Diagnostic Imaging Genitourinary 4th

Edition Ganeh Fananapazir

Visit to download the full and correct content document:
https://ebookmass.com/product/diagnostic-imaging-genitourinary-4th-edition-ganeh-fa
nanapazir/
More products digital (pdf, epub, mobi) instant
download maybe you interests ...

Diagnostic Imaging Gastrointestinal 4th Edition Atif

Zaheer

https://ebookmass.com/product/diagnostic-imaging-
gastrointestinal-4th-edition-atif-zaheer/

Diagnostic Imaging: Brain 4th Edition Miral D. Jhaveri

https://ebookmass.com/product/diagnostic-imaging-brain-4th-
edition-miral-d-jhaveri/

Diagnostic Imaging: Obstetrics 4th Edition Paula J.

Woodward Md

https://ebookmass.com/product/diagnostic-imaging-obstetrics-4th-
edition-paula-j-woodward-md/

Diagnostic Imaging: Pediatrics 4th Edition A. Carlson

Merrow Jr.

https://ebookmass.com/product/diagnostic-imaging-pediatrics-4th-
edition-a-carlson-merrow-jr/
Diagnostic Imaging: Head and Neck 4th Edition
Bernadette L. Koch Md

https://ebookmass.com/product/diagnostic-imaging-head-and-
neck-4th-edition-bernadette-l-koch-md/

Primer of diagnostic imaging Sixth Edition Chen

https://ebookmass.com/product/primer-of-diagnostic-imaging-sixth-
edition-chen/

Diagnostic Imaging: Spine 4th Edition Jeffrey S. Ross

Md And Kevin R. Moore Md Author

https://ebookmass.com/product/diagnostic-imaging-spine-4th-
edition-jeffrey-s-ross-md-and-kevin-r-moore-md-author/

Diagnostic Imaging: Gynecology 3rd Edition Akram M.

Shaaban

https://ebookmass.com/product/diagnostic-imaging-gynecology-3rd-
edition-akram-m-shaaban/

Diagnostic Imaging Oncology 2nd Edition Akram M.

Shaaban

https://ebookmass.com/product/diagnostic-imaging-oncology-2nd-
edition-akram-m-shaaban/
 FOURTH EDITION

Foster
Diagnostic
Genito
• •I
I?Fananabazir

ELSEVIER
FOURTH EDITION
 ■

и
 Diagnostic Imaging

Genitourinary
FOURTH EDITION

Ghaneh Fananapazir, MD
Professor
Department of Radiology
Mayo Clinic
Phoenix, Arizona

Bryan R. Foster, MD
Associate Professor
Department of Radiology
Oregon Health & Science University
Portland, Oregon

iii
 Elsevier
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899

DIAGNOSTIC IMAGING: GENITOURINARY, FOURTH EDITION ISBN: 978-0-323-79605-7

Inkling: 978-0-323-79607-1
Copyright © 2022 by Elsevier. All rights reserved.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical,
including photocopying, recording, or any information storage and retrieval system, without permission in writing from
the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our
arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be
found at our website: www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as
may be noted herein).

Notices

Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds or experiments described herein.
Because of rapid advances in the medical sciences, in particular, independent verification of
diagnoses and drug dosages should be made. To the fullest extent of the law, no responsibility is
assumed by Elsevier, authors, editors or contributors for any injury and/or damage to persons or
property as a matter of products liability, negligence or otherwise, or from any use or operation of
any methods, products, instructions, or ideas contained in the material herein.

Previous edition copyrighted 2016.

Library of Congress Control Number: 2021945935

Printed in Canada by Friesens, Altona, Manitoba, Canada

Last digit is the print number: 9 8765 4321

iv
 Dedications
To the rocks in my life: My wife, Melody, and children, Sameh and Nura, whose
love makes all things possible, as well as my parents and brother, Nafeh, for their
constant support and encouragement.
GF

To my wife, Sarah: Your support and love makes everything I do possible.

To my boys, Nolan and Bennett: You make it all worth it!
BRF
 Contributing Authors
Alice Fung, MD
Professor of Radiology
Department of Diagnostic Radiology
Oregon Health & Science University
Portland, Oregon

Zachary B. Jenner, MD
Resident Physician
Diagnostic & Interventional Radiology
University of California, Davis Medical Center
Sacramento, California

Kyle K. Jensen, MD
Assistant Professor
Department of Diagnostic Radiology
Oregon Health & Science University
Portland, Oregon

Kevin Kalisz, MD
Assistant Professor of Radiology
Duke University Hospital
Durham, North Carolina

Lori Mankowski Gettle, MD, MBA, FSRU

Assistant Professor of Radiology
Chief of Ultrasound
University of Wisconsin School of Medicine and Public Health
Madison, Wisconsin

Mark D. Sugi, MD
Assistant Professor of Radiology
Department of Radiology & Biomedical Imaging
University of California, San Francisco
San Francisco, California

Kanupriya Vijay, MD
Associate Professor of Radiology
UT Southwestern Medical Center
Dallas, Texas

Benjamin Wildman-Tobriner, MD
Assistant Professor of Radiology
Duke University Hospital
Durham, North Carolina

vi
Additional Contributing Authors
Shweta Bhatt, MD
Amir A. Borhani, MD
Michael P. Federle, MD, FACR
Alessandro Furlan, MD
Matthew T. Heller, MD, FSAR
R. Brooke Jeffrey, MD
Katherine E. Maturen, MD, MS
Jeffrey Dee Olpin, MD
Douglas Rogers, MD
Akram M. Shaaban, MBBCh
Ashraf Thabet, MD
Mitchell Tublin, MD
T. Gregory Walker, MD, FSIR
Paula J. Woodward, MD

vii
 Preface
Genitourinary imaging—with its focus on the adrenal glands, kidneys,
ureters, bladder, male genitourinary structures, and retroperitoneum—has
served as a core part of the scope of abdominal imagers, which also includes
gastrointestinal and gynecologic imaging. The breadth of anatomy, physiology,
and pathology that is incorporated within genitourinary imaging is vast, and
the increasing standardization of medicine with the ever-changing pathology
classification systems, radiology structured reporting schemes, staging
systems, and treatment options, as well as new and expanded use of imaging
tools, require the radiologist interpreting such images to be constantly learning
and updating their knowledge base.

With such a task in mind, we have built upon previous editions of this book by
recruiting a highly knowledgeable and respected author team of genitourinary
expert radiologists from multiple institutions that bring with them a wealth
of knowledge and experience. Image updates reflect the most contemporary
imaging techniques and also highlight new imaging technology, such as contrast-
enhanced ultrasound and dual-energy CT. We are pleased to present many new
chapters and sections that we feel make this edition more comprehensive. We
have added new chapters on IgG4 disease and transgender imaging, as well
as a new section on kidney transplantation that covers the imaging of normal
and pathologic states unique to kidney grafts, which a radiologist will likely
encounter. Updated classification systems are incorporated into this edition,
such as the Bosniak 2019 update, as well as the AJCC 8th edition tumor staging
systems for genitourinary cancers. We have heavily updated the prostate
section and incorporated many pages of new content on PI-RADS, as well as
many practical tips to approaching prostate MR, which we feel will be helpful,
regardless of whether you are just beginning or have interpretation experience.

As you may be accustomed to in the Diagnostic Imaging series, this book

serves as a rapid, easy-to-reference source in the typical bulleted format,
rich with illustrations, radiologic and pathologic images, and tables. This new
edition incorporates several hundred new radiologic images carefully selected
to show classic and nonclassic examples of both common and uncommon
manifestations of genitourinary disease, with hundreds more images available
in the electronic content.

Ghaneh Fananapazir, MD Bryan R. Foster, MD

Professor Associate Professor
Department of Radiology Department of Radiology
Mayo Clinic Oregon Health & Science University
Phoenix, Arizona Portland, Oregon

viii
Acknowledgments
LEAD EDITOR
Arthur G. Gelsinger, MA

LEAD ILLUSTRATOR
Laura C. Wissler, MA

TEXT EDITORS
Rebecca L. Bluth, BA
Nina Themann, BA
Terry W. Ferrell, MS
Megg Morin, BA
Kathryn Watkins, BA

IMAGE EDITORS
Jeffrey J. Marmorstone, BS
Lisa A. M. Steadman, BS

ILLUSTRATIONS
Richard Coombs, MS
Lane R. Bennion, MS

ART DIRECTION AND DESIGN

Tom M. Olson, BA

PRODUCTION EDITORS
Emily C. Fassett, BA
John Pecorelli, BS

ELSEVIER

xi
 Sections
SECTION 1:
Overview and Introduction
SECTION 2:
Retroperitoneum
SECTION 3:
Adrenal
SECTION 4:
Kidney and Renal Pelvis
SECTION 5:
Ureter
SECTION 6:
Bladder
SECTION 7:
Urethra/Penis
SECTION 8:
Testes
SECTION 9:
Epididymis
SECTION 10:
Scrotum
SECTION 11:
Seminal Vesicles
SECTION 12:
Prostate
SECTION 13:
Procedures

xiii
 TABLE OF CONTENTS

SECTION 1: OVERVIEW AND INFECTION

INTRODUCTION 56 Adrenal Tuberculosis and Fungal Infection
4 Imaging Approaches Mitchell Tublin, MD and Michael P. Federle, MD, FACR
Bryan R. Foster, MD and Ghaneh Fananapazir, MD
METABOLIC OR INHERITED
SECTION 2: RETROPERITONEUM 58 Adrenal Hyperplasia
12 Introduction to Retroperitoneum Ghaneh Fananapazir, MD
Bryan R. Foster, MD and Matthew T. Heller, MD, FSAR 60 Adrenal Insufficiency
Mitchell Tublin, MD and Michael P. Federle, MD, FACR
CONGENITAL
TRAUMA
16 Duplications and Anomalies of IVC
Bryan R. Foster, MD and Matthew T. Heller, MD, FSAR 62 Adrenal Hemorrhage
Ghaneh Fananapazir, MD, Mitchell Tublin, MD, and
INFLAMMATION Michael P. Federle, MD, FACR
20 Retroperitoneal Fibrosis
BENIGN NEOPLASMS
Alice Fung, MD and Matthew T. Heller, MD, FSAR
66 Adrenal Cyst
DEGENERATIVE Mitchell Tublin, MD
24 Pelvic Lipomatosis 70 Adrenal Adenoma
Bryan R. Foster, MD and Matthew T. Heller, MD, FSAR Mitchell Tublin, MD and Mark D. Sugi, MD
76 Adrenal Myelolipoma
TREATMENT RELATED Mitchell Tublin, MD and Michael P. Federle, MD, FACR
80 Pheochromocytoma
26 Retroperitoneal Hemorrhage
Mitchell Tublin, MD and Mark D. Sugi, MD
Alice Fung, MD and Matthew T. Heller, MD, FSAR
30 Postoperative Lymphocele MALIGNANT NEOPLASMS
Alice Fung, MD and Matthew T. Heller, MD, FSAR
86 Adrenal Cortical Carcinoma
BENIGN NEOPLASMS Mitchell Tublin, MD, Ghaneh Fananapazir, MD, and
Michael P. Federle, MD, FACR
32 Retroperitoneal Neurogenic Tumor
90 Adrenal Cortical Carcinoma Staging
Bryan R. Foster, MD and Matthew T. Heller, MD, FSAR
Akram M. Shaaban, MBBCh
MALIGNANT NEOPLASMS 102 Adrenal Lymphoma
Mitchell Tublin, MD and Mark D. Sugi, MD
36 Retroperitoneal Sarcoma 104 Adrenal Metastases
Alice Fung, MD Mitchell Tublin, MD and Mark D. Sugi, MD
40 Retroperitoneal and Mesenteric Lymphoma 108 Adrenal Collision Tumor
Alice Fung, MD and Matthew T. Heller, MD, FSAR Mitchell Tublin, MD and Mark D. Sugi, MD
44 Retroperitoneal Metastases
Bryan R. Foster, MD and Matthew T. Heller, MD, FSAR SECTION 4: KIDNEY AND RENAL PELVIS
48 Solitary Fibrous Tumor
112 Introduction to Renal Physiology and Contrast
Bryan R. Foster, MD
Alessandro Furlan, MD and Ghaneh Fananapazir, MD
SECTION 3: ADRENAL 114 Introduction to Kidney and Renal Pelvis
Alessandro Furlan, MD
52 Introduction to Adrenals
Mitchell Tublin, MD, Ghaneh Fananapazir, MD, and NORMAL VARIANTS AND PSEUDOLESIONS
Michael P. Federle, MD, FACR
120 Renal Fetal Lobation
Amir A. Borhani, MD and Michael P. Federle, MD, FACR

xiv
 TABLE OF CONTENTS
122 Junctional Cortical Defect 186 Localized Cystic Renal Disease
Amir A. Borhani, MD Alessandro Furlan, MD and Michael P. Federle, MD, FACR
124 Column of Bertin
Amir A. Borhani, MD and Michael P. Federle, MD, FACR BENIGN NEOPLASMS
188 Renal Angiomyolipoma
CONGENITAL Lori Mankowski Gettle, MD, MBA, FSRU and Matthew T.
126 Horseshoe Kidney Heller, MD, FSAR
Alessandro Furlan, MD, Mark D. Sugi, MD, and Michael P. 194 Renal Oncocytoma
Federle, MD, FACR Lori Mankowski Gettle, MD, MBA, FSRU and Matthew T.
130 Renal Ectopia and Agenesis Heller, MD, FSAR
Alessandro Furlan, MD, Michael P. Federle, MD, FACR, 198 Metanephric Adenoma
and Mark D. Sugi, MD Lori Mankowski Gettle, MD, MBA, FSRU, Ghaneh
134 Ureteropelvic Junction Obstruction Fananapazir, MD, and Matthew T. Heller, MD, FSAR
Alessandro Furlan, MD and Michael P. Federle, MD, FACR 200 Mixed Epithelial and Stromal Tumor Family
138 Congenital Megacalyces and Megaureter Ghaneh Fananapazir, MD and Matthew T. Heller, MD,
Alessandro Furlan, MD and Ghaneh Fananapazir, MD FSAR
140 Renal Lymphangiomatosis
Alessandro Furlan, MD and Ghaneh Fananapazir, MD INFLAMMATION
202 IgG4 Renal Disease
INFECTION
Kevin Kalisz, MD and Benjamin Wildman-Tobriner, MD
142 Acute Pyelonephritis 206 Histiocytic Diseases
Ghaneh Fananapazir, MD and Alessandro Furlan, MD Bryan R. Foster, MD
146 Chronic Pyelonephritis/Reflux Nephropathy
Alessandro Furlan, MD and Amir A. Borhani, MD MALIGNANT NEOPLASMS
148 Xanthogranulomatous Pyelonephritis 208 Renal Cell Carcinoma
Lori Mankowski Gettle, MD, MBA, FSRU, Alessandro Matthew T. Heller, MD, FSAR
Furlan, MD, and R. Brooke Jeffrey, MD 214 Renal Cell Carcinoma Staging
152 Emphysematous Pyelonephritis Lori Mankowski Gettle, MD, MBA, FSRU and Douglas
Lori Mankowski Gettle, MD, MBA, FSRU, Alessandro Rogers, MD
Furlan, MD, and R. Brooke Jeffrey, MD 234 Medullary Carcinoma
154 Renal Abscess Kevin Kalisz, MD
Lori Mankowski Gettle, MD, MBA, FSRU, Alessandro 236 Collecting Duct Carcinoma
Furlan, MD, and R. Brooke Jeffrey, MD Kevin Kalisz, MD
158 Pyonephrosis 238 Urothelial Carcinoma
Lori Mankowski Gettle, MD, MBA, FSRU and Alessandro Lori Mankowski Gettle, MD, MBA, FSRU and Matthew T.
Furlan, MD Heller, MD, FSAR
160 Opportunistic Renal Infections 242 Renal Pelvis and Ureter Carcinoma Staging
Alessandro Furlan, MD and Amir A. Borhani, MD Akram M. Shaaban, MBBCh
260 Renal Lymphoma
RENAL CYSTIC DISEASE Lori Mankowski Gettle, MD, MBA, FSRU and Matthew T.
162 Renal Cyst Heller, MD, FSAR
Kanupriya Vijay, MD and Alessandro Furlan, MD 262 Renal Metastases
166 Parapelvic (Peripelvic) Cyst Matthew T. Heller, MD, FSAR
Kanupriya Vijay, MD and Alessandro Furlan, MD
168 Bosniak Classification of Cystic Masses METABOLIC
Benjamin Wildman-Tobriner, MD and Kevin Kalisz, MD 264 Nephrocalcinosis
172 Autosomal Dominant Polycystic Kidney Disease Kevin Kalisz, MD
Bryan R. Foster, MD and Alessandro Furlan, MD 268 Urolithiasis
176 Acquired Cystic Kidney Disease Matthew T. Heller, MD, FSAR
Ghaneh Fananapazir, MD and Alessandro Furlan, MD 272 Paroxysmal Nocturnal Hemoglobinuria
178 von Hippel-Lindau Disease Matthew T. Heller, MD, FSAR
Alessandro Furlan, MD and Mark D. Sugi, MD
182 Medullary Cystic Diseases RENAL FAILURE AND MEDICAL RENAL
Ghaneh Fananapazir, MD and Michael P. Federle, MD, DISEASE
FACR
274 Hydronephrosis
184 Lithium Nephropathy
Lori Mankowski Gettle, MD, MBA, FSRU and Alessandro
Lori Mankowski Gettle, MD, MBA, FSRU, Alessandro
Furlan, MD
Furlan, MD, and Amir A. Borhani, MD

xv
 TABLE OF CONTENTS
276 Glomerulonephritis
TREATMENT RELATED
Ghaneh Fananapazir, MD and Michael P. Federle, MD,
FACR 344 Postoperative State, Kidney
278 Acute Tubular Injury Benjamin Wildman-Tobriner, MD
Alessandro Furlan, MD 348 Radiation Nephropathy
280 Renal Cortical Necrosis Benjamin Wildman-Tobriner, MD
Benjamin Wildman-Tobriner, MD 350 Contrast-Induced Nephropathy
282 Renal Papillary Necrosis Kevin Kalisz, MD, Benjamin Wildman-Tobriner, MD, and
Kevin Kalisz, MD Amir A. Borhani, MD
284 HIV Nephropathy
Alessandro Furlan, MD and Ghaneh Fananapazir, MD SECTION 5: URETER
286 Chronic Renal Failure 356 Introduction to Ureter
Alessandro Furlan, MD Bryan R. Foster, MD
288 Renal Lipomatosis
Alessandro Furlan, MD, Amir A. Borhani, MD, and Ghaneh CONGENITAL
Fananapazir, MD
358 Duplicated and Ectopic Ureter
Bryan R. Foster, MD and Amir A. Borhani, MD
VASCULAR DISORDERS
362 Ureterocele
290 Renal Artery Stenosis Bryan R. Foster, MD and Amir A. Borhani, MD
Amir A. Borhani, MD and Kanupriya Vijay, MD
294 Renal Infarction INFLAMMATION
Kanupriya Vijay, MD and Amir A. Borhani, MD
366 Ureteritis Cystica
300 Renal Vein Thrombosis
Bryan R. Foster, MD and Amir A. Borhani, MD
Kanupriya Vijay, MD and Amir A. Borhani, MD
368 Ureteral Stricture
304 Renal Vasculitis
Bryan R. Foster, MD and Amir A. Borhani, MD
Bryan R. Foster, MD
TRAUMA
TRAUMA
370 Ureteral Trauma
306 Renal Trauma
Bryan R. Foster, MD and Matthew T. Heller, MD, FSAR
Matthew T. Heller, MD, FSAR and Ghaneh Fananapazir,
MD NEOPLASMS
310 Urinoma
374 Fibroepithelial Polyp
Matthew T. Heller, MD, FSAR
Bryan R. Foster, MD and Amir A. Borhani, MD
TRANSPLANTATION 376 Ureteral Urothelial Carcinoma
Bryan R. Foster, MD and Amir A. Borhani, MD
312 Kidney Transplant Normal Anatomy
Ghaneh Fananapazir, MD MISCELLANEOUS
316 Vascular Thrombosis in Kidney Transplants
380 Ureterectasis of Pregnancy
Ghaneh Fananapazir, MD
Kyle K. Jensen, MD and Amir A. Borhani, MD
320 Transplant Renal Artery Stenosis
Ghaneh Fananapazir, MD
SECTION 6: BLADDER
324 Arteriovenous Fistulas Involving Kidney Transplants
Ghaneh Fananapazir, MD 384 Introduction to Bladder
326 Pseudoaneurysms Involving Kidney Transplants Kyle K. Jensen, MD, Amir A. Borhani, MD, and Paula J.
Ghaneh Fananapazir, MD Woodward, MD
328 Urinary Obstruction Involving Kidney Transplants
Ghaneh Fananapazir, MD CONGENITAL
330 Perinephric Fluid Collections Involving Kidney 388 Urachal Anomalies
Transplants Kyle K. Jensen, MD and Amir A. Borhani, MD
Ghaneh Fananapazir, MD
334 Posttransplant Lymphoproliferative Disease INFECTION
Involving Kidney Transplants 392 Cystitis
Ghaneh Fananapazir, MD Kyle K. Jensen, MD and Amir A. Borhani, MD
338 Acute Tubular Necrosis in Kidney Transplants 394 Bladder Schistosomiasis
Ghaneh Fananapazir, MD Bryan R. Foster, MD and Amir A. Borhani, MD
340 Rejection in Kidney Transplants 396 Malakoplakia
Ghaneh Fananapazir, MD Bryan R. Foster, MD and Amir A. Borhani, MD

xvi
 TABLE OF CONTENTS
474 Gender-Affirming Surgery: Female to Male
DEGENERATIVE
Kyle K. Jensen, MD
398 Bladder Calculi 478 Gender-Affirming Surgery: Male to Female
Bryan R. Foster, MD and Amir A. Borhani, MD Kyle K. Jensen, MD
400 Bladder Diverticulum
Bryan R. Foster, MD and Amir A. Borhani, MD SECTION 8: TESTES
404 Fistulas of Genitourinary Tract
Bryan R. Foster, MD and Amir A. Borhani, MD NONNEOPLASTIC CONDITIONS
408 Neurogenic Bladder 486 Approach to Scrotal Sonography
Bryan R. Foster, MD and Amir A. Borhani, MD Bryan R. Foster, MD
488 Cryptorchidism
TRAUMA Bryan R. Foster, MD and Paula J. Woodward, MD
410 Bladder Trauma 490 Testicular Torsion
Kyle K. Jensen, MD and Matthew T. Heller, MD, FSAR Bryan R. Foster, MD and Shweta Bhatt, MD
494 Segmental Infarction
TREATMENT RELATED Bryan R. Foster, MD and Mitchell Tublin, MD
414 Postoperative State, Bladder 496 Tubular Ectasia
Benjamin Wildman-Tobriner, MD and Amir A. Borhani, Alice Fung, MD and Mitchell Tublin, MD
MD 498 Testicular Microlithiasis
Alice Fung, MD and Mitchell Tublin, MD
BENIGN NEOPLASMS
NEOPLASMS
418 Inflammatory Myofibroblastic Tumor
Bryan R. Foster, MD and Amir A. Borhani, MD 500 Germ Cell Tumors
420 Bladder and Ureteral Intramural Masses Kyle K. Jensen, MD and Mitchell Tublin, MD
Bryan R. Foster, MD and Amir A. Borhani, MD 504 Testicular Carcinoma Staging
Akram M. Shaaban, MBBCh
MALIGNANT NEOPLASMS 520 Stromal Tumors
Kyle K. Jensen, MD and Shweta Bhatt, MD
424 Urinary Bladder Carcinoma Staging
524 Testicular Lymphoma and Leukemia
Akram M. Shaaban, MBBCh
Shweta Bhatt, MD and Kyle K. Jensen, MD
438 Squamous Cell Carcinoma
526 Epidermoid Cyst
Bryan R. Foster, MD and Amir A. Borhani, MD
Kyle K. Jensen, MD and Mitchell Tublin, MD
440 Adenocarcinoma
Bryan R. Foster, MD and Amir A. Borhani, MD SECTION 9: EPIDIDYMIS
SECTION 7: URETHRA/PENIS 530 Epididymitis
Bryan R. Foster, MD and Mitchell Tublin, MD
444 Introduction to Urethra
534 Adenomatoid Tumor
Bryan R. Foster, MD and Paula J. Woodward, MD
Bryan R. Foster, MD and Katherine E. Maturen, MD, MS
NEOPLASMS 536 Spermatocele/Epididymal Cyst
Alice Fung, MD and Katherine E. Maturen, MD, MS
446 Urethral Carcinoma Staging 538 Sperm Granuloma
Akram M. Shaaban, MBBCh Alice Fung, MD and Mitchell Tublin, MD

INFECTION SECTION 10: SCROTUM

460 Urethral Stricture 542 Hydrocele
Bryan R. Foster, MD and Matthew T. Heller, MD, FSAR Bryan R. Foster, MD
462 Urethral Diverticulum 544 Varicocele
Alice Fung, MD and Matthew T. Heller, MD, FSAR Bryan R. Foster, MD and Mitchell Tublin, MD
546 Pyocele
TRAUMA
Bryan R. Foster, MD and R. Brooke Jeffrey, MD
466 Urethral Trauma 548 Inguinal Hernia
Bryan R. Foster, MD Bryan R. Foster, MD
468 Erectile Dysfunction 554 Fournier Gangrene
Matthew T. Heller, MD, FSAR Bryan R. Foster, MD and Mitchell Tublin, MD
556 Fibrous Pseudotumor of Scrotum
TREATMENT RELATED Bryan R. Foster, MD and Paula J. Woodward, MD
470 Penile and Urethral Implants 558 Scrotal Trauma
Bryan R. Foster, MD Bryan R. Foster, MD and Mitchell Tublin, MD

xvii
 TABLE OF CONTENTS
SECTION 11: SEMINAL VESICLES
564 Congenital Seminal Vesicle Lesions
Bryan R. Foster, MD and Amir A. Borhani, MD
566 Acquired Seminal Vesicle Lesions
Bryan R. Foster, MD and Amir A. Borhani, MD

SECTION 12: PROSTATE

570 Prostatitis and Abscess
Bryan R. Foster, MD
572 Benign Prostatic Hyperplasia
Bryan R. Foster, MD
576 Prostatic Cyst
Bryan R. Foster, MD
578 Prostate Carcinoma
Bryan R. Foster, MD
584 PI-RADS Lexicon and Usage
Bryan R. Foster, MD
594 Prostate Carcinoma Staging
Jeffrey Dee Olpin, MD

SECTION 13: PROCEDURES

612 Native and Transplant Kidney Biopsy
Zachary B. Jenner, MD and Ghaneh Fananapazir, MD
618 Percutaneous Genitourinary Interventions
Matthew T. Heller, MD, FSAR, Ashraf Thabet, MD, and
Zachary B. Jenner, MD
630 Kidney Ablation
Mitchell Tublin, MD, Ashraf Thabet, MD, and Zachary B.
Jenner, MD
640 Kidney Embolization
Zachary B. Jenner, MD, Mitchell Tublin, MD, and Ashraf
Thabet, MD
650 Venous Sampling and Venography (Renal and
Adrenal)
Amir A. Borhani, MD, T. Gregory Walker, MD, FSIR, and
Zachary B. Jenner, MD

xviii
FOURTH EDITION
SECTION 1
 Imaging Approaches
Overview and Introduction
Renal Mass Evaluation
General concepts: Renal masses can be the cause of patient
symptomatology but are often discovered incidentally on
imaging. While the initial imaging can sometimes confidently
diagnose the lesion, often additional imaging is required to
characterize it as benign or of malignant potential. CT, MR,
and US (especially with the advent of contrast-enhanced US)
all play important roles in renal lesion characterization.
CT: CT is the most common imaging modality to characterize
indeterminate renal lesions. A homogeneous lesion on NECT
measuring -10 to 20 HU is highly likely to represent a cyst,
while those > 70 HU represent a benign, hyperdense cyst. On
portal venous-phase CT, cysts can confidently be diagnosed in
the 21-30 HU range. Cysts that are simple can be considered
benign, while those that are complex need to be evaluated
further using the Bosniak classification. Renal lesions < -10 HU
contain fat and almost always represent angiomyolipomas.
Renal lesions between 20-70 HU need to be further evaluated.
True enhancement (> 20 HU change between NECT and
nephrographic phase) indicates a solid mass [renal cell
carcinoma (RCC), oncocytoma, lipid-poor angiomyolipoma,
metastasis, etc.]. Lack of enhancement (< 10 HU change)
indicates a hyperdense cyst. Equivocal enhancement (10-20
HU change) may indicate pseudoenhancement of a cyst or
mild enhancement of a solid mass and may benefit from
contrast-enhanced US or MR, which are more sensitive in
detecting true enhancement.
Dual-energy CT is gaining traction in characterizing renal
masses using virtual monochromatic imaging. In addition to
potentially obviating the need for a noncontrast phase, dual­
energy CT potentially decreases pseudoenhancement.
MR: MR outperforms CT in the characterization of smaller
lesions (< 1.5 cm) given its lack of pseudoenhancement as well
as its high specificity for cysts on T2WI. Lesion enhancement
on MR is more sensitive than on CT. In the case of an
indeterminate renal lesion where the patient is unable to
receive contrast, unenhanced MR may still be able to provide
useful information, as a uniform, very high T2 signal lesion can
be diagnosed as a cyst. Homogeneous high T1 signal also
suggests a benign cyst. DWI may be useful in suggesting RCC
from oncocytoma.
US: US has historically been relegated to the characterization
of renal lesions based on whether or not they met the
characteristics of a cyst: Anechoic, thin, well-defined wall,
posterior acoustic enhancement, and no internal flow on
Doppler imaging. However, with the emergence of contrast-
enhanced US, previously indeterminate renal lesions can now
be characterized as vascularized (indicating a solid mass) or
not. Contrast-enhanced US is exquisitely sensitive, exceeding
the sensitivity of CT and probably MR in detecting internal
vascular flow, especially in patients where the kidney and the
lesion are sonographically readily visible.
Hematuria Evaluation
CT urography (CTU): All patients with macroscopic hematuria
should undergo CTU. Microscopic hematuria is a common
problem and, while CTU is highly sensitive and specific for
malignancy, historically the diagnostic yield of CTU for upper
tract cancer is only ~ 1%. Recently updated guidelines by the
American Urologic Association (AUA) risk stratify patients to
decrease unnecessary imaging and increase yield; only those
in the high-risk group should undergo CTU. All patients
4
undergoing CTU for hematuria should also be referred for
cystoscopy (typically performed after CTU). Therefore,
detection of a subtle bladder mass by CTU is less important.
CTU is performed primarily to detect upper tract cancers.
Many different techniques are used for CTU (number of
phases, number and timing of boluses) with no consensus.
Dose-reduction techniques include DECT, split bolus
technique, and low kVp imaging. While the delayed phase is
important to identify ureter filling defects, increasing
evidence suggests that corticomedullary or nephrographic
phase is equally important as urothelial carcinoma enhances
avidly and can be detected readily on these earlier phases.
Most institutions perform noncontrast, nephrographic, and
delayed phases at a minimum. Oral hydration is the easiest
patient preparation. Using IV hydration and IV Lasix, on the
other hand, adds complexity with questionable benefit.
MR urography (MRU): While MRU is attractive because it
avoids radiation, it is not widely utilized for hematuria. It is an
appropriate modality in a patient unable to undergo CTU due
to allergy or renal insufficiency. MRU is less sensitive for upper
tract malignancy compared to CTU. Additionally, stones are
poorly detected.
Intravenous urography, retrograde urography: Intravenous
urography has been abandoned for CTU. Retrograde (or
antegrade) urography remains important and is typically
performed after CTU to confirm abnormalities and obtain
biopsy or guide other interventions.
US: In some low-risk and all intermediate-risk groups with
microscopic hematuria, renal and bladder US is appropriate in
the work-up as it can detect stones, renal masses, and bladder
lesions.
Kidney Graft Evaluation
US: US serves as the 1st-line imaging modality given the
kidney graft's relative superficiality, need for repeat imaging,
lack of radiation, and ability to assess anatomy as well as
perfusion. Grayscale assessment of the kidney graft is used to
evaluate for hydronephrosis as well as the presence of
perigraft fluid collections. Color or power Doppler is used to
assess for graft perfusion, and spectral Doppler looks at renal
artery flow as well as intraparenchymal resistive indices.
Perfusional assessment can be supplemented with the use of
contrast-enhanced US.
CT: Perigraft collections may be difficult to fully evaluate by
US, and CT may be useful to fully assess deeper collections.
Iodinated contrast does not seem to confer any specific risks
to patients with kidney grafts and should be used when
clinically necessary. CTA can be employed to evaluate for the
presence of vascular abnormalities, including transplant renal
artery stenosis.
MR: MR can be utilized to evaluate for vascular abnormalities.
Both unenhanced MR techniques, as well as contrast-
enhanced MR, have been employed. The use of macrocyclic
gadolinium agents has mitigated the concern for nephrogenic
systemic fibrosis and can be used in patients with kidney
grafts.
Adrenal Mass Evaluation
General concepts: Adrenal masses are common and most
frequently represent benign adenomas. However, a subset
represents adrenal cortical carcinomas, pheochromocytomas,
and metastases. Therefore, correct follow-up and imaging
 Imaging Approaches
play an important role in the balance between the
overutilization of imaging and the underdiagnosis of clinically
important adrenal masses. In general, lesions < 1 cm do not
need to be pursued. Lesions > 4 cm usually require surgical
evaluation. Those between 1-4 cm may require further
imaging evaluation.
CT: CT serves as the main modality for assessing the adrenal
gland. The presence of macroscopic fat can be seen in the
setting of myelolipomas or, less commonly, in smaller
quantities with lipomatous metaplasia with adrenocortical
neoplasms. On NECT, If the adrenal mass measures < 10 HU, a
diagnosis of adrenal adenoma can be made with fair
confidence (although cyst or pseudocyst would be in the
differential). For those that have indeterminate characteristics
on NECT (> 10 HU), further evaluation can be performed using
contrast kinetics. Adenomas typically show brisk washout of
contrast as opposed to metastases, which tend to retain
contrast. However, a small percentage of
pheochromocytomas can also show brisk washout, and clinical
history may be important to avoid mischaracterization of
adrenal masses. Dual-energy CT utilizing virtual
monochromatic imaging has shown utility in diagnosing
adrenal adenomas utilizing the 10 HU cutoff.
MR: Chemical shift MR is employed to identify the lipid
content of adrenal adenomas and is useful to evaluate adrenal
masses in patients with allergies to iodinated contrast.
PET/CT or biopsy: For patients with a history of malignancy
and an enlarging adrenal mass, an indeterminate adrenal mass
on adrenal CT, or an adrenal mass > 4 cm, PET/CT or biopsy
should be considered due to concern for metastatic disease.
Bladder Mass Evaluation
CTU: While CTU can be highly sensitive for bladder cancer,
good technique is needed to opacify the bladder. However,
since all patients with hematuria need to undergo cystoscopy
based on current guidelines, CTU is not performed to detect
bladder cancer, rather it is performed to detect an upper tract
cancer, since this portion of the urinary tract is not readily
accessible with a scope. CT does however play a role in
bladder cancer staging by readily detecting nodal and distant
metastases. CT is more limited in tumor stage evaluation.
Advanced T3 or T4 disease may be detected by CT, but this is
generally a pathologic diagnosis obtained by transurethral
resection of bladder tumor (TURBT) through a cystoscope, a
procedure that is diagnostic and potentially therapeutic.
MR: The role of MR for the local staging of bladder cancer
continues to evolve. MR is highly accurate in local staging,
particularly when multiparametric imaging is used (T2WI, DWI,
and DCE sequences) and when combined with the Vesical
Imaging Reporting and Data System (VI-RADS). However,
prebiopsy MR prior to TURBT has not been adopted at many
high-volume centers, and its future role is uncertain at this
point.
Elevated PSA and Prostate MR
General concepts: Clinically significant prostate cancer is most
commonly defined as Gleason score > 7 (grade group > 2).
Most clinically significant cancer needs treatment, whereas
small-volume, clinically insignificant cancer in patients with
PSA < 10 may be able to avoid treatment and be placed on
active surveillance. Multiparametric prostate MR (mpMR) and
the Prostate Imaging Reporting and Data System (PI-RADS)
are currently optimized to detect clinically significant cancer
Overview and Introduction
and have rapidly become the standard in imaging evaluation
of the prostate.
Indications: Despite the increasingly recognized problem of
prostate cancer overdiagnosis by PSA screening, most
patients with significant prostate cancer are still detected due
to abnormal PSA or digital rectal exam. Historically, imaging of
the tumor within the prostate was not performed and only
detected and quantified by transrectal US-guided (TRUS)
biopsy obtaining > 12 cores randomly from the prostate.
mpMR has rapidly grown in the past 10 years and is now
performed for many indications due to its high accuracy.
mpMR is currently commonly performed in 4 scenarios, and it
is important to understand each.
First, mpMR is being increasingly performed in men with
elevated PSA who have not had a biopsy (so-called biopsy
naive). This is being driven mainly by 2 factors; first, targeted
biopsy of the prostate either by US fusion biopsy or in-bore
biopsy techniques is increasingly available, and second, there
is good evidence that MR-detected targets harbor the highest
grade cancer, and targeted biopsy is more likely to detect
clinically significant cancer compared to random TRUS biopsy.
Various society guidelines have recognized this accumulating
data and have made mpMR prior to biopsy and the targeted
biopsy approach a recommendation.
The second common indication for mpMR is evaluation of
men with elevated PSA who have had negative TRUS biopsy
previously. TRUS biopsy misses ~ 30% of clinically significant
cancer. Therefore, these men often harbor cancer readily
detected by mpMR, classically in the anterior transition zone
(TZ) or in the peripheral zone (PZ) apex, both locations that
are undersampled by TRUS biopsy. Targeted biopsy of these
lesions allows confirmation of cancer and the patient to
undergo appropriate treatment.
The third common indication for mpMR is evaluation of men
who have known prostate cancer but have chosen an active
surveillance pathway. mpMR may be done at the outset of
active surveillance to determine if there is a clinically
significant tumor that would need targeted biopsy and
preclude active surveillance. mpMR is also performed in these
patients if PSA is rising or to follow-up known lesions for
growth.
Finally, the fourth common indication for mpMR is local
staging of prostate cancer in men about to undergo
treatment, most commonly prior to robotic prostatectomy or
image-guided radiotherapy. mpMR has reasonable accuracy to
identify organ-confined disease (< T2) or extracapsular
extension (> T3), and knowing this may alter treatment
approach.
It is important to understand that mpMR however does not
have perfect NPV. Thus, a negative mpMR, at this point, does
not help men avoid TRUS biopsy.
Technical aspects: Adherence to excellent MR technique is
crucial to maintain high accuracy in mpMR. This is because
many cancers are small, and both high spatial resolution and
high SNR is needed to depict these. PI-RADS has set forth
minimal technical standards while allowing for flexibility
across different MR systems and field strengths. When
possible, mpMR should be performed at 3T. Endorectal coils,
while not widely utilized, improve signal several fold and
should be considered. mpMR is made up of 3 core sequences:
T2WI, DWI, and DCE.
5
 Imaging Approaches
Overview and Introduction

PI-RADS: The recent explosion of mpMR has in part been
driven by PI-RADS, which provides a validated framework for
interpretation and is designed to maximize detection of
clinically significant prostate cancer. PI-RADS has gone
through several iterations and is currently on version 2.1. PI-
RADS assigns lesions into 1 of 5 categories based on the
likelihood of clinically significant prostate cancer, similar to the
models of LI-RADS and BI-RADS. A detailed and practical guide
Selected References
1. Waisbrod S et al: Assessment of diagnostic yield of cystoscopy and
computed tomographic urography for urinary tract cancers in patients
evaluated for microhematuria: a systematic review and meta-analysis. JAMA
Netw Open. 4(5):e218409, 2021
2. Weinreb JC et al: Use of intravenous gadolinium-based contrast media in
patients with kidney disease: consensus statements from the American
College of Radiology and the National Kidney Foundation. Radiology.
298(1):28-35, 2021

to PI-RADS interpretation is laid out in other chapters.
PI-RADS differentiates scoring whether a lesion is located in
the TZ or PZ. In the TZ, T2WI is most important for scoring
with DWI used as a tiebreaker in some cases. In the PZ, DWI is
most important for scoring with DCE used as a tiebreaker.
Despite updates and changes to the scoring system, portions
of PI-RADS scoring are very much subjective. Several well-
known pitfalls are laid out in subsequent chapters. Thus,
radiologists need adequate, high-volume training and should
recognize that there is a learning curve to reading mpMR. At
many centers, prostate specialists interpret mpMR to maintain
high accuracy. Radiologists should track their cases and
3. Ahdoot M et al: MRI-targeted, systematic, and combined biopsy for prostate
cancer diagnosis. N Engl J Med. 382(10):917-28, 2020
4. Barocas DA et al: Microhematuria: AUA/SUFU guideline. J Urol. 204(4):778-
86, 2020
5. Lenis AT et al: Bladder cancer: a review. JAMA. 324(19):1980-91, 2020
6. Walker SM et al: Positron emission tomography (PET) radiotracers for
prostate cancer imaging. Abdom Radiol (NY). 45(7):2165-75, 2020
7. Walker SM et al: Prospective evaluation of PI-RADS version 2.1 for prostate
cancer detection. AJR Am J Roentgenol. 1-6, 2020
8. Roberts JL et al: Diagnosis, management, and follow-up of upper tract
urothelial carcinoma: an interdisciplinary collaboration between urology and
radiology. Abdom Radiol (NY). 44(12):3893-905, 2019
9. Turkbey B et al: Prostate Imaging Reporting and Data System Version 2.1:
2019 Update of Prostate Imaging Reporting and Data System Version 2. Eur
Urol. 76(3):340-51, 2019

correlate with biopsy results so that they become comfortable 10. Galgano SJ et al: Optimizing renal transplant Doppler ultrasound. Abdom
Radiol (NY). 43(10):2564-73, 2018
with what they are overcalling and undercalling. In the future,
11. Herts BR et al: Management of the incidental renal mass on CT: a white
imaging center accreditation and radiologist certification with paper of the ACR Incidental Findings Committee. J Am Coll Radiol.
minimum cases may become widespread. 15(2):264-73, 2018
12. Fananapazir G et al: Sonographic evaluation of clinically significant perigraft
PET/CT: Concurrent to the growth of mpMR, PET/CT of hematomas in kidney transplant recipients. AJR Am J Roentgenol.
prostate cancer has benefited from new radiotracers with 205(4):802-6, 2015
higher sensitivity and specificity as compared to FDG. F-18
fluciclovine and PSMA are the two most common tracers in
use which are prostate specific. Accumulating data indicates
high sensitivity with these tracers, detecting sites of
metastatic disease in biochemical recurrence, at very low PSA
values. They are also sensitive and specific for showing lymph
node and bone disease at initial staging, outperforming CT
and MR and often significantly altering the treatment plan.
In the future, combined imaging approaches may become
standard for some clinical scenarios. PET/MR units are
increasingly being installed in academic centers and are
appealing for rapid and complete anatomic and metabolic
imaging diagnosis and staging of prostate cancer.

(Left) Longitudinal US shows a

simple cyst involving the
superior pole of the kidney.
Classic US features include an
anechoic, well-defined back
wall, posterior acoustic
enhancementS, and lack of
Doppler flow. US can
confidently diagnose simple
cysts. (Right) Axial T1 FS MR
shows a renal lesion with
markedly bright signal S.
This can confidently be
diagnosed as a benign
hemorrhagic/proteinaceous
cyst.

6
Imaging Approaches

Overview and Introduction

(Left) Axial CECT shows a right
renal lesion S with
indeterminate enhancement
(10-20 HU). This needs further
characterization either by MR
or CEUS. (Right) Transverse
CEUS in the same patient
shows avid enhancement of
the lesion, which on CT was
equivocal. CEUS has excellent
sensitivity in assessing
vascularity of renal masses.
This was surgically removed
and pathologically proven to
represent papillary renal cell
carcinoma.

(Left) Longitudinal US shows a

well-defined, rounded,
isoechoic but heterogeneous
mass S involving the inferior
pole of the kidney. As this does
not demonstrate cyst
characteristics, it may
represent a complex cyst or
solid renal mass. (Right)
Coronal CECT in the same
patient shows avid
enhancement S. The mass
was surgically removed and
found to be clear cell renal cell
carcinoma.

(Left) Axial NECT shows an

incidentally detected right
adrenal lesion S with density
< 10 HU, consistent with
adrenal adenoma. Contrast
with washout kinetics was not
necessary to diagnose this
adrenal lesion. (Right) Axial
CECT shows a mass within the
left adrenal gland with large
amounts ofgross fat­
containing components,
findings diagnostic of
myelolipoma.

7
 Imaging Approaches
Overview and Introduction

(Left) Axial GRE MR shows a

left adrenal mass S that was
unable to be evaluated on CT.
The patient underwent MR
with both in- and opposed-
phase imaging. (Right) Axial
opposed-phase MR in the same
patient shows that the left
adrenal mass S drops in
signal, consistent with
intracellular fat, diagnostic of
adrenal adenoma.

(Left) Color Doppler US of the

kidney graft is important in
the assessment of graft
perfusion. Ensuring perfusion
extends to the cortex is
necessary to exclude cortical
infarction. (Right) Coronal CTU
shows a large, infiltrative right
renal mass S with a bean
shape typical of urothelial
carcinoma. A bladder mass В
is also present. Synchronous
and metachronous urothelial
carcinoma is not uncommon.
Left parapelvic cysts S are
also seen.

(Left) Axial CTU with split

bolus technique shows subtle,
circumferential wall
thickening and enhancement
of the right ureter S,
consistent with urothelial
carcinoma. The distal ureter is
the most common location
outside of the kidney. (Right)
Axial T2 MR shows a papillary
bladder mass S with an
intact, low-signal line S
representing muscularis,
unlikely to be muscle invasive.
mpMR has high accuracy for
local staging but is not widely
adopted at this point.

8
Imaging Approaches

Overview and Introduction

(Left) Axial T2 MR in a 64-year-
old man on active surveillance
for Gleason 3+3 prostate
cancer diagnosed by TRUS
biopsy 3 years prior is shown.
PSA is rising and currently 5.7
ng/mL. A homogeneous,
hypointense, lenticular
anterior TZ lesion S 2 1.5 cm
is seen. Note the lack of
capsule and the
noncircumscribed margins,
unlike the adjacent BPH
nodules B. T2 score is 5.
(Right) Axial DWI MR in the
same patient shows marked
increased signal abnormality
S.

(Left) Axial ADC map in the

same patient shows marked
decreased signal abnormality
S. DWI score is 5. (Right)
Axial DCE MR in the same
patient shows corresponding
early enhancement of the
lesion S. DCE score is
positive. Overall PI-RADS score
is 5. MR-guided biopsy showed
Gleason 4+3 cancer, and the
patient came off of active
surveillance and was treated.
This anterior TZ location is a
common place for a missed
tumor on TRUS biopsy.

(Left) Axial T2 MR in a 75-year-

old man with PSA 12 and
Gleason 3+4 cancer shows a
PI-RADS 5 lesion in the left
peripheral zone S with
extracapsular extension B.
MR is helpful in local staging
prior to surgery or
radiotherapy. (Right) Axial T1
C+ MR in a man with
biochemical recurrence of
prostate cancer shows a small
renal mass S. Fluciclovine
PET/CT shows focal uptake B
in this renal metastasis. While
a rare location, this case
highlights the sensitivity and
specificity of new prostate­
specific radiotracers.

9
 SECTION 2
Retroperitoneum

Introduction to Retroperitoneum 12

Congenital
Duplications and Anomalies of IVC 16

Inflammation
Retroperitoneal Fibrosis 20

Degenerative
Pelvic Lipomatosis 24

Treatment Related
Retroperitoneal Hemorrhage 26
Postoperative Lymphocele 30

Benign Neoplasms
Retroperitoneal Neurogenic Tumor 32

Malignant Neoplasms
Retroperitoneal Sarcoma 36
Retroperitoneal and Mesenteric Lymphoma 40
Retroperitoneal Metastases 44
Solitary Fibrous Tumor 48
 Introduction to Retroperitoneum
Retroperitoneum
Relevant Anatomy and Embryology
The parietal peritoneum separates the peritoneal cavity from
the retroperitoneum. The retroperitoneum contains all the
abdominal contents located between the parietal peritoneum
and the transversalis fascia. It is divided into 3 compartments
by 2 well-defined fascial planes: The renal and lateroconal
fasciae.
The perirenal space contains the kidney, adrenal, proximal
ureter, and abundant fat, and it is enclosed by the renal fascia,
a.k.a. Gerota fascia. The 2 perirenal spaces do not
communicate across the abdominal midline.
The anterior pararenal space contains the pancreas,
duodenum, colon (ascending and descending), and a variable
amount of fat.
The posterior pararenal space contains fat but no organs; it is
contiguous with the properitoneal fat along the flanks.
The anterior renal fascia separates the perirenal space from
the anterior pararenal space, and the posterior renal fascia
separates the perirenal space from the posterior pararenal
space.
The lateroconal fascia separates the anterior from the
posterior pararenal space and marks the lateral extent of the
anterior pararenal space.
The renal fascia joins and closes the perirenal space,
resembling an inverted cone with its tip in the iliac fossa.
Caudal to the perirenal space, in the pelvis, the anterior and
posterior pararenal spaces merge to form a single infrarenal
retroperitoneal space. Due to an opening in the cone of the
renal fascia caudally, the perirenal space communicates with
the infrarenal retroperitoneal space, which in turn
communicates directly with the extraperitoneal pelvic spaces.
Thus, all 3 retroperitoneal compartments communicate with
each other within the lower abdomen and pelvis. All of the
pelvic retroperitoneal compartments, such as the prevesical
(space of Retzius), perivesical, and presacral spaces,
communicate with each other, which is evident and clinically
relevant in cases of pelvic hemorrhage or tumor as well as
with extraperitoneal rupture of the urinary bladder.
The renal and lateroconal fascia are laminated planes, which
can split to form potential spaces as pathways of spread for
rapidly expanding fluid collections or inflammatory processes,
such as hemorrhage or acute pancreatitis. Splitting of the
anterior renal fascia creates a "retromesenteric plane" that
communicates across the midline; splitting of the posterior
renal fascia creates a "retrorenal plane," which also
communicates across the midline and anteriorly. There are
also radial bridging septa in the perirenal space that allow for
pathology to cross from the perirenal space to the pararenal
spaces or vice versa.
Imaging Techniques and Indications
Multiplanar CT and MR are ideally suited to display the
anatomy and pathology of retroperitoneal disease processes.
Use of IV contrast material allows easier recognition of fascial
plane landmarks and pathology and should be used unless
contraindicated.
12
Approach to Retroperitoneal Abnormalities
Perirenal Space
Disease within the perirenal space is usually the result of
diseases of the kidney. Common disease states include
hemorrhage, infection, inflammation, and neoplasia.
The renal fascia is very strong and is usually effective in
containing most primary renal pathology within the perirenal
space. Similarly, it usually excludes most other processes from
invading or involving the perirenal space.
Perirenal fluid may represent blood, urine, or pus or may be
simulated by inflammation of the perirenal fat (a common,
benign, and often age-related finding). Hemorrhage is often
due to trauma but may occur due to anticoagulation, rupture
of a renal tumor, or vasculitis. Pus or inflammation usually
originates from acute pyelonephritis, which may be associated
with an abscess. Perirenal urine collection ("urinoma") may
result from trauma with laceration through the renal
collecting system. Acute urine leak may also accompany
ureteral obstruction by a calculus due to forniceal rupture.
Renal cell carcinoma is common, and the renal fascia usually
confines the tumor, preventing invasion of contiguous
structures. However, renal cell carcinoma can invade through
the perirenal fascia (T4 tumor).
Other neoplasms can involve the perirenal space, classically
lymphoma or rarely extramedullary hematopoiesis.
Inflammatory processes may also rarely be seen, such as
Erdheim-Chester, IgG4, and retroperitoneal fibrosis.
Anterior Pararenal Space
Disease within the anterior pararenal space is common. For
example, acute pancreatitis results in peripancreatic
inflammation, necrosis, &/or fluid collections that often first
spread to the anterior pararenal space, surrounding the
duodenum and ascending and descending colon segments
that share this anatomic compartment. The spread of
inflammation is usually limited posteriorly by the anterior
renal fascia and laterally by the lateroconal fascia. Thickening
of these planes is a reliable clue as to the presence of
inflammatory diseases, which might otherwise be occult on
imaging. The perirenal space is usually not involved in acute
pancreatitis, sometimes resulting in the striking appearance of
a perirenal "halo" of fat density, while other retroperitoneal
spaces and planes are infiltrated. As the collections become
large (often in necrotizing pancreatitis), spread occurs from
the anterior pararenal to posterior and infrarenal spaces,
occasionally reaching the pelvis. The root of the mesentery
and transverse mesocolon originate from just ventral to the
3rd portion of duodenum and pancreas, and pancreatitis can
dissect along these planes beneath the parietal peritoneum.
Since the 2nd through 4th portions of the duodenum are
retroperitoneal, duodenal perforations (from ulcer, post-
ERCP, etc.) may result in extraluminal gas and fluid collections
in the right anterior pararenal space. As the collection grows, it
may extend into other spaces similar to necrotizing
pancreatitis collections. Only the duodenal bulb is
intraperitoneal; as such, a perforation of the bulb (the most
common type) shows pneumoperitoneum.
Posterior Pararenal Space
Disease originating within the posterior pararenal space is
uncommon, essentially limited to hemorrhage and tumor.
 Introduction to Retroperitoneum
"Retroperitoneal hemorrhage" is a misnomer since most
spontaneous, coagulopathic hemorrhage originates within
the abdominal wall, the iliopsoas compartment, or the rectus
sheath. Only when hemorrhage extends beyond these fascial
boundaries does it enter the retroperitoneum. Rectus sheath
hematomas enter the extraperitoneal pelvic spaces through a
defect in the caudal (infraumbilical) portion of the sheath.
Iliopsoas hemorrhage often extends into any or all of the
retroperitoneal compartments, predominantly along the main
fascial planes. The hallmarks of coagulopathic hemorrhage are
bleeding out of proportion to trauma, multiple sites of
bleeding, and the presence of the hematocrit sign, a fluid-
cellular debris level within the hematoma.
Retroperitoneal sarcomas, most commonly liposarcoma,
often originate within one of the retroperitoneal
compartments, and the site of origin can be determined by
the relative mass effect on various organs and structures, such
as the kidneys, colon, and great vessels. Most liposarcomas
have some identifiable fat within them and seem to be
encapsulated, allowing for excision, although recurrent
disease is common. Leiomyosarcomas originate typically
around the IVC.
If retroperitoneal nodes are included in the discussion, the
most common retroperitoneal tumor is non-Hodgkin
lymphoma (NHL). NHL often results in massive
lymphadenopathy. This characteristically involves the
mesenteric and retroperitoneal nodes that are confluent and
anteriorly displace the aorta and inferior vena cava from the
spine. Retroperitoneal nodes are also frequently involved by
malignancies originating in pelvic organs, such as the prostate,
rectum, and cervix.
The other large (though uncommon) group of primary
retroperitoneal tumors are of neurogenic origin, including
schwannoma, paraganglioma, and other nerve sheath tumors.
These often share the characteristics of appearing as well-
defined, moderately enhancing masses that do not appear to
arise from nodes nor abdominal viscera. Many, in fact, arise
along the nerves or ganglia, while others are part of a
syndrome, such as neurofibromatosis, that may involve
multiple nerves in a paraspinal or presacral distribution.
Retroperitoneum
The aorta and IVC are located in the central retroperitoneum
and are surrounded by fascia with the great vessel space.
Although primary disease of the IVC is rare, it may be the site
of primary tumor (leiomyosarcoma) or the site of intravascular
spread of renal or adrenal carcinoma. Anomalies of the IVC are
commonly seen incidentally in ~ 10% of the population,
usually at or below the level of the renal veins, resulting in
variations such as duplicated IVC and retro- and circumaortic
renal vein. While these are uncommonly of clinical significance
(limited to affecting surgical and interventional procedures),
they may be mistaken for pathologic conditions, most
commonly enlarged retroperitoneal lymph nodes.
Abdominal aortic aneurysm is a major health concern, and
rupture is usually fatal. Accurate diagnosis and precise
mapping of the size and shape of an aneurysm allows
effective, minimally invasive prophylactic treatment with
endovascular stenting.
Retroperitoneal fibrosis is an inflammatory disorder that may
be misinterpreted as a malignant process, as it envelops the
aorta and IVC, often causing displacement and encasement of
the ureters. It most commonly occurs as part of IgG4 disease
or less commonly due to medications or malignancy.
Selected References
1. Czeyda-Pommersheim F et al: Diagnostic approach to primary
retroperitoneal pathologies: what the radiologist needs to know. Abdom
Radiol (NY). 46(3):1062-81, 2021
2. Al-Dasuqi K et al: Radiologic-pathologic correlation of primary
retroperitoneal neoplasms. Radiographics. 40(6):1631-57, 2020
3. Shaaban AM et al: Fat-containing retroperitoneal lesions: imaging
characteristics, localization, and differential diagnosis. Radiographics.
36(3):710-34, 2016
4. Osman S et al: A comprehensive review of the retroperitoneal anatomy,
neoplasms, and pattern of disease spread. Curr Probl Diagn Radiol.
42(5):191-208, 2013
5. Goenka AH et al: Imaging of the retroperitoneum. Radiol Clin North Am.
50(2):333-55, vii, 2012
6. Tirkes T et al: Peritoneal and retroperitoneal anatomy and its relevance for
cross-sectional imaging. Radiographics. 32(2):437-51, 2012
7. Lee SL et al: Comprehensive reviews of the interfascial plane of the
retroperitoneum: normal anatomy and pathologic entities. Emerg Radiol.
17(1):3-11, 2010
8. Sanyal R et al: Radiology of the retroperitoneum: case-based review. AJR Am
J Roentgenol. 192(6 Suppl):S112-7 (Quiz S118-21), 2009
(Left) Axial graphic shows the
pancreas, duodenum, and left
colon in the anterior pararenal
space and fat in the posterior
pararenal space, separated
from the perirenal space by
the anterior S and posterior
S renal fascia, which join
laterally to form the
lateroconal fasciaB. (Right)
Axial CT analogous to the
previous graphic shows the
normal appearance of the
renal fascia. The anterior S
and posterior S renal fascia
and the lateroconal fascia B
are seen as a thin line in most
patients.
13
 Introduction to Retroperitoneum
Retroperitoneum

Pancreas Anterior pararenal space

Ascending colon Descending colon

Anterior renal fascia

Interfacial (retromesenteric) Lateroconal fascia

plane
Perirenal space

Interfascial (retrorenal) plane

Posterior renal fascia

Posterior pararenal space

Diaphragm

Adrenal gland
Liver

Anterior pararenal space Perirenal space

Posterior pararenal space

Transverse colon Iliac crest

Infrarenal retroperitoneal
space

(Top) The 3 main compartments of the retroperitoneum are the anterior pararenal space (yellow), perirenal space (purple), and
posterior pararenal space (blue). The interfascial planes (green) are potential spaces created by inflammatory processes that separate
the double-laminated layers ofthe renal and lateroconal fasciae. The posterior pararenal space communicates with the properitoneal
fat that extends along the lateral and anterior abdominal wall. (Bottom) Sagittal graphic through the right kidney shows the 3
retroperitoneal compartments. Note the confluence of the anterior and posterior renal fasciae at about the level of the iliac crest.
Caudal to this, there is only a single infrarenal retroperitoneal space.

14
Introduction to Retroperitoneum

Retroperitoneum
(Left) Axial CECT shows
thickening of the perirenal S
and lateroconal fascia В in a
patient with diverticulitis.
Thickening of the fascia can be
clues to disease. Since portions
of the colon are
retroperitoneal, pathology can
involve the retroperitoneum.
(Right) Axial CECT shows a
ruptured abdominal aortic
aneurysm with a large
hematoma in the posterior
pararenal space S. Thin wisps
of hematoma В track into
the perirenal space via
bridging septa that allow
communication between
spaces.

(Left) Axial CT cystogram in

the setting of trauma and
pelvic fractures shows large
prevesical (space of Retzius)
S and perivesical В space
hemorrhages. (Right) Axial CT
cystogram more superiorly in
the same patient shows
contiguous, large
hemorrhages in the infrarenal
spaces S. This case illustrates
the communication between
the pelvis and retroperitoneal
spaces. Hematoma can track
up in the setting of pelvic
fracture or downward in the
setting of spontaneous
retroperitoneal bleed.

(Left) Axial CECT in a patient

with necrotizing pancreatitis
shows a large, infected,
walled-off necrotic collection
S involving the anterior В
and posterior S pararenal
spaces. Extension into the
anterior pararenal space is
very common in pancreatitis
as the pancreas is located
within this retroperitoneal
space. (Right) Axial CECT in a
patient with retroperitoneal
fibrosis shows a periaortic soft
tissue mantle S and left
hydronephrosis S with
delayed nephrogram due to
obstruction of the proximal
ureter.

15
 Duplications and Anomalies of IVC

KEY FACTS
Retroperitoneum

TERMINOLOGY о Enlarged azygos vein empties into superior vena cava

• Congenital anomalies of inferior vena cava (IVC)
IMAGING
• Duplication of IVC (prevalence: ~ 1-3%)
о Left- and right-sided IVC are present inferior to renal
veins
о Left IVC typically drains into left renal vein, which crosses
anterior to aorta to join right IVC
о Recognition important prior to IVC filter placement
• Left IVC (prevalence: ~ 0.2-0.5%)
о Typically drains into left renal vein, which crosses anterior
to aorta to join normal right suprarenal IVC
о Important variant in repair of abdominal aortic aneurysm
and transjugular placement of IVC filter
• Azygos continuation of IVC (prevalence: ~ 0.6%)
о Absence of suprarenal IVC
о Blood flow enters azygous vein and enters thorax
posterior to diaphragmatic crus
(SVC) normally in right peribronchial location
о Hepatic veins drain directly into right atrium
о Important variant in planning cardiopulmonary bypass
• Circumaortic left renal vein (prevalence: ~ 2-3.5%)
о Important variant in nephrectomy planning
о Rare occurrence of hematuria and hypertension
TOP DIFFERENTIAL DIAGNOSES
• Retroperitoneal lymphadenopathy
• Varices/collaterals
• Gonadal vein
DIAGNOSTIC CHECKLIST
• Preoperative imaging may be important in planning
abdominal surgery, liver or kidney transplantation, or
interventional vascular procedures
о e.g., IVC filters, varicocele sclerotherapy, venous renal
sampling

(Left) Graphic shows

comparison between left IVC
S and duplicated IVCS. In
both, the left-sided IVC drains
through the left renal vein to
the right suprarenal IVC.
Images A through D show the
expected appearance of the
aorta and IVC at these levels
on cross-sectional axial
images. (Right) CoronalMIP
CECTshows a left-sided IVC
S, which ascends left of the
aorta, joins the left renal vein
S, crosses anterior to the
aorta to merge with the right
renal vein & and continues
along the conventional path
through the liver.

(Left) Axial CECTshows a

normal right IVCS and a
smaller accessory left IVC&
known as a duplicated IVC.
The 2 IVCs can be variable in
size and dominance. (Right)
Coronal MIP CT in the same
patient shows the normal
course of a duplicated IVC
with the left IVC& draining
into the left renal vein S,
crossing in front of the aorta,
and draining conventionally
into the right IVCS.

16
 Duplications and Anomalies of IVC
TERMINOLOGY
Definitions
• Congenital anomalies of inferior vena cava (IVC)
IMAGING
General Features
• Best diagnostic clue
о Malposition or duplication of IVC
• Morphology
о Types of IVC anomalies
- Duplicated IVC
- Left-sided IVC
- Azygos continuation of IVC
- Circumaortic left renal vein
- Retroaortic left renal vein
- Duplication of IVC with retroaortic right renal vein and
hemiazygos continuation of IVC
- Duplication of IVC with retroaortic left renal vein and
azygos continuation of IVC
- Circumcaval (retrocaval) ureter
- Absence of infrarenal or entire IVC
- Extrahepatic portocaval shunt (Abernethy
malformation)
- IVC webs
CT Findings
• Duplication of IVC
о Left- and right-sided IVC inferior to renal veins (variable
size and dominance)
о Left IVC typically drains into left renal vein, which crosses
anterior to aorta in normal fashion to join right IVC
о Duplicated IVCs may have significant asymmetry (left
usually smaller tan right)
• Left IVC
о Drains into left renal vein, which crosses anterior to aorta
in normal fashion to unite with right renal vein and form
normal right suprarenal IVC
о T enhancement of right renal vein relative to left renal
vein
- Due to dilution from unenhanced venous return from
lower extremities into left renal vein
• Azygos continuation of IVC
о Absence of suprarenal IVC
о Infrarenal IVC continues as azygous vein, which enters
thorax posterior to diaphragmatic crus
о Enlarged azygos vein empties into superior vena cava
(SVC) normally in right peribronchial location
о Hepatic veins drain directly into right atrium
о Enlarged azygos vein has similar attenuation to SVC
о Gonadal veins drain to ipsilateral renal veins
о Associated with polysplenia, left isomerism/heterotaxia
• Circumaortic left renal vein
о 2 left renal veins
- Superior renal vein joined by left adrenal vein and
crosses anterior to aorta
- Inferior renal vein, located 1-2 cm caudal to superior
renal vein, joined by left gonadal vein and ultimately
crosses posterior to aorta
• Retroaortic left renal vein
Retroperitoneum
о Solitary left renal vein that crosses posterior to aorta
lower than right renal vein
• Duplication of IVC with retroaortic right renal vein and
hemiazygos continuation of IVC
о Left and right IVCs inferior to renal veins
о Right IVC drains into right renal vein, which crosses
posterior to aorta to join left IVC
о Suprarenal IVC passes posterior to diaphragmatic crus to
enter thorax as hemiazygos vein
о In thorax, collateral pathways for hemiazygos vein
include these features
- Crosses posterior to aorta at T8-T9 to join azygos vein
- Continues superiorly to join coronary vein of heart via
persistent left SVC
- Accessory hemiazygos continuation to left
brachiocephalic vein
• Duplication of IVC with retroaortic left renal vein and
azygos continuation of IVC
о Combination of findings previously mentioned
• Circumcaval (retrocaval) ureter
о Proximal ureter courses posterior to IVC, emerges to
right of aorta, and lies anterior to right iliac vessels
о Ureter obstruction proximal to aberrant course
• Absence of infrarenal or entire IVC
о External and internal iliac veins join to form enlarged
ascending lumbar veins
о Venous return from lower extremities to azygos and
hemiazygos vein via anterior paravertebral collateral
veins
о ± suprarenal IVC formed by left and right renal veins
о May be acquired abnormality following thrombosis or
resection of IVC
о May present with acute thrombus of pelvic and leg veins
(KILT syndrome)
• IVC web
о Complete or incomplete membrane in suprahepatic or
intrahepatic IVC
о Dilated hepatic veins and intrahepatic collaterals
о Budd-Chiari changes may develop and lead to
hepatocellular carcinoma
• Abernethy malformation
о Shunt between portal system and IVC
о Type 1: Complete shunting of portal blood to IVC with
absence of portal vein
- Polysplenia and biliary atresia may coexist
о Type 2: End-to-side connection between portal vein and
IVC
MR Findings
• Flow voids or flow-related enhancement may distinguish
aberrant vessels from masses or lymph nodes
Ultrasonographic Findings
• Infrahepatic IVC at level of renal veins
о Suprarenal IVC continues as azygous or hemiazygos veins
• Hepatic veins drain directly into right atrium
• Right renal artery crossing anteriorly to azygos vein; may
demonstrate azygos continuation of IVC
Angiographic Findings
• Inferior vena cavography: Highly accurate method but
typically unnecessary because of cross-sectional imaging
17
 Duplications and Anomalies of IVC
Retroperitoneum

Imaging Recommendations
CLINICAL ISSUES
• Best imaging tool
Presentation
о CECT or MR with reformations in coronal plane
• Protocol advice • Most common signs/symptoms
о CT venogram: Pelvic veins and IVC are best opacified at 2 о Most patients are asymptomatic
minutes post contrast о Circumcaval ureter: Chronic ureteral obstruction or
- However, usually standard portal phase is sufficient recurrent urinary tract infections
for diagnosis о Absence of infrarenal or entire IVC: Venous insufficiency
of lower extremities or idiopathic deep venous
DIFFERENTIAL DIAGNOSIS thrombosis
• Diagnosis
Retroperitoneal Lymphadenopathy
о Usually diagnosed incidentally by imaging
• Malignancy: Metastases, lymphoma о Suspect duplicated IVC with recurrent pulmonary
• Granulomatous disease embolism after IVC filter
• Left-sided paraaortic adenopathy; may mimic duplication of • KILT syndrome
IVC or left IVC о Rare association of kidney and IVC anomalies associated
о Differentiate by renal vein drainage or contrast with leg thrombosis
enhancement of IVC о Typically presents in children with thrombosis of pelvic
• Retrocrural adenopathy; may mimic enlarged azygos vein in and lower extremity veins; present with leg pain
retrocrural space о IVC is absent, small, or anomalous
о Differentiate by tubular structure of azygos vein о Kidney absent or small
extending from diaphragm to azygos arch
о Retrocrural adenopathy enhances less than vessels Demographics
• Retroperitoneal adenopathy; may mimic circumaortic left • Age
renal vein о Congenital anomalies diagnosed at any age
• Epidemiology
Varices/Collaterals
о Prevalence
• Due to cirrhosis or IVC obstruction
- Duplication of IVC: ~ 1-3% of general population
• Left renal vein may appear dilated due to splenorenal
- Left IVC: ~ 0.2-0.5%
shunt, which is common
- Azygos continuation of IVC: ~ 0.6%
Gonadal Vein - Circumaortic left renal vein: ~ 2-3.5%
• May appear as paraaortic soft tissue "mass" or mimic left­ - Retroaortic left renal vein: ~ 2-3%
sided IVC, particularly when dilated as is common in Treatment
multiparous woman
• Usually no treatment required
• Follows inferior course toward ovary; does not
communicate with left iliac vein • Circumcaval ureter
о Surgical relocation of ureter anterior to IVC
PATHOLOGY
DIAGNOSTIC CHECKLIST
General Features
Consider
• Etiology
о Congenital • Duplicated IVC, left IVC, circumaortic renal vein, and
retroaortic renal vein all present challenges in IVC filter
о Risk factor: 1st-degree relatives
placement
о Pathogenesis
- Duplication of IVC Image Interpretation Pearls
□ Persistence of both supracardinal veins • Preoperative imaging may be important in planning
- Left IVC abdominal surgery, liver or kidney transplantation, or
□ Regression of right supracardinal vein with interventional procedures
persistence of left supracardinal vein о e.g., IVC filters, varicocele sclerotherapy, venous renal
- Azygos continuation of IVC sampling, cardiopulmonary bypass
□ Failure to form right subcardinal-hepatic • Anomalies of IVC can be confused with retroperitoneal
anastomosis, resulting in atrophy of right adenopathy, especially on NECT or if veins are thrombosed
subcardinal vein
- Circumaortic left renal vein SELECTED REFERENCES
□ Persistence of dorsal limb of embryonic left renal 1. Oliveira JD et al: Congenital systemic venous return anomalies to the right
vein and dorsal arch of renal collar atrium review. Insights Imaging. 10(1):115, 2019

- Retroaortic left renal vein
□ Persistence of dorsal arch of renal collar and
regression of ventral arch
2. Liu Y et al: Radiological features of azygos and hemiazygos continuation of
inferior vena cava: a case report. Medicine (Baltimore). 97(17):e0546, 2018
3. Doe C et al: Anatomic and technical considerations: inferior vena cava filter
placement. Semin Intervent Radiol. 33(2):88-92, 2016
4. Smillie RP et al: Imaging evaluation of the inferior vena cava. Radiographics.
35(2):578-92, 2015

18
Duplications and Anomalies of IVC

Retroperitoneum
(Left) AP venogram with
injection from the left iliac
vein shows 2 IVCfilters S in a
duplicated IVC. Contrast
opacifies the left IVC В and
drains into the left renal vein
S. Alternative treatment
strategies are needed for IVC
filter placement in some IVC
and renal vein anomalies.
(Right) Axial NECT shows 2
small, round lesions S on
either side of the aorta, which
proved to be a duplicated IVC.
IVC anomalies can
occasionally mimic
retroperitoneal LAD,
particularly on noncontrast
imaging.

(Left) Axial CECT in a young

patient shows a dilated
azygous vein S and absent
IVC, consistent with azygous
continuation of the IVC. Note
the right-sided polysplenia S
and midline liver В in this
patient with a left
isomerism/heterotaxia. (Right)
Axial CECT shows a dilated
azygous vein S extending
from the retroperitoneum into
the SVC. The infrahepatic IVC
is absent, and all blood from
the lower 1/2 of the body
drains through the azygous
with the exception of the liver,
which drains through an
intrahepatic IVC.

(Left) Coronal NECT shows a

severely dilated right ureter
S, which abruptly narrows
with fishhook appearance
before ascending and passing
behind and medial В to the
IVCS. This is the typical
course of a circumcaval
(retrocaval) ureter. (Right)
Coronal CECT shows a
retroaortic left renal vein S.
In both the retroaortic and
circumaortic renal vein, the
vein passes between the spine
and aorta at a level lower
than the conventional renal
vein insertion В.

19
 Retroperitoneal Fibrosis

KEY FACTS
Retroperitoneum

IMAGING • Retroperitoneal hemorrhage

• Irregular, periaortic soft tissue mass from renal vessels to
iliac bifurcation
о Aorta not displaced from spine
о Can surround IVC and medially displace ureters
о Soft tissue may extend to renal hila and into pelvis
• NECT: Isoattenuating to muscle
• CECT or MR: Enhancement varies with stage of disease
о Early/active disease: Avid enhancement
о Late/chronic disease: Minimal to no enhancement
• T1WI: Low signal intensity
• T2WI: Signal intensity varies with stage of disease
о Early/active disease: High signal intensity
о Late/chronic disease: Low signal intensity
• Favorable response to treatment: Decrease in T2 signal
intensity, enhancement, or size
TOP DIFFERENTIAL DIAGNOSES
• Retroperitoneal metastases and lymphoma
PATHOLOGY
• Primary (idiopathic): 75% of cases
о Manifestation of systemic autoimmune or inflammatory
diseases
о IgG4-related disease now known to cause 75% of
"idiopathic" retroperitoneal fibrosis (RPF)
• Secondary: 25% of cases
о Most commonly due to medications, neoplasms
CLINICAL ISSUES
• Difficult diagnosis: Insidious, nonspecific symptoms
• Benign RPF can be distinguished from malignant masses by
typical clinical, biochemical, and immunologic data and
typical imaging findings
DIAGNOSTIC CHECKLIST
• Percutaneous biopsy often requested to confirm diagnosis
and exclude malignancy

(Left) Graphic shows

encasement and medial
displacement of midureters by
a band offibrous tissue S.
Note the bilateral
hydroureteronephrosisВ. The
fibrous tissue is usually limited
to the inferior lumbar region.
(Right) Axial CECTin a patient
with secondary RPFshows
right hydronephrosis Sand a
distorted IVCВ due to
plaque-like soft tissue S
representing metastatic
urothelial cancer. Malignant
RPF is suggested based on the
patient's history and
contemporaneous widespread
metastatic disease.

(Left) Axial CECTin the same

patient more inferiorly shows
a medially deviated right
ureter S with a stenosed IVC
В. Retroperitoneal plaque­
like soft tissue Srepresents
metastatic urothelial cancer,
likely with desmoplastic
reaction. (Right) Axial CECT
just above the origin of the
inferior mesenteric artery in
the same patient shows
retroperitoneal plaque-like
soft tissue Srepresenting
metastatic urothelial cancer,
likely with desmoplastic
reaction.

20
 Retroperitoneal Fibrosis

TERMINOLOGY
Abbreviations
• Retroperitoneal fibrosis (RPF)
Synonyms
• Ormond disease, periaortitis
Definitions
• Spectrum of diseases resulting in proliferation of
fibroinflammatory tissue in infrarenal portion of
retroperitoneum
о IgG4-related disease (IgG4-RD)
о Systemic and organ-specific autoimmune diseases
о Chronic periaortitis: Inflammatory abdominal aortic
aneurysms
- Presumed etiology: Hypersensitivity to antigens in
atheromatous plaques
- Severe form: Perianeurysmal fibrosis
- Not always included in RPF since treatment and
prognosis are related to underlying vascular disease
IMAGING
General Features
• Best diagnostic clue
о Homogeneous, irregular periaortic soft tissue mass
causing hydronephrosis
• Location
о Extends from renal vessels inferior to iliac bifurcation
о Typically centered at L4-L5 level
о Atypical involvement: Throughout pelvis, mesenteric
root, mediastinum
Radiographic Findings
• Intravenous urography (IVU) triad
о Hydroureteronephrosis superior to L4-L5 and delayed
nephrogram
о Medial deviation of midureters
о Gradual tapering of ureters, extrinsic compression
• Retrograde pyelography (RGP)
о Hydroureteronephrosis, medial deviation of ureters
о Assesses extent and severity of ureteral obstruction
CT Findings
• Homogeneous, irregular, periaortic mass of variable
thickness
о Often, thin rind of soft tissue around otherwise normal
aorta
о Found anywhere between renal arteries and iliac vessels
- Typically centered at L4-L5 level
- Atypical involvement: Throughout pelvis; extension to
mesenteric root or into mediastinum
□ Worrisome for malignant or secondary RPF
о Envelopes aorta, inferior vena cava (IVC), and ureters
- Does not displace structures anteriorly from spine
(unlike lymphoma)
- May narrow but rarely invades aorta, IVC, and ureters
- Loss of tissue plane between fibrosis and muscles
- Medial ureteral deviation with ureteral stenosis and
upstream hydronephrosis
о Contrast enhancement varies with stage of fibrosis
Retroperitoneum
- T enhancement: Early/active fibroinflammatory
process
- J. enhancement: Chronic/inactive fibrosis
• Primary RPF: 25% cases have reactive subcentimeter
retroperitoneal lymph nodes
MR Findings
• T1WI
о Homogeneous low signal intensity (SI)
• T2WI
о SI varies with stage of fibrosis
- T T2 SI: Early/active fibroinflammatory process
- J T2 SI: Chronic/inactive fibrosis
• DWI
о Chronic RPF with higher apparent diffusion coefficients
(ADC) than active or malignant RPF
• T1WI C+
о Similar to CECT: Enhancement varies with stage of
fibrosis
о Late enhancement during fibrotic stage
Ultrasonographic Findings
• Grayscale ultrasound
о Iso- to hypoechoic, irregular mass anterior to spine
- Variable degrees of hydronephrosis
Nuclear Medicine Findings
• PET
о Not used for primary diagnosis due to low specificity
о Detects additional sites of disease, especially for RPF due
to IgG4-RD or malignancies
о May help guide biopsy
о Guides treatment
- Baseline PET with low FDG avidity predicts poor
response to medical therapy; early surgical
management may be considered
- Monitor for relapse
Imaging Recommendations
• Best imaging tool
о MR or CECT with multiplanar reformations
DIFFERENTIAL DIAGNOSIS
Retroperitoneal Metastases and Lymphoma
• Retroperitoneal metastases
о e.g., prostate, cervix, breast, lung carcinoma
о Additional pelvic and retroperitoneal nodes usually seen
о More discrete or asymmetrical nodal masses rather than
diffuse infiltrative tissue
о More heterogeneous and higher T2 SI
• Lymphoma
о Typically more cephalic location in retroperitoneum
о Generally presents larger and with avid enhancement
о Mass effect on vessels and viscera, lifting aorta/cava off
spine
о Rarely obstructs ureters
Retroperitoneal Hemorrhage
• Most commonly due to overanticoagulation
о Hematocrit sign (fluid-fluid level), involvement of
iliopsoas ± rectus sheath

21
 Retroperitoneal Fibrosis
Retroperitoneum

о Tends not to surround aorta • Sex

• Abdominal aortic aneurysm о M:F = 2-3:1
о 2nd most common cause of retroperitoneal bleed • Epidemiology
о Acutely ill and hypotensive patient о Prevalence: 1.3:100,000 population
• Spontaneous hemorrhage from neoplasm (surrounds
Natural History & Prognosis
organ or mass)
о Kidney: Renal cell carcinoma, angiomyolipoma, renal • Complications
vasculitis о Ureteral obstruction and renal vascular stenosis
о Adrenal: Carcinoma or myelolipoma - Renal failure
• CT findings - New-onset or worsening, preexisting hypertension
о Acute: High-attenuation fluid/hematoma о Worsening aortic aneurysm
о Chronic: Low-attenuation fluid collection о IVC stenosis/obstruction
о Associated renal/adrenal tumors or aortic aneurysm о Mesenteric ischemia if mesenteric and celiac arteries
• MR findings involved
о Varied SI (evolution of blood products) • Prognosis
о Idiopathic RPF as chronic-relapsing disorder
PATHOLOGY - Relapse rates up to 72%
- End-stage renal disease rarely develops
General Features
о Poor prognosis for malignant form (3- to 6-month
• Etiology survival)
о Primary/idiopathic (75% cases): Likely autoimmune
disease with antibodies
Treatment
- IgG4-RD now known to cause 75% of idiopathic RPF • Withdrawal of possible causative agent
- Ormond speculation: RPF is similar to collagen • Immunosuppression: Corticosteroids and other
vascular disease, supported by coexistence with other immunosuppressant agents
inflammatory processes • Surgery: Ureteral stent &/or ureterolysis/transposition
о Secondary (25% cases)
- Drugs: Methysergide, в-blockers, hydralazine, DIAGNOSTIC CHECKLIST
ergotamine, LSD Consider
- Conditions that stimulate desmoplastic reaction
• Percutaneous biopsy often requested to confirm diagnosis
□ Malignancy: Sarcoma, lymphoma, and metastases
and exclude malignancy
from stomach, colon, breast, lung, genitourinary,
and thyroid cancers Image Interpretation Pearls
□ Other: Surgery, radiation, trauma, infection, and • Irregular retroperitoneal soft tissue encasing great vessels
carcinoid tumor outside of retroperitoneum and ureters
• Associated abnormalities • Can be subtle rind around aorta
о Other IgG4-RD • Therapeutic response assessment
- Pseudotumor of orbit; Riedel thyroiditis о Favorable therapeutic response: Decrease in size, T2 SI,
- Sclerosing cholangitis; chronic fibrosing mediastinitis enhancement, or FDG avidity
- Autoimmune pancreatitis
SELECTED REFERENCES
Gross Pathologic & Surgical Features
1. Kurowecki D et al: Cross-sectional pictorial review of IgG4-related disease. Br
• Mass of woody fibrous tissue; whitish gray J Radiol. 92(1103):20190448, 2019
• Encases vessels and ureters 2. Morin G et al: Persistent FDG/PET CT uptake in idiopathic retroperitoneal
fibrosis helps identifying patients at a higher risk for relapse. Eur J Intern
Med. 62:67-71, 2019
CLINICAL ISSUES 3. Cohan RH et al: Imaging appearance of fibrosing diseases of the
retroperitoneum: can a definitive diagnosis be made? Abdom Radiol (NY).
Presentation
43(5):1204-14, 2018
• Most common signs/symptoms 4. Vaglio A et al: Idiopathic retroperitoneal fibrosis. J Am Soc Nephrol.
27(7):1880-9, 2016
о Nonspecific pain: Back, flank, abdomen
5. He Y et al: Spectrum of IgG4-related disease on multi-detector CT: a 5-year
о Renal insufficiency, hypertension: Ureteral obstruction or study of a single medical center data. Abdom Imaging. 40(8):3104-16, 2015
renal vascular involvement 6. Liang W et al: Imaging-based evaluation of retroperitoneal fibrosis: a
о Lower extremity edema: Deep vein thrombosis or challenge for radiologists. Radiology. 274(3):937-8, 2015

IVC/lymphatic compression 7. Bakir B et al: Role of diffusion-weighted MR imaging in the differentiation of

• Laboratory data: No specific or definitive test
о T ESR, C-reactive protein; 1 hematocrit; ± azotemia
о T serum IgG4
о ± rheumatoid factor, various autoimmune markers
benign retroperitoneal fibrosis from malignant neoplasm: preliminary study.
Radiology. 272(2):438-45, 2014
8. Caiafa RO et al: Retroperitoneal fibrosis: role of imaging in diagnosis and
follow-up. Radiographics. 33(2):535-52, 2013

Demographics
• Age
о Usually 40-65 years

22
Retroperitoneal Fibrosis

Retroperitoneum
(Left) Axial CECT in a patient
with primary RPF due to IgG4-
related disease shows plaque­
like periaortic soft tissue rind
S. Left hydronephrosis 3is
present with a delayed
nephrogram. (Right) Coronal
CECT in the same patient
shows typical distribution of
periaortic soft tissue from the
renal vessels to the aortic
bifurcation S. Medially
deviated and obstructed left
ureter 3 results in a delayed
nephrogram.

(Left) Axial CT urogram in a

patient with primary RPF
shows periaortic soft tissue S
without aortic displacement.
Severe atherosclerosis
suggests chronic periaortitis.
The dilated left ureter is
unopacifiedS, while the right
ureter is opacifiedS and
normal. (Right) Coronal CT
urogram in the same patient
shows periaortic soft tissue
extending past the aortic
bifurcation S. The left ureter
is dilatedS with abrupt
transition due to obstruction
by the fibrotic mass.

(Left) Axial CECT in a patient

with mantle cell lymphoma
shows significant
retroperitoneal soft tissue S
without hydronephrosis and
with mesenteric adenopathy
S, making RPF unlikely.
(Right) Axial T2 FS MR
demonstrates high signal
intensity of the soft tissue
mass S that surrounds the
iliac bifurcation, consistent
with an active stage of
retroperitoneal fibrosis.

23
 Pelvic Lipomatosis

KEY FACTS
Retroperitoneum

TERMINOLOGY • Chronic proctitis

• Uncommon, progressive overgrowth of benign, mature,
unencapsulated fat in perirectal and perivesical spaces
IMAGING
• Symmetrically distributed, nonencapsulated fat
surrounding pelvic organs
о No soft tissue component or enhancement of fat
• Superior displacement of bladder, prostate, seminal
vesicles, and sigmoid colon
• Inverted pear- or teardrop-shaped bladder
о Dilated, medially displaced ureters
• Elongated, narrowed rectum due to smooth, concentric
extrinsic compression
• Elongated, narrowed, straight rectosigmoid colon
TOP DIFFERENTIAL DIAGNOSES
• Normal variant
о Large pelvic muscles with narrow, bony pelvis
о e.g., IBD, radiation, lymphogranuloma venereum
о Fatty proliferation around rectum not involving bladder
• Postoperative colon
• Liposarcoma
CLINICAL ISSUES
• Compressed bladder (e.g., T frequency, dysuria, nocturia,
and hematuria)
• Compressed rectum (e.g., constipation, rectal bleeding,
tenesmus, ribbon-like stools, and nausea)
• Compressed veins (e.g., leg edema, thrombosis)
• Complications: Hydronephrosis, urolithiasis, renal failure,
colon obstruction, venous thrombosis, bladder
adenocarcinoma
• Patients may need urinary diversion or ureter
reimplantation

(Left) Coronal CECTin a 50-

year-old man shows an
elongated, narrow bladder S
with an inverted pear shape.
Notice the large amount offat
with mild stranding in the
perivesicularspaceВ. (Right)
Sagittal CECTin the same
patient shows the markedly
elongated, narrowed bladder
S due to mass effect from
pelvic lipomatosis. Also notice
the elongated, narrowed
rectosigmoid colon В.

(Left) Axial T2 MR shows a

large amount of pelvic fat
surrounding and compressing
the rectum S. The bladder В
is also displaced superiorly and
narrowed. These are typical
findings of pelvic lipomatosis.
(Right) Axial NECTshows an
abnormal shape of the
decompressed bladder S
with concave walls and
elongated narrow
configuration thought to be
due to mass effect from pelvic
lipomatosis.

24
 Pelvic Lipomatosis

Retroperitoneum
TERMINOLOGY PATHOLOGY
Abbreviations General Features
• Pelvic lipomatosis (PL) • Etiology
о Unknown
Definitions
о In large series, many patients had normal BMI; possible
• Uncommon, progressive overgrowth of benign, mature, that obesity does not contribute to disease
unencapsulated fat in perirectal and perivesical spaces
• Associated abnormalities
о Proliferative cystitis: Cystitis glandularis, cystitis cystica
IMAGING
- Affects ~ 75% of patients with PL and is of unknown
General Features etiology
• Best diagnostic clue - Multiple filling defects in contrast-filled bladder
о Overabundance of symmetrically distributed fat in - May be associated with intestinal metaplasia, which is
perivesical and perirectal spaces thought to be premalignant lesion of bladder
о Compression, elevation, and elongation of bladder and adenocarcinoma
rectosigmoid colon by extensive fat Gross Pathologic & Surgical Features
Radiographic Findings • Fat: Mature, whitish-yellow, lobular
• Radiography Microscopic Features
о AP view: Extensive lucent areas overlying pelvis
• Metaplasia: Mature cells, thin septa, lobular growth
о Lateral view: Increased size of presacral space

CT Findings CLINICAL ISSUES

• Symmetrically distributed, nonencapsulated fat Presentation
surrounding pelvic organs
• Most common signs/symptoms
• Homogeneous fat attenuation (-80 to -120 HU)
о Compressed bladder: T frequency, dysuria, nocturia, and
о Fat may contain occasional fibrous strands hematuria
о No soft tissue component or enhancement of fat о Compressed rectum: Constipation, rectal bleeding,
• Superior displacement of bladder, prostate, seminal tenesmus, ribbon-like stools
vesicles, and sigmoid colon о Compressed veins: Leg, scrotal edema, deep vein
• Inverted pear- or teardrop-shaped bladder thrombosis
о Medial displacement ± obstruction of ureters
• Elongated, narrowed, straight rectosigmoid colon Demographics
• Age
MR Findings
о Mean: 48 years (peak: 25-60 years)
• Homogeneous signal follows fat • Sex
• No enhancement or restricted diffusion о M:F = 18:1
Ultrasonographic Findings • Ethnicity
• Pear-shaped, nondistensible bladder compressed by о Predilection for Black patients (~ 67%)
extensive echogenic perivesical fat • Epidemiology
• Anterior and superiorly displaced bladder о Rare: Incidence of 1.7/100,000

Natural History & Prognosis

DIFFERENTIAL DIAGNOSIS
Normal Variant
• Large iliopsoas muscles may cause pear-shaped bladder
Chronic Proctitis
• e.g., ulcerative colitis, radiation, lymphogranuloma
venereum
• May cause fatty proliferation around rectum
Postoperative Rectosigmoid Colon
• Low anterior or abdominoperineal resection
• Colon appears stretched; bladder not affected
Liposarcoma
• Focal, heterogeneous, fatty mass rather than diffuse and
symmetric fat
• Complications: Hydronephrosis (seen in > 50%), urolithiasis,
renal failure, colon obstruction, venous thrombosis,
proliferative cystitis
• Up to 40% of patients progress to renal failure
Treatment
• Many therapies have proven ineffective, including weight
loss, steroids, antibiotics, and radiation therapy
• Ureteral stenting, ureter reimplantation, and urinary
diversion are most commonly performed
SELECTED REFERENCES
1. Bai X et al: Diagnostic accuracy of CT imaging parameters in pelvic
lipomatosis. Abdom Radiol (NY). 46(6):2779-88, 2021
2. Hermie I et al: Pelvic lipomatosis causing renal failure. J Belg Soc Radiol.
100(1):55, 2016
3. Sun Y et al: Value of multimode sonography for assessment of pelvic
lipomatosis compared with computed tomography. J Ultrasound Med.
35(6):1143-8, 2016

25
 Retroperitoneal Hemorrhage

KEY FACTS
Retroperitoneum

TERMINOLOGY о Active bleeding: Linear, flame-shaped density, isodense

• Hemorrhage in retroperitoneal (RP) or posterior abdominal
wall musculature
IMAGING
• Major causes and CT findings
о High-attenuation, poorly marginated collection that
initially accumulates near site of bleeding; can spread
throughout RP
- May extend into thigh, genitals, abdominal wall, and
peritoneum
о Coagulopathy/anticoagulation: High-density collection,
cellular-fluid level (hematocrit sign)
о Trauma: Pelvic fracture, spine trauma, renal/adrenal,
vascular injury
о Ruptured abdominal aortic aneurysm: Large, eccentric
aneurysm; draped aorta; disrupted calcs with periaortic
hematoma ± active extravasation contiguous with aorta
to vessels
о Sentinel clot sign: High-attenuation (60-80 HU) layering
along organ of origin
о Chronic hematoma: Lower density (20-40 HU) with rim
enhancement
• MR: Variable signal due to age of blood products
• US: Avoid; poor detection and often underestimates extent
• NECT is sufficient to diagnose RP hemorrhage
• If there is concern for active bleeding requiring
intervention, consider multiphase CTA
о Allows for detection and localization of active bleeding,
which can have management implications
DIAGNOSTIC CHECKLIST
• Hematocrit sign and bleeding into several spaces indicates
anticoagulation
• Spontaneous perirenal hemorrhage: Consider underlying
tumor, vasculitis, or coagulopathy

(Left) Axial NECT shows a

developing subcapsular and
perinephric hematoma S
during a microwave ablation
procedure for renal cell
carcinoma. Subsequent
imaging showed significant
enlargement of the hematoma
and extension throughout the
retroperitoneal spaces. (Right)
Axial NECTshows a large
retroperitoneal hematoma
with hematocrit level S
suggestive of coagulopathic
hemorrhage.

(Left) Axial T2 FS MR shows

hypoin tense, early subacute
retroperitoneal hematoma S
causing mass effect upon the
kidney Sand uncontrolled
hypertension (Page kidney).
(Right) AP angiogram of the
same patient shows
aneurysms/pseudoaneurysms
S throughout the distal
branches of the renal artery
and intrarenal arteries,
consistent with polyarteritis
nodosum.

26
Another random document with
no related content on Scribd:
Carency, where I became attached for quarters and rations to the
Sixteenth Canadian Scottish, which was one of the battalions of the
Third Canadian Infantry Brigade of which I was now R. C. chaplain.
My other battalions were the Thirteenth, Fourteenth and Fifteenth.
All, with the exception of the Fourteenth, were kilted battalions, and
each one had its own band of bag-pipes.
I was somewhat disappointed to find myself attached to the
Sixteenth as the Catholic chaplain who had proceeded me had been
quartered with the Fourteenth in which was an average of four
hundred Catholics; in the Sixteenth the average was about eighty.
There was some military reason for my appointment, so all I could do
was to obey orders.
We left Camblain L’Abbey and the motor went quickly over the well-
kept road. Soon the town, with all the houses still intact, was left far
behind, and presently, not far ahead, I saw a large sign-board
attached to two posts about fifteen feet high. At the top, in large
black block letters, were the words “Gas Alert,” and beneath were
words to the effect that from now on all troops must wear their gas
masks “at the alert.” This meant that instead of carrying the mask at
the side, with the bag closed, it must be tied about the chest, with the
bag open, so that in a moment the mask might be raised to the face.
A little nervousness came over me, for now on all sides were signs
of great devastation—broken and torn buildings, crumbled walls,
fields deeply marked with shell-holes; and the road became rough,
for it had been mended in many places after being rent by shells.
Less traffic appeared along our way; everything seemed quiet. On
our right, in the distance, I noticed what seemed to be a square
forest of miniature trees, which, as we drew nearer, became regular
in shape and equidistant from one another. As we came still nearer I
noticed low mounds, “row on row.” What had seemed to be trees
were crosses—a great forest of little low crosses—and between the
rows and rows of crosses were the long lines of “the little green tents
where the soldiers sleep.” We passed two or three other military
cemeteries, then the ruins of a small village or two, where many
soldiers looked out from cellar windows or low huts built of pieces of
broken stone and scraps of corrugated iron, with a piece of burlap
hanging and weighted at the end for a door. Dugouts were built into
the hill that sloped up from the roadside. The silence of the whole
countryside seemed uncanny. We came up a little hill where, on our
right a few hundred feet back from the road, were perhaps a dozen
corrugated iron stables, open at the sides, but with a partition the
whole length of the hut running through the middle. In the foreground
was the basement of what had once been a long, narrow dwelling-
house. Here we stopped, for we had come to headquarters of the
Sixteenth Battalion, or, to give them their full name, the Sixteenth
Canadian Scottish. They were a kilted battalion, hailing from British
Columbia.
The colonel told me to remain in the motor till he returned from the
orderly room, which I did. In a few minutes he came back with the
adjutant and two soldiers. The adjutant welcomed me kindly; the two
soldiers picked up my bed-roll and began to carry it towards
headquarters. I shook hands with the colonel as he said good-bye.
Then I accompanied the adjutant to headquarters. I had arrived at
the Western Front.
 Chapter XXXIX
A Strafe and a Quartet

My room was a partitioned off portion at the end of the cellar in which
was headquarters: there was no fire in it and the month was
December. Through cracks in the portion of the building that was
above ground, blew the cold, wintry wind.
That night at dinner in “the mess,” which was in the portion of the
cellar adjoining my billet, I met a number of the officers—though the
majority were still in the line—and they were among the finest men I
had ever met. The commanding officer, Colonel Peck, one of the
best-loved men on the Western Front, was a huge man with a black
drooping mustache which gave him a rather fierce appearance, but
there was a look of real kindness in his eyes. He possessed the
Distinguished Service Order Medal, and later he won the highest
decoration of the British army, the Victoria Cross. At that time,
although we did not know it till later, he had been elected a member
of the Canadian parliament.
When I returned to my billet I found a lighted candle sticking to the
bottom of an upturned condensed milk tin; some one had been
showing me an act of kindness. I had no sooner entered than there
was a knock on the door. A young soldier opened it and came in. He
said he had come to open my bed-roll and prepare my bed. I looked
at the berth, which was a piece of scantling about seven feet long
running the width of the room, to which was attached two
thicknesses of burlap about a yard wide that were fixed to the wall. I
wondered how I was going to sleep, for I was shivering then.
Suddenly the young soldier ceased tugging at the straps, listened
quietly for a second or two, then not looking at me, but keeping his
eye fixed on the bed-roll, he said slowly and solemnly, as if
addressing some imaginary person in the bed-roll: “All is quiet on the
Western Front.”
He neither smiled nor looked at me, but continued his work.
For months I had read those words in the daily papers of England;
but now there was something so comical in the lad’s manner of
saying them that I could not help laughing as he went on with his
unpacking.
But it was not for long that “all was quiet on the Western Front.”
Suddenly I heard a far-distant rumble which had the rhythmic roll of
snare-drums, yet the sound was much stronger and it was increasing
quickly in intensity and volume. Soon it was a great thundering roar
with a minor rattle. The earth seemed to be trembling.
I looked at the soldier. “A bombardment?” I questioned.
“No, sir,” he said quietly, “that’s just a strafe over on the LaBassée
front. Those are our guns. Fritzy’ll open up after they stop. You
should go outside and see it, sir.”
I stepped out, almost falling into a trench that was just outside my
door. Away to the northeast for about a mile flitted short, sharp
yellow flashes of light. Although the rumbling of the guns was so
loud, I judged them to be five or six miles distant. Everything was
quiet about where I stood. It was a moonlight night and along the
white road, as far as I could see, was a line of broken trees, with
here and there the irregular walls of a ruined village.
Presently there was a lull, then complete silence; in the clear
moonlight, the devastated countryside gave one a weird impression.
Then “old Fritzy opened up,” and although the rumble of his guns
was not so distinct, I judged that he was giving us about as much as
we had given him. I wondered how much harm would be done, and
whether many of our lads would be killed. Then slowly the firing
ceased and presently again “all was quiet on the Western Front.”
I was just about to reënter my quarters when I received another
surprise. From a hut just a few yards away came sounds of singing. I
listened: it was a low, sweet song that I had never heard before—a
quartet, and the harmony seemed perfect. I had never before heard
such sweet singing. An officer came out of the mess and stood near
me, listening in silence. Then he said: “That’s pretty good, Padre.” I
agreed with him, but I confessed I had never heard the song before.
“Why, Padre,” he said, “the name of that song is ‘Sweet Genevieve’.
Strange you never heard it! Wherever men are congregated one will
hear that song. It’s an old song, Padre. Strange you never heard it!”
So I had heard two sounds that I had never before heard: one was
the sound of a “strafe” on the Western Front; the other was the
singing of “Sweet Genevieve.”
 Chapter XL
The Valley of the Dead

When I reëntered my hut I found that the young soldier had opened
my bed-roll and removed the few little articles that were in it. The
bed-roll was arranged for the night on the burlap berth.
“You haven’t enough blankets, sir,” he said. Then he was gone; but
in about five minutes he was back again with two thick brown army
blankets. After I had thanked him, he looked around to see if he
could improve anything before leaving for the night. Not seeing
anything, he was just about to open the door when he turned and
said: “If old Fritz comes over to bomb us tonight, sir, the safest place
for you will be down in the trench. It’s a moonlight night and Fritzy
likes to be out in the moonlight.”
There was no bombing that night, but it was so extremely cold that I
could not sleep. I spent the night changing from one position to
another in the hope of getting warm, but I remained awake till
daylight.
About seven o’clock the following morning I heard a fumbling at the
latch of my door. I had just finished my prayers. I waited, for I knew
the door was not locked; then as the latch was raised the door
opened, assisted by the foot of the one entering. First there
appeared a large granite iron plate of steaming porridge and a
smoky hand holding it, then a granite iron mug of something
steaming, and another smoky hand holding it. Then appeared the
kindly soldier of the night before, his pleasant face a little begrimed,
but smiling, the arm of the hand which held the mug hugging to his
side a small earthen jar of sugar with a spoon in it. I went to his
assistance and soon we had the things spread out on an upturned
ration box which had been the seat. Now it was the table, and the
bed was my seat.
“How did you sleep, sir?” asked the soldier. I told him. Then he said
he must try to find something to make a stove. He went on to tell me
that he and the cook had built one, but that it was not working well.
He held up his hands as evidence, and I looked at his face. “The
cook is out there now,” he said, “trying to cook the breakfast, and
swearing, for there’s more smoke coming out around the stove than
there is going up the chimney.”
I poured from the earthen mug a little of the hot diluted condensed
milk over the steaming porridge, and the soldier told me to take all
the sugar I wanted as there was plenty. He stood beside me for a
while waiting to see if I would make any comment on the porridge. I
had never been in the habit of eating any cereal at breakfast, but this
morning I was very cold and also very hungry. I tasted the porridge; it
was hot, piping hot. It tasted slightly of smoke, but that didn’t matter.
“It’s fine,” I said.
“Not smoky?” he asked.
I assured him that if it was a little bit smoky it made no difference. He
went out again; but I had not quite finished the porridge before I
heard another fumbling at the latch, and in a moment he appeared
again with another granite iron plate on which were two rashers of
bacon and a large slice of toast; in the other hand was a large mug
of hot tea.
“Is this dinner?” I asked.
The lad smilingly told me to eat all I could, that when a man loses
sleep the best way to make up for it is by a good meal. He picked up
the empty porridge plate and the empty mug, leaving the sugar-bowl,
and went out again; but in about three minutes he was back with a
jar of compound jam, strawberry and gooseberry.
“Has the cook stopped swearing yet?” I asked.
“Yes,” replied the lad, “I told him you said the porridge was good. He
knew it wasn’t, and when he saw your empty plate he smiled. He’ll
be all right now for awhile.”
“What is the name of this place?” I asked.
“Carency,” he replied, “in the Souchez Valley. Just across the road,
on the other side of the valley, is where the sixty thousand French
soldiers and civilians were gassed. Their own turpinide gas that they
had sent over against the Germans came back on them. The wind
had changed. There are some of the victims in the wood that have
never been buried. The valley is called Valley of the Dead.”
He went on to tell me of the great battles that had already been
fought in the area where we now were. I learned that we were almost
at the base of Vimy Ridge.
“What is the difference between a ‘strafe’ and a ‘bombardment?’” I
asked him.
“Well,” he said, “a bombardment is usually all thought out
beforehand and a lot of preparations are made for it and it usually
lasts a long time. A ‘strafe’ is just a firing that might start up any time,
and it generally lasts only a few minutes. Sometimes a green hand in
the line brings off a ‘strafe’ that might last half an hour with the loss
of many lives and the cost of thousands of dollars. The first night in
the line every minute or two some fellow thinks he sees some one
coming across ‘No Man’s Land’ and sometimes he ‘gets the wind up’
pretty bad and fires. Then old Fritz thinks some one is coming
towards him and he fires back; then two or three of our fellows
answer, and immediately old Fritz comes back stronger. Then the
whole line opens up and the machine-guns begin to rat-tat-tat, and
an S. O. S. flare goes up for the artillery, and presently the earth is
rocking under a ‘strafe’ and everybody except one wonders who
started it all.”
As the lad then began to gather up the empty dishes, I made
apologies for having eaten so much; always my breakfast had been
just a little bread and jam. His only comment was, “Sorry, sir, I didn’t
have a couple of eggs for you.”
Long after he went out I kept thinking of the horrors of war; what
catastrophes might transpire through the changing of the wind or
through “getting the wind up.”
After I had returned home from the war I was giving a series of
lectures in a little town. In one of them I happened to mention the
terrible tragedy of the turpinide gas. Many among my audience found
it hard to believe that there had been so many victims. The following
day the priest with whom I was staying asked me many questions
about the Valley of the Dead. A day or two later, as we were sitting in
his office, one of his parishioners came in on some business. I was
about to leave the room when the priest motioned me to stay.
When the man had finished his business, he looked at me and said:
“So you have been to the war, Father?”
I said I had been there.
“Well,” continued the man, who had come a long distance, “I met a
lad who was through it all, and he told me he found the gas worse
than anything. He said he was in a place, one time, where thousands
and thousands had been froze stiff by a strange kind of gas. He said
that there was a church there, filled with people sitting in the pews,
and the windows were all up, and this gas came right in through the
windows and froze all the people in the pews. They’re all there yet,
and if you pay a quarter you can see them.”
The man was most serious. I did not dare look at the priest till he had
gone. For a moment the priest shook with laughter, then he said to
me: “Father, send for that returned man and make him your
assistant. He can tell the story much better than you.”
“Well,” I said, “considering that it was France, they might have made
the admission fee one franc instead of a quarter.”
However, my story had not been exaggerated.
 Chapter XLI
New Friends

Shortly after the young soldier left there was another knock on my
door, and as I stood up to go to open it I heard outside the voice of a
man speaking as if to a child. When I opened the door, there stood a
kilted officer over six feet in height, with the pleasant face of a boy.
He was accompanied by a billy-goat, the mascot of the battalion.
The officer greeted me warmly and then looked at the goat, saying:
“Shake hands, Billy, shake hands with the new Padre.” So Billy and I
shook hands, or rather, I shook Billy’s raised hoof.
In the afternoon I took a walk along the Valley of the Dead. Away in
the distance I noticed a large balloon far up in the air and, seemingly,
two men standing in the large basket attached to it. It was the first
time I had ever seen a balloon and I was a little surprised to find that
it was not round, but shaped like a sausage. It was a greyish-khaki
color.
The sun was just setting far away behind the broken trees when I
walked back from Neuville St. Vaast; the sky was pink with here and
there a pencil of red clouds. Along the skyline flew three homing
airplanes. As I turned to see if any more planes were coming, I
noticed the large balloon being hauled slowly down towards the
earth.
When I entered my little billet, I found the young soldier at work
putting up a stove that he had found and patched with a piece of tin.
I asked him what the great balloon was doing up in the air. He told
me that it was an observation balloon, and that the two men in the
aerial car were observing with field-glasses what was going on
behind Fritz’s line. The airplanes that I had seen wending their way
against the winter skyline were scout planes that had been patrolling
the sky for hours. “Now,” he said, “they are going home to roost.”
Before the stove was finished the Third Brigade interpreter—the men
always called the interpreter “the interrupter”—came to visit me. He
was the first Catholic I had met since coming to the Sixteenth. He
seemed very friendly and kind. The badge of his office was a sphinx.
It was Napoleon who designed this badge for interpreters—I
suppose to remind them that although they would learn much that
was occurring, it was part of their office not to divulge it. The
interpreter’s work was made very hard at times by the good
peasants of France. Sometimes, while marching through a rich
farmland, a soldier lad would “annex” a hen, or a head of cabbage,
or some grapes, or apples, etc.; then the irate owner would seek the
interpreter and oblige him to conduct him or her before the proper
military authorities, where compensation would be demanded from
the government.
The cook also came in to see me; he, too, was a Catholic and
seemed to be a lad full of energy. I was surprised to learn that in
private life he was a tailor. Before he left, he made arrangements for
going to confession. Then, by some strange association of ideas, I
asked him if his stove still smoked. It was going much better now, he
said.
That evening after dinner as I sat wiping my eyes with my
handkerchief, when it was not being applied to my nose—for besides
giving real warmth, the new stove emitted a quantity of smoke—an
officer knocked and came in, followed by two soldiers carrying his
bed-roll. I had been expecting him, for in the mess just before dinner
I had heard the officers planning the allotment of sleeping space for
the night. A number had been sleeping in their bed-rolls on the floor
of the mess; and now two or three other officers were coming back
from leave. I had heard an officer say: “We’ll put ‘Wild Bill’ with the
Padre.” The others had agreed to this.
I had been wondering who “Wild Bill” was. I did not think the officers
were playing a practical joke on me, for I had always found officers
most respectful to the priesthood. But now “Wild Bill” had entered,
and as I looked through the slight smoke-screen, my eyes rested on
one of the gentlest-mannered men I have ever met. Without being in
the least effeminate, he came quietly over and shook hands. I
understood now why they called him “Wild Bill” for I recalled that at
college one of the slowest moving lads I had ever met, had been
rechristened “Lightning.” I felt grateful to the other officers who had
billeted “Wild Bill” with me.
He slept in his bed-roll on the floor, after he had spread a rubber
ground sheet over it. Gradually the room became sufficiently warm to
sleep in. The soldier had found some coal. And as the smoke died
away I fell asleep and did not awake until morning.
 Chapter XLII
A Little Burlap Room

The following day was Saturday and I began to think of my duties for
the morrow. I had learned that the Thirteenth, Fifteenth and
Sixteenth battalions would remain in the trenches till Monday. I called
at the orderly room of the Fourteenth only to learn that they would be
moving Sunday. When I returned to my billet I found a letter from
Father MacDonnell, telling me to call to see him at the Transport
Section of the Seventy-second Battalion. I did, and found a little
man, dressed in Scotch military costume—tartan riding breeches,
round-cornered khaki tunic and glengarry cap. The Seventy-second
was a Scotch battalion from Canada, but its chaplain was a
Canadian from Scotland. He had been a member of the Benedictine
Monastery, at Fort Augustus, Scotland. He was then busy
composing a little work on the Holy Name, for he was anxious to
establish the Holy Name Society among not only the Catholic
soldiers, but also all other denominations. This was accomplished
later with the co-operation of the general commanding officer of the
Canadian Corps, Sir Arthur Currie. He was not a young man: his hair
was beginning to turn grey. I took him to be about fifty years old. He
wished me to work with him on Sunday. This I did, saying Mass in a
large Y. M. C. A. tent, while he said Mass some distance farther
down the valley. I did not have many at Mass, but a good number
came to Communion. Most of the men were in the trenches.
In the afternoon, towards three o’clock, I heard the inspiring strains
of a military march coming up the Valley of Death. I knew the march
well. It was “The Great Little Army,” one of the most popular marches
on the Western Front. I stepped outside and looked down the valley.
A battalion of infantry was marching back from the line.
“It’s the Fourteenth,” said a young soldier standing nearby.
I watched them carefully. The Fourteenth was one of my battalions. I
had heard of it before; it had been the sacrificed battalion in one of
the big battles. The men had advanced without support in order to
give the enemy the impression that we were stronger than we really
were. They had suffered terrible casualties, but their manoeuvre had
met with great success. I watched them till they disappeared round a
turn in the road—Hospital Corner, I think it was called—and still I
stood listening to the band. Very likely I would meet these lads on
Christmas Day—which meant within the week.
I had no sooner returned to my “room” when the young soldier who
had been so thoughtful of my interests came in. “Sir,” he said, “the
colonel and all the headquarters’ officers have gone to Chateau de la
Haie; the battalion is going there tomorrow. I think you should take
the colonel’s room before any one else gets it.”
In ten minutes all my belongings were in the room just vacated by
the colonel. It was a warm room completely lined with burlap: ceiling,
walls and floor were covered with it. There was a small burlap-
covered table and a low bench, about three feet long, also with a
covering of burlap, but above all else, there was a tiny stove with two
doors that slid back so that one could see the fire burning in it. Since
then I have been in very much worse quarters on the Western Front.
The following morning I said Mass on the little table, and the cook,
who had now only four officers to provide for, came to Holy
Communion. The next morning the interpreter, with a young soldier
who was being called home to Halifax to care for his wife and child
who had just passed through the terrible disaster, knelt reverently in
the little burlap room to receive their Lord.
 Chapter XLIII
Christmas at the Front

We had planned to have midnight Mass in one of the large moving-

picture huts at Chateau de la Haie, for here in reserve were four full
battalions: one belonging to Father MacDonnell, one to Father
Murray, a young chaplain whom I met just before Christmas, and
two, the Fourteenth and Sixteenth, belonging to me. My other
battalions were only about two miles beyond these, the Thirteenth at
Petit Servans and the Fifteenth at Grand Servans. But First
Divisional Headquarters, which was then at Chateau de la Haie,
reconsidered the matter. They thought the Catholic soldiers coming
in at such an early hour might disturb others who would wish to
sleep; and, also, that there might be too many lights used, so that
some aerial Santa Claus from across the line might wing his way
above the camp, dropping a few Christmas bombs in passing. We
then decided to have two Masses in the large hut at Chateau de la
Haie and one in the church at Petit Servans. Fathers Murray and
MacDonnell were to say the Masses at Chateau de la Haie and I
was to go to Petit Servans.
I found that not only had I to notify the men of my own battalions, but
also all the units in my area. As there were about ten other units—
labor groups, engineers, divisional trains, etc.—this took me quite a
while. In fact, it took all Monday afternoon. But the following morning,
which was Christmas, when I turned around after the gospel to say a
few words to the lads, I felt more than repaid for any inconvenience,
including my four mile walk from Carency to Petit Servans before
Mass, for the church was filled. All the seats were occupied and the
large space in the rear was packed with standing soldiers—kilted
laddies from the Thirteenth and Fifteenth, with their officers; soldiers
from the engineers; members of the labor groups; stretcher-bearers
from the First Field Ambulance. With a full heart I thanked the Christ
Child for bringing together all my Catholic men. It was the first time in
four months that I had been able to assemble such a large number.
At the hospital, naturally, the groups were small. And as I looked at
the sea of faces, so reverently attentive, many bearing marks of the
terrible conflicts through which they had passed, I felt a twitching at
the throat, so that it was a few seconds before I could begin to
speak.
It was a long while that Christmas Day before I finished giving Holy
Communion, for nearly all the men in the church came.
On my way home I learned from Father Murray that the Fourteenth
and Sixteenth had attended Mass in a body in the moving-picture hut
at Chateau de la Haie, and that great numbers had gone to Holy
Communion.
My Christmas dinner was a piece of dry roast beef, almost burnt,
some potatoes, bread and margarine, with a little apricot jam and a
cup of tea; that was all. Yet I think it was the happiest Christmas I
ever spent, for, as I thought of that first wonderful meeting with those
Canadian Catholic soldiers on the Western Front, I felt that in their
midst those words, written so long ago, “There was no room in the
inn,” could not be said that Christmas Day.
 Chapter XLIV
Back to Rest

Every morning for a week or two I was in the little church where I had
said Mass on Christmas Day, and every evening while I was there
men came to confession. Then one morning the young soldier who
had been so attentive to my wants, and whose name I had learned
was George, came into the burlap room in a state of evident
excitement and said: “We’re going back to rest, sir.”
I did not know exactly what “back to rest” really meant, but I judged
from George’s sparkling eyes that it was something very good.
“That’s good news,” I said. But one had to be a soldier of the line to
realize what good news it really was. One must be actually in the
trenches when the word comes to comprehend fully what those
words “back to rest” mean.
“We’re going back to rest, chummy,” somebody says, and the word is
relayed quickly down the front line trench. And tired-faced lads,
many of them with faint, dark rings around their eyes, smile broadly
as they stand half-crouching in the muddy trench. Onward the glad
tidings go, whispered or uttered in low voices: “Out to rest, Bo; the
relief’s coming in tonight at half-past ten. Hooray!” But the “hooray”
does not express adequately the feelings of the speaker. It must do,
however, as a loud cheer is not permitted in the front line trench.
When it is dark, the relief comes in very quietly and takes over the
different posts; then, as quietly, the lads go down the support
trenches till they slope up to the great wide road that seems so
spacious and airy after the deep, narrow trench they have been
standing in for days. On they go, past long rows of broken trees that
once were majestic, full-leafed elms, then through masses of ruined
buildings and broken stone walls, with here and there a small
corrugated iron hut or shack, built just lately. At times, not very far
away, a long yellow flash, followed by a thundering report, tells them
that our heavies are at work.
Somebody begins to whistle, “There’s a long, long trail a-winding,” or
“Over There,” then others catch the lilt, and in a few seconds
hundreds are whistling to the swinging, sweeping thud of marching
feet. When they get a little farther on their way, the whistling ceases
and a song is struck up, though not too loudly. Above them are the
silent stars peacefully shining. Away behind them shrapnel bursts
savagely and sprinkles its death-bearing message. But that is far
behind, and now they are going out—out to rest!
Perhaps they march all through the night, carrying their equipment
and their heavy packs on their backs, and as the dawn comes, they
notice at every cross-road a great cross, and nailed to the cross the
figure of the Crucified—white, blood-streaked, the thorn-crowned
head bent in the agony of suffering, the face livid with pain and
misery. And many a lad under his weight looks up. He understands it
all much better now than when he first came to the front. Some
breathe a little prayer. They are going out to rest—but they will be
coming back again!
They continue their march till the morning sunlight begins to brighten
all the land and the roar of the guns has become but a faint distant
rumble, then, perhaps, they sit on the roadside, or along the edge of
a field, the grass of which looks so fresh and green after the rolling,
shell-torn No Man’s Land they have been looking over for days,
where never a blade of grass could be seen; only the grey shell-
pitted earth, with here and there a line of white chalk which made
one think of a white-capped, angry sea. Birds begin to sing in field
and green wood, and from many field kitchens and little red fires built
on the roadside comes the odor of frying bacon.
Some of the lads take off their packs and go to sleep on the
roadside, their faces grey with the dust from marching feet. Much
traffic goes by—khaki motor lorries, general service wagons,
dispatch riders on motorcycles. Then from the distance come the
strains of a military march played by a brass band that is
approaching; it may be “Colonel Bogey” that they play, or “Sons of
the Brave,” etc. It is the band of the battalion coming to meet the lads
and play them back to rest.
When every one has eaten his bread and bacon and has finished his
pint of hot tea, they fall in, feeling much refreshed. Then there is a
rumble from the big drum and a rattle from the smaller ones and the
inspiring music of a military march breaks on the air. The lads
straighten momentarily under their packs, and there is a new swing
to their tired feet. Perhaps they pass through many fields lined with
tall elms. Perhaps they pass many French peasants, old and young,
going to work in the fields, who smile pleasantly. They may go
through a quiet little village or two till they come to a more flourishing
one in which is a large chateau. Then the band, which for the last
fifteen minutes has given place to a few buglers and drums, strikes
up the battalion’s own march and the order comes ringing down the
line, “March to attention.” Then the tired lads know that they are
coming into rest billets.
The organization in “rest” is done very quickly. One battalion takes
over from another, and in a very short time enamel signs are hung
out of billets which tell where are the different officers and orderly
rooms. If there is a curé in the village, and if it so happens that the
Catholic chaplain of the brigade is quartered with the battalion that
has come to rest here, a little sign hangs from the curé’s gate,
bearing the words “R. C. Chaplain,” for the soldiers’ priest is nearly
always billeted with the parish priest of the village; and on the church
door a paper is tacked giving the hours of Mass, confession, etc.
Sometimes there is no curé in the village; perhaps he has been
called to join the soldiers of France; perhaps at one time the village
has been heavily shelled and he has followed his people. In this
case, often it is necessary to renovate the little shell-torn church, but
this is quickly done. And in the morning, after Mass has been said, a
tiny lamp burns in the church which tells the soldiers that the Master
has come and is calling them.
At twelve o’clock the soldiers’ work for the day, when they are out in
rest, usually finishes, and they receive any papers and magazines
that may have come to them from friends across the sea. These are
very welcome arrivals, and so are the boxes of good things that
sometimes come from home. Then, as the lads sit under trees, or in
front of tents, or in low hay lofts to eat their dinner, papers are
opened and those who have received boxes or parcels from home
pass around candies, cake, etc., to those who have not, and so a
very pleasant hour passes.
The afternoon is usually given over to games and athletic sports. If
different troops happen to be quartered together in the same village
the competition between the two becomes very interesting. Perhaps
a baseball game is arranged between American and Canadian lads,
while English lads look on, it must be admitted, with irritation. They
cannot understand why one side should shout such things at the
other; why they should try to rattle the pitcher. To them it seems quite
abusive, and judging from their talk, they are disgusted. “Call that a
gaime,” one will say, “when one side keeps on ’ollerin’ at the blighter
bowlin’ that ball, so’s ’e caunt throw well?” “Call that sport?” “Call that
fair ply?” “I carn’t see where the fair ply comes hin when they tike
such bloomin’ hunderanded wys o’ tryin’ to win.” His mate agrees
with him, and presently they move off to some other scene of
amusement. Meanwhile, little French boys who have come to watch
the baseball game go racing about the field, imitating some of the
plays in the game which is so strange to them, and as they go sliding
to some imaginary home-plate, one can hear such expressions as
“Safe!” and “Hat a-boy.”
It was early in the morning when we left Chateau de la Haie, for we
were not under observation and it was not necessary to move by
night. We assembled on one of the squares near a long, tree-fringed
avenue which was one of the approaches to the chateau. For some
time before we fell in I heard from all quarters strange, unearthly
noises, and in every direction I turned I saw, at quite a distance from
each other, kilted figures walking up and down bearing their wide-
branched bag-pipes, each one emitting the weirdest wails
imaginable; they were the pipers of the Sixteenth pipe band tuning
up. However, when we started off the sound was quite different, for
the pipes and kettle-drums make merry marching music. I know of
no other music that can make tired men march so briskly and with