynamic instability
should be approached with heightened awareness for possible
intraabdominal bleeding.
■ Particularly in patients with recent pancreatic reconstructions,
bowel-associated leaks may compromise arterial/venous repairs
and can lead to acute catastrophic bleeding requiring urgent
intervention.
Methods to avoid lower ■ Patients are prone to increased lower extremity edema following
extremity edema lower extremity venous harvest or intraabdominal vena cava
reconstructions. For these patients, lower extremity elevation in
the immediate postoperative period is recommended.
■ Early compression therapy of the lower extremity can also
significantly minimize the extent of lower extremity edema in the
perioperative period. Arterial insufficiency should be ruled out
prior to initiation of compression therapy to avoid compromise of
already limited arterial inflow.
POSTOPERATIVE CARE
■
Patients are typically managed in a monitored setting where periodic vascular examination is
available and vasoactive agents are administered as necessary to maintain homeostatic arterial
perfusion pressure.
■
Intravenous fluid resuscitation is maintained in the short-term perioperative period until the patient
resolves an anticipated course of intestinal ileus.
■
All patients should be initiated and maintained on an antiplatelet agent, typically 325 mg aspirin
daily.
■
In patients who preoperatively received therapeutic anticoagulation, this should slowly be restarted
1 to 2 days following the patient’s operation to minimize perioperative bleeding complications.
■
Patients with large PTFE interposition caval grafts are typically anticoagulated for at least 6 months
postoperatively and potentially lifelong depending on risk factors, history of prior DVT, and extent
of reconstruction required to restore caval continuity.
■
Early mobilization and DVT mechanical and/or chemical prophylaxis should be initiated as soon as
safely possible in the postoperative period.
OUTCOMES
■
Abdominal tumor resection with vascular reconstruction is feasible for many malignancies
previously deemed unresectable.
■
In a series of 47 patients who underwent IVC reconstruction with en bloc tumor resection, there was
an 80% 5-year patency rate of the vascular reconstruction and a 45% 5-year survival.11
■
In a series of 17 patients with SMA and portal vein reconstructions with pancreatic mass resection,
there was an 88% primary patency rate. Two patients returned to the operating room for vascular-
related complications. Eighty-two percent of patients were reported alive over follow-up period
(4 to 48 months).12
■
In a series of 14 patients receiving retroperitoneal sarcoma resection and major arterial and venous
reconstruction, primary arterial patency was 58% and primary-assisted patency was 83%. Venous
patency was 78%. Local recurrence occurred in 21% of patients and 5-year disease-free survival
was 52%.13
■
In a series of 141 patients who underwent resection of retroperitoneal soft tissue sarcomas with
either major arterial or venous structure involvement, arterial continuity was retained in all
patients and venous continuity was retained in 80%. Perioperative morbidity was 36% and
mortality was 4%. Midterm arterial patency was 88.9% and venous patency was 93.8%. The
overall 5-year patient survival was 66.7%.14
COMPLICATIONS
■
Intraoperative bleeding
■
Perioperative infection
■
Thrombosis or occlusion of repair or graft site
■
Venous air embolism
■
Wound complications due to poor nutrition or possible radiation to operative field
■
DVT from hypercoagulable state
REFERENCES
1. De Vita VT, Lawrence TS, Rosenberg SA. DeVita, Hellman, and Rosenberg’s Cancer Principles & Practice of Oncology.
Philadelphia, PA: Lippincott Williams & Wilkins; 2011.
2. Feig BW, CD Ching. The MD Anderson Surgical Oncology Handbook. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins;
2012.
3. Wright EP, Glick AD, Virmani R, et al. Aortic intimal sarcoma with embolic metastases. Am J Surg. 1985;9:890–897.
4. Edge SB, Byrd DR, Compton CC, et al. AJCC Cancer Staging Manual. 7th ed. New York, NY: Springer; 2010.
5. Sigman DB, Hasnain JU, Del Pizzo JJ, et al. Real-time transesophageal echocardiography for intraoperative surveillance of patients
with renal cell carcinoma and vena caval extension undergoing radical nephrectomy. J Urol. 1999;161:36–38.
6. Kilkenny JW III, Bland KI, Copeland EM III. Retroperitoneal sarcoma: the University of Florida experience. J Am Coll Surg.
1996;182(4):329–339.
7. Ghosh J, Bhowmick A, Baguneid M. Oncovascular surgery. Eur J Surg Oncol. 2011;37:1017–1024.
8. Bandyk DF, Novotney ML, Johnson BL, et al. Use of rifampin-soaked gelatin-sealed polyester grafts for in situ treatment of
primary aortic and vascular prosthetic infections. J Surg Res. 2001;95:44–49.
9. Baumgartner F, Scudamore C, Nair C, et al. Venovenous bypass for major hepatic and caval trauma. J Trauma. 1995;39:671–673.
10. Klein SR, Baumgartner FJ, Bongard FS. Contemporary management strategy for major inferior vena caval injuries. J Trauma.
1994;37:35–41.
11. Quinones-Baldrich W, Alktaifi A, Eilber F, et al. Inferior vena cava resection and reconstruction for retroperitoneal tumor excision.
J Vasc Surg. 2012;55:1386–1393.
12. Song TK, Harris EJ Jr, Raghavan S, et al. Major blood vessel reconstruction during sarcoma surgery. Arch Surg. 2009;144:817–
822.
13. Tedesco MM, Norton JA, Cisco RM, et al. Pancreatic mass resection and revascularization. J Vascular Surgery. 2010;52(2):530.
14. Schwarzbach MH, Hormann Y, Hinz U, et al. Clinical results of surgery for retroperitoneal sarcoma with major blood vessel
involvement. J Vasc Surg. 2006;44:46–55.
Chapter 21 Hepatic- and Splenic-Based Renal Revascularization
Fred Weaver Sung Wan Ham Grace Huang
DEFINITION
■
The hepatic and splenic arteries represent suitable alternative inflow sources for renal artery
revascularization. The most common indications for basing bypass procedures from these arteries
include abdominal aortic occlusion or insufficiency or, alternatively, a scarred or hostile
periaortic retroperitoneum. Hepatic- or splenic-based renal revascularization also minimizes
increases in cardiac afterload induced by aortic cross-clamping, which may be of benefit in
patients with congestive heart failure. Alternative terms for hepatic- or splenic-based renal
revascularization include hepatorenal bypass, splenorenal bypass, splanchnorenal bypass, or
extraanatomic renal revascularization.
■
Renal revascularization is most commonly performed to alleviate “resistant” renovascular
hypertension. Resistant hypertension is defined by a systolic blood pressure greater than 140
mmHg in patients taking at least three antihypertensive medications, representing 5% to 10% of all
hypertensives. A subsegment of these patients has secondary hypertension due to renal artery
pathology or endocrine tumors. Alternative causes of resistant hypertension include
■
Renal artery
■
Atherosclerosis
■
Aneurysm
■
Arteriovenous fistula
■
Fibromuscular dysplasia
■
Takayasu arteritis
■
Other vasculitides involving the renal artery (i.e., Behçet’s syndrome, polyarteritis nodosa)
■
Trauma
■
Endocrine tumors associated with hypertension
■
Pheochromocytoma
■
Primary aldosteronism
■
Cushing’s syndrome
■
Primary adrenal hyperplasia
■
Hyperthyroidism
■
Acromegaly

■
Patient age: In younger patients, renovascular hypertension generally arises from nonatherosclerotic
pathologies, such as Takayasu’s arteritis or fibromuscular dysplasia. In patients older than 50
years of age, atherosclerosis is most common etiology.
■
Associated risk factors are those typical for all occlusive arterial disease: tobacco use, diabetes,
hyperlipidemia, and hypertension.
■
Length of the hypertensive diathesis: Was the hypertension easily controlled for a period of time,
with a recent increase in the difficulty of control? Is the hypertensive diathesis severe and recent in
onset? If either is true, the patient is more likely to have a secondary hypertension.
■
Recognition of the systemic burden of vascular disease present provides important perspective on
indications and treatment options. Many vascular maladies involve multiple vascular beds. Is there
evidence of disease involving the carotid artery, lower extremity arterial tree, and/or thoracic and
abdominal aorta?
■
A history of postprandial pain, significant unintentional weight loss, and food avoidance is
suggestive of mesenteric occlusive disease.
■
Prior pancreatitis may complicate attempts at splenic-based renal revascularization.
■
Prior Hodgkin’s disease or other neoplasms requiring mantle or midline abdominal radiation
■
For general operative risk considerations, recognition and documentation of the presence of
coronary artery disease, previous coronary stents, or surgical coronary revascularization as well
as valvular disease and congestive failure is fundamental to surgical planning.
■
Documentation of renal function as evidenced by increased serum creatinine, pedal edema, or recent
requirement for renal replacement therapy
■
Recognition of prior aortic procedures, or intraabdominal nonvascular procedures such as a
retroperitoneal lymphadenectomy for testicular cancer, which may complicate retroperitoneal
dissection and aortic exposure
■
Family history of syndromic aortic diseases such as Marfan’s, Ehlers-Danlos, and Loeys-Dietz
■
The specific antihypertensive regimen in place prior to surgery needs to be verified and
documented.
■
To obtain the most accurate baseline measurement, the highest pressure obtained from either arm
should be recorded and retained.
■
A complete vascular examination must be performed, with particular attention paid to pulse deficits
and bruits. In particular, diminished femoral pulses or an abdominal bruit may indicate significant
aortic or branch vessel occlusive disease, potentially complicating revascularization plans. The
presence of concomitant carotid bruits may suggest carotid occlusive disease that should be
assessed prior to renal revascularization. The presence of an aortic aneurysm should be excluded
by abdominal palpation.

■
Laboratory assessment of renal function should include, at a minimum, serum creatinine, blood urea
nitrogen (BUN), and electrolytes. Baseline glomerular filtration rate can be estimated from the
serum creatinine level and body mass index using the Cockcroft-Gault equation.
■
The co-occurrence of endocrine syndromes, such as pheochromocytoma or functional adrenal
tumors that potentially contribute to resistant hypertension should be evaluated with appropriate
serologic studies.
■
Renal artery duplex ultrasonography is performed to document existing renal artery disease, renal
mass, and intraparenchymal renal flow indices. Hemodynamically significant renal artery stenosis
(>60%) are determined by duplex-derived assessment of peak systolic velocity measurements
across lesions. Baseline characteristics (i.e., kidney size, velocity, spectral waveforms, resistive
indices) serve as reference points for future surveillance imaging following revascularization.
■
Selective visceral and renal arteriograms are obtained to define normal and variant vascular
anatomy, including lateral imaging of both the celiac and superior mesenteric arteries (FIGS 1 and
2).
■
Computed tomography (CT) arteriography of the abdomen and pelvis, with arterial and venous
pelvis, may provide additional useful information regarding the extent of aortic disease and other
associated abdominal pathology (FIGS 3 and 4). Catheter-based arteriography alone may not
identify significant arterial wall disease or the presence of aneurysmal lesions. However, the
expense, contrast load, and radiation associated with complementary arteriographic imaging
modalities may not be justified or appropriate in every patient, so anatomic information obtained
from these examinations should be integrated into the operative plan on an iterative basis.
Preoperative, imaging-based planning is combined with direct intraoperative assessment to create
the most effective and durable revascularization possible for each patient.
■
Documentation of celiac, hepatic, splenic, and superior mesenteric artery patency is a mandatory
prerequisite for these procedures. Significant stenosis of the celiac origin or hepatic or splenic
artery occlusive disease will prevent successful renal revascularization from these arteries.
Associated superior mesenteric artery disease also needs to be considered, particularly when the
gastroduodenal artery provides significant collateral flow from the celiac plexus to the mesenteric
bed. Renal artery anatomy, including branch vessel involvement and the presence of multiple renal
arteries also needs to be documented.
■
Bilateral lower extremity vein mapping is also necessary to identify potential graft conduit.
Standard vein mapping techniques, including imaging in a warm room with the patient in reverse
Trendelenburg position, should be employed to ensure accuracy and reproducibility.
■
For selected patients, a more extensive preoperative evaluation for coronary artery or valvular
disease should be considered. This may include both a transthoracic echocardiogram and cardiac
stress evaluation. Selective pulmonary evaluation may be required in patients with chronic
obstructive pulmonary disease (COPD)–associated respiratory compromise. Additional vascular
assessments should be performed as indicated, including carotid duplex ultrasonography to assess
the significance of carotid bruits identified on physical examination.
SURGICAL MANAGEMENT
■
The indications for hepatic and splenic artery–based renal revascularization are similar to those for
aorta-renal revascularization and are discussed elsewhere.1,4
■
Although aorta-renal bypass is most direct and generally most expeditious, extraanatomic renal
revascularization may be preferable in selected circumstances as previously noted.
■
Review of preoperative imaging is performed to determine variant vascular anatomy, if present.
Anatomy of the existing renal artery disease is assessed.
■
The hepatic–right renal bypass requires a conduit, preferably autogenous vein.
■
The spleno–left renal bypass may be performed with or without graft conduit. The native splenic
artery is sufficient length, usually to extend directly to the left renal artery, when fully mobilized.
When necessary due to variant anatomy, or prior inflammation or scarring around the pancreas,
venous conduit can also be employed.
■
Planning for availability of duplex ultrasonography in the operating room (OR) will facilitate
intraoperative confirmation of adequate target revascularization and renal perfusion.
Positioning
■
Patient is placed in supine position with both arms tucked.
■
A small bump is placed under the respective flank.
■
The operative field is prepped from the nipples to the knees.
TECHNIQUES
HEPATORENAL BYPASS
■
Optimal access is gained through a right subcostal incision extending from the midline to the tip of
the 12th rib. In large or obese patients, the medial extent of the incision can be extended across the
midline as a chevron (FIG 5).
■
When necessary, an upper midline incision may also provide sufficient exposure.
Hepatic Artery Exposure
■
The hepatoduodenal ligament is exposed by retracting the right lobe of the liver cephalad.
■
The right colon and duodenum are reflected anteriorly and to the left (Kocher maneuver). The small
intestine is packed toward the pelvis with moist laparotomy pads.
■
The hepatoduodenal ligament is incised longitudinally. The hepatic artery is located in the porta
hepatis medial to the common bile duct (FIG 6).
■
The gastroduodenal artery is identified as the first large branch coursing caudad and encircled with
a silastic loop. The gastroduodenal artery should be preserved in the presence of superior
mesenteric artery occlusive disease as it provides important collateral circulation to the small
intestines.
■
The hepatic artery is controlled proximally and distally with silastic loops (FIG 7).
Right Renal Artery Exposure
■
The right colon and duodenum are reflected as detailed earlier to expose the inferior vena cava and
right renal vein.
■
The right renal artery is located posterior and superior to the main renal vein. Depending on its
position, the renal vein is retracted either cephalad or caudad. To ensure the main renal artery is
exposed, the dissection should be carried to its aortic origin. This requires medial retraction of the
inferior vena cava and division of lumbar veins when necessary.
■
The right renal artery is controlled using a silastic loop.
■
The main renal artery is exposed circumferentially and then distally to the three segmental renal
artery branches. Each branch is identified and controlled with a silastic loop. This is a critical
operative maneuver that excludes the presence of branch disease and ensures a successful renal
artery revascularization (FIG 7).
Distal Anastomosis
■
The distal anastomosis is performed first to take advantage of the additional degrees of freedom
provided by the mobile graft.
■
An appropriate length of greater saphenous vein is harvested from the thigh. The patient is
heparinized 100 units/kg. The vein itself is reversed before placement.
■
The proximal renal artery is mobilized following its division from the aorta, at its origin. The
proximal stump is oversewn with 5-0 polypropylene suture.
■
Redundant renal artery is trimmed distally from its origin until the disease-free segment is reached.
The mobile renal artery is then transposed anterior to the inferior vena cava.
■
The vein graft and renal artery are spatulated and the end-to-end anastomosis created with
continuous 6-0 polypropylene suture, knotted at opposite ends of the anastomosis to prevent purse-
stringing. Alternatively, depending on renal artery diameter, eight interrupted sutures may be
distributed circumferentially around the lumen. The smaller the renal artery diameter, the more
advantageous the interrupted technique. Loupe magnification is necessary to ensure optimal results
regardless of which suture technique is chosen (FIG 7).
■
Once the distal anastomosis is completed, the vein graft is oriented longitudinally to prevent twisting
or kinking prior to completion of the proximal anastomosis.
Proximal Anastomosis
Hepatic artery
■
Small vascular clamps or removable clips are used to control the proximal and distal hepatic artery.
■
An arteriotomy is made on the hepatic artery and extended using Potts scissors.
■
The vein is spatulated and an end-to-side anastomosis is again performed with running
polypropylene suture (FIG 8A).
Gastroduodenal artery
■
The gastroduodenal artery may be used as an alternative inflow vessel if sufficiently large (4 to 6
mm in diameter). This anastomosis may be performed either end-to-end or end-to-side, but prior to
division of the gastroduodenal artery, consideration should be given toward its contribution to the
mesenteric circulation (FIG 8B).
Intraoperative Duplex Ultrasonography
■
We recommend insonation of the graft and both anastomoses using appropriately sized 7-MHz scan
heads to ensure technical proficiency following completion of the bypass. In recent years, our
practice has come to rely on duplex ultrasonography for intraoperative assessment of all small and
medium size autogenous reconstructions, especially in light of the reduced frequency of such
procedures in the era of endovascular and hybrid reconstructions. Renal artery reconstruction is
unforgiving in that failure in the perioperative period cannot be expeditiously addressed after the
abdomen is closed, almost always precipitating kidney infarction and permanent reductions in
creatinine clearance.
■
Spectral waveforms, velocities, and B-mode are all employed to detect technical errors requiring
immediate repair.
SPLENIC–RENAL BYPASS
■
Exposure is obtained through a left subcostal incision extending from the midline to the tip of the
12th rib. In large or obese patients, the medial extent of the incision can be extended across the
midline as a chevron (FIG 9).
■
As was the case on the right side, the upper midline incision may also provide sufficient access
depending on body habitus, prior surgeries, and operator experience.
Splenic Artery Exposure
■
The greater omentum is elevated exposing the transverse mesocolon. The ligament of Treitz is taken
down and the inferior mesenteric vein is ligated and divided. The plane between the pancreas and
kidney is entered and the pancreas elevated. The splenic vein is embedded in the body of the
pancreas—avoid injury during mobilization of the distal pancreas. The splenic artery should be
palpable along the cephalad border of the pancreas. It is mobilized free of surrounding parenchyma
moving medially and laterally until sufficient length is obtained to fashion either a primary bypass
or support an autogenous vein conduit (FIG 10).
Left Renal Artery Exposure
■
After mobilizing the distal pancreas, the left renal vein is located just inferior and slightly caudad.
■
The left renal vein is circumferentially mobilized. This requires division of its nonrenal tributaries:
the gonadal, adrenal, and lumbar veins. Dividing these veins greatly enhances renal vein mobility,
facilitating renal artery exposure from its position just cephalad and posterior to the vein.
■
As previously described on the right, the left renal artery is dissected to its aortic origin and
controlled with a silastic loop. The distal artery and its three segmental branches are identified and
encircled with silastic loops. The importance of mobilization is again emphasized (FIG 11).
Splenic–Renal Anastomosis
■
The patient is heparinized with 100 units/kg of unfractionated heparin. The left renal artery is
clamped at the origin and divided. The renal stump is oversewn with a 5-0 polypropylene suture.
The distal main renal artery is spatulated distal to the existing renal artery disease.
■
The mobilized splenic artery is divided with sufficient length to extend behind the pancreas to the
left renal artery without undue tension. The distal splenic artery is oversewn.
■
The mobilized splenic artery is spatulated and anastomosed end-to-end to the left renal artery, again
with either running or interrupted polypropylene suture depending on the respective arterial
diameters (FIG 12).
■
Alternatively, when splenic artery length is insufficient, reversed saphenous vein may be employed
as a bridge graft. Again, to optimize the degrees of freedom, the distal anastomosis is performed
first, followed by end-to-end or end-to-side anastomosis to the splenic artery. The vein graft is
positioned posterior and inferior to the body of the pancreas.
Intraoperative Duplex Ultrasonography
■
As described earlier
FINAL INSPECTION
■
With completion of the revascularization procedures, all anastomoses and oversewn renal artery
origins are inspected for hemostasis. Heparin anticoagulation is reversed with protamine, in a
quantity sufficient to normalize the activated clotting time (ACT). Palpation of the SMA at the base
of the mesentery is performed to confirm a pulse. Operative traction and/or preexisting disease
may compromise SMA flow or precipitate an occult dissection. If the SMA pulse is absent, or the
intestinal viability uncertain, mesenteric artery revascularization may be necessary.
PEARLS AND PITFALLS

Preoperative imaging ■ Surgical planning may require CT and catheter-based
arteriography as complementary references for surgical planning.
■ Celiac artery stenosis is an absolute contraindication for hepatic-
and splenic-based renal revascularization.
Preoperative vein mapping ■ Autogenous vein is the preferred conduit for renal
revascularization.
■ Lower extremity vein mapping allows assessment for suitable
conduit.
Exposure of the renal artery ■ Circumferential exposure of the entire main renal artery and the
three segmental branches is imperative for placement of the renal
anastomosis distal to existing disease
Graft orientation ■ Longitudinal orientation needs to be confirmed repeatedly during
graft tunneling and orientation. Excessive reliance on graft
marking or “striping” as the sole method of orientation may lead to
inadvertent kinking or twisting.
Intraoperative duplex ■ Completion duplex scanning is easy, quick, and invaluable in
identifying technical errors, which may compromise graft patency
and renal viability.
■ Unlike lower extremity bypass procedures, perioperative graft
occlusion cannot typically be identified expeditiously to prevent
end-organ compromise.
POSTOPERATIVE CARE
■
Postoperative care typically involves central venous and arterial pressure monitoring in an intensive
care unit (ICU) environment, at least for the first 24 to 48 hours.
■
Serial monitoring of serum creatinine, urine output, and acid–base status is essential in the early
postoperative period. Unexplained changes in acid–base or elevation of serum creatinine could
indicate occlusion of the revascularization itself or progressive mesenteric ischemic.
■
Blood pressure is maintained in a physiologic range with vasoactive medications as necessary. Oral
antihypertensives are resumed on postoperative day 1 and adjusted depending on the response to
renal revascularization.
■
Diet is resumed as bowel function returns; nasogastric suction is usually not required.
■
Blood pressure and antihypertensive medication requirements may decrease after renal
revascularization and should be adjusted prior to discharge.
■
Follow-up surveillance duplex ultrasonography is performed at 6 and 12 months then annually
thereafter. Detected abnormalities suggesting stenosis of the renal reconstruction may be addressed
with remedial endovascular intervention or surgical revision when indicated.
OUTCOMES
■
Large case series documenting the outcomes following isolated hepatorenal and splenorenal artery
bypass are sparse. Published results are derived from two relatively large series, generally
demonstrating acceptable perioperative morbidity and mortality with improved renal function and
blood pressure and durable patency.
■
Moncure et al. reported 77 patients who underwent 79 procedures (29 hepatorenal, 50 splenorenal
bypass) for the treatment of renovascular hypertension and renal preservation. The perioperative
mortality was 6%. Deterioration in renal function occurred on three occasions but only in patients
with bilateral simultaneous repair. Cure or improvement in hypertension was observed in 52 of 63
patients. Renal function was preserved or improved in 67 of 77 patients.2
■
Another series by Geroulakos et al. document similar outcomes with extraanatomic renal artery
revascularization for atherosclerotic renal artery disease. Forty-five hepatorenal and/or
splenorenal bypasses were performed in 38 patients for the treatment of renovascular
hypertension, renal preservation, or both. There was one postoperative death from myocardial
infarction and two cases of early graft thrombosis. There was a significant decrease in
postoperative mean serum creatinine as well as the average number of antihypertensives. Over a
median follow-up of 33 months, there were 10 deaths all from cardiac issues.3
COMPLICATIONS
■
Bypass graft thrombosis
■
Intestinal ischemia due to preexisting disease or traction injury to SMA during operative procedure
■
Bleeding from renal, hepatic, splenic anastomosis, ligated renal artery stump, portal vein if injured
■
Acute renal failure requiring temporary or permanent dialysis
■
Pancreatitis, splenic infarction, common duct injury
■
Incisional hernia
REFERENCES
1. Benjamin ME, Dean RH. Techniques in renal artery reconstruction: part II. Ann Vasc Surg. 1996;10(4):409–414.
2. Moncure AC, Brewster DC, Darling RC, et al. Use of the splenic and hepatic arteries for renal revascularization. J Vasc Surg.
1986;3(2):196–203.
3. Geroulakos G, Wright JG, Tober JC, et al. Use of the splenic and hepatic artery for renal revascularization in patients with
atherosclerotic renal artery disease. Ann Vasc Surg. 1997;11(1):85–89.
4. Weaver FA, Kumar SR, Yellin AE, et al. Renal revascularization in Takayasu arteritis–induced renal artery stenosis. J Vasc Surg.
2004;39:749–757.
Advanced Aneurysm Management Techniques: Open
Chapter 22 Surgical Anatomy and Repair
Elizabeth Blazick Mark F. Conrad
DEFINITION
■
An aneurysm is defined as a permanent, focal dilation of an artery to a size that is greater than 50%
of the normal or expected transverse diameter of the vessel. Although dimensions differ slightly
for men and women, practically speaking the normal diameter for the abdominal aorta is 2 cm;
therefore, the abdominal aorta is considered aneurysmal when it reaches 3 cm in transverse
dimensions.
■
Fusiform aneurysms are the most common configuration and are a symmetric enlargement of the
entire vessel, whereas a saccular aneurysm is a focal outpouching that results in an asymmetric
bulge of the vessel wall.
■
Aneurysms may occur in virtually any vessel in the body but are most commonly seen in the
infrarenal abdominal aortic aneurysm (AAA). The neck is the length of normal aorta between the
osteum of the lowest renal artery and the beginning of the aneurysmal aorta. The term juxtarenal is
used to describe AAAs that do not involve the renal arteries but because of proximity (<1 cm
neck) require clamping above the renal arteries to complete the proximal aortic anastomosis. In a
suprarenal aneurysm, at least one of the renal arteries arises from aneurysmal aorta, implying the
need not only for a proximal clamp but also renal artery reconstruction at the time of the repair
(FIG 1). This chapter will focus on the indications and techniques for repair of infrarenal and
juxtarenal AAA.
■
AAA size and/or expansion rate is an important predictor of rupture, and as such guides indication
for repair in asymptomatic patients.1
■
Other predictors for increased risk rupture include female gender, positive family history of
aneurysms, smoking status (higher for current smokers versus never smokers and previous
smokers), hypertension, and chronic obstructive pulmonary disease (COPD).2–5

■
A thorough history and physical exam is imperative in the evaluation of a patient being considered
for aneurysm repair.
■
History of present illness: Determine how the aneurysm was discovered. Often, AAAs are an
incidental discovery on an imaging test done for another purpose. Be sure to ask about abdominal
or back pain, which may indicate this is a symptomatic aneurysm that would require more urgent
repair.
■
Past medical history: Patients with concomitant renal, cardiac, or lung disease tend to have more
complications perioperatively and should be medically optimized prior to proceeding with
elective repair. Although there is no benefit to preoperative cardiac revascularization in
asymptomatic patients, those with known cardiac disease or risk factors should be evaluated by a
cardiologist.6
■
Family history: Close to 15% of patients with AAA will have a first-degree relative with
aneurysmal disease. Patients with AAA should be counseled to alert their siblings and children to
this condition, so they may be screened appropriately.3
■
Social history: Smoking has been linked to increased risk of aneurysm formation and rate of
expansion. Patients should be counseled on smoking cessation.
■
Review of systems: In addition to the generalized systems review appropriate for all patients
undergoing major surgery, particular attention should be directed to other vascular comorbidities.
In particular, query about previous cerebrovascular accident (CVA) or transient ischemic attack
(TIA) symptoms, amaurosis fugax, mesenteric ischemia, lower extremity ischemic symptoms
(claudication, rest pain, ulcers), and work up positive symptoms as appropriate.
■
On physical exam, perform a thorough abdominal exam, although be aware that the positive
predictive value for localizing a small- to moderate-sized AAA on exam is poor. A small
proportion (1% to 10%) of patients with AAA will have a concomitant aneurysm elsewhere, so be
cognizant that those patients with known AAA and a prominent femoral or popliteal pulse may
need further imaging to exclude an aneurysm in these locations.7
■
Conversely, patients who initially present with peripheral aneurysms such as femoral (85%) or
popliteal aneurysms (60%) have a much higher rate of concomitant AAA and aortic screening
should be performed in these patients.7,8

■
Of all imaging techniques used for AAA surveillance, B-mode ultrasonography is the least
expensive and does not expose the patient to radiation. Currently, the U.S. Preventative Services
Task Force (USPSTF) recommends an ultrasound as a screening test for males between the ages of
65 and 75 years who have ever smoked 100 or more cigarettes over a lifetime. There are no
official recommendations for women. It is generally accepted that a negative screening ultrasound
exonerates the patient from further screening or surveillance imaging, as the likelihood of new
aneurysm development of clinical significance after the age of screening is extremely low. If a
screening ultrasound detects a small aneurysm, yearly ultrasounds are indicated until the sac
approaches a size where repair may be indicated, at which time further imaging with computed
tomography (CT) is recommended.7,9
■
Computed tomography angiography (CTA) provides a more accurate assessment of aneurysm size,
extent, branch vessel proximity and involvement (which may determine if the aneurysm is
amenable to endovascular or open repair, and if open repair is to be done, where the proximal
clamp should be applied) and is the test that should be used for planning open AAA repair. A
thorough exam should include thin (1.5 cm or smaller) cuts of the chest, abdomen, and pelvis with
contrast administered in the arterial phase (FIG 2).
■
It is important to note the location of the aneurysm and its relationship to the renal arteries. Renal
anatomy should be noted as well, including any accessory renal arteries and the presence of a
pelvic or horseshoe kidney. The renal vein usually travels anterior to the aorta but can be posterior
and this should be noted as it may influence operative approach. Other venous anatomy such as a
duplicated or left-sided inferior vena cava (IVC) should be noted as well.
SURGICAL MANAGEMENT
■
The decision to operate on an asymptomatic patient is based on three primary factors: the risk of the
aneurysm’s rupturing, the risk associated with aneurysm repair, and the patient’s life expectancy.
The operative risk and overall life expectancy should be assessed. Assuming that a patient is fit
enough to proceed with repair, size is currently our best predictor of rupture. The UK Small
Aneurysm Trial and ADAM VA Trial recommend treatment for all patients with an infrarenal
AAA larger than 5.5 cm in size, with consideration for repair in women with AAA of 5.0 cm given
their higher risk of rupture and likely smaller baseline aortic size. These studies also support
repair for those patients who have an increase in diameter of greater than 0.5 cm over a 6-month
period (Table 1).10,11
■
Although there are no large trials looking specifically at iliac aneurysms, repair is generally
recommended when they reach 4 cm or greater in size. Iliac aneurysms are more often seen in
patients with a concomitant aortic aneurysm and only a quarter of patients with iliac aneurysms
will have isolated disease.
■
All open repairs should be performed under general anesthesia. It is preferable for the anesthesia
team to evaluate the patient prior to the day of surgery so that appropriate time for developing an
anesthetic plan, lines, and other means of hemodynamic monitoring is allowed. The use of an
epidural for pain control in the postoperative period is useful. In addition, arrangements should be
made for autotransfusion given the unavoidable amount of intraoperative blood loss.
■
Preoperative understanding of anatomy is of the utmost importance. The surgeon must understand the
proximity of the aneurysmal aorta to the renal and visceral vessels and if these branch vessels are
affected, as this will impact where the proximal cross-clamp will be applied. If at all possible,
clamping should only be done on nonaneurysmal aorta with minimal thrombus or calcification to
minimize risk of distal embolization of debris or clamp injury, and all aneurysmal aorta should be
resected even if this means involvement of the visceral or iliac segment. If the aorta contains a
significant amount of debris or there is little space between branch vessels, a more proximal
clamp site in the supraceliac aorta should be considered. It is important to discuss the proposed
clamp site with anesthesia preoperatively, as this will affect their management of the patient. The
choice of clamp site should be made during the preoperative stage, as the intraoperative need to
move the clamp higher is associated with adverse outcomes.
■
Planning for the distal anastomosis requires review not only of the aortic bifurcation but the iliacs as
well. If there is aneurysmal or occlusive disease within the iliac arteries, concurrent repair with a
bifurcated graft may be appropriate; otherwise, the majority of AAAs are repaired with a tube
graft to the iliac bifurcation. Anastomosis may predicate method of distal control, which can be
obtained with a single clamp across the bifurcation or both iliac origins, or occlusion balloons
(Foley catheters or Pruitt occlusion balloons) for heavily diseased vessels.
■
Key pre-operative planning concerns are summarized in Table 2.
TECHNIQUES
■
There are two approaches for the open repair of the infrarenal or juxtarenal aortic aneurysm:
transperitoneal or retroperitoneal (FIG 3). Which approach is used for an infrarenal AAA is based
on several factors: body habitus (obese patients are often best approached via retroperitoneal),
prior surgery (concern for intraperitoneal adhesions), and location of clamp (above the renal
arteries may favor a retroperitoneal approach), whereas planned intervention on the right renal or
iliac artery would be better approached from the front (transperitoneal).
TRANSPERITONEAL APPROACH
■
Positioning: The patient is positioned supine on a standard operating room (OR) table with both
arms extended. The area from the nipple line to midthighs should be included in the prep field to
allow exposure for a high incision as well as the groins should access to the femoral vessels be
needed. The hair is clipped and a towel is placed over the perineum. Any previous incisions
within the prep field are marked. A Steri-Drape or Ioban is used to secure the drapes in position.
Once in position, check pulse volume recording (PVRs) and/or distal pulses.
■
Incision: A generous midline incision from the xiphoid to the pubis is made and dissected until the
peritoneal cavity is entered (FIG 3). It may be necessary to extend the incision cephalad lateral
alongside the xiphoid if higher exposure is needed or in emergent situations such as a rupture
where immediate supraceliac control is needed. A self-retaining retractor system should then be
positioned. We prefer the Omni retractor as the open configuration of the system does not limit the
width of exposure.
■
Dissection: Reflect the greater omentum and transverse colon cephalad and pack these structures
away in a moistened towel or lap pad on top of the patient’s chest. The small bowel should be
retracted to the right and packed within a separate moistened towel. The small bowel is gently
placed behind a self-retaining retractor, taking care not to compromise the superior mesenteric
artery (SMA). This exposes the ligament of Treitz, which can be divided along the jejunum to the
level of the aorta (FIG 4). Reposition the retractor to allow as much small bowel to be out of the
field as possible, and take down the ligament of Treitz with electrocautery, taking care not to injure
the bowel. The inferior mesenteric vein is usually ligated during this dissection. This allows
access to the infrarenal aorta where the overlying retroperitoneal tissue can be dissected free.
Depending on how much aorta is needed for an adequate cuff of the proximal anastomosis, an
anterior renal vein may need to be mobilized cephalad, with ligation of the gonadal and/or adrenal
vein for better exposure (FIG 5).
■
Exposure of the supraceliac aorta (FIG 6): The maneuver is only needed in cases where high
abdominal aortic exposure is needed, such as in a rupture. The left lobe of the liver must be
retracted laterally by taking down the triangular ligament. Next, identify and dissect free the
gastroesophageal junction after dividing the gastrohepatic ligament, which is most expeditiously
done by palpating for the nasogastric tube and applying caudal traction. Division of the
gastrohepatic ligament must be done with the thought that a replaced left hepatic artery would be
coursing beneath this structure. The esophagus can be retracted to the patient’s left, and this
maneuver will expose the aorta. An aortic compressor can be used in extreme circumstances;
however, dissection of the aorta circumferentially and surrounding the aorta with a shoestring if the
patient’s condition allows is preferable. This exposure, although useful when urgent supraceliac
control is needed, will not allow access to the visceral segment of the aorta. In order to gain this
exposure, a right or left medial visceral rotation should be incorporated into the dissection. The
use of a right medial visceral rotation will allow access to the right renal artery, as well as placing
the SMA on 90-degree tension and is useful for clearing a clamp site in those patients with a
juxtarenal aneurysm who have very little room between the renals and SMA (FIG 7). The use of a
left medial visceral rotation also allows for exposure to the entire visceral segment of the aorta as
well as the left renal artery. Care in this approach must be made to avoid injury to the spleen and
tail of the pancreas.
RETROPERITONEAL APPROACH
■
Positioning: Once asleep, position the patient in the lateral position with the left side up at an
approximately 60-degree angle (FIG 8). Extend the right arm on an armboard, being sure to leave
room for an Omni or other self-retaining retractor post. The upper left arm should be placed on
another armboard and padded to prevent neural injury. The bed should be flexed at the patient’s
flank to open up the area between the ribs and the anterior superior iliac spine. Position the legs so
that the lower leg is straight and the upper leg is bent. Use two pillows as padding between legs. A
beanbag can be inflated to keep the patient in place, and use thick cloth tape over the hip to secure
the patient on his or her side. Ideally, the patient should be placed on a beanbag; however, blanket
rolls can be used anteriorly and posteriorly to further secure the patient. Be sure to allow access to
prep from the spine posteriorly to the umbilicus anteriorly and from the nipple line to the groins.
All bony prominences and pressure points should be well padded to avoid injury. Use clippers to
remove hair within the prep area. Prep from the axilla and nipple line to the upper thigh. Mark all
previous incisions and use a Steri-Drape or Ioban over the entire prepped area to secure the
drapes. Once in position, check PVRs and/or distal pulses.
■
Incision: Unless clamping is planned at or above the level of the SMA, a standard retroperitoneal
incision over the 11th rib will provide adequate exposure (FIG 3). Carry the incision from the
posterior axillary line to the anterior border of the rectus. Avoid entry into the pleural cavity if
possible, being cognizant that the further posterior the incision is carried, the higher likelihood this
will occur.
■
Divide the transversalis fascia and enter the retroperitoneal space down to but not violating
Gerota’s fascia. This space can be more easily identified by resecting a distal segment of the 11th
rib, as the tranversalis fascia and transversus abdominal musculature inserts along the inferior
border of this rib. It is possible to stay entirely within a retroperitoneal plane; however, if the
peritoneum is violated, the abdominal contents can be packed away with retractors or the
peritoneum can be repaired with a running 3-0 chromic suture. The aorta may be approached via
an anterorenal (colloquially referred to as “leaving the kidney down”) or retrorenal plane (“taking
the kidney up”) (FIG 9). Generally, the aorta is approached via a retrorenal approach unless there
is a renal vein running posterior to the aorta. As the retroperitoneal dissection continues, the left
ureter should be identified and swept toward the midline and placed behind a retractor to avoid
injury during dissection of the aorta. The renal artery is identified and dissected back to its origin
to identify the aorta
■
Dissection: The renal artery should be cephalad to the vein, and once this is identified, it can be
used as a landmark and dissected back to the aorta.The renal lumbar vein should be identified and
ligated to avoid injury and excessive bleeding. Once the origin of the renal artery is identified, a
right angle can be placed along the surface of the aorta and the overlying retroperitoneal tissue
divided with electrocautery. It is imperative here to get on the aorta and stay on the aorta to avoid
excessive bleeding from the retroperitoneal tissue. The aorta is exposed to the bifurcation and can
be dissected circumferentially here if a clamp site is planned; however, the left iliac vein can
course posterior to the bifurcation and should be avoided. It is often easier to expose an area of the
left common iliac artery for clamping and control the right common iliac artery with an occlusion
balloon from within. It is unwise to gain circumferential control of the iliacs in this situation as the
iliac veins are often adherent to the posterior aspect of the artery and are easily injured, leading to
rapid exsanguinating blood loss. Identify and isolate the inferior mesenteric artery (IMA) with a
vessel loop. Pay particular attention to identifying and not injuring the ureters, which will
eventually cross anterior to the iliac vessels. If necessary and if the incision is placed along a
higher rib space, the dissection can be carried caudal to expose the entire visceral segment if need
be (FIG 10).
AORTIC CLAMPING AND REPAIR
■
Regardless of approach, it is important during circumferential dissection of the aorta to avoid injury
to the posterior lumbar arteries, which are usually paired. If they are encountered and require
ligation, carefully circumferentially dissect out the artery, tying the proximal side of the vessel, and
using another tie, double clip on the distal side prior to dividing. When dissecting on the aorta,
care must be taken to minimize aggressive manipulation and subsequent atheroembolization,
particularly if preoperative imaging shows extensive mural debris.
■
Choice of graft: There are several choices for conduit during repair. Generally, a
polytetrafluoroethylene (PTFE) or Dacron tube graft is sewn from the proximal aorta to the
bifurcation. In those patients with extensive bifurcation or iliac disease, a bifurcated graft may be
used. If this is the case, the proximal single lumen portion of the graft should be as short as
possible to prevent kinking, ideally less than 4 cm. Tunneling the limb to the femoral level should
be done only if necessary, and if so, care must be taken to run the graft posterior to the ureter. The
aorta can be measured for the appropriate graft with aortic sizers, but often, an estimation of size
can be made from the preoperative CTA. Regardless, the majority of patients can be repaired with
an 18- to 22-mm graft (FIG 11).
■
Choosing the site of the proximal anastomosis: This will depend on the quality of the proximal neck
of the aneurysm and the vicinity of the visceral vessels. In the most straightforward scenario, an
adequate cuff of normal aorta is present below the renals to allow for infrarenal clamping and an
end-to-end anastomosis. A suprarenal clamp can be used to provide space to sew to a short
infrarenal cuff. If aneurysmal tissue extends to the visceral branches, or if there is significant
antherosclerotic disease of the branches, a beveled anastomosis may be required, possibly
including an endarterectomy of the origin of a branch vessel or a bypass to the left renal artery
(FIG 12). This should be apparent based on careful review of preoperative imaging and planned
for well before clamping of the aorta. From the retroperitoneal approach, every effort should be
made to incorporate the right renal artery into the anastomosis.
■
In preparation for clamping, the patient should be systemically heparinized at a dose of 70 units of
heparin per kilogram and allowed to circulate for 3 to 5 minutes. It is important to communicate
with anesthesia prior to clamping and unclamping so they may anticipate and address subsequent
hemodynamic shifts. Generally, the systemic pressure should be dropped in preparation for the
proximal clamping. If the visceral segment is involved, bulldog clamps should be applied to the
visceral vessels prior to aortic clamping to avoid embolization. The proximal clamp is carefully
applied and secured with a shoestring around the clamp. The aortic sac is then opened with
electrocautery and heavy scissors proximally and distally. Mural debris should be carefully
removed to identify all patent lumbar arteries. Distal control can then be obtained with balloon
occlusion into each iliac with Foley catheters if external control was not previously done due to
calcific disease. All lumbar vessels with back-bleeding into the aorta should be suture ligated with
2-0 silk in a figure-of-eight fashion. In heavily calcified aortas, focal endarterectomies may be
necessary for effective ligation of each vessel.
■
Sewing of the proximal anastomoses: There are several ways to complete the anastomosis, and
choice is based on a combination of surgeon preference and tissue quality. Regardless of
technique, the posterior row of sutures should be done first. Ensure that there is adequate exposure
of the proximal aorta; this may require the use of a self-retaining retractor within the opened sac or
stay sutures on the edges of the sac. Place the graft on the patient’s chest upside down, so the
posterior aspect of the graft lies anteriorly. If the posterior row is to be done in an interrupted
fashion, the first mattress suture is placed in the middle of the graft from outside to in, placing a
snap on the needled ends of the sutures. Place four more mattresses, two on each side, working
your way to the 3 o’clock and 9 o’clock positions on the graft. Care must be taken to ensure there
are no gaps between sutures; all travel must be within a mattressed stitch and not between stitches.
Once all sutures are placed in the graft, begin placing the aortic sutures from inside to outside on
the aorta. The proximal aorta is usually not completely transected and the posterior wall can be
used to create a Creech bite that uses the aortic wall as a pledget. Once all sutures are placed, each
individual stitch is pledgeted and tied down snugly. The anterior row is then completed, starting
from each side and working your way to the center, such that the anterior-most stitch is the final
stitch placed. These are also pledgeted and tied into place. Once the proximal anastomosis is
completed, an atraumatic clamp should be applied to the body of the graft, and the proximal aortic
clamp slowly released to test for integrity of the repair. Any leaks in the suture line should be
addressed at this time, particularly along the posterior row, as this will be inaccessible once the
distal anastomosis is in place. It is unwise to attempt to place stitches on a fully perfused aorta,
and the proximal clamp should be reapplied if repair stitches are necessary. In addition, pledgets
should be used with these stitches. A running anastomosis can also be performed with a 3-0
Prolene and an atraumatic needle. The back row is again began in the middle of the graft with deep
Creech bites on the aorta. The graft can be parachuted in to make the suture line taut. The back row
should be inspected to ensure that it is snug and additional sutures are used at the 3 o’clock and 9
o’clock positions to secure the back row and run to the top of the aorta (FIGS 13 and 14).
■
IMA implantation: Although the IMA can generally be ligated without clinical consequence, there
are certain situations where it may be beneficial to reimplant the vessel to avoid bowel ischemic
complications. Patients with altered pelvic blood flow, such as those with prior gastrointestinal
surgery or occluded hypogastric arteries, should especially be considered for IMA reimplantation.
Furthermore, visual inspection of the sigmoid colon prior to closure should be done, and IMA
reimplantation done if there appears to be questionable viability of the bowel. Additionally, prior
to IMA ligation, an assessment of back-bleeding (and thus the collateral circulation to the IMA
territory) should be performed and reimplantation considered in cases where the back-bleeding is
poor.
■
Creating the distal anastomosis: After the proximal anastomosis is completed and hemostasis is
ensured, the graft should be pulled taut to the location of the distal anastomosis (or anastomoses if
a bifurcated graft is to be used). The graft should be measured to ensure no redundancy or kinking
occurs but not so tight as to put undue strain on the proximal anstomosis. The distal can be done in
a running or interrupted fashion, as described previously. When sewing, the assistant should use a
forceps to pull the graft distally and remove tension on the anastomosis, decreasing the chance the
sutures will be too loose.
■
Flushing and unclamping: Just prior to the completion of the distal anastomosis, the graft will need
to be flushed proximally and distally to remove clot, air, and debris. After flushing, irrigate the
graft with heparinized saline and complete the anastomosis. Once both anastomoses are completed,
communicate with the anesthesiologist that the clamps are ready to be removed. There is often a
substantial drop in systemic blood pressure as the lower extremities are reperfused, and they will
need to prepare to react accordingly. It is more appropriate to tolerate a slightly longer clamp time
and allow the anesthesiologist to regulate the blood pressure accordingly then unclamp a
hypotensive patient. As the surgeon slowly unclamps, the assistant can hold manual pressure at the
level of the femoral arteries to allow any debris to flush into the pelvis, which may tolerate
embolization better due to the extensive collateral network. Pressure is then released on the
femoral vessels and systemic pressure is monitored. If there is a substantial hypotensive response,
partial or complete reclamping may need to be performed to allow the anesthesia team time to treat
the hemodynamics. Once unclamped, inspect the anastomosis and sac for bleeding. There may be
new lumbar bleeding as a result of pelvic reperfusion that was not apparent during the graft
placement. Diffuse oozing can be treated with Surgicel and Gelfoam. Once unclamped, check
pulses and Doppler signals in iliacs and any clamped branch vessels, as well as distal pulses
and/or PVRs. If lower extremity PVRs are significantly worse than preoperatively, this should
raise concern for embolization and may warrant a groin exploration and thrombectomy.
■
Sac closure: This is especially important during the transperitoneal approach, as an uncommon but
disastrous late complication from open aortic surgery is the aortoenteric fistula, which occurs
when graft and/or anastomosis erodes into the bowel. To help prevent this, the walls of the now
decompressed aortic sac should be closed over the graft, and sewed in a running fashion with a
long 3-0 silk or chromic suture. If there is insufficient sac to close, a flap of omentum can be
mobilized and placed over the graft prior to returning the visceral to its anatomic location. The sac
of the aorta can be a not insignificant source of bleeding, so electrocautery should be used along
the cut edge of the sac to ensure hemostasis prior to sac closure, and persistent bleeding should be
suture ligated.
■
Drainage and closure: If the pleural cavity was entered, drainage will be required either by use of a
red rubber suction catheter placement during diaphragmatic repair or postoperative chest tube
placement. Additional placement of a closed suction Jackson-Pratt (JP) or Blake drain in the
peritoneal or retroperitoneal (RP) cavity can be done on a selective basis; we generally place a
drain if there is some concern over excessive mobilization near the tail of the pancreas and thought
a pancreatic leak may occur, or in coagulopathic patients where ongoing bleeding may be of
concern. Special attention should be paid to inspecting the spleen, and we have a low threshold for
splenectomy if there is any injury to the organ. The abdominal wall should then be closed in layers.
PEARLS AND PITFALLS

■ Ideally, proximal clamp time should be less than 30 minutes. It is therefore imperative to have all
tools and grafts ready and all team members briefed on the operative plan prior to clamping.
However, for an infrarenal clamp, the operator will have several hours if necessary to complete
the anastomosis. If the clamp is suprarenal, complications begin with more than 40 minutes of
ischemia.
■ Injury to the common iliac vein or distal IVC during dissection is a potentially lethal
complication. It is important to completely mobilize the vein and perform a primary repair under
direct vision. Blind suturing in a bleeding field will only lead to disaster. If exposure cannot be
obtained, it is acceptable to transect the overlying artery (aorta or iliac) to allow access to the
vein. This is a complication that is much better to avoid than treat.
■ The ureters can be injured during the transperitoneal or retroperitoneal approach, and every time
the retractors are repositioned or as you begin to dissect a new plane, the ureters should be
identified.
POSTOPERATIVE CARE
■
Patients should be monitored in an intensive care unit (ICU) postoperatively, with blood pressure
goals generally of a systolic blood pressure from 100 to 140 mmHg for a straightforward
infrarenal or juxtarenal repair. Blood pressure goals should be higher for thoracoabdominal
repairs to promote spinal cord perfusion.
■
Patient may be weaned to extubated as soon as possible after the operation, even in the OR if
appropriate.
■
An NGT is kept in place given the bowel manipulation, and this is left in place for the first
postoperative day. Although it is not imperative to keep in place until there is full return of bowel
function, we will keep in place an additional day if outputs are unusually high. We generally start
standing rectal suppositories on the first postoperative day.
■
If there is a chest tube in place, we leave this to suction until removal, which is done when output is
less than 150 mL per 24 hours and the chest x-ray (CXR) shows no large effusion.
■
Mobilization should be done as soon postoperatively as possible. These patients will require
physical therapy and many will ultimately require inpatient rehab.
OUTCOMES
■
Mortality for an elective, open infrarenal AAA repair is less than 5%, and although the risk
increases for those with a juxtarenal or suprarenal repair, our recent experience shows that 30-day
mortality in patients with juxtarenal repair is 2.5%. Mortality increases in the instance of an urgent
or rupture to as high as 70%.1,5
■
Patient-specific predictors of postoperative complications include older age, COPD, chronic renal
disease (creatinine >1.8) or history of myocardial infarction (MI)/congestive heart failure (CHF).1
■
Operative-specific predictors of postoperative complications include long OR or clamp times,
hypothermia, high blood turnover, and a high perioperative fluid requirement.
COMPLICATIONS
■
Bleeding
■
Infection
■
Splenic injury (consider adding splenectomy to operative consent)
■
Renal failure
■
MI
■
CVA
■
Spinal cord ischemia (increased risk with suprarenal and thoracoabdominal repairs)
■
Anastomotic breakdown
■
Aortoenteric fistula
■
Pancreatitis
REFERENCES
1. Brewster DC, Cronenwett JL, Hallett JW Jr, et al. Guidelines for the treatment of abdominal aortic aneurysms. Report of a
subcommittee of the Joint Council of the American Association for Vascular Surgery and Society for Vascular Surgery. J Vasc
Surg. 2003;37:1106–1117.
2. Cronenwett JL, Sargent SK, Wall MH, et al. Variables that affect the expansion rate and outcome of small abdominal aortic
aneurysms. J Vasc Surg. 1990;11(2):260–269.
3. Darling RC III, Brewster DC, Darling RC, et al. Are familial abdominal aortic aneurysms different? J Vasc Surg. 1989;10(1):39–
43.
4. Strachan DP. Predictors of death from aortic aneurysm among middle-aged men: the Whitehall study. Br J Surg. 1991;78(4):401–
404.
5. Tsai S, Conrad MF, Patel VI, et al. Durability of open repair of juxtarenal abdominal aortic aneurysms. J Vasc Surg. 2012;56(1):2–
7.
6. McFalls EO, Ward HB, Moritz TE, et al. Clinical factors associated with long-term mortality following vascular surgery: outcomes
from the Coronary Artery Revascularization Prophylaxis (CARP) Trial. J Vasc Surg. 2007;46(4):694–700.
7. 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.
8. Dawson I, Sie RB, van Bockel JH. Atherosclerotic popliteal aneurysm. Br J Surg. 1997;84(3):293.
9. Johnston KW, Rutherford RB, Tilson MD, et al. Suggested standards for reporting on arterial aneurysms. Subcommittee on
Reporting Standards for Arterial Aneurysms, Ad Hoc Committee on Reporting Standards, Society for Vascular Surgery and North
American Chapter, International Society for Cardiovascular Surgery. J Vasc Surg. 1991;13(3):452–458.
10. Lederle FA, Johnson GR, Wilson SE, et al. The aneurysm detection and management study screening program: validation cohort
and final results. Aneurysm Detection and Management Veterans Affairs Cooperative Study Investigators. Arch Intern Med.
2000;160:1425–1430.
11. Lederle FA, Wilson SE, Johnson GR, et al. Immediate repair compared with surveillance of small abdominal aortic aneurysms. N
Engl J Med. 2002;346(19):1437–1444.
Advanced Aortic Aneurysm Management:
Endovascular Aneurysm Repair—Standard and
Chapter 23 Emergency Management
Vinit N. Varu Ronald L. Dalman
DEFINITION
■
An abdominal aortic aneurysm (AAA) is defined as a localized enlargement of more than 1.5 times
the diameter of the most adjacent, proximal uninvolved aorta; by consensus, this represents more
than 3.0 cm in most persons. Definitions vary somewhat between men and women, most likely
normalized by body surface area or body mass index (BMI).
■
The most common etiology of AAAs is progressive, transmural degeneration of the aortic wall. The
full scope of pathogenetic considerations and relevant mechanisms is beyond the scope of this
chapter but, in summary, although aneurysm disease shares many important risk factors for aortic
and peripheral vascular occlusive disease, important differences exist, and current thinking
regarding pathogenesis recognizes that aneurysmal and occlusive disease of the aorta are distinct
pathologic processes. Hence, the colloquial term “atherosclerotic aneurysm,” although in common
use, is an inaccurate and potentially misleading characterization of the most common clinical
presentation for AAA.
■
Risk factors for development, expansion, and rupture are multifactorial1 (Table 1). Smoking is the
only modifiable risk factor that has been associated with all three.
■
The risk of AAA rupture increases with progressive diameter enlargement.2 Rupture and subsequent
aneurysm-related mortality may be prevented by elective surgical repair, either by open
interposition grafting or endovascular aneurysm repair (EVAR).
■
EVAR provides similar long-term survival versus traditional open repair, as well as enhanced
perioperative survival. The perioperative survival benefit is sustained for several years following
surgery.3 EVAR is now the de facto standard of care for both elective and ruptured AAA repair in
patients who are anatomically suited to receive currently available devices.

■
Patients may be entirely asymptomatic despite suffering from large, advanced AAAs. Most
commonly, AAAs are found incidentally on imaging studies obtained for other reasons.
Occasionally, they may be identified by the presence of prominent aortic pulse, proximal to the
umbilicus, on physical exam. Less frequently, AAAs may cause distal limb ischemia secondary to
embolization, or fulminate congestive heart failure if they rupture into the adjacent inferior vena
cava, creating an acute aortocaval fistula. Only 30% to 40% are noted on physical examination,
with detection of pulsatile abdominal mass dependent on aneurysm size. As noted by Sir William
Osler, prior to the era of ubiquitous availability and use of cross-sectional abdominal imaging in
the evaluation of abdominal pain: “There is no disease more conducive to clinical humility than
aneurysm of the abdominal aorta.”
■
Patients with a ruptured AAA may present with moderate or extreme back and abdominal pain,
syncope, hypotension, and mottling of the lower extremities, in conjunction with progressive
abdominal distension. When sufficiently stable to remain conscious and conversant, pain is
reproducibly elicited by direct palpation of the abdominal aorta. Many patients with ruptured
AAA present in extremis, others with progressively hemodynamic deterioration and pain of
several hours duration. Patients may actually linger for several days with “contained”
retroperitoneal hemorrhage following AAA rupture.
■
A thorough vascular history should be noted and modifiable risk factors, including smoking,
hyperlipidemia, and hypertension, addressed in patients with AAAs. Smoking cessation is
recommended to reduce the risk of aneurysm growth and rupture, and statins may also be
beneficial in this regard.
■
AAAs occur almost exclusively in the elderly (mean age of repair 72 years of age) and male
patients outnumber female by 4 to 6 is to 1.1 When AAA is recognized in younger patients, it is
usually in association with hereditary risk, syndromic aortic conditions such as Marfan syndrome,
or in the setting of focal aortitis or mycotic aneurysms. The latter tend to occur most frequently in
the suprarenal abdominal aorta, at or directly proximal to the origin of the celiac artery,
underneath the crus of the diaphragm. Aneurysmal degeneration of the abdominal aorta may also
occur late following thoracic and abdominal aortic dissection.
■
Factors associated with increased risk of rupture include female gender, large initial diameter, low
forced expiratory volume in 1 second (FEV1), current smoking history, and elevated mean blood
pressure.

■
Screening decreases aneurysm-related mortality in AAA disease.4 Current guidelines recommend a
screening ultrasound for 65- to 75-year-old at-risk individuals, defined as men who have smoked
more than 100 cigarettes in their lifetime or men or women with a family history of AAAs.5
■
Thin-slice computed tomography (CT) imaging, with intravenous contrast injection timed to opacify
the abdominal aorta and runoff vessels, remains the standard modality for operative planning. The
extent, morphology, and accessibility of the aneurysm via retrograde iliofemoral access determine
the suitability for an endovascular repair. Other relevant anatomic considerations include the
location and volume of laminar intraluminal thrombus in the region of the “surgical” neck (defined
as the length between the lowest renal artery and the start of the aneurysm); angulation of the
surgical neck, size and tortuosity of access vessels; presence and significance of anomalous and
accessory renal arteries; diameter at the aortic bifurcation; and diameter of the more proximal
abdominal aorta (provides useful guidance as to the likely long-term diameter of the surgical
neck).
■
For cases of suspected AAA rupture, bedside transcutaneous ultrasonography may be used to detect
the presence of intra- or retroperitoneal fluid (or blood) or assess for confounding conditions
eliciting abdominal pain. When sufficiently hemodynamically stable, however, CT aortography
should be obtained to assess for suitability for endovascular repair.6
SURGICAL MANAGEMENT
Indications
■
Patients with “symptomatic” AAAs (e.g., pain likely originating from the aneurysm despite absence
of retroperitoneal hemorrhage on CT aortography) are at increased risk of rupture and urgent
intervention is recommended. Of those AAAs that rupture, more than half will die prior to
hospitalization. Of those that undergo attempted operative repair, approximately 50% mortality is
to be expected. The latter estimate is highly dependent on hemodynamic conditions, duration of
symptoms, and comorbid conditions present at the time of surgery and is not useful in predicting
survival of individual patients.1
■
For asymptomatic AAAs, management is determined by the maximal orthogonal transverse diameter
at the time of evaluation or rate of aneurysm enlargement over time. AAAs less than 4.0 cm are at
low risk of rupture and should be monitored with serial imaging; those larger than 5.4 cm are at
high risk of rupture and should be repaired. Surveillance is recommended for most patients in the
range of 4.0 to 5.4 cm, although young healthy patients and especially women may benefit from
repair in AAAs between 5.0 and 5.4 cm.1
■
Anatomic measurement obtained from high-quality CT aortography, preferably reconstructed with
millimeter or submillimeter slices, is paramount to successful endovascular repair. Ideally,
precise diameter and path length measurements are derived from three-dimensional (3-D)
reconstruction of the two-dimensional (2-D) source images (via TeraRecon™, OsiriX™, or
similar software).
■
Precision is most essential in determining diameter throughout the surgical neck and common iliac
landing zones proximal to the bilateral iliac bifurcations. Graft oversizing of 10% to 20% is
typically used in the region of the surgical neck. Length measurements are obtained from the lowest
renal artery to the iliac bifurcation, using path lengths, when available, from image reconstruction
software noted earlier.
■
Multiple aortic endografts are approved for use in the United States at the current time, and device
selection should be tailored to individualized anatomic requirements. Contraindications to
endovascular repair may include inadequate neck length, diameter, and angulation; thrombus
volume and distribution in the neck; insufficient iliac artery diameter, and excessive iliac or aortic
tortuosity. It is the responsibility of the operating surgeon to ensure that for each selected device,
the instructions for use (IFU) are understood and appropriate for the planned repair. Experienced
operators, with careful planning, may knowingly place devices in off-label circumstances,
depending on the patient-specific anatomic and physiologic risk assessment, with the expectation
of reasonably long-term results. In off-label applications, however, the onus is on the surgeon to
confirm that sufficient proximal and distal fixation and sealing zones exist to ensure a reasonable
result.7
■
Femoral access must also be evaluated with ultrasound or CT imaging to determine if the patient is a
candidate for percutaneous repair. The “preclose” technique (see the following text) can be used
for arteriotomy closure for devices up to 21 French (Fr) in diameter. Contraindications to
percutaneous repair include calcification of the anterior femoral artery wall, diameter less than 7
mm, the presence of an aneurysmal femoral artery, and excessive scaring at the access site.
■
The superior mesenteric artery (SMA) and celiac arteries should be examined for patency and the
presence of flow-limiting stenosis or occlusion; if found, revascularization of the SMA and celiac
artery should be considered prior to attempted EVAR, or open repair is considered as an
alternative approach. In planning for EVAR, attention must be paid to the status of the inferior
mesenteric artery and the total visceral vascularity assessed in terms of consequences of obligate
inferior mesenteric artery (IMA) coverage during EVAR. Occasionally, depending on anatomic
circumstances, custom fenestration or parallel grafting options may be considered as alternatives,
allowing for EVAR management despite the presence of significant celiac or SMA disease. The
latter options again, however, should only be considered by operators experienced in these
techniques or facile with rapid open conversion when indicated to preserve intestinal perfusion.
■
Facilities are an essential consideration. Fixed imaging is the preferred option for procedural
guidance and aortography, preferably when available in a “hybrid” operating room configuration.
This is especially true when tolerances are low regarding IFU status and related anatomic
considerations. Anesthesia can be either general or local with conscious sedation, depending on
the habitus of the patient, their suitability for conscious sedation, and the potential likelihood of
open conversion. In our practice, all patients are consented for open conversion, even though in
practice this happens in less than 1% of cases.
TECHNIQUES
ENDOVASCULAR ANEURYSM REPAIR STANDARD

Percutaneous Access
■
Using ultrasound guidance to determine the location of the femoral bifurcation and potential
presence of anterior calcified atherosclerotic plaque, bilateral common femoral arteries (CFAs)
are accessed with 0.018-in micropuncture kits. Femoral arteriography is performed to confirm
suitability of the selected access site within the CFA prior to serial dilation.
■
A 0.035-in general purpose wire (e.g., Bentson, Cook Medical, Bloomington, IN) is advanced into
the aorta through the micropuncture sheath and 11-cm, 7-Fr sheaths are exchanged over the Bentson
into the external iliac arteries (EIA) under continuous fluoroscopic guidance. Full intravenous
anticoagulation is established with unfractionated heparin (at least 100 units/kg) and confirmed by
subsequent determination of activated clotting time (ACT) greater than 250 seconds.
Preclose Technique
■
In all circumstances, the surgeon should consult the respective IFUs for all devices employed during
these procedures.
■
While the assistant maintains direct compression proximal to the inguinal ligament to maintain
hemostasis, the 7-Fr sheaths are individually removed over each respective wire and replaced
with a Perclose ProGlide™ (Abbott, Abbott Park, IL) device. This is back-loaded on the wire and
advanced until the guidewire exit line on the device. The wire is then temporarily removed and the
device advanced until pulsatile blood is visualized through the pilot tube lumen. The first device is
turned to the 10 o’clock position and foot plate activated. Holding back tension on the device, the
suture is deployed, and the ends are removed from the device and controlled with a padded suture
clamp. After the wire is repositioned through the wire port into the aorta under fluoroscopic
guidance, the foot plate is released and the device is backed out of the femoral artery. Pressure is
reapplied over the puncture site during this maneuver (FIG 1).
■
A second Perclose ProGlide™ (Abbott) device is back-loaded on the wire and the aforementioned
steps are repeated with the device turned to the 2 o’clock position.
■
After both ProGlides™ (Abbott) are deployed, the 7-Fr sheath is reformed and replaced over the
wire to maintain hemostasis. The suture clamps are positioned consistent with the clockface
orientation of each suture placement.
■
The procedure is then repeated for the contralateral femoral access site.
Delivery and Deployment of Endograft
■
Wire exchange is performed through a guiding catheter (e.g., 100-cm Glidecath™, Terumo Medical,
Somerset, NJ) for a stiffer access wire (e.g., Lunderquist™, Cook Medical). Serial dilation is
preformed over the stiff wire, under fluoroscopic guidance, to gently distend and enlarge the
respective arteriotomy sites. Following dilation to at least 14 Fr, the primary and secondary access
sheaths are advanced under fluoroscopic guidance into the aorta.
■
The main body endograft is placed up the ipsilateral iliac artery to the level of the renal arteries.
Laterality of main body deployment is determined based on the tortuosity and diameter of the
access arteries, as well as the desired angle at which the main body will interface with the renal
arteries. The main body should be oriented so that the gate deploys in anterolateral fashion for easy
contralateral limb access. The image intensifier should be adjusted to limit parallax by accounting
for some degree of anterior angulation (usually in the range of 10%, occasionally more) and lateral
angulation in the surgical neck, based on preprocedural assessment from the reformatted CT
aortogram (FIG 2A).
■
An Omni Flush catheter (AngioDynamics, Latham, NY) is placed up the contralateral iliac artery to
the level of the renal arteries. The gantry position is then confirmed to be appropriate for the
patient’s anatomy, ensuring that the image plane is orthogonal to the takeoff of the lowest renal
artery. Usually, a “20 for 10” contrast run is performed during breath-hold under magnification
views, delivering 10 mL of contrast at a rate of 20 mL per second, to confirm the device position
vis-a-vis the renal artery origins.
■
The main body endograft is then deployed according to the IFU, with the proximal fabric margin
positioned just below the lowest renal artery. Deployment continues until the contralateral gate is
fully open (although techniques may vary between devices). Depending on the device-specific IFU,
the main body may be resheathed and repositioned, if necessary, to obtain optimal positioning
(FIG 2B).
■
Repeat aortography is performed to ensure adequate placement. The side-hole, aortic flush catheter
is withdrawn into the aneurysm through the proximal landing zone, over a wire. If the device uses
suprarenal stent fixation, the suprarenal stents are deployed when main body placement is deemed
sufficient. Care should be taken to prevent pulling the main body of the endograft down into the
aneurysm.
Gate Cannulation
■
The contralateral sheath is placed 1 to 2 cm distal to the contralateral gate. Using an Omniflush™
(Angiodynamics) or Glide™ catheter (Terumo), the gate is cannulated with an angled Glidewire™
(Terumo). When successful, the Omniflush catheter should be exchanged over a wire and
reintroduced into the endograft. The tip is allowed to reform by withdrawing the wire and the
curled flush catheter is spun 360 degrees several times to confirm gate cannulation. Failure to
confirm this step may result in deployment of the contralateral limb outside of the gate, likely
generating “endotrash” (e.g., graft limb free in the aneurysm, outside the main body, which will not
remain in circulation) (FIG 2C).
■
If the contralateral gate cannot be successfully cannulated using standard guidewire and catheter
techniques (different-shaped catheters should be employed, as well as repositioning the sheath in
relation to the contralateral gate), cannulation may be accomplished by advancing a snare up the
contralateral sheath into the aneurysm and engaging the main body endograft bifurcation with a Sos
Omni or similar curved catheter. The ipsilateral wire is then advanced through the gate, to be
snared from the contralateral side. Once the wire is withdrawn through the contralateral sheath, a
catheter may be back-loaded and advanced into the main body, which in turn allows an exchange to
a stiffer wire through the gate. When necessary, a wire can also be advanced from brachial artery
access for the same purpose.
Limb Extension
■
Retrograde iliac angiography is performed through the sheath, with the gantry position in the
contralateral oblique position. This will identify the origin of the internal iliac artery. Once this is
confirmed, distance from the gate to the internal iliac is measured using a marker catheter and an
appropriately sized limb is chosen. For three-piece bifurcated devices (e.g., TriVascular
Ovation™, Cook Zenith™), this procedure has to be performed on both sides. Optimal limb
deployment maintains sufficient contact with the gate to maintain seal (see respective IFU) and
sufficient distal coverage to completely exclude the common iliac artery without impinging on the
origin of the internal iliac artery (FIG 2D).
■
Occasionally, when the distance required for proper limb placement does not precisely correlate
with the sizes available, the next size–longer limb may be deployed into the gate and slowly along
its length. During deployment (once out of the gate), continued upward pressure on the deployment
handle is maintained to encourage the graft to take a somewhat more serpiginous route, taking up
some of the additional leak. Partial coverage of the ipsilateral internal iliac artery orifice is also
appropriate when deployment can be precisely monitored in the contralateral oblique gantry
position.
Balloon Molding
■
An appropriately sized semicompliant balloon (e.g., Coda™, Cook Medical) is expanded with
dilute contrast solution at all three landing zones and overlap areas within the gate(s) as
appropriate for the specific device (FIG 3). When existing common iliac artery stenosis is present,
kissing balloons should be deployed to obtain optimal internal diameter and prevent limb kinking
or occlusion. Similarly, the aortic bifurcation should also be dilated when necessary.
Occasionally, self-expanding bare metal nitinol stents may be deployed at areas of stenosis or from
the distal limb into external iliac artery, to prevent kinking of the endograft or native external iliac
artery distal to the device.
Completion Arteriography
■
Completion arteriography is performed with higher volume and longer injection time to completely
fill the endograft, ensure limb patency, and identify endoleaks (FIG 4). All type I or III endoleaks,
when present at the end of the case, should be addressed with additional maneuvers to ensure seal.
This may include deployment of proximal endograft cuffs, prolonged molding balloon inflation
time, or, on occasion, placement of embolism coils in recalcitrant leaks. When small leaks persist,
even when anatomic coverage seems adequate, anticoagulation should be reversed and sheaths
removed with the plan for follow-up CT aortography within a few days. Care should be taken to
carefully evaluate the nature of all leaks (type, volume, location in regard to lumbar branches,
status of graft limb deployment, adequacy of molding, etc.) before secondary interventions are
considered for persistent leaks. The majority of type II endoleaks resolve in the first year. In our
practice, we never resort to deployment of a large diameter, balloon-expandable stent in the
proximal neck—accurate sizing and deployment of this stent may be difficult and “stretching” the
proximal orifice of the main body in this way may damage the graft, without sufficient assurance
that the proximal type I leak will be adequately addressed.
Closure
■
The contralateral sheath is removed over the wire and manual pressure is held. The previously
placed preclose polypropylene sutures are deployed sequentially in each access site and cinched
down with a knot pusher over a wire. When initial hemostasis appears adequate, the wire is
removed and slightly more pressure is applied to the knot pusher. After both sutures are deployed
in one groin, determination is made as to which of the two appears to provide more effective
hemostasis and manual pressure is held to this suture for 5 additional minutes. This is repeated for
the ipsilateral side.
■
Procedural anticoagulation is reversed once all sheaths and clamps are removed. It is essential to
wait for final introducer device removal before reversing the anticoagulation, because the large
diameter sheaths used to deliver EVAR devices may almost entirely occlude the ipsilateral
external iliac artery, causing potentially catastrophic graft limb and iliac artery thrombosis in the
absence of full anticoagulation.
ENDOVASCULAR ANEURYSM REPAIR FOR RUPTURED ANEURYSMS,

OR REVAR
Percutaneous Access
■
Bilateral CFA access is obtained under local anesthesia. The preclose technique (described in the
previous section) can be employed when time and conditions permit, but if not possible, the case
can proceed percutaneously initially, with conversion to open femoral closure when the endograft
is fully deployed and internal bleeding has stopped.
■
Rapid catheter and guidewire exchanges are performed, with sheath upsizing as noted in the
previous section. The use of intravenous anticoagulation is controversial in this setting—again it is
highly dependent on the hemodynamic status of the patient, presence of active bleeding, and
existing consumptive coagulopathy. Often when treating ruptured aneurysms, the case begins
without anticoagulation, which is subsequently instituted once the main body and extension limbs
are deployed.
■
In the case of rupture procedures, preoperative CT aortography may not exist or may not provide
sufficient anatomic detail to guide deployment. In this circumstance, catheter arteriography with a
marker flush catheter should be employed to determine path lengths, landing zones, and optimal
graft sizing.
Aortic Balloon Control
■
Following access and wire exchange, a Lunderquist™ (Cook Medical) or similar stiff wire is
advanced into the aorta, over which a 14-Fr × 55-cm braided sheath is advanced to the level of the
renal arteries. Once localization is confirmed, the sheath is sutured to the skin at the access site.
■
A semicompliant balloon (Coda™, Cook Medical) or similar aortic occlusion balloon is directed to
a position immediately proximal to the visceral arteries under fluoroscopic guidance (FIG 5).
Once positioned, it can be maintained in the deflated site until or unless the patient’s hemodynamic
status requires inflation and aortic occlusion.
■
Once bilateral therapeutic sheath access is obtained and the deflated occlusion balloon is positioned
properly, general anesthesia may be induced.
Endograft Delivery and Deployment
■
Aortography is performed through the contralateral sheath below the balloon to localize the origins
of the renal arteries.
■
The main body endograft is placed up the ipsilateral sheath to the level of the renal arteries. It
should be oriented so that the gate deploys in anterolateral fashion.
■
The main body endograft is then deployed according to the IFU, just distal to the lowest renal artery.
Deployment continues until the contralateral gate is fully deployed (FIG 6).
■
The ipsilateral limb of the endograft is cannulated and the sheath advanced into the main body of the
endograft.
■
A second Coda balloon is placed in the ipsilateral sheath and inflated in the main body (FIG 7). The
first balloon is deflated and removed through the contralateral sheath. Balloon placement should be
performed in such a way that time without balloon coverage is kept to an absolute minimum.
Retroperitoneal hemorrhage can continue at a rapid rate throughout this procedure, and in the
absence of external bleeding, neither the surgeons nor the anesthesiologists may appreciate true
magnitude of blood loss and circulatory reserve. Under these circumstances, hemodynamic
collapse can be precipitous and, unfortunately, calamitous, unless an occlusion balloon is properly
positioned and immediately inflated at the first indication of rapid hemodynamic deterioration.
Gate Cannulation
■
Gate cannulation proceeds in a standard fashion during REVAR.
Limb Extension
■
Limb extension proceeds in a standard fashion during REVAR. Time awareness is critical during
standard EVAR steps to ensure that aneurysm sealing is accomplished in the most expeditious
manner possible.
Balloon Molding
■
Coda™ balloon (Cook Medical) molding is performed at all seal zones to optimize hemostasis.
Only after molding is complete is hemostasis assured.
Completion Aortography
■
Completion aortography is performed as previously described. Attention should be paid to all the
usual considerations, including presence and nature of endoleaks, iliac limb or arterial kinking,
sufficient overlap in the landing zones to meet IFU, and so forth (FIG 8).
Closure
■
Closure proceeds as indicated for standard EVAR, with caveat that if ProGlides were not deployed
prior to percutaneous access, then surgical incisions will need to be made to expose the femoral
artery sites for control and closure under direct vision as the therapeutic sheaths are withdrawn.
PEARLS AND PITFALLS

Access ■ Ultrasound guidance is essential to limiting access complications.
Visualize the needle tip entering the anterior artery wall, in an
area deemed appropriate for access.
Gate cannulation ■ In general, main body should be advanced through the more
tortuous of the two iliac arteries to allow a more “straight shot”
for the contralateral gate cannulation. This preference is not
always practical, however, and laterality may need to be decided
based on more practical considerations (e.g., Is the tortuosity
sufficient to prevent main body positioning and deployment
altogether?).
Tortuous iliacs ■ Perform the completion aortogram with soft catheters instead of
stiff wires in place. Stiff wires may straighten out a tortuous
vessel, which may end up kinked when the wires are removed and
lead to limb occlusion. Also, retention of stiff wires at the time of
completion aortography may mask the development of type I
proximal endoleaks, which may develop situationally when stiff
wires are removed.
Closure ■ Tie down the sutures of the closure device with the wire in place.
If there is still significant bleeding, either deploy another closure
device or place an occlusive sheath and proceed with open
conversion of the femoral artery closure under more controlled
circumstances.
Ruptures ■ Outcomes are vastly improved when REVAR protocols are
established and practiced. Abdominal compartment syndrome is a
real and frequent complication following REVAR—if there is any
indication that ventilation pressures are rising or abdominal
pressures are significantly elevated at the end of the procedure by
measuring bladder pressure, strong consideration should be given
to decompressive laparotomy at the initial setting.
POSTOPERATIVE CARE
■
Patients should remain supine for a minimum of 3 hours and are free to ambulate thereafter. Most
elective EVARs can be discharged on postoperative day 1 or 2. For cases well within the IFU,
same-day surgery is now a reality and can safely be offered to patients who can remain in
reasonably close proximity to the hospital the evening after surgery.
■
Following REVAR, consideration should be given to decompressive laparotomy whenever
abdominal pressures are elevated at the end of the initial procedure. When decompressive
laparotomy is performed, free peritoneal blood should be evacuated but retroperitoneal
hematomas should not be explored or evacuated. Abdominal wound suction systems should be
deployed to control drainage and provide a moist environment for intestinal viability. Dressing
changes should be performed daily or every other day until the wound can be safely closed.
■
Initial postprocedural CT aortography is performed at 1 month to document presence or absence of
endoleaks and graft position and confirm visceral perfusion (FIG 9). Follow-up imaging is
performed with either ultrasound +/− noncontrast CT scanning or by CT aortography, based on the
last known status of endoleaks (presence or absence), symptomatic status, and comorbid
conditions such as chronic renal insufficiency. In general, we prefer serial ultrasound evaluations,
with CT scanning reserved for aneurysms which are enlarging following endografting or evidence
of significant changes in endoleak volume or location.
OUTCOMES
■
All-cause mortality is similar in patients undergoing open or EVAR for AAA at 2 years.3,8,9
■
There is higher perioperative survival in patients undergoing EVAR, which is sustained for several
years.3 The loss of this is due to late ruptures in the EVAR group.
■
Secondary interventions are similar in open and EVAR.3
COMPLICATIONS
■
Endoleak
■
Delayed rupture
■
Renal dysfunction
■
Thromboembolism
■
Limb occlusion
■
Colon ischemia
■
Abdominal compartment syndrome (ruptured EVAR)
REFERENCES
1. Chaikof EL, Brewster DC, Dalman RL, et al. The care of patients with an abdominal aortic aneurysm: the Society for Vascular
Surgery practice guidelines: executive summary. J Vasc Surg. 2009;50(4):880–896.
2. Lederle FA, Johnson GR, Wilson SE, et al. Rupture rate of large abdominal aortic aneurysms in patients refusing or unfit for elective
repair. JAMA. 2002;287(22):2968–2272.
3. Lederle FA, Freischlag JA, Kyriakides TC, et al. Long-term comparison of endovascular and open repair of abdominal aortic
aneurysm. N Engl J Med. 2012;367(21):188–197.
4. Lindholt JS, Norman PE. Meta-analysis of postoperative mortality after elective repair of abdominal aortic aneurysms detected by
screening. Br J Surg. 2011;98(5):619–622.
5. Guirguis-Blake JM, Beil TL. Ultrasonography screening for abdominal aortic aneurysms: a systematic evidence review for the U.S.
Preventive Services Task Force. Ann Intern Med. 2014;160(5):321–329.
6. Mehta M. Endovascular aneurysm repair for the ruptured abdominal aortic aneurysm: the Albany Vascular Group approach. J Vasc
Surg. 2010;52(6):1706–1712.
7. Lee JT, Ullery BW, Zarins CK, et al. EVAR deployment in anatomically challenging necks outside the IFU. Eur J Vasc Endovasc
Surg. 2013;46(1):65–73.
8. De Bruin JL, Baas AF, Buth J, et al. Long-term outcome of open or endovascular repair of abdominal aortic aneurysm. N Engl J
Med. 2010;362:1881–1889.
9. Greenhalgh M, Allison DJ, Bell PRF, et al. Endovascular versus open repair of abdominal aortic aneurysm. The United Kingdom
EVAR Trial Investigators. N Engl J Med. 2010;362:1863–1871.
Advanced Aneurysm Management Techniques:
Chapter 24 Management of Internal Iliac Aneurysm Disease
W. Anthony Lee
DEFINITION
■
Iliac aneurysm is defined as an iliac artery whose diameter is 20 mm or more. Iliac aneurysms are
present in up to 20% of abdominal aortic aneurysms,1 and common iliac aneurysms occur far more
frequently than internal iliac aneurysms.
■
Isolated iliac aneurysms represent less than 5% of all aortoiliac aneurysms.
■
External iliac aneurysms are extremely rare and mostly either associated with underlying connective
tissue disorders or represent traumatic pseudoaneurysms.
■
Differential diagnoses of iliac aneurysm are limited to true degenerative aneurysms, which are most
common; mycotic, traumatic, or surgical pseudoaneurysms; or aneurysmal enlargement of the false
lumen from a primary dissection.

■
Most iliac aneurysms are clinically silent (asymptomatic). Rarely, in very thin individuals with
large aneurysms, a pulsatile aneurysm may be palpable on physical examination. Even more
rarely, a patient being evaluated for hydroureter may be determined to have an iliac aneurysm.
Ureteral obstruction in this circumstance derives from perianeurysmal inflammation (similar to
retroperitoneal fibrosis) rather than mechanical compression by the aneurysm.

■
Although a plain abdominal x-ray can detect an aortoiliac aneurysm if there is heavy mural
calcification, the most common imaging modalities include ultrasound, computed tomography
(CT), and magnetic resonance imaging (MRI).
■
Thin-cut (1 mm), intravenous contrast-enhanced, spiral CT (CT arteriogram) represents the “gold
standard” for diagnosis and anatomic evaluation of abdominal aneurysms. Even in patients with
stage III/IV chronic kidney disease, high-quality imaging may be obtained relatively safely using
reduced volumes of isoosmolar, nonionic contrast with multidetector (32, 64, 128, or 220)
scanners, particularly following preprocedural intravenous hydration. The CT dataset is rendered
into three-dimensional (3-D) images for dimensional postprocessing, a critical requirement for
complex endovascular case planning.
■
Conventional arteriography adds little to the identification and analysis of iliac aneurysms;
penetrating ulcers may appear like saccular aneurysms, and large aneurysms with circumferential
mural thrombus may appear to have a normal contour.
SURGICAL MANAGEMENT
■
In general, iliac aneurysms are repaired when they reach 30 mm in diameter, become symptomatic,
or rupture.
■
Due to the relatively inaccessible location of iliac aneurysms, situated deep in the pelvis, as well as
densely adherent pelvic veins posterior to the arteries and frequent co-occurrence of calcific
occlusive disease, conventional surgical repair is challenging and fraught with risk of significant
hemorrhage. Thus, evolving endovascular methods of repair have largely supplanted open surgical
reconstruction.
■
A variety of off-label devices and hybrid techniques have been applied to iliac aneurysm
management. The variability derives, in large part, from uncertainty regarding the need to preserve
antegrade internal iliac artery flow in most patients. Indications for internal iliac preservation
remain controversial due to the added complexity, cost, and uncertain benefit derived from such
procedures; analysis of the relative merits of intentional unilateral occlusion versus preservation
in the management of iliac aneurysm disease is beyond the scope of this chapter.
■
As in all things endovascular, high-quality imaging is critical for precase planning and, as
previously mentioned, CT arteriography is optimal for this purpose. Using a combination of axial
imaging and 3-D postprocessing, complete evaluation should, note the following:
■
Locations, diameter, and length of proximal and distal landing zones
■
Iliac artery tortuosity and angulation
■
Presence and severity of associated occlusive disease
■
Ipsilateral and contralateral internal iliac artery patency
■
Status of the ipsilateral deep femoral artery
■
Concomitant abdominal or thoracic aortic pathology
■
In general, landing zones are sited in nonaneurysmal arterial segments, manifesting minimal
occlusive disease, with relative absence of angulation or tortuosity. The allowable diameter range
for treatment may vary, depending on the particular device to be deployed. In all circumstances,
reference should be made to the “Instructions for Use” included in the package insert.
■
Device selection is based on the need for durable aneurysm exclusion and endograft fixation,
accomplished with the fewest component pieces possible.
■
This chapter focuses on endovascular and hybrid management strategies for the iliac bifurcation in
the context of large common or internal iliac aneurysms. Standard techniques suffice for
management of smaller (<24 mm) aneurysms that do not involve the bifurcation, either in isolation
or associated with larger proximal aortic aneurysms.
Positioning
■
Nearly all endovascular aortoiliac aneurysm repairs are performed with the patient in the supine
position, with both arms tucked. The operative team stands on the patient’s right, with the C-arm
brought in from the left. Although some operators prefer to access the left groin from the left side
of the table, for a right-handed operator, it is ergonomically more natural to access both groins
from the right.
■
Electrocardiogram (EKG) leads and other monitoring cables and lines are positioned so that they
are not in the x-ray beam and do not entangle the C-arm gantry.
■
The left arm should be available for brachial artery access when necessary; it is not routinely
prepped into the surgical field.
TECHNIQUES
TECHNIQUES
ENDOVASCULAR COMMON ILIAC ARTERY ANEURYSM REPAIR WITH

INTERNAL ILIAC ARTERY OCCLUSION
■
After obtaining bilateral femoral access, a shepherd’s hook–type (e.g., Omni™ Flush) side-hole
catheter is advanced from the contralateral side for pelvic arteriography. Typical injection
technique is 10 to 15 mL contrast at 15 mL per second. Following satisfactory anatomic
delineation, a steerable hydrophilic 0.035 guidewire (e.g., angled Glidewire®, Terumo) is
advanced through the same catheter into the ipsilateral external iliac artery. Following exchange
for a stiffer guidewire (e.g., Rosen®), the flush catheter and contralateral femoral sheath are
removed and replaced with a 45-cm 6-French (Fr) guide sheath (e.g., Balkan® or similar braided
sheath), positioning the tip in the distal third of the common iliac aneurysm (FIG 1).
■
A 65-cm 4-Fr angled catheter (e.g., Kumpe®) is advanced through the sheath and, under digital
subtraction roadmapping guidance, directs the hydrophilic guidewire into the ipsilateral internal
iliac artery (FIG 2). The catheter is then advanced securely into either the anterior or posterior
divisions. The C-arm gantry is positioned at approximately 30 degrees contralateral anterior-
oblique for optimal visualization during this maneuver. With access secured, the 6-Fr sheath is
then advanced over the 4-Fr catheter into the proximal internal iliac artery.
■
A selective internal iliac arteriogram is obtained through the 6-Fr sheath, and the angle catheter is
retracted to the first bifurcation of the internal iliac artery. Typically, distal access is maintained
with the wire during this maneuver.
■
[Alternate technique] Depending on anatomic considerations (e.g., tortuosity, iliac bifurcation angle,
internal iliac branch anatomy, etc.), ipsilateral access may be feasible. In this case, a 25-cm, 6-Fr
sheath is advanced from the ipsilateral femoral artery. A 4- or 5-Fr appropriately shaped catheter
(curve or reverse curve) directs the hydrophilic guidewire into the internal iliac artery (FIG 3). If
a shepherd’s hook catheter type is employed, the hook may be reformed either in the iliac aneurysm
or in the aorta, depending on their respective luminal diameters. The ipsilateral approach is more
demanding technically and is not recommended when concomitant internal iliac aneurysm
embolization is also indicated.
■
Size-appropriate platinum occlusion coils are deployed through the 4-Fr catheter into the main
internal iliac artery trunk, with care taken to avoid placement or distal migration into arborizing
branches or reflux back into the main iliac circulation. Alternative vascular occlusion devices may
also be used for internal iliac embolization, including hydrogel coils and nitinol mesh (e.g.,
Amplatzer®) plugs. Interval arteriograms are obtained using small volume hand injections through
the sheath or catheter to guide deployment and confirm positioning. Complete occlusion of the
target artery during deployment is not necessary or even desirable. Following subsequent endograft
deployment over the internal iliac artery orifice, in the absence of antegrade flow, the extensive
surface area of the coils induces rapid thrombosis following reversal of anticoagulation at the end
of the procedure. Usually less than five coils will suffice to ultimately induce complete occlusion.
■
[Alternate technique] The presence of an internal iliac aneurysm, either with or without an
associated proximal common iliac aneurysm, deserves special consideration. In these situations,
more extensive embolization of the internal iliac circulation will be necessary to prevent
retrograde (type II) endoleak. Individual internal iliac branches must be separately embolized at
the initial procedure (FIG 4). If left untreated, due to collateral pelvic flow, these branches
unfortunately remain patent following endograft deployment, severely limiting options for
secondary procedures. Complete branch vessel embolization can be time consuming and tedious,
due to the sheer number, anatomy and sizes of the branches that must be occluded, requiring
patience, expert catheter and guidewire skills, and excellent intraoperative imaging.
■
[Alternate technique] When the common iliac aneurysm tapers to a funnel near the iliac bifurcation,
the so-called sleeve technique may be employed to occlude the adjacent internal iliac artery. In
this method an appropriately sized aortic cuff is deployed into the distal common iliac artery and
over the internal iliac artery origin. The distal end of this cuff is partially extended into the external
iliac artery. The iliac limb is next passed through the aortic cuff and deployed normally from its
proximal landing zone and into the external iliac artery 20 mm distal to the aortic cuff (FIG 5). The
putative benefit of this technique is avoidance of potential atheroembolization that may occur
during standard coil occlusion techniques from catheter manipulation, which some speculate is the
cause of ischemic complications following internal iliac artery occlusion.
■
Following internal iliac occlusion, subsequent aneurysm exclusion procedures vary as functions of
landing zone and aneurysm anatomy. Endograft deployment nearly always follows management of
the internal iliac artery in some form or another. In the typical scenario, following internal iliac
embolization, the endograft positioning and deployment proceeds in the standard fashion except for
extension of the ipsilateral distal landing zone beyond the iliac bifurcation to the external iliac
artery. At least 20 mm of purchase into the external iliac artery is recommended.
■
In the unusual case of an isolated common iliac aneurysm without aortic involvement, with a
proximal uninvolved segment at least 20 mm in diameter and 15 mm in length, a short endograft
may be deployed to bridge the proximal common and external iliac arteries.2 Device options for
this approach include either the “off-label” deployment of an aortouniiliac converter graft or
placement of a flared or “bell bottom” iliac endograft limb that has been previously deployed,
reversed, and reloaded into the delivery sheath at the back table (way off-label). These adaptations
are often necessary because although nonaneurysmal, the common iliac artery is still too large to
securely seat the proximal end of most iliac limbs. To obtain a satisfactory proximal seal, the
distal flared segment, commonly available in diameters up to 24 mm, is deployed proximally by
simply reversing the limb in the sheath (FIG 6).
ENDOVASCULAR COMMON ILIAC ARTERY ANEURYSM REPAIR WITH
INTERNAL ILIAC PRESERVATION
■
These techniques specifically pertain to common iliac aneurysms without an associated ipsilateral
internal iliac aneurysm. In cases of an internal iliac aneurysm (see exception below), preservation
methods are not possible and selective branch occlusion (see above) and endovascular exclusion
are necessary.
■
Indications for internal iliac artery preservation may include the following:
■
Routine revascularization as procedural preference
■
The presence of contralateral internal iliac occlusion
■
Active patient with concern/potential for buttock claudication
■
Diabetic with diseased ipsilateral deep femoral artery (reduced potential collateral supply)
■
Prior thoracic endograft repair (concern regarding anterior spinal artery collateral flow arising
from the internal iliac circulation and potential for postoperative paraplegia)
■
The simplest internal iliac preservation technique involves deployment of flared or so-called bell-
bottom devices. Although anecdotally applied to larger aneurysms, conventionally, this technique
is limited to common iliac artery aneurysms with 24-mm or shorter diameter distal landing zones.
As an off-label modification of this technique, for common iliac aneurysms with larger or poorly
defined distal landing zones, the maximal diameter flared iliac limb is intentionally deployed
approximately 2 cm proximal to the internal iliac artery orifice. An aortic extension cuff without a
proximal uncovered stent (typically 28 mm) is then deployed halfway into the unsecured iliac limb
and flared out into the distal aneurysm, essentially creating a larger landing zone than that
conventionally available (FIG 7). Although strictly speaking, cuff deployment is essentially in the
aneurysm itself; late outcomes from these procedures appear favorable, with a low reported
incidence of migration or type Ib endoleak.
■
Direct internal iliac artery revascularization can also be accomplished by surgical bypass from or
transposition to the ipsilateral external iliac artery distal to the ipsilateral endograft limb. Like all
open vascular procedures, exposure is the most critical requirement for technical success.
■
Proper incision placement and entry into the retroperitoneal space is tantamount to gaining adequate
and safe iliac bifurcation exposure and minimizing postoperative discomfort. For these exposures,
the primary surgeon stands on opposite side of the table. The incision is centered over either lower
quadrant and starts at a paramedian location at level of the umbilicus and gently curves toward the
midline over the first third of the distance from the umbilicus to the symphysis pubis (FIG 8).
Exposure proceeds through the anterior rectus sheath following the hockey-stick shape of the skin
incision. Care is taken not to divide the rectus muscle—this is a complete “muscle-sparing”
technique. The sheath itself is incised at least 3 to 5 cm medial to the semilunar line. Keeping the
rectus muscle intact reduces incisional hernia risk and decreases postoperative pain.
■
The rectus muscle is dissected away from the sheath and retracted medially. The retroperitoneal
space is developed below the arcuate line (linea semicircularis) just superior to the inferior
epigastric vessels, which are preserved and gently swept inferiorly. In women without prior
hysterectomy, the round ligament of the uterus is often encountered as a fibrous cord during this
exposure and is divided between ties. The peritoneal sac is swept bluntly medially until the
external iliac artery and the distal half of the common iliac aneurysm are exposed. The ureter is
visualized crossing the iliac artery and should be left undisturbed. Self-retaining retractors (e.g.,
Bookwalter®) are placed at this point.
■
Choice of retractors and proper placement are essential for procedural success. The retractor post is
placed on the opposite side about the level of the costal margin, and a small round ring is fixed and
centered directly over the incision. A Balfour® blade is placed over the inguinal ligament, and a
medium Kelly® blade oriented toward the opposite shoulder. A narrow malleable blade is
oriented medially to retract the bladder. Following retractor placement, if the incision was sited
properly, the iliac bifurcation should be positioned directly in the center of the surgical field.
■
The midsegment of the external iliac artery is exposed and controlled. The internal iliac artery is
next isolated from the surrounding tissue, from its origin to the bifurcation of the anterior and
posterior divisions, which are individually controlled. No attempt should be made to expose
anything more than a small anterior aspect of the distal common iliac aneurysm during this
maneuver.
■
The internal iliac artery origin is ligated with 0-polypropylene suture, and the anterior and posterior
divisions of the internal iliac artery are controlled independently. Additional small branches
arising from the main trunk are clipped for hemostasis. The internal iliac artery is divided as
proximally as possible, and the stump closure is reinforced and imbricated with a 5-0
polypropylene suture (FIG 9). The distal internal iliac artery is then mobilized from the subjacent
internal iliac vein.
■
The patient is systemically anticoagulated at this point. An 8-mm × 10-cm graft knitted, collagen-
impregnated polyester graft is anastomosed to the distal stump of the internal iliac artery in an end-
to-end manner. The graft is occluded at its open end and distal control released to test anastomotic
leaks. The graft is then recontrolled just proximal to the distal anastomosis.
■
A segment of the ipsilateral, adjacent external iliac artery, at least 5 cm distal to its origin, is next
mobilized and controlled. Following creation of a posteromedial arteriotomy, the graft is trimmed
and beveled to length and anastomosed to the external iliac artery in an end-to-side manner. The
graft is flushed routinely and flow restored to the internal and external iliac arteries (FIG 10).3
■
A large clip is sewn transversely at the heel of the external iliac artery anastomosis to establish a
fiducial point for the internal iliac bypass. After hemostasis is confirmed, the retractor system is
removed and retroperitoneal contents allowed to collapse back into the wound. The endovascular
portion of the procedure completed through femoral artery access sites in a standard fashion.
■
After endograft deployment and satisfactory completion aortography, the retroperitoneum is
reinspected for hemostasis following reversal of anticoagulation. The anterior rectus sheath is
closed with a running 1-0 PDS suture, followed by closure of Scarpa’s layer and skin.
■
[Alternate technique] Occasionally, the common trunk of the internal iliac artery is long and runs
parallel to the course of the external iliac artery for some distance. If sufficient length is present,
the internal iliac artery may be transposed to the external iliac artery, as long as the anastomosis is
tension-free.
■
[Alternate technique] Another hybrid approach is available to preserve internal iliac flow. In this
method, a covered self-expanding stent (e.g., Viabahn®, W. L. Gore, Flagstaff, AZ) is deployed to
provide retrograde flow from the external to internal iliac artery, ipsilateral to the common iliac
aneurysm to be excluded. An aortouniiliac endograft is then deployed from the contralateral side,
and the procedure completed with a femoral–femoral bypass graft (FIG 11). Several
circumstances limit the general applicability of this technique, including an acute external–internal
iliac bifurcation angle and significant diameter discrepancy (>2 mm) between the two arteries.
Also, the durability of this technique is not well established and may be limited by the propensity
of the covered stent to back out of either the origin or destination artery or kink. This technique
also requires advanced catheter and guidewire skills and a large device inventory to reliably
complete the procedure.
■
[Alternate technique] More recently, a variation of the chimney (parallel) stenting technique has
been described for complete endovascular repair of common iliac aneurysms.4 In this technique,
the proximal brachial artery is exposed through an axillary incision to allow safe introduction of a
long (90 cm) braided 9-Fr sheath. Briefly, after the bifurcated main body endograft is deployed,
the long 9-Fr sheath is advanced from the left brachial artery, through the main body, and
positioned into the ipsilateral common iliac artery. The internal iliac artery is catheterized,
followed by wire exchange for a stiff wire. A covered self-expanding stent graft (e.g., Viabahn®),
sized for the target internal iliac artery diameter, is deployed from the ipsilateral iliac gate to the
internal iliac artery landing zone. A second covered self-expanding stent graft is advanced from the
ipsilateral femoral artery access retrograde into the aneurysm and proximal external iliac artery
and deployed at the same level as prior internal iliac artery stent graft. Both stent grafts are
expanded within the ipsilateral iliac limb of the aortic endograft using a kissing-balloon technique.
This procedure can be repeated for the contralateral side in cases of bilateral common iliac
aneurysms (FIG 12). Care should be taken during this maneuver to deploy each stent graft
sequentially, rather than simultaneously, in order to position the covered stents accurately relative
to each other.
■
[Alternate technique] Although only available under an investigational device exemption (IDE), U.S.
Food and Drug Administration (FDA)–approved clinical trial at the current time, an iliac branch
device (IBD) is under development for total endovascular repair of common iliac aneurysms (FIG
13). Briefly, this bifurcated device is inserted ipsilateral to the common iliac aneurysm prior to
main body deployment. It is designed to be used in conjunction with a standard bifurcated aortic
endograft. The partially constrained branch in the investigational device and adjacent internal iliac
artery are catheterized from the contralateral side employing a preloaded catheter in the delivery
system and cross-femoral guidewire access. A bridging covered stent is advanced from the branch
to the internal iliac artery. Following this, a standard bifurcated endovascular aneurysm repair is
completed in the usual manner.5
PEARLS AND PITFALLS

Choose the right procedure ■ Although perfusion is optimally maintained to at least one internal
for the right patient. iliac artery, preservation should be attempted selectively,
weighing the risks and benefits of potential ischemic
complications associated with intentional occlusion vs. the
additional complexity and long-term durability issues associated
with preservation techniques.
External-to-internal iliac ■ Make sure the longitudinal segment of the skin incision is
bypass exposure sufficiently medial to the lateral edge of the rectus to
accommodate a single layer fascial closure. The preserved rectus
muscle provides a natural barrier against postoperative abdominal
wall hernia formation.
Use a cross-over introducer ■ The cross-over sheath allows for intermittent contrast injection
sheath for internal iliac and stabilization of the embolization catheter. Internal iliac sheath
embolization. access also minimizes the probability that deployed coils may
reflux retrograde into the axial iliac circulation, requiring often
prolonged and frustrating attempts at retrieval.
Pelvic bleeding ■ The internal iliac vein is posterior and adherent to the artery and
may be the source significant, unanticipated hemorrhage if injured
during circumferential arterial dissection.
Inflow to the internal iliac ■ Choose a site on the external iliac artery sufficiently distal to its
bypass origin so that the stent graft can land in a segment free from kinking
and prevent subsequent development of an ipsilateral type Ib
endoleak.
POSTOPERATIVE CARE
■
Postoperative care is similar to a standard endovascular aneurysm repair. A complete blood count
and a basic metabolic panel are checked the following morning.
■
If the procedure was performed entirely using endovascular techniques, oral intake is started
immediately, Foley catheter is removed, and patient is encouraged to ambulate and discharged on
following postoperative day.
■
If the procedure involved a surgical internal iliac revascularization, the patient is started on clear
liquids and advanced as tolerated. The retroperitoneal approach is not typically associated with a
clinically significant ileus, and the muscle-sparing exposure is well tolerated. Patients may be
discharged typically on the second postoperative day.
OUTCOMES
■
Ipsilateral hip and buttock claudication develops in as many as 40% of patients following acute
internal iliac artery occlusion. Fortunately, more severe forms of postprocedural pelvic ischemia,
although potentially lethal, occur extremely rarely. Although claudication symptoms, when present,
are reported to improve within 6 months following the procedure, this improvement may be
attributable to lifestyle alteration (e.g., walking less) rather than collateral vessel formation. It is
generally agreed, however, that complete symptom resolution rarely occurs.
■
Internal iliac bypass grafting (surgical or endovascular) effectively maintains pelvic perfusion, with
excellent long-term patency. Most patients enjoy a symptom-free postoperative course in
perpetuity. Thus, in active individuals, as a general recommendation, internal iliac circulation
should be preserved whenever possible.
COMPLICATIONS
■
Complications for management of common iliac aneurysms can be a result of internal iliac
revascularization or occlusion techniques.
■
The main complication associated with revascularization is bleeding. This can occur
intraoperatively from venous injury and/or postoperative anastomotic or other arterial sources.
Other less common complications include ureteral injury, bowel injury, ipsilateral leg ischemia,
and early graft thrombosis.
■
Complications associated with acute occlusion of internal iliac artery include the spectrum of
ischemic symptoms ranging from hip and buttock claudication to more severe forms such as
perineal necrosis, ischemic sacral plexopathy, and vasculogenic impotence.
■
The internal iliac artery serves as an important outflow branch in maintaining patency of the iliac
limb after endovascular aneurysm repair. Iliac limbs whose distal landing zone is placed in the
external iliac artery may have an increased risk of thrombosis. However, this is not an indication
for any additional antiplatelet or anticoagulation treatments beyond what is customary.
REFERENCES
1. Armon MP, Wenham PW, Whitaker SC, et al. Common iliac artery aneurysms in patients with abdominal aortic aneurysms. Eur J
Vasc Endovasc Surg. 1998;15(3):255–257.
2. Boules TN, Selzer F, Stanziale SF, et al. Endovascular management of isolated iliac artery aneurysms. J Vasc Surg. 2006;44(1):29–
37.
3. Lee WA, Nelson PR, Berceli SA, et al. Outcome after hypogastric artery bypass and embolization during endovascular aneurysm
repair. J Vasc Surg. 2006;44(6):1162–1168.
4. Lobato AC. Sandwich technique for aortoiliac aneurysms extending to the internal iliac artery or isolated common/internal iliac
artery aneurysms: a new endovascular approach to preserve pelvic circulation. J Endovasc Ther. 2011;18(1):106–111.
5. Parlani G, Verzini F, De Rango P, et al. Long-term results of iliac aneurysm repair with iliac branched endograft: a 5-year
experience on 100 consecutive cases. Eur J Vasc Endovasc Surg. 2012;43(3):287–292.
Occlusive Disease Management: Isolated Femoral Reconstruction,
Aortofemoral Open Reconstruction, and Aortoiliac Reconstruction
Chapter 25 with Femoral Crossover for Limb Salvage
Nathan Itoga E. John Harris, Jr.
DEFINITION
■
Aortoiliac occlusive disease falls under the umbrella of peripheral artery disease where
atherosclerosis and chronic plaque accumulation leads to diminished blood supply to distal
arterial beds.
■
The aortic bifurcation near the level of the L4 disc space is one of many areas of decreased shear
stress and is an area of early atherosclerosis.
■
Peripheral arterial disease (PAD) is usually classified into inflow and outflow disease.
■
The infrarenal aorta and iliac vessels are of larger caliber and are classified as inflow vessels.
■
The infrainguinal outflow from the common femoral artery is via the profunda femoral and
superficial femoral arteries.
■
The patterns of arterial stenosis and occlusion can be broken up into five types (Table 1). When a
combination of both inflow and outflow disease exists, treatment is focused on the aortoiliac
system first or femoral artery occlusive disease. Outflow occlusive disease is addressed in
Chapters 26–28, 31–33.
■
Neurogenic claudication is frequently confused for arterial claudication. Neurogenic claudication is
variable—some good days, some bad—whereas arterial claudication is very consistent.
Neurogenic claudication can be relieved by the use of spinal support while walking, such as a
shopping cart, or wheeled walker. These aids do not influence arterial claudication symptoms.
■
Osteoarthritis of the hips can be frequently confused with arterial claudication. Like arterial
claudication, pain is brought on by activity and relieved by rest and is more common with
increasing age.
■
Venous claudication from chronic venous outflow obstruction is described as a bursting type pain,
comes on at longer distances, requires a longer rest period that requires leg elevation, and is
frequently associated with leg swelling and discoloration.

■
The diagnosis of aortoiliac occlusive disease can readily be made from a patient’s clinical history
and physical examination.
■
Patient’s with aortoiliac disease have up to a 50% risk of concomitant coronary artery disease with
the same risk factors of smoking, hypertension, lipid abnormalities, diabetes mellitus, male gender,
increased age, and family history.
■
The disease burden in the internal and external iliac blood supply leads to a variety of clinical
presentations which is most notable for Leriche syndrome which comprises the symptoms of
buttock claudication, impotence in men, muscle atrophy, and absent or diminished femoral pulses.
■
Claudication is the most common presenting symptom and is not limited to the buttocks but can
occur in the hip, thigh, and, rarely, in the calf muscles.
■
Impotence as an isolated symptom in men should be evaluated for other possible causes.
Impotence is only seen in 30% of men with decreased hypogastric perfusion as there are
abundant collaterals from the mesenteric, profunda, and lumbar arteries.
■
Ankle–brachial indices (ABI) are usually diminished but rarely lower than 0.5 in isolated
aortoiliac occlusive disease for the same reason cited earlier. It is rare to see critical limb
ischemia, which encompasses rest pain and/or tissue loss, in the setting of isolated aortoiliac
disease as there are multiple collaterals through the ilioprofunda system.
■
Severe common femoral disease, with both superficial femoral and profunda femoral artery high-
grade stenosis or occlusion, can mimic aortoiliac occlusive disease.

■
Ultrasound studies available in noninvasive vascular laboratories can help aid in diagnosis and
assess the degree of PAD.
■
ABI measurements can be supplemented by exercise, where a decrease in 15% of the ABI is
considered significant as a decrease in peripheral resistance during exercise leads to diminished
blood flow distal to the point of stenosis or obstruction.
■
Duplex ultrasound for the aortoiliac system is difficult and is limited by body habitus and bowel
gas. With an experienced technician, arterial disease of the intraabdominal vessels can be detected
with greater sensitivity.
■
For vascular surgeons, computed tomography angiography (CTA) is the noninvasive imaging study
of choice for preoperative planning. Considerations for kidney disease and contrast dye allergies
need to be taken into account. The evaluation usually involves the abdomen pelvis and runoff to the
feet. It is difficult, especially in tall patients, to evaluate the thoracic aorta during one contrast
bolus due to timing of the contrast injection. A CTA study provides accurate estimation of luminal
flow and with good visualization of degree of calcification.
■
Magnetic resonance (MR) angiography is also useful but is found to, at times, overestimate the
degree of stenosis, and motion artifacts may limit the quality of the study.
■
Direct arteriography under fluoroscopy is considered the gold standard, but improvements in CTA
approach this accuracy in evaluating PAD.
■
Arteriography may be difficult in the setting of an iliac occlusion and may need to be performed
through the descending thoracic artery using a radial or brachial artery approach.
■
Some surgeons may forego computed tomography (CT) studies and proceed with a contrast digital
subtraction angiogram in the setting of a reliable history and physical and/or noninvasive
ultrasound testing. This may limit the amount of contrast dye the patient is exposed to by
proceeding directly with endovascular intervention. Like CTA, catheter-based arteriographic
studies should include infrainguinal outflow of the femoral, popliteal, and tibial vessels, in
addition to the abdominal and pelvic views.
■
Although rarely used, pressure catheters can also be used during arteriography to identify significant
lesions with a mean arterial pressure drop of 5 to 10 mm Hg across the stenosis considered
significant.
■
Preoperative imaging is essential in preoperative planning. The degree of aortoiliac disease in
combination with infrainguinal and tibial occlusive disease needs to be considered in choosing the
appropriate intervention for the patient.
■
Graft selection, location of cross-clamping, and enlarged collaterals need to be accounted for prior
to surgery.
■
Identifying the degree and extent of arterial occlusive disease also enlightens the decision between
an open or endovascular approach.
■
The Trans-Atlantic Inter-Society Consensus (TASC) Classification (FIG 1) is a multispecialty
consensus approach to managing aortoiliac occlusive disease. Routinely, TASC A and B lesions
are treated with endovascular approaches with balloon angioplasty and/or stenting. TASC C and
D lesions have a better outcome with an open approach.
SURGICAL MANAGEMENT
■
Before surgical management is pursued, medical management should be initiated due to the high
incidence of coronary artery disease with peripheral artery disease.
■
Patients should be advised to quit smoking; placed on a regular walking program, ideally
supervised; and started on statin therapy and aspirin when appropriate and tolerated.
■
Preoperative anesthesia visits should include inquiries into cardiac, lung, and renal systems to
evaluate overall operative risk.
■
Age and comorbidities should be factored into decisions regarding an open versus endovascular
approach, as should procedural durability and invasiveness of the intervention.
■
The aims of therapy in aortoiliac occlusive disease are to relieve symptoms and, in cases of critical
limb ischemia, prevent limb loss. Revascularization of the aortoiliac system can be done in a
variety of endovascular and open approaches. The choice of procedure depends on the disease
pattern, patient risk factors, available resources, and surgeon experience.
■
We describe three common operative interventions for inflow disease: aortobifemoral bypass,
femoral–femoral bypass, and femoral endarterectomy.
TECHNIQUES
ISOLATED FEMORAL RECONSTRUCTION FOR LIMB SALVAGE WITH

POSSIBLE ENDOVASCULAR INTERVENTION
First Step—Landmarks
■
The patient is placed prone on the operating table, with a soft bump under the knee and the leg
slightly abducted and externally rotated. The inguinal ligament marks the transition point from the
external iliac artery to the common femoral artery and is identified by connecting the anterior
superior iliac spine to the pubic symphysis. The common femoral artery is usually located over the
medial third of the femoral head but may be difficult to palpate in aortoiliac occlusive disease.
Pre- or intraoperative ultrasound can be used to identify the common femoral as well as the
bifurcation into the superficial and profunda arteries.
Second Step—Incision and Exposure
■
Two types of incisions can be made to expose the common femoral artery. A vertical incision above
the common femoral artery and bifurcation allows for greater access to the proximal and distal
vessels in extensive disease. An oblique incision is better for cosmesis and is made cephalad to
the groin crease and is acceptable in focal isolated lesions and in obese patients.
■
After a skin incision is made, the subcutaneous tissue is then dissected with electrocautery with
careful attention to ligate superficial crossing vessels to control bleeding and ligating lymphatics to
prevent seroma formation. A self-retaining retractor is used to help expose the tissues and is
repositioned as the dissection proceeds deeper. Once the femoral sheath is identified and entered
the femoral artery lies lateral to the femoral vein. The distal external iliac artery, the common
femoral artery, the proximal profunda femoral and superficial femoral arteries are
circumferentially dissected with scissors and tagged with a vessel loop or moist umbilical tape
using a right angle. Other arterial side branches may be identified and are controlled with vessel
loops or temporary clips but rarely ligated in occlusive disease.
Third Step—Clamping
■
Before clamping of the arteries, heparin is given intravenously as a weight-based bolus at 100
units/kg and allowed to circulate for 3 minutes. Heparin has a half-life of approximately 90
minutes and is checked periodically with activated clotting time (ACT) measurements. A range of
250 to 350 is desirable and 1,000 to 3,000 units boluses can be given periodically to maintain this
level of anticoagulation. Gaining proximal and distal control of the femoral arteries can be done
with a variety of clamps. An angled Novare clamp or femoral C-clamp can be used at the proximal
common femoral artery. Next, a profunda clamp is used to clamp the profunda femoral artery and
the superficial femoral artery. Clamps are placed on soft areas of the artery past the area of the
high plaque burden. Side branches can be controlled with vessel loops pulled tightly around the
artery and clamped with a hemostat or temporarily clamped with a medium or large clip.
Fourth Step—Endarterectomy, Tacking sutures
■
A longitudinal incision is made along the exposed common femoral artery using a no. 11 blade
scalpel followed by Potts scissors. The adventitia is grasped with vascular forceps and a freer
elevator is used to dissect the plaque away from the adventitia. The plaque is removed with blunt
dissection unless sharp dissection is needed to dissect the plaque off the posterior wall. Tacking
sutures with 7-0 Prolene are used to secure the remaining plaque to the posterior wall to avoid a
dissection plane and emboli (FIG 2).
Fifth Step—Patch Angioplasty

■
Rarely is the common femoral artery closed primarily after endarterectomy as this decreases the
artery diameter. Patch angioplasty with bovine pericardium, polyester (Dacron), or saphenous vein
is used. A patch is cut out to match the length of the endarterectomy incision with tapering at the
proximal and distal edges to facilitate a curved end of the ellipse. The patch is secured with 6-0
Prolene suture. A parachute technique or three knots is used to anchor the patch at the proximal or
distal end. The patch is then sewn with a running suture line. Before the patch is completely sewn
in, back-bleeding is performed from the profunda artery, superficial femoral artery, and common
femoral artery. Repair sutures with 6-0 or 7-0 sutures can be made in the case of suture line
bleeding. Once the patch is in place, a micropuncture kit can be used to access the common
femoral artery if endovascular therapies in a retrograde fashion are planned for the iliac arteries
(FIG 3). In the case of extensive profunda femoral arterial occlusive disease, this artery should be
exposed beyond the extent of any palpable plaque, and a separate arteriotomy, endarterectomy, and
patch angioplasty of the superficial femoral and the profunda femoral arteries are performed (FIG
4). In the situation where extensive endarterectomy yields an adventitia that is too thin, the femoral
bifurcation can be reconstructed with prosthetic graft material (FIG 5).
Sixth Step—Closure
■
If an endovascular technique is performed in the same operation, simple Prolene stitches can be
used to close the sheath access site. Careful attention is then made to ensure hemostasis. The
femoral sheath may or may not be closed over the vessels, but careful attention must be made to
approximate tissues to close dead space to prevent seroma formation. Usually, a three-layer
closure is used. At the end of the operation, femoral and distal flow should be checked with pulse
palpation and continuous wave Doppler insonation. We do not routinely employ completion
angiography or duplex ultrasonography. Protamine may be given, depending on the time of last
heparin bolus or according to the intraoperative ACT reading. Approximately 10 mg is given for
every 1,000 units of heparin given, adjusted for time decay and the heparin half-life or can be
estimated off the last ACT measurement.
AORTOFEMORAL OPEN RECONSTRUCTION

Positioning
■
The patient is supine, with a soft bump under the left hip for a retroperitoneal exposure and the table
slightly flexed, or straight supine on a flat table for a transabdominal approach. The entire
abdomen; the perineum, blocked with a sterile drape; and the groins and both legs are
circumferentially prepped and draped into the sterile field.
First Step—Exposure of Femoral Vessels
■
The femoral vessels are typically exposed first through bilateral longitudinal or oblique incisions to
minimize the time which the abdomen is open. The crossing vein off the femoral vein beneath the
inguinal ligament must be ligated or carefully avoided as this may be injured when the graft is
tunneled from the abdomen later in the operation. After a soft spot is identified for anastomosis in
the common femoral artery, or the profunda femoral artery when the superficial femoral artery is
occluded, and adequate circumferential exposure is achieved, the common femoral artery along
with superficial femoral and profunda artery are tagged with vessel loops or moist umbilical tape.
The groin incision is then packed with an antibacterial saline-soaked gauze to avoid desiccation.
Second Step—Exposure of the Aorta
■
A transperitoneal approach is routinely used to expose the infrarenal aorta, although a
retroperitoneal approach may also be used. A longitudinal midline incision is made from just
below the xiphoid process to a few centimeters below the umbilicus or down to the symphysis
pubis when iliac arterial exposure will be required. Subcutaneous tissue is dissected and the
abdomen is entered between the rectus muscles. With routine CTA preoperatively, a thorough
abdominal exploration is discouraged, which will minimize postoperative ileus. The transverse
colon is retracted cephalad, and the small bowel is shifted to the patient’s right side and packed in
soft, moist lap sponges to the right. The ligament of Treitz is taken down and the duodenum is
mobilized to the right. A self-retaining retractor is then placed to sweep the bowel to the right with
a moist laparotomy pad. The retroperitoneal tissue overlying the aorta is dissected, and the aorta is
exposed superiorly to the level of the left renal vein. Extra retractors are used as needed for
exposure. Distal control of the infrarenal aorta will be necessary if an end-to-side aortic
anastomosis is planned. Preoperative imaging and manual palpation of the aorta identify a soft spot
for the proximal anastomosis. Accessory renal arteries and the inferior mesenteric artery should be
identified and be evaluated if reimplantation is necessary. Endarterectomy of the origin of the
reimplanted visceral vessels is recommended, and extra aortic tissue is used as a Carrel patch.
Lumbar arteries should also be identified and controlled with suture ligation or a vessel loop with
care to avoid excessive bleeding. Depending on the type of aortic occlusive disease, an end-to-
side or an end-to-end anastomosis will be fashioned and the dissection necessary is dictated by
this decision. In general, an end-to-end anastomosis is more favorable hemodynamically, yet with
preserved inferior mesenteric or iliac arteries, an end-to-side anastomosis may be more feasible.
Third Step—Tunneling
■
After adequate exposure of the aorta is achieved, focus turns to making tunnels for the femoral limbs
of the bypass. Tunnels should track directly along the anterior aspect of the external iliac artery
and by elevating soft tissues and ensuring ureters remain anterior. Moist umbilical tapes or
Penrose drains are passed with a smooth aortic clamp to mark the tunnels.
■
Graft selection can also be made at this time with an 18 × 9-mm or a 16 × 8-mm graft used for males
and a 14 × 7-mm or 12 × 6-mm graft typically used for females. Typically, a polyester (Dacron)
graft is used, although others prefer polytetrafluoroethylene (PTFE). Prior to aortic clamping,
heparin is given intravenously, as explained earlier with a target ACT range of 250 to 350.
Fourth Step—Clamp Placement
■
The choice of clamp depends on the approach if end-to-side anastomosis or an end-to-end is chosen.
The patency is similar for both approaches and, in most cases, is made by surgeon preference. For
an end-to-end anastomosis, the proximal clamp is placed just below the renal arteries if the
disease pattern does not obligate suprarenal clamping, with as little dissection of the renal artery
origins as possible. The distal infrarenal aorta is then divided and oversewn in two layers with 4-
0 Prolene suture. The proximal aortic cuff may require endarterectomy, which is performed up to
the proximal clamp. For an end-to-side anastomosis, two aortic clamps are used or a side-biting
Satinsky clamp is used to obtain proximal and distal control. With flush occlusion of the aorta at
the level of the renal arteries (FIG 6), suprarenal dissection is required, with mobilization and
control of the origins of the renal arteries, which are controlled with doubly passed silastic loops
so that they may be occluded during endarterectomy to prevent atheroma embolization. A
suprarenal clamp is placed to allow thromboendarterectomy of the infrarenal aortic cuff, then the
clamp is moved caudally prior to graft anastomosis.
Fifth Step—Proximal Anastomosis
■
In the case of the end-to-end anastomosis, the technique is straight forward and the graft diameter
should match the remaining aortic diameter. In the side-to-side anastomosis, the graft is cut at a
bevel to maximize the amount of blood flow and the arteriotomy is laterally placed to allow the
graft to enjoy a more retroperitoneal position to minimize the chance for development of an
aortoenteric fistula (FIG 7). The graft is sewn in place with running 3-0 or 4-0 Prolene sutures
using a parachute technique or securing the suture with three knots, starting from the posterior wall
to visualize the placement of each stitch. The graft limbs are then clamped and the proximal clamp
is then released to check for suture line bleeding. Repair sutures can be used for any suture line
bleeding with 4-0 or 5-0 sutures on a pledget as needed. The abdomen is then packed and attention
is then turned to the femoral anastomoses. In some instances, where a single internal iliac artery is
patent, but the distal aorta or proximal common iliac artery is diseased, we will directly
revascularize the internal iliac artery with the bifurcated graft limb and then jump graft down to the
femoral position (FIG 8).
Sixth Step—Graft Tunneling
■
Using the umbilical tape or Penrose drain as a guide, a smooth aortic clamp is then used to tunnel
each graft limb from the abdomen into the femoral incision. The graft is then pulled gently through
the tunnel above the external iliac vessels and below the ureter. Care must be taken to minimize
kinking and redundancy in the graft tunnels. Once tunneled the graft limbs are flushed to confirm
adequate inflow, reclamped in the abdomen and flush with heparinized saline solution.
Seventh Step—Distal Anastomosis
■
Clamping of the femoral artery is then performed as described earlier so that the common femoral
artery, superficial femoral artery, and profunda femoral artery are controlled. A longitudinal
incision is then made with a no. 11 blade followed by Potts scissors to approximate the graft limb.
The graft is then cut on a taper to allow a natural reimplantation angle into the common femoral
artery with minimal tension. The anastomosis is then completed as an end-to-side fashion with 5-0
or 6-0 Prolene suture in a running fashion. In some situations, where retrograde external iliac flow
is not possible, an end-to-end femoral anastomosis is preferred to either the common femoral or
the profunda femoral artery (FIG 8). The same procedure is completed for the contralateral limb.
Eight Step—Closure
■
After hemostasis is achieved, careful attention is made to ensure the anastomoses are securely done
and dead space is closed to prevent seroma formation and minimize groin infections. Protamine
may be given as described earlier.
AORTOILIAC RECONSTRUCTION WITH FEMORAL CROSSOVER

■
This technique can be used to restore blood flow to a lower limb when one of the iliac arteries is
obstructed and the contralateral iliac arteries are patent. The surgical procedure can also be used
in conjunction with an endovascular procedure, for example, angioplasty and/or stenting of the
nonoccluded iliac vessels. Groin incisions are made in an oblique or longitudinal fashion. Control
of the common, superficial femoral, and profunda femoral arteries are performed as previously
described. Endarterectomy of the common femoral artery is performed as necessary if there is
significant plaque burden. The suprapubic tunnel is made with blunt dissection using a blunt-ended
hemostat or one’s fingers. The key is to create the tunnel just anterior to the abdominal fascia.
Either a blunt tunneling device or a long aortic clamp can be used to pass the graft from one side to
the other in the subcutaneous tissue, avoiding entry into the peritoneal cavity. The anastomosis is
performed so the graft sits in a curved configuration over the suprapubic tissue (FIG 9).
Meticulous attention is given to closure to avoid kinking or compression of the graft and to avoid
dead space that can lead to problematic seromas and the possibility of soft tissue infection, with
subsequent graft infection.
PEARLS AND PITFALLS
Isolated femoral ■ Care must be taken to be certain that proximal and distal
reconstruction atherosclerotic plaque is not causing residual stenosis.
■ Patch angioplasty is critical to the success of this procedure.
■ Distal tacking sutures should be employed generously.
Aortofemoral reconstruction ■ Adequate exposure is critical to success.
■ Localized endarterectomy at both proximal and distal anastomotic
sites is generally required.
■ Tunneling errors can lead to late complications and early graft
failure.
Femoral–femoral crossover ■ Adequate inflow and outflow must be assured for success.
■ Concomitant femoral endarterectomy should be used freely.
■ Tunneling and closure errors frequently cause early graft failure.
POSTOPERATIVE CARE
■
Patients are admitted to a cardiac monitored floor postoperatively as patients are at high risk for or
have documented coronary artery disease. Immediately, postoperative vascular checks are
performed with high frequency to assess early graft thrombosis requiring reintervention or
initiation of anticoagulation. Patients are encouraged to ambulate 4 to 6 hours after the operation,
with adequate pain control a point of focus. When the abdomen is entered, in the case of
aortobifemoral grafting, patients are kept from an oral diet until bowel function returns. While
anticoagulation is not routinely used for graft patency, aspirin is standard, and subcutaneous
heparin is given for secondary prevention of deep vein thrombosis (DVT).
OUTCOMES
■
See Table 2.
COMPLICATIONS
■
Early
■
Hemorrhage
■
Early thrombosis
■
Infections
■
Colon ischemia
■
Femoral nerve injury
■
Late
■
Aortoenteric fistula
■
Restenosis, thrombosis of graft
■
Anastomotic pseudoaneurysm
■
Sexual dysfunction
■
Spinal cord ischemia
■
Graft infection
SUGGESTED READINGS
1. Cronenwett JL, Johnston KW. Rutherford’s Vascular Surgery. 7th ed. Philadelphia, PA: Elsevier; 2010.
2. Mulholland MW, Lillmoe KD, Doherty GM, et al. Greenfield’s Surgery: Scientific Principles and Practices. 5th ed. Philadelphia,
PA: Lippincott Williams & Wilkins; 2011.
3. Rasmussen TE, Clouse WD, Tonnessen BH. Handbook of Patient Care in Vascular Diseases. 5th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2008.
4. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society consensus for the management of peripheral arterial disease. Int Angiol.
2007;26(2):81–157.
Occlusive Disease Management: Iliac Angioplasty
Chapter 26 and Femoral Endarterectomy
Venita Chandra
DEFINITION
■
Multilevel atherosclerotic occlusive disease involving the distal aorta, iliac vessels, and common
femoral arteries is a common occurring pathology seen often by vascular surgeons. Traditional
approaches to this disease process involved open surgical reconstruction with an aortobifemoral
bypass or iliofemoral bypass. Recently, however, there has been a paradigm shift toward
endovascular and hybrid approaches. Combining femoral endarterectomy with endovascular iliac
stenting is an increasingly common minimally invasive approach to this problem, providing an
effective alternative to open strategies with the potential of shorter hospitalizations and decreased
morbidity. Compared to iliac stenting alone, proper evaluation of femoral disease and, if
indicated, a hybrid approach with concomitant femoral endarterectomy have been associated with
increased durability of endovascular aortoiliac interventions.1

■
Aortoiliac and femoral occlusive disease can present, as with all peripheral arterial diseases
(PADs), in a variety of ways.
■
The typical presentation of aortoiliac occlusive disease includes claudication of the buttock and
upper thigh and erectile dysfunction. When multilevel vascular disease occurs, as in the case of
combined aortoiliac and femoral occlusive disease, distal lower extremity symptoms such as calf
claudication, rest pain, and tissue loss may ensue.
■
Typical physical exam includes the absence or diminution of femoral pulses. Other than the
peripheral pulse assessment, the physical exam can demonstrate other signs of PAD such as cool
digits and active wounds.

■
The initial evaluation of a patient with PAD should involve noninvasive evaluation of peripheral
blood flow with arterial waveforms and ankle–brachial indices (ABIs) (FIG 1). These studies
provide objective data regarding the extent of occlusive disease; however, they do not provide
adequate anatomic data for preoperative planning.
■
Once the degree and physiologic impact of the disease are determined by noninvasive testing, high-
resolution anatomic imaging via either computed tomographic angiography (CTA) or magnetic
resonance angiography (MRA) should be obtained for surgical planning.
■
CTAs are currently the gold standard for preoperative planning. They have the advantage of
providing information regarding the degree and location of stenosis as well as the anatomy of the
arterial wall (including degree of calcification and presence of aneurysms). Three-dimensional
reformatting can provide additional valuable information (FIG 2). CTAs, however, are limited by
the fact that they involve the use of contrast as well as radiation exposure. MRAs avoid radiation
exposure and contrast often, however, at the risk of reduced anatomic precision. Gadolinium
magnetic resonance (MR) contrast also entails risk of long-term renal dysfunction.
■
Catheter-based diagnostic aortography also provides anatomic data; however, this study has a
number of limitations including the fact that it is an invasive procedure with potential
complications. In addition, arteriograms only provide an understanding of the luminal anatomy,
occasionally obscuring features such as aneurysms, inclusion cysts, or periarterial inflammation.
Particularly for aorto-iliac-femoral disease, preprocedural CTA has the ability to identify
significant common femoral disease that may benefit from concomitant open endarterectomy at the
time of catheter-based intervention. Alternatively, relying on catheter-based arteriography as the
primary diagnostic modality may reduce overall contrast burden, radiation exposure, and need for
additional procedures if common femoral level intervention is not required. In general, careful
preprocedural physical examination and duplex imaging may suffice to help determine whether the
additional cost, risk, and inconvenience of CTA are justified prior to catheter-based intervention
for aortoiliac arterial occlusive disease.
SURGICAL MANAGEMENT
■
As with all patients with PAD, initial treatment approach should include comprehensive assessment
and management of concomitant cardiovascular disease risk factors. Details regarding maximal
medical management of PAD are beyond the scope or purpose of this chapter; at a minimum,
however, consideration should be given to beginning statin and antiplatelet therapy prior to
intervention, along with consideration of beta blockade and angiotensin receptor blocker or
converting enzyme inhibitor therapy in selected patients.
■
Regardless of medical or anesthetic risk, however, all patients with critical limb ischemia should be
considered candidates for revascularization when limb loss is a distinct possibility. Despite
platitudes to the contrary, major limb amputation above or below the knee is not necessarily a
“safer” surgical alternative to multilevel hybrid revascularization. Indications for intervention for
intermittent claudication are somewhat more complicated, however. The risks of a procedure are
weighed against the potential gain; typically, only patients with severe lifestyle-limiting
claudication who have failed nonoperative strategies are offered surgical revascularization.
■
Determining the anatomic distribution of disease is essential to obtaining optimal results. The
imperative for precision imaging cannot be emphasized enough—if you cannot appreciate the full
extent of disease, you cannot expect to comprehensively address it. As in all aspects of vascular
surgery, the biggest disappointments, both during and after the procedure, usually arise from
underestimating the extent of underlying disease.
■
The Trans-Atlantic Inter-Society Consensus (TASC) II guidelines provide a classification scheme
based on anatomic patterns of disease (FIG 3).2 The recommendations of the TASC II guidelines
is an endovascular management for TASC A and B iliac lesions, whereas open surgical
reconstruction is recommended for TASC C and D lesions in good-risk patients. Frequently,
however, patients with multilevel disease as seen in TASC C and D lesions have more virulent
atherosclerotic processes that often make them poorer surgical candidates. In addition, the
development of an increasingly sophisticated armamentarium of endovascular tools and strategies
are leading more and more vascular surgeons to attempt endovascular revascularization, even for
patients with TASC C or D lesions. Further updates of the TASC classification guidelines are
under review and will likely be published in the near future, highlighting the dynamic nature of
surgical management of this challenging condition.
■
Targeted perioperative risk assessment should be undertaken in appropriate patients, particularly
those with reduced exercise tolerance, known or suspected congestive heart failure, clinically
significant pulmonary disease, exercise-induced angina, arrhythmias, or those with recent history
of myocardial infarction. The presence of additional relevant comorbidities, including diabetes,
reduced glomerular filtration rate, iodinated contrast allergies, thrombophilia or coagulopathic
disorders, concomitant bacterial infection, or liver disease should also be identified and, when
present, evaluated.
Positioning
■
Patients are generally placed in the supine position, either in a hybrid operating suite with fixed
imaging capabilities or on a radiolucent table with a mobile imaging unit (C-arm) in a traditional
operating room environment.
■
Positioning should be arranged in such as way as to ensure adequate exposure of the entire
aortoiliac and femoral vasculature, with room on either side of the patient to rotate the imaging
unit to various angles in order to obtain appropriate oblique images. In angiographic parlance, in
many important circumstances (such as identifying and protecting the origin of the ipsilateral
internal iliac artery), “one view is no view.”
TECHNIQUES
FEMORAL ENDARTERECTOMY
First Step
■
For extended femoral endarterectomy (often requiring exposure of the proximal deep femoral artery
as well as the entire length of common femoral artery), optimal exposure is obtained via a
longitudinal incision placed directly over the femoral artery (FIG 4). The inguinal ligament should
be identified by palpation of the pubic tubercle and anterior superior iliac spine (an oblique line
between these two structures is the typical course of the inguinal ligament) and used as a guide for
femoral localization. Typically, the femoral artery is located approximately one-third the distance
from the pubic tubercle to anterior superior iliac crest. Even when no pulse is palpable, a firm
calcified linear mass can usually be palpated in this area. Alternatively, duplex ultrasound or
fluoroscopic imaging may be used to ensure accurate placement of the incision. Failure to incise
directly over the common femoral artery may increase risk for chronic lymphatic drainage, delayed
or complicated wound healing, and femoral nerve or venous injury. Although oblique femoral
incisions have gained in popularity, especially when used to obtain femoral access for proximal
aneurysm repair, these often do not provide exposure sufficient for comprehensive endarterectomy
as previously detailed.
■
The subcutaneous tissues are divided, ligating any lymphatic channels that are encountered. The
inferior edge of the inguinal ligament is identified and the common femoral artery is exposed
through the femoral sheath as it exits underneath the inguinal ligament.
Second Step
■
Full circumferential dissection of the distal external iliac artery (under the inguinal ligament), the
common femoral artery, the superficial femoral artery, and the origin of the deep femoral artery
and its initial branches are obtained sequentially (FIG 4).
■
The individual arteries should be assessed for areas of calcification and extensive plaque burden.
Soft sections with minimal calcification, or plaque limited to the posterior arterial wall, should be
identified for consideration of clamp placement as appropriate for the planned procedure.
■
The inguinal ligament may be divided for adequate exposure of the distal external iliac artery when
necessary to ensure adequate endarterectomy When considering the relative margin of distal
endarterectomy versus proximal stent placement, it is important to avoid stent placement across the
inguinal ligament, as this may greatly reduce long-term patency of the procedure as well as
complicate stent delivery through an ipsilateral retrograde sheath. In general, operators should err
of the side of more extensive proximal endarterectomies as opposed to distal extension of external
iliac stents.
■
Careful ligation of the circumflex iliac vein as it crosses over the external iliac artery under the
inguinal ligament should be considered to prevent accidental tearing of the vessel during clamping.
■
External iliac collaterals, like the epigastric artery or circumflex iliac artery, should be preserved
during dissection and endarterectomy whenever possible to ensure optimal long-term outcome.
Third Step
■
Once exposure is complete, the common femoral artery can be punctured under direct vision with
advancement of a wire under fluoroscopic guidance across the iliac lesion (FIG 5).
■
This eliminates the possibility of creating a retrograde dissection when a wire is passed after the
endarterectomy is performed, as well as the need to puncture the endarterectomy patch to gain
access.
■
If the disease burden is confined to the common iliac artery or only the proximal external iliac
artery, then iliac stenting can proceed at this point, prior to proceeding with the endarterectomy.
Occasionally, however, the amount of femoral disease burden is so great that the sheath will be
occlusive or otherwise impair runoff, which may limit the ability to obtain digital subtraction
angiography (DSA) images during or after stent placement. So consideration should be given to
initial endarterectomy depending on individual anatomic circumstances.
■
When retrograde wire passage is not possible due to extensive proximal plaque burden, tortuosity,
or other anatomic considerations, antegrade passage from the contralateral iliofemoral system
(obtained via either percutaneous or open femoral access) or left axillary or brachial access may
be attempted. Obviously, longer sheath/catheter/guidewire combinations will be needed for these
procedures and positioning considerations will be affected as well (e.g., arm will need to be
exposed and prepped on a radiolucent surface). Once antegrade wire is accomplished, this may be
used to deliver treatment devices directly or snared and externalized through the ipsilateral
femoral access for retrograde intervention as originally planned.
Fourth Step
■
Leaving the wire in place, systemic anticoagulation is accomplished with sufficient doses of
unfractionated intravenous heparin administration and proximal and distal femoral control is
obtained with vascular clamps. Especially proximally, a padded clamp should be chosen to allow
the external iliac artery to be clamped over the existing wire to prevent or minimize wire-related
injury.
■
A longitudinal common femoral arteriotomy is performed to expose the full extent of femoral
disease that needs to be addressed to ensure adequate runoff from the iliac intervention. This can
almost always be accomplished within the femoral incision itself without need for additional distal
femoral bypass procedures, unless extensive forefoot gangrene is present as a consequence of
multilevel arterial occlusive disease. Extended deep femoral endarterectomy is highly effective in
achieving suitable runoff when few other revascularization options may be available (FIG 4).
■
The arteriotomy can extend onto either the superficial or deep femoral artery. Occasionally, an
eversion endarterectomy of the deep femoral artery can be performed when the arteriotomy extends
onto the superficial femoral artery. Alternatively, the arteriotomy may be extended down the deep
femoral artery when the superficial femoral artery is chronically occluded. Selection of the
reconstruction technique is influenced by the occlusive pathology, level of debility, indications for
revascularization, and optimal revascularization strategy (FIG 6).
Fifth Step
■
Carefully, an endarterectomy plane is developed between the plaque and remaining mural media or
adventitia using a Penfield dissector or Beaver blade. The plane most typically is developed
within or exterior to the media, leaving the adventitia intact. Failure to appreciate the appropriate
endarterectomy plane may weaken the adventitia, leading to bleeding or postoperative hematoma
or pseudoaneurysm formation. Care should be taken to dissect the plaque away from the remaining
arterial wall, not vice versa. The endarterectomy plane is developed on each side of the vessel and
advanced posteriorly until the planes meet in the midline. Following this maneuver, the plaque is
transected flush with the arterial wall. Care should be taken to achieve good quality and minimally
diseased endpoints in both the superficial and deep femoral arteries as necessary (FIG 7). Tacking
sutures, as commonly employed during carotid endarterectomy, may also be necessary in the
femoral artery to ensure adequate endpoints. Particularly in the case of the deep femoral artery,
care should be taken to extend the endarterectomy well past the mass of common femoral artery–
related plaque. This may require exposing the deep femoral artery well beyond its initial branches,
dividing crossing branches of the deep femoral vein, and avoiding excessively deep placement of
self-retaining retractors to limit the possibility of traction injury to femoral nerve branches.
■
Often, significant posterior plaque extends proximally well into the external iliac arteries. As
previously discussed, care should be taken in deciding at which point the endarterectomy should
end versus distal extension of iliac stents (FIG 5).
Sixth Step
■
Once the full extent of plaque has been removed and suitable irrigation performed to identify and
eliminate remaining mobile fragments of residual media, patch angioplasty should be performed
typically using running 5-0 polypropylene suture initiated at both the proximal and distal endpoints
and tied in the middle. Bovine pericardium, extruded polytetrafluoroethylene (ePTFE), and
polyester or autogenous vein segments all may represent reasonable patch options, depending on
individual circumstances. In general, autogenous vein is more resistant to infection, whereas
prosthetic patch options are available off the shelf in a variety of configurations. ePTFE patches
tend to bleed more through their suture holes following placement, although this tendency may be
tempered by use of ePTFE patches. Currently, our preference is to use bovine pericardial patch as
the default choice in the absence of infection or other contraindication (e.g., patient objection due
to religious reasons) (FIG 6).
■
Rarely, when arterial wall integrity appears compromised following endarterectomy, femoral
interposition grafting may be performed in lieu of patch angioplasty. Interposition grafting may also
be a good choice when the femoral plaque burden is so great that endarterectomy is impractical; in
this case, an interposition graft (ePTFE or knitted polyester) can be placed instead of a patch. This
can be configured in any number of ways:
■
Distal anastomosis to distal common femoral artery
■
Distal anastomosis to syndactylized superficial and deep femoral arteries (FIG 6)
■
Distal anastomosis to superficial femoral artery with reimplantation of the deep femoral artery
■
Distal anastomosis to the deep femoral artery with reimplantation of superficial femoral artery
■
Distal anastomosis to the deep femoral artery only, when the superficial femoral artery is already
occluded
Seventh Step
■
Before completion of patch closure, the middle or distal portion of the patch is punctured with an
18-gauge needle and the back of the previously placed wire is routed through the needle. Patch
closure is then completed and the clamps removed; at this point, an appropriately sized sheath can
be advanced over the wire, through the patch, in preparation for iliac stenting.
COMMON ILIAC STENTING

First Step
■
Typically, a 6- or 7-Fr sheath is adequate for iliac stenting. Once the sheath is placed after
completion of the patch, appropriate arteriogram images are obtained.
■
For distal aorta and proximal common iliac disease, often the best approach is passage of a flush
catheter into the aorta and a power-injected aortogram.
■
For primarily iliac disease, retrograde arteriography through the femoral sheath is usually sufficient
to obtain adequate iliac opacification.
■
Contralateral anterior oblique (15- to 30-degree) projections are typically chosen for visualization
of the respective iliac systems to ensure identification of the origin of the ipsilateral internal iliac
arteries. Also, the full extent of disease burden may be most adequately addressed by multiple
obliquities in any circumstance.
■
A marking catheter may be used to assist in length measurements and “buddy” wires may also be
placed from contralateral femoral access. Every effort should be made to maintain perfusion to the
hypogastric arteries.
Second Step
■
Selection of the appropriate balloon and stent diameter is of great importance. Slight oversizing of
5% to 10% is recommended, except in the case of heavily calcified lesions, where oversizing may
predispose to arterial rupture.
■
Optimal target vessel diameter may be estimated preoperatively by measurements from the CTA,
particularly looking at the diameter of adjacent or contralateral normal arterial segments.
Similarly, diameter and length measurements may also be obtained during the hybrid procedure
itself. Generally speaking, common iliac artery target diameters may range from 7 to 10 mm,
depending on gender, body habitus, and burden of disease. External iliac artery diameters range
from 5 to 8 mm under similar qualifications.
■
Balloon “predilation” may facilitate stent placement and assist with stent sizing.
■
Mild pain during dilation is to be anticipated and indicates stretching of the adventitia; excessive or
persistent pain, however, may indicate arterial compromise or rupture. In the latter circumstance,
consideration should be given to additional placement of a covered stent when contrast
extravasation is present on arteriography and not immediately controlled with extended balloon
deployment. In the retroperitoneum, unlike the lower extremities, tamponade will not likely limit
further bleeding and extended balloon deployment may not be advisable as definitive treatment.
When general anesthesia is required for the concomitant endarterectomy, this warning sign may not
be present and completion arteriography should be carefully scrutinized for indications of iliac
artery compromise or contrast extravasation.
■
There are numerous commercially available stents to choose from, many of which are specifically
indicated for iliac arterial intervention (e.g., “on label”). Appropriate diameter and length stents
generally fall into two categories, balloon-expandable or self-expanding and can be covered or
uncovered (e.g., with adherent graft material).
■
The length of the balloon or stent should cover the entire length of the diseased area.
■
Balloon-expandable stents have the advantage of higher precision of placement and greater radial
strength; however, they are less flexible than self-expanding stents. As a general rule of thumb,
balloon-expandable stents are best suited for common iliac artery lesions where “kissing” stents in
the contralateral iliac artery may be needed to deal with excessive plaque burden or calcification
or the aortic bifurcation may need to be “advanced” into the distal aorta to completely ensure
adequate luminal recanalization. Alternatively, external iliac lesions are often best treated with
self-expanding stents, which by their nature are more flexible and compliant with the radius of
curvature present in this artery. Exceptions exist for both indications, however, and device
placement should be individualized to specific anatomic and clinical requirements.
Third Step
■
In the setting of bilateral or even unilateral proximal common iliac artery disease or distal aortic
disease, bilateral aortic bifurcation balloon dilation and stenting should be completed
simultaneously to protect the contralateral common iliac artery from dissection, plaque
dislodgement, or subsequent embolization. This is generally referred to as “kissing” stents.
■
Balloon-expandable stents are typically used for these proximal common iliac lesions and they may
be deployed well into the distal aorta, essentially “advancing the aortic bifurcation.”
Fourth Step
■
For common iliac lesions immediately adjacent to the aortic bifurcation, after precise arteriographic
localization of the aortic and iliac bifurcations and extent of plaque burden, appropriately sized
stents are selected. Uni- or bilateral sheaths of sufficient diameter for the selected stents are
advanced into the distal aorta. When common iliac lesions are not strictly “orificial,” concomitant
contralateral stenting is generally not required. Again, careful angiographic assessment should be
made to determine the extent of plaque burden present at the origin of the common iliac arteries to
make this determination.
■
Appropriately sized balloon-expandable stents are advanced within the sheaths and positioned
across the respective lesions. The sheaths are then pulled back to expose the entire stent; this
sequence prevents accidental dislodgement of the stent off the balloon, attempting to cross the
lesion, and limits the risk of plaque embolization during stent passage.
■
Once both stents are positioned appropriately, they are inflated simultaneously to achieve the kissing
configuration (FIG 8).
Fifth Step
■
Completion arteriography, typically through a pressure injection in the distal aorta through “side-
hole” or flush catheters, is obtained to confirm stent placement, evaluate degree of residual
stenosis, and rule out complications such as dissection or thrombus/embolization.
■
When pressure measurement are required, pull-back pressures are obtained with the goal of
eliminating pressure gradients across the treated lesion at rest or limiting to less than 15 mmHg
following injection of a distal vasodilator such as papaverine.
EXTERNAL ILIAC ARTERY STENTING

First Step
■
When the external iliac artery is diseased, particularly the distal segment, self-expanding stents are
typically used due to the increased tortuosity of these vessels and the increased flexibility of self-
expanding stents as opposed to balloon-expandable stents.
■
The same principles exist in terms of sizing, although for self-expanding stents, 10% to 20%
oversizing is typically recommended in the respective instructions for use (IFU).
Second Step
■
Deployment of self-expanding stents does not require advancement of the introducer sheath past the
lesion. The self-expanding stents usually are mounted on a carrier and constrained. The stents
should be positioned across the lesion and deployed.
■
Close fluoroscopic monitoring should occur during deployment, as self-expanding stents tend to be
far less precise in positioning in comparison to balloon-expandable stents and typically may
advance across the lesion during deployment.
Third Step
■
Predilation and postdilation may be performed as necessary with appropriately sized balloons
before and after stent deployment.
■
In the setting of very distal external iliac artery disease or incomplete distal external iliac
endarterectomy (as described earlier), the distal end of the stent may be carried down to the level
of the endarterectomy, again with care to be taken to avoid crossing the inguinal ligament as
previously described (FIG 5).
Fourth Step
■
Just as in common iliac stenting, completion arteriograms should be performed, and pressure
gradients may be obtained as necessary to confirm sufficient resolution of the stenosis.
Fifth Step
■
Usually, a single-repair stitch can be used to close the patch sheath access site, regardless of the
diameter of the sheath used for stent deployment.
■
Once hemostasis is achieved, the sheaths removed, and anticoagulation reversed with protamine
injection, the femoral exposure should be closed with a multilayer, anatomic closure with
absorbable suture.
PEARLS AND PITFALLS

Occluded iliac artery
strategies
Reentry devices ■ When attempting to cross an occluded segment with catheter-
guidewire combinations, a subintimal plane may be developed.
This subintimal technique is appropriate as long as the true lumen
can once again be regained prior to entering the aorta. In some
circumstances, this reentry may be challenging. In these situations,
reentry devices can be employed. These devices have nitinol
cannula that can be advanced through the device and used to
puncture into the true lumen; a 0.014-in wire is then advanced.
Free passage of the wire indicates true lumen access, which is
confirmed by contrast injection. The passage can then be dilated
and stented in a conventional manner (FIG 9). Care should be
taken to attempt reentry before the dissection plane is advanced
too far proximally into the distal aorta, as this may compromise
the ability to properly deploy balloon-expandable stents and/or
compromise inferior mesenteric arterial flow. Similarly, reentry
systems should be used with caution in the iliac arterial system to
avoid perforation and retroperitoneal bleeding.
Alternative approach ■ Antegrade approach from either a brachial or contralateral

femoral access sometimes provides more “pushability” across
recalcitrant lesions and may be more successful at obtaining wire
access. This is particularly true when a small invagination is
apparent angiographically in the ipsilateral common iliac artery
(when totally occluded). Once the occlusion or stenosis is
traversed, the wire can be snared from the ipsilateral femoral and
an ipsilateral sheath can still be advanced to complete the
procedure as previously described from the ipsilateral femoral
access. This is generally advisable as compared to attempted stent
placement from left brachial access, due to proximity and control
issues, as well as the availability of suitably sized stents on long
delivery catheters.
Severe calcified disease ■ In patients with significant atherosclerotic burden, care should be
strategies taken during the intervention to minimize atheroembolization. Use
of covered stent grafts can be considered in these scenarios.
Additionally, as an added benefit of the hybrid approach, flushing
maneuvers of the patch angioplasty site may be performed to
eliminate embolic debris.
Arterial rupture ■ Cover with stent graft. Consider proximal balloon occlusion.
Arterial dissection ■ Extend stent if flow limiting dissection.
POSTOPERATIVE CARE
■
Following femoral endarterectomy and iliac stents, patients are usually monitored in the hospital for
1 to 2 days.
■
Postoperative antithrombotic management is not well studied in this population; however, most
surgeons treat patients with dual antiplatelet therapy such as aspirin and clopidogrel, with a
loading dose of clopidogrel followed by a daily dose, for the first 6 weeks following the
procedure. Long-term antiplatelet management is usually achieved with acetylsalicylic acid (ASA)
alone, except in circumstances of aspirin allergy.
■
Routine follow-up with arterial duplex and ABIs is important to monitor for continued patency and
potential need for secondary intervention.
OUTCOMES
■
Early and long-term results of concomitant common femoral artery endarterectomy and iliac stenting
have been excellent. One-year primary patency and primary-assisted patency rates have been
reported to be 84% and 97%, respectively.3 Five-year primary, primary-assisted, and secondary
patency rates were 60%, 97%, and 98% in a recent report of 171 patients.4
■
There is some evidence that covered stent grafts may have improved patency compared to bare
metal stents, particularly in TASC C and D lesions.4,5
■
Iliac artery stenting combined with open femoral endarterectomy also appears to be equally
effective as open surgical revascularization. Piazza and colleagues6 found similar 30-day
morbidity and mortality as well as primary patency at 3 years when comparing a 10-year cohort of
patients treated in both manners. These similarities were maintained even after stratification for
TASC group.
COMPLICATIONS
■
Contrast nephropathy
■
Wound complications, including infection, dehiscence, seroma formation, and nerve entrapment
■
Arterial rupture
■
Arterial dissection
■
Embolization
REFERENCES
1. Rzucidlo EM, Powell RJ, Zwolak RM, et al. Early results of stent-grafting to treat diffuse aortoiliac occlusive disease. J Vasc Surg.
2003;37(6):1175–1180.
2. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II).
J Vasc Surg. 2007;45(suppl S):S5–S67.
3. Nelson PR, Powell RJ, Schermerhorn ML, et al. Early results of external iliac artery stenting combined with common femoral artery
endarterectomy. J Vasc Surg. 2002;35(6):1107–1113.
4. Chang RW, Goodney PP, Baek JH, et al. Long-term results of combined common femoral endarterectomy and iliac stenting/stent
grafting for occlusive disease. J Vasc Surg. 2008;48(2):362–367.
5. Mwipatayi BP, 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.
6. Piazza M, Ricotta JJ II, Bower TC, et al. Iliac artery stenting combined with open femoral endarterectomy is as effective as open
surgical reconstruction for severe iliac and common femoral occlusive disease. J Vasc Surg. 2011;54(2):402–411.
Chapter 27 Management of the Infected Femoral Graft
Matthew Mell

■
The symptoms of an infected femoral graft can vary widely, from a chronically draining wound to
sepsis and hemodynamic collapse.
■
Symptoms may have been present from hours to weeks.
■
Physical examination should include inspection of the surgical wounds and graft tunnels for
induration, erythema, tenderness, open wounds, aneurysmal degeneration of the graft or
anastomosis, or drainage.

■
When possible, causative organisms should be identified prior to surgery to aid in choosing
appropriate systemic antibiotics and the optimal surgical approach.
■
Prior to surgery, detailed imaging with computed tomographic angiography (CTA) can provide
critical information for developing a cohesive plan for surgical exploration and graft removal and
replacement.
■
Computed tomography (CT) can accurately identify anatomic signs of infection, including abscess or
anastomotic aneurysm. CT can also provide clues to the extent of infection.
■
CTA provides high-resolution imaging of the aorta and runoff vessels, which will aid in determining
the options for revascularization, including in situ reconstruction, obturator bypass, or ilioprofunda
bypass.
■
Radionuclide scans may provide evidence for graft infection when other imaging studies are
nondiagnostic.
SURGICAL MANAGEMENT
■
Aggressive and wide debridement of devitalized or infected tissue must accompany graft excision
and replacement in the setting of infection.
■
Partial or complete excision of infected prosthetic grafts is generally required to eliminate the
infection.
■
Excision of infected autogenous graft infections may be necessary when associated with sepsis
caused by Escherichia coli, Pseudomonas, Klebsiella, or Proteus spp.
■
Graft excision without reconstruction: Infected thrombosed grafts with adequate collateral
circulation may require only excision without reconstruction.
■
Excision and extraanatomic bypass is preferred with presence of severe sepsis and/or hemorrhage.
Examples of extraanatomic bypasses include axillary-to-femoral bypass (FIG 1), obturator
bypass, or cross-femoral bypass.
■
In situ replacement: Low-grade infections without sepsis or invasive infection and those with distal
occlusive disease may be best treated with in situ graft replacement.
■
Graft replacement material
■
Graft material should be considered prior to surgery to ensure availability.
■
Potential options for graft material include the following:
■
Autogenous vein (saphenous vein, cephalic vein, basilic vein, superficial femoral vein [SFV])
■
Cryopreserved tissue (aorto-iliac-femoral artery, femoral vein, saphenous vein)
■
Prosthetic graft (rifampin-soaked Dacron™, polytetrafluoroethylene [PTFE])
■
Consider the need for wound coverage:
■
Debridement of an infected groin wound may result in a large defect that either cannot be covered
or closed. Muscle flaps can provide coverage of healthy well-vascularized tissue to protect the
repair.
■
Small to medium defects can be covered with a sartorius muscle flap, which is divided from its
attachment to the anterior superior iliac spine and mobilized medially to cover the wound.
■
A pedicled flap from the leg or abdominal wall may be required for larger wounds. These flaps
include rectus femoris, rectus abdominis, tensor fasciae latae, or gracilis.
TECHNIQUES
GENERAL CONSIDERATIONS
■
It is desirable when considering an extraanatomic reconstruction to revascularize before excising the
infected graft. This can be accomplished with a bypass and tunnel performed across clean tissue
planes. Once the bypass is completed and wounds closed, the groin can be explored and the
infected graft removed. With this approach, the continuity between the superficial femoral and
deep femoral arteries should be maintained by either oversewing the distal common femoral artery
or anastomosing the profunda femoris artery (PFA) to the superficial femoral artery with proximal
ligation (FIG 2).
■
Debridement of the infected site must include removal of infected or necrotic tissue and complete
excision of the anastomosis. Dissection may be aided by lack of incorporation of the infected graft
but also may prove challenging from extensive scarring in the reoperative field. Sharp dissection
techniques are critical to minimizing the risk of inadvertent injury to vessels or adjacent structures.
■
It is important to send cultures of the perigraft fluid, tissue, and graft.1 Instructions should be given to
the microbiology lab to perform sonication of the graft to separate biofilm from graft and maximize
the bacteriology yield.
OBTURATOR BYPASS
■
Using the obturator foramen may be a useful approach for bypassing an infected groin through a
sterile field.2 A reinforced PTFE graft is best suited for this technique and can be used if sepsis
has been controlled and the bypass can be performed without violating the infected field.
■
The proximal anastomosis can be performed to the common iliac artery, external iliac artery
(ipsilateral or contralateral), or previous graft if not infected (FIG 3). Exposure can be obtained
through a standard retroperitoneal incision, by dividing the external and internal oblique and
transversus abdominis muscles, identifying the preperitoneal space, and retracting the peritoneum
medially with blunt dissection techniques. The obturator foramen is just posterior to the anterior
ramus of the pelvis, although it may not be easily palpated due to the overlying obturator
membrane.
■
Distal anastomosis can be performed to the distal superficial femoral artery, the midportion of the
PFA (see the following section, lateral approach to the Lateral Profunda Femoris Artery
Exposure), or the popliteal artery. During this dissection, the adductor longus and magnus can be
identified with the leg abducted and externally rotated. The tunnel will be placed deep to these
muscles, which insert on the external surface of the obturator foramen.
■
The tunnel should be performed in a cranial direction with a long aortic clamp or tunneling
instrument (FIG 4). The instrument is passed deep to the adductor magnus while a hand is placed
over the obturator foramen from the retroperitoneal incision. The instrument can be directed
through the obturator foramen. The tunnel should be made through the lateral portion of the
obturator foramen to avoid the obturator artery and nerve, which traverse anteromedially.
■
Once the tunnel is made, the graft can be placed and the bypass performed. Once completed, the
incisions should be closed and protected before proceeding with excision of the infected graft.
LATERAL PROFUNDA FEMORIS ARTERY EXPOSURE
■
Another option for remote revascularization is to use the second portion of the PFA, exposed
through a lateral incision.3 This approach may be useful if the superficial femoral artery is
occluded and the goal is to establish flow from the axillary artery via a tunnel medial to the
anterior iliac spine and lateral to the femoral infection.
■
The PFA is exposed through an incision placed along the lateral border of the sartorius muscle 4 to
6 cm below the anterior superior iliac spine (FIG 5). The sartorius and superficial femoral vessels
can be retracted medially to expose the adductor longus. Its overlying fascia is divided, and with
medial retraction, the PFA is exposed.
SUPERFICIAL FEMORAL VEIN HARVEST

■
SFV can be a suitable graft for reconstruction, with a low incidence of recurrent or uncontrolled
infection.4 Preoperative evaluation should include duplex imaging of the SFV to exclude deep
venous thrombosis and to determine the vessel diameter.
■
Dissection can be performed through a standard anteromedial leg incision, or placed over the lateral
border of the sartorius (FIG 6). The vein should be dissected from its confluence with the
profunda femoris vein distally to obtain sufficient length for reconstruction. Care should be taken
to preserve the profunda femoris vein and the common femoral vein and to stop the dissection at
the adductor canal. These limits will preserve important collateral circulation between the
profunda femoris and the popliteal vein, which will minimize postoperative leg edema.
■
Once harvested, branches of the SFV should be doubly ligated or suture ligated a distance 2 mm
from their junction with the SFV to prevent slippage of the ligature once the conduit is pressurized.
The SFV can be used in a reversed manner or nonreversed after disrupting the valves.
CRYOPRESERVED GRAFTS
■
Some studies have shown favorable results for cryopreserved allografts with regard to limb loss,
recurrent infection, and survival compared with other in situ replacements.5
■
When considering an allograft, greater than 24 hours may be required to locate suitable graft
material and length if there is no on-site inventory.
■
Grafts should be prepared immediately before implantation. The thaw-and-rinse process takes
approximately 45 minutes.
■
Ligated braches should be tested for hemostasis and suture ligatures placed if necessary. If using an
aortoiliac homograft, it is easier to confirm hemostasis if the graft is placed with the lumbar
branches facing anterior.
■
Graft length should allow for a tension-free anastomosis. When possible, avoid allograft-to-allograft
anastomoses.
PEARLS AND PITFALLS

Preoperative considerations ■ When possible, consideration should be made prior to surgery for
the best option(s) of graft material, allowing time to obtain it if
required. For autogenous vein, preoperative duplex is essential to
determine the size and quality of the proposed conduit.
Proximal and distal vessel ■ When possible, proximal and distal vessel control should be
control obtained through extension of the original incision or through
separate incisions before dissecting the infected vessels. Remote
bypass with subsequent removal of infected material may be
preferable to in situ repair.
Intraoperative cultures ■ It is important to obtain Gram stain, aerobic, and anaerobic
cultures of the perigraft fluid, perigraft tissue, and graft. The yield
of the graft will be increased if sonication of the graft is
performed in the microbiology lab prior to incubation.
Tunnels ■ Tunnels, when possible, should be placed in sterile fields.
Systemic antibiotic treatment ■ Broad-spectrum antibiotics should be initially considered for
patients with severe sepsis. For those without sepsis, blood and
wound cultures should be performed prior to starting antibiotics.
Initial antibiotics should include coverage for methicillin-resistant
Staphylococcus aureus (MRSA). After surgery, parenteral
antibiotics should be considered for 4–6 weeks, especially for
invasive infections or in situ repair.
POSTOPERATIVE CARE
■
Antibiotics should be continued for at least 2 to 6 weeks, depending on the type of organism, and
should be chosen based on antimicrobial sensitivity when available.
■
Patients should be inspected daily for signs of infection, which may include fever, leukocytosis,
erythema or drainage from the wound, or wound breakdown. Persistent infection should trigger
consideration of wound exploration and reevaluation of the antibiotic regimen.
■
Drains, if placed, should be removed as soon as possible, based on quantity and appearance of
fluid. Ongoing purulent drainage or continued fever and leukocytosis may indicate lack of source
control, which may require wound exploration and washout.
■
Arterial surveillance should be performed prior to discharge to confirm the integrity of the repair
and establish a baseline for future surveillance examinations.
COMPLICATIONS
■
Bleeding from the wound should raise immediate concerns of arterial disruption from persistent
infection leading to tissue destruction. If present, patients should undergo arterial duplex and be
considered for reexploration. Under these circumstances, complete evaluation of the arterial
reconstruction (even if remote) is advisable as vascular resection and reconstruction may be
required. At times, arterial ligation may be the only option for local control of sepsis.
■
If not already performed, patients requiring reexploration and debridement for persistent infection
will most often benefit from muscle flap coverage of the defect.
REFERENCES
1. Bandyk DF, Bergamini TM, Kinney EV, et al. In situ replacement of vascular prostheses infected by bacterial biofilms. J Vasc
Surg. 1991;13(5):575–583.
2. Pearce WH, Ricco JB, Yao JS, et al. Modified technique of obturator bypass in failed or infected grafts. Ann Surg.
1983;197(3):344–347.
3. Bridges R, Gewertz BL. Lateral incision for exposure of femoral vessels. Surg Gynecol Obstet. 1980;150(5):732–733.
4. Smith ST, Clagett GP. Femoral vein harvest for vascular reconstructions: pitfalls and tips for success. Semin Vasc Surg.
2008;21(1):35–40.
5. Kieffer E, Gomes D, Chiche L, et al. Allograft replacement for infrarenal aortic graft infection: early and late results in 179 patients.
J Vasc Surg. 2004;39(5):1009–1017.
Chapter 28 Surgical Exposure of the Lower Extremity Arteries
Luke X. Zhan Joseph L. Mills, Sr.
DEFINITION
■
Chronic lower extremity ischemia, also known as peripheral artery disease (PAD), is a common
condition managed by vascular specialists. The primary etiology is atherosclerosis.
Atherosclerotic stenosis or occlusion of the peripheral arterial tree results in arterial insufficiency
and end-organ (limb) ischemia. PAD is a major contributor to morbidity, reduced quality of life
(QOL), and mortality in an increasing elderly demographic in the Western world.
■
The challenge for the vascular specialist is to determine whether the nature and severity of
presenting symptoms correlate with the degree of chronic arterial insufficiency present or whether
alternative etiologies, such as neuropathy, inflammation, infection, lymphatic or venous disease,
and repetitive trauma, are more likely responsible. Definitive diagnosis is derived from detailed
historic and physical examination findings correlated with appropriately directed noninvasive
vascular laboratory and adjunctive imaging studies.

■
Patients with PAD may present with a spectrum of symptoms ranging in severity from none to
varying degrees of claudication to severe or “critical” limb ischemia (“CLI” = ischemic rest pain,
ulceration, and gangrene). Pulse palpation is an integral component of the physical examination.
Femoral, popliteal, posterior tibial, and dorsal pedal pulses should be noted and graded (0 =
absent; 1 = present but diminished; 2 = normal; 3 = enlarged, aneurysmal). Claudication is defined
as muscular pain, cramping, aching, or discomfort in the lower limb, reproducibly elicited by
exercise and relieved within 10 minutes of cessation. CLI has been traditionally defined as (1)
persistent, recurring ischemic rest pain requiring opiate analgesia for more than 2 weeks and (2)
ankle systolic pressure less than 50 mmHg or toe systolic pressure less than 30 mmHg (or absent
pedal pulse in patients with diabetes).1 Ischemic rest pain typically is nocturnal, worsens with
elevation, and is relieved by dependency. Pedal pulses are absent; dependent rubor, elevation
pallor, and calf muscle atrophy are frequent accompaniments. CLI also includes ischemic foot
ulceration and gangrene in the setting of ankle systolic pressure less than 50 to 70 mmHg or toe
systolic pressure less than 40 mmHg in patients without diabetes (<50 mmHg in diabetics).
SURGICAL MANAGEMENT
Indication
■
All patients with PAD require comprehensive medical management and risk factor modification.
Revascularization (either open bypass or endovascular intervention) is indicated in patients who
remain symptomatic and significantly limited despite adequate risk factor modification, exercise,
and medical management. The primary goal of intervention, in patients with lifestyle-limiting
claudication, is to improve exercise tolerance and hence QOL. Patients with rest pain, tissue loss,
and gangrene are at greater risk for limb loss and cardiovascular mortality (stroke, myocardial
infarction) associated with systemic atherosclerosis than those who present with claudication
alone. Revascularization in the CLI cohort is focused on wound healing and functional limb
salvage as well as symptomatic relief and improvement in QOL.2,3
Preoperative Planning: Imaging and Risk Assessment/Mitigation
■
The vascular specialist must first determine, given the underlying disease burden, the severity of
ischemic and infectious complications as well as the patient’s comorbidities, functional status, and
anticipated longevity. Once it is decided that revascularization will improve the patient’s
functional status and QOL, these same variables, in concert with anatomic assessment of the
location, extent, and severity of occlusive arterial lesions will determine whether endovascular,
open, or hybrid revascularization options are indicated. When bypass is selected as the preferred
revascularization option, the goals of preoperative planning involve delineation of diseased
arterial segment(s), identification of the most appropriate arterial inflow source, selection of the
optimal bypass target for maximal outflow and target bed perfusion, and selection of the best
available conduit. In practice, conduit availability is almost always a critical, rate-limiting factor
because good quality, autogenous vein conduit is preferred in almost every circumstance.
■
Adequate preoperative planning depends on a thorough history and detailed physical examination.
■
The delineation of the relevant arterial anatomy on the index limb is facilitated by high quality,
noninvasive vascular laboratory studies (ankle–brachial index and toe pressure measurements).
These are supplemented by arterial color duplex ultrasound imaging. Arterial duplex is extremely
accurate in the assessment of iliofemoral and femoropopliteal arterial occlusive disease but less
so for infrageniculate (tibial–peroneal) lesions. Duplex enables differentiation of stenosis from
occlusion and determination of lesion length and degree of calcification. Cross-sectional imaging
studies such as computed tomography angiography (CTA) or magnetic resonance arteriography
(MRA) may add complementary information, but most experienced operators prefer the precision
and resolution inherent in catheter-based, intraarterial contrast arteriography for definitive
preoperative planning, especially when bypass will be required to distal calf or pedal targets.
■
PAD is a coronary artery disease equivalent. Therefore, preoperative risk evaluation for overall
cardiovascular-related mortality represents a component of preoperative planning. In most patients
with stable or minimally symptomatic coronary disease, preoperative risk-reduction efforts are
best focused on optimizing medical management. Frequently, this includes statin and antiplatelet
therapy, β-blockade, and optimization of hypertension management.
■
The surgical plan should be tailored to each patient’s needs based on extent of disease, conduit
availability, and realistic long-term functional potential. Infrainguinal bypass may originate from
the common, superficial, or deep femoral artery or the popliteal artery with a bypass target of the
popliteal, tibial, or pedal/plantar arteries. The positioning, choice of incisions, and surgical
techniques are dictated by type of bypass procedure deemed most appropriate under the
circumstances.
TECHNIQUES
■
Refer to references 4 through 9 for this section.
FEMORAL VESSEL EXPOSURE

Positioning
■
The patient is placed in supine position. A Foley catheter is inserted. Arms may be tucked to
facilitate intraoperative prebypass and completion angiography.
■
The common femoral artery (CFA) is located on a line between the pubic tubercle and anterior iliac
spine, two fingerbreadths lateral to pubic tubercle. Palpation of the inguinal ligament and femoral
pulse or direct arterial visualization with duplex imaging can localize the CFA bifurcation and
guide optimal incision placement. Even when pulseless due to excessive calcification or occlusive
disease, the CFA may be localized by reliance on anatomic landmarks and direct palpation,
recognized as a firm tubular structure positioned within the femoral sheath.
■
The vertical groin incision is most commonly employed to provide optimal access to the entire
length of the CFA. This should be created coaxially along the artery itself, continued from the
inguinal ligament distally, and aimed at the medial aspect of the knee. The incision can be extended
superiorly or inferiorly to increase arterial exposure as necessary to achieve optimal inflow (FIG
1, dashed line A).
■
Alternatively, especially in obese patients with substantial abdominal pannus, a curvilinear incision
can be placed 1 cm below and parallel to the inguinal ligament to avoid potential skin maceration
and wound complications that may accompany vertical incisions in this situation (FIG 1, dashed
line B). Although the proximal superficial femoral and deep femoral arteries can be exposed via
this incision, such a curvilinear or oblique incision limits further distal arterial exposure. It
therefore would not be selected if an extensive common and deep femoral artery endarterectomy is
anticipated as potentially necessary to optimize inflow.
■
The incision is carried sharply through the subcutaneous tissue and superficial fascia.
Dissection and Control of the Common, Superficial, and Proximal Deep Femoral Arteries
■
Deep to the subcutaneous tissue and superficial fascia, the dissection is extended longitudinally,
even when using an oblique incision, to optimize the length of femoral exposure. Depending on the
depth of dissection and subcutaneous adiposity, self-retaining Weitlaner or cerebellar retractors
are carefully placed to optimize exposure while avoiding traction injury to femoral nerve branches
or the common femoral vein. Further dissection through the femoral sheath exposes the anterior
surface of the femoral artery.
■
The dissection plane should remain centered directly over the femoral artery. Encountering venous
structures indicates medial deviation from the optimal plane; exposure of the iliopsoas muscle,
femoral nerve fibers, or lymphatic vessels is an indication of lateral deviation. An increasing
incidence of femoral incisional complications, including wound edge necrosis and separation,
lymphatic leaks, femoral neuropraxia, and venous injuries are associated with incorrectly placed
inguinal incisions for femoral exposure.
■
Dissect directly along the CFA both proximally and distally. Placement of silastic vessel loops
around the femoral artery and its larger branches aids in retraction, dissection, and mobilization.
■
Proximal dissection is continued along the CFA to the inguinal ligament. The inguinal ligament may
be divided to aid in exposure or to enable extended endarterectomy. Caution is necessary in this
area, as a prominent femoral vein tributary crosses anteriorly over the CFA in this area and is
prone to injury if not identified, ligated, and divided early in the dissection. Inadvertent injury to
this “vein of pain” produces retraction and troublesome bleeding. The medial and lateral femoral
circumflex arteries, important collaterals in iliofemoral arterial occlusive disease, are identified at
level of the inguinal ligament and individually controlled with removable clips or silastic vessel
loops. Use of the former reduces clutter in the wound during endarterectomy or creation of the
proximal anastomosis.
■
As the dissection proceeds distally, an abrupt change in caliber marks the femoral bifurcation and
the origins of the deep (also known as “profunda femoris” in Latin) and superficial femoral
arteries (SFA). The latter continues distally in the same plane; the former usually courses
posteriorly and laterally away from the femoral bifurcation. After silastic loops are placed on each
vessel, gentle upward traction on the CFA or SFA may help bring the deep femoral artery into
view. The lateral circumflex iliac vein may course anteriorly over the origin of the deep femoral
artery and should be ligated and divided to optimize exposure and control of the first segment of
this vessel (FIG 2A).
■
Medial and distal dissection provides extended exposure of the proximal SFA (FIG 1, dashed line
F). This vessel only occasionally has small branches in its proximal segment. A sensory branch of
the femoral nerve may be present crossing the SFA from lateral to medial. Transection may result
in medial thigh discomfort. Even extended femoral bifurcation dissections rarely require division
of femoral nerve branches, which should be avoided to minimize postoperative paresthesias and
dysesthesias.
Exposure of the Middle and Distal Segments of Deep Femoral Artery
■
Exposure of the distal portions of the deep femoral artery often enables use of shorter vein conduit
in distal leg bypass or may improve outflow from proximal revascularization procedures (iliac
angioplasty and stenting or aortofemoral bypass). These segments are easily exposed from either
posteromedial or anteromedial approaches (FIG 1, dashed line C–F). The approach should be
dictated by the indication (inflow sources or outflow target); an additional consideration is the
necessity to obtain exposure in a native field, either in the setting of prior dissection or femoral
graft infection.
■
Incisions are placed along either the medial (anteromedial approach; dashed line C and F in FIG 1)
or lateral borders (posterolateral approach) of the sartorius muscle (FIG 1, dashed line D and E).
The dissection plane is developed through the subcutaneous tissue and fascia, passing lateral or
medial to the sartorius, respectively. Mobilize and retract sartorius muscle laterally or medially,
depending on approach.
■
The dissection is continued posteriorly, passing lateral to the superficial femoral vessels and
accompanying nerve, to the space between the adductor longus muscle (medially) and vastus
medialis (laterally) (FIG 2B, incisions C–E). The deep femoral artery and vein pass directly
underneath.
■
Dissection between adductor longus and vastus medialis muscle exposes the middle segments of the
deep femoral artery. Crossing venous tributaries should be ligated and divided as necessary to
provide optimal exposure. The more distal segments of deep femoral artery begin to course
posterior to the femur beyond this point and are therefore less useful for bypass origination or
destination.
■
Alternatively, exposure between the adductor longus (anteriorly) and gracilis muscle
(posteromedially) enables medial exposure of the deep femoral artery in the distal thigh (FIG 1,
dashed line F; FIG 2B, incision F).
POPLITEAL ARTERY EXPOSURE

Medial Exposure of the Above-Knee Popliteal Artery
■
Place patient in supine position. Rotate leg laterally, flex the leg, and place a bump underneath the
knee joint.
■
Place a 10- to 12-cm longitudinal incision along the groove formed between the edges of the vastus
medialis (anteriorly) and the sartorius muscles (posteromedially) (dashed line A in FIG 3A). The
incision is carried through the subcutaneous tissue and fascia. Place self-retaining retractor. Take
care not to trap and injure the great saphenous vein and the saphenous nerve. The great saphenous
vein is likely to be encountered more posteromedially to the incision in the subcutaneous tissue.
The saphenous nerve may be encountered at distal end of the incision as it joins the saphenous vein
near the medial aspect of the knee.
■
Incise the deep fascia longitudinally and above the sartorius muscle to enter the popliteal fossa. The
popliteal artery can be palpated up against the posterior surface of the femur (FIG 3B).
■
The popliteal artery is often surrounded by multiple venous collaterals, or “venae comitantes” in
Latin; the popliteal vein is usually posterolateral to the artery in this location. The popliteal and/or
superficial femoral veins may be duplicated throughout the popliteal fossa and distal thigh.
Isolation and control of the artery usually requires ligation and division of surrounding collateral
veins.
Lateral Exposure of the Above-Knee Popliteal Artery
■
Lateral exposure of the above-knee (AK) popliteal artery is useful in a variety of circumstances—
for instance, axillopopliteal bypass or when the medial approach has previously been developed
or is complicated by infection or injury.
■
Place patient in supine position. Rotate leg medially, flex the knee, and place a bump underneath the
knee joint.
■
Place 10- to 12-cm longitudinal incision between the vastus lateralis and the biceps femoris muscles
(dashed line A in FIG 4A). The incision is carried through the subcutaneous tissue and fascia.
■
Make a generously cruciate incision (“T-ed”) at both ends on the fascia lata to prevent bypass graft
impingement by its dense fibers.
■
Place retractor and enter the popliteal space. Sciatic nerve then popliteal vein will be encountered
first before popliteal artery. Gently retract sciatic nerve downward. Then mobilize and retract
popliteal vein to expose and control the popliteal artery.
Posterior Exposure of the Popliteal Vessels
■
Posterior exposure may be the preferred approach for management of popliteal artery entrapment,
popliteal cyst, focal popliteal artery aneurysm, or arterial injury following traumatic posterior
knee dislocation. Although direct and relatively uncomplicated, posterior access is limited by the
heads of the gastrocnemius muscle distally and the biceps femoris/“hamstring” muscles
proximally; only focal, limited popliteal artery access is achievable through this incision.
■
Patient is placed in prone position with pillow to prop up the lower leg and foot.
■
The incision is S-shaped, across the posterior crease of the knee joint, with its superior extent
beginning medially.
■
The incision is carried anteriorly through the subcutaneous tissue and superficial fascia to enter the
popliteal fossa. Exposure is maximized by mobilizing the popliteal artery between the two heads
of the gastrocnemius muscle inferiorly and between semimembranosus and biceps femoris muscle
superiorly.
■
The muscles are gently retracted to expose the entire popliteal fossa. The tibial and common
peroneal nerves are encountered superficially in this exposure. The popliteal artery is anterior, or
deep to the vein, in the depths of the wound.
■
It may be necessary to mobilize the popliteal vein with ligation and division of popliteal venous
tributaries to fully expose the artery. Once the appropriate segment is exposed, silastic vessel
loops are placed proximally and distally.
INFRAGENICULAR EXPOSURE
Medial Exposure of the Infragenicular Popliteal Artery and Its Branches
■
The most common approach is a medial one (FIG 3A).
■
Place patient in supine position. Rotate leg laterally, flex the leg, and place a bump underneath the
knee joint.
■
Make a longitudinal incision from below the edge of the tibia along the course of the great
saphenous vein (dashed line B in FIG 3A).
■
Carry the incision through subcutaneous tissue and fascia into the deep posterior compartment. The
below-knee (BK) popliteal vessels reside deep in the wound and are partially covered by the
origin of the soleus muscle.
■
Division of the soleus origin medially (FIG 3C) will facilitate exposure of the tibioperoneal trunk,
and origin of the anterior tibial artery, but is not really necessary for exposure of the popliteal
artery itself. As was described for the posterior approach, the artery lies in close proximity to the
popliteal vein and tibial nerve. Mobilization of the popliteal vein from the adjacent artery is
necessary for sufficient exposure of all relevant structures, including the anterior tibial artery,
tibioperoneal trunk, and derivative branches (posterior tibial and peroneal arteries). It is usually
necessary to ligate and divide the anterior tibial vein at its confluence with the (often paired)
popliteal vein to gain sufficient exposure to isolate and mobilize the more distal branches.
■
Dissection must proceed deliberately to avoid injury to the neighboring tibial nerve and its distal
branches.
Lateral Exposure of the Infragenicular Popliteal Artery and Its Trifurcation
■
The lateral approach is rarely required but may be particularly useful to avoid scarring from a
previous medial approach.
■
Place the incision posterior to the head of the fibula and extend along the course of the fibula.
Dissect directly onto fibula (incision is marked as dashed line B in FIG 4A). Note the location of
the common peroneal nerve, which courses from posterior to anterior around the neck of the upper
fibula just below its head, before it branches into the superficial and deep peroneal nerves.
■
Circumferentially elevate the periosteum of the fibula and excise the exposed segment of the fibula
with a saw. The popliteal vessels and branches are found directly beneath the fibular periosteum,
with the artery usually located anterior to the posterior tibial nerve and the popliteal vein.
■
Extending the dissection distally allows exposure and control of distal popliteal artery, as well as
the origins of the anterior tibial and the tibioperoneal trunk.
Exposure of the Anterior Tibial Artery
■
Proximal segment
■
The proximal segment of the anterior tibial artery is exposed in a fashion similar to the exposure
for the infragenicular popliteal artery and its branches.
■
Middle segment
■
The middle segment exposure of the anterior tibial artery is useful when there is limited length of
autogenous vein.
■
Place an axial incision in a vertical plane about two fingerbreadths lateral to the anterior edge of
the tibia (FIG 5A).
■
Deepen the incision between the tibialis anterior and the extensor hallucis longus muscles.
■
The anterior tibial artery is superficial to the interosseus membrane between the cleft formed by
these two muscles.
■
Dissecting away the overlying collateral veins allows exposure and control of the middle segment
of the anterior tibial artery. Use of a proximal sterile tourniquet during exposure of all the crural
arteries may significantly accelerate the dissection while limiting bleeding from the numerous
and redundant collateral veins.
Exposure of the Posterior Tibial Artery
■
Proximal segment
■
The proximal segment of the posterior tibial artery is approached in a similar fashion to the
exposure for the infragenicular popliteal artery and its branches and requires taking down the
soleus muscle from the tibia.
■
Middle segment
■
The middle segment exposure of the posterior tibial artery is useful when there is limited length
of vein graft to bypass to the posterior tibial artery.
■
Incision is made just anterior to the soleus muscle. Divide the overlying soleus to expose the
underlying vessels (FIG 5B).
■
The posterior tibial artery lies anterior to soleus muscle with the peroneal artery located
laterally, in the same plane, between the soleus and tibialis posterior muscles.
■
Avoid injury to the tibial nerve, which commonly runs between the posterior tibial and peroneal
vessels.
Exposure of the Peroneal Artery
■
Proximal and middle segments
■
Exposure of the proximal segment of the peroneal tibial artery is via distal extension of the
infragenicular popliteal artery approach.
■
Middle segment
■
The middle segment may also be approached anterolaterally. The following description relates to
lateral exposure requiring fibulectomy.
■
Place a vertical incision over the fibula at the desired level (FIG 5C).
■
Carry down the incision through the overlying muscle down to the fibula. Elevate the periosteum
of the fibula circumferentially.
■
Transect the overlying segment of fibula. Incise the inner periosteal membrane. The peroneal
vessels are found immediately beneath. The artery usually is anterior to flexor hallucis longus
and posterior to the tibialis posterior muscles.
■
The peroneal artery is exposed and controlled after mobilization from circumferential collateral
veins and the main peroneal vein.
EXPOSURE OF PEDAL VESSELS

Exposure of the Inframalleolar Posterior Tibial Artery
■
Distal posterior tibial exposure enables pedal bypass at or below the ankle, which may be
especially useful in patients with advanced diabetes.
■
Make a longitudinal incision through skin and fascia at the midpoint between the medial malleolus
and the Achilles tendon. If this exposure is used for an in situ bypass procedure, the incision
should be sighted slightly more anteriorly to accommodate the anterior course of the great
saphenous vein as it crosses the medial malleolus.
■
Identify and divide the flexor retinaculum as needed to provide optimal exposure. The posterior
tibial vessels are located between the flexor digitorum longus and flexor hallucis longus
muscles/tendons.
■
Place a small Weitlaner self-retaining retractor. The neurovascular bundle is usually enveloped by
fatty tissue below the fascia.
■
Dissection proceeds along the neurovascular bundle. The posterior tibial artery is usually anterior to
the tibial nerve. There is typically a rich network of venous collaterals present. These may either
be mobilized or (more commonly) divided to facilitate distal posterior tibial artery exposure.
■
When more distal bypass targets are needed (e.g., prohibitive burden of disease in the posterior
tibial artery itself), the dissection may be continued along the posterior tibial artery distally to the
bifurcation of the medial and lateral plantar arteries. In all such cases, however, preoperative
imaging is paramount to immediate and long-term surgical success, and only in rare circumstances
should the operative plan be changed by unexpected findings at the time of surgery. The presence
of luminal calcification alone, without substantial compromise to the target lumen diameter, is not
a contraindication to bypass construction. When uncertainty is present regarding the optimal bypass
target despite adequate preoperative imaging, consideration should be given to on-table,
intraoperative arteriography to guide surgical decision making and confirm outcome. To this end,
we perform all open bypass procedures in a hybrid operating room environment with high-quality
imaging capabilities to ensure the optimal outcome of all procedures, regardless of the initial
operative plan.
Exposure of the Supramalleolar Anterior Tibial Artery
■
The distal anterior tibial artery may serve as a suitable distal bypass target, especially when
substantial disease is present more proximally. It may also be preferable to bypass to this segment
in the presence of a dorsal foot wound.
■
The incision is placed between the tibialis anterior medially and extensor hallucis longus and the
extensor digitorum longus laterally (FIG 6B).
■
Anterior tibial artery and peroneal nerve usually course through the groove between them.
■
Dissect between these tendons and retract them to expose the supramalleolar segment of anterior
tibial artery.
Exposure of the Dorsal Pedal Artery
■
The dorsal pedal artery (or “dorsalis pedis” in Latin) is the extension of the anterior tibial artery as
it passes beneath the extensor retinaculum. It can serve as a suitable distal bypass target, especially
in patients with diabetes.
■
The artery is best exposed beyond the inferior extensor retinaculum. Place an incision between the
1st and 2nd metatarsal shafts and distal to the extensor retinaculum (FIG 6B).
■
The dorsalis pedis artery resides in the groove between the 1st and 2nd metatarsal heads, usually
just lateral to the extensor hallucis longus tendon, which is readily identified by dorsiflexion of the
great toe, and medial to extensor hallucis brevis.
■
Carry down dissection through subcutaneous tissue and longitudinally divide the fascia to expose
and control the artery.
PEARLS AND PITFALLS
■ Preoperative ultrasound duplex mapping aids the selection and placement of the incision.
Dissection can be guided by palpation of the underlying arterial pulse. In most cases, because
distal pulses are frequently absent or difficult to palpate, use of an intraoperative Doppler probe
will aid the localization and dissection of vessel. Nonetheless, knowledge of appropriate
anatomic landmarks will greatly facilitate careful and expeditious exposure. In all circumstances,
dissection should be directly targeted on and around the artery. This guidance is similar in many
ways to the orthopedic axiom to “stay on the bone” during dissection—keeping exposure
centered on the target artery minimizes venous bleeding and damage to surrounding structures.
Placement of an encircling silastic vessel loop will aid in further mobilization.
■ In the exposures of the thigh arteries, the sartorius muscle serves as an important landmark for the
exposure of the common, superficial, and profunda femoral arteries.
■ In the setting of reoperation, alternative surgical exposures allow operation in a virgin field that
is unscarred by previous operation.
COMPLICATIONS
■
Bleeding complication: Aim to achieve satisfactory hemostasis for surgical bleeding prior to skin
closure. Full anticoagulation from heparin can be reversed with protamine to reduce the risk of
postoperative bleeding.
■
Vessel injury: Vascular clamps or silastic loops can lift atherosclerotic plaques and create
dissection and arterial injury in the presence of arterial calcification. The vascular clamp should
be placed at a relatively soft, disease-free segment. Occasionally, this requires lateral positioning
of a clamp to provide anterior/posterior rather than lateral compression of a vessel. In the CFA,
the accumulation of significant posterior plaque often mandates modification of “atraumatic”
clamp placement. In the tibial vessels, care should be taken to obtain control in the least traumatic
fashion possible to limit compression of inelastic runoff vessels and the potential for clamp injury
and restenosis. Often, alternative devices such as “flow arresters” or intraarterial no. 2
embolectomy catheters attached to stopcocks may provide sufficient control to maintain a
hemostatic field during completion of the distal anastomosis without exerting undue force on the
target artery. In any extent, pressure is reduced to begin with in distal tibial arteries, so the amount
of force exerted to obtain control should be modified accordingly. As previously mentioned,
strategic use of proximal thigh tourniquets and Esmarch bandage, deployed following creation of
the proximal anastomosis and graft tunneling, may also be useful in limiting bleeding and the risk
of clamp injury and dissection in diseased tibial vessels.
■
Distal embolization: Most frequently, periprocedural embolization is due to fragmentation of
atherosclerotic plaque fragments or thrombus during dissection or clamping. Full systemic
anticoagulation with intravenous (IV) heparin prior to clamping the vessel and intraoperative
monitoring of active coagulation time (ACT) will minimize the risk of graft or native vessel
thrombosis. Prior to closure of arteriotomy and clamp release, all involved arteries must be
meticulously and repeatedly flushed and back-bled to remove residual thrombus or loosen plaque
fragments. Attention to this portion of the procedure, as well as to the precise course of graft
tunneling, will optimize outcome and eliminate the need for reanticoagulation, embolectomy, and
revision at the end of an often long procedure.
■
Nerve injury: Nerves and vessels are often intimately associated. Nerve injury can be caused by
dissection, a poorly placed retractor, injudicious spreading and clamp placement, and thermal
energy from the electrocautery. These injuries can be reduced by knowledge of appropriate
anatomic landmarks, accurate incision placement, and meticulous sharp dissection directly down
to and immediately around the intended artery. Importantly, excessively deep placement of self-
retaining retractors in an extended common or deep femoral artery exposure can cause traction
injuries to motor branches of the femoral nerve, significantly limiting the ability of patients to
stand or bear weight for weeks following the procedure. In general, to avoid nerve injury,
retractors should be placed in the most superficial plane possible to obtain sufficient exposure of
target vessels. In all circumstances, retractors should be removed immediately as soon as they are
no longer needed or if attention is turned to alternative sites or other portions of the procedure that
do not require continuous exposure.
■
Lymphatic leakage: Lymphatic vessels usually course close to the arteries and veins. Avoid
transection of lymph nodes. If necessary, cauterize the divided end of lymphatics. Visible
lymphatic vessels should be suture ligated. Careful dissection respecting tissue planes allows
layered closure to eliminate dead space and lymphatic accumulation, formation of seroma, or
hematoma. When lymph nodes are injured, extra time should be taken to control, ligate, and divide
afferent and efferent vessels and remove the node completely.
POSTOPERATIVE CARE
■
Following bypass, patients should be maintained on a comprehensive medical regimen to optimize
their cardiopulmonary status. Lower extremity bypass operations are often performed on patients
with diabetes and debilitating symptoms of claudication or CLI. Postoperative care should also
aim to optimize nutritional status, functional status, and control of blood sugar level.
■
Most surgeons routinely employ routine antiplatelet and selective anticoagulation therapy to
improve graft patency in lower extremity bypass patients. The Dutch Bypass Oral Anticoagulants
or Aspirin (BOA) trial suggested that oral anticoagulation improved vein graft patency compared
with aspirin, whereas aspirin improved prosthetic graft patency compared with anticoagulation.
The antiplatelet and/or anticoagulation regimen must be tailored to individual patient with lower
extremity bypass considering their risk for graft failure and risk of bleeding. We routinely
administer aspirin to bypass patients and reserve warfarin for high-risk situations (redo bypass,
marginal or alternative vein conduits, spliced vein grafts, poor outflow, prior graft thrombosis)
due to the increased bleeding risk associated with anticoagulation.
■
Wound care: Considerable efforts on wound care are required to achieve wound healing after lower
extremity revascularization in patients with CLI with tissue loss. Meticulous nursing care and early
ambulation are also crucial to prevent decubitus ulcer in the lower extremities and the sacrum,
creating new wounds in patients with lower extremity ischemia.
OUTCOMES
■
Outcomes of revascularization should be reported and interpreted through the reporting standards
created and updated by the Society for Vascular Surgery.
■
In general, autogenous vein conduits are superior to all others for infrainguinal bypass, even for the
AK popliteal insertion site, where vein has proven superior to polytetrafluoroethylene (PTFE)
beyond 2 to 3 years. Ipsilateral and contralateral greater saphenous vein (GSV) conduits exhibit
patency rates superior to alternative veins such as small saphenous vein, arm vein, and spliced
veins. Vein graft primary patency rates for femoral BK popliteal bypasses are approximately 70%
to 75% at 5 years, and assisted primary patency can be improved even further by a duplex vein
graft surveillance protocol. Infrapopliteal vein graft primary patency rates range from 60% to 70%
at 5 years. Multiple randomized trials have shown no benefit of reversed versus in situ vein
configurations. PTFE grafts have acceptable short- and intermediate-term patency rates only in the
AK popliteal position and therefore should only be used in limb salvage situations if autologous
vein is truly unavailable. When PTFE must be used, an adjunctive venous Miller cuff or Taylor
patch may improve results. The primary factors influencing graft patency are indication, conduit
type, and conduit quality. Poor runoff adversely impacts prosthetic graft patency.
■
The reader is further referred to standard textbook sources such as Cronenwett et al.’s Rutherford’s
Vascular Surgery, 7th edition, Chapter 109 for a more detailed discussion of the expected
outcomes after surgical revascularization for infrainguinal disease.
REFERENCES
1. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-society consensus for the management of peripheral arterial disease (TASC II). J
Vasc Surg. 2007;45(suppl S):S5–S67.
2. Mills JL. Infrainguinal bypass. In: Cronenwett JL, Johnston KW, Rutherford RB, eds. Rutherford’s Vascular Surgery. 7th ed.
Philadelphia, PA: Saunders/Elsevier; 2010:1682–1703.
3. London NJM. Surgical intervention for lower extremity arterial occlusive disease: femoropopliteal and tibial interventions. In: Hallett
JW, Mills JL, Earnshaw J, et al, eds. Comprehensive Vascular and Endovascular Surgery. 2nd ed. Philadelphia, PA: Mosby,
Inc; 2009:192–214.
4. Netter FH. Atlas of Human Anatomy. 5th ed. Philadelphia, PA: Saunders/Elsevier; 2010.
5. Ouriel K, Rutherford RB. Atlas of Vascular Surgery : Operative Procedures. Philadelphia, PA: Saunders; 1998.
6. Rohen JW, Yokochi C, Lutjen-Drecoli E. Color Atlas of Anatomy: A Photographic Study of the Human Body. 7th ed.
Baltimore, MD: Lippincott Williams & Wilkins; 2011.
7. Zarins CK, Gewertz BL. Atlas of Vascular Surgery. New York, NY: Churchill Livingstone; 1989.
8. Mills JL, ed. Management of Chronic Lower Limb Ischemia. London, United Kingdom: Arnold Publishing Inc and New York,
NY: Oxford University Press; 2000.
9. Mills JL, Lucas LC. Reversed vein bypass grafts to popliteal, tibial and peroneal arteries. In: Fischer JE, ed. Mastery of Surgery.
6th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.
Percutaneous Femoral–Popliteal Reconstruction
Chapter 29 Techniques: Reentry Devices
Danielle E. Cafasso Peter A. Schneider
DEFINITION
■
Reentry devices facilitate true lumen reentry after subintimal recanalization for endovascular
treatment of complex lesion morphologies and occlusions in the femoral–popliteal segment.
■
Subintimal recanalization and reconstruction of the femoral and popliteal arteries have diminished
reliance upon femoral–popliteal bypass. Reentry into the true lumen can be challenging and is
often the rate-limiting factor for the success of this procedure. Improved wires and support
catheters, and also reentry devices, have been developed for crossing chronic total occlusions
(CTOs).
■
Tools for managing CTOs are listed in Table 1. CTO support catheters may be used to support the
guidewire that is being used to cross the occlusion. These typically have lubricious surface and a
stiff tip. Distal access may be used to recanalize infrainguinal occlusions from a retrograde
direction. Reentry catheters may be used to reenter the true lumen. CTO crossing catheters are not
discussed in the chapter. These are relatively new and use either mechanized or hand power to
manipulate through an occlusion in hopes of remaining in the true lumen.
■
Planning and performing subintimal recanalization and reentry into the true lumen of the femoral and
popliteal arteries are described herein.

■
Patients with clinical symptoms and signs of lower extremity ischemia may benefit from subintimal
recanalization and the use of reentry techniques in the course of their clinical care.
■
Patients present with claudication, rest pain, nonhealing ischemic ulcers, or gangrene. The history
and physical examination is consistent with these lower extremity presentations and is described
elsewhere in this atlas.

■
Patients who might benefit from subintimal recanalization and reentry typically have complex lesion
morphology, such as arterial occlusion, that may be managed by creating a new channel outside of
the potential space offered by the subintimal area. Imaging studies that define the anatomy and
lesion morphology are useful prior to revascularization. This may include duplex scanning,
magnetic resonance angiography, or computerized tomographic angiography. We usually perform
duplex mapping prior to any lower extremity intervention. Long lesions, occlusions, and complex
lesions are typically identifiable with preoperative imaging.
■
Patients with lower extremity ischemia should have objective physiologic confirmation of the
degree to which perfusion is diminished. This may be accomplished by ankle–brachial indices or
toe pressures.
SURGICAL MANAGEMENT
■
Preoperative planning includes identifying the best access site for arterial entry. Subintimal
recanalization of the femoral–popliteal segment may be performed using an up and over approach,
from the contralateral common femoral artery, or using an antegrade approach from the ipsilateral
common femoral artery. A reentry catheter may be used through either of these access choices.
Preoperative noninvasive imaging is very helpful in making this plan for approach.
■
The location of lesion helps determine access site and approach. Many patients with superficial
femoral artery (SFA) and/or popliteal artery disease are treated with an up and over approach. If
the patient has inflow iliac artery disease or has an SFA lesion that begins near the origin of the
SFA, an up and over approach is warranted. Reentry devices require placement of a 6-Fr sheath. If
an up and over approach is anticipated, the aortic bifurcation should also be assessed to make sure
that the reentry device can be passed.
■
Patients with extensive disease below the knee and without iliac or proximal SFA disease and who
are not obese can be treated using an antegrade approach.
TECHNIQUES
RECANALIZATION STRATEGY
■
In managing complex lesions of the femoral and popliteal arteries, it is quite common to attempt to
recanalize the true lumen. Stenosis can almost always be crossed transluminally using a wire
supported by a catheter. A steerable, hydrophilic, low-profile wire is best. Long lesions,
especially if occluded, may not be possible to cross in the true lumen. In this case, subintimal
recanalization and reentry is the best option.
■
Strategy is based on selection of a reentry site where the artery has an acceptable lumen, collaterals
can be preserved, calcification is avoided, and potential bypass sites remain intact. Staying in the
true lumen when possible offers the shortest reconstruction and preservation of most collaterals.
When subintimal passage is required, reenter the true lumen as close to the distal reconstitution as
possible. The most common method of subintimal recanalization is using a loop of hydrophilic
wire to dissect the subintimal space and the loop can also be used to reenter the true lumen.
■
There is typically a large incoming collateral feeding the reconstituted segment. If the reentry site is
calcified, the success rate for loop passage is lower and use of a reentry catheter is more likely to
be indicated.
■
If there is a substantial plaque at the intended reentry site, consider a site more distal than the initial
reconstitution site. If there is another lesion distal to but near the reentry site, this can pose a
challenge for passing the guidewire distally after it has popped into the true lumen.
■
The operator must decide in this case whether it would be appropriate to reenter distal to all the
lesions, given that it might negatively affect bypass options. If the reentry fails and the patient
needs a bypass, target sites for distal anastomosis should be anticipated, although failed reentry
usually does not result in thrombosis of that segment.
TREATMENT PLATFORM
Sheath Placement
■
Place sheath tip close to the origin of the occlusion. Contrast administered through sheath fills the
distal reconstitution site through collaterals. For an SFA occlusion, the tip of the sheath is usually
positioned near the femoral bifurcation and the distal artery is visualized with contrast flowing
through profunda collaterals. Use a sheath that is one size larger than that used for angioplasty and
stenting, usually 7 Fr. This permits contrast administration even if a reentry device is being
positioned (FIG 1).
Entering the Subintimal Space

■
Place an angled tip catheter pointing toward the artery wall at the origin of the occlusion. Point it
opposite the location where the largest runoff collateral is located. Advance a Glidewire™ into
the wall. Push it and the tip will catch and a loop will form (FIG 2).
LOOP MANAGEMENT
Loop Advancement
■
Visualization, loop management, and assessment of the reentry site are the maneuvers that enhance
success. The looped hydrophilic wire is advanced past the lesion (FIG 3). The loop is kept
narrow and is optimal if less than the diameter of the artery lumen, and this is done by closely
following the loop with a supporting catheter. Because the loop is in the subintimal space, keeping
the loop narrow keeps the subintimal space tight. This helps to direct the wire in a straighter
trajectory toward its target and also makes the knuckle of the wire loop a more effective tool for
piercing tissue to get into the true lumen.
■
The standard Glidewire™ (Terumo) has a directional tip with a soft shaft. If subintimal passage is
being performed past a heavily calcified lesion, the artery wall may be more adherent to the
calcified segment, making wire passage alone more difficult. Catheter support is required, and
sometimes a low-profile balloon must be used to create space in the subintimal plane. Typically, a
standard Glidewire™ is used, but when passing a very calcified lesion, a stiff Glidewire™ should
be considered. A nylon catheter, 4 or 5 Fr, with an angled tip and a hydrophilic coating is best.
■
A recent development is the availability of CTO support catheters, such as the Quick-Cross™
(Spectranetics) or the CXI™ (Cook Medical) offering more support and low profile. The loop
usually seeks the weakest point in the tissue and breaks across the membrane from subintimal
potential space to true lumen more than 70% of the time in our experience. Orthogonal views are
helpful in assessing the trajectory of the loop and whether it is progressing toward the reentry site.
■
Even if the reentry site is calcified, a wire loop or a stiff wire with catheter support may reenter the
true lumen and it is worth an attempt. If this approach is unsuccessful, select a reentry catheter as
the next step. This saves time and the reentry site is best for success before too much manipulation
has taken place.
REENTRY DEVICE
Reentry Device Placement
■
The subintimal wire is exchanged for a stiff 0.014-in guidewire.
■
The reentry device is advanced.
■
If the proximal part of the subintimal space is too tight to allow passage of a 6-Fr reentry catheter
(approximately 2 mm), a long, low-caliber balloon may be used to slightly enlarge the
subintimal space. Do not dilate the area intended for reentry. If the subintimal space at the
reentry site is enlarged, it prevents the reentry needle from having adequate support to puncture
the true lumen.
Reentry into True Lumen
■
After the catheter is in place, a needle in the tip of the catheter is advanced into the true lumen.
■
A 0.014-in guidewire is advanced from the reentry catheter into the true lumen.
■
The direction of the needle is oriented using fluoroscopy.
■
Orthogonal views are obtained to locate the juxtaposition of the true and false lumens.
■
The image intensifier is positioned so that the catheter and an acceptable target vessel segment
are viewed side-by-side.
■
Rotate the catheter until the “L” shape appears at the tip.
■
Advance the needle into the true lumen
■
Multiple needle passes may be required. The risk of a needle pass is low.
■
The needle may only require a partial advancement to get into the true lumen. A full advancement
may go through the true lumen and into the wall on the opposite side.
■
Multiple small adjustments are often required before the true lumen is reentered, especially if the
reentry site is diseased.
■
The needle throw is oriented with intravascular ultrasound (IVUS) when using the Pioneer™
catheter (Medtronic). The needle is at 12 o’clock position on the IVUS image and the catheter is
rotated to face the true lumen. Using color ultrasound, the true and false lumens can be
distinguished and the wire passed into true lumen.
■
After passing the wire, the needle is retracted and the reentry catheter is removed over the wire.
■
Some commercially available reentry catheters are listed in Table 1. Reentry catheters may be
guided by fluoroscopy or IVUS, and reentry is achieved by passage of a needle, stiff wire tip, or
drill. Orthogonal views are obtained to locate the juxtaposition of the true and false lumens and the
image intensifier is positioned so that the catheter and an acceptable target vessel segment are
viewed side-by-side (FIG 4).
ALTERNATIVE REENTRY OPTIONS

Reentry Device Cannot Be Used
■
Use a catheter with a stiff tip to bluntly push on the reentry site or use low-profile balloon
angioplasty to break up the tissue membrane in hopes of achieving a fenestration as shown by
active blood return.
■
This approach is sometimes successful but it enlarges and occasionally perforates the subintimal
space at the reentry site and will render the reentry catheters less efficacious because they rely on
a tight subintimal space to provide leverage for the needle passage into the true lumen.
■
Another option is to consider a straight 0.035-in Glidewire™ or a straight 0.014 in, or 0.018 in
CTO wire and push on the location desired for reentry and see if it can be drilled into place.
Retrograde Approach
■
Retrograde puncture can be performed on a distal artery, such as a tibial or pedal artery. Retrograde
passage of a wire is often possible, even when antegrade passage across the same lesion was not.
This is especially the case for occlusions of the popliteal and proximal tibial level where there are
collaterals that an antegrade wire tends to follow blindly along and where reentry devices are not
as applicable.
■
Contrast is administered through the proximal access to obtain a roadmap of the distal puncture
site or ultrasound used to guide the access.
■
A 4-cm 21-gauge micropuncture needle is used.
■
A V18 wire (Boston Scientific) is introduced.
■
Sheath placement is avoided if possible to keep the arteriotomy small.
■
If the retrograde wire cannot break into the true lumen, a coronary balloon catheter is passed over
it.
■
A balloon introduced from the antegrade direction and the balloon introduced retrograde are
juxtaposed and inflated and are usually able to split the dissection flap to open the true lumen (FIG
5).
PEARLS AND PITFALLS

Staying in true lumen ■ Shortest reconstruction
■ Preservation of most collaterals
■ May increase risk of embolization at time of recanalization
Subintimal passage ■ Intraluminal contents are excluded.
■ The subintimal space often can be converted to a smooth, large
diameter conduit. Usually, the entry and reentry sites require extra
angioplasty or mechanical support from implants.
Optimal reentry site ■ Minimal calcifications
■ Healthy true lumen
■ Shortest subintimal channel
Collaterals ■ Reenter as close to distal reconstitution as possible
■ Typically large incoming collateral feeding reconstituted segment
■ Subintimal space (flow channel)—no collaterals and can fail
suddenly
Reentry catheters more ■ Calcified reentry site
likely ■ Worse disease morphology
POSTOPERATIVE CARE
■
Postoperative care involves standard care after endovascular procedures. True lumen
recanalizations have collaterals, whereas subintimal passages do not. The subintimal
recanalization should be monitored with duplex because they may fail suddenly in a manner
similar to a bypass. We typically perform duplex surveillance every 6 months.
OUTCOMES
■
Loop reentry using standard technique is successful in about 70% to 80% of cases.1,2
■
Patients that failed loop reentry were treated with reentry catheters and approximately 80% of these
were successful.2
■
Reentry success was 90% successful in a study using the Outback™ (Cordis) reentry catheter for
all-comers.3
COMPLICATIONS
■
Complications are similar to other endovascular procedures.
■
Access site complications are the most common and include bleeding, hematoma, pseudoaneurysm,
and arteriovenous fistulae.
■
Embolism to the runoff may be slightly more common in this patient population because it involves
treatment of the most complex infrainguinal lesions.
■
Perforation may also occur with greater frequency because angioplasty and manipulation in the
subintimal space are key maneuvers in this procedure. However, when perforation occurs, it is
only rarely clinically significant.
REFERENCES
1. Bolia A, Brennan J, Bell PR. Recanalisation of femoro-popliteal occlusions: improving success rate by subintimal recanalisation.
Clin Radiol. 1989;40(3):325.
2. Setacci C, Chisci E, de Donato G, et al. Subintimal angioplasty with the aid of a re-entry device for TASC C and D lesions of the
SFA. Eur J Vasc Endovasc Surg. 2009;38(1):76–87.
3. Bausback Y, Botsios S, Flux J, et al. Outback catheter for femoropopliteal occlusions: immediate and long-term results. J Endovasc
Ther. 2011;18(1):13–21.
Percutaneous Femoral–Popliteal Reconstruction
Chapter 30 Techniques: Antegrade Approaches
F. Gallardo Pedrajas Peter A. Schneider
DEFINITION
■
Overview: Femoral–popliteal revascularization, for indications of limb salvage or claudication, is
performed using open, endovascular, or hybrid approaches. Advanced open surgical techniques
are detailed elsewhere. Guidewire-catheter combinations are particularly effective and widely
used to cross femoral–popliteal stenoses or occlusions. Once across, reconstructions are
performed with any combination of angioplasty, stenting, stent grafting, or atherectomy.
■
Basic procedural goals: Improve functional status, quality of life, and, in the setting of ischemic
tissue loss, augment wound healing and limb preservation.
■
Challenges influencing long-term clinical success: (1) superficial femoral and popliteal artery
movement during activities of daily living, including flexion, compression, torsion, and stretching;
(2) compromised runoff; (3) the generally diffuse nature of femoral–popliteal disease, requiring
angioplasty of long segments of diseased and stiffened artery; (4) complex pathology, including
ostial lesions, luminal thrombus accumulation, and mural calcification.
■
Indications for intervention:
■
Rutherford class 1, 2, and 3 ischemia—exercise therapy and medical management are pursued as
primary intervention.1
■
Rutherford class 4, 5, and 6 ischemia—rest pain, ischemic ulcer, and gangrene warrant
revascularization as initial therapy.
■
Technical approach: Utilization patterns are trending toward percutaneous-first approaches to
management of Inter-Societal Consensus for the Management of Peripheral Arterial Disease
(TASC II) type A, B, and C lesions.2 Full consideration of current indications for open versus
percutaneous interventions is beyond the scope of this text; reference should be made to most
recent TASC updates.3

■
History includes a detailed description of ischemic symptoms pertaining to claudication, rest pain,
or tissue loss. The progression of symptoms and timeframe are helpful in determining the urgency
of therapy.
■
The presence and severity of cardiovascular disease risk factors should be assessed and managed to
ensure optimal perioperative and long-term clinical results, including tobacco use, diabetes,
hypertension, hyperlipidemia, renal dysfunction, and sedentary lifestyle.
■
Previous vascular or endovascular surgery procedures should be reviewed in detail, including
obtaining operative notes, prior imaging and surveillance studies, and prior physiologic testing
results whenever possible.
■
For claudicants, the potential presence and contribution of nonvascular causes of leg pain with
exercise should be considered; for example, neurologic claudication secondary to lumbar
radiculopathy and other degenerative spine diseases.4
■
Physical examination should document peripheral pulses at all levels, both lower extremities,
including the strength and quality of femoral pulses and skin integrity at potential access sites.
■
The severity and extent of ischemia, degree of existing tissue damage, and presence of infection are
documented prior to initiating intervention.

■
Physiologic vascular testing provides objective determination of the location and severity of
disease, assists in procedural planning, and provides documentation of baseline conditions.
■
Ankle–brachial index (ABI): ratio of the continuous wave Doppler–determined blood pressure in
the anterior or posterior tibial arteries (whichever is higher) to the blood pressure in the
brachial artery (>0.9 = normal; 0.5 to 0.9 = usually consistent with mild to severe claudication;
<0.5 = present in patients with very short distance claudication, rest pain, or tissue loss)
■
Toe pressures: The ABI may be artifactually elevated in diabetic patients with calcified tibial
arteries. Toe pressures may provide more reliable assessment of pedal and forefoot perfusion
when the ABI is greater than 1.2. Hallux pressure less than 50 mmHg may predict delayed or
inadequate wound resolution, 50 to 80 mmHg is indeterminant, and greater than 80 mmHg is
generally sufficient to promote healing.
■
Duplex arterial imaging: Direct insonation provides insight into the location and severity of
disease. The ratio of the peak systolic velocities (PSV) obtained from the most compromised
location divided by PSV from the most adjacent, proximal noninvolved segment provides
additional guidance regarding the severity of disease; greater than or equal to 2.5:1 usually
identifies a stenosis greater than 50% (FIG 1).
■
Computed tomographic arteriography (CTA): CTA has assumed an increasing role in guiding
peripheral vascular intervention, particularly in regard to choosing appropriate devices and
optimal interventional approach (e.g., ipsilateral antegrade vs. contralateral retrograde). This
additional guidance, however, comes at the cost of substantially more iodinated contrast and
radiation exposure than that provided by catheter-directed, intraarterial contrast arteriography,
augmented by direct ultrasonic visualization and physiologic testing (FIG 2).
■
Magnetic resonance arteriography (MRA): MRA may also assist preoperative planning. Although
MRA does not expose patients to ionizing radiation, artifactual overestimation of disease severity
is common in low flow conditions. Also, gadolinium contrast administration is contraindicated in
patients with a glomerular filtration rate of less than 30 mL per minute due to risk of contrast-
associated glomerulosclerosis (FIG 3).
SURGICAL MANAGEMENT
■
Overview—Success in percutaneous management of femoral–popliteal occlusive disease has
catalyzed a reciprocal decline in the use of open bypass for definitive revascularization. Key
features of percutaneous management include detailed preoperative planning, choice of access site
and closure techniques, and familiarity and facility with a wide range of complementary
intraluminal wire-guided devices.4
■
The operative plan includes access site selection, planned method of crossing, and options for
arterial reconstruction.
■
Endovascular inventory: An essential element of endovascular success is a robust and redundant
device inventory. In contrast to open reconstruction techniques, where similar instruments will
suffice for all lower extremity bypass configurations, regardless of routing, a unique and task-
specific repertoire is required for almost every endovascular approach. Procedural success
requires that the necessary devices, including guidewires, sheaths, catheters, angioplasty balloons,
stents, reentry devices, stent grafts, and atherectomy catheters are identified and available before
intervention is attempted.
■
Appropriate radiation protection must be available for all individuals involved in interventional
procedures. All team members must conscientiously wear a radiation dosimeter, submitted
monthly for aggregate exposure documentation. Leadership ensures that all team members adhere
to basic radiation safety tenants, including limiting the length and intensity of exposure to the
minimum required for precision imaging and intervention (the “as low as reasonably achievable”
[ALARA] principle). Safety principles, including distance from the radiation source, appropriate
shielding and optimal table height, and source-image intensifier distance, must be understood and
applied during every procedure.
■
Antibiotic prophylaxis is administered prior to the initiation of the procedure, whenever permanent
implants are considered.
■
Percutaneous procedures are performed under local anesthesia with appropriate sedation. Care
should be taken to avoid oversedation to ensure that patients can cooperate with instructions and
imaging requirements during the procedure. When hybrid open endovascular procedures are
contemplated, general anesthesia may facilitate more rapid and accurate device deployment, with
reciprocally less radiation exposure for the patient, cath lab team, and operator.
■
An important initial consideration is the approach and optimal puncture site. The common femoral
artery (CFA) is the most frequent access site. The approach is typically either up and over the
aortic bifurcation from the contralateral femoral artery or ipsilateral antegrade femoral puncture.
The transbrachial, transthoracic approach may also provide optimal antegrade access under
certain circumstances.
Positioning
■
Surgeon position should provide forehand access, whenever possible (FIG 4).
■
Retrograde femoral puncture: This is the most common type of access for all endovascular
procedures, including femoral–popliteal revascularization (FIG 5). The needle is placed in the
CFA and the guidewire is advanced retrograde into the iliac artery.
■
The femoral area is examined prior to puncture of the artery. The inguinal ligament extends from the
anterior superior iliac spine to the pubic tubercle. The best puncture site is inferior to the inguinal
ligament and at least a centimeter superior to the femoral bifurcation. Ultrasound provides useful
guidance for arterial puncture (FIG 6). Following needle insertion, spot fluoroscopy from an
ipsilateral oblique angle is obtained to confirm position. If arterial insertion is determined to be
proximal to the femoral head, the access attempt is aborted before larger devices are inserted to
minimize the risk of retroperitoneal hematoma formation due to inadequate compression or control
following the procedure. Common femoral access also enables closure devices to be employed
with confidence when necessary.
■
Closure devices: recommended for retrograde femoral access site management following insertion
of greater than or equal to 6-French (Fr) sheaths. Sheath puncture less than 6 Fr is best managed by
compression for 10 to 15 minutes, with or without adjuncts such as a thrombin-impregnated
dressing (e.g., D-stat® patch).
■
When pulses are not palpable at the desired access site, ultrasound or fluoroscopic guidance
(assisted by mural femoral artery calcification) may provide valuable assistance. Under these
circumstances, bilateral femoral access and ipsilateral iliac intervention may be required for
procedural success. Ideally, this eventuality is anticipated based on the results of preprocedural
examination and physiologic testing. Fortunately, the pulseless femoral artery is often palpable
based on mural calcification alone. Patience and spot fluoroscopic images to confirm needle and
artery position following failed needle passes often ensures ultimate success.
■
Secondary puncture of the postoperative groin presents special challenges. Whenever possible, scar
tissue and anastomoses should be avoided. Access in native artery is preferable to prosthetic or
autogenous grafts. Considerable force may be required for needle and micropuncture set access;
consideration should be given to using “stiff” 0.018-in wires and micropuncture sets specifically
manufactured to facilitate difficult groin access.
■
Antegrade femoral puncture: The femoral pulse and inguinal ligament are carefully marked (FIG 7).
Needle placement is directed proximal to the femoral artery bifurcation under real-time ultrasound
guidance.
■
Guidewire placement into the superficial femoral artery (SFA) requires patience and practice.
Ultrasound imaging in a longitudinal view may facilitate SFA wire intubation. When using a
micropuncture set with a “steerable” 0.018-in wire (e.g., one with a slight curve placed at the tip),
fluoroscopic control may also be employed. If repeated attempts result in deep femoral artery
placement, the micropuncture set should be exchanged for an 11 cm 4- or 5-Fr sheath over a
standard multipurpose (e.g., Bentsen) wire. Once safe antegrade deep femoral access is obtained,
the 5-Fr sheath may be gradually withdrawn with sequential fluoroscopic contrast “puffs” of 1 mL
or less performed until the femoral bifurcation is imaged (but while the sheath tip is still in the
CFA). At this juncture, roadmapping or last-image-hold digital subtraction angiography from an
ipsilateral oblique angle is performed to outline femoral bifurcation anatomy, after which a
steerable hydrophilic guidewire and, ultimately, the 5-Fr sheath is directed under fluoroscopic
imaging into the SFA.
■
Antegrade femoral access should be avoided in the obese, in patients with a short CFA, or in
patients with extreme proximal or orificial SFA disease. Although antegrade access improves
“pushability” across total occlusions and enables usage of a wider inventory of guidewire-catheter
combinations, there is no option for inflow disease management using this approach. Also, the
safety of current generation closure device placement is uncertain in antegrade approaches and
should be avoided whenever possible.
■
Brachial puncture and transaortic sheath placement may provide an alternative option for
“antegrade” femoral access. Upper extremity arteries are smaller, less forgiving, more prone to
spasm, and less predictably managed with compression following access. Notoriously, small
amounts of arterial extravasation may catalyze debilitating and permanent neurapraxia, even when
brachial access is obtained well distal to the axillary fossa. Debilitating nerve injury from
“axillary” sheath hematomas may occur at any location proximal to the antecubitum. In our
practice, we minimize this risk by defaulting to surgical exposure and direct arterial puncture with
suture closure for essentially all brachial artery access procedures. Exposure is easily obtained
with local anesthetic in most patients.
■
The longer guidewires and catheters required to access the femoral and popliteal arteries are also
less responsive to surgeon manipulation from a brachial approach and also limit the available
inventory of appropriate devices for femoral or popliteal intervention.
■
When brachial access is required, the level of access is determined by the diameter of the largest
sheath required to complete the procedure. For 6- or 7-Fr sheaths, the segment immediately
proximal to the antecubital fossa is sufficient. For larger sheaths, access should be obtained in the
distal axillary artery, proximal to the bifurcation of the deep brachial artery. The left arm should
be used whenever possible to minimize risk for embolic iatrogenic stroke. During micropuncture
access, even under direct vision, back-bleeding may not be pulsatile due to the smaller caliber of
the brachial artery. Sheaths should be managed with frequent flushing with 100 units/mL heparin,
as well as systemic anticoagulation once definitive interventional sheaths (6 to 7 Fr, 55 to 90 cm
from the arm) are positioned in the target artery, or whenever sheaths appear to be occlusive.
Intraarterial nitroglycerine injection may reduce arterial vasospasm to the distal extremity when
necessary.
TECHNIQUES
■
Percutaneous femoral–popliteal revascularization techniques include balloon angioplasty alone, or
self-expanding stent graft implantation as an adjunct to angioplasty. These techniques require
placement of interventional-grade sheaths, braided when required to cross the aortic arch or
bifurcation to prevent kinking as well as sufficient length to reach the treatment site without
limiting device selection. Sheath access also permits serial angiographic imaging to guide device
positioning, deployment, and confirm procedural success.
SHEATH PLACEMENT
■
Ensure that the appropriate sheath is selected and that alternatives are available should plans or
needs change.
■
Decide on optimal sheath positioning. Usually, placement immediately adjacent to the target lesion
maximizes the ability to cross the lesion, control the procedure, and minimize contrast usage. In
many circumstances, it may not be possible or practical to advance the sheath past the femoral
bifurcation when approaching from the contralateral femoral artery.
Up and Over Approach
■
Crossing the aortic bifurcation (FIG 8): Through a contralateral retrograde puncture, an infrarenal
aortogram is performed to evaluate aortic bifurcation anatomy and location. Usually located at the
level of the iliac crest, vascular calcifications may outline the bifurcation and guide positioning.
The aortic bifurcation must be free of occlusive or aneurysmal disease to ensure safe sheath
passage. Occasionally, iliac artery lesions must be treated prior to femoral intervention to ensure
optimal outcome.
■
Selective catheterization of the aortic bifurcation is performed, followed by antegrade
catheterization of the contralateral iliac artery system, either with the flush or pigtail catheter used
for the aortogram or an exchange catheter advanced at least to the femoral bifurcation.
■
The sheath tip is placed somewhere between mid-iliac artery and the mid- to distal SFA, depending
on lesion location and interventional intention. A 6-Fr sheath may be adequate for this purpose, but
7 Fr may be required for many devices (read the package insert). The angioplasty catheter length
for proximal SFA lesions is 75 to 80 cm; for more distal lesions, 90 to 110 cm.
■
Access to the deep femoral artery may be required to safely advance the “up and over” sheath over a
stiff exchange wire (e.g., Rosen®). After flushing and dilator placement, ensure that the sheath
sidearm stopcock is turned to the “off” position. The skin incision may need to be enlarged to
facilitate placement. Consider serial dilator exchanges when upsizing a sheath by two or more
French sizes. Occasionally, depending on the angle of the aortic bifurcation, sheath placement may
be facilitated by passage over a stiff, exchange length hydrophilic wire. When using hydrophilic
wires for this purpose, care should always be taken to keep the tip of the wire in the image screen
field to prevent inadvertent arterial puncture and extravasation from wire injury. Similarly, when
confronted by extreme tortuosity in the iliac arterial system, interval advancement of the sheath into
the internal iliac artery may be required to gain access to the contralateral iliac artery with a
second or “buddy” wire, following which, standard catheter and guidewire techniques may be
used to advance the sheath to its ultimate desired location.
■
Regardless of procedure or access approach, it is always advisable to keep the wire tip in the
imaging field whenever sheaths are exchanged or advanced—arterial perforation and extravasation
may limit procedural options, or the ability to initiate systemic anticoagulation, and may increase
compartment pressures to the point of requiring surgical release if not recognized and managed
promptly.
Ipsilateral Approach
■
See prior recommendations for securing access (Table 1). Obesity and excessive abdominal pannus
may significantly limit the use of this approach. Before initiating treatment, obtain angiographic
documentation of existing ipsilateral anatomy, including infrapopliteal runoff.
■
Shorter guidewires and devices improve the efficiency of the ipsilateral antegrade approach.
■
If balloon angioplasty alone is planned, 4- or 5-Fr sheath can be used to treat ipsilateral SFA
lesions. More complex reconstructions require 6 Fr and occasionally 7-Fr sheaths.
CROSSING OCCLUSIVE LESIONS

■
Guidewire-catheter skills form the basis of all endovascular procedures. Successful guidewire
positioning requires familiarity with a range of devices and guidewire-catheter pairings. The
guidewire required for crossing the lesion could not be adequate for working or deploying a stent
or a stent graft. Familiarity with and access to a wide selection of wires (depending on length,
diameter, tip pressure, and hydrophilic qualities) is essential for success (FIG 9).
■
Guidewire features to be considered:
■
Length: Must be adequate to cover the cumulative distance, both inside and outside the patient, to
perform the procedure and support the catheter. Guidewire lengths vary from 145 to 300 cm.
For an ipsilateral antegrade approach, 145- to 180-cm guidewires are adequate, but for
contralateral or brachial access, 260- to 300-cm lengths are necessary. As a general rule of
thumb, guidewire length must be at least twice that of the coaxial device to be positioned over
the wire.
■
Diameter: Most femoral–popliteal procedures are performed with 0.035-in guidewires, but
smaller caliber angioplasty is generally performed with 0.018-in or 0.014-in guidewires.
■
Stiffness: An inner steel core confers different magnitudes of stiffness on the shaft of the wire. A
stiffer wire may help to cross a calcified lesion, but it is also easier to injure the vessels. In
wires specifically designed to cross femoral–popliteal lesions, tip pressure may also vary
across wires with similar stiffness along the majority of their length.
■
Coating: Hydrophilic guidewires may reduce the coefficient of friction. Typically, they are
passed in conjunction with purpose-specific crossing catheters.
■
Crossing catheters support guidewire passage and, depending on design, confer varying degrees of
support and directionality. After the guidewire is used to cross the lesion, the catheter may be
advanced so that the choice working wire may be placed. Crossing catheter technology has
advanced considerably in the last 5 to 10 years. Options abound for torsionality (braided or
unbraided), tip taper, tip shape, length, and diameter. Examples include the Quick-Cross® and
CTX® catheter families. Some experience is required to learn how to use these catheters optimally
in most situations.
BALLOON ANGIOPLASTY
■
The angioplasty process enlarges the lumen by compressing and rupturing the plaque, as well as
stretching and, in some cases, damaging the media and adventitia (FIG 10).
■
Heparin is typically administered, 50 to 100 units/kg following sheath placement and prior to
intervention.
■
The balloon length and diameter are typically selected to treat the entire lesion, with minimal
proximal or distal overlap, to restore original diameter as determined by proximal or distal
measurement. The balloon catheter is positioned over the guidewire and inflated to nominal
pressure to achieve the specified diameter. Occasionally, higher pressures may be required to
reduce lesion “waisting.”
■
Inflate slowly. Balloon inflation is maintained for 2 minutes.
■
Deflate slowly, and ensure full deflation fluoroscopically before withdrawal.
■
The balloon angioplasty catheter may be used repeatedly during the same procedure; however, its
capacity to recover the predeployment diameter following deflation degrades with sequential use.
■
Balloon diameters range from 4 to 7 mm for the SFA and 3 to 6 mm in the popliteal artery.
■
Conventional angioplasty is limited somewhat by target artery dissection. Not all dissections need
further treatment. In general, only flow-limiting dissections as judged by sequential contrast
injections through the interventional sheath need additional treatment. Dissections may be managed
by prolonged periods of inflation followed by gradual deflation to “tack” the plaque up to the
arterial wall. Persistent flow obstruction following angioplasty is the most common indication for
subsequent secondary stenting.
STENTS
■
Although all vascular-compatible, size-appropriate, self-expanding (nitinol) stents may be deployed
in the superficial femoral or popliteal arteries as clinically indicated, select devices have obtained
specific indications for this application from the U.S. Food and Drug Administration. The operator
is encouraged to familiarize himself or herself with this designation and to use application-
approved devices whenever appropriate to ensure optimal outcome.
■
Material and characteristics of peripheral stents have evolved in recent years. Self-expanding
nitinol stents are most appropriate for SFA and popliteal applications. The ideal stent should have
the ability to adapt to the vessel with a precise deployment and without kinking, collapsing, or
fracturing as well as limit long-term arterial injury and restenosis. More recently, drug-eluting
stents have been developed and are approved for use in the United States to limit chronic
restenosis of the stent arterial segment following deployment. The potential clinical benefits
derived from these devices are offset to a significant degree by their substantial increase in cost
over “bare metal” stents.
■
Femoral–popliteal stents may be placed routinely or selectively. Selective stent placement may be
considered for significant postangioplasty dissection, long lesions (>15 cm), residual stenosis
postangioplasty, pressure gradient (>10 mmHg) after angioplasty, recurrent stenosis, occlusion, or
to prevent or limit postangioplasty embolization of plaque.
■
Localization: A stent is typically deployed to span the distance between relatively healthy artery
proximal and distal to the target lesion. “Healthy” is a relative term in this sense, and care should
be taken to limit stent coverage to the minimal distance required to achieve an optimal result. Long
lesions in the SFA are the most commonly stented segment, but be aware that stents in the distal
superficial femoral and popliteal arteries may be damaged by stress from knee flexion (FIG 11).
Excessive stent coverage may accelerate long-term restenosis and luminal compromise, regardless
of the degree of initial success or the type or size of deployed stent.
■
Sheath size: Most stents for infrainguinal deployment require a 6- or 7-Fr sheath. Refer to the
individual instructions for use for each individual device.
■
Deployment: Most infrainguinal nitinol stents are deployed using a pin and pull maneuver that
retracts the cover from the constrained stent and the underlying mandrel. A ratcheting mechanism
may also be integrated into the deployment process. Typically, these may be removed for basic
pin/pull deployment if the ratchet becomes jammed or disabled. After deployment, completion
angioplasty is performed to bring the stent to profile.
■
Complications of stent deployment:
■
Acute: arterial dissection, occlusion, rupture, stent migration or embolization, embolization of
atherosclerotic material, thrombosis
■
Chronic: intimal hyperplasia, recurrent stenosis, infection, stent damage, thrombosis
STENT GRAFTS
■
Nitinol-based, flexible stent grafts may be deployed over long and calcified SFA lesions as an
alternative to bare metal or drug-eluting stents. As a general rule of thumb, the longer and more
complex the target lesion(s) and length of required coverage, the more suitable the indication for
covered stent placement.
■
Stent grafting may require exchange of a 0.035-in wire system for smaller guidewires (e.g., 0.025 in
or 0.018 in); the operator is again cautioned to refer to the instructions for use for each device
considered for placement. Stent grafts must be deployed over the specific guidewire adequate for
the stent graft. Sheath upsizing may also be required, depending on the diameter selected. Choosing
a larger sheath at the outset will minimize the need for awkward or inefficient sheath exchange
after the procedure is well underway. Aggressive predilatation is also often necessary in order to
create sufficient space for bulkier covered stent to pass the lesion prior to deployment. Similar to
bare metal stents, covered stent deployment is usually followed by completion angioplasty to bring
the covered lumen to profile (FIG 12).
■
Relative advantages of stent grafting, compared to bare metal stents, include the ability to create an
entirely new lining for a disease arterial segment. This coverage obviates the possibility of in-stent
stenosis within the graft. However, experience has shown that unlike surgically placed prosthetic
bypass grafts, covered stents in the superficial femoral and popliteal arteries tend to incite
restenosis at the proximal end. Thus, placement usually requires coverage up to the origin of the
SFA. Any uncovered artery in this region is likely to develop critical restenosis. Disadvantages
include the necessary coverage of all collateral vessels encompassed in the covered segment, as
well as the increased risk for graft infection inherent in fabric-covered metal stents. Also, although
some stent grafts are heparin-bonded, the thrombogenicity of covered stents varies directly with
the length of segment covered, such that complete SFA coverage from the origin to the adductor
canal necessitates long-term oral anticoagulation therapy in patients treated in our practice.
Anticoagulation in this circumstance is designed to limit thrombus extension following future graft
occlusion rather than increasing long-term graft patency. Anticoagulation does not typically extend
prosthetic graft patency in the lower extremity, regardless of open or endovascular placement.
PEARLS AND PITFALLS
Indications A complete vascular history is essential to accurately confirm the
diagnosis. Objective evidence of ischemia is required to justify
intervention and to provide a baseline for future comparison.
Artery puncture The puncture is planned prior to the procedure. Access site issues are
the most common type of complication. A well-performed access
will set the procedure up for success.
Specific material In planning the procedure, check to make sure that all the necessary
inventory is available prior to the procedure.
Crossing the lesion Do not force the wire across the lesion.
Closure Closure devices can simplify the procedure and allow for more
patient comfort and earlier discharge, but accurate CFA access
should be confirmed, typically at the outset of the procedure, before
therapeutic sheaths are placed.
Follow-up The patient is evaluated after the procedure at 1 week and 1 month
and then 6-month intervals after that. We typically obtain some
assessment of perfusion (ABI). Duplex mapping may also be
performed for surveillance.
POSTOPERATIVE CARE
■
The patient should remain at bedrest for at least 6 hours after the procedure. After use of a closure
device, usually 2 hours of bedrest is required.
■
Puncture site management: Obtaining hemostasis is made safer and simpler when the arteriotomy
site is carefully managed during the procedure. Ensure the patient is comfortable prior to removing
the sheath.
■
Holding pressure: After ipsilateral antegrade puncture, use two hands to hold pressure, one is
placed proximal to the inguinal ligament to apply pressure over distal external iliac artery to
decrease the pressure flowing through the puncture. The other hand applies pressure over the area
of arterial puncture just distal to the inguinal ligament. There are no approved closure devices for
antegrade puncture. Following a retrograde puncture, digital pressure is held at the location of
arteriotomy, proximal to the skin puncture site.
■
Closure devices: Closure devices are used whenever possible to reduce risk of access site
complications and limit patient immobility following the procedure. Newer generations of closure
devices are easier to use and are considered a good option for closing the arteriotomy in puncture
procedures for 6 Fr and larger.
■
The patient should be encouraged to
■
Avoid smoking
■
Walk daily
■
Follow best medical treatment
■
Follow-up with the vascular clinic
OUTCOMES
■
Patients with peripheral artery disease (PAD) and critical limb ischemia (CLI) have a shorter life
expectancy than the general population. The most effective method of revascularization that returns
patients to their premorbid functional state in the shortest period of time, with the least amount of
surgical risk, is considered ideal. In this regard, most centers have adopted a percutaneous-first
approach to lower extremity revascularization, when intervention is indicated.5 This rubric
reserves open surgical reconstruction for patients who fail percutaneous intervention. More
recently, controversy has arisen as to how many unsuccessful secondary interventions constitute
“failure.”
■
Successful percutaneous revascularization is considered equivalent to traditional standard
management strategy—that is, bypass surgery—in providing freedom from major and minor
amputation, in patients with severe limb ischemia, up to 2 years following revascularization. To
date, the Bypass versus Angioplasty in Severe Ischemia of the Leg (BASIL) trial remains the only
randomized prospective trial comparing the success of open surgical bypass versus endovascular
therapy for CLI. When life expectancy extends beyond 2 years, bypass patency is superior.6
■
Although percutaneous transluminal angioplasty (PTA) provides superior limb salvage rate and
assisted patency rates than prosthetic bypass, care should be taken to avoid outcomes that limit
future bypass options (e.g., injury or occlusion of significant infrageniculate arteries that could
serve as future bypass targets). Modern surgical practice should incorporate a full range of
postprocedural outcomes, beyond arterial patency alone, in the assessment of procedural success.
As such, consideration to postoperative ambulatory status, potential for independent living, wound
care requirements, and pain management is essential and comparable to the impact on graft patency
on long-term patient satisfaction and quality of life.7
■
A comparison of self-expandable stents versus femoral–popliteal above-the-knee bypass had been
published by Kedora et al., reporting similar limb salvage, with comparable primary (73.5% vs.
74.2%) and secondary patency rates (83.9% vs. 83.7%) at 1 year with both techniques.8
■
Others studies reported that despite the reduced primary patency, limb salvage rates remain
comparable to surgical bypass and range from 74% at 5 years to 84.7% at 8 years.9
■
Lower limb revascularization of diabetic patients affected by intermittent claudication, in addition
to improved walking performance, is associated with a reduction in the incidence of future major
cardiovascular events when accompanied by increased physical exercise and improved glucose
management and weight control.10
COMPLICATIONS
■
Artery puncture: hematoma, occlusion, dissection, pseudoaneurysm, arteriovenous fistula (FIG 13)
■
Failure of recanalization: intimal dissection, branch occlusion, thrombosis, embolization, vessel
rupture, remote hemorrhage
■
Stent/stent graft complications: stent embolization, stent will not expand lesion, stent kink, stent
thrombosis
■
Infection
REFERENCES
1. 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.
2. Faglia E, Dalla Paola L, Clerici G, et al. Peripheral angio-plasty as the first-choice revascularization procedure in diabetic patients
with critical limb ischemia: prospective study of 993 consecutive patients hospitalized and followed between 1999 and 2003. Eur J
Vasc Endovasc Surg. 2005;29:620–627.
3. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II).
J Vasc Surg. 2007;45(suppl S):S5–S67.
4. Issack PS, Cunningham ME, Pumberger M, et al. Degenerative lumbar spinal stenosis: evaluation and management. J Am Acad
Orthop Surg. 2012;20(8):527–535.
5. Giugliano G, Perrino C, Schiano V, et al. Endovascular treatment of lower extremity arteries is associated with an improved
outcome in diabetic patients affected by intermittent claudication. BMC Surg. 2012;12(suppl 1):S19.
6. Nice C, Timmons G, Bartholemew P, et al. Retrograde vs. antegrade puncture for infra-inguinal angioplasty. Cardiovasc Intervent
Radiol. 2003;26:370–374.
7. Adam DJ, Beard JD, Cleveland T. Bypass versus angioplasty in severe ischaemia of the leg (BASIL): multicentre, randomised
controlled trial. Lancet. 2005;366:1925–1934.
8. Kedora J, Hohmann S, Garrett W, et al. Randomized comparison of percutaneous Viabahn stent grafts vs. prosthetic femoral–
popliteal bypass in the treatment of superficial femoral arterial occlusive disease. J Vasc Surg. 2007;45:10–16.
9. Houbballah R, Raux M, LaMuraglia G. Trans-Atlantic debate: lower extremity bypass versus endovascular therapy for young
patients with symptomatic peripheral arterial disease. Part two: against the motion. Endovascular therapy is the preferred treatment
for patients <65 years old with symptomatic infrainguinal arterial disease. Eur J Vasc Endovasc Surg. 2012;44:116–119.
10. Conrad MF, Crawford RS, Hackney LA, et al. Endovascular management of patients with critical limb ischemia. J Vasc Surg.
2011;53:1020–1025.
Chapter 31 Maximizing Vein Conduit for Autogenous Bypass
Gregory J. Landry
DEFINITION
■
Autogenous conduit is preferred for all lower extremity bypasses when available. The greater
saphenous vein (GSV) is the most frequently used conduit. Other options for native conduit include
the short saphenous vein, arm vein (basilic, cephalic, brachial), and femoral vein.
■
The majority of patients for whom autogenous vein bypass is necessary will have atherosclerotic
peripheral vascular disease.
■
Other conditions for which autogenous vein bypass may be necessary include aneurysms (e.g.,
femoral, popliteal), trauma, and vasculitis.

■
A history of cardiovascular risk factors should be elicited in all patients undergoing lower extremity
bypass, including smoking history and history of cardiac and cerebrovascular disease and history
of diabetes, chronic kidney disease, hyperlipidemia, and chronic obstructive pulmonary disease.
■
Upper and lower extremity pulse exam should be performed. Because atherosclerosis is a systemic
disorder, the following pulses should be assessed bilaterally: carotid, brachial, radial, femoral,
popliteal, dorsalis pedis, and posterior tibial. Both the presence and strength of pulses should be
recorded.
■
If lower extremity pulses are absent, which is usually the case in patients undergoing surgery for
peripheral vascular disease, ankle–brachial indices should be measured. The highest ankle
pressure is divided by the highest brachial pressure.
■
Lower extremities should be evaluated for the presence of ulcerations or gangrene.
■
A history of prior vein use or removal should be elicited. Veins may have previously been used for
prior lower extremity or coronary artery bypass. Patients with varicose veins may have undergone
prior vein stripping or ablation. Patients with chronic kidney disease may have had prior upper
extremity arteriovenous fistula placement. In dialysis-dependent patients, upper extremity veins
should be used judiciously as they may be necessary for future arteriovenous access.

■
All patients considered for lower extremity bypass should undergo arteriography to define the
proximal (inflow) and distal (outflow) targets.
■
Digital subtraction angiography remains the gold standard and provides the greatest anatomic
detail for operative planning.
■
Alternative imaging modalities include computed tomography (CT) and magnetic resonance (MR)
angiography or duplex ultrasonography.
■
Duplex ultrasonography should be used for preoperative vein mapping to identify suitable
autogenous conduit (FIG 1). If the patient has good-quality GSV, no further vein mapping is
typically necessary. If the GSV is of poor quality or absent, small saphenous vein and arm vein
should be mapped (FIG 2).
■
Ideal conduit diameter is 3.5 mm or greater.
■
Vein should be easily compressible. Thick-walled or noncompressible vein indicates prior
superficial venous thrombosis and vein is likely not suitable for bypass.
■
Mapping should ideally immediately precede surgery with vein course marked with an indelible
marker on the skin. This allows precise placement of incisions, which avoids the creation of
skin and tissue flaps that might impede wound healing.
SURGICAL MANAGEMENT
■
Preoperative planning
■
If not previously marked or if marks have faded, it is useful to remark the intended venous conduit
with ultrasound guidance prior to surgery (FIGS 3 and 4).
■
Open foot lesions or gangrene should be covered with sterile adhesive to prevent contamination
of sterile incisions.
■
Prophylactic intravenous antibiotics should be administered to reduce risk of perioperative
infection.
■
If arm vein is to be harvested, it is important to avoid blood draws or intravenous lines in the
intended arm(s). If veins from both arms are necessary, central venous access may be necessary.
■
Positioning
■
The majority of the procedures are performed with the patient supine. If small saphenous vein is
the intended conduit, it is often easier to perform this part of the procedure with the patient
prone and then to reprepare and drape with the patient supine.
■
If arm vein is to be harvested, the arms should be abducted and placed on arm boards.
TECHNIQUES
■
Open vein harvest: GSV
■
A longitudinal incision is made directly over the marked vein. Either a single incision or multiple
skip incisions can be used, with some evidence of fewer wound infections with the latter
approach (FIG 5).
■
The necessary length of vein is unroofed. Using blunt and sharp dissection with Metzenbaum
scissors, the vein is freed from surrounding structures. Side branches are ligated and divided
with silk ligatures and hemoclips.
■
The GSV is divided proximally at the saphenofemoral junction (FIG 6), distally according to the
length of vein needed.
■
It is helpful distally to identify a branch point in the vein that can subsequently be used for the
proximal anastomosis if the graft is placed in reversed configuration (FIG 7A,B).
■
Open vein harvest: small saphenous vein
■
The same technique is used as for the GSV, except typically with the patient prone.
■
Proximally, the vein is typically divided at the saphenopopliteal junction. Some patients will
have continuation of the small saphenous vein in the thigh (Giacomini vein) which allows
harvesting additional length of vein in the thigh.
■
Open vein harvest: arm vein
■
Both the cephalic and basilic veins can be harvested through longitudinal arm incisions. The same
technique is used as for leg vein; however, care must be taken as the arm veins tend to be more
thin walled and fragile than leg vein.
■
The cephalic vein can frequently be harvested as a single conduit from the wrist to the
deltopectoral groove (FIG 8A–C). A single segment is frequently adequate for a femoral–
popliteal or femoral to proximal tibial bypass.
■
The basilic vein tends to be larger in diameter than the cephalic vein, although often, only a short
segment in the upper arm is available. The basilic vein is well suited for use as an extension
graft when revision of a previously placed bypass is necessary. When used as a new bypass, a
composite graft composed of two or more vein segments is frequently necessary.
■
The basilic vein often has large branches that communicate medially with the brachial vein. These
branches are often broad based and are better ligated with a running monofilament suture than
simple ligation.
■
The median antebrachial cutaneous nerve frequently interdigitates with the basilic vein. With
meticulous dissection, this nerve can be preserved (FIG 9).
■
Brachial vein is intimately associated with both the brachial artery and median nerve. This vein
can also be harvested as conduit, but great care needs to be taken to avoid injury to adjacent
structures (FIG 10).
■
Open harvest: femoral vein
■
Although typically used for larger vessel reconstruction, femoral vein can be used for autogenous
lower extremity bypass if necessary.
■
Proximal femoral vein is harvested medial to Sartorius muscle. Vein is adjacent to superficial
femoral artery. Vein can be harvested proximally up to the profunda femoral vein.
■
Distally, the femoral vein is easier to harvest with the Sartorius muscle reflected posteriorly. The
vein can easily be harvested as far as the adductor canal.
■
If a longer segment is needed, the vein can be further harvested caudal to the adductor tendon into
the popliteal fossa.
■
Endoscopic harvest: GSV
■
Endoscopic harvest works best for veins within the saphenous fascial envelope (FIG 11A). It is
technically more difficult in cases where the vein leaves this fascial envelope and is situated
more superficially or in the subcutaneous fatty tissue (FIG 11B).
■
Available harvesting systems are described in Table 1.
■
A 2-cm incision is made at the level of the knee and the GSV dissected free at this site and
encircled with a silastic vessel loop (FIG 12).
■
The vein is dissected from the knee to the saphenofemoral junction using a conical dissecting tip
(FIG 13). CO2 insufflation is performed through an inflatable trocar.
■
The vein is held in place with the C-ring or V-lock mechanism and side branches are divided
with bipolar electrocautery or harmonic scissors depending on the manufacturer (FIG 14).
■
Harvesting can also be performed in the calf; however, this is more technically challenging due to
multiple geniculate venous branches, subcutaneous position of vein, and close approximation
with saphenous nerve.
■
If an incision in the groin is going to be made for the proximal anastomosis of the graft, the
incision can be made at this point to complete the proximal harvest. If an incision is not going to
be made in the groin, a stab incision is made in the groin and the vein grasped under direct
vision with a tonsil clamp. The vein is then pulled through the incision and ligated and divided
with silk ligatures.
■
After proximal division, the vein can be pulled out of the tunnel through the knee incision.
■
A below-knee incision can be made to harvest the distal vein if this incision is already intended
for the distal anastomotic site.
■
Back-table vein preparation
■
Harvested veins are prepared on a back table (FIG 15). Veins are distended with the surgeon’s
solution of choice. The author prefers using chilled, heparinized autologous blood, although
heparinized saline is also sufficient.
■
Any side branches not ligated during the initial harvest are ligated with silk ligatures or, if too
small or short, with 7-0 polypropylene suture.
■
For endoscopically harvested veins, because the side branches are not ligated during the initial
harvest, they are ligated at a back table with silk ligatures or 7-0 polypropylene suture after vein
removal.
■
Composite graft creation
■
A venovenostomy can be performed with two (or more) venous segments to create a single
conduit of adequate length. The vein of larger diameter should be placed proximally. The veins
are spatulated and sewn end-to-end with running 7-0 polypropylene suture (FIG 16A–E).
Additional vein segments can be added as necessary with the same technique to create a conduit
of adequate length.
■
Graft tunneling
■
Grafts are best tunneled using a hollow tube tunneler, such as a Scanlan tunneler, in order to
avoid unnecessary tension on the vein as it is pulled through the subcutaneous tissue. This is
particularly important in a composite graft where suture line disruption can potentially occur.
■
Tunneling performed after the proximal anastomosis allows the graft to be passed under pressure,
which lessens the likelihood of twisting or kinking during tunneling.
■
In a first-time bypass, tunneling anatomically through the popliteal fossa for below-knee targets
provides the most direct route to maximize vein length (FIG 17). In redo procedures in which
previous grafts were tunneled through the popliteal fossa, a subcutaneously tunneled graft may
be necessary.
■
Two options exist for grafts tunneled to the anterior tibial artery. For grafts based on the common
femoral artery, a lateral, subcutaneously tunneled graft is the most straightforward. For grafts
based further distally on the superficial femoral or profunda femoral arteries, an anatomic tunnel
through the popliteal fossa and interosseous membrane is more direct and maximizes vein
length. The interosseous membrane should be directly visualized and a cruciate incision made to
prevent graft stricture. Grafts to the posterior tibial or peroneal artery are tunneled either
through the popliteal fossa or medially and subcutaneously (FIG 18).
■
Choice of proximal anastomotic site
■
The choice of proximal anastomotic site depends on the anatomy and vein length and quality.
■
If adequate vein length is present, an anastomosis to the common femoral artery is generally
preferred.
■
If vein length is insufficient, the graft can be based on either the superficial or profunda
femoral artery. For patients with atherosclerotic lower extremity arterial occlusive disease,
the profunda femoral artery is more likely to be better preserved than the superficial femoral
artery, which is more likely to be affected by atherosclerosis (FIG 19A,B).
■
In the presence of common femoral or proximal profunda femoral artery stenosis, a common
and/or profunda femoral endarterectomy with placement of a vein or prosthetic patch (Linton
patch) can provide adequate inflow for the graft, with the proximal anastomosis to the distal
end of the patch (FIG 20).
■
In patients with patent superficial femoral arteries and more distal tibial artery disease, as is
often seen in patients with diabetes, grafts may be based on either the above- or below-knee
popliteal artery.
■
For patients requiring tibial or pedal bypasses with insufficient vein length, the superficial
femoral artery can be treated with angioplasty with or without stenting to provide inflow for
a graft based on the above- or below-knee popliteal artery. This is ideally performed either
in a hybrid operating room (OR) suite or in a standard OR with C-arm fluoroscopy.
■
Choice of distal anastomotic site
■
In general, the shortest bypass configuration that provides adequate distal flow is chosen.
■
If direct runoff to the foot can be achieved through a bypass to the popliteal artery, this is
preferred.
■
If the popliteal artery is occluded and a tibial artery serves as the distal target, a direct
angiosome revascularization should be chosen if possible in cases of foot ulcers or ischemia.
For rest pain or claudication, the dominant tibial vessel should be chosen.
■
Proximal anastomosis
■
Proximal and distal arterial control is obtained with atraumatic vascular clamps, silastic
loops, or Fogarty catheters as needed and per surgeon’s choice.
■
The anastomotic arteriotomy is made with a no. 11 scalpel and extended with Potts scissors.
The arteriotomy length should be about 1.5 to 2 times the diameter of the vein.
■
The proximal anastomosis is ideally performed using a vein branch as the heel in order to
avoid heel stricture (FIG 21). The vein is spatulated through the heel (FIG 22A–C).
■
The anastomosis is performed with running polypropylene rule. As a rule of thumb, suture
diameter is 4-0 in the iliac artery, 5-0 femoral, 6-0 popliteal, and 7-0 tibial (FIG 23).
■
Distal anastomosis
■
This is performed in similar fashion to the proximal anastomosis, although spatulation through
a side branch is generally not possible and less necessary as for the proximal anastomosis,
because the graft toe geometry is more important for patency than the heel geometry in the
outflow (FIG 24).
■
Intraoperative assessment
■
Augmentation of Doppler signals at the ankle with the graft open compared to the graft
occluded generally indicates graft patency with improved arterial perfusion. Intraoperative
duplex or arteriography should also be considered to rule out technical problems with the
graft.
PEARLS AND PITFALLS

Open vein harvest ■ Preoperative vein mapping is important to localize the site of the
incision to avoid tissue flaps that can lead to poor wound healing.
■ Vein branches should not be ligated flush with the vein as
“dimpling” can occur when the vein is distended. It is good to
ligate the vein branch at least 1 mm away from the vein to allow
proper vein expansion (FIG 25).
■ Arm veins tend to be more fragile than leg veins, requiring gentler
handling during harvest.
Endoscopic vein harvest ■ Avoid harvesting veins that are subcutaneous or not enclosed
within a fascial envelope as these are technically more difficult to
harvest and therefore more prone to injury.
Vein preparation ■ Avoid overdistending the vein during preparation. A good
technique is to inject a small amount of fluid into the vein and then
manually distending the vein in segments rather than trying to
inflate the vein with the syringe.
Graft tunneling ■ Passing the graft while distended reduces the risk of twisting or
kinking.
■ Using a sterile marking pen, a line can be drawn on the anterior
surface of the vein to help orient the graft distally and prevent
twisting.
Anastomotic placement ■ Severely diseased vessels tend to delaminate when handled. Great
care must be taken to include all layers in the anastomosis to
prevent dissection.
■ In severely calcified vessels, vessel loops may not provide
adequate control and vascular clamps may cause a crush injury. In
these cases, Fogarty balloons may be needed for arterial control.
POSTOPERATIVE CARE
■
Patients should be monitored postoperatively in either an intensive care unit or a surgical ward.
Hourly vascular checks should be performed with continuous wave Doppler.
■
Early ambulation, generally on the first postoperative day, is encouraged, particularly in patients
with claudication or rest pain. Patients with ulcers or gangrene may require a longer period of
non–weight bearing if lesions are on a weight-bearing surface.
OUTCOMES
■
Anticipated 3-year primary patency rates for reversed saphenous vein grafts are 70% to 80% for
femoral–popliteal and 60% to 75% for femoral–tibial. Comparable patency rates for arm vein
bypasses are 60% to 70% and 50% to 60%, respectively, and for prosthetic grafts, 45% to 65%
and 20% to 30%, respectively. Anticipated 5-year limb salvage in patients with critical limb
ischemia is 80% to 90%, with 5-year survival in 40% to 70%.1–5
■
Reversed and in situ vein grafts have been shown to have comparable patency rates in multiple
studies.6
■
Ambulatory function and independent living status is preserved in the majority of patients who
undergo successful revascularization.
■
Quality of life measures are improved in the majority of patients who undergo successful
revascularization.7
■
Up to 20% of patients will develop vein graft stenoses requiring either open or endovascular
revision during follow-up.
■
Data on patency rates of open versus endoscopically harvested vein grafts are mixed, making
definitive recommendations on the preferred approach difficult.
COMPLICATIONS
■
Wound infection
■
Seroma
■
Hematoma
■
Graft occlusion
■
Myocardial infarction
REFERENCES
1. Chew DK, Owens CD, Belkin M, et al. Bypass in the absence of ipsilateral greater saphenous vein: safety and superiority of the
contralateral greater saphenous vein. J Vasc Surg. 2002;35(6):1085–1092.
2. Curi MA, Skelly CL, Woo DH, et al. Long-term results of infrageniculate bypass grafting using all-autogenous composite vein. Ann
Vasc Surg. 2002;16(5):618–623.
3. Faries PL, Arora S, Pomposelli FB, et al. The use of arm vein in lower-extremity revascularization: results of 520 procedures
performed in eight years. J Vasc Surg. 2000;31(1):50–59.
4. Gentile AT, Lee RW, Moneta GL, et al. Results of bypass to the popliteal and tibial arteries with alternative sources of autogenous
vein. J Vasc Surg. 1996;23(2):272–279.
5. Taylor LM Jr, Edwards JM, Porter JM. Present status of reversed vein bypass: five-year results of a modern series. J Vasc Surg.
1990;11(2):193–206.
6. Harris PL, Veith FJ, Shanik GD, et al. Prospective randomized comparison of in situ and reversed infrapopliteal vein grafts. Br J
Surg. 1993;80(2):173–176.
7. Nguyen LL, Moneta GL, Conte MS, et al. Prospective multicenter study of quality of life before and after lower extremity vein
bypass in 1404 patients with critical limb ischemia. J Vasc Surg. 2006;44(5):977–983.
Tibial Interventions: Tibial-Specific Angioplasty
Chapter 32 Considerations and Retrograde Approaches
Georges E. Al Khoury Rabih A. Chaer
DEFINITION
■
Endovascular tibial intervention is a minimally invasive, endoluminal revascularization of the
infrapopliteal vessels. It is an accepted treatment of critical limb ischemia (CLI) in patients with
tibial occlusive disease. It is usually performed from a transfemoral access (antegrade approach)
and, in selected cases, from transpedal or tibial access (retrograde approach).
■
Therapeutic interventions performed in tibial arteries include balloon angioplasty, drug-eluting
balloon angioplasty, stenting, and atherectomy.
■
Procedures are most commonly performed under local anesthesia with moderate conscious sedation
in a fixed-imaging hybrid operating room or in the interventional angiography suite. Portable
imaging systems may also provide sufficient resolution for precise, image-guided intervention
depending on circumstances.
■
Neuropathic pain is commonly described as burning sensation, stabbing, or aching pain that is
commonly accompanied by numbness or hypoesthesia. Diabetic neuropathy is probably most
common and is frequently nocturnal as well. The symptom complex of diabetic neuropathy may be
confused with ischemic rest pain or metatarsalgia, given the similar dermatomal distribution and
overlapping risk factors.
■
Venous ulcers are associated with skin pigmentation, induration from chronic venous hypertension,
and inflammation. They develop primarily in the perimalleolar region of the ankle and usually do
not involve the forefoot.
■
Musculoskeletal pain resulting from mechanical etiology, stress fracture, arthritis, and plantar
fasciitis
■
Soft tissue infection and malperforans ulcers in diabetic patients with advanced sensory neuropathy
and/or Charcot deformity of the foot
■
Chronic, nondiabetic peripheral neuropathies such as dorsal foot paresthesias and dysesthesias
following long saphenous vein harvest

■
Patients with infrainguinal occlusive disease present with symptoms of claudication (Rutherford
ischemia classification categories 1, 2, and 3), ischemic rest pain, or tissue loss (Rutherford
categories 4, 5, and 6). When the atherosclerotic disease is limited to the infrapopliteal arterial
segments, pain is mainly located in the forefoot. Advanced arterial insufficiency can also lead to
ischemic ulceration, gangrenous changes, and nonhealing wounds. This constellation of symptoms
represents CLI and typically occurs when the ankle pressure is less than 50 mmHg, the ankle–
brachial index (ABI) is less than 0.4, and the great toe pressure is less than 30 mmHg (FIG 1A,B).
■
CLI with tissue loss often occurs in the setting of multilevel arterial occlusive disease. In the case of
isolated diabetic tibial occlusive disease, femoral, and frequently popliteal, pulses remain
palpable. In either circumstance, limb-threatening ischemia may ensue. In the latter circumstance,
multilevel approaches to complete revascularization, either staged or simultaneous, should be
pursued.
■
Neurovascular exam, with particular focus on the wound location and the extent of tissue loss,
should be evaluated and documented. Probably, the most deterministic variable is the extent of
tissue loss—Wagner wound classification, the presence and severity of osteomyelitis, exposure or
involvement of the calcaneus bone, residual intact skin on either the dorsal or plantar foot. These
conditions all impact decision making and clinical outcome.
■
Patient functional capacity also plays an important role in the therapeutic strategy. Options and
outcome goals vary substantially between ambulatory and nonambulatory patients.

■
Pulse volume recordings (PVRs) (FIG 2)
■
Duplex (FIG 3)
■
Computed tomography (CT) and magnetic resonance (MR) angiograms can be obtained; however,
their diagnostic use in planning tibial interventions is frequently limited by the imprecision of
bolus timing with distal extremity cross-sectional imaging techniques, heavy medial calcification
frequently present in target arteries, and the diminutive size of reconstituted target arteries, which
may be present in the peri- and inframalleolar regions.
■
Catheter-directed, intraarterial angiography remains the gold standard imaging study for tibial
occlusive disease for both diagnostic and therapeutic purposes (FIG 4).
SURGICAL MANAGEMENT
■
Technical skills, careful planning, and knowledge of the relevant arterial anatomy determine tibial
revascularization strategies for limb salvage. Current controversies include the potential value of
restoring patency in more than one tibial vessel to optimize blood flow and maximize the chances
of wound healing. Proponents of this approach reference the “angiosome” concept of the foot or
the idea that specific skin regions derive primary perfusion from end-arterioles arising primarily
from either the dorsal pedal or posterior tibial arteries as they cross the ankle. This practice is
pursued in marked contradistinction to the open surgical imperative to restore in-line flow to the
foot in the single largest, most continuous crural artery. The many advantages of endovascular
reconstruction techniques in tibial reconstruction include restoring partial flow in multiple target
arteries as compared to a single artery following surgical bypass, as well as opportunities to
repeat procedures with relatively simple outpatient interventions as needed, to maintain patency
and skin integrity. Treatment decisions regarding revascularization strategy in individual
circumstances should be guided by patient-specific anatomic considerations, arterial runoff into
the foot, patient habitus and ambulatory status as well as patency and feasibility considerations
related to either open or endovascular options.
■
Currently available endovascular technology facilitates successful treatment of complex occlusive
lesions at and below the malleolar level. Technical limitations remain, however, highlighted by
risks of arterial perforation (FIG 5), difficulty in true lumen reentry in complete occlusions (FIG
6), procedure-related distal arterial embolization, and limited pedal vessel outflow in certain
circumstance.
■
The retrograde or SAFARI (SubintimAl Flossing with Antegrade-Retrograde Intervention) tibial
intervention technique may improve technical results in challenging lesions, particularly those
resistant to ipsilateral antegrade access, including flush occlusions at the origin of the target artery
or with large collateral arteries adjacent to the occluded origin. In nearly every circumstance, even
chronic and recalcitrant occlusions may be crossed more easily from the retrograde rather than
antegrade approach; this is true regardless of the chronicity of the lesion in question, degree of
calcification, or length of occlusion.
■
Preoperative vein mapping prior to the diagnostic angiogram is helpful in handicapping potential
surgical alternatives and determining the extent to which interventional alternatives to be pursued.
■
Patients should be medically optimized prior to their procedure: Preventive strategies are advised
to reduce the risk of kidney injury in patients at risk for contrast nephropathy; smoking cessation is
encouraged as well as antiplatelet and statin therapy.
■
Tibial interventions can entail significant radiation exposure. Protective shields, lead glasses, and
judicious use of fluoroscopy are recommended to protect all participants in the procedure.
Ultrasound-guided access can minimize radiation exposure, particularly for pedal access; needle
extenders allow the operator to puncture remotely and minimize hand exposure.
■
Micropuncture and pedal access kits are essential access tools.
■
Sheaths: 5 and 6 Fr, braided, 90 cm or 110 cm from contralateral femoral access; 45- to 55-cm
sheath from the ipsilateral transfemoral access
■
Wires: 300-cm, 0.014-in or 0.018-in wires; 260-cm, 0.035-in floppy Glidewire™
■
Catheters: 150- to 170-cm catheters and balloons
■
Medications: heparin (or other anticoagulant), clopidogrel, nitroglycerin, papaverine, alteplase, and
calcium channel blockers. Consider preprocedural perioperative antibiotics prior to procedures
potentially requiring prosthetic implants.
Positioning
■
The patient is placed supine on the angiographic table with both groins prepped and draped.
Consider preparing the foot and the leg in anticipation for retrograde approach if needed.
Stockinette can be placed over the involved foot and the leg is covered with the angiographic
drape (FIG 7).
TECHNIQUES
ANTEGRADE TIBIAL REVASCULARIZATION

First Step: Femoral Access and Anticoagulation
■
Contralateral femoral access with standard up and over technique is our routine approach for
diagnostic arteriograms and most tibial interventions.
■
Antegrade femoral approach has distinct advantages for tibial or pedal interventions, especially in
the setting of a hostile and narrow aortic bifurcation or occluded or severely diseased contralateral
iliofemoral system. Antegrade access generally provides easier pushability and reduced radiation
to the patient and procedural team.
■
Ultrasound-guided access may minimize risk for access site complications.
■
Diagnostic arteriogram to image the inflow is performed.
■
A 5- or 6-Fr sheath is advanced over a stiff wire to the popliteal artery, positioned as close as
possible to the tibial trifurcation. (Sheath: 90 to 110 cm from the contralateral femoral access and
45 to 55 cm from the ipsilateral femoral access) (FIG 8).
■
Sheath tip positioning close to the target vessel maximizes pushability across total occlusions. Also,
improved visualization of tibial vessels is achieved with reduced contrast volumes.
■
Anticoagulation is established using unfractionated heparin or other alternatives to achieve an
activated clotting time (ACT) of more than 250 seconds.
Second Step: Selective Angiogram
■
Imaging of the tibial outflow is obtained from sheath injections or through diagnostic catheters (5- to
10-mL power or hand injection). To reduce contrast load, contrast may be diluted 50% for all but
the most distal arterial beds.
■
Anteroposterior or ipsilateral anterior oblique projections are obtained to visualize the popliteal
“trifurcation” and separate the tibia and fibula. True lateral oblique projections are obtained to
visualize pedal outflow.
■
Arteriographic images must be carefully examined to optimize outcome; multiple projections may be
required to sufficiently opacify tibial and pedal vascular anatomy, especially distal to extended or
serial occlusions. Delayed views (prolonged digital subtraction angiography [DSA] time) may
improve opacification of patent tibial or pedal vessels distal to occluded segments (FIG 9).
Withdrawing the sheath to the femoral bifurcation may uncover reconstitution of distal tibial artery
segments through extended deep femoral artery collateral pathways.
Third Step: Crossing the Occlusion
■
Angled catheters and guidewires are typically used to select the respective tibial arteries.
■
The catheter/guidewire combination is advanced into the target tibial artery proximal to the
occlusion or stenosis.
■
Anatomy is confirmed with magnified arteriographic views.
■
“Road mapping” may improve guidance across occlusions. The wire leads through the occlusion,
followed by the crossing catheter (e.g., Quick-Cross™ or Cook CXI™, 0.014 in or 0.018 in) (FIG
10).
■
Transluminal passage is preferred to subintimal access, because reentry into the true lumen may be
unpredictable and challenging.
■
Soft-tipped hydrophilic guidewires are used to negotiate and traverse tibial stenosis with the
support of crossing catheters under magnified road map guidance.
■
Heavier weighted tip, chronic total occlusions (CTO) guidewires (either 0.014-in or 0.018-in
platforms) are designed to provide improved performance and penetration across total occlusions.
■
For longer occlusions, leading with a 2-mm percutaneous transluminal angioplasty (PTA) balloon as
an alternative to low-profile crossing catheters (e.g., Quick-Cross™ or CXI™) can improve
access by extending or reestablishing the recanalization plane during transit.
Fourth Step: Reentry into the True Lumen
■
Reenter into the true lumen under road map guidance (FIG 11).
■
Advance the catheter over the wire into the true lumen beyond the target lesion and remove the wire.
■
Aspirate to check for back-bleeding and subsequently perform a selective angiogram through the
catheter to confirm the proper intraluminal position (FIG 12).
■
Advance a stiff wire with long, soft tip into the target vessel as distal as possible (FIG 13).
■
Remove the catheter carefully under fluoroscopic guidance while maintaining wire access into the
distal patent artery.
■
Reentry devices can be used to select the true lumen from a dissection plane. Alternatively, if failure
to reenter the true lumen persists despite the use of reentry devices or balloon angioplasty to
disrupt the dissection membrane, access into the distal true lumen can be reattempted in a staged
future setting.
Fifth Step: Treatment with Balloon Angioplasty
■
The proximal and distal ends of the lesion are demarcated by a repeat contrast injection through the
sheath. The use of radiopaque adhesive rulers applied on the affected leg may help with
measurement and device selection.
■
Deliver the appropriate size balloon (typically 2 to 3.5 mm in diameter) to the target lesion and
perform the balloon angioplasty for 2- to 3-minute inflation time (FIG 14).
■
Single inflation using a long balloon decreases the procedural time and reduces the risk of
postangioplasty dissection requiring reintervention (FIG 15). Tapered balloons can help treat
lesions across vessels of variable size.
■
Heparin flush, continuous or intermittent, through the sheath is recommended during balloon inflation
and throughout the procedure.
■
Selective injection of intraarterial nitroglycerin through the sheath will minimize the effects of
spasm at or distal to the intervention.
Sixth Step: Angiogram Post–Balloon Angioplasty
■
The treatment balloon is retracted back over the wire to the popliteal artery level.
■
The completion arteriogram is performed from a sheath injection to assess the angioplasty outcome
and pedal runoff (FIG 16).
■
Recoil or dissections are treated with sustained reinflation of the balloon for 3 to 5 minutes or by
upsizing the balloon, followed by more gradual deflation.
■
Flow-limiting dissections in the proximal tibioperoneal trunk and proximal tibial arteries may be
resolved with stent placement when necessary.
■
Distal embolization can be managed by aspiration through the existing catheter or aspiration with a
purpose-specific catheter such as the Export™.
■
Other modalities may be useful in restoring patency, such as atherectomy devices and can be used as
stand-alone therapy or as adjuncts to balloon angioplasty.
■
The routine use of tibial stenting is not advocated at this stage. Although there is some evidence to
suggest that drug-eluting stents may result in improved durability, these are subject to cost
restrictions, regulatory approvals, and availability depending on the country of practice.
Seventh Step: Reconstruction of Another Tibial Vessel
■
The ultimate goal is to reestablish direct, in-line arterial flow to the ischemic part of the foot. A
secondary goal is to optimize flow by reconstructing more than one occluded tibial artery, when
possible.
■
The wire is redirected into another tibial vessel and recanalization is performed as described
earlier (FIG 17).
■
When the peroneal artery is the sole outflow vessel, revascularization to the level of the peroneal
collaterals at ankle is needed.
■
Ostial lesions at the bifurcation of anterior tibial artery and tibioperoneal trunk can be treated with
kissing balloon technique to prevent plaque shifting.
Eighth Step: Completion Angiogram and Hemostasis
■
If the completion angiography is satisfactory (FIG 18), the sheath is pulled back to the common
femoral artery and injection from that level is recommended to rule out any complications in the
femoropopliteal segment related to sheath position.
■
The sheath is removed and hemostasis is obtained at the access site either by using closure device or
manual compression without heparin reversal unless necessary.
RETROGRADE TIBIAL RECANALIZATION

First Step: Retrograde Access
■
Antegrade access is obtained first as described earlier. This is used for initial imaging and delivery
of treatment devices.
■
Retrograde tibial arterial access is performed under ultrasound or fluoroscopic guidance using a
micropuncture 21-gauge needle; a 300-cm, 0.018-in or 0.014-in wire; and balloon or support
catheter. An introducer dilator, although potentially useful, is not essential.
■
Sedation should be managed to minimize movement when road mapping is used to identify target
arteries.
■
Local anesthesia is infiltrated at the intended puncture site.
■
Access to the posterior tibial artery is obtained in the region of the medial malleolus. Dorsiflexion
and/or eversion of the foot may facilitate access.
■
Access to the anterior tibial artery is obtained on the dorsum of the foot or the distal aspect of the
leg anteriorly, where the target artery may be larger. Dorsalis pedis access is facilitated by plantar
flexion of the foot.
■
The peroneal artery should be approached laterally through the interosseous membrane.
■
More proximal access to the posterior or anterior tibial arteries may be obtained with road map
guidance when necessary.
■
Inadvertent venous puncture may occur during attempts at retrograde access, and when it does,
consider leaving the wire in place to help guide further attempts at arterial access.
■
Ultrasound-assisted retrograde access, as an adjunct to road map guidance alone, may help to define
the three-dimensional orientation of the needle in relation to the target artery (FIG 19).
■
Image quality is optimized by incorporating a sufficient delay following contrast injection to
maximize opacification of the target artery. Selective use of intraarterial vasodilators through the
antegrade may reduce the severity of access-related vasospasm, when present, distally.
■
The C-arm is adjusted to best align the needle to the target vessel, typically using an ipsilateral
oblique projection.
■
Surgical exposure may become necessary to ensure adequate access for retrograde tibial
reconstruction. Retrograde access may also be obtained concomitant with planned transmetatarsal
amputation by identifying and cannulating the open end of transected distal dorsal pedal artery.
Second Step: Retrograde Angiogram
■
Once good back-bleeding is achieved, the wire is advanced under fluoroscopic guidance (FIG 20),
followed by an appropriately sized support catheter, balloon, or the inner dilator of the 4-Fr
microsheath.
■
In most cases, retrograde sheaths are generally not deployed to minimize trauma to the puncture site
and distal target artery (FIG 21). When sheaths are required, use of a radial access sheath will
facilitate atraumatic access.
■
Intraluminal position is confirmed by retrograde angiography through the catheter or dilator (FIG
22).
Third Step: Recanalization of Tibial Occlusion
■
Antegrade sheath arteriography is used to delineate the extent of the target lesion.
■
The occlusion is crossed using 0.018-in or 0.014-in wires, supported by a crossing catheter or low-
profile angioplasty balloon (FIG 23).
■
The wire and crossing catheter combination is advanced from distal to proximal and into the
popliteal artery if possible. The wire is removed.
■
Following aspiration to confirm luminal position, a selective arteriogram is performed from the
retrograde catheter.
Fourth Step: Exteriorization of the Wire from the Femoral Access Site
■
Next, an attempt is made to advance the guidewire into the antegrade sheath.
■
When this proves difficult on its own, a snare is deployed through the antegrade sheath to capture
and externalize the distal retrograde wire (FIG 24).
■
Following successful externalization of the retrograde wire, “wire access” is available from both
ends.
■
A crossing catheter is then advanced from the antegrade access site over the wire to the patent tibial
vessel distal to the occlusion.
■
Distal intraluminal position is confirmed with arteriography through the crossing catheter.
■
Next, the through and through wire is removed from the antegrade sheath, leaving the crossing
catheter across the lesion. The wire is exchanged for a 300-cm working wire, advanced distally
through the antegrade crossing catheter.
■
The retrograde access catheter or micropuncture 4-Fr access dilator is subsequently removed from
the distal target artery. Hemostasis is obtained and maintained by manual pressure at the access
site (FIG 25), the application of a blood pressure cuff across the site (FIG 26), or a radial
compression device (Dstat™ Radial Hemostat Band).
■
Removing all devices from the retrograde access site as quickly as possible reduces instrumentation
time and potential for arterial injury and distal thrombosis.
■
Inflating a balloon advanced from the antegrade access sheath across the retrograde access site (FIG
27) may affect hemostasis but can also increase traumatic injury and access site bleeding and is
thankfully rarely needed.
Fifth Step: Treatment with Balloon Angioplasty

■
The intervention is then performed in the standard fashion from the antegrade approach (FIG 28).
Antegrade-Retrograde Approach
■
If the retrograde wire is not able to cross the lesion and regain access to the true lumen, an
antegrade-retrograde approach may be used to create adjacent subintimal planes in opposing
directions (FIG 29).
■
The dissection flap separating the adjacent subintimal spaces may be disrupted by simultaneous
inflation in both directions.
■
This allows visualization and recanalization of true lumen from either or both directions. The two
PTA balloons selected for this maneuver should be sized appropriately to minimize risk for target
arterial rupture.
PEARLS AND PITFALLS
Goals for percutaneous ■ Achieve direct in-line flow to the ischemic foot and, when
tibial revascularization possible, optimize pedal perfusion by recanalizing more than one
occluded tibial artery.
Contralateral or antegrade ■ Choice based on inflow anatomy and target lesion. Advancement
femoral access of the antegrade sheath tip into the popliteal artery is key for
successful tibial revascularization.
Ultrasound-guided access ■ Can help access the anterior wall of the vessel in a relatively
disease-free spot and minimize access site complications. It is
recommended in antegrade femoral access and retrograde pedal
access.
Retrograde approach ■ Should not be regarded as the first option for tibial interventions.
It is selectively considered after failed attempts at antegrade
access and in the setting of flush occlusions of the antegrade artery
with large, adjacent collaterals.
Sheathless retrograde ■ Is preferred to minimize tibial artery access complications such as
technique dissection and thrombosis. Recanalization is achieved with a wire
and support catheter. Hemostasis with manual compression is
usually sufficient.
Crossing total occlusions ■ The intraluminal plane is attempted first with a stiff wire and
crossing catheter. The proper catheter position should be
confirmed with a selective arteriography prior to definitive
angioplasty.
Balloon-assisted ■ Inflation of a 2-mm balloon may assist with the recanalization of
recanalization long calcified occlusions.
Kissing balloon technique ■ Is sometimes needed to treat the ostial lesions at the origin of the
anterior tibial or posterior tibial artery, depending on the amount
of plaque in the adjacent peroneal artery or tibioperoneal trunk.
Anticoagulation ■ Maintain an ACT of greater than 250 seconds throughout the
intervention. Continuous or intermittent flushing of the popliteal
sheath with heparinized solution is recommended.
Vasodilators ■ Are used from the antegrade sheath and at the pedal access site to
prevent vasospasm and to allow better visualization of tibial
vessels distal to the occlusion
POSTOPERATIVE CARE
■
Following the procedure, the patient is observed in the recovery unit with serial postarterial
intervention, neurovascular exams, and intravenous and oral hydration.
■
A clopidogrel loading dose (usually 300 mg) is administered when the patient is not already on dual
antiplatelet therapy. Dual antiplatelet therapy is recommended for at least 3 months; longer when
stents are used.
■
Clinical follow-up is obtained 2 to 4 weeks after the procedure is performed, including vascular lab
studies (usually PVRs, segmental pressures, and Duplex arterial insonation) (FIG 30).
■
Close follow-up is essential to ensure optimal symptom resolution and limb salvage.
OUTCOMES
■
Tibial balloon angioplasty carries a relatively low primary patency rate but can greatly augment
long-term limb salvage rates. The minimally invasive nature of the procedure is especially
advantageous in high medical risk patients. One year primary patency rates in experienced hands
range from 30% to 40%; secondary patency rates approach 60%, with ultimate limb salvage
greater than 70%.1,2
■
Use of a drug-eluting balloon may improve patency rates.
■
Primary stenting does not appear to offer any advantage over tibial angioplasty alone.3 There may be
some patency advantage associated with drug eluting, as compared to bare metal stents.4 Stenting
under all circumstances should be considered as a “bailout,” used to improve suboptimal results
of angioplasty alone.5
■
Patients with significant tissue loss and gangrene should be followed very closely after successful
tibial angioplasty. Lesional restenosis rates trend higher in patients at increased risk for limb
loss.6
■
Multilevel interventions, when necessary, are associated with improved limb salvage rate and
wound healing compared to isolated tibial interventions.2
■
Postangioplasty arterial restenosis may portend less clinical significance once healing is achieved
in the distal limb or forefoot. The temporary increase in blood flow following angioplasty is often
sufficient to heal small ulcerations.7
■
There is some evidence of improved patency with drug-eluting stents and drug-eluting balloons.4,8
COMPLICATIONS
■
Access site complications (hematoma, bleeding, pseudoaneurysm) are more common with the
ipsilateral antegrade femoral approach.
■
Contrast-induced nephropathy can be avoided by sufficient preoperative, intraoperative, and
postoperative hydration as well as judicious use of contrast at all times.
■
Vessel thrombosis can be avoided by maintaining a therapeutic anticoagulation level throughout the
procedure. The use of nitroglycerin can help prevent vasospasm and a low-flow state. Dual
antiplatelet therapy is recommended to avoid early postprocedural target artery thrombosis.
■
Outflow embolization may be successfully treated with aspiration embolectomy or alteplase if
needed.
■
Retrograde access site bleeding, dissection, and vessel thrombosis are described after the
retrograde pedal access. Using ultrasound-guided access, sheathless technique and the use of local
vasodilators may minimize the risk of retrograde access site complications.
■
Compartment syndrome may develop either from reperfusion injury following successful
intervention or, more commonly, perforation of tibial arteries in the deep compartments of the leg.
■
Limb loss may result from failed intervention, iatrogenic vessel thrombosis, distal arterial occlusion
following embolization, and compartment syndrome.
REFERENCES
1. Fernandez N, McEnaney R, Marone LK, et al. Predictors of failure and success of tibial interventions for critical limb ischemia. J
Vasc Surg. 2010;52:834–842.
2. Fernandez N, McEnaney R, Marone LK, et al. Multilevel versus isolated endovascular interventions for critical limb ischemia. J
Vasc Surg. 2011;54:722–729.
3. Randon C, Jacobs B, De Ryck F, et al. Angioplasty or primary stenting for infrapopliteal lesions: results of a prospective randomized
trial. Cardiovasc Intervent Radiol. 2010;32:260–269.
4. Bosiers M, Scheinert D, Peeters P, et al. Randomized comparison of everolimus-eluting versus bare-metal stents in patients with
critical limb ischemia and infrapopliteal arterial occlusive disease. J Vasc Surg. 2012;55:390–398.
5. Donas K, Torsello G, Schwindt A, et al. Below knee bare nitinol stent placement in high-risk patients with critical limb ischemia is
still durable after 24 months of follow-up. J Vasc Surg. 2010;52:356–361.
6. Sagib NU, Domenick N, Cho JS, et al. Predictors and outcomes of restenosis following tibial artery endovascular interventions for
critical limb ischemia. J Vasc Surg. 2013;57(3):692–699.
7. Schmidt A, Ulrich M, Winker B, et al. Angiographic patency and clinical outcome after balloon-angioplasty for extensive
infrapopliteal arterial disease. Catheter Cardiovasc Interv. 2010;76:1047–1054.
8. Schmidt A, Piorkowski M, Werner M, et al. First experience with drug-eluting balloons in infrapopliteal arteries: restenosis rate and
clinical outcomes. J Am Coll Cardiol. 2011;58;1105–1109.
Chapter 33 Perimalleolar Bypass and Hybrid Techniques
Geetha Jeyabalan Rabih A. Chaer
DEFINITION
■
Perimalleolar bypasses are defined by the anatomic location of the distal target outflow vessel.
Perimalleolar bypasses refer to any bypass in which the distal target vessel of revascularization is
the posterior tibialis, anterior tibialis, or peroneal arteries at the level of the ankle. The pedal
vessels (dorsalis pedis, posterior tibialis, lateral or medial plantar artery) are also target vessels
in some patients with very distal disease.
■
These bypasses are performed in patients with advanced critical limb ischemia (CLI), which
includes tissue loss, or ischemic rest pain for which there is not a durable or feasible
endovascular option. With the advent of advanced endovascular techniques, the indications for
perimalleolar or tibial bypasses are evolving. The inflow vessel and conduit chosen are tailored
to individual patients and their anatomic limitations.
■
The three major etiologies of lower extremity ulceration include ischemic, neuropathic, and venous
stasis disease. Although all of these can have poor perfusion as a primary contributing factor, the
diagnostic workup and management may be slightly different. Arterial ulcerations typically have a
punched-out dry appearance and usually occur on the distal forefoot and toes, whereas neuropathic
ulcerations often occur on pressure points and are associated with calluses. Venous stasis
ulcerations are typically located on the medial or lateral malleolus and have associated skin
changes and brawny induration in addition to serous drainage.

■
Patients with CLI typically present with ischemic rest pain and/or tissue loss or forefoot gangrene.
Most of these patients have significant comorbid conditions such as diabetes mellitus, coronary
artery disease, hyperlipidemia, and hypertension that will be important for risk stratification and in
deciding between different revascularization modalities. Additionally, managing and optimizing
these risk factors are keys to successful outcomes following lower extremity revascularization,
regardless of the technique used. As such, optimizing lipid profile, glycemic control, smoking
cessation; minimizing renal dysfunction; and managing hypercoagulable states are all essential
components to the perioperative medical management, in addition to managing any concomitant
coronary disease. The majority of patients are already followed by a team of physicians for their
comorbidities (primary care physician, cardiologist, endocrinologist, nephrologist), whereas the
surgical team is evaluating the peripheral vascular disease. It is imperative that these consultants
remain actively involved in the perioperative period for both the short-term and long-term success
of limb salvage and overall survival. The age of the patient, functional status, and comorbidities
guide the vascular surgeon’s decision making in terms of the type of revascularization offered to
the patient.
■
Most patients presenting as outpatients will have a history of symptoms of disabling claudication,
rest pain, or tissue loss. Taking a careful history noting duration of symptoms, level of
pain/claudication, areas of tissue loss, and history of traumatic neuropathic ulceration will guide
the workup. Young patients, younger than 60 years of age, or patients with multiple arterial/venous
thromboses should undergo a thrombophilia evaluation. Physical examination should include a
thorough peripheral vascular examination, including assessment of the potential presence of a
palpable aortic aneurysm on abdominal exam. The quality and symmetry of pulses and/or handheld
Doppler signals between both legs at the femoral, popliteal, and pedal levels assist in determining
the anatomic level of disease. Wound documentation, when present, should note location, depth,
presence of infection, bone exposure, and extent of soft tissue defects. Neuropathic deformities of
the foot should also be taken into careful consideration for offloading purposes. If there is gross
purulence or systemic signs of infection, a debridement of the affected area is required prior to
revascularization, even if the area is malperfused, for source sepsis control.
■
The location and appearance of ulcerations will often assist in differentiating ischemic, neuropathic,
or decubitus wounds. Location of the ischemic wound is important in determining which target
vessel will be chosen for revascularization. If the history and physical examination suggest
peripheral vascular disease as the primary diagnosis, then noninvasive vascular testing is the next
step in determining need for revascularization and level of disease.

■
After a thorough history and physical examination, the diagnostic workup of patients with ischemic
ulcerations, rest pain, or significant claudication involves noninvasive vascular testing. This
involves calculation of ankle–brachial indices and pulsed volume recordings in addition to duplex
imaging of the extremity. An ankle–brachial index (ABI) of less than 0.4 is typically seen in
patients with CLI (FIG 1). Toe pressures of less than 40 mmHg suggest inadequate perfusion for
wound healing. In cases of severely calcified vessels, it is important to obtain associated pulsed
volume recordings and toe pressures because ABIs can be falsely elevated due to vessel
incompressibility. Transcutaneous oxygen tension (TcPO2) measurement can also be used to
determine the severity of ischemia and probability of wound healing.
■
Once the history, physical examination, and noninvasive testing are complete, the surgeon must
determine the next step in imaging, which may be both diagnostic and therapeutic. The patient’s
functional status, cardiac risk profile, and other comorbidities (ambulatory status, etc.) will all
play an important role in determining whether any revascularization attempt is even feasible. If
femoral pulses are not palpable on physical examination and noninvasive testing is also suggestive
of inflow disease, computed tomography arteriography (CTA) may be instrumental in evaluating
the extent of aortoiliac disease, taking into account renal function and risk of contrast-induced
nephrotoxicity. Alternatively, aortography obtained from contralateral femoral access or upper
extremity arterial access may suffice. General management approaches to aortoiliac versus
infrainguinal disease are discussed elsewhere in this book.
■
Once the clinical determination is made that the level of disease is infrainguinal, digital subtraction
angiography is an excellent diagnostic test and provides access for therapeutic intervention as
well. This chapter focuses on patients with multilevel infrainguinal disease who, presumably, have
either failed endovascular revascularization, prior open bypass, or who have no endovascular
options for revascularization. Therefore, the primary goal of diagnostic angiography is to assess
the caliber and quality of inflow vessels and bypass targets.
■
The contralateral femoral artery is accessed and an aortogram with oblique pelvic views is
obtained to rule out the presence of inflow disease that may need treatment prior to evaluating the
infrainguinal segment. An ipsilateral oblique magnified projection will be helpful in determining if
there is any significant common femoral or profunda femoris stenosis, which is especially
important if these vessels are to be chosen as the source of inflow for an open bypass (FIG 2).
■
Deciding on which type of intervention to perform, endovascular versus open, and how aggressive
to be about either approach is determined by multiple considerations as outlined earlier and
elsewhere in this section. Patients requiring open bypass typically have multilevel disease. As
such, it is critically important to image the runoff with the catheter placed proximal to the profunda
origin, as the distal runoff will likely be filling from profunda collaterals that are communicating
with geniculate collaterals. With common femoral or profunda disease, the catheter will need to be
placed in the common iliac artery to evaluate internal iliac collaterals that are in communication
with the profunda and more distal collaterals. Performing magnified, time-delayed digital
subtraction angiography will assist in revealing which tibial vessels are patent and filling through
collateral networks. It is also essential to identify the primary named crural artery that is in
continuity to the foot that will perfuse the tissue affected by ischemic ulceration (FIG 3).
■
Using full-strength contrast, magnified projections of the foot will help delineate which pedal
vessels are patent, which fill the tarsal and plantar branches, and confirm the status of the plantar
arch. Occasionally, there are situations in which no suitable target (e.g., “named” artery) is
identifiable and exploration of a tibial vessel at the time of operative intervention may be
required. This exercise is fraught with risk, however, especially in the setting of a desperately
ischemic foot, and should rarely be undertaken without conclusive pre- or intraoperative
arteriography. Duplex ultrasonography may assist in further defining quality, caliber, and patency
of tibial vessels in these situations. Choosing a patent posterior tibialis or anterior tibialis artery
in direct continuity with the pedal arteries is preferred over a peroneal artery as a distal target
when the former is available, especially in cases of forefoot wounds; however, peroneal arteries
are perfectly suitable and serviceable in this situation in the absence of other alternatives.
■
The decision to proceed with open perimalleolar bypass is made in the context of the patient’s
overall clinical functional status, cardiopulmonary and renal comorbidities, presence of
autogenous saphenous vein conduit, and options for endovascular revascularization. Preoperative
autogenous conduit assessment is best performed by detailed ultrasonographic imaging along the
length of the vein. Preference is always given to a single segment of greater saphenous vein (GSV)
from the ipsilateral leg that is at least 2.5–3 mm in diameter, compressible, and free of thrombus
throughout. Assessment of the contralateral GSV is useful in case ipsilateral vein is found to be of
poor quality during operative exploration.
■
Inflow artery selection is usually based on length of available conduit and location of proximal
disease. The common, superficial, or deep femoral or popliteal arteries may all serve as suitable
inflow arteries in circumstances where minimal or insignificant occlusive disease is present
proximally. This determination is best made during diagnostic angiography. The need for
concomitant inflow endarterectomy should also be evaluated at this time.
SURGICAL MANAGEMENT
■
Type of anesthesia to be used is determined by the type of cardiopulmonary comorbidities and the
anatomic level of arterial occlusive disease. Preoperative consultation with anesthesiology and
cardiology is customary in this patient population to assess the appropriate amount of surgical risk.
General anesthesia, peripheral nerve block, and spinal anesthesia are all potential options in this
group of patients. Intraoperative fluid administration should be used judiciously and preoperative
preparation should include blood type determination and crossmatching as necessary. It is our
practice to hold therapeutic anticoagulation for at least a few days prior to the procedure, but most
patients remain on antiplatelet agents through the day of surgery and continue through the
perioperative period.
Positioning
■
Any lower extremity bypass might require intraoperative angiography and, as such, all such
procedures should be performed on a radiolucent table. The patient is positioned supine, with the
leg slightly abducted and externally rotated to provide optimal exposure of the ipsilateral GSV
harvest site (FIG 4). It is our practice to localize the GSV by ultrasound to assist in incision
planning. This also helps determine whether the contralateral leg should also be prepped as an
alternative site for vein harvesting.
■
Other items that should be available in the room include a sterile pneumatic tourniquet and surgical
bump. Both are useful when the below knee popliteal artery or tibioperoneal trunk is used for
arterial inflow for the graft. Open forefoot wounds are excluded from the operative field with
adhesive or Ioban drapes.
TECHNIQUES
PERIMALLEOLAR BYPASS TO THE DISTAL POSTERIOR TIBIALIS

ARTERY
First Step: Exposure of the Posterior Tibialis Artery at the Ankle
■
Simultaneous dissection of the inflow and outflow targets increases the efficiency of the operative
approach. The distal incision is marked by palpating posterior to the medial malleolus, taking care
to avoid injury to adjacent GSV (FIG 5). Dissection is carried sharply through skin and
subcutaneous tissues and through the flexor retinaculum. The tendons of the flexor digitorum longus
muscle and flexor hallucis longus pass anteriorly and posteriorly, respectively, to the
neurovascular bundle at this level. The paired tibial veins are often seen first as overlying the
artery. The tibial nerve travels posterior to the artery and may not be seen clearly during this
exposure. The tibial artery does not need to be dissected circumferentially if a pneumatic
tourniquet is deployed for proximal control. Use of a tourniquet minimizes risk for venous injury at
the dissection site and trauma to the arterial endothelium from vessel loops and vascular clamps.
For exposure of the medial and lateral plantar arteries, the same incision is typically carried
further distally onto the medial aspect of the foot.
Second Step: Exposure of the Inflow Artery

■
Concurrent dissection of the arterial inflow should be performed while the tibial target is being
exposed. If the common femoral artery is chosen, then a longitudinal vertical incision just below
the inguinal ligament will allow for simultaneous exposure of the femoral bifurcation in addition to
the saphenofemoral junction for dissection of the GSV (FIG 6). If the deep femoral artery is to be
used as inflow, then division of the lateral femoral circumflex vein may be helpful in controlling
the first-order branches past the origin. If the deep femoral origin is truly deep, the muscle bellies
of the adductor longus and vastus medialis should be divided to limit the angle from which the
graft originates from the arterial anastomosis. If the below knee popliteal artery is to be used as the
inflow, which might be the case in diabetic patients with severe tibial disease not amenable to
endovascular revascularization, this exposure is best obtained through a medial calf incision.
Third Step: Harvest and Preparation of Autogenous Vein
■
The course of the GSV is marked on the skin prior to prepping. The shortest segment of suitable
caliber and quality GSV is harvested. Incision placement is partially determined by the location of
the arterial access incisions. Care should be taken to avoid creating skin flaps during vein
exposure. Harvesting vein through skip incisions may help to minimize wound complications but is
not necessary for a good result. Minimal vein manipulation, with care being taken to accurately
ligate side branches with 4-0 braided permanent suture (or silk), is important. Minimal dissection
of the vein is typically required when in situ bypass in planned. The vein can be left in its bed,
with limited dissection of the anastomotic segments. Skip incisions provide access to ligate large
side branches.
■
After an adequate length of saphenous is exposed, it is removed from its bed for bypass placement
or transposed into position after valve lysis for in situ bypass. When removed and repositioned,
we generally try to use the largest diameter segment for bypass. The saphenofemoral junction is
oversewn or suture ligated. The vein is then reversed and distended gently with heparinized saline
or plasmalyte solution. Other vein preservative solutions can be used at the discretion of the
surgeon. Any untied branches are carefully clamped and tied with silk suture. Small tears or holes
are oversewn in a longitudinal fashion, taking care not to narrow the vein, using 7-0 polypropylene
suture (FIG 7). Depending on institutional expertise, endovein harvest is an alternative method to
minimize incisional length and potential wound complications.
■
Once prepared, veins can be used in reversed or nonreversed configurations. We generally prefer
reversed as to minimally disrupt the endothelium. If the distal portion of the vein is significantly
smaller and concern exists regarding size mismatch at either end, then veins may be positioned in a
nonreversed fashion by lysing the valve. To lyse the vein valves, a valvulotome is gently passed up
the vein after the proximal anastomosis is complete and the vein is perfused and distended. It is
critically important to have the first assistant provide gentle countertraction on the vein as the
valvulotome is hooked on the valves in order to lyse them (FIG 8A). Care must also be taken to
not hook the valvulotome on any ligated branches to avoid tearing the vein. Other commercially
available valvulotomes can be used at the discretion of the surgeon.
■
Tunneling the vein: The tunnel is created using a hollow tunneler (e.g., Gore, Scanlan, Jenkner) with
a blunt appropriately sized tip (6 mm at least) in a subcutaneous plane away from the
saphenectomy incision, if possible, to avoid wound complications. The vein is carefully inspected
at the entry and exit site of the tunnel to ensure it is in a loose plane and not constrained by fascial
or muscular bands (FIG 8B).
■
After systemic anticoagulation is achieved with unfractionate heparin, the proximal anastomosis is
performed after controlling the inflow artery with vessel loops or vascular clamps. The loops or
clamps are released and the anastomosis is confirmed to be hemostatic. Once this is assured, the
vein is perfused and distended, the valves are lysed if applicable, and the vein is marked for
orientation. It is then passed through the tunneler to exit the distal incision and clamped proximally
with an atraumatic bulldog clamp or Yasargil clip. The length of vein needed is determined after
the vein has already been tunneled and distended, with the leg in a maximally extended position.
The leg can be manipulated in various positions with knee flexion to make sure any excess or
redundant vein is appropriately trimmed prior to embarking on the distal anastomosis.
Fourth Step: Distal Anastomosis Creation
■
If a tourniquet is to be used for distal control, then the lower leg is exsanguinated using an Esmarch
bandage. The tourniquet is placed around the thigh if the inflow is at the level of the common
femoral, profunda femoris, or proximal superficial femoral arteries. It is inflated to 250 to 300
mmHg. The target is then identified. Care is taken to identify the artery instead of the vein because
they can appear deceptively similar when exsanguinated under tourniquet hemostasis. The distal
anastomosis is created using a 6-0, 7-0, or 8-0 polypropylene suture depending on the size of the
target artery. Loupe magnification is helpful and generally mandatory in this setting. The first
assistant should sit beside the operating surgeon to maintain suture tension around the anastomosis
and suction away blood and debris from the operative field (FIG 9).
■
If the tourniquet fails to maintain sufficient hemostasis due to medial calcification in the larger
proximal arteries, other options for hemostasis include vessel loops and vascular clamps for tibial
control, use of vessel stoppers, or use of a carbon dioxide (CO2) blower suction device.
Circumferential tibial artery dissection must be done with care to avoid injury to the adjacent
paired tibial veins, or venae comitantes, that give off several crossing branches above and below
the target artery. Newer dissolving endoluminal occlusion gels are available for temporary
hemostasis as well and may provide a less traumatic method of control in smaller arteries.
■
Prior to completion of the anastomosis, the tourniquet is deflated and flushed. The proximal graft
clamp or bulldog is released and the anastomosis is thoroughly flushed prior to tying down and
completing the anastomosis. Topical agents such as thrombin/Gelfoam, Surgicel®, or Floseal®
may be helpful in obtaining hemostasis following reversal of anticoagulation with protamine.
■
Wound closure is a key component of the operation. Most of the morbidity from these procedures
arises from wound complications. The vein harvest bed should be irrigated, inspected for
hemostasis, and closed in multiple layers of running or interrupted absorbable suture. Care is taken
to avoid injury to the saphenous nerve. At the ankle and around points of flexion, such as the knee,
it is useful to use vertical mattress nylon suture. It is also important to close the ankle incision first
before reperfusion edema makes tension-free closure challenging. It is often difficult to get more
than one layer of subcutaneous tissue over the bypass and distal anastomosis at the perimalleolar
level (FIG 10).
■
The patency of the bypass is assessed intraoperatively by multiple potential methods. Feeling a
strong bypass pulse in the tunnel and in the target vessel distal to the anastomosis is reassuring.
Listening with a handheld Doppler to assess the quality of the Doppler signal of the artery distal to
the distal anastomosis is also helpful. A multiphasic strong Doppler signal that augments
significantly when the graft is first compressed and then released is suggestive of a patent bypass.
In the absence of strong clinical signs of graft patency (e.g., palpable distal pulse), an
intraoperative color flow duplex scan may be used to identify potential flow limiting defects, such
as retained valves, focal velocity elevations, and low flow in the graft itself. However,
intraoperative duplex scanning is not available in all operating rooms with sufficient resolution to
recognize these defects. Finally, on-table arteriography also provides useful detail regarding
potential problems, including the status of the anastomoses, tunneling issues, and the presence of
retained valves, if any. Completion arteriography can be performed either through an up-and-over
approach from the contralateral femoral artery or with a puncture in the ipsilateral inflow artery
just above the proximal anastamosis (FIG 11). Some degree of spasm may be seen at the site of
clamp placement or vessel loop manipulation. When tunneling concerns arise, dynamic
arteriography with the leg flexed and extended in various positions can be helpful to prevent
kinking of the bypass in the early postoperative period.
PERIMALLEOLAR BYPASS TO THE DISTAL ANTERIOR TIBIALIS
ARTERY
First Step: Exposure of the Anterior Tibialis Artery at the Ankle
■
Simultaneous dissection of the vein and proximal inflow artery should occur while the distal bypass
target is identified and controlled as described earlier. The distal exposure of the anterior tibial
above the ankle is performed by identifying the tendon of the extensor hallucis longus and creating
an incision just lateral to this and medial to the tibialis anterior tendon. Plantar flexing the ankle
and palpating the space that opens between the two tendons often easily identify this groove in
which the artery runs. The extensor retinaculum is divided at the malleolus and the vascular bundle
should be easily identified at this level lying along the anterior surface of the tibia (FIG 12).
Second Step: Tunneling the Vein to the Anterior Tibialis Artery

■
The GSV is harvested and either reversed or used in a nonreversed fashion depending on factors
described earlier. The tunnel from the inflow artery to the anterior tibial can be maintained in a
subcutaneous plane across the anterior surface of the tibia medial to the exposure site. A
counterincision may be needed at the ankle to allow for a gentler curvature of the vein graft toward
the dorsum of the foot. If there is concern about potential compression of the vein graft in this
region because of its superficial nature, the alternative is to tunnel through the interosseus
membrane. This tunnel is created higher in the calf between the deep posterior and anterior
compartments (FIG 13). Because the GSV harvest incision is already on the medial calf, the
dissection can be extended deeper by retracting the gastrocnemius muscles posteriorly and
partially dividing the soleus to reach the posterior tibial vessels. These are protected and gently
retracted posteriorly while the fibers of the tibialis posterior muscle are separated and the tunneler
is bluntly passed through the interosseus membrane here. Once the vein graft is in the anterior
compartment, it can be tunneled in a subcutaneous or subfascial plane to reach the exposed anterior
tibialis artery just above the ankle.
Third Step: Exposure of the Dorsalis Pedis Artery

■
If the dorsal pedal artery is the target vessel, then the exposure distally is on the dorsum of the foot
and the tunneling techniques remain similar to what is outlined earlier for the anterior tibial artery
at the ankle. An incision is created on the dorsum of the foot just lateral to the extensor hallucis
longus tendon and carried down through the fascia. The dorsal pedal artery lies lateral to the deep
peroneal nerve here (FIG 14).
■
Care should be taken to not leave self-retaining retractors in for too long in these smaller distal
incisions to avoid tension on the wound edges and potential skin necrosis.
EXPOSURE OF THE PERONEAL ARTERY AT THE ANKLE

First Step: Peroneal Artery Anatomy
■
The peroneal artery comes off the tibioperoneal trunk at the upper calf and then distally branches
into two perforating branches, termed anterior and posterior perforating peroneal arteries, which
supply the anterior and lateral compartments and communicate with the anterior tibial artery and
some tarsal branches.
Second Step: Exposure of the Distal Third of the Peroneal Artery
■
Because the proximal segment of the peroneal artery can be accessed easily from a medial
approach, the perimalleolar or distal third of the artery needs to be approached from a lateral
approach and requires resection of a portion of the fibula. An incision is created along the lateral
border of the fibula and dissection is carried down through the fascia to the fibula after which the
periosteum is cleared proximally and distally (FIG 15). The peroneal arteries are in close
proximity to the fibula medially and care should be taken to avoid injury to the vascular bundle
when clearing the bone medially (FIG 16). The bone can then be excised and the peroneal artery is
identified behind the interosseus membrane. The bone can be transected using a Gigli saw or
oscillating power saw. The advantage of either a traditional bone cutter or power saw is that the
bone does not necessarily have to be circumferentially dissected.
■
The peroneal artery can also be exposed posteriorly, but this is somewhat challenging to do when
the patient is supine. An incision just above the ankle posterolaterally between the tendons of the
flexor hallucis longus and the flexor digitorum longus reveals the artery in its most distal segment
(FIG 17). This approach is favored when the small saphenous vein will also be harvested for the
graft conduit.
Third Step: Additional Procedure: Spliced Vein
■
Despite careful preoperative planning and efforts to fully interrogate adequate conduit, the greater
saphenous vein may prove to be unsuitable for the intended purpose once exposed. If length of vein
is a concern, then careful consideration should be given to either moving the inflow anastomosis
more distally or moving the target artery more proximally. An additional alternative is to create a
shorter tunnel, harvest the greater saphenous vein from the contralateral leg, or harvest arm vein
when other options are not available or advisable.
■
Occasionally, if no suitable autogenous vein conduit exists (especially in the case of redo bypass);
consideration may be given to cadaveric cryopreserved vein or prosthetic bypass with vein cuffs
or patches distally. The limitations of these nonautogenous options must be weighed against the
known patency limitations of spliced vein or arm vein grafts.
PEARLS AND PITFALLS

Preoperative planning ■ The bypass target is chosen to provide the best option for direct
in-line perfusion to area of tissue loss on the forefoot.
Placement of incision ■ Using ultrasound in the operating room to identify the GSV in
relation to the proximal and distal incisions can help avoid raising
flaps or creating postoperative wound complications.
■ Use of a tourniquet above the knee can assist in avoiding
unnecessary manipulation and potential injury to distal tibial
vessels.
Tunneling ■ Tunneling the bypass away from the vein harvest incision can help
protect the bypass from exposure and infection in case of wound
complications and wound dehiscence postoperatively.
Intraoperative assessment of ■ Manipulating the leg in slightly different positions can assist with
bypass evaluating the course of the vein bypass in the tunnel during
intraoperative assessment with on-table angiography.
Wound closure ■ Avoid leaving self-retaining retractors in distal incisions for
prolonged periods to avoid skin edge necrosis.
■ Closure of distal wounds is best accomplished with nylon suture
in a vertical mattress fashion in order to avoid tension on the
wound. Wounds over the dorsum of the foot can be closed with
horizontal mattress sutures. Occasionally, a counterincision may
be necessary to provide adequate coverage over the exposed
artery at the ankle.
Postoperative care ■ A gently placed soft cast can prevent significant lower leg edema
and subsequent wound breakdown in the immediate postoperative
period.
■ Predischarge duplex assessment of the graft is important if
intraoperative assessment of the bypass was not performed with
angiography or duplex.
POSTOPERATIVE CARE
■
Because of the length and location of incisions for inflow, vein harvest, and distal anastomosis, the
patient will undoubtedly have significant edema postoperatively throughout the affected leg. To
prevent blistering and potential wound breakdown, the foot, ankle, and lower leg may be wrapped
in a soft cast consisting of an inner layer of Webril® and outer layer of gently compressive
Coban®. Care needs to be taken to minimize external compression on the vein graft itself,
especially in the areas around the ankle. The soft case is changed on postoperative day 3. The
patient can ambulate starting on postoperative day 1, but the leg should be elevated when the
patient is sitting or in bed. Patients are left on antiplatelet therapy perioperatively. There is some
data supporting therapeutic anticoagulation in patients with high-risk vein bypasses (poor runoff,
suboptimal conduit, etc.); however, this must balanced against the risk of bleeding in individual
patients.
■
For perimalleolar bypass patients who did not get an intraoperative assessment of their bypass with
an on-table angiography, a predischarge duplex is performed to document patency and pedal
perfusion. If a significant abnormality is identified on duplex (significantly low flows in the
bypass or focally high velocities), then this should be addressed prior to discharge with
angiography or exploration of the area with appropriate intervention.
■
Once discharged, patients either return weekly for a change of their soft cast until their edema has
sufficiently resolved or follow-up at the 1-month interval for formal duplex interrogation of the
bypass. Certainly, more frequent visits may be warranted in patients with wound concerns.
■
Surveillance duplex of vein bypasses is obtained at the 3-month, 6-month, 9-month, and 12-month
postoperative time points with both ABI and graft duplex (FIG 18). After the 1-year time point,
provided everything is stable clinically with the patient and there are no previous abnormalities on
postoperative imaging, the surveillance can be moved to once a year. Occasionally, the
surveillance interval is shortened for high-risk bypasses or prosthetic tibial bypasses.
OUTCOMES
■
Primary patency of perimalleolar vein bypasses can be as high as 77% at 1 year, and limb salvage
rates up to 85% at 1 year as well. Given the significant comorbidities in many patients with CLI,
the rate of hospital readmission and poor functional outcome can be very high. Wound healing is
adversely impacted by the presence of diabetes mellitus and renal failure.
COMPLICATIONS
■
Early complications of distal bypasses include bleeding, wound infection/breakdown, and graft
occlusion. Late complications include graft stenosis, limb swelling, graft occlusion, and
aneurysmal degeneration of the vein bypass. Most patients with CLI have concomitant coronary
disease and the rate of perioperative myocardial infarction can be as high as 5%. It is very
important to maintain patients on their cardiac medications in the perioperative period and manage
fluids judiciously to avoid precipitating coronary events.
SUGGESTED READINGS
1. Cronenwett JL, Johnston KW, Rutherford BS, eds. Rutherford’s Vascular Surgery. 7th ed. Philadelphia, PA: Saunders/Elsevier;
2010.
2. Wind GG, Valentine RJ, eds. Anatomic Exposures in Vascular Surgery. Philadelphia, PA: Lippincott Williams & Wilkins; 2013.
3. Zarins CK, Gewertz BL. Atlas of Vascular Surgery. 2nd ed. New York, NY: Churchill Livingstone; 2005.
4. Netter FH. Atlas of Human Anatomy. 5th ed. Philadelphia, PA: Saunders/Elsevier; 2010.
5. Zwiebel WJ, Pellerito JS. Introduction to Vascular Ultrasonography. 5th ed. Philadelphia, PA: Saunders; 2005.
Acute Iliofemoral Deep Vein Thrombosis and May-
Thurner Syndrome: Surgical and Interventional
Chapter 34 Management
Sharon C. Kiang Brian G. DeRubertis
DEFINITION
■
Acute iliofemoral occlusion is defined as complete or partial thrombosis of any part of the iliac vein
and/or the common femoral vein (CFV), with or without associated femoropopliteal thrombosis, in
which symptoms have been present for 14 days or less or for which imaging indicates that
thrombosis has occurred within the past 14 days or less.1 Acute iliofemoral occlusion may occur
de novo following unprovoked deep vein thrombosis (DVT) or may occur (or reoccur) in the
setting of prior ipsilateral DVT or external compression (May-Thurner syndrome or neoplasia).
Treatment options include (1) systemic anticoagulation alone; (2) open surgical venous
thrombectomy; or (3) percutaneous intervention, including catheter-directed thrombolysis,
pharmacomechanical thrombectomy, and stenting of intrinsic or extrinsic obstructive lesions or
masses.
■
Iliofemoral DVT most commonly presents with unilateral leg swelling and pain. Although patient
history and simple diagnostic testing can generally distinguish from other causes, differential
diagnoses include cellulitis or worsening of chronic conditions such as venous insufficiency or
lymphedema.

■
There are three objectives in the treatment of iliofemoral thrombotic occlusion: (1) Prevent
propagation of DVT and subsequent pulmonary embolism (PE), (2) provide symptomatic relief for
the patient, and (3) prevent the development of postthrombotic syndrome (PTS).
■
A thorough history must be obtained prior to treatment because decisions regarding choice of
treatment modality are impacted by severity of symptoms as well as the patient’s overall
functional status.
■
Specific risk factors that merit individualized questioning include history of trauma, current or past
episodes of DVT or PE, history of thrombophilia, history or current diagnosis of cancer, and a
history of tobacco or substance use. Family history of DVT or PE is important to ascertain. A
thorough investigation of current medications should be undertaken, making note of any
contraceptive therapy, hormone replacement therapy, or use of anticoagulation (i.e., warfarin,
enoxaparin, etc.).
■
Symptoms of iliofemoral occlusion can range from nondescript mild symptoms to severe disabling
symptoms, and manifestations of symptoms can vary widely. Commonly reported symptoms of
iliofemoral occlusion include limb edema, heaviness, pain, lifestyle-limiting venous claudication,
stasis dermatitis, and in advanced cases, venous ulcerations.2 Duration of symptoms and
consideration of inciting events at the time of symptom development will help differentiate acute
occlusion from exacerbation of chronic disease.
■
Symptom severity is an important differentiating variable in the management rubric of acute
iliofemoral occlusion; severe and persistent symptoms, especially those continuing following the
initiation of therapeutic anticoagulation, increase the likelihood of long-term disabling sequelae.
The more severe and persistent the symptoms, the more justified the indication for aggressive
thrombus removal.
■
A detailed physical examination is essential. Conditions that produce symptoms mimicking those
associated with iliofemoral occlusion should be excluded. A thorough abdominal and lower
extremity pulse examination, with noninvasive physiologic testing if necessary, will exclude
possibility of arterial insufficiency. Comprehensive assessment of peripheral motor and sensory
nerve function and of the spine and lower limb joints can rule out these confounding etiologies.
■
The affected limb(s) should be examined for evidence of chronic venous insufficiency and/or stasis
dermatitis, as well as signs and symptoms of acute DVT. Signs of acute iliofemoral occlusion may
include pain, swelling, and bluish discoloration. Extensive thrombus propagation throughout the
ipsilateral venous system may lead to phlegmasia alba dolens, characterized by profound painful
swelling and a pale, milklike skin hue. Further thrombus propagation from the deep to the
superficial venous system increases outflow obstruction to the point of impeding arterial inflow,
precipitating phlegmasia cerulea dolens, limb threat, and tissue loss.
■
In patients with either acute or chronic venous disease, objective evaluation and prognostic
stratification is best accomplished by using the CEAP (Clinical, Etiology, Anatomy,
Pathophysiology) system and venous clinical severity score (VCSS).3,4
■
Because multiple interventions may be required to optimize outcome in acute iliofemoral disease,
patients’ expectations should be managed accordingly. In addition, iliac and femoral venous
intervention commonly requires extended periods of postoperative anticoagulation (warfarin
and/or low-molecular-weight heparin) to ensure long-term procedural success. The likelihood of
patient compliance thus represents an additional important prognostic indicator.
■
Long-term functional outcomes are discouraging for patients who refuse interventional management
of acute iliofemoral occlusive disease. Forty-four percent of patients treated with medical therapy
alone will experience venous claudication, and up to 60% will develop PTS within 2 years.5–7

■
Imaging provides important prognostic and interventional guidance to surgical management of acute
iliofemoral occlusive disease. Current modalities include duplex ultrasonography; catheter-based
contrast phlebography; and reconstructed, cross-sectional, contrast-based whole body (computed
tomography [CT] and magnetic resonance [MR]) imaging.
Duplex Ultrasonography
■
In experienced hands, duplex ultrasonography (US) provides extremely sensitive and specific
information regarding the chronicity and extent of infrainguinal venous obstruction. Diagnostic
accuracy in the iliocaval venous system is less predictable due to the presence of overlying bowel
gas and abdominal adiposity.
■
Duplex-derived criteria for acute venous occlusion include incompressibility under direct vision,
partial luminal obstruction within the normally echo-free lumen, and absent or abnormal venous
flow characteristics with respiration or following a Valsalva maneuver or distal compression.8
■
The primary advantages of duplex imaging include its noninvasive nature, avoidance of ionizing
radiation or nephrotoxic contrast agents, easy reproducibility, portability, and accessibility in the
outpatient setting. Additionally, substantial cost savings are realized compared to other imaging
modalities. Other advantages include the ability of duplex scanning to differentiate hematomas,
lymphatic system obstruction, superficial thrombophlebitis, and other soft tissue abnormalities
from deep venous obstruction. Thus, duplex scanning is the initial imaging modality of choice in
all patients with suspected iliofemoral DVT. When sufficient imaging parameters are met,
definitive therapeutic intervention may be safely performed based on duplex-derived anatomic and
diagnostic imaging alone.
Computed Tomography Venography
■
CT phlebography is frequently ordered for assessment of limb swelling in the inpatient setting.
Advantages of this modality include nearly universal availability day or night, less reliance on
skill and experience of the technical staff performing the procedure, outstanding spatial resolution,
reproducibility and sensitivity throughout the entire venous system, the simultaneous ability to
image pulmonary arterial flow and lung perfusion, freedom from limb pain induced by direct
probe compression during ultrasound examinations, and the ability to incidentally diagnose
concurrent conditions (such as solid organ neoplasia) that may influence thrombogenicity or
suitability for treatment with open versus endovascular techniques.
■
The modern helical CT phlebogram provides a diagnostic sensitivity and a specificity of nearly
100% per year and was found to detect previously unsuspected venous thrombosis at a prevalence
of 1.1%.9,10
■
CT phlebography also provides useful information regarding thrombus density (and thus chronicity),
the presence of residual luminal patency in obstructed veins, and the nature and severity of
extrinsic iliac vein compression when present.
■
The applicability of CT phlebography to the diagnosis of venous obstruction is limited by the
volume of iodinated intravenous contrast required to obtain optimal spatial resolution in target
vessels, as well as considerable whole-body radiation exposure inherent in CT imaging. On
average, the radiation dosage delivered by diagnostic CT phlebography is equivalent to that of
over 1,200 chest x-rays or over 10 years environmental exposure at sea level (dosage equivalents
courtesy of Radiation Physics Department, Stanford Hospital & Clinics). This is particularly true
in patients with reduced creatinine clearance, women of childbearing age who may be pregnant, or
in children. For many reasons, including the considerable expense associated with the study, CT
phlebography should not be considered a first-line study but rather reserved for patients in whom
duplex scanning does not provide sufficient anatomic guidance or where additional diagnoses
(e.g., pulmonary embolization, solid organ malignancy, or external iliac vein compression, etc.)
merit evaluation or exclusion.
Magnetic Resonance Venography
■
MR phlebography shares many of the advantages and disadvantages of CT-derived cross-sectional
imaging, including the ability to obtain high-quality, high-resolution images of surrounding soft
tissues and delineate the extent of accompanying lymphadenopathy, soft tissue sarcomas, venous
aneurysms, malformations, and compression syndromes that may influence treatment and long-term
management considerations. MR phlebography also provides a sensitivity and specificity of nearly
100%, respectively, in the diagnosis of acute iliofemoral venous occlusion.11
■
However, unlike computed tomography venography (CTV), magnetic resonance venography (MRV)
can be used during pregnancy and provide reduced risk of nephrotoxicity in patients with reduced
creatinine clearance (although gadolinium is contraindicated in patients with an estimated
glomerular filtration rate [eGFR] of more than 60 mL per minute).
■
Contraindications for MR-based venous imaging include the presence of implantable
pacemakers/defibrillators/infusion systems or other ferromagnetic devices and surgical
clips/endografts, as well as claustrophobia in affected patients. MR studies are also expensive
compared to duplex US, and dedicated personnel and equipment are less widely available than are
modern, multirow-detector CT imaging capabilities. Thus, MR phlebography is considered most
appropriate as a secondary examination in the absence of suitable duplex imaging or in the
presence of contraindications to CT phlebography. MR phlebography may be particularly useful in
the evaluation of coexisting or complicating ipsilateral or central venous vascular malformations.
Catheter-Based Contrast Phlebography

■
Despite continuing improvements in the quality and widespread availability of noninvasive imaging,
catheter-based contrast phlebography remains the gold standard for iliofemoral venous evaluation.
Sensitivity and specificity are also nearly 100%, and in addition to anatomic information,
physiologic venous pressure and flow information are also provided throughout the iliocaval
system when accessed in a retrograde fashion from the CFV.
■
Typical fluoroscopic findings include abrupt vessel cutoff in the case of total occlusion or
visualization of a filling defect with residual luminal flow around the margins, a phenomenon
known as “tram tracking.”
■
An obvious limitation is the relatively high degree of operator dependency, both in terms of
physician and facility capabilities. Catheter-based contrast phlebography may be nondiagnostic in
up to 18% of cases due to misinterpretations, artifacts, or superimposition of overlying
structures.12 Thus, experience and suitable infrastructure are necessary to ensure accuracy and
precision.
■
Other major drawbacks include the inherent invasiveness of the procedure and attendant procedural
risk, radiation and contrast exposure (although significantly less than that required for CT
imaging), and cost. Thus, contrast phlebography is also inappropriate as the initial diagnostic
modality for most patients and best employed in conjunction with planned interventions directed at
active thrombus removal.
Intravascular Ultrasound
■
Intravascular ultrasound (IVUS) with the 9F Volcano IVUS catheter (Volcano Corporation, San
Diego, CA) provides direct intraluminal visualization during catheter-based phlebographic
assessment and intervention.
■
IVUS-based imaging allows for precise measurement of cross-sectional area and maximum and
minimum lumen diameter. Flow within the residual lumen may be determined, as well as precise
analysis of residual luminal irregularities. The superior two-dimensional imaging characteristics
of IVUS compared to contrast phlebography make this modality the measurement instrument of
choice when assessing extrinsic iliac vein compression from tumors or overlying iliac arteries
(e.g., May-Thurner syndrome).
INTERVENTIONAL AND SURGICAL MANAGEMENT

■
Serologic and hematologic evaluation should include the basic metabolic panel (to assess renal
function and concomitant electrolyte abnormalities), complete blood count, and a coagulation
profile. It is also important to ascertain the status of antiplatelet or anticoagulation therapies when
present (e.g., dose, dosing frequency, prior complications, etc.).
■
Prior to operative intervention, the index treatment limb should be marked as required for World
Health Organization’s preoperative checklist and “time-out” requirements and extent and severity
of edema “baselined” for future comparison.
■
When appropriate access requires multiple sites (e.g., bilateral femoral and/or internal jugular vein
approaches), those should be marked and initialed as well.
Positioning
■
Patients can be placed supine or prone depending on the site necessary for access. On the operating
table, the patient should be placed supine, with their arms secured at the side to facilitate ancillary
access from the groin or neck. When popliteal access is required, prone positioning is required.
TECHNIQUES
PERCUTANEOUS MANAGEMENT OF ILIOFEMORAL DEEP VEIN

THROMBOSIS(+/− VENOUS COMPRESSION SYNDROMES)
Duplex-Guided Femoral Vein Access
■
Access site is chosen based on duplex US findings, proximal (peripheral) to the site of thrombotic
occlusion. This may be the CFV in patients with isolated iliac DVT or the popliteal or tibial veins
in patients with iliofemoral DVT.
■
Under ultrasound guidance, a 0.018-in micropuncture set is used to access the target vein. In the
setting of proximal obstruction, the vein is typically large and easily identified. Wire and catheter
exchanged is performed to upsize to a 5-Fr interventional sheath.
Baseline Phlebography
■
The initial phlebogram is performed either through the interventional sheath or through a diagnostic
catheter advanced to the suspected site of occlusion. When using digital subtraction angiography, a
mixture of 50% Visipaque and 50% saline provides adequate volume and visualization while
minimizing contrast load.
■
The ease with which guidewire passage is accomplished, as well as historical information
regarding duration of symptoms, informs interventional decision making. Patients with symptoms
of less than 7 days duration are frequently conclusively treated with single-session
pharmacomechanical thrombectomy, whereas patients with longer duration will more frequently
require pretreatment with multiday courses of catheter-directed thrombolytic therapy. The initial
phlebogram is instrumental in determining the course of therapy in this regard. Regardless of
approach, the goal of therapy is to achieve rapid thrombus removal, minimize venous obstruction,
reduce the likelihood of venous valvular damage, uncover underlying venous compression
syndromes, and at least theoretically, reduce likelihood of symptomatic recurrence.
Catheter-Directed Thrombolysis
■
Until recently, catheter-directed thrombolysis has been the mainstay of interventional management
for iliofemoral DVT. Following guidewire traversal of thrombus, treatment length is determined
via insertion of a marker catheter. Subsequently, an appropriately sized side-hole infusion catheter
is positioned over the occluding thrombus. Infusion catheters come with infusion (perforated
segment lengths) ranging from 5 to 50 cm or longer, and infusion segment length should be selected
to direct infusate specifically into luminal thrombus only—for example, not into patent luminal
segments where it will be rapidly dissipated into the venous and systemic circulation. Prior to
initiating infusion, the multipurpose guidewire used to position the catheter is exchanged for a
purpose and catheter-specific end-occlusion wire, which typically forces the infusate to exit
through the side holes rather than leak out coaxially along the guidewire lumen.
■
Once proper positioning is obtained, a continuous infusion of tissue plasminogen activator (tPA or
alteplase, Genentech, San Francisco, CA) is initiated at the rate of 0.25 to 1.0 mg per hour,
depending on the extent of thrombus burden and perceived chronicity. A concurrent, coaxial
heparin infusion (400 to 700 units per hour) is administered through the sheath to prevent thrombus
accumulation around the infusion system.
■
Monitoring in a step-down or intensive care environment is an essential safety requirement during
extended periods of catheter-directed intravenous thrombolysis outside of the cath lab. Fibrinogen
levels, coagulation profile, and hematocrit are assessed every 4 to 6 hours. Typically, tPA infusion
is halted if/when fibrinogen levels drop below 200 mg/dL or evidence of bleeding is present.
Repeat phlebography is performed every 12 to 24 hours to assess therapeutic progress and
residual thrombus load. As thrombus burden recedes, replacement catheters with shorter infusion
segments are typically chosen to concentrate drug delivery within the remaining clot. Infusion
rarely continues beyond 48 hours regardless of progress, as experience has demonstrated that
complication rates vary directly with total tPA dosage and length of infusion. Also, infusion rates
may be reduced when significant progress is noted during periodic phlebographic assessment,
again to reduce risks of dosage-related bleeding complications while still pursuing complete
dissolution of clot.
■
Ultrasound-assisted thrombolysis using the EKOS infusion catheter (EKOS Corporation, Bothell,
WA) may reduce the duration of infusion and total tPA dose. This 6-Fr catheter is also available in
multiple infusion lengths and contains a core wire producing ultrasound energy that may disrupt
fibrin bonds and increase tPA diffusion within thrombus. Clinical studies have demonstrated
equivalent clinical outcomes with reduced infusion times using the EKOS system.
Pharmacomechanical Thrombectomy
■
Pharmacomechanical thrombectomy (PMT) uses mechanical forces to assist tPA dispersion within
the thrombus, typically during a single treatment session. Concurrent aspiration capabilities help
remove thrombus fragments during treatment sessions. Devices currently used for this purpose in
the venous system include the AngioJet catheter (MEDRAD, Warrendale, PA) and Trellis
(Covidien, Mansfield, MA) infusion systems.
■
The AngioJet systems comprise an infusion catheter and dedicated reusable drive unit. Radially
oriented infusion ports generate high-pressure jets to disperse heparinized saline, with or without
tPA, into the thrombus and an adjacent aspiration port to export fragments and debris.
■
The AngioJet catheter is most commonly used in acute iliofemoral occlusion in the “power pulse”
mode; in this setting, the aspiration function of the catheter is temporarily disabled, whereas tPA
pulsation is delivered directly into the thrombus. Typically, 6 to 8 mg of tPA is delivered in this
fashion at the beginning of a treatment session. With power pulse activated, the catheter is
repeatedly advanced and withdrawn through the thrombus over the guidewire (FIG 1). After
allowing the tPA to dwell for 10 to 15 minutes, the aspiration function is activated and thrombus
removed to the greatest extent possible.
■
The Trellis system is composed of an infusion catheter of either 15- or 30-cm infusion length, with
compliant occlusion balloons at either end of the infusion ports (FIG 2). Following placement
over the guidewire, the end occlusion balloons are inflated in order to isolate the area of planned
pharmacomechanical thrombolysis (FIG 3). A sinusoidal dispersion wire is then advanced through
the core of the catheter and attached to a disposable drive unit, which when activated uses
mechanical forces to disperse the tPA through the thrombus. After an infusion of 6 mg of tPA over
the span of 10 minutes, aspiration of thrombus and debris is performed from the treated segment.
The occlusion balloons concentrate tPA within the treatment segment, enabling multiple infusion
and dispersal sessions during the same procedure with minimal systemic delivery of thrombolytic
agent (FIG 4).
Stenting of Underlying Venous Stenoses or Venous Compression Syndromes
■
Following clearance of acute thrombus from the iliofemoral system, underlying venous lesions that
provoked DVT formation, or focal external compression may become apparent on completion
phlebography. These lesions should be addressed during the same treatment session to minimize
the risk of recurrence. IVUS may be particularly useful in this regard.
■
Although fixed stenoses may occur throughout the venous system, the most common location for
extrinsic compression occurs at the point where the left common iliac vein passes beneath the
overlying right common iliac artery (RCIA) (FIG 5). After recognizing this compression and
successful removal of thrombus proximal or distal to this lesion, the stenosis may be safely
resolved with stenting (FIG 6). This is best performed by upsizing the interventional sheath to at
least 10 Fr followed by deployment of a self-expanding, braided, stainless steel Wallstent (Boston
Scientific, Watertown, MA). In conjunction with completion venography, IVUS is then used to
quantify the extent of residual compression.
■
Stent diameter is chosen based on IVUS-obtained measurements, but diameters commonly chosen for
common iliac vein placement in May-Thurner patients range from 16 to 20 mm. In this application,
it is important to choose longer stents that provide additional surface apposition in the common or
even external iliac veins to present stent dislodgement and migration. Wallstents are particularly
appropriate in this regard as they will shorten or extend in proportion to the ultimate treatment
diameter and feature exposed wires at either end to optimize vein wall engagement.
■
Once appropriately sited and deployed, poststent dilation is necessary to ensure optimal deployment
and migration resistance. Some discomfort will be experienced by the “awake” patient during
these procedures, and stenting molding should be guided by patient tolerance under these
circumstances.
Completion Imaging
■
Completion phlebography documents resolution of target stenosis and reciprocal reduction in
collateral venous flow.
■
The presence of persistent collaterals suggests residual venous stenosis or compression; IVUS
should be reperformed in this circumstance to confirm wall apposition and stent expansion. Repeat
balloon dilation may be necessary in these circumstances until sufficient expansion is achieved.
Closure of the Femoral Vein Access
■
Following sheath removal, manual pressure is held over the venous puncture site. Closure devices
are not appropriate or indicated for management of venous access.
■
Patients need to remain supine for at least 1 hour following sheath removal.
■
Therapeutic intravenous anticoagulation with unfractionated heparin is initiated at the completion of
the procedure. Maintenance of full anticoagulation without interruption throughout the early
postoperative period is imperative to procedural success.
OPERATIVE MANAGEMENT OF ILIOFEMORAL DEEP VEIN

THROMBOSIS
Iliac Venous Thrombectomy
■
For most clinical scenarios, open venous thrombectomy has largely been supplanted by the
interventional, image-guided techniques described in the preceding sections. In patients with limb-
threatening phlegmasia cerulean dolens or those with contraindications to lytic therapy or contrast
administration, open surgical thrombectomy remains an effective and necessary treatment modality.
■
Whenever possible, surgical thrombectomy is performed under general anesthesia with positive
pressure ventilation to reduce the risk of intraoperative PE.
■
A vertical inguinal incision is made to allow exposure and control of the CFV, femoral vein,
saphenofemoral junction, and the profunda femoris vein. Once these venous structures have
exposed, the patient is systemically anticoagulated with 100 units/kg of intravenous heparin.
■
A longitudinal venotomy is made in the CFV, and a no. 8 or no. 10 venous thrombectomy catheter is
then passed up to the level of the common iliac vein and thrombectomy is performed. Attempts are
made to clear the majority of the iliac thrombus before passing the thrombectomy catheter into the
vena cava in order to reduce the likelihood of pulmonary embolization.
■
Back-bleeding may not be present due to competent iliac vein valves, or back-bleeding can occur
from the hypogastric vein even without clearance of the thrombus within the common iliac vein.
Therefore, back-bleeding should not be used as an indicator of effective thrombus clearance and
venography should be performed as a routine after completion of iliac and infrainguinal
thrombectomy.
Infrainguinal Femoral Venous Thrombectomy
■
Following iliac venous thrombectomy, heparinized saline should be used to flush the iliac vein, the
proximal external iliac vein (or distal CFV) should be clamped, and then any thrombus at the
proximal (peripheral) aspect of the venotomy should be extracted with forceps.
■
Infrainguinal thrombus can then be removed by manual massage or by exsanguinating the leg with an
Esmarch bandage, sequentially applied from the foot to the groin, with sufficient overlap to
provide continuous compression (FIG 7). Clot is delivered through the venotomy at the groin.
■
Balloon thrombectomy can be performed using a no. 3 thrombectomy catheter passed from the
venotomy in the CFV in a retrograde fashion down toward the popliteal and tibial veins.
Following thrombectomy, the infrainguinal venous circulation should be flushed vigorously with
heparinized saline before closure of the venotomy.
■
If infrainguinal thrombus persists after thrombectomy, additional techniques for thrombus removal
include on-table tPA administration. For on-table tPA administration, 6 mg of alteplase in 200 mL
saline is infused retrograde into the femoral vein through the venotomy in the CFV, then the vein is
clamped and the solution is allowed to dwell for 10 to 30 minutes.
■
If the infrainguinal venous thrombectomy is not successful due to chronic thrombus in the femoral
vein, the femoral vein is then ligated below the profunda, and balloon thrombectomy is then
performed on the profunda vein and its branches.
■
After open thrombectomy is complete, the venotomy is closed with running continuous monofilament
suture, avoiding postclosure stricture of the CFV by precision suture placement. If narrowing is
apparent, vein or bovine pericardial patch angioplasty may be performed as necessary to restore
luminal diameter.
Adjunct Arteriovenous Fistula Creation
■
Rates of rethrombosis following surgical thrombectomy can be as high as 80%. Creation of an
arteriovenous fistula (AVF) may significantly reduce this risk and are incorporated in the
procedure by most surgeons.
■
The same groin incision may be employed for AVF creation, transposing the proximal segment of the
ipsilateral greater saphenous vein to the superficial femoral artery (FIG 8).
■
Surgical ligation or interventional occlusion of the AVF is ultimately required for optimal long-term
outcome, usually employed within 6 weeks following the procedure. Documented patency of the
venous system should be demonstrated on follow-up duplex imaging. Failure to close this fistula
may result in significant long-term limb and cardiovascular complications, and follow-up is
essential to ensure that this part of the procedure is completed.
■
Open thrombectomy procedures by their nature are associated with significant blood loss from the
central venous system, and preparations should be made both to crossmatch and bank sufficient
packed red blood cells (RBCs), as well as employ operative scavenging systems to recycle and
reinfuse lost blood to ensure that appropriate hemodynamic conditions may be maintained
throughout the procedure.
Completion Imaging
■
Completion venography of the iliac venous system should be performed following open surgical
thrombectomy to assess the adequacy of the thrombectomy.
■
Following closure of the venotomy and reestablishment of venous flow through the iliofemoral
venous system, an 18-gauge access needle and guidewire can be used to puncture the CFV and
place a 5-Fr sheath. Contrast injection directly through this sheath is performed to evaluate the
iliac veins and assess for residual thrombus. Following venography, the sheath is removed, and a
single monofilament stitch can be used to close the puncture site.
Wound Closure
■
A careful search for any transected lymphatics should be conducted prior to wound closure.
■
A closed suction drain should be placed in the groin wound to prevent seroma formation.
■
The wound is then closed with multilayered running absorbable sutures for hemostatic and
lymphostatic closure.
POSTOPERATIVE CARE
■
Following open surgical thrombectomy, full therapeutic anticoagulation is imperative to prevent
rethrombosis. An intravenous heparin infusion is immediately initiated and maintained for 24 to 48
hours before the patient is transitioned to oral anticoagulation with a low-molecular-weight
heparin bridge prior to discharge.
■
Ambulation should begin on the first postoperative day. Patients may usually be discharged within
48 to 72 hours following thrombectomy.
■
On discharge, the patient should be placed in elastic compression stockings (30- to 40-mmHg ankle
gradient), and the importance of compression should be stressed to the patient in the discharge
instructions.
OUTCOMES
Endovascular Intervention
■
Pharmacomechanical venous thrombectomy provides clinical success rates of 70% to 100% and
may reduce the incidence of the PTS, although this latter conclusion remains controversial.
■
Following successful procedures, long-term venous patency is reported at 84% in 5 years.
■
Valvular competence is preserved at 80% in 5 years and 56% in 10 years in recent series.
Surgical Thrombectomy
■
Surgical thrombectomy provides long-term iliac venous patency, with rates approaching 80% when
combined with inclusion of a temporary AVF.
■
At 5 years, over one-third of patients can be expected to be symptom free and have retained valvular
competence.
REFERENCES
1. Vedantham S, Grassi CJ, Ferral H, et al. Reporting standards for endovascular treatment of lower extremity deep vein thrombosis. J
Vasc Interv Radiol. 2005;17:417–434.
2. Kahn SR, Ginsberg JS. Relationship between deep venous thrombosis and the postthrombotic syndrome. Arch Intern Med.
2004;164:17–26.
3. Porter JM, Moneta GL. Reporting standards in venous disease: an update. International Consensus Committee on Chronic Venous
Disease. J Vasc Surg. 1995;21:635–645.
4. Rutherford RB, Padberg FT, Comerota AJ, et al. Venous severity scoring: an adjunct to venous outcome assessment. J Vasc Surg.
2000;31:1307–1312.
5. Prandoni P, Lensing AW, Prins MH, et al. Below-knee elastic compression stockings to prevent the postthrombotic syndrome. Ann
Intern Med. 2004;141:249–256.
6. Brandjes DP, Buller HR, Heijboer H, et al. Randomized trial of effect of compression stockings in patients with symptomatic
proximal-vein thrombosis. Lancet. 1997;349:759–762.
7. Delis KT, Bountouroglou D, Mansfield AO. Venous claudication in iliofemoral thrombosis: long-term effects on venous
hemodynamics, clinical status, and quality of life. Ann Surg. 2004;239:118–126.
8. Kearon C, Ginsberg JS, Hirsh J. The role of venous ultrasonography in the diagnosis of suspected deep venous thrombosis and
pulmonary embolism. Ann Intern Med. 1998;129:1044–1049.
9. Weinmann EE, Salzman EW. Deep-vein thrombosis. N Engl J Med. 1994;15:1630–1641.
10. Zontsich T, Turetschek K, Baldt M. CT-phlebography. A new method for the diagnosis of venous thrombosis of the upper and
lower extremities. Radiology. 1998;38:586–590.
11. Burke B, Sostman HD, Carroll BA, et al. The diagnostic approach to deep venous thrombosis. Which technique? Clin Chest Med.
1995;16:253–268.
12. Allie DE, Hebert CJ, Lirtzman MD, et al. Novel simultaneous combination chemical thrombolysis/rheolytic thrombectomy therapy
for acute limb ischemia: the power pulse spray technique. Catheter Cardiovasc Interv. 2004;63(4):512–522.
Chapter 35 Transjugular Intrahepatic Portosystemic Shunt
Ranjith Vellody Narasimham L. Dasika
DEFINITION
■
Transjugular intrahepatic portosystemic shunt (TIPS) is a channel created within the liver
parenchyma to divert blood from the portal circulation to the systemic circulation. The aim of
TIPS is to reduce portal venous pressure and treat the complications of portal hypertension, such
as refractory bleeding varices and ascites. The shunt is created percutaneously between the
intrahepatic portal vein and a hepatic vein through internal jugular venous access, by minimally
invasive endovascular techniques under image guidance. The TIPS procedure is now widely
accepted as an alternative to surgically created portosystemic shunts, which are associated with
greater morbidity and mortality.
■
TIPS can also serve as a bridge to liver transplantation and offers the benefit of not altering the
anatomy of the portal and mesenteric veins. Preservation of this anatomy reduces operative risk
during subsequent transplantation. Other advantages of TIPS include controlled decompression of
portal hypertension, thus minimizing the risk of hepatic encephalopathy, and the ability to embolize
and sclerose bleeding varices and other competing portosystemic shunts at the time of placement.
PATIENT SELECTION, HISTORY, AND PHYSICAL FINDINGS

■
There is level 1A evidence by systematic review of randomized controlled trials to support TIPS
placement for the management of variceal bleeding refractory to endoscopic management and
ascites refractory to medical management, which are the most common indications for TIPS
placement.1
■
Clinical benefits of TIPS creation have been reported for other indications with limited evidence. A
comprehensive list of indications and contraindications for the TIPS procedure and their
associated level of evidence are listed in Table 1.1,2
■
Details of prior upper and lower gastrointestinal (GI) bleed, findings of upper GI endoscopy to
exclude other causes of nonvariceal upper GI bleeding, history of prior endoscopic management of
bleeding varices, and frequency of paracentesis or thoracentesis should be obtained. Specific
attention should be paid to the history of recent changes in mentation or memory loss indicating
encephalopathy.
■
Patients with the preexisting encephalopathy and bleeding gastric varices should be evaluated for
balloon-occluded retrograde transvenous obliteration (BRTO) of gastric varices because TIPS can
worsen encephalopathy.
■
History of hepatobiliary disease and prior biliary and GI surgery should be documented. Prior
surgeries may alter anatomy and can increase the complexity of TIPS placement.
■
History of prior liver resection or liver transplantation and the details of altered anatomy from these
surgeries including the type of venous anastomosis must be obtained. Prior liver resection or
transplantation is not a contraindication for TIPS. However, knowledge of altered portal and
hepatic venous anatomy is essential for proper procedure planning.
■
History pertaining to heart disease, deep vein thrombosis, prior pulmonary embolism and pulmonary
hypertension require additional preprocedural cardiac workup because pulmonary hypertension
and right heart failure are contraindications to TIPS.
■
History of prior pancreatitis with splenic vein thrombosis may result in focal left upper quadrant
portal hypertension and gastric varices. TIPS is not indicated for isolated gastric varices from
splenic vein occlusion. Transhepatic recanalization of the splenic vein, BRTO, partial splenic
arterial embolization, or splenectomy should be considered to treat this condition.
■
Focal physical examination is performed with special emphasis on assessing the patient’s nutritional
status, jaundice, lower extremity edema, splenomegaly, ascites, hydrothorax, and encephalopathy.
■
Detailed and extensive discussion of the risks and benefits of the procedure (in particular
encephalopathy) should be carried out with the patient and the family.

■
Complete blood count (CBC), comprehensive metabolic panel, and coagulation profile are essential
to evaluate the need for correction of thrombocytopenia or coagulopathy and to evaluate the
severity of liver disease.
■
A Model for End-Stage Liver Disease (MELD) score that does not include additional points for
cause of liver disease is widely accepted to predict survival following TIPS placement.3 A MELD
score of greater than 18 is associated with significantly higher mortality rate at 3 months following
TIPS.1
■
Preprocedural imaging of the liver and the portal venous system with ultrasound or other imaging
modalities such as computed tomography (CT) and magnetic resonance imaging (MRI) to
document patency of the hepatic veins, portal vein, and intrahepatic portal branches should be
performed. Chronic occlusion of the portal vein is a relative contraindication of TIPS placement.
Contrast-enhanced CT or MRI scans of the liver and portal venous system allow greater
understanding of the spatial relationship between the hepatic veins and intrahepatic portal venous
branches and should be considered for planned TIPS creation. Cross-sectional imaging with CT
and MRI are especially helpful for planned TIPS in patients with prior liver resections.
■
In patients with history of long-term central venous access catheters, ultrasound examination of the
internal and external jugular veins bilaterally should be considered.
■
Electrocardiogram (EKG) and surface echocardiography should be performed to assess cardiac
function and right heart pressures if there is any suspicion of associated heart disease on history
and physical examination.
■
Preprocedure liver biopsy is not essential before TIPS placement. However, if prior liver biopsy is
available, it may be useful to differentiate presinusoidal and postsinusoidal causes of liver
disease.
■
Evaluation of ascitic fluid should be performed in patients with clinical suspicion of spontaneous
bacterial peritonitis.
■
TIPS is contraindicated in the presence of significant intrahepatic biliary dilation. However, TIPS
can be performed safely following decompression of the bile ducts.
■
Patients with hepatitis C liver disease should be tested for α-fetoprotein elevation, and if elevated,
should have cross-sectional imaging when feasible to rule out intrahepatic tumors.
■
It is common practice to type and crossmatch for blood products prior to TIPS.
SURGICAL MANAGEMENT
■
Risks and benefits of TIPS placement are thoroughly discussed with the patient and family, and
informed consent is obtained in the clinic setting. For emergent procedures, the family should be
made aware of the morbidity, mortality, and risk of encephalopathy associated with the procedure.
■
Laboratory data and all previous imaging studies should be reviewed to access the extent of liver,
renal, and cardiac disease present; to document patency of the portal venous system; and to
identify altered anatomy from prior surgeries.
■
Preexisting thrombocytopenia and coagulopathy should be corrected. Blood products should be
made available at the blood bank.
■
Patients with active upper GI variceal bleeding should have Blakemore tubes placed for balloon
tamponade of varices before transfer to interventional radiology. TIPS can be performed while the
esophageal and gastric balloons are inflated. However, the authors recommend deflation of
balloons during post-TIPS placement splenoportogram to assess variceal filling and the need for
embolization of varices.
■
Thoracentesis and paracentesis followed by recommended albumin infusion is performed the
evening prior to the procedure in elective cases.
■
Preprocedural prophylactic broad-spectrum antibiotics are recommended.
Positioning
■
Patient is placed supine on the angiographic table.
■
Preliminary ultrasound examination of the internal and external jugular veins should be performed
bilaterally.
■
Following the initiation of conscious sedation or induction of general anesthesia, the planned jugular
venous access site is prepped and draped in sterile fashion. Prepping the right upper quadrant
(RUQ) and lower abdomen is recommended if paracentesis or transhepatic portal vein access for
guidance is anticipated.
■
Paracentesis or thoracentesis should be performed first if there is significant ascites or hydrothorax.
Significant ascites reduces fluoroscopic visibility during the procedure and at the same time
increases the radiation dose to the patient. Displacement of the liver due to hydrothorax or massive
ascites may also result in unfavorable anatomy for portal vein access.
■
An arterial line for continuous pressure monitoring during the procedure is indicated following large
volume paracentesis in patients with active GI bleeding or hemodynamic instability.
TECHNIQUES
VENOUS ACCESS
■
TIPS is most commonly performed through right internal jugular vein access. Using standard
Seldinger technique, access to the right internal jugular vein is obtained with ultrasound guidance.
Over a guidewire, the access is dilated and a 10-Fr dedicated vascular sheath is placed into the
inferior vena cava (IVC).
■
Some practitioners prefer the use of the left internal jugular vein, as it may provide more stable
access to the right hepatic vein. Alternatively, the right and left external jugular veins can be
used.
■
In cases of superior vena cava (SVC) obstruction, right and left common femoral venous access
can be used for recanalization of the SVC to facilitate more standard venous access from above.
Common femoral access can also be used directly for TIPS creation in extreme situations.
■
Care is taken with guidewires, dilators, and sheaths to prevent cardiac dysrhythmias and right
atrial perforation while crossing the right atrium.
■
Right atrial and IVC pressures are not routinely obtained unless there is a clinical reason such as
history of cardiac or pulmonary disease.
HEPATIC VEIN SELECTION

■
Selection of an appropriate vein of suitable diameter is important. TIPS creation through the right
hepatic vein is most common. A standard nonglide, 5-Fr appropriately shaped catheter (based on
prior imaging) is then advanced through the sheath into the mid-IVC. As the catheter is withdrawn,
the hepatic vein is cannulated.
■
When the right hepatic vein is considered not suitable due to smaller caliber or other anatomic
reason, TIPS can be performed through the middle or even left hepatic veins.
■
It can be difficult to distinguish between the right and middle hepatic veins (MHVs), but it is
important to do so. When a wedged hepatic venogram is performed in a steep right anterior
oblique (RAO) projection (see Visualization of the Portal Venous System), the right hepatic
vein will be posterior and the MHV will be anterior to the right branch of portal vein (FIG 1).
VISUALIZATION OF THE PORTAL VENOUS SYSTEM

■
Indirect visualization of the intrahepatic and extrahepatic portal veins during the TIPS procedure can
dramatically decrease procedure time. This can be done in multiple ways.
■
Most commonly, wedged portography using contrast or carbon dioxide (CO2) gas is performed
(FIG 2A). CO2 gas is an excellent agent for imaging of the hepatic veins, portal veins, and
varices because CO2 can easily flow through the venules and sinusoids due to its low viscosity.
CO2 is the contrast agent of choice for wedged hepatic venography and in patients with
associated renal impairment. However, use of CO2 is contraindicated in patients with right-to-
left intracardiac shunting and should be used with caution in patients with hepatopulmonary
syndrome.
■
The right hepatic vein catheter is wedged into a central hepatic venule. Wedge hepatic venogram
and indirect portogram is then performed with injection of CO2 gas or contrast. CO2 or contrast
will flow through the sinusoids to the portal side resulting in filling of the main portal vein and
its branches. Peripheral wedging should be avoided to prevent extravasation and even capsular
perforation. Imaging should be performed in both anteroposterior (AP) and steep RAO
projections to properly assess the anatomic relation of the hepatic vein and the right branch of
the portal vein (FIG 1).
■
Similarly, the intrahepatic portal branches can also be visualized using an occlusion balloon
catheter. In this method, the 5-Fr catheter is exchanged over a guidewire for an occlusion
balloon catheter. The balloon catheter is inflated in a branch of the hepatic vein and not wedged.
The balloon is inflated to obstruct venous outflow from the segment. The injection pressure of
CO2 is dissipated in a larger segment of liver minimizing complications and with better filling
of the portal branches and the main portal vein.
■
Occasionally, wedge portography may fail to visualize portal vein especially in patients with
veno-occlusive disease and intrahepatic portal vein branch thrombosis.
■
When indirect visualization of the portal vein is unsuccessful, direct visualization can be attempted
(see “The Difficult Transjugular Intrahepatic Portosystemic Shunt ”).
■
Under ultrasound guidance, a 22-gauge needle can be inserted percutaneously into the intrahepatic
portal venous system for injection of contrast or CO2. This method will require embolization of
the parenchyma traversed during portal vein access at the end of the procedure with Gelfoam or
coils to ensure hemostasis.
■
Other methods include percutaneous cannulation of a paraumbilical vein or trans-splenic access
to the portal vein, both of which also require embolization of the access tract at the conclusion
of the procedure.
PORTAL VEIN ACCESS

■
A number of commercially available device sets are available for TIPS placement. The most
important component of the set is a directional needle with a 30-degree angulated tip and an
external marker to show the direction of the tip of the needle developed by Colapinto. Several
modifications have been made to this original set, and the commonly used modified set is the
Rösch-Uchida set (Cook Medical, Bloomington, IN) and is shown in FIG 2B. This set is designed
to be more flexible with a needle tip of smaller caliber to minimize trauma to liver. The original
Colapinto needle (Cook Medical, Bloomington, IN) is modified to an angulated blunt end cannula
covered with a sheath and is used to direct a smaller Rösch-Uchida trocar needle-catheter
combination for portal vein access.
■
The Colapinto cannula is advanced through the sheath and into the right hepatic vein over a
guidewire. The outer sheath and directable cannula are slowly retracted to within 2 cm from the
IVC while rotating the tip in the direction of portal vein.
■
The cannula is rotated anteromedially from the right hepatic vein, aiming for the right portal vein as
seen on portography (typically seen at the level of the 11th rib approximately 0.5 to 1.5 vertebral
body widths from the spine). The trocar needle-catheter combination is then advanced through the
cannula and into the expected location of the right portal vein. The depth of the pass is most
commonly 5 cm or less. After removal of the trocar, aspiration of the catheter is performed as it is
gradually withdrawn back toward the right hepatic vein. When blood is aspirated, contrast is
injected to confirm portal vein access and to assess the suitability of the accessed portal branch for
TIPS creation (FIG 2C).
■
Access into the right branch of the portal vein within 2 to 3 cm from the portal vein bifurcation is
desired. The portal vein bifurcation is extrahepatic in up to 50% of patients and puncture in this
area may lead to exsanguination. Punctures that are too peripheral in the right portal vein are
also not optimal because they result in turbulent flow in the TIPS from undesirable angulation.
■
The right branch of the portal vein is posterior in relation to the MHV, necessitating posterior
rotation of the cannula for portal vein access. MHV to left portal vein access may need
anteromedial rotation of the cannula. It is extremely important to assess the spatial relationship
of the chosen hepatic vein and the portal anatomy visualized on portogram to guide the needle
pass.
■
Following confirmation of proper access into the portal venous system, a hydrophilic guidewire is
advanced into the superior mesenteric or splenic vein. The catheter is exchanged for a multi–side-
hole marking catheter over the guidewire (FIG 2D).
■
The 10-Fr sheath is then withdrawn to the right atrium. Dual pressure measurements are obtained in
the portal venous system and the right atrium. The difference between the measurements is the
portosystemic pressure gradient.
■
A portosystemic gradient (PSG) of 5 to 7 mm is normal and a PSG of greater than 12 mmHg is
abnormal. Note that the measured PSG could be lower in the setting of partial portal
decompression from extensive portosystemic collaterals such as spontaneous splenorenal shunt.
PSGs are also low when the right atrial pressure is transiently elevated from resuscitative
measures with intravenous (IV) fluids and blood products, but the absolute portal pressure may
remain high from portal hypertension.
■
Direct splenoportography is then performed in AP and oblique projections with iodinated contrast to
delineate the portal anatomy, evaluate the presence of competitive shunts and varices as well as to
determine the hepatic parenchymal tract length (FIG 2D).
■
In cases of hepatofugal flow, additional venography is performed through the sheath placed within
the parenchymal tract to get an accurate measurement of tract length.
■
If the IVC/hepatic vein confluence cannot be clearly visualized during portography, direct
contrast injection in that region should be performed to localize the hepatocaval junction for
accurate measurement of tract length.
DILATION OF THE TRACT

■
A 180-cm long Amplatz Super Stiff guidewire (Boston Scientific, Natick, MA) is then advanced into
the splenic vein and the marker pigtail catheter is removed. The 10-Fr sheath dilator is replaced
into the sheath and both the sheath and dilator are advanced over the stiff wire and into the portal
vein. When the liver is sclerotic and hard, some operators prefer to predilate the hepatic
parenchymal tract with a 6- to 8-mm balloon to facilitate advancement of the sheath through the
parenchymal tract (FIG 2E).
STENT SELECTION
■
Historically, TIPS was performed with no stent placement within the hepatic parenchymal tract.
Tracts were created using only balloon dilation, but patency rates were poor.4 With the
development of bare metal stents, long-term patency rates improved to the point that TIPS could be
considered a viable alternative to surgical portal decompression. Patency rates improved further
with the introduction of polytetrafluoroethylene (PTFE)-covered stent grafts.
■
The most commonly used stent for TIPS placement is the Gore Viatorr PTFE-covered stent graft.
The stent is covered with PTFE graft material except for the caudal most 2 cm. The junction
between the PTFE covered portion and the bare metal portion is marked with a gold band. The
bare stent portion should be placed within the portal vein to allow uninterrupted flow through the
interstices and the covered portion is meant to extend through the parenchymal tract and back to the
hepatic vein/IVC confluence (FIG 2F). The graft material limits the permeability of bile and mucin
into the tract and also eliminates intrastent tissue growth, leading to improved patency rates.5
■
There is still a role for placement of self-expanding bare metal stents, particularly in patients in
whom early transplant is expected, when there is single hepatic venous outflow, or when there is
concomitant spontaneous bacterial peritonitis.
■
Even though TIPS were created with balloon expandable bare metal stents in the past, their role is
currently limited to pediatric TIPS creation to preserve the ability to increase shunt diameter with
the growth of the child.6 They can also be used to eliminate kinks during TIPS revision.
■
Typically, a stent diameter of 10 mm is used for all TIPS indications.
■
The stent length is equal to the distance of the hepatic parenchymal tract plus the distance of the
hepatic outflow vein to the IVC confluence. One centimeter is often added to this number to
account for the loss of length that occurs when a stent is deployed in a curved tract and to
compensate for minimal foreshortening during deployment.
STENT PLACEMENT
■
The Gore Viatorr stent graft is advanced through the sheath and into the portal vein. The sheath is
then withdrawn to expose the uncovered distal 2 cm. The sheath and stent graft are then retracted
as a unit until the gold band marking the covered portion of the stent graft is at the edge of
parenchymal tract. The gold band should be held exactly at the junction of the portal vein with the
parenchymal tract with gentle traction until deployment. With the stent graft held in this position,
the sheath is retracted to the right atrium and the release cord is pulled. The stent graft is now
deployed. Following deployment, the stent graft shows an hourglass constriction within the
parenchymal tract. The stent graft is then expanded completely by dilating with a balloon of the
same diameter as the deployed stent graft.
■
In some patients, such as those with preexisting portal vein stenosis or occlusion, it may be
necessary to extend the TIPS into the portosplenic confluence, superior mesenteric vein, or
splenic vein to allow effective outflow through the TIPS. This should be performed with self-
expanding bare metal stents to preserve inflow into the stent from branches. This may
complicate liver transplantation and should be discussed with the transplant team.
■
A correctly placed Gore Viatorr stent graft is easily grasped and removed by a transplant surgeon
at the time of liver transplant.
■
The multi–side-hole catheter is readvanced into the portal vein in order to calculate the post-TIPS
PSG.
■
When bleeding is the indication, the target PSG is less than 12 mmHg. In the setting of ascites or
hydrothorax, gradients under 8 mm are recommended by the Society of Interventional Radiology
(SIR) and American Association for the Study of Liver Disease guidelines.2 The risk of hepatic
encephalopathy increases significantly when the final gradient is below 5 mmHg. It may be
difficult to obtain a truly accurate gradient immediately following emergency TIPS procedure
due to the hemodynamic shifts and fluid overload from resuscitative efforts.
■
A final portal venogram is then obtained to ensure proper flow into and out of the TIPS (FIG 2G).
ADJUNCT PROCEDURES
■
When TIPS is performed emergently for refractory variceal bleeding, embolization and sclerosis of
gastric and esophageal varices with coils, vascular plugs, or liquid embolic agents such as alcohol
should be considered (FIG 2H).
THE DIFFICULT TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC
SHUNT
■
The left hepatic vein is used for creation of TIPS (FIG 3) in only exceptional circumstances such as
when right liver lobe resection is planned in the presence of mild portal hypertension.
■
If no hepatic veins can be accessed (such as in Budd-Chiari syndrome), a direct IVC to portal vein
communication can be created through the caudate lobe (direct intrahepatic portocaval shunt
[DIPS]). Transplant surgeons should be made aware of the DIPS anatomy as it may alter surgical
approaches for future transplantation.
■
If targeting the portal system is proving to be difficult with fluoroscopy alone, access under real-
time transabdominal or intravascular ultrasound guidance can be used. Other methods of portal
vein localization for targeting the access point include percutaneous placement of a metallic
marker under ultrasound guidance just anterior to the right portal vein or placement of a balloon
(FIG 4A) or catheter within the portal vein from direct transhepatic or paraumbilical vein access
(FIG 4B–D). Similarly, a snare can be placed via direct transhepatic access and can be targeted in
the same manner as a balloon. In special situations, a technique frequently described as “gunsight”
can be used to create the TIPS tract. In this method, a second snare inserted from the hepatic
venous circulation can provide gunsight targeting whereby a needle can be percutaneously
advanced through both snares to create the TIPS (FIG 4E,F). Gunsight is particularly useful when
the hepatic and portal veins are at the same level due to asymmetric shrinkage of the liver or in
pediatric patients.
PEARLS AND PITFALLS
Patient history and physical ■ There is level 1 evidence for TIPS placement for variceal
exam bleeding and for ascites refractory to medical management.
■ Altered anatomy from prior surgeries may increase the complexity
of TIPS placement.
Imaging and other diagnostic ■ Preprocedure imaging of the liver to evaluate hepatic and portal
studies venous anatomy, portosystemic collateral pathways, ascites, and
intrahepatic tumors is essential.
■ MELD score should be calculated for risk stratification.
Preoperative planning ■ Paracentesis improves ventilation, fluoroscopic visibility, and
reduces radiation to the patient and operator.
■ Gastroesophageal balloon tamponade tubes should be placed in
unstable patients with active upper GI variceal hemorrhage.
Positioning ■ Surgical preparation of RUQ and anterior abdominal wall should
be considered for transhepatic access to the portal vein and for
draining ascites if needed.
Venous access ■ Although the right internal jugular vein is most commonly used,
TIPS creation is feasible through alternative venous access.
Hepatic vein selection ■ The right hepatic vein is most commonly used for TIPS creation.
■ AP and steep RAO projections can help identify the right hepatic
vein by noting its spatial relationship with the right portal vein.
Visualization of the portal ■ CO2 is the contrast agent of choice for wedge hepatic venography.
venous system ■ Anatomic localization of the intrahepatic portal vein for access
significantly reduces procedure time.
Portal vein access ■ Direction of rotation of the Colapinto cannula varies based on
hepatic vein selected.
■ Access within 2 to 3 cm of the portal vein bifurcation is most
desirable.
■ Measurement of PSG is essential prior to TIPS placement.
Dilation of the tract ■ Balloon dilation of the tract facilitates advancement of the sheath
into the portal vein.
Stent selection ■ The Gore Viatorr endoprosthesis is the desired stent for TIPS
creation whenever feasible.
Stent placement ■ The gold band of the Gore Viatorr must be placed at the junction
of the portal vein entry site and the hepatic parenchymal tract.
■ A post-TIPS PSG of less than 12 should be achieved in all
bleeding patients.
Adjunct procedures ■ In patients with refractory variceal bleeding, embolization of
varices should be considered.
The difficult TIPS ■ When preprocedural imaging and wedged portography depicts
unfavorable anatomy, alternative TIPS creation strategies should
be considered.
POSTOPERATIVE CARE
■
Following emergency TIPS for active variceal bleeding, patients are admitted to the intensive care
unit (ICU) until they are hemodynamically stable. Following elective TIPS, patients are admitted
overnight for inpatient observation.
■
Immediate postoperative care for emergent TIPS placement consists of continued resuscitation and
hemodynamic monitoring. Shunt placement immediately elevates right atrial (central venous)
pressure, increasing cardiac preload, which can lead to heart failure. Variceal bleeding may
continue with incomplete reduction of absolute portal pressure secondary to elevated central
venous pressures. Steps should be undertaken to reduce right atrial pressure.
■
Patients with continued bleeding should have repeat upper GI endoscopy to rule out nonvariceal
source of bleeding. Reevaluation of the TIPS shunt and embolization of residual bleeding
varices should be performed for continued variceal bleed.
■
Repeat CBC and coagulation panel should be performed every 4 hours. Urine output is monitored.
Serum creatinine level and liver function tests are checked at 12 and 24 hours. Patients are
periodically checked for altered mentation. Transient alterations in liver function tests are usually
noted immediately following TIPS. Progressive worsening of liver function with encephalopathy
is a cause for concern.
■
A liver ultrasound with complete Doppler evaluation of the TIPS shunt is obtained 2 to 3 days
following TIPS placement.
■
Lactulose administration can be considered in encephalopathic patients.
OUTCOMES
■
Technical success is greater than 95% in most centers. SIR TIPS quality improvement guidelines
recommend thresholds of 95% for technical success and 90% for clinical success.2
■
Following emergent TIPS for variceal hemorrhage, bleeding control is achieved greater than 90% of
patients. Mortality rates range from 27% to 50% following TIPS placement and is related to risk
classification scores, hemodynamic instability at the time of placement, and the presence of other
comorbidities.7 Mortality rates are significantly higher than in patients undergoing elective TIPS
placement. Rebleeding rates are lower after TIPS shunt placement with adjunctive variceal
embolization and sclerosis.8
■
Following elective TIPS, there is significantly higher survival rate in patients treated for variceal
bleeding compared to those treated for ascites (>60 months vs. 29 months).9
■
TIPS creation is superior to large volume paracentesis with albumin infusion to treat refractory
ascites. However, TIPS patients have higher rates of encephalopathy and no definite survival
benefit has been shown.10
■
Early, 3 months and 6 months, mortality rates are significantly higher in patients with MELD
scores of 18 or greater who are undergoing elective TIPS placement. (In addition, 6-month
survival for patients with MELD scores less than 10 is 100% compared to 25% for patients
with scores over 24.10)
■
TIPS created using PTFE-covered stents compared to bare metal stents demonstrate a lower rate
of TIPS dysfunction (15% vs. 44%), higher primary patency rate (76% vs. 36%), decreased
likelihood of developing encephalopathy (33% vs. 49%), and a lower rate of clinical relapse
(10% vs. 29%).7
■
De novo or worsening encephalopathy may be seen in 20% to 31%. However, most can be
managed medically and shunt occlusion is only required in less than 5%.2
COMPLICATIONS
■
Although TIPS is a relatively safe procedure, complications can arise during every step of TIPS
placement due to the complexity of the procedure. In addition, early and delayed nonprocedure-
related complications are also associated with significant morbidity.
■
Procedure-related complications
■
Procedure-related mortality in published series is 0.6% to 4.3%, but the procedure-related
mortality in most major centers is about 1.4%.2 Major procedural complication rate should be
no more than 3%. Most procedure-related complications can be minimized by careful
preprocedural evaluation of cross-sectional images, proper portal vein localization, having a
clear understanding of the procedure, and by the use of meticulous technique.
■
Intraperitoneal hemorrhage, a serious complication associated with procedure-related mortality,
can occur due to liver capsule perforation during needle passes or from puncture of the portal
vein in an extrahepatic location. Rarely, bleeding occurs from hepatic artery pseudoaneurysm or
arteriovenous fistula formation, hepatic artery laceration, IVC perforation, or gallbladder
perforation. Additional intervention such as arteriography and embolization may be required to
treat extrahepatic source of bleeding and hepatic artery lacerations.11
■
Other procedure-related complications include jugular access–related hematoma, cardiac
arrhythmias during advancement of devices through the right atrium, nontarget organ puncture,
and injury to the bile ducts.
■
Periprocedural complications
■
Liver enzyme elevation is noted frequently after shunt placement but is usually transient.
Persistent elevation may indicate liver failure from the reduction of blood flow into the liver
caused by the TIPS. Persistent hyperbilirubinemia has been noted from chronic hemolysis.
■
Infectious complications, such as liver abscess formation and graft infection (endotipsitis), are
uncommon (FIG 5). At present, there is no evidence that the use of prophylactic antibiotics is
beneficial before TIPS placement.11 Treatment usually consists of long-term antibiotic therapy
coupled with percutaneous abscess drainage as needed. Attempts to reopen the TIPS should not
be performed until all signs of infection have resolved.
■
Rapid deterioration of liver function following TIPS, worsening encephalopathy, and elevated
blood ammonia is rare. Reduction of shunt caliber and, in extreme cases, closure of TIPS
should be considered. Right liver lobe infarction due to obstruction of the right branch of portal
vein preventing inflow to or outflow from the right liver lobe is a very rare complication.
Reduction in hepatic sinusoidal perfusion due to reduced compensatory hepatic artery inflow
from any cause can potentially increase the risk of ischemic complications.
■
Delayed complications
■
Hepatic encephalopathy can be caused or worsened by TIPS placement in up to a third of patients
undergoing TIPS. Most patients respond to medical management with elimination of
precipitating factors, dietary modification, administration of nonabsorbable disaccharides such
as lactulose, and antibiotics. Reduction in shunt diameter or even occlusion of TIPS is needed
in very few patients.
■
Recurrent variceal bleeding or recurrence of ascites may suggest TIPS dysfunction (see TIPS
Dysfunction).
■
Rarely, when a TIPS shunt is ineffective in adequately reducing the PSG, a second TIPS (parallel
TIPS) (FIG 6) placement should be considered to reduce the PSG further.
■
Radiation injury to the skin can occur with prolonged procedural times. The risk of radiation
injury can be significantly reduced with periodic changes in angulation of the image intensifier.
TRANSJUGULAR INTRAHEPATIC PORTOSYSTEMIC SHUNT

DYSFUNCTION
■
Recurrent portal hypertension with stenosis or occlusion of the shunt is a significant drawback of
TIPS creation. Better primary and secondary patency rates are now achieved with the introduction
of PTFE-covered stents.
■
Early TIPS dysfunction is seen secondary to technical and biologic factors resulting in occlusion or
stenosis of the TIPS. The technical causes include inadequate coverage, stent shortening, and stent
migration. The biologic factors include communication of bile ducts with the shunt tract resulting
in stent thrombosis and parenchymal tract stenosis from intrastent tissue growth from cellular
hyperplasia (FIG 7A). PTFE-covered grafts have mostly eliminated the biologic factors.12
■
Inadequate extension of the stent to the junction of the IVC and hepatic vein confluence leaves a
segment of the hepatic vein uncovered. This predisposes the hepatic venous end of the TIPS to
stenosis from intimal hyperplasia. Extension of the stent to the IVC is an important determinant of
shunt patency (FIG 7B,C).
■
Dysfunction may also result from poor portal venous inflow into the shunt because of competitive
shunts or kinking of the TIPS stent.
■
Secondary interventions are usually successful in the salvage of dysfunctional TIPS. Completely
occluded TIPS (FIG 7D) can be salvaged with mechanical or pharmacomechanical thrombolysis
and relining with a stent to the hepatocaval junction as needed. Stenosis of the hepatic venous end,
and occasionally, the portal venous end of the TIPS is treated with repeat balloon dilation and
placement of a new stent to cover the lesion if needed. Inflow-related dysfunction from
competitive shunts is treated by embolization and sclerosis of the competitive shunts to redirect the
blood flow toward the liver. Care should be taken to prevent infolding of a Gore Viatorr PTFE-
covered stent graft when the stent graft is placed inside a preexisting Wallstent (Boston Scientific,
Natick, MA) during revision by adequately dilating with high-pressure balloons to the appropriate
diameter.
FOLLOW-UP OF TIPS TRANSJUGULAR INTRAHEPATIC

PORTOSYSTEMIC SHUNTS
■
Periodic screening of TIPS with Doppler ultrasound is an effective noninvasive method to recognize
TIPS dysfunction early.
■
Although there is no consensus about the timing of TIPS screening, Doppler ultrasound at 1 month, 3
months, 6 months, 1 year, and then biannual is performed at many major centers. Ultrasound should
also be performed if there is a return of pre-TIPS symptoms. The findings of TIPS dysfunction on
ultrasound examination are listed in Table 2.13
■
Clinical or Doppler ultrasound evidence of TIPS dysfunction should be followed by catheterization
of the TIPS with direct portography and pressure measurements. Dysfunctional shunts can be
revised on an outpatient basis with balloon dilation of stenosis, extension of the stent, or relining
of the stent as needed based on the portogram and pullback pressures to restore acceptable PSGs.
REFERENCES
1. Fidelman N, Kwan SW, LaBerge JM, et al. The transjugular intrahepatic portosystemic shunt: an update. AJR Am J Roentgenol.
2012;199:746–755.
2. Boyer TD, Haskal ZJ. The role of transjugular intrahepatic portosystemic shunt (TIPS) in the management of portal hypertension:
update 2009. Hepatology. 2010; 51:306.
3. Salerno F, Merli M, Cazzaniga M, et al. MELD score is better than Child-Pugh score in predicting 3-month survival of patients
undergoing transjugular intrahepatic portosystemic shunt. J Hepatol. 2002;36:494–500.
4. Colapinto RF, Stronell RD, Gildiner M, et al. Formation of intrahepatic portosystemic shunts using a balloon dilation catheter:
preliminary clinical experience. AJR Am J Roentgenol. 1983;140:709–771.
5. 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.
6. Lorenz JM. Placement of transjugular intrahepatic portosystemic shunts in children. Tech Vasc Interv Radiol. 2008;11:235–240.
7. Loffroy R, Estivalet L, Cherblanc V, et al. Transjugular intrahepatic portosystemic shunt for the management of acute variceal
hemorrhage. World J Gastroenterol. 2013;19:6131–6143.
8. Qi X, Liu L, Bai M, et al. Transjugular intrahepatic portosystemic shunt in combination with or without variceal embolization for the
prevention of variceal rebleeding: a meta-analysis. J Gastroenterol Hepatol. 2014;29(4):688–696.
9. Heinzow HS, Lenz P, Köhler M, et al. Clinical outcome and predictors of survival after TIPS insertion in patients with liver
cirrhosis. World J Gastroenterol. 2012;18:5211–5218.
10. Ferral H, Gamboa P, Postoak DW, et al. Survival after elective transjugular intrahepatic portosystemic shunt creation: prediction
with model for end-stage liver disease score. Radiology. 2004;231:231–236.
11. Gaba RC, Khiatani VL, Knuttinen MG, et al. Comprehensive review of TIPS technical complications and how to avoid them. AJR
Am J Roentgenol. 2011;196:675–685.
12. Cura M, Cura A, Suri R, et al. Causes of TIPS dysfunction. AJR Am J Roentgenol. 2008;191:1751–1757.
13. Valji K. Vascular and Interventional Radiology. 2nd ed. Philadelphia, PA: Elsevier; 2006:290–291.
Surgery for Portal Hypertension in Children and
Chapter 36 Adults
Michael J. Englesbe Amit K. Mathur
DEFINITION
■
Portal vein (including splenic and superior mesenteric vein) pressure ranges between 1 and 4 mmHg
higher than the hepatic vein free pressure and not more than 6 mmHg greater than central venous
pressures (CVPs). Pressures that exceed these limits define portal hypertension. More commonly,
portal hypertension is used to define a constellation of symptoms related to elevated mesenteric
venous pressures, including ascites, gastrointestinal bleed due to varices, and the development of
mesenteric venous collaterals. Portal hypertension may be caused by liver disease or prehepatic
or posthepatic venous obstruction.

■
The first step in the management of a patient with portal hypertension is to assess liver function.
Most children and adults with portal hypertension have cirrhosis. Complete an extensive history to
investigate for risk factors of liver disease. In children, neonatal history is important including
exposure to umbilical catheterization.
■
Patients with noncirrhotic portal hypertension usually present with a variceal hemorrhage. Many
patients have chronic abdominal pain, especially in the left upper quadrant.
■
Assess for signs of liver disease and portal hypertension on physical examination. Measure the
spleen relative to the costal margin and umbilicus.
■
Malnutrition, jaundice, encephalopathy, frailty, or coagulopathy are signs of decompensated liver
disease. Patients with noncirrhotic portal hypertension usually have only splenomegaly.

■
Assessment should include blood tests and serologies. Attention to synthetic liver function and
platelet count is important. A complete hypercoagulable workup is needed. Results should be
interpreted with care; many patients with abnormal liver function will have abnormal levels, such
as protein C and protein S.
■
Complete a liver ultrasound to assess the patency of the vasculature in the right upper quadrant and
liver morphology. Importantly, a recanalized, thrombosed portal vein may be mistakenly
appreciated as “normal” on ultrasound.
■
Arterial and venous phase magnetic resonance imaging (MRI) or computed tomography (CT) scan
(both require intravenous contrast) provides an excellent anatomic assessment.
■
Do an endoscopy to assess for varices, with particular attention to gastric varices.
■
Assess for liver pathology with a liver biopsy. This can be done via the transjugular approach. At
the same time, an assessment can be made of pressures within the right atrium, inferior vena cava,
hepatic veins, and wedged portal pressures. Patients with mesenteric veno-occlusive disease
(such as portal vein thrombosis) and portal hypertension usually have normal wedged hepatic vein
pressures.
■
Complex patients will merit a comprehensive angiographic assessment, which may include imaging
of the inferior vena cava, abdominal arterial system, and mesenteric venous system with or without
direct access to these veins.
■
Patients with severe portal hypertensive complications and a portal to systemic gradient of greater
than 12 mmHg merit intervention.
SURGICAL MANAGEMENT
■
Patients with cirrhosis and portal hypertension–related complications should have a transjugular
intrahepatic portosystemic shunt (TIPS) procedure unless contraindicated.
■
A multidisciplinary committee should review all complex cases. The committee must include
pediatric and adult hepatologists, pediatric and adult radiologists, interventional radiologists, and
surgeons.
■
Endovascular procedures (including TIPS) can provide durable management of portal hypertension.
These percutaneous interventions to shunt and/or recanalize are the first-line therapy. Percutaneous
procedures to embolize the spleen are poorly tolerated by most patients, although occasionally,
splenic embolization is the best option.
■
Indications for surgery in adults are the following:
■
At least one life-threatening complication of portal hypertension. This usually includes a large
gastrointestinal bleed.
■
Adults with complications of portal hypertension related to decompensated cirrhosis should have
a liver transplant or TIPS procedure; shunt surgery is rarely indicated in these patients.
■
Severe and long-standing thrombocytopenia
■
Severe and disabling abdominal pain. This is usually from massive splenomegaly. Many patients
with mesenteric veno-occlusive disease will have abdominal pain and no other complications;
few of these patients should have surgery.
■
Massive splenomegaly affecting lifestyle. The spleen crosses the abdominal midline and occupies
much of the pelvis.
■
Indications for surgery in children are the following:
■
Two life-threatening complications of portal hypertension.
■
Massive splenomegaly or severe thrombocytopenia affecting lifestyle.
■
No viable or durable endovascular procedure available.
■
Children with complications of portal hypertension related to decompensated cirrhosis should
have a liver transplant and not shunt surgery.
■
All patients having surgery should have immunizations for pneumococcus, meningococcus, and
Haemophilus influenzae.
Positioning
■
The patient is placed in the supine position on the operating table with arms at sides for smaller
children. Operative exposure to the neck and/or groin for vein procurement is needed in many
cases.
■
An arterial line and central line should be placed in most cases. The central line will be used to
assess the CVP in calculations of the portal-systemic pressure gradient. Additional tubing and
anesthesia equipment will be needed for intraoperative mesenteric venous pressure measurements.
■
All members of the operative team (surgical, nursing, and anesthesia) should be prepared for
significant intraoperative bleeding, as is frequently experienced during liver transplantation or
open abdominal vascular surgery. Overresuscitation will worsen this bleeding; the goal CVP
during the dissection should be 5 mmHg. This requires frequent communication between the
anesthesiologists and surgeons.
TECHNIQUES
INCISION AND RETRACTION

■
Do a midline incision.
■
Retract aggressively in the superior direction to facilitate access to the short gastric veins in the
upper abdomen. This is best achieved with an Omni™ or Thompson™ retractor.
OPERATIVE DECISION MAKING

■
The final surgical approach to manage severe portal hypertension is determined by operative
findings. The surgeon must understand the patient’s physiology and how to best assure long-term
management of portal hypertension with reasonable operative risks. Consideration must be made
for future options for management if the current surgical procedure fails.
■
Prosthetic graft material or cryopreserved vein should be reserved for patients in severe extremis
from acute portal hypertensive complications.
■
Assessment of portal pressures. Ask the anesthesiologist to hand pressure tubing onto the field.
Select a vein that will be easy to ligate following cannulation; omental branches work well for
this. Cannulate the vein with an angiocatheter and measure pressures (FIG 1). Pressures are low
and variations in transducer location can have marked effects on pressures. Fix the transducer in a
location so that subsequent measures can be reliably compared to this baseline measure.
SPLENECTOMY WITH PROXIMAL SPLENIC ARTERY LIGATION AND
ESOPHAGOGASTRIC DEVASCULARIZATION
■
The indications for this procedure include patients with a life-threatening complication from portal
hypertension and complex mesenteric veno-occlusive disease or poor venous drainage of the
spleen (left-sided portal hypertensive physiology) (FIG 2).
■
Patients with long-standing thrombocytopenia (platelets <35,000/μL) and massive splenomegaly
needs a splenectomy. The spleen is fibrotic and will remain large (and platelet counts will
remain low) following shunt surgery alone. Also, a massive spleen will make many portal
hypertension surgical procedures impossible and, as a result, splenectomy is the first portion of
the procedure (FIG 3).
■
The procedure can be done with a laparoscope. If there is significant portal hypertension and
collaterals, preoperative splenic embolization should be done immediately prior to the procedure.
If done more than a few hours before the splenectomy, the patient will have significant adverse
symptoms and the spleen will become soft and easy to injure during surgery. The size of the spleen
and the severity of the portal hypertension usually favor an open procedure.
■
Key steps include the following:
■
Exposure above the spleen with generous retraction of the abdominal wall superiorly
■
Keep dissection to a minimum. Use hands instead of metal retractors for operative exposure.
Collateral veins are best ligated using a “no-touch” technique and either surgical clips or an
electrosurgical device (such as a LigaSure or Harmonic scalpel) (FIG 4).
■
Divide enough short gastric vessels to expose the splenic vein.
■
Ligate the splenic artery with surgical clips. Identify the splenic artery proximally, but more
importantly, in a location that is easy to dissect. Do not circumferentially dissect the splenic
artery; the splenic vein and branches are posterior to the artery and injury to these veins can be
extremely difficult to manage. Ligation of the artery will decompress the spleen, lower portal
pressures, and profoundly reduce bleeding.
■
Mobilize the spleen by taking down collaterals to the retroperitoneum with the LigaSure device
and clips.
■
Use the argon beam coagulator to mobilize the planes around the spleen. This effectively manages
the innumerable small collaterals.
■
Leave the short gastric vessels at the upper pole of the spleen to the end of the procedure after the
hilum has been divided.
■
Achieve circumferential control of the splenic hilum as close to the spleen as possible. Advance
a surgical stapler across the hilum. Make sure the stapler is designed to traverse thick tissue
loads. Fire the stapler after assuring no pancreas tissue will be transected with the stapler.
■
Once the hilum is transected, divide the remaining short gastric veins either with the stapler or
surgical clips (FIG 5).
■
Place clips on the splenic artery close to the celiac artery. Once again, circumferential dissection
of the artery should not be done.
■
Complete the esophagogastric devascularization. Identify any collateral vessels behind the
stomach and in the gastrohepatic ligament. Ligate these veins with clips (FIG 6).
■
Repeat portal pressure measurements to determine whether a shunt is needed. Cannulate
collateral veins prior to ligation. Direct pressure measurements of the splenic vein may be
necessary. Multiple measurements may be needed.
■
A shunt should be done if there is a viable target for mesenteric venous inflow and central venous
outflow and a postsplenectomy mesenteric-systemic gradient of 12 mmHg.
PROXIMAL SPLENORENAL SHUNT

■
This procedure is indicated for persistent portal hypertension following splenectomy and functions
as a nonselective shunt. The confluence of the superior mesenteric vein and splenic vein should be
patent with a patent splenic vein. A pressure gradient between the splenic vein and central venous
system of 12 is needed to maintain shunt patency. If pressure monitoring during the case seems
unreliable, a small, easy to repair venotomy in the splenic vein to gauge the pressure in the splenic
vein will inform the decision on whether a proximal splenorenal shunt is needed following
splenectomy.
■
Generous mobilization of the splenic vein is needed to this procedure. This is not always technically
possible and alternative approaches include minimal dissection of the splenic vein and use of a
vein conduit or an alternative shunt procedure.
■
Key steps to the procedure
■
Find the left renal vein. The location of the renal vein anterior to the aorta should be confirmed on
preoperative imaging.
■
Mobilize the splenic flexure of the colon to expose the left kidney. The collaterals in this are
best managed with the argon beam photocoagulator.
■
Enter Gerota’s fascia. This plane is less vascular than the plane anterior to the kidney and
posterior to the colon mesentery. Dissect toward the renal hilum until the vein is identified.
■
In some patients, the renal vein can be dissected freely, directly through the colon mesentery
(without mobilization of the colon).
■
The left renal vein may have numerous large collateral veins (FIG 7). Dissect a sufficient
amount of the vein to place a vascular clamp. Only divide these collateral veins if necessary;
they are extremely thin walled and difficult to manage.
■
Mobilize the splenic vein and pancreas. Only dissect as much as needed to create an
anastomosis between the renal vein and the splenic vein. The dissection is difficult and is
best managed with a needle tip electrocautery, small surgical clips, and meticulous gentle
dissection. Bleeding from the splenic vein or other veins in this area is best repaired with
Prolene suture and pledgets.
■
Administer systemic heparin. Skip this step if there is ongoing bleeding. Much of this bleeding
will stop once the shunt is created.
■
Place a clamp on the left renal vein, usually in the anterior and superior location.
■
Depending on how the vessels line up, the anastomosis to the splenic vein can occur to the end
of the vein (FIG 8A) or, more commonly, to the side of the splenic vein (FIG 8B). Clamp
placement on the splenic vein is among the most challenging aspects of the case. It is critical
that an easy, tension-free anastomosis is possible. If this is not possible, a vein graft conduit
(such as the saphenous vein) should be considered.
■
Complete the back wall of the anastomosis and tie with a small air knot to permit growth.
Prolene suture is used in adults and polydioxanone (PDS) suture in children. Check shunt
inflow from the splenic vein. Clot can form within the vein following splenectomy; if this
occurs, perform a thrombectomy. Complete the front wall of the anastomosis, leaving a small
growth knot.
■
Remove the renal vein clamp first and assess for bleeding. Remove the splenic vein clamp.
■
Check flow with a Doppler and flow probe. Flow is usually about 10% of the estimated
cardiac output, although it can be quite high (FIG 8C).
■
Flow can be augmented by further ligation of collateral veins and/or a reduction in the CVPs.
Collateral veins around the stomach and esophagus should be ligated in all cases.
■
Leave a drain near the area of the splenic vein dissection. Recheck mesenteric venous
pressures.
INFERIOR MESENTERIC VEIN TO LEFT RENAL VEIN SHUNT

■
The inferior mesenteric vein (IMV) is too small to provide adequate inflow for a shunt in most
patients. In some patients with complex mesenteric veno-occlusive disease, the IMV can be large
and spared of chronic occlusive disease. These patients should have a splenectomy. If there is
significant mesenteric venous pressure following splenectomy and there are not better inflow
vessels available, the IMV to left renal vein shunt is a good option.
■
■
Assure the IMV is large (about 50% the diameter of the left renal vein) and has sufficient pressure
to maintain shunt patency. Check pressure in the IMV, making sure not to injure any areas of the
vein that might affect flow through the shunt.
■
Mobilize the left renal vein directly through the colon mesentery, if possible. If not, expose the
left renal vein as described in the earlier section describing the proximal splenorenal shunt.
■
The left renal vein may have numerous large collateral veins (FIG 7). Dissect a sufficient amount
of the vein to place a vascular clamp. Only divide these collateral veins if necessary; they are
extremely thin walled and difficult to manage.
■
Mark the course of the IMV to assure proper orientation upon creation of the shunt.
■
Administer systemic heparin.
■
Place a clamp in the proper location on the left renal vein to facilitate a properly aligned and easy
to sew anastomosis.
■
Ligate and divide the IMV. Check inflow and do a thrombectomy, if necessary. Place a clamp as
close to the pancreas as possible maintaining proper vein alignment.
■
Create an anastomosis between the IMV and left renal vein (FIG 9). Prolene suture is used in
adults and PDS suture in children. Complete the back wall and once again check inflow. Flush
with heparinized saline. Leave a small growth knot to allow the anastomosis to expand.
■
Remove the renal vein clamp and check for bleeding. Remove the clamp on the IMV.
■
Check flow with a Doppler and flow probe. Flow can be augmented by further ligation of
collateral veins and/or a reduction in the CVPs.
DISTAL SPLENORENAL SHUNT

■
The indications for this procedure include the following:
■
Severe portal hypertension with life-threatening complications. The splenic vein must be patent
and the spleen cannot be too large. Patients with persistent thrombocytopenia (platelets
<35,000/μL) and massive splenomegaly need a splenectomy.
■
Patients with significant ascites should not have a selective shunt such as a distal splenorenal
shunt.
■
■
Divide enough short gastric vessels to expose the splenic vein and pancreas. Keep dissection to a
minimum. Use hands instead of pickups for operative exposure. Collateral veins are best ligated
using a no-touch technique and either surgical clips or the LigaSure device (FIG 4). The splenic
vein can also be approached through the transverse mesocolon by following the IMV toward the
splenic vein.
■
Mobilize the splenic flexure of the colon to expose the left kidney. The collaterals in this are best
managed with the argon beam photocoagulator.
■
Enter Gerota’s fascia. This plane is less vascular than the plane anterior to the kidney and
posterior to the colon mesentery. Dissect toward the renal hilum until the vein is identified.
■
If the splenic vein was exposed directly through the transverse mesocolon, the renal vein can be
dissected freely, directly through the colon mesentery (without mobilization of the colon). If
extensive mobilization of either the splenic vein or the renal vein is needed, this approach is not
recommended.
■
The left renal vein may have numerous large collateral veins (FIG 7). Dissect a sufficient amount
of the vein to place a vascular clamp. Only divide these collateral veins if necessary; they are
extremely thin walled and difficult to manage.
■
Mobilize a sufficient amount of the splenic vein to reach the renal vein. Place a vessel loop
around the splenic vein during the dissection and location that provides easy access. Use the
vessel loop to administer gentle traction to improve exposure of the small branches of the
splenic vein.
■
A needle-tipped electrocautery can facilitate this gentle dissection. Provide the small branches
with electrocautery or microvascular clips. Placing ties around the small veins is more likely
to tear the vein and cause bleeding.
■
If an injury occurs to the splenic vein, place repair sutures (frequently with pledgets) only after
the splenic vein has been decompressed with gentle pressure on the splenic hilum.
■
In small number of patients, it is impossible to safely mobilize the splenic vein out of the
pancreas. Decide early whether this is the case and move on to an alternative portal
hypertension procedure.
■
Only mobilize enough splenic vein as needed for a tension-free anastomosis. Mobilization of
the pancreas will bring the splenic vein closer to the renal vein and will help minimize how
much splenic vein needs to be dissected.
■
Administer systemic heparin. Skip this step if there is ongoing bleeding. Much of this bleeding
will stop once the shunt is created.
■
Ligate and divide the medial splenic vein. This can be done with a silk tie or surgical clips to
reinforce the closure of the vein.
■
Place a small vascular clamp (a Heifetz or bulldog clamp) on the splenic vein toward the spleen.
Make sure the clamp does not distort the anatomic course of the vein.
■
Place a clamp on the left renal vein, usually in the anterior and superior location.
■
Complete the back wall of the anastomosis and tie with a small air knot to permit growth. Prolene
suture is used in adults and PDS suture in children. Check shunt inflow from the splenic vein and
flush with heparinized saline. Complete the front wall of the anastomosis leaving a small growth
knot.
■
Remove the renal vein clamp first and assess for bleeding. Remove the splenic vein clamp (FIG
10).
■
Check flow with a Doppler and flow probe. Flow is usually about 10% of the estimated cardiac
output, although it can be quite high.
■
Ligate additional portal-systemic collateral vessels. These veins can be found around the spleen,
stomach, and esophagus. Simply placing a surgical clip on these veins is sufficient to ligate
them.
■
Leave a drain near the area of the splenic vein dissection.
■
Follow-up with ultrasound. If shunt cannot be seen on ultrasound, do a CT scan or MRI of the
abdomen with mesenteric vein reconstructions (FIG 11).
MESO-REX SHUNT
■
The indications for this procedure include the following:
■
Severe portal hypertension with life-threatening complications.
■
Portal vein thrombosis with a patent superior mesenteric vein (or splenic vein) and intrahepatic
portal veins, including the junction between the right and left lobes of the liver.
■
Patients with persistent thrombocytopenia (platelets <35,000/μL) and massive splenomegaly need
a splenectomy.
■
A meso-Rex shunt restores normal physiology and has been reported to be associated with
improved liver and cognitive function.1,2
■
Vein conduit is required for this procedure. The jugular vein is favored.
■
The intrahepatic portal vein is not always adequate for an anastomosis. Be prepared to do an
alternative shunt procedure, and do not procure conduit until the portal vein in the Rex recess is
determined to be patent and suitable for anastomosis.
■
■
Dissect into the Rex recess by following the round ligament. Use a needle tip electrocautery and
small clips/ties to divide small vessels entering the liver. Expose a sufficient amount of the
segment 2 or 3 portal vein for placement of a side-biting clamp and creation of an anastomosis.
■
Confirm patency of this vein by duplex or intraoperative ultrasound. A venogram can be done if
there is concern for lack of patency after less invasive testing.
■
Expose the superior mesenteric vein. Find the middle colic vein in the medial colon mesentery.
Follow the middle colic vein toward the root of the mesentery. Numerous collateral veins will
be present; ligate these with clips and/or a small LigaSure device.
■
Expose a sufficient amount of superior mesenteric vein to facilitate placement of a vascular clamp
on the anterior vein and an anastomosis (FIG 12).
■
Once both veins are confirmed to be suitable for a meso-Rex shunt, procure a vein conduit. The
internal jugular vein is the preferred conduit.
■
Administer systemic heparin.
■
Place a side-biting vascular clamp on the segment 2 or 3 portal vein in the Rex recess. A small
“C” clamp or a baby Satinsky clamp works well for this.
■
Fashion an anastomosis between the portal vein and the end of the vein conduit. Leave a small
growth knot in the anastomosis when tying. Release the portal vein clamp and repair any
bleeding.
■
Flush the conduit with heparinized saline to confirm patency and low resistance to flow. Replace
the vascular clamp on the conduit near the anastomosis, making sure not to affect the anatomic
lie of the conduit and that there is not a column of blood in the conduit.
■
Run the conduit either in front of or behind the antral/pyloric region and through a small defect in
the transverse colon mesentery toward the superior mesenteric vein.
■
Confirm the correct length of the conduit. Make sure the liver is in the anatomic location (without
retraction) when sizing the conduit.
■
Fashion an end-to-side anastomosis between the conduit and superior mesenteric vein, usually
creating a 45-degree bevel in the conduit. Check flow in the superior mesenteric vein before
completing the anastomosis.
■
Release the clamp on the portal vein side before trying to assure no clot formed in the
liver/conduit and to allow the conduit to expand. Tie down the anastomosis only until bleeding
stops.
■
Remove the clamp on the superior mesenteric vein (FIG 13).
■
Tie the anastomosis with a small growth knot.
■
Check flow with a Doppler and flow probe. Flow is usually about 15% of the estimated cardiac
output, although it can be quite high.
■
Ligate additional portal-systemic collateral vessels. These veins can be found around the spleen,
stomach, and esophagus. Simply placing a surgical clip on these veins is sufficient to ligate
them.
■
Follow up with ultrasound. Early diagnosis of changes in flow within the conduit is critical to
assure early angiographic intervention and shunt salvage.
OTHER SHUNTS
■
Surgery for portal hypertension requires novel approaches to unique patient problems and a
willingness to change the plan during surgery depending on intraoperative findings.
■
Numerous variations on the surgical procedures detailed earlier should be considered. Large
collateral vessels are occasionally appropriate for shunt creation. These vessels tend to be thin
walled and meticulous technique is paramount. For example, a large coronary vein can be used for
anastomosis to the portal vein in the Rex recess or to the retrohepatic inferior vena cava to create
an Inokuchi shunt (FIG 14).
PEARLS AND PITFALLS
Patient selection ■ Assess liver function; most patients have cirrhosis.
■ Noncirrhotic portal hypertension: Patients usually only have
splenomegaly and history of bleeding.
■ Many children had an umbilical catheter.
Imaging ■ Patients with mesenteric vein thrombosis need hypercoagulable
workup.
■ Arterial and venous phase MRI or CT scan provides an excellent
anatomic assessment.
Indications for surgery in ■ One life-threatening complication of portal hypertension
adults ■ No angiographic option for a durable solution
■ Preserved liver function. If cirrhotic, no decompensation
■ Massive splenomegaly, profound thrombocytopenia, or severe
pain profoundly affecting lifestyle
Indications for surgery in ■ Two life-threatening complications of portal hypertension
children ■ Massive splenomegaly or severe thrombocytopenia affecting
lifestyle
■ No viable or durable endovascular procedure available.
Operative decision making ■ Plan frequently changes based on operative findings.
■ Assess mesenteric venous pressures during surgery to help with
decision making.
Splenectomy ■ Keep dissection to a minimum.
■ No-touch technique with use of clips, argon beam, and LigaSure
device
■ Early ligation of the splenic artery with clips
■ Staple across the hilum
Proximal splenorenal shunt ■ Central shunt done following splenectomy
■ Enter Gerota’s fascia to find the renal vein; only dissect enough
renal vein to place a clamp.
■ Repair injuries to these veins with pledgeted Prolene sutures.
■ Use systemic heparin.
■ Augment flow through the shunt by ligating other collaterals.
IMV-left renal vein shunt ■ The IMV is usually too small to adequately decompress the
mesenteric system.
■ For patients with mesenteric venous occlusive disease
■ Mobilize the left renal vein directly through the colon mesentery.
Distal splenorenal shunt ■ Only dissect enough splenic vein to reach the renal vein.
■ Only dissect enough renal vein to enable clamping.
■ Ligate competing collateral veins to augment flow.
Meso-Rex shunt ■ Restores normal hepatic flow
■ Jugular vein is the favored conduit.
■ Confirm patency of the intrahepatic portal vein preoperatively and
during surgery.
■ Do not procure conduit until certain can complete the shunt.
■ Use systemic heparin.
■ Make sure liver is in anatomic position when positioning the
conduit.
POSTOPERATIVE CARE
■
A typical hospitalization may be between 3 and 7 days.
■
Avoid volume overload; it will affect shunt flow.
■
Carefully monitor liver function.
■
Many patients have a preoperative propensity for thrombosis; consider postoperative fractionated or
unfractionated heparin. Discharge these patients on systemic anticoagulation.
■
All splenectomy patients need a postoperative aspirin. If the platelet count goes over 300,000/μL,
inpatient and outpatient systemic anticoagulation is required for 3 months or greater.
■
Patients do not need nasogastric tubes and diets can be advanced quickly.
■
A surveillance abdominal ultrasound is obtained prior to discharge to verify patency of the shunt. If
the shunt cannot be visualized, more advanced imaging can be considered on a case-by-case basis.
■
Patients with preoperative ascites will need to continue diuretics for several weeks.
■
Endoscopy to assess for stigmata of portal hypertension and follow-up imaging of the shunt should
be done at scheduled intervals for several years as an outpatient.
■
Early diagnosis and intervention by interventional radiology will facilitate long-term shunt patency.
OUTCOMES
■
Excellent long-term survival is reported in children, although continuous monitoring and early
intervention of flow changes within a shunt is necessary to maintain patency.2,3
■
Less data is available in adults. They frequently have more complex disease, including
hypercoagulable states.
■
With attentive care, death from a portal hypertensive complication is rare for these patients.
COMPLICATIONS
■
Liver decomposition
■
Shunt thrombosis
■
Bleeding
■
Thrombocytosis in splenectomy patients
■
Pancreatic leak
REFERENCES
1. Superina R, Shneider B, Emre S, et al. Surgical guidelines for the management of extra-hepatic portal vein obstruction. Pediatr
Transplant. 2006;10(8):908–913.
2. Shneider BL, Bosch J, de Franchis R, et al. Portal hypertension in children: expert pediatric opinion on the report of the Baveno v
consensus workshop on methodology of diagnosis and therapy in portal hypertension. Pediatr Transplant. 2012;16(5):426–437.
3. Shneider B, Emre S, Groszmann R, et al. Expert pediatric opinion on the Report of the Baveno IV consensus workshop on
methodology of diagnosis and therapy in portal hypertension. Pediatr Transplant. 2006;10(8):893–907.
Index
Page numbers followed by f and t indicated figures and tables, respectively.
A
AAA. See Abdominal aortic aneurysm
Abdominal aortic aneurysm (AAA), 192, 192f, 203, 203t
etiology of, 203
EVAR for, 203
balloon molding for, 207, 207f
closure of, 207
completion arteriography for, 207, 208f
complications with, 211
endograft delivery and deployment, 205–206, 206f
gate cannulation for, 206, 206f
imaging and diagnostic studies for, 204
indications for, 204
limb extension for, 206–207, 206f
outcomes with, 211
patient history and physical findings for, 203–204
pearls and pitfalls of, 210
percutaneous access for, 205
postoperative care for, 210–211, 211f
preclose technique for, 205, 205f
preoperative planning for, 204
imaging and diagnostic studies of, 193, 193f
patient history and physical findings of, 192–193
preoperative planning for, 194, 194t
REVAR for
aortic balloon control for, 209, 209f
balloon molding for, 210
closure for, 210
completion aortography for, 210, 210f
endograft delivery and deployment for, 209, 209f
gate cannulation for, 210
limb extension for, 210
outcomes with, 211
percutaneous access for, 208–209
postoperative care for, 210–211
risk factors for, 203t
surgical management of, 193, 193t
aortic clamping and repair for, 199–201, 199f–201f
outcomes with, 202
postoperative care for, 202
retroperitoneal approach to, 194, 194f, 197–198, 197f–198f
transperitoneal approach to, 194–195, 194f–196f
Acute iliofemoral deep vein thrombosis, 313
differential diagnosis for, 313
imaging and diagnostic studies for, 314–315
operative management of
adjunct arteriovenous fistula creation for, 319–320, 319f
completion imaging for, 320
iliac venous thrombectomy for, 318
infrainguinal femoral venous thrombectomy for, 319, 319f
outcomes with, 320
positioning for, 315
wound closure for, 320
patient history and physical findings for, 313
percutaneous management of
baseline phlebography for, 315
catheter-directed thrombolysis for, 315–316
completion imaging for, 318
duplex-guided femoral vein access for, 315
femoral vein closure for, 318
outcomes with, 320
pharmacomechanical thrombectomy for, 316–317, 316f–317f
venous compression syndrome stenting, 317–318, 318f
venous stenoses stenting, 317–318, 318f
Acute iliofemoral occlusion, 313
Acute mesenteric ischemia (AMI), 156
hybrid repair of, 163, 164f
patient selection with, 157–158
Adjunct arteriovenous fistula creation, for acute iliofemoral deep vein thrombosis, 319–320, 319f
Adson’s test, for neurogenic TOS, 46
AMI. See Acute mesenteric ischemia
Aneurysm
of aorta
abdominal. See Abdominal aortic aneurysm
paravisceral. See Paravisceral aortic aneurysms
thoracic. See Thoracic aortic aneurysms
thoracoabdominal. See Thoracoabdominal aortic aneurysm
of aortic arch, 1
fusiform, 192
Angiography. See also Computed tomographic angiography; See also Magnetic resonance angiography
for antegrade tibial interventions, 292, 293f
for autogenous vein bypass, 279
digital subtraction, for perimalleolar bypass, 303, 303f
for tibial interventions, 290, 290f–291f
of upper extremity, 86–87, 87f
Angioguard, 24, 24f
AngioJet thrombectomy system, 316–317, 316f
Angioplasty. See also Patch angioplasty
balloon
for antegrade tibial interventions, 294–295, 294f–295f
for CAS, 29, 29f
for femoral–popliteal reconstruction, 273, 274f
for retrograde tibial interventions, 299, 300f
for CAS, 29, 29f
of renal arteries, 159–161, 160f–161f
for vertebrobasilar insufficiency, 43
of visceral arteries, 162–163, 162f
Ankle–brachial indices (ABI)
with aortoiliac occlusive disease, 221–222
in CLI, 302, 303f
for femoral–popliteal reconstruction, 265
Antegrade tibial interventions. See Tibial interventions
Anterior tibial artery, exposure of, 253–254, 253f
supramalleolar, 255, 255f
Anterior tibialis artery
exposure of, 308, 308f
perimalleolar bypass to, dorsalis pedis artery exposure for, 309, 309f
tunneling to, 308–309, 309f
Anticoagulation
in arterial reconstruction, 77
after lower extremity artery exposure, 256–257
for vTOS, 68, 73
Antihypertensive medications, for carotid angioplasty and stenting, 26
Antiplatelet therapy
for carotid angioplasty and stenting, 26, 31
after lower extremity artery exposure, 256–257
Aorta
aneurysm of. See Aneurysm
eggshell, 25
in retroperitoneal aortic exposure, 124–125
shaggy, 25
visceral, in retroperitoneal aortic exposure, 125, 125f–126f
Aortic aneurysm
juxtarenal. See Juxtarenal aortic aneurysm
paravisceral. See Paravisceral aortic aneurysms
thoracic. See Thoracic aortic aneurysms
Aortic arch
aneurysm of, 1
angiography of, 24–25, 25f
debranching of, 7
Aortic arch reconstruction, 1
debranching technique for, 2–4, 3f–5f
endovascular second stage of, 5
imaging and diagnostic studies for, 1, 1f
outcomes with, 6
pearls and pitfalls of, 5–6
positioning for, 2
preoperative planning for, 1–2
Aortic dissection
TEVAR for
completion aortogram for, 113
complications with, 116–117
initial aortogram for, 111–113, 112f
outcomes with, 116
pearls and pitfalls for, 116
sheath removal and arteriotomy closure for, 113
special considerations for, 114, 114f
subclavian artery revascularization, 113, 113f
thoracic stent graft selection and sizing for, 109–111, 110f–111f
vascular access for, 111
Aortic exposure, retroperitoneal. See Retroperitoneal aortic exposure
Aortic reconstruction, 171–173, 172f–174f
Aortic repair, in TAAA, 102–103, 102f–103f
Aortic transection, traumatic. See Traumatic aortic transection
Aortofemoral open reconstruction
aorta exposure in, 226
clamp placement in, 226–227, 227f
distal anastomosis in, 227–228, 228f
femoral vessel exposure in, 226
graft tunneling in, 227
outcomes with, 226t
proximal anastomosis in, 227, 227f–228f
tunneling in, 226
Aortography
for aortoiliac occlusive disease, 232
for common iliac stenting, 236–237
for perimalleolar bypass, 303, 303f
retroperitoneal aortic exposure and, 123
for REVAR, for AAA, 210, 210f
for TEVAR
completion, 113
initial, 111–113, 112f
Aortoiliac occlusive disease, 221, 221t, 231
aortofemoral open reconstruction for
outcomes with, 226t
tunneling in, 226
aortoiliac reconstruction with femoral crossover, 228–229, 229f
common iliac stenting for
aortogram for, 236–237
balloon and stent selection for, 237
completion arteriography for, 237
kissing stent technique for, 237, 238f
outcomes with, 239
pearls and pitfalls for, 238–239, 239f
external iliac stenting for, 234f, 238–239
femoral endarterectomy for
closure for, 235, 235f
endarterectomy plane creation, 235–236, 236f
femoral artery exposure for, 233, 234f
iliac artery dissection for, 234, 234f
outcomes with, 239
patch angioplasty for, 236
patch closure for, 236
wire advancement for, 234–235, 234f
imaging and diagnostic studies for, 222, 223f, 231–232, 231f
isolated femoral reconstruction for
clamping in, 224
closure for, 224, 226
endarterectomy, tacking sutures in, 224, 224f
incision and exposure for, 223–224
landmarks for, 223
outcomes with, 226t
patch angioplasty for, 224, 225f
patient history and physical findings for, 221–222, 231
surgical management of, 222, 232
preoperative planning for, 232, 233f
Aortoiliac reconstruction with femoral crossover, 228–229, 229f
Arch aortography, for CAS, 26, 27f
Arm vein
back-table preparation of, 283, 283f
mapping of, 279, 280f
open vein harvest of, 281, 281f
Arterial occlusive disease, 74
Arterial oncologic pathologies, 169t
Arterial reconstruction
for aTOS decompression, 72
distal to wrist, 91
hand fasciotomy, 96–97, 96f
imaging and diagnostic studies for, 92–93, 92f
outcomes of, 97–98
positioning for, 93–94, 93f
postoperative care for, 97, 97f
snuffbox, 95–96, 95f–96f
ulnar artery, 94–95, 94f–95f
proximal to wrist, 74, 74t
brachial artery, 81–84, 82f–83f
mid-distal axillary artery, 79–80, 79f–81f
operating room setup for, 76, 76f–77f
outcomes with, 89
proximal axillary artery, 76f–77f, 77–79
radial artery, 83f, 84–85, 85f
ulnar artery, 83f, 85f, 86
Arterial stenosis, 221, 221t
Arterial TOS (aTOS), 66, 66f
decompression for
arterial reconstruction for, 72
outcomes with, 73
positioning for, 69
supraclavicular approach to, 71–72, 71f–72f
differential diagnosis for, 66–67
neurogenic TOS compared with, 46, 59–60
Arteriography. See also Computed tomographic arteriography
for common iliac stenting, 237
for EVAR, for AAA, 207, 208f
for iliac aneurysm, 212
Atherosclerotic aneurysm. See Abdominal aortic aneurysm
aTOS. See Arterial TOS
Autogenous vein
preparation of, 283, 283f, 305–307, 306f
Autogenous vein bypass, 279
back-table vein preparation for, 283, 283f
composite graft creation for, 283, 283f
distal anastomosis for, 285, 287f
distal anastomotic site selection for, 284
endoscopic vein harvest for, 281–283, 282f–283f, 282t
graft tunneling for, 283–284, 284f
imaging and diagnostic studies for, 279, 279f–280f
intraoperative assessment for, 285
open vein harvest for, 280–281, 280f–281f
outcomes with, 288
pearls and pitfalls of, 287, 287f
preoperative planning for, 279–280, 280f
proximal anastomosis for, 284–285, 286f
proximal anastomotic site selection for, 284, 285f
Axillary artery
interposition grafting for, 76
open surgical bypass for, 76
reconstruction of
mid-distal, 79–80, 79f–81f
proximal, 76f–77f, 77–79
thromboembolectomy for, 75–76
B
Balloon angioplasty
for antegrade tibial interventions, 294–295, 294f–295f
for CAS, 29, 29f
for retrograde tibial interventions, 299, 300f
Balloon molding
for EVAR
for AAA, 207, 207f
periscope technique, 141, 142f–143f
snorkel/chimney technique, 140, 140f
for REVAR, for AAA, 210
Beach chair position, for internal carotid artery exposure, 35, 35f
Biopsy
of liver
TIPS and, 322
Bleeding
after lower extremity artery exposure, 256
with TIPS, 329–330
Bovine arch, 24
Brachial artery
interposition grafting for, 76
open surgical bypass for, 76
reconstruction of, 81–84, 82f–83f
thromboembolectomy for, 75–76
Brachial plexus
mobilization of, for supraclavicular decompression of NTOS, 51–52, 52f–53f
neurolysis of, for supraclavicular decompression of NTOS, 52–53, 55f
Brachiocephalic vessels, debranching of, 1
Branch dissection, 155
Branched repair. See Endovascular aortic repair
Branch perforation, 155
Buerger’s disease, 91
C
Cancer management, visceral reconstruction for, 169
aortic reconstruction, 171–173, 172f–174f
IVC reconstruction, 178–180, 179f–180f
operating room setup for, 171
outcomes with, 181–182
patient selection for, 170
SMA reconstruction, 174–176, 175f
SMV reconstruction, 176–178, 177f
Cannulation
gate
for EVAR for AAA, 206, 206f
for REVAR for AAA, 210
renal, for EVAR, 138–139, 139f
visceral, for EVAR, 138–139, 139f, 141, 141f–142f
Carotid angioplasty and stenting (CAS), 24, 24f
access hemostasis for, 30
arch aortography for, 26, 27f
common carotid catheterization for, 27, 27f–28f
completion angiogram for, 30, 30f
contraindications for, 26, 26t
EPD for, 24
deployment of, 29, 29f
retrieval of, 30, 30f
guiding sheath placement for, 28, 29f
for hostile neck anatomy, 34
percutaneous retrograde femoral artery access for, 26
positioning for, 26
predilatation with angioplasty balloon, 29, 29f
stenting and postdilatation for, 30, 30f
Carotid artery. See also Common carotid artery; See also Internal carotid artery exposure and control
angiography of, 24–25, 25f
in aortic arch debranching, 3–4, 4f
dissection and control
for carotid artery interposition bypass, 21
for carotid artery ligation, 21
for carotid endarterectomy, 20
exposure of
for carotid–carotid bypass, 11–12
for carotid–subclavian bypass, 8–9, 9f
vertebral transposition to, 41–42, 42f
Carotid artery interposition bypass, 15
indications for, 15–16
pearls and pitfalls, 22
technique for
anastomosis, 21, 21f
carotid artery dissection and control, 21
closure, 21
incision, 21
Carotid artery ligation, 15
indications for, 16
technique for
closure, 21
endarterectomy, 21, 22f
incision, 21
Carotid–carotid bypass, 7
outcomes with, 14
positioning for, 7
technique for
bilateral carotid arteries exposure, 11–12
closure, 12
graft tunneling and anastomosis, 12, 12f–13f
Carotid duplex scanning, for extrathoracic revascularization, 7
Carotid endarterectomy (CEA), 15
alternative to, 24
candidates for, 26
eversion technique
anastomosis, 20, 20f
closure, 20
eversion endarterectomy, 20, 20f
incision, 20
indications for, 15
patch angioplasty technique
carotid exposure and control, 16–17, 17f
closure, 18
conventional endarterectomy, 18, 19f
incision for, 16, 17f
patch placement, 18, 19f
Carotid Revascularization Endarterectomy versus Stenting Trial (CREST), 32
Carotid stump syndrome, carotid artery ligation for, 16
Carotid–subclavian bypass, 7
in aortic arch debranching, 4, 5f
outcomes with, 14
positioning for, 7
technique for
bypass, 9–10, 9f–10f
carotid artery exposure, 8–9, 9f
closure, 10
subclavian artery exposure, 8, 8f
Carpal tunnel release, in hand fasciotomy, 97
CAS. See Carotid angioplasty and stenting
Catheter-based phlebography, for acute iliofemoral deep vein thrombosis, 314–315
Catheter-directed thrombolysis, for acute iliofemoral deep vein thrombosis, 315–316
Catheterization, of CCA, for CAS, 27, 27f–28f
CEA. See Carotid endarterectomy
Celiac artery
aneurysms of, 156
angioplasty and stenting for, 162–163, 162f
embolization for, 164–166, 165f–166f
in EVAR, 204
fenestrated graft creation for, 133–134, 134f
Cerebral arteries, angiography of, 24–25, 25f
Cerebral hyperperfusion syndrome, with CAS, 33
CFA. See Common femoral artery
Chest radiography
for neurogenic TOS, 46, 48f
Chimney EVAR. See Endovascular aortic repair
Chronic lower extremity ischemia. See Peripheral arterial disease
Chronic mesenteric ischemia (CMI), 156
hybrid repair of, 163, 164f
patient selection with, 157
Chronic total occlusions (CTOs), tools for managing, 258, 258t
Claudication
with aortoiliac occlusive disease, 221
of lower limbs, 265
with PAD, 247
CLI. See Critical limb ischemia
CMI. See Chronic mesenteric ischemia
Common carotid artery (CCA)
bovine arch with, 24
catheterization of, for CAS, 27, 27f–28f
Common femoral artery (CFA)
exposure of, for PAD management, 248–250, 248f–249f
infrainguinal outflow from, 221
retrograde access for CAS, 26
Common femoral vein (CFV), acute iliofemoral occlusion of, 313
Common iliac stenting
aortogram for, 236–237
balloon and stent selection for, 237
completion arteriography for, 237
kissing stent technique for, 237, 238f
outcomes with, 239
Compartment syndrome, 91
Complete visceral debranching and endovascular tube graft repair
anticoagulation, 131
endograft deployment, 132
exposure, 129–131, 130f
intravascular ultrasound, 132
multivisceral bypass, 131–132, 131f
outcomes with, 135
percutaneous access, 132
stiff wire exchange, 132
Complex regional pain syndrome (CRPS), with NTOS, 46
Computed tomographic angiography (CTA)
of AAA, 193, 193f
for aortoiliac occlusive disease, 222, 231, 231f
for arterial reconstruction proximal to wrist, 75
for carotid angioplasty and stenting, 24–25, 25f, 30, 30f
for extrathoracic revascularization, 7
for internal carotid artery exposure, 34, 34f
for TAAA treatment, 99–100, 99f, 100f
for TEVAR, 108
for tibial interventions, 290
Computed tomographic arteriography (CTA)
for retroperitoneal aortic exposure, 123
Computed tomography (CT). See also Multidetector computed tomography
for AAA, 204
for aortic arch reconstruction, 1, 1f
for arterial reconstruction proximal to wrist, 75
for iliac aneurysm, 212
TIPS and, 322
Computed tomography phlebography, for acute iliofemoral deep vein thrombosis, 314
Computed tomography venography (CTV), for acute iliofemoral deep vein thrombosis, 314
Crawford classification, 118, 118f
CREST. See Carotid Revascularization Endarterectomy versus Stenting Trial
CREST syndrome, 91
Critical limb ischemia (CLI)
ABI in, 302, 303f
with PAD, 247
percutaneous femoral–popliteal reconstruction for, 277
perimalleolar bypass for, 302
tibial intervention for, 289
CRPS. See Complex regional pain syndrome
Cryopreserved grafts, for femoral graft infection, 245
CT. See Computed tomography
CTA. See Computed tomographic angiography; See Computed tomographic arteriography
CTOs. See Chronic total occlusions
CTV. See Computed tomography venography
D
DASH questionnaire. See Disabilities of the Arm, Shoulder, and Hand
DeBakey classification, 118, 119f
Debranching
of aortic arch, 7
for aortic arch reconstruction, 2–4, 3f, 4f–5f
of brachiocephalic vessels, 1
Deep femoral artery. See Profunda femoris artery
Deep vein thrombosis (DVT), 313
Descending aortic dissections
diaphragm exposure for, 118
abdominal exposure for, 120, 121f
closure for, 122
division of, 121, 121f
incision for, 119–120, 120f
outcomes with, 122
positioning for, 119, 119f
thoracic exposure for, 121
differential diagnosis for, 118, 119f
Diaphragm
exposure and surgical management of, 118
closure for, 122
differential diagnosis for, 118, 118f–119f
outcomes with, 122
in retroperitoneal aortic exposure, 125–126, 125f
Digital subtraction angiography, for perimalleolar bypass, 303, 303f
Disabilities of the Arm, Shoulder, and Hand (DASH) questionnaire, for neurogenic TOS, 46
Dissection
aortic. See Aortic dissection
Distal aortic perfusion, for TAAA, 102, 102f
Distal embolization, after lower extremity artery exposure, 256
Distal EPD, 24, 24f
CAS deployment of, 24, 29, 29f
Distal splenorenal shunt, for portal hypertension surgery, 339–340, 340f
Dorsalis pedis. See Dorsal pedal artery
Dorsal pedal artery, exposure of, 255, 255f
for perimalleolar bypass, 309, 309f
Duplex arterial imaging, for femoral–popliteal reconstruction, 265, 266f
Duplex ultrasound
for acute iliofemoral deep vein thrombosis, 314
for autogenous vein bypass, 279, 279f–280f
for carotid angioplasty and stenting, 24
during hepatorenal bypass, 187–188
for neurogenic TOS, 46
for perimalleolar bypass, 304
for renal artery disease, 157
for tibial interventions, 289, 290f
DVT. See Deep vein thrombosis
E
EAST. See Elevated arm stress test
ECG. See Electrocardiogram
Echocardiography. See also Transesophageal echocardiography
Effort thrombosis. See Venous TOS
Eggshell aorta, 25
Electrocardiogram (ECG)
TIPS and, 322
Electrophysiologic tests, for neurogenic TOS, 46
Elevated arm stress test (EAST), for neurogenic TOS, 46, 47f, 59
Embolic protection devices (EPD), distal, CAS deployment of, 24, 29, 29f
Embolization
of renal or visceral arteries, 164–166, 165f–166f
Embolization devices, size/shape of, 159
Endarterectomy. See also Femoral endarterectomy
inadequate endpoint for, 127
injury during, 127
in isolated femoral reconstruction, 224, 224f
Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis (EVA-3S), 32
Endograft
for AAA
EVAR, 205–206, 206f
REVAR, 209, 209f
for endovascular tube graft repair, 132
Endoleaks
with EVAR, 155
with TEVAR, 117
Endoscopic vein harvest, of GSV, 281–283, 282f–283f, 282t
Endovascular aneurysm repair for ruptured aneurysms (REVAR), for AAA
aortic balloon control for, 209, 209f
balloon molding for, 210
closure for, 210
completion aortography for, 210, 210f
endograft delivery and deployment for, 209, 209f
gate cannulation for, 210
limb extension for, 210
outcomes with, 211
percutaneous access for, 208–209
Endovascular aortic repair (EVAR)
for AAA, 203
balloon molding for, 207, 207f
closure of, 207
completion arteriography for, 207, 208f
endograft delivery and deployment, 205–206, 206f
gate cannulation for, 206, 206f
limb extension for, 206–207, 206f
outcomes with, 211
percutaneous access for, 205
postoperative care for, 210–211, 211f
preclose technique for, 205, 205f
with branched stent grafts, 145
ancillary tools for, 146, 147t
arterial access for, 147–148
diagnostic imaging for, 145–146
with fenestrated stent grafts, 152, 153f
outcomes with, 154
perioperative measures for, 146–147
stent graft design for, 146
technique for, 150–152, 151f
with fenestrated stent grafts, 145
ancillary tools for, 146, 147t
arterial access for, 147–148
with branched stent grafts, 152, 153f
diagnostic imaging for, 145–146
outcomes with, 154
perioperative measures for, 146–147
stent graft design for, 146, 146f
technique for, 148–150, 148f–150f
periscope technique for, 136
deployment and balloon molding for, 141, 142f–143f
femoral access for, 141, 141f
imaging and diagnostic studies for, 136–137, 136f–137f
stent graft positioning for, 141, 142f
visceral branch cannulation for, 141, 141f–142f
snorkel/chimney technique for, 136
arm access for, 138, 138f
completion of, 140, 140f
renal/visceral cannulation in, 138–139, 139f
stent graft deployment and balloon molding, 140, 140f
stent graft positioning for, 139–140, 139f
thoracic. See Thoracic endovascular aortic repair
Endovascular common iliac artery aneurysm repair
with internal iliac artery occlusion
catheter advancement for, 213, 213f
embolization for, 214–215, 214f
endograft deployment for, 215, 215f
ipsilateral access for, 213–214, 214f
occlusion for, 214
sleeve technique for, 215, 215f
with internal iliac preservation
anastomosis for, 217, 217f
bell-bottom devices for, 216, 216f
chimney stenting technique for, 218, 218f
division for, 217, 217f
endograft deployment for, 217–218, 217f–218f
iliac branch device for, 218–219, 219f
retroperitoneal access for, 216–217, 216f
surgical bypass for, 216
pearls and pitfalls with, 219
Endovascular tube repair. See Complete visceral debranching and endovascular tube graft repair; See Partial visceral debranching and
physician-modified endovascular repair
EPD. See Embolic protection devices
Esophagogastric devascularization, for portal hypertension surgery, 335–336, 335f–337f
EVA-3S. See Endarterectomy Versus Angioplasty in Patients with Symptomatic Severe Carotid Stenosis
EVAR. See Endovascular aortic repair
External iliac stenting, 234f, 238
Extrathoracic revascularization, 7
outcomes with, 14
positioning for, 7
techniques for
carotid–carotid bypass, 11–12, 12f–13f
carotid–subclavian bypass, 8–10, 8f, 9f–10f
subclavian artery transposition, 10, 11f
F
FBE. See Fenestrated and branched EVAR
Femoral artery. See also Common femoral artery
aneurysm of, autogenous vein bypass for, 279
in antegrade tibial interventions, 292, 292f
aortofemoral open reconstruction
tunneling in, 226
exposure of
for femoral endarterectomy, 233, 234f
for PAD management, 248–250, 248f–249f
isolated reconstruction of
clamping in, 224
landmarks for, 223
subintimal recanalization of, 258
complications of, 246
cryopreserved grafts for, 245
lateral profunda femoris artery exposure for, 244, 244f
obturator bypass for, 242–243, 243f
postoperative care of, 246
sheath placement for, 259, 259f
strategy for, 259
superficial femoral vein harvest for, 244, 245f
superficial, dissection and control of, 248–249, 248f–249f
Femoral endarterectomy
closure for, 235, 235f
endarterectomy plane creation, 235–236, 236f
femoral artery exposure for, 233, 234f
iliac artery dissection for, 234, 234f
outcomes with, 239
patch angioplasty for, 236
patch closure for, 236
wire advancement for, 234–235, 234f
Femoral graft infection
surgical management of, 241–242, 241f–242f
cryopreserved grafts for, 245
lateral profunda femoris artery exposure for, 244, 244f
obturator bypass for, 242–243, 243f
superficial femoral vein harvest for, 244, 245f
Femoral–popliteal reconstruction, percutaneous, 258, 258t, 265
antegrade femoral puncture for, 269, 270f
balloon angioplasty for, 273, 274f
brachial puncture for, 269–270
complications with, 277, 277f
crossing occlusive lesions, 272–273, 272f–273f
guidewire placement for, 269, 272–273, 272f–273f
imaging and diagnostic studies for, 258, 265–266, 266f–267f
outcomes with, 277
patient history and physical findings for, 258, 265
postoperative groin puncture for, 268–269
preoperative planning for, 258, 266–267
retrograde femoral puncture for, 267–268, 269f
sheath placement for, 269–270
ipsilateral approach to, 271, 272t
up and over approach to, 271, 271f, 272t
stent grafts for, 275–276, 276f
stent placement for, 274–275, 275f
subintimal recanalization of
catheter for, 262
loop management for, 260–261, 261f
outcomes with, 264
reentry device placement for, 261
retrograde approach to, 262–263, 263f
strategy for, 259
subintimal space entry in, 259, 260f
true lumen reentry, 261–262, 262f
Femoral vein. See also Superficial femoral vein
common, acute iliofemoral occlusion of, 313
open vein harvest of, 281
Fenestrated and branched EVAR (FBE), 136
Fenestrated repair. See Endovascular aortic repair
Fenestration misalignment, 154–155
Fibromuscular dysplasia (FMD), 156
FilterWire, 24, 24f
FMD. See Fibromuscular dysplasia
Fusiform aneurysms, 192
G
Gastroduodenal artery (GDA)
anastomosis of, in hepatorenal bypass, 187, 187f
Gate cannulation, for AAA
EVAR, 206, 206f
REVAR, 210
GDA. See Gastroduodenal artery
Graft tunneling
for aortofemoral open reconstruction, 227
for autogenous vein bypass, 283–284, 284f
for carotid–carotid bypass, 12, 12f–13f
Greater saphenous vein (GSV)
endoscopic harvest of, 281–283, 282f–283f, 282t
mapping of, 279, 279f–280f, 304, 304f
open vein harvest of, 280, 280f–281f
preparation of, 283, 283f, 305–307, 306f
tunneling to anterior tibialis artery, 308–309, 309f
Great vessel reconstruction. See Aortic arch reconstruction
GSV. See Greater saphenous vein
H
Hand fasciotomy, for arterial reconstruction distal to wrist
carpal tunnel release, 97
incision placement for, 96–97, 96f
wound care for, 97
Hematology
for TIPS, 321
Hematoma
with femoral–popliteal reconstruction, 277, 277f
Hemothorax
with vTOS decompression, 73
Heparin
in aortic arch debranching, 3
in arterial reconstruction, 75
for vTOS, 68, 73
Hepatic arteries
anastomosis of, in hepatorenal bypass, 187, 187f
exposure of, in hepatorenal bypass, 185, 186f–187f
in renal revascularization. See Hepatorenal bypass
Hepatic encephalopathy, TIPS and, 331
Hepatic vein
TIPS selection of, 323, 323f
Hepatorenal bypass
distal anastomosis in, 185–187, 186f–187f
duplex ultrasonography during, 187–188
final inspection of, 190
hepatic artery exposure in, 185, 186f
proximal anastomosis in, 187, 187f
renal artery exposure in, 185, 186f–187f
Hostile neck anatomy, CAS for, 34
Hypertension. See also Portal hypertension
Hypotension, with CAS, 32
I
ICA. See Internal carotid artery
Iliac aneurysm, 212
differential diagnosis of, 212
endovascular repair
with internal iliac artery occlusion, 213–215, 213f–215f
with internal iliac preservation, 216–219, 216f–219f
surgical management of, 212
Iliac arteries. See also Aortoiliac occlusive disease
dissection of
for femoral endarterectomy, 234, 234f
Iliac branch device (IBD), 218–219, 219f
Iliac veins
acute iliofemoral occlusion of, 313
Iliac venous thrombectomy, for acute iliofemoral deep vein thrombosis, 318
Iliofemoral arterial injury, with TEVAR, 117
Iliofemoral deep vein thrombosis. See Acute iliofemoral deep vein thrombosis
Iliofemoral occlusion, acute, 313
IMA. See Inferior mesenteric artery
Impotence, with aortoiliac occlusive disease, 221
IMV. See Inferior mesenteric vein
Incision
for portal hypertension surgery, 335
Infection
femoral graft. See Femoral graft infection
Infectious disease
TIPS and, 330–331, 330f
Inferior mesenteric artery (IMA)
in EVAR, 204
Inferior mesenteric vein (IMV)
to left renal vein shunt, 339, 339f
Inferior vena cava (IVC)
reconstruction of, for cancer management, 178–180, 179f–180f
Infrageniculate popliteal artery, exposure of
lateral, 251–253, 252f
medial, 250–251, 250f–251f, 253
posterior, 252
Infrainguinal femoral venous thrombectomy, for acute iliofemoral deep vein thrombosis, 319, 319f
Infrainguinal occlusive disease, 289, 289f
Infrainguinal outflow, from common femoral artery, 221
Inframalleolar posterior tibial artery, exposure of, 254, 255f
Infrarenal aortic aneurysm
imaging and diagnostic studies of, 193, 193f
patient history and physical findings of, 192–193
preoperative planning for, 194, 194t
outcomes with, 202
Innominate artery
bovine arch with, 24
position of, 24–25, 25f
Innominate vein, in aortic arch debranching, 3, 3f
Internal carotid artery (ICA), distal filter placement in, 24, 24f
Internal carotid artery exposure and control, 34
anterior approach to
exposure distal to bifurcation, 35–37, 36f–37f
outcomes with, 39
patient history and physical findings for, 34, 34f
retrojugular approach to
retrojugular dissection, 37
spinal accessory nerve identification, 37, 38f
superior laryngeal nerve identification, 37, 38f
Interposition graft
for axillary or brachial artery, 76
Intraabdominal oncological pathologies, 169, 169t
visceral reconstruction for
Intravascular ultrasound (IVUS), for acute iliofemoral deep vein thrombosis, 315
Isolated femoral reconstruction
clamping in, 224
landmarks for, 223
outcomes with, 226t
IVC. See Inferior vena cava
IVUS. See Intravascular ultrasound
J
JAA. See Juxtarenal aortic aneurysm
Juxtarenal aortic aneurysm (JAA)
EVAR for, 136
imaging and diagnostic studies of, 136–137, 136f–137f, 193, 193f
patient history and physical findings of, 136, 192–193
periscope EVAR/TEVAR for
preoperative planning for, 137, 194, 194t
snorkel/chimney EVAR for
arm access for, 138, 138f
completion of, 140, 140f
renal/visceral cannulation in, 138–139, 139f
stent graft deployment and balloon molding, 140, 140f
stent graft positioning for, 139–140, 139f
surgical management of
outcomes with, 202
K
Kissing stent technique, 237, 238f
L
LAP. See Laparotomy
Laparotomy (LAP)
thoraco-phreno-, for TAAA, 101, 101f
Latissimus dorsi muscle
in retroperitoneal aortic exposure, 125, 125f
Limb ischemia, 74–75
Liver biopsy
TIPS and, 322
Liver transplantation
TIPS and, 321
Lower extremity
bypass. See Autogenous vein bypass
venous anatomy and mapping of, 279, 279f–280f
Lower extremity disease patterns, 221t. See also Peripheral arterial disease
Lower extremity ischemia, femoral–popliteal reconstruction for, 258, 265
Low-molecular-weight heparin, for vTOS, 68, 73
Lung injury, with aTOS and vTOS decompression, 73
Lymphatic leakage, after lower extremity artery exposure, 256
M
Machine perfusion. See Renal machine perfusion
Magnetic resonance angiography (MRA)
for aortoiliac occlusive disease, 222, 231, 231f
for carotid angioplasty and stenting, 24–25, 25f, 30, 30f
for internal carotid artery exposure, 34
for tibial interventions, 290
for vertebrobasilar insufficiency, 41, 41f
Magnetic resonance arteriography (MRA), for femoral–popliteal reconstruction, 266, 267f
Magnetic resonance imaging (MRI)
for vascular tumors, 170
TIPS and, 322
Magnetic resonance phlebography, for acute iliofemoral deep vein thrombosis, 314
Magnetic resonance venography (MRV), for acute iliofemoral deep vein thrombosis, 314
May-Thurner syndrome. See Acute iliofemoral deep vein thrombosis
MDCT. See Multidetector computed tomography
MELD. See Model for End-Stage Liver Disease
Mesenteric arteries. See Acute mesenteric ischemia; See Chronic mesenteric ischemia; See Inferior mesenteric artery; See Superior
mesenteric artery
Mesenteric veins. See Superior mesenteric vein
Mesenteric vessels. See also Inferior mesenteric vein
Meso-Rex shunt, for portal hypertension surgery, 340–341, 341f
MI. See Myocardial infarction
Mid-distal axillary artery, reconstruction of, 79–80, 79f–81f
Model for End-Stage Liver Disease (MELD)
TIPS and, 322
MRA. See Magnetic resonance angiography; See Magnetic resonance arteriography
MRI. See Magnetic resonance imaging
MRV. See Magnetic resonance venography
Multidetector computed tomography (MDCT), for vascular tumors, 170
Myocardial infarction (MI), with CAS, 33
N
Nasotracheal intubation, for internal carotid artery exposure, 34–35
Nerve injury
after lower extremity artery exposure, 256
after neurogenic TOS decompression, 65
Neurogenic TOS (NTOS), 45–46, 45f, 59
diagnostic studies for, 46–48, 48f, 60
differential diagnosis of, 46, 46t, 59
imaging for, 46–48, 48f
patient history and physical findings for, 46, 47f, 59–60
pectoralis minor tenotomy for
incision and exposure for, 55, 56f
pectoralis minor muscle tendon division for, 55–56, 56f
surgical approach, 60
preoperative evaluation of, 60
supraclavicular decompression of
anterior scalenectomy for, 50–51, 51f
brachial plexus mobilization for, 51–52, 52f–53f
brachial plexus neurolysis for, 52–53, 55f
first rib resection for, 52, 53f–54f
middle scalenectomy for, 51–52, 52f–53f
outcomes with, 58
scalene fat pad incision and mobilization, 49–50, 49f–50f, 50t
transaxillary decompression of
closure, 64
exposure for, 61–63, 62f–63f
incision for, 61
outcomes of, 65
postoperative care, 65
rib resection for, 63, 64f
surgical anatomy, 60, 61f
NTOS. See Neurogenic TOS
O
Obturator bypass, for femoral graft infection, 242–243, 243f
Occlusive disease. See Aortoiliac occlusive disease
Open surgical bypass, for axillary or brachial arteries, 76
Open vein harvest
of arm vein, 281, 281f
of femoral vein, 281
of greater saphenous vein, 280, 280f–281f
of small saphenous vein, 280
P
PAD. See Peripheral arterial disease
Paget-Schroetter syndrome. See Venous TOS
Paracentesis, TIPS and, 322, 330
Paravisceral aortic aneurysms, hybrid revascularization strategies for, 128, 128f
complete visceral debranching and endovascular tube graft repair, 129–132, 130f–131f
outcomes with, 135
partial visceral debranching and physician-modified endovascular repair, 131f, 132–134, 134f–135f
surgical management for, 128
Partial visceral debranching and physician-modified endovascular repair
access site closure, 134
anticoagulation for, 133
exposure for, 132–133
fenestrated graft creation, 133–134, 134f
multivisceral bypass, 131f, 133
outcomes with, 135
percutaneous access, 134
stiff wire exchange, 134
target vessel cannulation, 134, 134f, 135f
target vessel marking and graft deployment, 134, 134f
Patch angioplasty, for isolated femoral reconstruction, 224, 225f
Peak systolic velocities (PSV), for femoral–popliteal reconstruction, 265, 266f
Pectoralis minor tenotomy, for NTOS
incision and exposure for, 55, 56f
pectoralis minor muscle tendon division for, 55–56, 56f
Pedal artery, exposure of, 255, 255f
Pedal vessels, exposure of, 254–255, 255f
Perfusion
renal machine. See Renal machine perfusion
Perimalleolar bypass, 302
to distal anterior tibialis artery
anterior tibialis artery exposure, 308, 308f
dorsalis pedis artery exposure for, 309, 309f
vein tunneling to anterior tibialis artery, 308–309, 309f
to distal posterior tibialis artery
autogenous vein preparation, 305–307, 306f
distal anastomosis creation for, 307–308, 307f–308f
inflow artery exposure, 305, 305f
posterior tibialis artery exposure, 305, 305f
peroneal artery exposure, 310, 310f–311f
Peripheral arterial disease (PAD), 221, 231, 247
autogenous vein bypass for, 279
evaluation of, 231, 231f
femoral vessel exposure for, 248–250, 248f–249f
infragenicular exposure for, 253–254, 253f
outcomes with, 257
popliteal artery exposure for, 250–252, 250f–252f
Periscope EVAR/TEVAR. See Endovascular aortic repair
Peroneal artery, exposure of, 253f, 254
for perimalleolar bypass, 310, 310f–311f
PFA. See Profunda femoris artery
Pharmacomechanical thrombectomy (PMT), for acute iliofemoral deep vein thrombosis, 316–317, 316f–317f
Phlebography, for acute iliofemoral deep vein thrombosis, 314–315
Physical therapy, for supraclavicular decompression of NTOS, 58–59
PMT. See Pharmacomechanical thrombectomy
Pneumothorax
with aTOS and vTOS decompression, 73
after neurogenic TOS decompression, 65
Popliteal artery
aneurysm of, autogenous vein bypass for, 279
exposure of
lateral, 251–253, 252f
medial, 250–251, 250f–251f, 253
posterior, 252
subintimal recanalization of, 258
catheter for, 262
outcomes with, 264
strategy for, 259
Portal hypertension
surgery for, 334
distal splenorenal shunt, 339–340, 340f
incision and retraction for, 335
inferior mesenteric vein to left renal vein shunt, 339, 339f
meso-Rex shunt, 340–341, 341f
operative decision making for, 335, 335f
other shunts for, 342, 342f
outcomes with, 343
pearls and pitfalls for, 342–343
proximal splenorenal shunt for, 337–338, 338f
splenectomy and esophagogastric devascularization, 335–336, 335f–337f
TIPS for, 321
Portal vein (PV)
TIPS and
access for, 324f–325f, 325–326
visualization of, 323–324, 324f–325f
Postdilatation, for CAS, 30, 30f
Posterior tibial artery, exposure of, 253f, 254, 305, 305f
inframalleolar, 254, 255f
Posterior tibialis artery, perimalleolar bypass to, 305, 305f
autogenous vein preparation, 305–307, 306f
distal anastomosis creation for, 307–308, 307f–308f
inflow artery exposure, 305, 305f
Postoperative bleeding. See Bleeding
Postrevascularization compartment syndrome, in arm or hand, 89
Predilatation, for CAS, 29, 29f
Profunda femoris artery (PFA)
dissection and control of, 248–249, 248f–249f
exposure of, 248f–249f, 250
for femoral graft infection, 244, 244f
Protamine, in aortic arch debranching, 4
Proximal axillary artery, reconstruction of, 76f–77f, 77–79
Proximal splenorenal shunt, for portal hypertension surgery, 337–338, 338f
PSV. See Peak systolic velocities
Pulse volume recordings (PVRs), for tibial interventions, 289, 290f
PV. See Portal vein
PVRs. See Pulse volume recordings
R
Radial artery, reconstruction of, 83f, 84–85, 85f
Radiography. See also Chest radiography
RAS. See Renal artery stenosis
Raynaud’s syndrome, 91
Reentry device, for femoral–popliteal reconstruction, 261
true lumen entry of, 261–262, 262f
Reflex sympathetic dystrophy, with NTOS, 46
Renal arteries. See also Paravisceral aortic aneurysms
arterial disease of, 156, 156t
renal revascularization for, 183
exposure of
in hepatorenal bypass, 185, 186f–187f
in splenic–renal bypass, 189, 189f
intervention for
angioplasty and stenting of, 159–161, 160f–161f
embolization of, 164–166, 165f–166f
outcomes with, 168
patient selection for, 157–158
in retroperitoneal aortic exposure, 125, 125f
Renal artery aneurysms (RAAs), 156
angioplasty and stenting for, 159–161, 160f–161f
Renal artery stenosis (RAS), 156
Renal cannulation, for EVAR, snorkel/chimney technique, 138–139, 139f
Renal machine perfusion
renal artery cannulation for
of multiple renal arteries 20f
Renal revascularization
hepatorenal bypass, 183
distal anastomosis in, 185–187, 186f–187f
duplex ultrasonography during, 187–188
hepatic artery exposure in, 185, 186f
proximal anastomosis in, 187, 187f
renal artery exposure in, 185, 186f–187f
splenic–renal bypass, 183
renal artery exposure for, 189, 189f
splenic artery exposure for, 188, 188f
Renovascular hypertension (RVH), 156
renal revascularization for, 183
Restenosis, with CAS, 33
Retrograde tibial interventions. See Tibial interventions
Retroperitoneal aortic exposure
for AAA repair, 194, 194f, 197–198, 197f–198f
for endovascular common iliac artery aneurysm repair, with internal iliac preservation, 216–217, 216f
instrumentation for, 123
technique for, 124–126, 125f–126f
REVAR. See Endovascular aneurysm repair for ruptured aneurysms
Rib
middle, for aTOS decompression, 68, 71–72, 71f–72f
in neurogenic TOS decompression
exposure of, 61–63, 62f–63f
resection of, 52, 53f–54f, 63, 64f
in vTOS decompression, 68, 70, 70f
Rutherford ischemia classification, 289
RVH. See Renovascular hypertension
S
SA. See Splenic artery
SAFARI. See SubintimAl Flossing with Antegrade-Retrograde Intervention
Saphenous vein. See also Greater saphenous vein; See also Small saphenous vein
Scalenectomy
anterior
for aTOS decompression, 68, 71, 71f
for supraclavicular NTOS decompression, 50–51, 51f
for vTOS decompression, 68, 70
middle
for aTOS decompression, 68, 71, 71f
for supraclavicular NTOS decompression, 51–52, 52f–53f
for vTOS decompression, 68, 70
Scalene fat pad, in supraclavicular decompression of NTOS, 49–50, 49f–50f, 50t
Scalenus anticus syndrome. See Thoracic outlet syndrome
Serologic tests, for arterial reconstruction proximal to wrist, 75
SFA. See Superficial femoral artery
SFV. See Superficial femoral vein
Shaggy aorta, 25
SMA. See Superior mesenteric artery
Small saphenous vein
mapping of, 279, 279f–280f
open vein harvest of, 280
SMV. See Superior mesenteric vein
Snorkel/chimney EVAR. See Endovascular aortic repair
Snuffbox radial arterial reconstruction, for arterial reconstruction distal to wrist
incision placement for, 95, 95f–96f
resection/bypass of diseased segment, 96, 96f
vein graft interposition, 96, 96f
Soleus origin, division of, 251f, 253
SPACE. See Stent-Supported Percutaneous Angioplasty of Carotid Artery versus Endarterectomy
Spinal cord ischemia, with TEVAR, 117
Splenectomy
for portal hypertension surgery, 335–336, 335f–337f
Splenic arteries
ligation of, for portal hypertension surgery, 335–336, 335f–337f
Splenic artery (SA)
exposure of, in splenic–renal bypass, 188, 188f
in renal revascularization. See Splenic–renal bypass
Splenic–renal bypass, 183
renal artery exposure for, 189, 189f
splenic artery exposure for, 188, 188f
Splenorenal shunt, portal hypertension surgery
distal for, 339–340, 340f
proximal for, 337–338, 338f
Stanford classification, 118, 119f
Stenosis, renal artery. See Renal artery stenosis
Stent graft. See also Thoracic stent graft
branched, for EVAR, 147t
for femoral–popliteal reconstruction, 275–276, 276f
fenestrated, for EVAR, 146, 146f, 147t
kinks and narrowing with, 155
in periscope EVAR/TEVAR, 141, 142f
size/shape of, 159
in snorkel/chimney EVAR, 139–140, 139f–140f
Stenting
of common iliac, 236–237, 238f
of external iliac, 234f, 238
of renal arteries, 159–161, 160f–161f
of venous compression syndrome, 317–318, 318f
of venous stenoses, 317–318, 318f
of visceral arteries, 162–163, 162f
Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial, 32
Stent placement
for CAS, 30, 30f
for femoral–popliteal reconstruction, 274–275, 275f
in upper extremity, 86–87, 87f
for TIPS, 325f, 327
Stent restenosis. See Restenosis
Stent-Supported Percutaneous Angioplasty of Carotid Artery versus Endarterectomy (SPACE), 32
Sternotomy incision
for aortic arch debranching, 2
Stroke
carotid endarterectomy for, 15
with CAS, 32
with TEVAR, 116–117
Subclavian artery
division of, for subclavian artery transposition, 10, 11f
exposure of, for carotid–subclavian bypass, 8, 8f
revascularization of, in TEVAR, 113, 113f
Subclavian artery transposition, 7
outcomes with, 14
positioning for, 7
technique for
carotid–subclavian anastomosis, 10, 11f
closure, 10
exposure, 10
subclavian artery division, 10, 11f
SubintimAl Flossing with Antegrade-Retrograde Intervention (SAFARI), 291. See also Tibial interventions
Subintimal recanalization, 258
of femoral and popliteal arteries
catheter for, 262
outcomes with, 264
strategy for, 259
Superficial femoral artery (SFA)
dissection and control of, 248–249, 248f–249f
guidewire placement in, 269
Superficial femoral vein (SFV), harvest of, for femoral graft infection, 244, 245f
Superior mesenteric artery (SMA)
aneurysms of, 156
in EVAR, 204
fenestrated graft creation for, 133–134, 134f
reconstruction of, for cancer management, 174–176, 175f
in retroperitoneal aortic exposure, 125–126, 125f–126f
Superior mesenteric vein (SMV)
reconstruction of, for cancer management, 176–178, 177f
Suprageniculate popliteal artery, exposure of
lateral, 251–252, 252f
medial, 250–251, 250f–251f
posterior, 252
Supramalleolar anterior tibial artery, exposure of, 255, 255f
T
TAAA. See Thoracoabdominal aortic aneurysm
TAAs. See Thoracic aortic aneurysms
TEE. See Transesophageal echocardiography
Temporomandibular subluxation, for internal carotid artery exposure, 35
Tenotomy, of pectoralis minor, for NTOS, 55–56, 56f
TEVAR. See Thoracic endovascular aortic repair
Thoracentesis, TIPS and, 322
Thoracic aortic aneurysms (TAAs)
TEVAR for
outcomes with, 116
Thoracic endovascular aortic repair (TEVAR), 107
with aortic arch repair, 1
aortogram
completion, 113
initial, 111–113, 112f
carotid–carotid bypass with, 7
outcomes with, 116
periscope technique for, 136
special considerations for
aortic dissection, 114, 114f
aortic transection, 114, 115f
Thoracic outlet
anatomy of, 45, 45f, 60, 61f
exposure of
closure, 64
for neurogenic TOS decompression, 61–63, 62f–63f
Thoracic outlet syndrome (TOS), 45, 45f, 59
arterial. See Arterial TOS
neurogenic. See Neurogenic TOS
venous. See Venous TOS
Thoracic stent graft, for TEVAR, selection and sizing of, 109–111, 110f–111f
Thoracoabdominal aortic aneurysm (TAAA), 99, 99f
diaphragm exposure for, 118
closure for, 122
outcomes with, 122
differential diagnosis for, 118, 118f
imaging and diagnostic studies for, 99–100, 99f–100f, 118–119
aortic repair for, 102–103, 102f–103f
closure, 104, 104f
distal aortic perfusion for, 102, 102f
postoperative care, 105
preoperative workup and patient optimization, 100
thoraco-phreno-laparotomy for, 101, 101f
Thoracoabdominal exposure, 124, 124f
Thoraco-phreno-laparotomy, for TAAA, 101, 101f
Thrombectomy. See Iliac venous thrombectomy; See Infrainguinal femoral venous thrombectomy; See Pharmacomechanical
thrombectomy
Thromboembolectomy, for axillary or brachial arteries, 75–76
Thrombolysis
catheter-directed, for acute iliofemoral deep vein thrombosis, 315–316
for vTOS, 68
Tibial artery, exposure of, 253–254, 253f
inframalleolar, 254, 255f
supramalleolar, 255, 255f
Tibial interventions, 289
antegrade
angiogram for, 292, 293f
angiogram post–balloon angioplasty, 295, 295f
balloon angioplasty for, 294–295, 294f–295f
completion angiogram and hemostasis, 295, 296f
occlusion crossing in, 292–293, 293f
tibial vessel reconstruction, 295, 296f
true lumen reentry, 293–294, 293f–294f
outcomes with, 301
retrograde, 291
antegrade-retrograde approach, 299, 300f
balloon angioplasty for, 299, 300f
recanalization of tibial occlusion, 297, 297f–298f
retrograde access for, 296–297, 297f
retrograde angiogram for, 297, 297f–298f
wire exteriorization, 298–299, 299f
surgical management of, 290–291, 291f
Tibialis artery
anterior. See Anterior tibialis artery
posterior. See Posterior tibialis artery
Tibioperoneal trunk, 253
Toe pressures, for femoral–popliteal reconstruction, 265
TOS. See Thoracic outlet syndrome
Trans-Atlantic Inter-Society Consensus (TASC) Classification, 222, 223f, 232, 233f
Transection, traumatic aortic. See Traumatic aortic transection
Transesophageal echocardiography (TEE), for TEVAR, 108
Transjugular intrahepatic portosystemic shunt (TIPS), 321
adjunct procedures for, 327
complications with, 330–331, 330f–331f
difficult, 327–328, 327f–328f
dysfunction of, 331, 332f
follow-up for, 331–332, 332t
hepatic vein selection for, 323, 323f
patient selection, history, and physical findings for, 321, 321t
for portal hypertension, 334
portal vein access for, 324f–325f, 325–326
portal venous system visualization for, 323–324, 324f–325f
stent placement for, 325f, 327
stent selection for, 325f, 326–327
tract dilation for, 325f, 326
venous access for, 322
Transperitoneal approach, to AAA repair, 194–195, 194f–196f
Transplantation
of liver. See Liver transplantation
Traumatic aortic transection
TEVAR for
outcomes with, 116
special considerations for, 114, 115f
Trellis infusion system, 317, 317f
True lumen reentry
in antegrade tibial interventions, 293–294, 293f–294f
in percutaneous femoral–popliteal reconstruction, 261–262, 262f
U
Ulnar artery reconstruction, 83f, 85f, 86
for arterial reconstruction distal to wrist
incision placement, 94, 94f
resection for, 94–95, 94f–95f
vein graft interposition for, 94f–95f, 95
Ultrasound (US)
for AAA, 204
of AAA, 193
duplex. See Duplex ultrasound
EUS. See Endoscopic ultrasonography
intravascular, 315
for TIPS, 329, 331–332, 332t
ULTT. See Upper limb tension test
Upper extremity
angiography and stenting of, 86–87, 87f
arterial reconstruction and revascularization of. See Arterial reconstruction
venous anatomy and mapping of, 279, 280f
Upper extremity arterial insufficiency, 74
Upper extremity ischemia, 74
Upper limb tension test (ULTT), for neurogenic TOS, 46, 47f, 59
US. See Ultrasound
V
Vascular injury, after neurogenic TOS decompression, 65
Vascular tumors, 169, 169t
visceral reconstruction for
Venous compression syndrome, stenting of, 317–318, 318f
Venous occlusive disorders, 74
Venous oncologic pathologies, 169t
Venous reconstruction, for vTOS decompression, 70, 70f
Venous stenoses, stenting of, 317–318, 318f
Venous TOS (vTOS), 66, 66f
decompression for
closure for, 70
infraclavicular approach to, 69–70, 69f
outcomes with, 73
positioning for, 69
venous reconstruction for, 70, 70f
neurogenic TOS compared with, 46, 59
Vertebral transposition, 40
to common carotid, 41–42, 42f
complications with, 43–44, 44f
differential diagnosis for, 40, 40t
outcomes of, 43
Vertebrobasilar insufficiency, 40
differential diagnosis for, 40, 40t
complications with, 43–44, 44f
outcomes of, 43
vertebral artery angioplasty and stent placement, 43
vertebral transposition to common carotid, 41–42, 42f
Vessel injury, after lower extremity artery exposure, 256
Visceral aorta, in retroperitoneal aortic exposure, 125, 125f–126f
Visceral arteries. See also Paravisceral aortic aneurysms
arterial disease of, 156, 156t
intervention for
embolization of, 164–166, 165f–166f
outcomes with, 168
patient selection for, 157–158
Visceral artery aneurysms, 156
Visceral cannulation, for EVAR
periscope technique, 141, 141f–142f
snorkel/chimney technique, 138–139, 139f
Visceral debranching
complete. See Complete visceral debranching and endovascular tube graft repair
partial. See Partial visceral debranching and physician-modified endovascular repair
Visceral reconstruction
of aorta, 171–173, 172f–174f
for cancer management, 169
of IVC, 178–180, 179f–180f
of SMA, 174–176, 175f
of SMV, 176–178, 177f
vTOS. See Venous TOS
W
Wright/Salm classification, 169
Wrist
arterial reconstruction distal to, 91
hand fasciotomy, 96–97, 96f
snuffbox, 95–96, 95f–96f
ulnar artery, 94–95, 94f–95f
arterial reconstruction proximal to, 74, 74t
brachial artery, 81–84, 82f–83f
mid-distal axillary artery, 79–80, 79f–81f
operating room setup for, 76, 76f–77f
outcomes with, 89
proximal axillary artery, 76f–77f, 77–79
radial artery, 83f, 84–85, 85f
ulnar artery, 83f, 85f, 86
X
X-ray. See Chest radiography

Operative Techniques in Vascular Surgery

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Operative Techniques in Vascular Surgery

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Acquisitions Editor: Keith Donnellan

Product Development Editor: Brendan Huffman

Copyright © 2015 Wolters Kluwer Health

Library of Congress Cataloging-in-Publication Data

Ramin E. Beygui, MD, FACS

Julie Ann Freischlag, MD

Sung Wan Ham, MD

E. John Harris, Jr., MD

Alexander Kulik, MD, MPH, FRCSC

Peter H. U. Lee, MD, MPH

W. Anthony Lee, MD, FACS

Joseph L. Mills, Sr., MD

Mark D. Morasch, MD, FACS

Benjamin W. Starnes, MD, FACS

Fred Weaver, MD, MMM

Mohamed A. Zayed, MD, PhD, RPVI

Luke X. Zhan, MD, PhD

Section I Cerebrovascular Arterial Surgery/Intervention

1 Arch and Great Vessel Reconstruction with Debranching Techniques

Section II Management of the Thoracic Outlet

Section III Upper Extremity Reconstruction/Revascularization

Section IV Thoracic Aorta Distal to the Pericardium

Section V Hybrid, Open and Endovascular Approaches to the

15 Retroperitoneal Aortic Exposure

19 Stenting, Endografting, and Embolization Techniques: Celiac, Mesenteric,

Section VII The Abdominal Aorta and Iliac Arterial System

Section VIII Infrainguinal Arterial Disease Management/Limb

27 Management of the Infected Femoral Graft

Section IX Surgical Management of Venous Disease

W. Anthony Lee Alexander Kulik

PATIENT HISTORY AND PHYSICAL FINDINGS

IMAGING AND OTHER DIAGNOSTIC STUDIES

AORTIC ARCH DEBRANCHING

ENDOVASCULAR SECOND STAGE

PEARLS AND PITFALLS

Edward Y. Woo Scott M. Damrauer

PATIENT HISTORY AND PHYSICAL FINDINGS

IMAGING AND OTHER DIAGNOSTIC STUDIES

Exposure of Carotid Artery

SUBCLAVIAN ARTERY TRANSPOSITION

PEARLS AND PITFALLS

Vinit N. Varu Wei Zhou

PATIENT HISTORY AND PHYSICAL FINDINGS

IMAGING AND OTHER DIAGNOSTIC STUDIES

CAROTID ENDARTERECTOMY—PATCH ANGIOPLASTY

Carotid Exposure and Control

CAROTID ARTERY INTERPOSITION BYPASS

CAROTID ARTERY LIGATION (CAROTID STUMP SYNDROME)

PEARLS AND PITFALLS

Zhen S. Huang Darren B. Schneider

IMAGING AND OTHER DIAGNOSTIC STUDIES

PERCUTANEOUS RETROGRADE FEMORAL ARTERY ACCESS

SELECTIVE COMMON CAROTID CATHETERIZATION

PLACEMENT OF GUIDING SHEATH

CROSSING THE LESION WITH DISTAL EMBOLIC PROTECTION

STENTING AND POSTDILATATION

PEARLS AND PITFALLS

PATIENT HISTORY AND PHYSICAL FINDINGS

IMAGING AND OTHER DIAGNOSTIC STUDIES

ANTERIOR APPROACH TO THE DISTAL INTERNAL CAROTID ARTERY

RETROJUGULAR APPROACH TO THE DISTAL INTERNAL CAROTID

Identification of the Superior Laryngeal Nerve

PEARLS AND PITFALLS

PATIENT HISTORY AND PHYSICAL FINDINGS