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 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.

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may be noted herein).

Notices

Practitioners and researchers must always rely on their own experience and knowledge in
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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:
"she may be dead, but you did not kill her. No one would kill Mary
Legs. Killing Mary Legs would be like killing the sun and the stars and
the sky, and even if a man could kill these things he would not do so,
and neither would he kill Mary Legs."
"I did not kill her on purpose," he introduced himself and told the King
about the Fly by Night's encounter with the Lambda-Xi field, of how
he had locked Saint Annabelle Leigh in the starboard storeroom to
die. "If I had not been so selfish," he concluded, "she would still be
alive today."
The King looked at him pityingly. "And now your hands are bloodied,
and you must seek her ghost."
"Yes," said Drake. "Now I must seek her ghost—and destroy it."
The King shook his head. "You may seek it all you want, and you may
even find it. But you will never destroy it, Nathaniel Drake. It will
destroy you. Knowing this, I will help you find it. Come with me."

He spoke a few words into an intercom at his elbow, then came

around the bar and led the way down a spiral staircase into a
subterranean room. Their entry brought vein-like ceiling lights into
luminescence, and the room turned out to be a large hall. Cushioned
chairs were arranged in rows on either side of a narrow ramp that
protruded from a velvet-curtained stage, and to the right of the stage,
a chromium piano stood.
"It is fitting that I tell you about her here," King Tutankhamen said, "for
this is where she danced. Come, we will take the best seats in the
house."
Drake followed him down the aisle to the juncture of stage and ramp.
The King seated him in the chair nearest the juncture and took the
adjacent chair for himself. Leaning back, he said, "Now I will begin.
"It was over three galactic years ago when she first walked into my
establishment. The tourists had not entirely forsaken Worldwellost in
those days, and I was still enjoying prosperity. The bar was bright and
bustling, but I saw her nevertheless the minute she stepped upon the
premises. Thin, she was, and pale, and I thought at first that she was
sick. When she sat down at the table by the door, I went immediately
over to her side.
"'Wine, would you like?' I asked, knowing as I do the revivifying
qualities of the grape. But she shook her head. 'No,' she said, 'I want
work.' 'But what can you do?' I asked. 'I can take off my clothes,' she
replied. 'Is there something else I need to know?' Looking at her more
closely, I saw that indeed there was nothing else she needed to
know; nevertheless, there is an art of sorts to bumps and grinds, and
this I told her. 'You have other girls who can show me the rudiments,'
she said. 'After that, it will be up to me.' 'What is your name?' I asked
then. 'Mary Legs,' she answered. 'It is not my real name, however,
and you will have to pay me in cash.' I took one more look at her, and
hired her on the spot.
"It developed that she had no aptitude for bumps and grinds. It also
developed that she did not need to have. The first time she danced,
only a dozen men sat here in this room and watched her. The second
time she danced, two dozen sat here. The next time she danced, the
room was packed, the bar was overflowing, and there was a line of
men waiting in the street. Some girls dance simply by walking. She
was one of them. She had what is called 'poetry of motion', but I think
it was her legs, really, that most men came to see. I will let you judge
for yourself. Incidentally, the piano which you will hear accompanying
her was played by me."
King Tutankhamen leaned forward, slid aside a small panel just
beneath the edge of the proscenium, and depressed several
luminescent buttons. Instantly the lights went out, and the velvet
curtains parted. A stereo-screen leaped into bright life, and a moment
later, Mary Legs, nee Annabelle Leigh, appeared upon it. So flawless
was the illusion that it was as though she had stepped upon the
stage.
Perfume reminiscent of the vineyards of Azure infiltrated the room.
Drake found breathing difficult.
She was wearing a standard stripper's outfit that could be removed
piece by piece. Hardly had she "appeared" upon the stage when the
first piece fluttered forth and disappeared. Three more followed in
swift succession. A fifth went just as she stepped, seemingly, out
upon the ramp.
"She was always that way," the King whispered. "I told her that she
should be coy, that she should tease, but she paid no attention. It was
as though she couldn't get her clothes off fast enough."
Drake barely heard him.

Mary Legs was moving down the ramp now, and now another
garment drifted forth and winked out of sight. He saw her breasts.
Chords sounded in the background. A progression of ninths and
elevenths. Her face was glowing; her eyes were slightly turned up.
Glazed.
Drake watched the final garment disappear into the mists of time. She
was down to sandals and cache-sexe now. Her slow walk down the
ramp continued.
There was poetry in the play of light upon her flesh, there was poetry
in her every motion. The flabby pectorals of beauty queens, she knew
not. Here was firmness; depth. Her hair burned with the yellow fires of
fall. An arpeggio like the tinkling of glass chimes leaped up and
formed a brief invisible halo over her head. At the base of the ramp
she went through a series of contemptuous bumps and grinds, then
returned casually the way she had come. Now there was a subtle
difference in her walk. Sweat broke out on Drake's face. His breath
burned in his throat. Eyes turned up, she saw no one, then or now;
knew no one, knew nothing but the moment. Her body writhed
obscenely. Notes fell around her like cool rain. Suddenly Drake
realized that she had not been flaunting her sex to the audience, but
to the worlds.
She began a second series of bumps and grinds. While it lacked
finesse, it was obscene beyond belief, and yet, in another sense, it
was somehow not obscene at all. There was something tantalizingly
familiar about it, so tantalizingly familiar that he could have sworn that
he had seen her dance before. And yet he knew perfectly well that he
had not.
His mind ceased functioning, and he sat there helplessly, a prisoner
of the moment. Presently she began a series of movements, a dance
of sorts that had in it the essence of every orgy known to mankind,
and yet simultaneously possessed a quality that had nothing
whatsoever to do with orgies, a quality that was somehow
transcendent ... and austere. She paused transiently just above him,
and her legs were graceful pillars supporting the splendid temple of
her body and her head was the rising sun, then she stepped back into
the screen, the lights went on, and the curtain closed.

I am a wall, and my breasts like the towers thereof:

Then was I in his eyes as one that found peace.

It was some time before either man spoke. Then Drake said, "I'd like
to buy it."
"The realitape? Why—so you can destroy it?"
"No. How much do you want?"
"You must understand," said the King, "that it is very precious to me,
that—"
"I know," Drake said. "How much?"
"Six hundred Rockefellows."
The amount came perilously close to the figure to which Drake's
capital had dwindled. Nevertheless, he did not haggle, but counted
the hundred-credit notes out. The King removed the realitape from
the proscenium projector, and the exchange was made. "You are
getting a bargain, Mr. Drake," the King said. "For a collector's item
like that, I could get twice six hundred Rockefellows."
"When did she leave here?" Drake asked.
"About a year after she arrived. A big year. I went to her room after
one of her dances and found her gone. Her clothes, everything.... For
all her willingness to exhibit herself, she was never really one of us.
She would never permit any of us to get close to her in any sense of
the word. There was something tragic about her. She said once that
she could not bear children, but I do not think that this had very much
to do with her unhappiness. She was unhappy, you know, although
she was very careful never to let on." The King raised his eyes, and
Drake was dumfounded to see tears in them. "You have told me that
after she left Worldwellost she became a saint. Somehow this does
not surprise me. There is an exceedingly thin line between good and
evil. Most of us manage to walk this line with a greater or lesser
degree of equilibrium, but I think Mary Legs could not walk it at all:
with her, I think it had to be one side or the other. Evil, she found
intolerable after a while, and she ran away, crossing the line to good.
But good, she eventually found intolerable too, and she ran away
again. She told you that she wished to be put down on Iago Iago to
witness a resurrection. This, I do not believe. Real or not, the
resurrection was an excuse for her. I believe that she was searching
for a way of life that would combine the two extremes of good and evil
and that she hoped to find it among the primitive Polysirians. And I
think that she also hoped to find a man who would understand her
and accept her for what she was. Do you think I may be right,
Nathaniel Drake?"
"I don't know," Drake said. Abruptly he stood up. "I'll be on my way
now."
King Tutankhamen touched his arm. "The question which I am about
to ask is an exceedingly delicate one, Nathaniel Drake. I hope you
will not take offense?"
Drake sighed wearily. "Ask it then, and get it over with."
"By any chance, are you of Dutch descent?"
"No," Drake said, and left.

Three of the six months which Pastelsilks, Inc. had given Drake to
sell his cargo had now passed, and his cargo was undiminished by so
much as a single bolt of blue. His capital, on the other hand, was
virtually exhausted. Even Der Fliegende Holländer had never had it
so bad.
Drake had not expected to be able to sell any of the pastelsilk on
Worldwellost, nor, he realized in retrospect, had he expected to be
able to sell any of it on Azure. It was imperative, however, that he sell
it somewhere and sell it soon, for, unredeemed or not, he still
intended to go on living, and in order to go on living he needed a
means by which to make his daily bread, and while a ghost-ship left
much to be desired, it was better than no ship at all. He had known all
along that there was one place in the Sirian Satrapy where the people
were naive enough to barter worthwhile goods for "bolts of blue and
pastel nothingness", and that place was Iago Iago. However, he had
deferred going there for two reasons. The first reason had been his
eagerness to discredit Saint Annabelle Leigh, and the second had
been his fear that fencing the goods he procured on Iago Iago might
get him into trouble with the authorities and lead to the loss of his
pilot's license. But for all his seeming success in blackening the face
of the woman he wanted to hate, he had failed so completely to
evoke the desired emotion that he knew by now that the cause was
hopeless; and in view of the fact that his pilot's license would be
worthless if he lost his ship, the second objection was no longer valid.
It had been in the books all along for him to go to Iago Iago.
He lifted up from Heavenly and found the stars again, and the stars
were good. Madame Gin, he left behind. After turning over the ship to
the automatic pilot, he got out the realitape he had purchased from
King Tutankhamen and fitted it into the girlie realitape projector.
Presidently Mary Legs stepped out of the past. He propped the
stereo-snapshot Penelope had given him against the base of the
chart lamp, then he turned on the intercom. "I have chosen to speak
to you this day of the Potomac Peregrination, of the walking of His
ghost upon the land," said Saint Annabelle Leigh. Mary Legs cast her
final garment into the mists of time and walked lewdly down the ramp.
Perfume reminiscent of the vineyards of Azure permeated the room.
Cancelling out the background music, Drake discovered that her
dance blended with the words Saint Annabelle Leigh was uttering.
No, not Saint Annabelle's words exactly, but the rhythm and the
resonance of her voice. What the one was trying to express, the other
was trying to express also. Look at me, they "said" in unison. I am
lonely and afraid, and full of love. Yes, yes! cried the girl on the hill.
Full of love, full of love, full of love!... And in the cabin, vineyards
blossomed, flowers bloomed; there rose a blue-bright sun, and in its
radiance the boy and the girl walked, the boy Nathaniel and the girl
Annabelle Leigh, and the wind blew and the grass sang and the trees
put their heads together in rustling consultations ... and all the while,
the hull-beams creaked and the grav generator murmured, and the
spectral Fly by Night sped on its way to Iago Iago.
It was fitting that a ghost should fall in love with a ghost.

Iago Iago
Iago Iago is like a massive ball of yarn left lying in the hall of the
universe by some capricious cosmic cat. It is emerald in hue, and
when it is viewed from a great distance its atmosphere lends it a soft
and fuzzy effect. This effect diminishes as the distance decreases,
finally ceases to be a factor, and the planet emerges as a bright
green Christmas-tree ornament hanging upon the star-bedight spruce
of space.
The Polysirians were expecting Nathaniel Drake. They had been
expecting him for many months. "I will arise and come back to you,"
he had said. "I will appear in your sky, and come down to you, and
you will know then that His ghost did truly walk, and that it did not
walk in vain." Nathaniel Drake did not know that they were expecting
him, however, nor did he know that he had said these words.
He brought the Fly by Night down in a grassy meadow, parked it on
extended anti-grav jacks, and drifted down to the ground. He heard
the shouts then, and saw the Polysirians running toward him out of a
nearby forest. He would have re-boarded his ship and closed the lock
behind him, but the tenor of their shouts told him that he had nothing
to fear, and he remained standing in the meadow, tall and gaunt and
ghostly, waiting for them to come up.
They halted a dozen yards away and formed a colorful semicircle.
They wore flowers in their hair, and their sarongs and lap-laps were
made of pastelsilk. The pastelsilk was decades-old. Had another
trader come down out of the heavens in times past and defiled this
virgin ground?
Presently the semicircle parted, and an old woman stepped into the
foregound. Drake saw instantly that she was not a Polysirian. Her
Church of the Emancipation uniform stood out in jarring contrast to
the colorful attire of the natives, but it was not one of the mass-
produced uniforms worn by her compeers in the civilized sections of
the satrapy. It had been spun and cut and sewn by hand, and in its
very simplicity had attained a dignity that its civilized cousins could
never know. Somehow he got the impression that she was wearing it
for the first time.
She began walking toward him through the meadow grass. There
was something tantalizingly familiar about the way she moved;
something nostalgic. The brim of her kepi kept her eyes in shadow,
and he could not see into them. Her cheeks were sere and thin, yet
strangely lovely. She stopped before him and looked up into his face
with eyes into which he still could not see. "The people of Iago Iago
welcome you back, Nathaniel Drake," she said.
The heavens seemed to shimmer; the terrain took on an unreal cast.
The semicircle knelt and bowed its be-flowered heads. "I don't
understand," he said.
"Come with me."

He walked beside her over the meadow, the ranks of the people
parting, and the people falling in behind; over the meadow and
through the park-like forest and down the street of an idyllic village
and up a gentle hill that swelled like a virgin's breast into the sky. The
people began to sing, and the tune was a thrilling one, and the words
were fine and noble.
On top of the hill lay a lonely grave. The old woman halted before it,
and Drake halted beside her. Out of the corner of his eye he saw a
tear flash down her withered cheek. At the head of the grave there
was a large stone marker. The marker was intended for two graves,
and had been placed in such a way that when the second grave was
dug the stone face would be centered behind both.
"Mine eyes have seen the glory of the coming of the Lord;" the
Polysirians sang. "He is trampling out the vintage where the grapes of
wrath are stored; HE hath loosed the fearful lightning of his terrible
swift sword, His truth is marching on."
Nathaniel Drake looked at the marker's stone face. One half of it was
blank. On the other half—the half that overlooked the grave—the
following letters had been inscribed:
SAINT NATHANIEL DRAKE
Drake knew the answer then, and knew what he must do—
What, in a sense, he had done already....
He turned to the old woman standing beside him. "When did I first
come here?" he asked.
"Fifty-two years ago."
"And how old was I when I died?"
"You were eighty-three."
"Why did I become a saint?"
"You never told me, Nathaniel Drake."
Gently, he touched her cheek. She raised her eyes then, and this
time he saw into them—saw the years and the love and the laughter,
the sorrow and the pain. "Were we happy together?" he asked.
"Yes, my darling—thanks to you."
He bent and kissed her upon the forehead. "Good by, Mary Legs," he
said, and turned and walked down the hill.
"Glory, glory hallelujah," the Polysirians sang, as his ship rose up into
the sky. "Glory, glory, hallelujah. Glory, glory, hallelujah, his truth is
marching on."

To what may a warp seepage be likened?

It may be likened to a leak in the roof of a twentieth-century dwelling.
The roofs of twentieth-century dwellings were supported by rafters,
and whenever a leak occurred, the water ran along these rafters and
seeped through the ceiling in unexpected places. While the "rafters"
of man-made spacewarps are of a far more complex nature than the
rafters of such simple dwellings, the basic analogy still holds true: the
spatio-temporal elements that escape from spacewarps such as the
Suez Canal never emerge in the immediate vicinity of the rift.
Even in Nathaniel Drake's day, the Suez Canal techs knew this, but
what they did not know was that such seepages do not pose a threat
to the continuum, but only to whoever or whatever comes into contact
with their foci. Neither did the Suez Canal techs—or anyone else, for
that matter—know that the effect of these foci varies in ratio to the
directness of the contact, and that in the case of partial contact, the
effect upon a human being or an object is seemingly similar to the
hypothetical preliminary effect of a Lambda-Xi bombardment. Hence
it is not surprising that no one, including Drake himself, had tumbled
to the true cause of his "ghosthood": i.e., that he and the major part of
his ship, in coming into partial contact with a focus, had been partially
transmitted into the past. Simultaneously, the rest of the ship—and
Annabelle Leigh—had come into direct contact with the focus and
had been totally transmitted into the past.
Here then was the situation when Drake left Iago Iago:
Part of himself and part of his ship and all of Saint Annabelle Leigh
were suspended in a past moment whose temporal location he knew
to be somewhere in the year 3614 but whose location, although he
knew it to be within displacement-drive range of Iago Iago, he could
only guess at, while the preponderance of himself and the
preponderance of his ship hurtled toward the region of space that
was responsible for his "ghosthood" and whose co-ordinates he had
jotted down in the Fly by Night's log over three months ago. In the
light of the knowledge with which his visit to Iago Iago had endowed
him, he quite naturally assumed that once he and the ship made
direct contact with the force that had partially transmitted them, the
rest of the transmission would automatically take place—as in a
sense it already had. But what Drake did not know, and had no way
of knowing, was that spatio-temporal inconsistencies must be
balanced before they can be eliminated, and that before total
transmission could be effected, his three months-plus sojourn in the
future had to be compensated for by a corresponding sojourn in the
past, the length of said sojourn to be in inverse ratio to the spatio-
temporal distance he would be catapulted. Consequently he was
shocked when, following the Fly by Night's coincidence with the
focus, he emerged, not in the spatio-temporal moment he was
prepared for, but in the war-torn skies of a planet of another era and
another system.
At the instant of emergence, every warning light on the ship began
blinking an angry red, and the scintillometric siren began wailing like
an enfant terrible. Drake's conditioned reflexes superseded his shock
to the extent that he had the anti-fission field activated before the
automatic pilot had finished processing the incoming sensoria.
Although he did not know it at the time, the shield that the ship threw
out cleansed nearly an entire hemisphere of radioactivity and
engulfed half an ocean and a whole continent. All of which brings up
another aspect of time that was undreamed of in Drake's day:
Expansion.

Neanderthal man stood knee-high to a twentieth-century

grasshopper, and the woolly mammoth that he hunted was no longer
than a twentieth-century cicada. The universe expands on a temporal
as well as a spatial basis, and this expansion is cumulative. Over a
period of half a century, the results are negligible, but when millennia
are involved, the results are staggering. Look not to fossils to dispute
this seeming paradox, for fossils are an integral part of the planets
they are interred upon; and do not point with polemic fingers to such
seemingly insuperable obstacles as mass, gravity, and bone tissue,
for the cosmos is run on a co-operative basis, and all things both
great and small co-operate. Nor are there any discrepancies in the
normal order of events. A six-foot man of a past generation is the
equivalent of a six-foot man of a future generation: it is only when you
lift them from their respective eras and place them side by side that
the difference in relative size becomes manifest. Thus, in the eyes of
the inhabitants of the planet he was about to descend upon,
Nathaniel Drake would be a figure of heroic proportions, while his
ship would loom in the heavens like a small moon—
Or a small planet....
Beneath him lay the ruins of a once-magnificent structure. Not far
away from the ruins, a pale river ran, and across the river, a city
burned brightly in the night. Nathaniel Drake knew where he was then
—and when. Looking down upon the ruins, he had an inkling of his
destiny.
What I do now, he thought, has already been done, and I cannot
change it one iota. Therefore, what I do I am destined to do, and I am
here to fulfill my destiny.
He still wore his anti-grav belt. He parked the Fly by Night on
extended jacks, and drifted down to the ground.
Here, cherry trees grew, and the cherry trees were in blossom.
Towering above the pink explosions, Nathaniel Drake knew his heroic
proportions.
He approached the ruins he had seen from above. The noble
columns lay broken; the stately roof had fallen in. The walls,
blasphemed not long ago by the hate-steeped scrawls of
segregationists, were rivened. Was that a marble hand protruding
over there?
A hand. A marble arm. A shattered white-marble leg. Drake knew his
destiny then, and began to dig.
No one saw him, for men had become moles, and cowered in dark
places. Above him in the sky, missiles struck the anti-fission shield
and winked out like gutted glowworms. Interceptors blazed up, then
blazed back down again, and died. The flames of the burning capital
painted the Potomac blood-red.
He continued to dig.
A fallen column lay across the broken marble body. He rolled the
column aside. The noble head lay broken on the floor. He picked it up
with gentle hands and carried it out and laid it on the spring-damp
ground. Piece by piece, he carried the broken statue out, and when
he was sure that not a single fragment remained among the ruins, he
brought his ship down and loaded the pieces into the hold. Lifting, he
set forth for the sea.

Some distance inland from the shores of Chesapeake Bay, he left the
ship and drifted down to the bank of the river and began walking
along the river to the sea. Above him, the automatic pilot held the
ship on the course.
He felt like a giant, Nathaniel Drake did, walking down the Potomac to
the sea, and in this long-ago age a giant he was. But all the while he
walked, he knew that compared to the giant he was impersonating,
he was a pygmy two feet tall.
... and if you cannot believe in the walking of His ghost upon the land
and in His ascension to the stars, then you are as one dead, without
hope, without love, without pity, without kindness, without humanity,
without humility, without sorrow, without pain, without happiness, and
without life ...
"Amen," said Nathaniel Drake.
He came to a village untouched by the destruction around it, and saw
people crawling out of underground shelters. Looking down upon
them, he proclaimed "Lo, I have arisen. Lo, I walk again! Look at Me,
ye peoples of the earth—I have come to emancipate you from your
shackling fears, and I have summoned the Planet of Peace from out
of the immensities of space and time to transport My ghost to the
stars. Lo, I force peace upon you, ye peoples of the earth, and I
command you to remember always this terrible day when you drove
Kindness from your doorsteps and threw wide your portals to
Perdition."
On the shore of Chesapeake Bay he halted, and when the automatic
pilot brought the ship down, he removed the fragments of the statue
from the hold and laid them gently on the beach.... And the Planet of
Peace absorbed His ghost and bore it from the face of the earth.
A moment later, complete transmission occurred.

The cabin was a lonely place. He left it quickly and hurried down the
companionway to the starboard storeroom. The bulkheads no longer
shimmered, and the deck was solid beneath his feet. His
translucence was no more. He opened the storeroom lock and
stepped across the threshold. Mary Legs, nee Annabelle Leigh, was
huddled on the floor. She looked up when she heard his step, and in
her eyes was the dumb and hopeless misery of an animal that is
cornered and does not know what to do.
He raised her gently to her feet. "Next stop, Iago Iago," he said.
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