Teaching Atlas of Abdominal Imaging 1588906566, 9781588906564

Comprehensive review of diseases of the abdomen and pelvis Teaching Atlas of Abdominal Imagingis a case-based reference

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Teaching Atlas of Abdominal Imaging
 1588906566, 9781588906564

Table of contents :
Title Page......Page 2
Copyright......Page 3
Contents
......Page 4
Foreword......Page 9
Preface......Page 10
Acknowledgments......Page 11
CASE 1 Hepatic Hemangioma......Page 12
CASE 2 Focal Nodular Hyperplasia......Page 16
CASE 3 Liver Adenoma......Page 20
CASE 4 Hydatid Disease......Page 25
CASE 5 Pyogenic Liver Abscess......Page 29
CASE 6 Hepatic Venous Malformation......Page 32
CASE 7 Intrahepatic Cholangiocarcinoma......Page 36
CASE 8 Hepatic Lymphoma......Page 40
CASE 9 Liver Metastasis from Primary Pancreatic Cancer......Page 43
CASE 10 Calcifi ed Hepatic Metastases in a Patient with Breast Cancer......Page 46
CASE 11 Hepatocellular Carcinoma......Page 49
CASE 12 Acute Acalculous Cholecystitis......Page 53
CASE 13 Gallbladder Polyp......Page 58
CASE 14 Porcelain Gallbladder......Page 61
CASE 15 Adenomyomatosis of Gallbladder......Page 64
CASE 16 Biliary Ascariasis......Page 67
CASE 17 Gallbladder Carcinoma......Page 70
CASE 18 Choledochocele......Page 73
CASE 19 Mirizzi Syndrome......Page 76
CASE 20 Choledocholithiasis......Page 79
CASE 21 Primary Sclerosing Cholangitis......Page 82
CASE 22 Bile Leak Secondary to Bile Duct Injury......Page 85
CASE 23 Pancreas Divisum......Page 88
CASE 24 Intraductal Papillary Mucinous Neoplasia......Page 90
CASE 25 Pancreatic Lymphangioma......Page 94
CASE 26 Acute Necrotizing Pancreatitis......Page 97
CASE 27 Pancreatic Abscess......Page 100
CASE 28 Autoimmune Pancreatitis......Page 103
CASE 29 Pancreatic Transection......Page 106
CASE 30 Extramedullary Plasmacytoma......Page 109
CASE 31 Microcystic Adenoma (Serous Cystadenoma) of the Pancreas......Page 112
CASE 32 Ductal Adenocarcinoma of the Pancreatic Head......Page 115
CASE 33 Islet Cell Tumor of the Pancreas (Insulinoma)......Page 118
CASE 34 Metastatic Renal Cell Carcinoma to the Pancreas......Page 121
CASE 35 Solid Papillary Epithelial Neoplasm......Page 124
CASE 36 Pancreatic Mucinous Cystadenocarcinoma......Page 128
CASE 37 Primary Pancreatic Lymphoma (Non-Hodgkin Type)......Page 131
CASE 38 Nonfunctioning Neuroendocrine Tumor of the Pancreas......Page 134
CASE 39 Groove Pancreatitis......Page 137
CASE 40 Acinar Cell Carcinoma of the Pancreas......Page 140
CASE 41 Accessory Spleen in the Pancreatic Tail......Page 143
CASE 42 Hemangioma of the Spleen......Page 146
CASE 43 Splenic Sarcoidosis......Page 150
CASE 44 Wandering Spleen......Page 153
CASE 45 Infl ammatory Splenic Pseudotumor......Page 157
CASE 46 Autosplenectomy from Sickle Cell Disease......Page 160
CASE 47 Thorotrast Accumulation in the Liver, Spleen, and Lymph Nodes......Page 163
CASE 48 Splenic Arteriovenous Fistula with Features of Portal Hypertension......Page 166
CASE 49 Secondary Involvement of the Spleen in Lymphoma......Page 168
CASE 50 Septic Emboli Causing Infarcts in the Spleen and Left Kidney......Page 171
CASE 51 Splenosis......Page 174
CASE 52 Autosomal Dominant Polycystic Kidney Disease......Page 177
CASE 53 Renal Angiomyolipoma......Page 180
CASE 54 Lipid-poor Angiomyolipoma......Page 183
CASE 55 Atrophic Right Kidney Secondary to Refl ux Nephropathy......Page 186
CASE 56 Renal Infarct......Page 189
CASE 57 Pyelonephritis of the Right Kidney......Page 192
CASE 58 Oncocytoma......Page 195
CASE 59 Metanephric Adenoma......Page 198
CASE 60 Renal Changes from Lithium Toxicity......Page 201
CASE 61 Localized Cystic Disease of the Kidney......Page 203
CASE 62 Multilocular Cystic Nephroma......Page 206
CASE 63 Von Hippel-Lindau Disease......Page 209
CASE 64 Cystic Renal Cell Carcinoma......Page 212
CASE 65 Renal Abscess......Page 215
CASE 66 Renal Cell Carcinoma......Page 218
CASE 67 Renal Metastases from Primary Lung Adenocarcinoma......Page 222
CASE 68 Lymphoma (Non-Hodgkin Type) Involving the Kidney......Page 225
CASE 69 Retroperitoneal Fibrosis......Page 228
CASE 70 Left Adrenal Cyst......Page 231
CASE 71 Myelolipoma......Page 235
CASE 72 Pheochromocytoma......Page 238
CASE 73 Adrenal Hemorrhage......Page 242
CASE 74 Metastic Renal Cell Carcinoma to the Left Adrenal Gland......Page 245
CASE 75 Adrenocortical Carcinoma......Page 248
CASE 76 Adrenal Ganglioneuroma......Page 251
CASE 77 Abberrant Right Subclavian Artery......Page 254
CASE 78 Gastric Mucosa-associated Lymphoid Tissue Lymphoma......Page 257
CASE 79 Gastric Adenocarcinoma......Page 261
CASE 80 Gastrointestinal Stromal Tumor......Page 265
CASE 81 Organoaxial Gastric Volvulus in a Large Hiatal Hernia......Page 268
CASE 82 Duodenal Diverticulum Arising from the Lateral Wall of the Duodenum......Page 272
CASE 83 Abdominal Wall Hernia......Page 276
CASE 84 Acute Mesenteric Ischemia......Page 281
CASE 85 Infectious Colitis......Page 285
CASE 86 Acute Appendicitis......Page 288
CASE 87 Crohn Disease......Page 292
CASE 88 Intussusception......Page 296
CASE 89 Bowel Pneumatosis with Portal Venous Gas......Page 300
CASE 90 Malignant Mucocele of the Appendix with Pseudomyxoma Peritonei......Page 304
CASE 91 Diverticulosis......Page 307
CASE 92 Sigmoid Colon Adenocarcinoma with Hepatic Metastasis......Page 310
CASE 93 Sigmoid Colonic Polyp......Page 313
CASE 94 Ulcerative Colitis......Page 316
CASE 95 Rectal Adenocarcinoma with Perirectal Extension of Tumor......Page 320
CASE 96 Lymphoma of the Sigmoid Colon......Page 323
CASE 97 Acute Abdominal Attack in Familial Mediterranean Fever......Page 326
CASE 98 Pedunculated Gastric Carcinoid, Type III (Sporadic Subtype)......Page 330
CASE 99 Gastric Fundal Diverticulum......Page 333
CASE 100 Gossypiboma (Textiloma or Retained Surgical Sponge)......Page 336
CASE 101 Spigelian Hernia......Page 339
CASE 102 Subhepatic Abscess Secondary to Dropped Gallstones......Page 341
CASE 103 Dedifferentiated Retroperitoneal Liposarcoma......Page 344
CASE 104 Small Bowel Carcinoid with Mesenteric Metastases......Page 347
CASE 105 Juxtacortical Chondrosarcoma Mimicking a Pelvic Visceral Mass......Page 351
CASE 106 Retroperitoneal Lymphangioma......Page 354
CASE 107 Metastatic Liposarcoma with Pseudocystic Sign......Page 357
CASE 108 Misty Mesentery......Page 360
CASE 109 Small Bowel Obstruction Secondary to Obturator Hernia......Page 362
CASE 110 Multilocular Mesothelial (Peritoneal) Inclusion Cyst......Page 365
CASE 111 Porcelain Appendix Secondary to an Appendiceal Mucocele......Page 368
CASE 112 Radiation Enteritis......Page 371
CASE 113 Retroperitoneal Schwannoma......Page 374
CASE 114 Mechanical Small Bowel Obstruction Secondary to Phytobezoar......Page 377
CASE 115 Perforated Meckel Diverticulum......Page 379
CASE 116 Focal Omental Infarction......Page 383
CASE 117 Anterior Abdominal Wall Desmoid Tumor......Page 387
CASE 118 Dedifferentiated Retroperitoneal Liposarcoma......Page 390
CASE 119 Lumbar Hernia of Grynfeltt......Page 393
CASE 120 Bladder Stone......Page 396
CASE 121 Emphysematous Cystitis......Page 399
CASE 122 Schistosomiasis......Page 402
CASE 123 Urinary Bladder Hernia......Page 405
CASE 124 Lipoma of the Urinary Bladder......Page 408
CASE 125 Transitional Cell Carcinoma......Page 410
CASE 126 Urachal Adenocarcinoma......Page 414
CASE 127 Colovesical Fistula......Page 417
CASE 128 Urethral Diverticulum......Page 420
CASE 129 Adenomyosis......Page 423
CASE 130 Gartner Duct Cyst......Page 427
CASE 131 Leiomyoma......Page 430
CASE 132 Pelvic Infl ammatory Disease with Tubo-ovarian Abscess......Page 435
CASE 133 Polycystic Ovary Syndrome......Page 439
CASE 134 Gestational Trophoblastic Disease......Page 443
CASE 135 Endometrioma (Chocolate Cyst)......Page 447
CASE 136 Bicornuate Uterus......Page 451
CASE 137 Adnexal Torsion Secondary to Ovarian Dermoid......Page 455
CASE 138 Ovarian Mucinous Cystoadenocarcinoma......Page 458
CASE 139 Endometrial Adenocarcinoma......Page 462
CASE 140 Cervical Carcinoma......Page 466
CASE 141 Mature Cystic Teratoma (Dermoid Cyst)......Page 470
CASE 142 Cervical Lymphoma (Large B-Cell, Follicular Type)......Page 473
CASE 143 Undescended Testis (Cryptorchidism)......Page 476
CASE 144 Segmental Testicular Infarct......Page 479
CASE 145 Left Malignant Germ Cell Tumor of the Testis with Metastatic Bulky
Retroperitoneal Adenopathy......Page 482
CASE 146 Left Extratesticular Adenomatoid Tumor......Page 485
CASE 147 Testicular Lymphoma......Page 488
CASE 148 Testicular Microlithiasis with Multifocal Seminoma in the Left Testis......Page 491
CASE 149 Tuberculous Epididymo-Orchitis......Page 494
CASE 150 Prostate Carcinoma with Extracapsular and Seminal Vesicle Extension......Page 497
CASE 151 Penile Fracture......Page 499
CASE 152 Penile Metastases from Primary Prostate Cancer......Page 501
CASE 153 Tubular Ectasia of the Rete Testes......Page 503
CASE 154 Pelvic Arteriovenous Malformation......Page 506
CASE 155 Dedifferentiated Spermatic Cord Liposarcoma......Page 509
APPENDIX 1 64-Slice Protocol for Routine Abdomen and Pelvic CT Scan......Page 512
APPENDIX 2 64-Slice Protocol for Dual-Phase Liver CT Scan......Page 514
APPENDIX 3 64-Slice CT Protocol for Evaluation of Hematuria......Page 517
APPENDIX 4 64-Slice Protocol for Pancreatic CT Scan......Page 519
APPENDIX 5 64-Slice CT Protocol for Evaluation of Adrenal Mass......Page 521
Index......Page 524

Citation preview

Teaching Atlas of Abdominal Imaging Editors Mukesh G. Harisinghani, MD Associate Professor of Radiology; Director, Abdominal MRI, Department of Radiology Division of Abdominal Imaging and Interventional Radiology Massachusetts General Hospital Boston, Massachusetts Peter R. Mueller, MD Professor of Radiology, Department of Radiology Division of Abdominal Imaging and Interventional Radiology Massachusetts General Hospital Boston, Massachusetts Assistant Editor Alejandro M. Heffess, MD Division Chief, Ultrasound Mount Auburn Hospital Department of Radiology Cambridge, Massachusetts

Thieme New York • Stuttgart

Thieme Medical Publishers, Inc. 333 Seventh Avenue New York, NY 10001 Editor: Timothy Y. Hiscock Editorial Assistants: David Price, Dominik Pucek Vice President, Production and Electronic Publishing: Anne T. Vinnicombe Production Editor: Martha L. Wetherill Vice President, International Marketing and Sales: Cornelia Schulze Sales Director: Ross Lumpkin Chief Financial Officer: Peter van Woerden President: Brian D. Scanlan Compositor: Macmillan Solutions Printer: The Maple-Vail Book Manufacturing Group Library of Congress Cataloging-in-Publication Data Teaching atlas of abdominal imaging / editors, Mukesh G. Harisinghani, Peter R. Mueller ; assistant editor, Alejandro M. Heffess. p. ; cm. Includes bibliographical references and index. ISBN 978-1-58890-656-4 1. Abdomen—Imaging—Atlases. I. Harisinghani, Mukesh G. II. Mueller, Peter R. III. Heffess, Alejandro M. [DNLM: 1. Radiography, Abdominal—Atlases. 2. Abdomen—anatomy & histology—Atlases. 3. Abdomen—pathology—Atlases. WI 17 T253 2009] RC944'.T43 2009 617.5'50754—dc22 2008036820 Copyright © 2009 by Thieme Medical Publishers, Inc. This book, including all parts thereof, is legally protected by copyright. Any use, exploitation, or commercialization outside the narrow limits set by copyright legislation, without the publisher’s consent, is illegal and liable to prosecution. This applies in particular to photostat reproduction, copying, mimeographing or duplication of any kind, translating, preparation of microfilms, and electronic data processing and storage. Important note: Medical knowledge is ever-changing. As new research and clinical experience broaden our knowledge, changes in treatment and drug therapy may be required. The authors and editors of the material herein have consulted sources believed to be reliable in their efforts to provide information that is complete and in accord with the standards accepted at the time of publication. However, in view of the possibility of human error by the authors, editors, or publisher of the work herein, or changes in medical knowledge, neither the authors, editors, or publisher, nor any other party who has been involved in the preparation of this work, warrants that the information contained herein is in every respect accurate or complete, and they are not responsible for any errors or omissions or for the results obtained from use of such information. Readers are encouraged to confirm the information contained herein with other sources. For example, readers are advised to check the product information sheet included in the package of each drug they plan to administer to be certain that the information contained in this publication is accurate and that changes have not been made in the recommended dose or in the contraindications for administration. This recommendation is of particular importance in connection with new or infrequently used drugs. Some of the product names, patents, and registered designs referred to in this book are in fact registered trademarks or proprietary names even though specific reference to this fact is not always made in the text. Therefore, the appearance of a name without designation as proprietary is not to be construed as a representation by the publisher that it is in the public domain. Printed in the United States of America 54321 ISBN 978-1-58890-656-4

CONTENTS

Foreword . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xi Preface. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiii Acknowledgments . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . xiv SECTION I Liver CASE 1 Hepatic Hemangioma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 CASE 2 Focal Nodular Hyperplasia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 5 CASE 3 Liver Adenoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 9 CASE 4 Hydatid Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 14 CASE 5 Pyogenic Liver Abscess . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 18 CASE 6 Hepatic Venous Malformation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 21 CASE 7 Intrahepatic Cholangiocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 25 CASE 8 Hepatic Lymphoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 29 CASE 9 Liver Metastasis from Primary Pancreatic Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 32 Calcified Hepatic Metastases in a Patient with Breast Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . 35 CASE 10 CASE 11 Hepatocellular Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 SECTION II Gallbladder and Bile Ducts CASE 12 Acute Acalculous Cholecystitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 13 Gallbladder Polyp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 14 Porcelain Gallbladder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 15 Adenomyomatosis of Gallbladder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 16 Biliary Ascariasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 17 Gallbladder Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 18 Choledochocele . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 19 Mirizzi Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 20 Choledocholithiasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 21 Primary Sclerosing Cholangitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 22 Bile Leak Secondary to Bile Duct Injury . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

42 47 50 53 56 59 62 65 68 71 74

SECTION III Pancreas CASE 23 Pancreas Divisum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 24 Intraductal Papillary Mucinous Neoplasia. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 25 Pancreatic Lymphangioma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 26 Acute Necrotizing Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 27 Pancreatic Abscess . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . CASE 28 Autoimmune Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

77 79 83 86 89 92

v

vi

CONTENTS

CASE 29 CASE 30 CASE 31 CASE 32 CASE 33 CASE 34 CASE 35 CASE 36 CASE 37 CASE 38 CASE 39 CASE 40

Pancreatic Transection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 95 Extramedullary Plasmacytoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 98 Microcystic Adenoma (Serous Cystadenoma) of the Pancreas . . . . . . . . . . . . . . . . . . . . . . . . 101 Ductal Adenocarcinoma of the Pancreatic Head . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 104 Islet Cell Tumor of the Pancreas (Insulinoma) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107 Metastatic Renal Cell Carcinoma to the Pancreas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110 Solid Papillary Epithelial Neoplasm . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113 Pancreatic Mucinous Cystadenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 117 Primary Pancreatic Lymphoma (Non-Hodgkin Type) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 120 Nonfunctioning Neuroendocrine Tumor of the Pancreas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 123 Groove Pancreatitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 126 Acinar Cell Carcinoma of the Pancreas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 129

SECTION IV Spleen CASE 41 Accessory Spleen in the Pancreatic Tail . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 132 CASE 42 Hemangioma of the Spleen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 CASE 43 Splenic Sarcoidosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 139 CASE 44 Wandering Spleen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 142 CASE 45 Inflammatory Splenic Pseudotumor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 146 CASE 46 Autosplenectomy from Sickle Cell Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 149 CASE 47 Thorotrast Accumulation in the Liver, Spleen, and Lymph Nodes . . . . . . . . . . . . . . . . . . . . . 152 CASE 48 Splenic Arteriovenous Fistula with Features of Portal Hypertension . . . . . . . . . . . . . . . . . . . 155 CASE 49 Secondary Involvement of the Spleen in Lymphoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157 CASE 50 Septic Emboli Causing Infarcts in the Spleen and Left Kidney. . . . . . . . . . . . . . . . . . . . . . . . . 160 CASE 51 Splenosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 163 SECTION V Kidneys and Ureters CASE 52 Autosomal Dominant Polycystic Kidney Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 166 CASE 53 Renal Angiomyolipoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 169 CASE 54 Lipid-poor Angiomyolipoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 172 Atrophic Right Kidney Secondary to Reflux Nephropathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175 CASE 55 Renal Infarct . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 178 CASE 56 Pyelonephritis of the Right Kidney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181 CASE 57 CASE 58 Oncocytoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 184 CASE 59 Metanephric Adenoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 187 Renal Changes from Lithium Toxicity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 190 CASE 60 Localized Cystic Disease of the Kidney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 192 CASE 61 Multilocular Cystic Nephroma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195 CASE 62 Von Hippel-Lindau Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198 CASE 63 Cystic Renal Cell Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201 CASE 64 Renal Abscess . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 204 CASE 65 Renal Cell Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 207 CASE 66 Renal Metastases from Primary Lung Adenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211 CASE 67 CASE 68 Lymphoma (Non-Hodgkin Type) Involving the Kidney . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 214 CASE 69 Retroperitoneal Fibrosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 217

CONTENTS

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SECTION VI Adrenal Glands CASE 70 Left Adrenal Cyst . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220 CASE 71 Myelolipoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 224 CASE 72 Pheochromocytoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 227 CASE 73 Adrenal Hemorrhage . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 231 CASE 74 Metastic Renal Cell Carcinoma to the Left Adrenal Gland . . . . . . . . . . . . . . . . . . . . . . . . . . . . 234 CASE 75 Adrenocortical Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 237 CASE 76 Adrenal Ganglioneuroma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 240 SECTION VII GI Tract, Peritoneal Cavity, and Retroperitoneum CASE 77 Abberrant Right Subclavian Artery . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 243 CASE 78 Gastric Mucosa-associated Lymphoid Tissue Lymphoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 246 Gastric Adenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 250 CASE 79 Gastrointestinal Stromal Tumor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 254 CASE 80 Organoaxial Gastric Volvulus in a Large Hiatal Hernia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 257 CASE 81 CASE 82 Duodenal Diverticulum Arising from the Lateral Wall of the Duodenum . . . . . . . . . . . . . . . 261 CASE 83 Abdominal Wall Hernia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 265 Acute Mesenteric Ischemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 270 CASE 84 Infectious Colitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 274 CASE 85 Acute Appendicitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 277 CASE 86 CASE 87 Crohn Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 281 CASE 88 Intussusception. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285 Bowel Pneumatosis with Portal Venous Gas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289 CASE 89 Malignant Mucocele of the Appendix with Pseudomyxoma Peritonei . . . . . . . . . . . . . . . . . . 293 CASE 90 Diverticulosis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 296 CASE 91 CASE 92 Sigmoid Colon Adenocarcinoma with Hepatic Metastasis . . . . . . . . . . . . . . . . . . . . . . . . . . . . 299 CASE 93 Sigmoid Colonic Polyp . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 302 CASE 94 Ulcerative Colitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305 CASE 95 Rectal Adenocarcinoma with Perirectal Extension of Tumor . . . . . . . . . . . . . . . . . . . . . . . . . . 309 CASE 96 Lymphoma of the Sigmoid Colon. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 312 CASE 97 Acute Abdominal Attack in Familial Mediterranean Fever . . . . . . . . . . . . . . . . . . . . . . . . . . . . 315 CASE 98 Pedunculated Gastric Carcinoid, Type III (Sporadic Subtype) . . . . . . . . . . . . . . . . . . . . . . . . . 319 CASE 99 Gastric Fundal Diverticulum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 322 CASE 100 Gossypiboma (Textiloma or Retained Surgical Sponge) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 325 CASE 101 Spigelian Hernia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 328 CASE 102 Subhepatic Abscess Secondary to Dropped Gallstones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 330 CASE 103 Dedifferentiated Retroperitoneal Liposarcoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333 CASE 104 Small Bowel Carcinoid with Mesenteric Metastases . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 336 CASE 105 Juxtacortical Chondrosarcoma Mimicking a Pelvic Visceral Mass . . . . . . . . . . . . . . . . . . . . . . 340 CASE 106 Retroperitoneal Lymphangioma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 343 CASE 107 Metastatic Liposarcoma with Pseudocystic Sign . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 346 CASE 108 Misty Mesentery. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 349 CASE 109 Small Bowel Obstruction Secondary to Obturator Hernia . . . . . . . . . . . . . . . . . . . . . . . . . . . . 351 CASE 110 Multilocular Mesothelial (Peritoneal) Inclusion Cyst. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 354

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CONTENTS

CASE 111 CASE 112 CASE 113 CASE 114 CASE 115 CASE 116 CASE 117 CASE 118 CASE 119

Porcelain Appendix Secondary to an Appendiceal Mucocele . . . . . . . . . . . . . . . . . . . . . . . . . . 357 Radiation Enteritis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 360 Retroperitoneal Schwannoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 363 Mechanical Small Bowel Obstruction Secondary to Phytobezoar. . . . . . . . . . . . . . . . . . . . . . 366 Perforated Meckel Diverticulum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 368 Focal Omental Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 372 Anterior Abdominal Wall Desmoid Tumor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 376 Dedifferentiated Retroperitoneal Liposarcoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 379 Lumbar Hernia of Grynfeltt . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 382

SECTION VIII Bladder CASE 120 Bladder Stone . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 385 CASE 121 Emphysematous Cystitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 388 CASE 122 Schistosomiasis. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 391 CASE 123 Urinary Bladder Hernia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 394 CASE 124 Lipoma of the Urinary Bladder . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 397 CASE 125 Transitional Cell Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 399 CASE 126 Urachal Adenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 403 CASE 127 Colovesical Fistula . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 406 SECTION IX Pelvis (Female Genital Pelvis) CASE 128 Urethral Diverticulum . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 409 CASE 129 Adenomyosis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 412 CASE 130 Gartner Duct Cyst . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 416 CASE 131 Leiomyoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 419 CASE 132 Pelvic Inflammatory Disease with Tubo-ovarian Abscess . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 424 CASE 133 Polycystic Ovary Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 428 CASE 134 Gestational Trophoblastic Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 432 CASE 135 Endometrioma (Chocolate Cyst). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 436 CASE 136 Bicornuate Uterus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 440 CASE 137 Adnexal Torsion Secondary to Ovarian Dermoid . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 444 CASE 138 Ovarian Mucinous Cystoadenocarcinoma. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 447 CASE 139 Endometrial Adenocarcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 451 CASE 140 Cervical Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 455 CASE 141 Mature Cystic Teratoma (Dermoid Cyst) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 459 CASE 142 Cervical Lymphoma (Large B-Cell, Follicular Type) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 462 (Male Genital Pelvis) CASE 143 Undescended Testis (Cryptorchidism) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 465 CASE 144 Segmental Testicular Infarct . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 468 CASE 145 Left Malignant Germ Cell Tumor of the Testis with Metastatic Bulky Retroperitoneal Adenopathy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 471 CASE 146 Left Extratesticular Adenomatoid Tumor . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 474 CASE 147 Testicular Lymphoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 477 CASE 148 Testicular Microlithiasis with Multifocal Seminoma in the Left Testis . . . . . . . . . . . . . . . . . . 480 CASE 149 Tuberculous Epididymo-Orchitis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 483

CONTENTS CASE 150 CASE 151 CASE 152 CASE 153 CASE 154 CASE 155

ix

Prostate Carcinoma with Extracapsular and Seminal Vesicle Extension . . . . . . . . . . . . . . . . 486 Penile Fracture . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 488 Penile Metastases from Primary Prostate Cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 490 Tubular Ectasia of the Rete Testes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 492 Pelvic Arteriovenous Malformation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 495 Dedifferentiated Spermatic Cord Liposarcoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 498

SECTION X Appendixes APPENDIX 1 64-Slice Protocol for Routine Abdomen and Pelvic CT Scan . . . . . . . . . . . . . . . . . . . . . . . . 501 APPENDIX 2 64-Slice Protocol for Dual-Phase Liver CT Scan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 503 APPENDIX 3 64-Slice CT Protocol for Evaluation of Hematuria . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 506 APPENDIX 4 64-Slice Protocol for Pancreatic CT Scan . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 508 APPENDIX 5 64-Slice CT Protocol for Evaluation of Adrenal Mass . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 510

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 513

FOREWORD Thirty years ago, when Dr. Joseph Ferrucci Jr. and I began the concept of radiology rounds, computed tomography was just beginning to be added to our usual imaging armamentarium of plain films, fluoroscopy, and ultrasound. This expansion took both of us daily to different locations in the Department of Radiology at Massachusetts General Hospital, so that it was difficult to conveniently share in each other’s experiences. These late afternoon teaching rounds were begun to be sure we exchanged “pearls” not only with each other but also with residents and fellows. This forum provided the opportunity to see the same patient’s radiologically displayed pathology by more than one technique, thereby providing immediate congruent feedback and potential redundancy, along with unique comparative additional information. It was really the beginning of a practical technique for sorting out what imaging technique best serves a patient’s presenting signs and symptoms, notwithstanding the ability to accurately recognize the abnormalities, so that a concise differential diagnosis could be made. Fast forward to the present world of magnetic resonance, positron emission tomography, and interventional radiology. The appropriate first examination imaging triage has now become rather clear. What remains is the ever-present challenge to precisely diagnose the disease and to decide whether additional imaging/radiologic intervention is necessary. The basis of the latter decision rests on a comprehensive knowledge of the common and esoteric disease processes we daily encounter and their therapeutic solutions. Mastering both imaging and clinical expertise is no trivial task, realistically taking years, if not decades, to accomplish. Teaching Atlas of Abdominal Imaging is a successful effort to reduce that time frame to years rather than decades. Its format is essentially that which we use for discussion in our daily rounds and has found wide acceptance among our residents, fellows, and visiting radiologists. In fact, most of the cases have been selected from those rounds for the quality of imaging and educational potential. In a comprehensive and concise fashion, this image-based case review takes you through the gamut of common (and a few uncommon) disease diagnoses that we abdominal imagers encounter. The findings are the classic ones we would feel remiss in failing to make the likely specific diagnosis. The discussion is meaty but brief enough so that an informed exchange can be had with the referring physician and decisions can be made as to what follows, either radiologically or therapeutically. For those of you who possess the time and/or curiosity for seeking further information, suggested readings are provided. Drs. Harisinghani and Mueller combine an experience of over 50 years of academic, multimodal, cutting-edge abdominal imaging. The Division of Abdominal Imaging and Interventional Radiology at Massachusetts General Hospital is unique in that all of the technologies’ interpretations and their applications to interventional work are undertaken by its members. This diversity of experience is ideally represented in our rounds and transposed to this atlas. You can almost hear Drs. Harisinghani and Mueller conducting the sessions. Not only have they seen it all, but they have taught it all as well. Jack Wittenberg, MD August 2008

xi

PREFACE The idea behind this book really began 30 years ago when the Abdominal Division at Mass General under the auspices of Dr. Joseph Ferrucci Jr and Dr. Jack Wittenberg initiated our “daily rounds” review. These rounds, which meet at the end of every day, give everyone who works in the division a chance to see the interesting cases in areas that they might not have spent covering. Thus, the radiologist assigned to fluoroscopy is able to see the “good” cases from ultrasound or magnetic resonance imaging, and the radiologist assigned to MRI is able to see the “good” cases from computed tomography, ultrasound, and fluoroscopy. It is a win-win situation for all, with everyone benefiting from this arrangement, and many research projects, journal discussions, and teaching points have originated from these daily meetings. We have attempted not only to show some of the interesting cases that have come from these rounds, but also to reproduce, in a written form, the salient teaching points that often come out during the review. Teaching Atlas of Abdominal Imaging, as the table of contents indicates, reviews all areas of abdominal imaging with cases that span the gastrointestinal and genitourinary tract. We tried to cover every organ and anatomical area that we are routinely asked to be “experts” in, on a daily basis. From the liver to the pancreas; from the kidney to the bladder, we hope we have added to your teaching collection and education with good examples and discussions. We want you to enjoy the book as much as we did in putting it together. Mukesh G. Harisinghani, MD Peter R. Mueller, MD August 2008

xiii

ACKNOWLEDGMENTS We would like to acknowledge the following individuals for their valuable contribution to this atlas. • • • • • • • • • • • • • • •

Jack Wittenberg, MD Peter F. Hahn, MD, PhD Stephanie M. Ford, MB, BCh, BAO, MSc, MRCPI, FFR(RCSI) Amol Katkar, MD Elisa Ventura, MD Christine L. Cooley, MD Amy M. Oliveira, MD Tinoosh Zand, MD Leila Khorashadi, MD Nidhi Kacholiya, MD Lejla Aganovic, MD Jerome Pierce, MD Daniel T. Cohen, MD Jonathan Bojarkski, MD Omar Sahagun, MD

xiv

I

Liver

CASE 1 Clinical Presentation A 54-year-old man presents with nonspecific abdominal discomfort.

A

B

Fig. 1.1 Hepatic hemangioma. (A) Contrast-enhanced axial CT image of the liver shows a well-defined hypodense lesion with peripheral, nodular contrast enhancement (arrows) during the portal phase. The density of the nodular enhancement is similar to the density of the opacified aorta. (B) Delayed contrast-enhanced axial CT image of the liver shows irregular fill-in of contrast within the lesion.

Radiologic Findings Contrast-enhanced computed tomography (CT) scan images of the liver show a large hypodense lesion with peripheral nodular enhancement with density of nodules similar to the density of the opacified aorta (Fig. 1.1A); there is centripetal enhancement and retention of contrast on the more delayed series (Fig. 1.1B).

Diagnosis Hepatic hemangioma

Differential Diagnosis •

Liver metastases

Discussion Background Hemangioma is the most common tumor of the liver. The incidence of hemangioma in the general population is reported to be ~20%.

1

2

TEACHING ATLAS OF ABDOMINAL IMAGING

Clinical Findings Typically, hemangiomas are found in middle-aged women and are usually asymptomatic. When large they can cause symptoms secondary to complications.

Complications Large hemangiomas can undergo spontaneous or traumatic rupture. There can be spontaneous bleeding within these lesions. Large hemangiomas can exert mass effect on adjacent structures, resulting in obstruction of hepatic vessels or the biliary tree, or can lead to Kasabach-Merritt syndrome, which is a form of consumptive coagulopathy due to thrombocytopenia. High-output congestive cardiac failure has also been reported related to large lesions. Pedunculated hemangiomas, regardless of size, can torse, leading to thrombosis and necrosis.

Etiology Hemangiomas arise from the endothelial lining of the hepatic blood vessels. They are considered to be congenital in origin. Hemangiomas arising in the liver are invariably of the cavernous pathological subtype.

Imaging Findings •





• •

Hemangiomas do not show any lobar predilection. They can be either solitary or multiple. Calcifications within the lesion are uncommon and typically seen in large lesions, contrary to the cavernous hemangiomas at other sites. On noncontrast CT, hemangiomas most commonly appear hypodense relative to normal liver. On noncontrast magnetic resonance imaging (MRI), hemangiomas appear hypointense on T1weighted and intensely hyperintense on T2-weighted imaging. Contrast enhancement characterizes hemangiomas, and they show peripheral discontinuous nodular enhancement, with or without focal central enhancement during arterial phase of contrast administration, dense globular enhancement isodense to aorta, and delayed fill-in, making the lesion isodense or hyperdense to the liver parenchyma (Figs. 1.2 and 1.3). On angiography, hemangiomas show puddling of contrast material in large vascular spaces and dense, peripheral opacification of vascular lakes, clusters, or lobules. On ultrasound, hemangiomas appear as well-defined, discrete hyperechoic liver lesions with or without peripheral feeding vessels recognized on color Doppler imaging.

Treatment • • •

Giant hemangiomas may require treatment if symptomatic or if complicated. Surgical resection as a treatment option is advocated only in cases of complications, such as rupture, rapid increase in size, and Kasabach-Merritt syndrome. Transcatheter arterial embolization, surgical ligation of feeding vessels, and hepatic irradiation are other treatment options.

Prognosis •

Prognosis depends on the severity of the complications caused by the hemangioma. The majority of hemangiomas are asymptomatic and of no clinical significance.

I LIVER

A

3

B

Fig. 1.2 Hepatic hemangioma. (A) T2-weighted axial MRI of the liver shows two well-defined hyperintense lesions (arrows) in the liver. (B) The lesions (arrows) are hypointense on a T1-weighted image. (C) Gadolinium enhanced axial T1-weighted image of the liver shows a peripheral nodular contrast enhancement (arrows) in the lesions.

C

B

A

Fig. 1.3 Giant hepatic hemangioma. Postcontrast CT images of the liver in a 54-year-old patient with a history of rectal cancer show (A) a large dominant hepatic mass with peripheral contrast enhancement (arrows) with partial fillin during the venous phase and (B) more fill-in during delayed phase imaging. Smaller lesions are also seen in the left lobe of the liver in A.

PE ARL



Typical contrast enhancement characteristics in a liver lesion in the absence of known primary malignancy are strongly suggestive of hemangioma. MRI is best for characterization, given the intensely bright T2 appearance of hemangiomas compared with other hepatic lesions.

4

TEACHING ATLAS OF ABDOMINAL IMAGING

PITFALL



Hemangiomas < 1.5 cm in size can demonstrate homogeneous arterial enhancement rather than peripheral nodular enhancement and can therefore be more difficult to characterize.

Suggested Readings Kim S, Chung JJ, Kim MJ, et al. Atypical inside-out pattern of hepatic hemangiomas. AJR Am J Roentgenol 2000;174(6):1571–1574 Leslie DF, Johnson CD, Johnson CM, et al. Distinction between cavernous hemangiomas of the liver and hepatic metastases on CT: value of contrast enhancement patterns. AJR Am J Roentgenol 1995;164(3):625–629 McFarland EG, Mayo-Smith WW, Saini S, et al. Hepatic hemangiomas and malignant tumors: improved differentiation with heavily T2-weighted conventional spin-echo MR imaging. Radiology 1994;193(1):43–47 Perkins AB, Imam K, Smith WJ, Cronan JJ. Color and power Doppler sonography of liver hemangiomas: a dream unfulfilled? J Clin Ultrasound 2000;28(4):159–165 Quinn SF, Benjamin GG. Hepatic cavernous hemangiomas: simple diagnostic sign with dynamic bolus CT. Radiology 1992;182(2):545–548 Tung GA, Vaccaro JP, Cronan JJ, Rogg JM. Cavernous hemangioma of the liver: pathologic correlation with high-field MR imaging. AJR Am J Roentgenol 1994;162(5):1113–1117 Vilanova JC, Barceló J, Smirniotopoulos JG, et al. Hemangioma from head to toe: MR imaging with pathologic correlation. Radiographics 2004;24:367–385 Vilgrain V, Boulos L, Vullierme MP, et al. Imaging of atypical hemangiomas of the liver with pathologic correlation. Radiographics 2000;20(2):379–397. Vilgrain V, Boulos L, Vullierme MP, Denys A, Terris B, Menu Y. Imaging of atypical hemangiomas of the liver with pathologic correlation. Radiographics 2000;20:379–397

CASE 2 Clinical Presentation A 42-year-old woman presents with upper right quadrant tenderness and hepatomegaly.

Fig. 2.1 Abdominal contrast-enhanced CT scan shows an ill-defined, homogeneously enhancing lesion within the caudate lobe of the liver (arrow) with a hypodense central scar (dashed arrow).

Radiologic Findings Abdominal computed tomography (CT) scan (Fig. 2.1) reveals a poorly defined lesion within the caudate lobe with a low-density central scar. Abdominal magnetic resonance imaging (MRI) (Fig. 2.2) was subsequently performed. The liver mass appears isointense to normal liver parenchyma on T2- and T1-weighted images with a central scar that is T2 hyperintense. Arterial enhancement is noticed within the lesion as well as delayed enhancement of the scar.

Diagnosis Focal nodular hyperplasia (FNH)

Differential Diagnosis • • • • •

Fibrolamellar hepatocellular carcinoma Hepatocellular carcinoma (HCC) Hypervascular liver metastasis Adenoma Hemangioma

Discussion Background FNH is the second most common hepatic benign tumor after hemangioma and is found in 1% of the population (mainly middle-aged women). It is most frequently seen as a solitary lesion even though multiple masses have been described in 20% of patients. Histologically, FNH is characterized by the presence of normal hepatocytes with a malformed biliary draining system. Prompt diagnosis is man-

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Fig. 2.2 Abdominal MRI in the same patient shows the lesion (arrow) to be isointense on (A) T1- and (B) T2weighted images. Also seen is the hyperintense central scar on the T2-weighted image (dashed arrow). (C) On an axial T1 fat-saturated postcontrast image (arterial phase), the lesion (arrow) shows a diffuse homogeneous enhancement only sparing the central scar. (D) On an axial T1 fat-saturated delayed image, the lesion (arrow) becomes isointense to the liver parenchyma, whereas the central scar shows delayed enhancement (dashed arrow in E).

E

datory to distinguish this lesion from malignant hepatic masses such as fibrolamellar carcinoma, HCC, cholangiocarcinoma, and hypervascular metastasis.

Clinical Findings FNH is usually asymptomatic and is almost always an incidental finding.

Complications FNH is a benign lesion with no malignant potential. Rarely described complications include rupture and hemorrhage.

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Fig. 2.3 Abdominal MRI with gadolinium benzyloxypropionictetraacetate (BOPTA) (hepatobiliary contrast agent) in a patient with multiple focal nodular hyperplasia. (A) Precontrast T1-weighted image shows multiple faintly hypointense lesions in the liver. (B) In the arterial phase after contrast, the lesions (arrows) show vivid homogeneous enhancement. (C) Equilibrium phase image shows rapid washout with lesions almost isointense to liver. (D) Delayed (1 hour) image shows retention of contrast with lesions (arrows) appearing hyperintense compared with normal parenchyma.

Etiology The etiology is still uncertain, but recent studies have shown FNH to be the result of a hyperplastic response to abnormal hepatic vasculature.

Imaging Findings FNH is usually found on CT or ultrasound, but MRI is the most accurate modality to characterize it. It is typically a T1 isointense, T2 isointense to slightly hyperintense lesion with a hyperintense central scar on T2 images. Such lesions show diffuse and homogeneous arterial enhancement sparing the central scar, early washout of contrast, and classically delayed enhancement of the central scar. Technetium 99m–labeled sulfur colloid scintigraphy can be helpful in the assessment of equivocal lesions felt to be FNH, as half to two thirds of these lesions show uptake of the radiopharmaceutical. More recently, hepatobiliary MR contrast agents have been used to characterize FNH (Fig. 2.3).

Treatment •

FNH is a benign lesion; therefore, it should be treated conservatively.

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PE ARL



The pattern of enhancement is the most important clue for FNH diagnosis, as the central scar is not always noticed.

PITFALL



FNH can present different radiologic features so that the diagnosis needs histologic proof. Efforts have been undertaken to refine MRI technique to ease radiologic diagnosis.

Suggested Readings Grazioli L, Morana G, Kirchin MA, Schneider G. Accurate differentiation of focal nodular hyperplasia from hepatic adenoma at gadobenate dimeglumine-enhanced MR imaging: prospective study. Radiology 2005;236:166–177 Hussain SM, Terkivatan T, Zondervan PE, et al. Focal nodular hyperplasia: findings at state-of-the-art MR imaging, US, CT, and pathologic analysis. Radiographics 2004;24(1):3–19 Martin DR, Semelka RC. Imaging of benign and malignant focal liver lesions. Magn Reson Imaging Clin N Am 2001;9:785–802 Mortele KJ, Praet M, Van Vlierberghe H, De Hemptinne B, Zou K, Ros PR. Focal nodular hyperplasia of the liver: detection and characterization with plain and dynamic-enhanced MRI. Abdom Imaging 2002;27(6):700–707 Terkivatan T, van den Bos IC, Hussain SM, Wielopolski PA, de Man RA, Ijzermans JN. Focal nodular hyperplasia: lesion characteristics on state-of-the-art MRI including dynamic gadolinium-enhanced and superparamagnetic iron-oxide-uptake sequences in a prospective study. J Magn Reson Imaging 2006;24(4):864–887

CASE 3 Clinical Presentation A 38-year-old woman presents with mild right upper quadrant pain.

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Fig. 3.1 Hepatic adenoma. (A) Gradient echo in-phase T1-weighted image fails to delineate the lesion. (B) On the out-ofphase image, there is signal dropout within the lesion (arrow), indicating the presence of intralesional fat. (C) The lesion is isointense on the T2-weighted image. (D) There is arterial enhancement seen in the lesion (arrow) with gadolinium.

Radiologic Findings Magnetic resonance imaging (MRI) of the liver shows an isointense lesion on T2-weighted image with signal drop on the out-of-phase gradient echo sequence and showing brisk homogenous enhancement on the arterial phase images (Fig. 3.1).

Diagnosis Liver adenoma

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Differential Diagnosis • • • •

Benign hepatic lesions: focal nodular hyperplasia (FNH), hemangioma. Nodular regenerative hyperplasia Hepatocellular carcinoma Metastases (hypervascular)

Discussion Background Hepatic adenomas are uncommon benign neoplasms, mostly occurring in young women with a history of oral contraceptive use. Although typically solitary, multiple hepatic adenomas have been described in patients with glycogen storage disease and adenomatosis (Fig. 3.2); the latter is a distinct pathologic entity defined by the presence of more than 10 hepatic adenomas in patients without known risk factors. Adenomatosis is encountered both in men and women and is more often associated with impaired liver function and hepatic enzyme abnormalities (elevated level of alkaline phosphatase). The histology of hepatic adenomas consists of disorganized cords of hepatocytes without biliary ducts or portal areas. Kupffer cells may be present in small number but are not functional.

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Fig. 3.2 Multiple adenomas in a patient with glycogen storage disease. (A–E) Contrast-enhanced CT images show multiple enhancing adenomas (arrows) within the liver.

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Clinical Findings Adenomas do not typically cause clinical symptoms; some patients may experience right upper quadrant pain or tenderness when these lesions achieve considerable size or hemorrhage.

Complications Adenomas are benign lesions with a small risk of progression to hepatocellular carcinoma; therefore they must be recognized at cross-sectional imaging and periodically followed to exclude malignant degeneration. The risk of spontaneous bleeding and hemoperitoneum is higher for large subcapsular lesions and these patients can present severe acute abdominal pain and signs of shock (hypotension, tachycardia, diaphoresis, etc.) (Fig. 3.3).

Etiology Several studies strongly suggest a causal relationship between liver adenomas and oral contraceptive use; in fact, the risk of developing these neoplasms is directly associated with both the dose and duration of the therapy. Hepatic adenomas have also been described in the setting of anabolic steroid use. Still the precise pathogenesis remains unknown.

Imaging Findings •



Multidetector computed tomography (MDCT) with multiphase acquisition technique is helpful in the assessment of these lesions. Most adenomas typically appear well marginated, rarely calcified and isodense to liver parenchyma before the administration of intravenous contrast material (as they mainly consist of hepatocytes); then they become hyperattenuating on arterial phase and nearly isoattenuating on portal-venous phase and delayed phase. Unenhanced CT scans may add important diagnostic clues as they reveal the presence of hypodense fat or hyperdense blood, possibly with fluid-fluid levels that can be frequently seen within these neoplasms. Calcifications may be found in adenomas in areas of necrosis or old hemorrhage. MR plays an important role in the diagnosis of these neoplasms, as it is able to best characterize them.

Fig. 3.3 Bleeding adenoma in a male patient with a history of steroid abuse. Contrast-enhanced CT shows a large left lobe lesion (arrow) with heterogeneous density consistent with intralesional bleeding.

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Fig. 3.4 Large hepatic adenoma. (A) Gradient echo in-phase T1-weighted image shows a large faintly hyperintense lesion in the right lobe of the liver (arrow). (B) On the out-of-phase image, there is signal dropout within the lesion (arrow), indicating the presence of intralesional fat. (C) The lesion (arrow) is minimally hyperintense to liver on the T2-weighted image. (D) There is arterial enhancement seen in the lesion (arrow) with gadolinium.



Adenomas have a characteristic appearance: on T1-weighted images they can be bright (fat or recent hemorrhage) or partially hypointense in the presence of calcifications, necrotic areas, or old hemorrhage. They may show signal dropout on the out-of-phase gradient echo images owing to fat content. They are usually T2 isointense to slightly hyperintense and demonstrate arterial enhancement and early washout. (Fig. 3.4)

Treatment •

Treatment is controversial: some clinicians have suggested serial radiologic follow up after contraceptive therapy discontinuation whereas others have proposed surgical resection of adenomas to avoid the possibility of malignant degeneration, rupture, or hemorrhage. Hepatic arterial embolization has proved to be extremely effective in case of acute bleeding. Patients with adenomatosis may be eligible for liver transplantation due to the higher risk of malignancy.

Prognosis •

Prognosis is extremely variable: some lesions remain stable, others become smaller after oral contraceptive therapy withdrawal, and others may undergo malignant transformation.

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PE ARL



Hepatic adenomas should be considered in young women presenting with hepatic masses and a known history of oral contraceptive use.

PITFALL



Cross-sectional imaging is not always able to exclude a malignant neoplasm; some lesions may still require a biopsy.

Suggested Readings Basaran C, Karcaaltincaba M, Akata D, et al. Fat-containing lesions of the liver: cross-sectional imaging findings with emphasis on MRI. AJR Am J Roentgenol 2005;184:1103–1110 Casillas VJ, Amendola MA, Gascue A, Pinnar N, Levi JU, Perez JM. Imaging of nontraumatic hemorrhagic hepatic lesions. Radiographics 2000;20:367–378 Grazioli L, Federle MP, Brancatelli G, Ichikawa T, Olivetti L, Blachar A. Hepatic adenomas: imaging and pathologic findings. Radiographics 2001;21:877–894 Grazioli L, Federle MP, Ichikawa T, et al. Liver adenomatosis: clinical, histopathologic, and imaging findings in 15 patients. Radiology 2000;216:395–402 Horton KM, Bluemke DA, Hruban RH, Soyer P, Fishman EK. CT and MR imaging of benign hepatic and biliary tumors. Radiographics 1999;19:431–451 Ichikawa T, Federle MP, Grazioli L, et al. Hepatocellular adenoma: multiphasic CT and histopathologic findings in 25 patients. Radiology 2000;214:861–868 Ruppert-Kohlmayr AJ, Uggowitzer MM, Kugler C, Zebedin D, Schaffler G, Ruppert GS. Focal nodular hyperplasia and hepatocellular adenoma of the liver: differentiation with multiphasic helical CT. AJR Am J Roentgenol 2001;176:1493–1498

CASE 4 Clinical Presentation A 46-year-old man presents with right upper quadrant pain and tenderness.

Fig. 4.1 An axial nonenhanced CT image of the liver shows a well-defined, round-shaped, hypodense lesion in the right lobe with hyperdense internal septa demonstrating a spokewheel pattern.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) image (Fig. 4.1) shows a hypodense, welldefined, round cystic lesion in the liver; thin, mildly enhancing internal septations arranged in a spoke-wheel pattern within the lesion are noted.

Diagnosis Hydatid disease

Differential Diagnosis • • •

Liver cyst Liver abscess (pyogenic, fungal, amebic) Metastases

Discussion Background Hydatid disease is a worldwide parasitic infestation caused by different species of a tapeworm belonging to the genus Echinococcus; this zoonosis, quite uncommon in the United States and northern Europe, is otherwise widely present in the Mediterranean areas, the Middle East, the southern part of South America, Iceland, Africa, Australia, and New Zealand. Hydatid disease occurs in both sexes usually in their 3rd to 5th decade and affects the liver (75%), the lungs (15%), and, less commonly, the brain, kidney, spleen, and bone. Unusual locations (< 1%) include the gastric wall, orbit, heart, mediastinum, and adrenal glands. Hydatid cysts have a unique structure that can almost always be

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easily recognized at cross-sectional imaging. They present three different layers: the outer pericyst, the middle laminated layer, and the inner germinative membrane. Small, round vesicles (daughter vesicles) containing protoscolices are found within the mother cyst firmly attached to the germinative membrane.

Clinical Findings Clinical presentation mostly relies on parasite load, size, and location of the hydatid cysts. Some patients can be completely asymptomatic despite the presence of these lesions; other patients can present with abdominal pain and tenderness, fever, and jaundice due to the mass effect of the cysts in the liver.

Complications Rupture of hydatid cysts represents the most threatening complication; not only can these lesions easily rupture into the biliary tree, but they can spill their antigenic content directly into the host’s bloodstream, causing anaphylaxis or subsequently spreading to the lungs, kidneys, bones, and brain. Exophytic hydatid cysts can grow beyond the liver’s capsule boundaries and rupture into the peritoneal cavity, thoracic cavity (pleural effusion and pulmonary consolidation), and hollow viscera. Portal vein compression and thrombosis are unusual complications and have been reported in cases of hydatid cysts located in the caudate lobe.

Etiology Echinococcosis is a parasitic disease caused by the larval stage of three different species of Echinococcus, the most commonly involved in human hydatidosis being E. granulosus. E. alveolaris, the most virulent species, and E. vogeli account for only a small percentage of cases. The life cycle of these tapeworms involves a permanent host, usually a dog, and an intermediate host; the adult tapeworm inhabits the proximal small bowel of the permanent host and releases its eggs in the feces. Hydatid disease can develop in humans after ingestion of contaminated water and raw vegetables or through contact with dogs. Once in the human bowel, ingested embryos pass through the gastrointestinal wall and settle into the liver via the portal venous system.

Imaging Findings The appearance of hydatid cysts can vary depending on the developmental stage of these lesions. At CT, hydatid cysts, most commonly located in the right lobe, are usually hypodense (water attenuation fluid) with a mildly hyperattenuating peripheral rim even on nonenhanced scans. They can be either unilocular or multilocular, with lower density daughter vesicles located peripherally within the mother cyst. Healing, recently treated lesions typically display peripheral, ring-shaped calcifications of the outer pericyst and can present as slightly higher density due to the rupture of the daughter vesicles and release of scolices within the cyst. Dense, complete calcification of these lesions implies the death of the parasite. Ultrasound still remains the most sensitive imaging technique to detect these lesions and follow them up after treatment. In fact, ultrasound can depict better than CT the inner components of hydatid cysts: the contour appears as a double echogenic lining separated by a hypoechogenic layer, and internal septa are arranged in a typical honeycomb or spoke-wheel pattern. Complete detachment of the endocyst from the outer pericyst is the result of trauma, rupture, or treatment and is commonly described as the water lily sign (a serpentine membrane floating

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within the hydatid fluid). Calcified cysts are surrounded by a cone-shaped acoustic shadow and can be better seen at CT.

Treatment •

Surgical resection is advised but cannot always be safely performed due to the high risk of complications. Some patients can benefit from a CT- or ultrasound-guided percutaneous treatment (known as PAIR: puncture, aspiration, injection, and reaspiration), a recently introduced technique that has been gaining increasing acceptance in the last few years. This approach allows direct injection of an albendazole solution (usually albendazole and hypertonic saline) into the hydatid cysts so that the drug can concentrate within the lesions.

Prognosis •

Prognosis is mostly affected by the accurate selection of the best treatment option for each patient according to the characteristics of the hydatid cysts.

PE ARL



The presence of small, round vesicles peripherally attached to the cystic wall (daughter vesicles) is very helpful in distinguishing hydatid cysts from other infectious hepatic lesions.

PITFALL



The appearance of hydatid cysts depends on their stage of growth; thus, a unilocular cyst (without the typical internal septa or daughter vesicles) can be mistaken for other hepatic lesions more often than for abscesses.

Suggested Readings Abu-Eshy SA. Clinical characteristics, diagnosis and surgical management of hydatid cysts. West Afr J Med 2006;25(2):144–152 Doyle DJ, Hanbidge AE, O’Malley ME. Imaging of hepatic infections. Clin Radiol 2006;61(9):737–748 Kabaalioglu A, Cecken K, Alimoglu E, Apaydin A. Percutaneous imaging-guided treatment of hydatid liver cysts: do long-term results make it a first choice? Eur J Radiol 2006;59(1):65–73 Epub 2006 Mar 2. Marani SA, Canossi GC, Nicoli FA, Alberti GP, Monni SG, Casolo PM. Hydatid disease: MR imaging study. Radiology 1990;175:701–706 Mortelé KJ, Ros PR. Cystic focal liver lesions in the adult: differential CT and MR imaging features. Radiographics 2001;21:895–910 Mortelé KJ, Segatto E, Ros PR. The infected liver: radiologic-pathologic correlation. Radiographics 2004;24:937–955 Paksoy Y, Odey K, Sahin M, Arslan A, Koc O. Percutaneous treatment of liver hydatid cysts: comparison of direct injection of albendazole and hypertonic saline solution. AJR Am J Roentgenol 2005;185(3):727–734

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Pedrosa I, Saíz A, Arrazola J, Ferreirós J, Pedrosa CS. Hydatid disease: radiologic and pathologic features and complications. Radiographics 2000;20:795–817 Taori K, Sanyal R, Rathod J, et al. CT appearances of hydatid disease at various locations. Australas Radiol 2006;50(4):298–305 Yagci G, Ustunsoz B, Kaymakcioglu N, et al. Results of surgical, laparoscopic, and percutaneous treatment for hydatid disease of the liver: 10 years’ experience with 355 patients. World J Surg 2005;29(12):1670–1679

CASE 5 Clinical Presentation A 25-year-old man presents with fever and right upper quadrant pain.

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Fig. 5.1 (A) Utrasound of the abdomen shows a heterogeneous hypoechoic lesion in the right lobe of the liver (arrow). (B) Contrast-enhanced CT in the same patient shows a hypodense lesion with multiple enhancing septa (arrow).

Radiologic Findings Ultrasound of the abdomen (Fig. 5.1A) demonstrates a heterogeneous hypoechoic lesion in the right lobe of the liver with posterior acoustic enhancement. The lesion is hypodense on contrast-enhanced computed tomography (CT) (Fig. 5.1B) with multiple enhancing septa. No other lesions are seen.

Diagnosis Pyogenic liver abscess

Differential Diagnosis • • • • •

Amebic abscess Echinococcal cyst Solitary liver metastasis Hepatocellular carcinoma Biliary cystadenoma/cystadenocarcinoma

Discussion Background Pyogenic hepatic abscesses have become less common due to early recognition and treatment of sepsis related to abdominal inflammatory processes, such as appendicitis and diverticulitis. In fact, no obvious source is identified in many patients with liver abscesses. Most infections are polymicrobial,

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with Escherichia coli the most common cultured bacterium. Abscesses may be solitary or multifocal. Larger collections often contain multiple septa and a surrounding fibrotic rim.

Clinical Findings The clinical manifestations of hepatic abscess are highly variable. Patients may present with high fever, rigors, and severe right-sided abdominal pain or may have clinically occult (“cold”) abscesses that manifest with nonspecific symptoms, such as weight loss and vague abdominal pain. Laboratory abnormalities are also nonspecific but may include slightly elevated total bilirubin and transaminase levels in addition to hypoalbuminemia.

Complications Complications are usually associated with delays or errors in diagnosis, such as when multiple small abscesses are misdiagnosed as hepatic metastases. Other complications may occur at the time of percutaneous drainage or at the time of surgical intervention.

Etiology In general, abscesses may be caused by bacteremia, ascending cholangitis, or superinfection of necrotic tissue, such as primary or metastatic hepatic tumors.

Imaging Findings On ultrasound, small abscesses may be seen as focally hypoechoic with little or no posterior acoustic enhancement. Larger abscesses may be hypoechoic or hyperechoic, or they may appear as large areas of markedly heterogeneous liver echotexture. Gas-containing foci within the abscess may appear hyperechoic and produce dirty shadows. On CT, the abscess is typically hypodense with respect to the background liver and may have a thick rim of fibrous tissue that demonstrates various degrees of enhancement. At magnetic resonance imaging (MRI), pyogenic abscesses have variable signal intensity on T1- and T2-weighted images. However, most lesions have intermediate to high signal intensity on T2-weighted images with perilesional edema. Transient hepatic attenuation or intensity differences can be seen associated with abscesses on CT and MRI, respectively.

Treatment • •



Prompt diagnosis, coupled with percutaneous drainage, has significantly reduced both the mortality rates and the need for surgery. Antibiotic therapy may be the only required treatment for small abscesses. Initial antibiotic regimens should include metronidazole until amebic abscess is ruled out serologically, cover the most common bacterial pathogens, and continue for a minimum of 6 weeks. Larger abscesses require percutaneous catheter drainage with follow-up imaging to ensure resolution. Abscesses > 5 cm may also require surgical drainage for optimal results.

Prognosis •

Generally good, unless the abscess is secondary to an underlying disease, such a primary malignancy

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PE ARL



Posterior acoustic enhancement may be a tip-off on ultrasound that the otherwise nonspecific hepatic lesion is not solid and may be an abscess.

PITFALL



There is imaging overlap in the appearance of hepatic abscesses and necrotic or solid hepatic masses.

Suggested Readings Mendez J, Schiebler ML, Outwater EK, et al. Hepatic abscesses: MR imaging findings. Radiology 1994;190:431–436 Mortelé KJ, Segatto E, Ros PR. The infected liver: radiologic-pathologic correlation. Radiographics 2004;24:937–955

CASE 6 Clinical Presentation A 36-year-old man presents with mild abdominal pain.

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Fig. 6.1 (A–E) Axial contrast-enhanced CT images show an irregular linear, hyperattenuating lesion located peripherally within the liver. The lesions appear in close proximity to hepatic veins and portal venous branches and show similar attenuation as the opacified vessels. These findings are indicative of venous malformation.

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Radiologic Findings Axial contrast-enhanced computed tomography (CT) images (Fig. 6.1) show two different hyperattenuating, irregularly shaped lesions located peripherally within the hepatic parenchyma, in close proximity to the hepatic veins and the branches of the portal vein. These vessels do not taper peripherally as they are supposed to do but appear otherwise quite prominent. There is early opacification of hepatic veins. Both the lesions present the same attenuation of vessels consistent with vascular perfusion anomalies.

Diagnosis Hepatic venous malformation

Differential Diagnosis • • • •

Hepatocellular carcinoma (HCC) Benign hypervascular lesions (adenoma, focal nodular hyperplasia [FNH], hemangioma) Hypervascular metastases (neuroendocrine neoplasms: islet cell tumors, carcinoid; breast carcinoma, renal cell carcinoma) Perfusion anomalies of hepatic parenchyma due to inflammatory changes or arteriovenous fistulas as described after percutaneous catheter procedures (radiofrequency thermal ablation [RFTA], transarterial chemoembolization) or transplantation

Discussion Background The liver benefits from a dual blood supply: the arterial system accounts for 25% of the total amount, and the portal vein provides the remaining 75%. These two systems are not independent but intimately connected by means of transsinusoidal, transvasal, and transplexal routes. As soon as vascular disorders occur, the dual blood supply undergoes hemodynamic changes concerning both volume and direction of the blood flow. Perfusion alterations represent a relatively common cause of pseudolesions at cross-sectional imaging; thus, radiologists should be aware of these vascular disorders when reading liver CT.

Clinical Findings Patients are usually asymptomatic, but some of them can experience right upper quadrand pain, hepatomegaly, and jaundice related to bile duct compression.

Complications Patients with significant liver lesions are at high risk of developing high-output heart failure due to shunting from the hepatic artery to hepatic veins or from portal veins to hepatic veins. Arterioportal shunts can lead to liver arterialization of the portal venous system and therefore to a nodular transformation of the hepatic parenchyma (pseudocirrhosis). Patients can also present portosystemic shunts, causing portal hypertension, gastrointestinal bleeding, ascites, and encephalopathy.

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Etiology Congenital perfusion abnormalities are seen in patients with hereditary hemorrhagic telangiectasia (HHT or Rendu-Osler-Weber syndrome); this autosomal dominant transmitted disease mostly occurs in the subcutaneous tissues, but any site of the body can be affected. In fact, hepatic involvement is not only quite common but also more frequent than previously estimated. Most of the vascular disorders described at cross-sectional imaging are acquired after interventional procedures and abdominal trauma or related to portal vein obstruction (neoplastic invasion or compression) and hepatic vein obstruction (Budd-Chiari syndrome, right-sided heart failure). Vascular malformations have also been noticed in cirrhosis, a major predisposing factor to HCC; the presence of perfusion abnormalities in this group of patients represents a great challenge for radiologists, as these lesions can be mistaken for neoplastic foci of HCC.

Imaging Findings CT is a very useful imaging tool to assess the presence of vascular malformations; triple-pass technique (acquisition of multiple phases of contrast enhancement) and three-dimensional reconstructions of hepatic vessels provide a very accurate depiction of the vascular anatomy of the liver. Besides, if compared with conventional catheter angiography, CT is a safer, noninvasive imaging technique. Perfusion abnormalities are typically seen during arterial phase imaging as transient, hyperattenuating, peripheral, wedge-shaped foci that return isodense to the surrounding hepatic parenchyma on portal venous phase images. This finding is related to the passage of contrast medium from highpressure arterial blood into a low-pressure venous branch before the hepatic parenchyma is enhanced via the portal venous system. Early enhancement of peripheral portal vein branches occurring before portal vein enhancement is also highly suggestive of arteriovenous malformations.

Treatment •

Embolization of the feeding vessels with or without subsequent surgery represents the best therapeutic option for arteriovenous malformations. If this procedure fails to control the disease, liver transplantation is the only possible alternative treatment.

Prognosis •

Poor outcome in patients affected by HHT is associated with pulmonary arteriovenous malformations; long-term hepatic involvement can increase the risk of developing hyperdynamic circulation and consequent right-sided heart failure.

PE ARL



The peripheral location within hepatic parenchyma, the wedge-shaped appearance, and the typical transient arterial enhancement highly suggest the presence of arteriovenous malformations.

PITFALL



Vascular malformations present as transient arterial enhancement as well as hepatocellular carcinoma foci.

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Suggested Readings Buscarini L, Civardi G, Arruzzoli S, Bossalini G, Piantanida M. Hepatic vascular malformations in hereditary hemorrhagic telangiectasia: imaging findings. AJR Am J Roentgenol 1994;163:1105–1110 Gallego C, Miralles M, Marín C, Muyor P, González G, García-Hidalgo E. Congenital hepatic shunts. Radiographics 2004;24:755–772 Ianora AS, Memeo M, Sabbà C, Cirulli A, Rotondo A, Angelelli G. Hereditary hemorrhagic telangiectasia: multi-detector row helical CT assessment of hepatic involvement. Radiology 2004;230:250–259 Lane MJ, Jeffrey RB Jr, Katz DS. Spontaneous intrahepatic vascular shunts. AJR Am J Roentgenol 2000;174:125–131 LuDS, Lin J, Kadell BM. Congenital or idiopathic hepatic vascular malformations: CT findings. AJR Am J Roentgenol 1996;167:1155–1157 Quiroga S, Sebastià C, Pallisa E, Castellà E, Pérez-Lafuente M, Alvarez-Castells A. Improved diagnosis of hepatic perfusion disorders: value of hepatic arterial phase imaging during helical CT. Radiographics 2001;21:65–81 Winter TC III, Nghiem HV, Freeny PC, Hommeyer SC, Mack LA. Hepatic arterial anatomy: demonstration of normal supply and vascular variants with three-dimensional CT angiography. Radiographics 1995;15:771–780 Yakes WF, Luethke JM, Parker SH, et al. Ethanol embolization of vascular malformations. Radiographics 1990;10:787–796 Yu JS, Kim KW, Jeong MG, Lee JT, Yoo HS. Nontumorous hepatic arterial-portal venous shunts: MR imaging findings. Radiology 2000;217:750–756 Yu JS, Kim KW, Sung KB, Lee JT, Yoo HS. Small arterial-portal venous shunts: a cause of pseudolesions at hepatic imaging. Radiology 1997;203:737–742

CASE 7 Clinical Presentation A 68-year-old man presents with jaundice, weight loss, and anorexia.

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Fig. 7.1 (A–E) Contrast-enhanced CT image of liver parenchyma reveals an extensive, ill-defined, hypodense mass located within segment IVa with a mild peripheral, rimlike enhancement. The lesion is also associated with dilatation of the left intrahepatic biliary ducts.

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Radiologic Findings Axial contrast-enhanced computed tomography (CT) images (Fig. 7.1) show an irregularly shaped, low-attenuation mass within the left lobe of the liver with a peripheral, rimlike enhancement. Note the associated dilatation of the left peripheral intrahepatic ducts.

Diagnosis Intrahepatic cholangiocarcinoma

Differential Diagnosis • • • • •

Benign biliary tumors: papilloma, adenoma Benign diseases of the biliary system: cholangitis, primary sclerosing cholangitis Hepatocellular carcinoma Unusual primary malignant tumors: embryonal sarcoma, neuroendocrine carcinoma Metastases

Discussion Background Cholangiocarcinoma is a highly malignant tumor of the biliary duct system and represents nowadays the second most common hepatobiliary malignancy. Its incidence is increasing worldwide, but it is higher in Asian countries (especially in Japan), where this neoplasm is commonly related to longstanding inflammation of the bile ducts due to chronic parasitic infestation. Although cholangiocarcinoma may occur in patients with a history of chronic biliary tree disease (primitive sclerosing cholangitis, chronic choledocolithiasis, parasitic biliary infestation, etc.), most of the cases arise in patients without any known predisposition. Cholangiocarcinoma can be classified according to the site of origin as intrahepatic or extrahepatic and can be further classified as either peripheral or hilar. Hilar cholangiocarcinoma, also known as Klatskin tumor, is the most frequent and arises from the confluence of the left and right common bile ducts. Although Klatskin neoplasms have been previously included in the group of intrahepatic cholangiocarcinomas, their clinical and radiologic features resemble more those of extrahepatic cholangiocarcinomas. A further classification based on the growth pattern identifies three different categories of cholangiocarcinoma: exophytic (mass forming), infiltrating (periductal), and polypoid (intraductal). At histology these neoplasms are almost always well to moderately differentiated tubular adenocarcinomas, and their growth within the biliary system is often associated with a diffuse desmoplastic reaction (fibrosis); squamous cell or mucoepidermoid carcinomas, signet ring carcinomas, and papillary adenocarcinomas represent rare histologic variants.

Clinical Findings Clinical presentation is related to tumor anatomical location. Patients with hilar or distal extrahepatic neoplasms usually present with signs and symptoms of obstruction (pruritus and jaundice). Intrahepatic cholangiocarcinomas do not typically cause obstructive symptoms and are therefore

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discovered in an advanced stage; this group of patients may experience anorexia, weight loss, and upper quadrant pain.

Complications Patients with cholangiocarcinoma associated with severe biliary obstruction may develop infection of the biliary tree and secondary biliary cirrhosis (< 20% of cases). All the other complications are usually the result of surgical and interventional procedures.

Etiology Several studies show a causal relationship between cholangiocarcinoma and chronic biliary tree inflammation; in fact, primitive sclerosing cholangitis, chronic choledocolithiasis, recurrent pyogenic cholangitis, biliary papillomatosis, Caroli disease, and parasitic biliary infestation (more frequently caused by Opisthorchis viverrini, O. sinensis, and Ascaris lumbricoides) represent all major predisposing factors for cholangiocarcinoma. Chronic hepatitis C virus (HCV) infection is considered a risk factor, as HCV core protein has been identified in cholangiocarcinoma samples. Recently, molecular studies have been performed to understand the different molecular pathways leading to cholangiocarcinogenesis.

Imaging Findings Cholangiocarcinomas present a wide spectrum of radiologic findings according to their different anatomical localization and growth pattern. At CT, mass-forming intrahepatic cholangiocarcinomas (Fig. 7.1) have been described as irregular, low-attenuation masses within the hepatic parenchyma; after intravenous injection of contrast material, they typically show a thin, minimal, rimlike enhancement during the arterial and portal venous phases with a progressive centripetal enhancement in the delayed phase (this finding is mostly due to the presence of a fibrotic component). Other findings include capsular retraction, dilatation, and irregular thickening of the peripheral intrahepatic ducts; in the advanced stage, CT is very helpful in assessing vascular encasement (portal vein and hepatic arteries), distant metastases, and regional lymphadenopathy. Magnetic resonance imaging (MRI) allows an accurate evaluation of bile duct malignancies. At MRI, intrahepatic cholangiocarcinomas appear hypointense on T1-weighted images and hyperintense on T2-weighted images, with a typical central hypointensity corresponding to fibrotic tissue. On dynamic MR images, these tumors present a mild peripheral enhancement with progressive centripetal filling of contrast material. Magnetic resonance cholangiopancreatography (MRCP) is extremely helpful, as it has a very high sensitivity in differentiating benign from malignant biliary tree abnormalities.

Treatment •



Complete surgical resection represents the only curative therapeutic option; nonetheless, only a small percentage of patients are eligible for surgery at the time of diagnosis. Several neoadjuvant therapies, such as chemotherapy, radiation, and photodynamic therapy, have been studied, but none of these have shown a clear benefit. Patients with unresectable neoplasms and biliary obstruction are candidates for palliative therapy aimed at relieving symptoms and improving the quality of life. Endoscopic and percutaneous biliary stenting represent the most common procedures performed in this group of patients.

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Prognosis •

Prognosis is extremely poor for patients with unresectable disease who are eligible only for palliative stent placement.

PE ARL



The early peripheral enhancement followed by the central delayed filling of contrast material represents the most typical radiologic feature of cholangiocarcinomas.

PITFALL



Benign biliary diseases as described above may present radiologic findings similar to those of infiltrative cholangiocarcinoma. Clinical history should always be carefully considered.

Suggested Readings Acalovschi M. Cholangiocarcinoma: risk factors, diagnosis and management. Rom J Intern Med 2004;42(1):41–58 Feydy A, Vilgrain V, Denys A, et al. Helical CT assessment in hilar cholangiocarcinoma: correlation with surgical and pathologic findings. AJR Am J Roentgenol 1999;172:73–77 Han JK, Choi BI, Kim AY, et al. Cholangiocarcinoma: pictorial essay of CT and cholangiographic findings. Radiographics 2002;22(1):173–187 Keogan MT, Seabourn JT, Paulson EK, McDermott VG, Delong DM, Nelson RC. Contrast-enhanced CT of intrahepatic and hilar cholangiocarcinoma: delay time for optimal imaging. AJR Am J Roentgenol 1997;169:1493–1499 Lee WJ, Lim HK, Jang KM, et al. Radiologic spectrum of cholangiocarcinoma: emphasis on unusual manifestations and differential diagnoses. Radiographics 2001;21:S97–S116 Loyer EM, Chin H, DuBrow RA, David CL, Eftekhari F, Charnsangavej C. Hepatocellular carcinoma and intrahepatic peripheral cholangiocarcinoma: enhancement patterns with quadruple phase helical CT—a comparative study. Radiology 1999;212:866–875 Maetani Y, Itoh K, Watanabe C, et al. MR imaging of intrahepatic cholangiocarcinoma with pathologic correlation. AJR Am J Roentgenol 2001;176:1499–1507 Malhi H, Gores GJ. Cholangiocarcinoma: modern advances in understanding a deadly old disease. J Hepatol 2006;45(6):856–867 Park MS, Kim TK, Kim KW, et al. Differentiation of extrahepatic bile duct cholangiocarcinoma from benign stricture: findings at MRCP versus ERCP. Radiology 2004;233:234–240 Patel T. Cholangiocarcinoma. Nat Clin Pract Gastroenterol Hepatol 2006;3(1):33–42 Slattery JM, Sahani DV. What is the current state-of-the-art imaging for detection and staging of cholangiocarcinoma? Oncologist 2006;11(8):913–922 Soyer P, Bluemke D, Reichle R, et al. Imaging of intrahepatic cholangiocarcinoma: 1. Peripheral cholangiocarcinoma. AJR Am J Roentgenol 1995;165:1427–1431 Soyer P, Bluemke D, Reichle R, et al. Imaging of intrahepatic cholangiocarcinoma: 2. Hilar cholangiocarcinoma. AJR Am J Roentgenol 1995;165:1433–1436

CASE 8 Clinical Presentation A 57-year-old man presents with abdominal pain, anorexia, and weight loss.

Fig. 8.1 Axial contrast-enhanced CT scan show a large, lobulated, hypodense lesion centered in the right lobe of the liver with heterogeneous enhancement. There is no biliary dilatation. No calcification or internal septa are noticed within the lesion.

Radiologic Findings An axial contrast-enhanced computed tomography (CT) image (Fig. 8.1) shows within the right lobe of the liver a large, hypodense markedly lobulated lesion with a mildly enhancing peripheral wall; the surrounding liver parenchyma appears slightly hypodense probably due to the presence of edema. There is no vessel displacement or biliary tree dilatation.

Diagnosis Hepatic lymphoma

Differential Diagnosis • • •

Metastases (hypovascular) Hepatocellular carcinoma Liver abscess (pyogenic, parasitic, or fungal infection)

Discussion Background Secondary hepatic involvement is often described in patients affected by non-Hodgkin and Hodgkin lymphoma, whereas a primary liver lymphoma is a very rare malignancy that has been increasingly reported in patients with chronic hepatitis C virus (HCV) infection. The most common histology of these lesions is non-Hodgkin B cell lymphoma, usually the diffuse large cell type.

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Clinical Findings Patients usually experience abdominal pain and tenderness, anorexia, weight loss, and night sweating.

Complications Complications are commonly related to the size and location of the lymphoma: prominent or multiple liver lesions can cause biliary tree obstruction and jaundice. Moreover, these lesions occasionally bleed, and patients may experience signs of acute abdominal pain.

Etiology Primary hepatic lymphoma is seen in Caucasian, middle-aged males affected by acquired immunodeficiency syndrome (more than half of the reported cases) or chronic liver diseases. Recent studies have suggested the possible role of HCV infection in the pathogenesis of diffuse large B cell lymphoma.

Imaging Findings Primary hepatic lymphoma can present different CT features and is therefore difficult to detect at cross-sectional imaging. Lymphoma commonly appears as a solitary, hypodense (hypovascular) lesion barely distinguishable from metastatic disease or a hepatocellular carcinoma. Some of these lesions can also display a mildly enhancing peripheral rim. The size of the lymphoma can vary from a few millimeters to several centimeters; calcifications are hardly ever described within these lesions unless patients have undergone prior radiotherapy. Multiple liver lesions are also seen in patients affected by hepatic primary lymphoma, but again, these findings are not pathognomonic. Diffuse infiltration of the liver probably represents the most difficult finding to detect at CT, as lymphomatous lesions have the same density of the surrounding liver parenchyma and therefore cannot be easily distinguished. The presence of pathologic lymphadenopathy can suggest the diagnosis of a hematologic malignancy.

Treatment •

Patients are treated with chemotherapy or a multimodality approach (surgery, chemotherapy, or radiotherapy).

Prognosis •

The prognosis is variable. Patients treated with early aggressive combination chemotherapy usually have a more favorable outcome.

PE ARL



Hepatic lymphoma should always be considered in the differential diagnosis of liver lesions, especially in patients with liver disease or acquired immunodeficiency.

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PITFALL



Hepatic lymphoma does not present typical imaging features and thus can be easily mistaken for other lesions that more commonly affect liver parenchyma.

Suggested Readings Coenegrachts K, Vanbeckevoort D, Deraedt K, Van Steenbergen W. MRI findings in primary nonHodgkin’s lymphoma of the liver. JBR-BTR 2005;88(1):17–19 Fishman EK, Kuhlman JE, Jones RJ. CT of lymphoma: spectrum of disease. Radiographics 1991;11:647– 669 Fukuya T, Honda H, Murata S, et al. MRI of primary lymphoma of the liver. J Comput Assist Tomogr 1993;17(4):596–598 Gazelle GS, Lee MJ, Hahn PF, Goldberg MA, Rafaat N, Mueller PR. US, CT, and MRI of primary and secondary liver lymphoma. J Comput Assist Tomogr 1994;18:412–415 McDermott RS, Maher MM, Dunleavy K, O’Keane CJ, Stack JP, Carney DP. Unusual presentations of lymphoma: case 2. Non-Hodgkin’s lymphoma presenting as liver disease. J Clin Oncol 2002;20(7):1943– 1946 Mohan C, Alurkar SS, Sharma OP, Advani SH. Primary liver lymphoma: a diagnostic dilemma. AJR Am J Roentgenol 1991;157:413 Rizzi EB, Schinina V, Cristofaro M, David V, Bibbolino C. Non-Hodgkin’s lymphoma of the liver in patients with AIDS: sonographic, CT, and MRI findings. J Clin Ultrasound 2001;29:125–129

CASE 9 Clinical Presentation A 71-year-old man presents with abdominal pain, anorexia, and weight loss over the last few months.

A

B

Fig. 9.1 (A) An axial contrast-enhanced CT scan shows a small hypoattenuating lesion in the right lobe of the liver (arrow). There is biliary ductal dilatation. (B) Axial image at a lower level shows a hypodense primary pancreatic neoplasm (arrow).

Radiologic Findings An axial contrast-enhanced computed tomography (CT) scan (Fig. 9.1) shows a small hypoattenuating lesion in the right lobe of the liver. There is biliary ductal dilatation accompanied by a hypodense mass in the pancreatic head.

Diagnosis Liver metastasis from primary pancreatic cancer

Differential Diagnosis • • •

Liver cysts Liver abscess Hepatocellular carcinoma

Discussion Background The liver represents the most common organ affected by metastatic disease. Gastrointestinal (GI) malignancies, especially colorectal carcinoma, and other primary tumors (more often breast, lung, and pancreas carcinoma and melanoma) can easily spread to the liver parenchyma.

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Clinical Findings Liver metastases are usually not clinically significant.

Complications Prominent multiple metastases can cause obstruction of the biliary system and therefore jaundice. Hemoperitoneum caused by spontaneous rupture of hepatic metastases is uncommon but has been reported in patients with lung carcinoma, renal cell carcinoma, and melanoma.

Etiology Hepatic involvement in liver metastases is probably related to the unique anatomy of the endothelial lining: fenestrated end vessels (sinusoids) serve as an open connection with the extracellular space (space of Disse) and thus make the liver more susceptible to metastatic disease. Moreover, experimental data show that the liver hosts a considerable amount of humoral factors that can support tumoral cell growth. The main pathway used by neoplastic cells to seed liver parenchyma is the portal venous system, whereas neoplastic emboli have rarely been noticed within the hepatic artery.

Imaging Findings Liver metastases can mimic almost every kind of hepatic lesion; at CT, their features depend on the primary origin of the tumors: metastases from GI malignancies (usually colon carcinoma) often appear as solitary, hypodense, peripherally enhancing lesions. Several primary tumors, including melanoma, renal cell carcinoma, neuroendocrine tumors, and thyroid carcinoma, are known to cause hypervascular, hyperattenuating lesions. Moreover, liver metastases, regardless of their site of origin, can present different features after treatment (both chemotherapy and radiation therapy). Previously hypervascular lesions can appear hypodense for the presence of areas of cystic or necrotic degeneration, whereas hypodense lesions may undergo fibrotic changes and appear densely hyperattenuating on delayed images. Radiation therapy frequently causes a complete calcification of liver metastases, so that they may resemble granulomas or healed hydatid cysts. CT, ultrasound, and magnetic resonance imaging (MRI) are all sensitive and specific techniques widely performed to assess metastatic disease and to follow it up. Recent studies have reported that 18F-fluorodeoxyglucose positron emission tomography (FDG PET) can also be used for the detection of liver metastases, especially from GI tract tumors; this technique may be particularly useful in patients with increasing carcinoembryonic antigen (CEA) levels but normal imaging studies.

Treatment •

Radiofrequency thermal ablation (RFTA) has been increasingly approved as an alternative therapeutic option to surgery in select patient populations. This percutaneous procedure is more successfully performed in patients with unresectable liver lesions from colorectal carcinoma and provides in these patients longer survival if compared with chemotherapy alone. Nonetheless, RFTA requires advanced skills and must be performed only by highly trained staff. Possible complications include abdominal infection, bleeding, and injury to the biliary system.



Chemotherapy remains the only option in cases of metastatic disease.

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Prognosis •

Patients with metastatic liver disease usually have a poor prognosis; nonetheless, solitary liver lesions (especially colorectal liver metastases) have been successfully treated, extending patients’ survival rates.

PE ARL



CT protocol in patients with hypervascular metastatic lesions must include an arterial phase of acquisition. Radiologists should be informed of patients’ clinical history and treatment.

PITFALL



Metastatic lesions can present a wide range of different imaging features.

Suggested Readings Baker ME, Pelley R. Hepatic metastases: basic principles and implications for radiologists. Radiology 1995;197:329–337 Bipat S, van Leeuwen MS, Comans EF, et al. Colorectal liver metastases: CT, MR imaging, and PET for diagnosis—meta-analysis. Radiology 2005;237(1):123–131 Blake SP, Weisinger K, Atkins MB, Raptopoulos V. Liver metastases from melanoma: detection with multiphasic contrast-enhanced CT. Radiology 1999;213:92–96 Bluemke DA, Paulson EK, Choti MA, DeSena S, Clavien PA. Detection of hepatic lesions in candidates for surgery: comparison of ferumoxides-enhanced MR imaging and dual-phase helical CT. AJR Am J Roentgenol 2000;175:1653–1658 Kinkel K, Lu Y, Both M, Warren RS, Thoeni RF. Detection of hepatic metastases from cancers of the gastrointestinal tract by using noninvasive imaging methods (US, CT, MR imaging, PET): a metaanalysis. Radiology 2002;224:748–756 Raptopoulos VD, Blake SP, Weisinger K, Atkins MB, Keogan MT, Kruskal JB. Multiphase contrastenhanced helical CT of liver metastases from renal cell carcinoma. Eur Radiol 2001;11(12):2504– 2509 Rhim H, Goldberg SN, Dodd GD III, et al. Essential techniques for successful radio-frequency thermal ablation of malignant hepatic tumors. Radiographics 2001;21:S17–S39 Soyer P, Poccard M, Boudiaf M, et al. Detection of hypovascular hepatic metastases at triple-phase helical CT: sensitivity of phases and comparison with surgical and histopathologic findings. Radiology 2004;231:413–420 Valls C, Andia E, Sanchez A, Guma A, Serrano T. Hyperenhancing focal liver lesions: differential diagnosis with helical CT. AJR Am J Roentgenol 1999;173:605–611 Van Erkel AR, Pijl ME, van den Berg-Huysmans AA, Wasser MN, van de Velde CJ, Bloem JL. Hepatic metastases in patients with colorectal cancer: relationship between size of metastases, standard of reference, and detection rates. Radiology 2002;224:404–409 Ward J, Robinson PJ, Guthrie JA, et al. Liver metastases in candidates for hepatic resection: comparison of helical CT and gadolinium- and SPIO-enhanced MR imaging. Radiology 2005;237:170–180

CASE 10 Clinical Presentation A 56-year-old woman presents with abdominal pain.

B

A

Fig. 10.1 (A) Ultrasound image shows multiple hyperechoic foci in the liver. (B) Axial non-contrast-enhanced CT demonstrates multiple calcified lesions within the liver (arrow). In addition, calcified lymph nodes are seen in the peripancreatic and retroperitoneal location (dashed arrows).

Radiologic Findings An ultrasound image shows multiple hyperechoic foci in the liver (Fig. 10.1). Axial non-contrastenhanced computed tomography (CT) demonstrates multiple calcified lesions within the liver. In addition, calcified lymph nodes are seen in the peripancreatic and retroperitoneal location.

Diagnosis Calcified hepatic metastases in a patient with breast cancer

Differential Diagnosis • • • • • • •

Hepatocellular carcinoma or adenoma Granulomatous disease Echinococcal cysts Multiple calcified hemangiomas Treated lymphoma Treated metastases Peliosis hepatis

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Discussion Background The liver is a common site of metastatic disease. Calcified metastases can occur from many primary sites, but they are particularly common with mucinous adenocarcinoma of the colon, adenocarcinoma of the stomach, adenocarcinoma of the breast, and neuroendocrine tumors of the pancreas. Less commonly, soft tissue sarcomas, osteosarcoma, and medullary thyroid cancer metastases may calcify. In children, neuroblastoma is the most common metastasis to contain calcifications.

Clinical Findings The diagnosis of liver metastases in patients at high risk is straightforward. An enlarged or tender liver on physical examination or abnormal alkaline phosphatase and transaminases point to liver metastases in the proper clinical context. Multiple lesions are the rule, but single metastases may be seen. It may be impossible to distinguish metastatic liver disease from multicentric hepatocellular carcinoma in patients without a known primary tumor. The diagnosis should be confirmed histologically by percutaneous liver biopsy if treatment will be changed on the basis of the biopsy results.

Complications Most complications in patients with hepatic metastases occur as a result of surgery or chemotherapy. In addition, complications may occur during diagnostic evaluation, especially when percutaneous biopsy is required. Hepatic metastases may become superinfected or may be a cause of pain. Finally, certain lesions may cause focal or diffuse biliary dilatation that predisposes the patient to life-threatening infections, such as cholangitis.

Etiology Some tumors, such as mucin-secreting tumors of the ovary and colon, calcify due to inherent tumor characteristics. In other cases, the tumor calcification is the sequela of treatment.

Imaging Findings • • •

The imaging findings are often nonspecific. Ultrasound demonstrates single or multiple lesions. Calcified metastases will appear echogenic on ultrasound and may shadow. Calcified lesions are best seen on non-contrast-enhanced CT, where they appear hyperdense with respect to the background liver.

Treatment •

In certain settings, metastases may be surgically resected or treated by means of ablation techniques. Imaging plays a vital role in the diagnosis of liver metastases and in the assessment of the response to treatment. However, most cancers are considered inoperable when liver metastases are found. In these cases, the only available treatment includes systemic chemotherapy.

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Prognosis •

The prognosis varies depending on the type of primary lesion and the number of hepatic metastases.

PE ARL



Without treatment, calcified hepatic metastases most commonly suggest mucinous adenocarcinomas of the gastrointestinal tract, breast, or ovary.

PITFALL



If solitary, calcified hepatic metastases can be confused with infectious etiologies.

Suggested Readings Paley MR, Ros PR. Hepatic calcification. Radiol Clin North Am 1998;36:391–398 Stoupis C, Taylor HM, Paley MR, et al. The rocky liver: radiologic-pathologic correlation of calcified hepatic masses. Radiographics 1998;18:675–685

CASE 11 Clinical Presentation A 71-year-old man with long-standing cirrhosis and chronic hepatitis B presents with general malaise, weight loss, and increased serum levels of alpha fetoprotein.

Fig. 11.1 Arterial phase CT image shows multiple arterially enhancing lesions (arrows) within the hepatic parenchyma.

Radiologic Findings Arterial phase computed tomography (CT) image (Fig. 11.1) shows multiple arterially enhancing lesions within the hepatic parenchyma.

Diagnosis Hepatocellular carcinoma (HCC)

Differential Diagnosis • • • • • •

Benign and dysplastic regenerative nodule (cirrhosis) Benign nodular hyperplasia Arteriovenous shunts (transient hepatic attenuation differences) Adenoma Metastases Hemangioma

Discussion Background HCC represents the most common hepatic primary malignancy, mostly occurring in the elderly population (6th–7th decade) and earlier in patients with underlying hepatic disease. In the United States, the prevalence of HCC has been increasing in the last few years and is currently estimated at 4 cases per 100,000 (0.2–0.8%). Worldwide, this neoplasm is more common

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(in particular in Asia and Africa) and is usually associated with either chronic hepatitis B and C or aflatoxin exposure.

Clinical Findings Early HCC is a silent, completely asymptomatic lesion. Patients with advanced stage disease may experience abdominal pain, general malaise, and fever. The aggressive form of HCC as seen in highincidence countries may present with bleeding, hepatic rupture, and hemoperitoneum. Laboratory test findings may include an increased level of alpha fetoprotein.

Complications HCC is locally invasive and tends to grow within the portal vein system rather than metastasize in a distant organ, typically causing portal vein thrombosis. However, distant metastases have also been described in lung, adrenal glands, lymph nodes, and bone. Invasion of the biliary tree is less common, although large lesions may present with jaundice. HCC may also be associated with paraneoplastic syndromes, resulting in hypercalcemia, erythrocytosis, hypoglycemia, and hirsutism.

Etiology Several predisposing factors have been identified, including alcoholic cirrhosis, chronic hepatitis B and C, exposure to toxin (aflatoxin, Thorotrast, and oral contraceptive), and metabolic diseases, which usually account for the majority of cases seen in younger patients (galactosemia, glycogen storage disease, congenital biliary atresia, and hemochromatosis).

Imaging Findings Ultrasound often represents the initial imaging modality for the detection of HCC in patients at high risk (cirrhosis, chronic hepatitis). The sonographic appearance is extremely variable: small foci of HCC typically appear hypoechoic, whereas larger lesions may be more heterogeneous. At nonenhanced CT scan, HCC may be either hypodense or hyperdense (fatty infiltration of the liver). At magnetic resonance imaging (MRI), these lesions are usually T2 hyperintense but may exhibit T1 signal hyperintensity due to the presence of blood product, copper, or fat. At dynamic CT and MRI, small foci of HCC usually demonstrate early arterial enhancement with rapid washout in the portal venous phase; conversely, larger lesions often present heterogeneous contrast enhancement in the arterial phase (mosaic pattern) with delayed enhancement of the external capsule in the portal venous phase. Invasion of the portal venous system (Fig. 11.2) and, to a lesser extent, of the hepatic veins (Fig. 11.3) has been frequently described in HCC; the thrombus is hyperdense on nonenhanced CT and appears as a filling defect on enhanced CT. Cavernous transformation results from subacute/chronic portal vein thrombosis and is associated with dilatation of the periportal veins.

Treatment • •

Surgical treatment represents the best therapeutic option but is often precluded by extensive disease and poor hepatic functional reserve. Radiofrequency thermal ablation, percutaneous ethanol injection, and percutaneous microwave coagulation therapy have been increasingly performed as alternative therapeutic options to surgery in select populations.

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B

A

Fig. 11.2 Portal venous thrombus in a patient with hematoma. (A) Arterial phase image shows a linear focus of enhancement (arrow). (B) Postal venous phase image shows a filling defect (arrow) within the portal venous branch corresponding to the arterial enhancement, suggesting tumor thrombus within the portal vein.

Fig. 11.3 Axial contrast-enhanced dynamic fat-suppressed MRI demonstrates a large, round, subcapsular, peripherally enhancing hepatocellular carcinoma (arrow) within the liver parenchyma; a filling defect is also observed within the entire length of the right hepatic vein and is suggestive of thrombosis. The liver presents a diffusely nodular appearance as seen in long-standing cirrhosis. There is a large amount of ascites.

• •

Transcatheter arterial chemoembolization (TACE) is usually performed in patients with multifocal HCC. Liver transplantation is reserved for patients with small HCC lesions and Child-Pugh class C disease.

Prognosis •

Prognosis depends on the size of the tumor and on the hepatic function at the time of the diagnosis. A prompt identification of this tumor is mandatory to improve the overall survival.

PE ARL S

• •

Patients with long-standing hepatic cirrhosis are at higher risk of developing HCC. HCC lesions typically demonstrate an early arterial enhancement with a rapid washout of contrast material in the delayed images.

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PITFALL



Both benign and dysplastic regenerative nodules in cirrhotic patients may simulate HCC, as they usually enhance on arterial phase imaging. Arteriovenous shunts, frequently resulting from interventional procedures (biopsy, TACE, etc.), may also mimic HCC, as they appear as round, arterial enhancing lesions. A small minority of HCC is hypovascular and lacks the typical imaging features of this tumor.

Suggested Readings Baron RL, Oliver JH III, Dodd GD III. Hepatocellular carcinoma: evaluation with biphasic, contrastenhanced, helical CT. Radiology 1996;199(2):505–511 Baron RL, Peterson MS. From the RSNA refresher courses: screening the cirrhotic liver for hepatocellular carcinoma with CT and MR imaging: opportunities and pitfalls. Radiographics 2001;21:S117– S132 Bruix J, Sherman M. Management of hepatocellular carcinoma. Hepatology 2005;42(5):1208–1236 Clark HP, Carson WF, Kavanagh PV, Ho CP, Shen P, Zagoria RJ. Staging and current treatment of hepatocellular carcinoma. Radiographics 2005;25:S3–S23 Fernandez MP, Redvanly RD. Primary hepatic malignant neoplasms. Radiol Clin North Am 1998;36(2):333–348 Gore RM, Levine MS. Textbook of Gastrointestinal Radiology. 2nd ed. Philadephia: WB Saunders Co; 2000 Hussain SM, Zondervan PE, Ijzermans JN, Schalm SW, de Man RA, Krestin GP. Benign versus malignant hepatic nodules: MR imaging findings with pathologic correlation. Radiographics 2002;22:1023– 1039 Ito K, Mitchell DG, Honjo K. Biphasic contrast-enhanced multisection dynamic MR imaging of the liver: potential pitfalls. Radiographics 1997;17(3):693–705 Jeong YY, Yim NY, Kang HK. Hepatocellular carcinoma in the cirrhotic liver with helical CT and MRI: imaging spectrum and pitfalls of cirrhosis-related nodules. AJR Am J Roentgenol 2005;185:1024– 1032 Larcos G, Sorokopud H, Berry G, Farrell GC. Sonographic screening for hepatocellular carcinoma in patients with chronic hepatitis or cirrhosis: an evaluation. AJR Am J Roentgenol 1998;171:433–435 Lim HS, Jeong YY, Kang HK, Kim JK, Park JG. Imaging features of hepatocellular carcinoma after transcatheter arterial chemoembolization and radiofrequency ablation. AJR Am J Roentgenol 2006;187:W341–W349 Mathieu D, Grenier P, Lardé D, Vasile N. Portal vein involvement in hepatocellular carcinoma: dynamic CT features. Radiology 1984;152:127–132 Rossi S, Rosa L, Ravetta V, et al. Contrast-enhanced versus conventional and color Doppler sonography for the detection of thrombosis of the portal and hepatic venous systems. AJR Am J Roentgenol 2006;186:763–773 Takizawa D, Kakizaki S, Sohara N, et al. Hepatocellular carcinoma with portal vein tumor thrombosis: clinical characteristics, prognosis, and patient survival analysis. Dig Dis Sci 2007;52:3290–3295

II Gallbladder and Bile Ducts CASE 12 Clinical Presentation A 45-year-old woman complains of unremitting right upper quadrant pain.

Fig. 12.1 Axial contrast-enhanced CT image showing a distended gallbladder with wall thickening and pericholecystic fat stranding. No gallstones are seen in this case of acalculous cholecystitis.

Radiologic Findings Axial computed tomography (CT) image shows a distended gallbladder with wall thickening and pericholecystic inflammatory fat stranding (Fig. 12.1).

Diagnosis Acute acalculous cholecystitis

Differential Diagnosis • • • •

Peptic ulcer disease Colonic diverticulitis Acute pancreatitis Liver abscess

Discussion Background Cholecystitis is a common complication of gallstones. Although gallstones are more frequently encountered in women, male patients with gallstones are more likely to have cholecystitis than female patients.

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Clinical Findings Most common symptoms are right upper quadrant pain radiating to the back or right scapula (usually brought about by having fatty food), associated with fever, nausea, and vomiting. Patients typically have a history of similar episodes in the past with symptoms resolving after some time.

Complications • • • • • • • • • • •

Gangrenous cholecystitis Gallbladder perforation Empyema Cholangitis Pancreatitis Gallstone ileus Liver abscess Emphysematous cholecystitis Septicemia Cholecystoenteric fistula (Bouveret syndrome; gallstone eroding into the duodenum, causing an obstruction) Chronic calculus cholecystitis

Etiology Cholecystitis is usually the result of an acute obstruction of the gallbladder by calculi (calculus cholecystitis). Acalculus cholecystitis can be seen in enteric fever, diabetes, acquired immunodeficiency syndrome (AIDS), certain vascular diseases, burns, and sepsis; hospitalized fasting patients on total parenteral nutrition and critically ill patients are at risk. Emphysematous cholecystitis is an infection caused by gas-forming organisms and can be seen in older men, people with type 2 diabetes, and immunocompromised patients.

Imaging Findings •



Ultrasound is the most commonly used imaging modality and shows a distended gallbladder with calculi obstructing the cystic duct. The gallbladder wall shows thickening (> 3 mm), edema, and pericholecystic fluid. A discontinuous wall with a collapsed gallbladder suggests gallbladder perforation, which is a surgical emergency. The presence of hyperechoic specks of gas within the gallbladder wall with comet tail and reverberation artifacts indicate emphysematous cholecystitis, where the presence of gas interferes with a complete assessment of the pathology and necessitates use of CT for further evaluation. Sonographically, Murphy sign is tenderness elicited by probe pressure when the gallbladder is directly visualized under the ultrasound probe. A false-negative Murphy sign can be seen in gangrenous cholecystitis (Fig. 12.2). In cases of chronic cholecystitis, ultrasound shows a thickened gallbladder wall with a nondistended gallbladder even after fasting.

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A

B

C

D

Fig. 12.2 (A–D) Axial and coronal images from contrast-enhanced CT show diffuse circumferential wall thickening of the gallbladder in a patient with gangrenous cholecystitis. Note the extension of inflammation to the abdominal wall (arrow).











CT is better for visualizing the common bile duct and assessing contrast enhancement characteristics of associated lesions due to complications (Fig. 12.3). Emphysematous cholecystitis can be better diagnosed and assessed on CT than on ultrasound (Fig. 12.4). Gallstones may not always be visualized on CT if they are of the same density as bile. Magnetic resonance imaging (MRI) in acute cholecystitis is superior to ultrasound in detecting gallbladder neck and cystic duct calculi, which can be missed or overlooked on ultrasound. MR findings of cholecystitis include significant wall thickening and enhancement on contrast administration and transient increased pericholecystic hepatic enhancement during arterial phase imaging, which can also be seen on CT. Combined functional and morphological assessment of the biliary tree can be obtained with heavily T2-weighted MR cholangiography and with manganese-enhanced T1-weighted MR cholangiography. Radioscintigraphy (cholescintigraphy) with hepatobiliary iminodiacetic acid (HIDA) scans provide functional assessment of gallbladder pathologies with fewer false-negative results with the use of morphine and show nonvisualization of tracer in the area of the gallbladder at 60-minute study. The im sign is the presence of radiotracer seen as a rim surrounding the gallbladder at 1-hour study and is present in gangrenous cholecystitis.

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Fig. 12.3 Axial contrast-enhanced CT image of the

Fig. 12.4 Coronal reformatted CT image in a diabetic patient with

gallbladder in a patient with gangrenous cholecystitis shows a distended gallbladder with an irregular discontinuous wall, pericholecystic fat stranding, and fluid collection. Gallstones are not visualized in this section.

right upper quadrant pain shows a collapsed perforated gallbladder and the presence of gas in the gallbladder wall, lumen, and hepatic ducts. This is a case of emphysematous cholecystitis.



Endoscopic retrograde cholangiopancreatography (ERCP) is advantageous in cases of choledocholithiasis where it can be diagnostic as well as therapeutic.

Treatment •

In acute cholecystectomy, conservative treatment is the preferred option with further planned laparoscopic or open cholecystectomy. Emergency cholecystectomy is performed for patients with complications of cholecystitis. In patients who are poor candidates for surgery but who need emergency decompression of the gallbladder, percutaneous imaging-guided cholecystostomy is a better option.

Prognosis •

Uncomplicated cholecystitis has a good prognosis. In complicated cases, especially emphysematous cholecystitis, the prognosis is bad, with higher rates of mortality.

PE ARL



Stone impacted in the cystic duct with a sonographic Murphy sign is indicative of cholecystitis.

PITFALL



Ultrasound is less sensitive for the diagnosis of gallbladder neck and cystic duct stones as well as choledocholithiasis. It also does not give information about the enhancement characteristics of the gallbladder wall and adjacent structures. CT can miss gallstones with a similar density to bile. Magnetic resonance cholangiopancreatography (MRCP) can miss very small gallstones in maximum intensity projection images and can artifactually produce findings of ductal disconnection

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TEACHING ATLAS OF ABDOMINAL IMAGING

or duplication of the ductal system if breath hold sequences are not properly performed. Also, false-positive ductal stenosis can be apparent on MRCP due to artifacts from adjacent metallic clips, coils, or gas.

Suggested Readings Bennett GL, Balthazar EJ. Ultrasound and CT evaluation of emergent gallbladder pathology. Radiol Clin North Am 2003;41:1203–1216 Gill KS, Chapman AH, Weston MJ. The changing face of emphysematous cholecystitis. Br J Radiol 1997;70(838):986–991

CASE 13 Clinical Presentation A 28-year-old woman presents with ill-defined abdominal pain.

Fig. 13.1 Ultrasound image of the gallbladder showing a well-defined, rounded, hyperechoic nonshadowing polyp in the gallbladder lumen.

Radiologic Findings Ultrasond image of the gallbladder shows a well-defined hyperechoic nonshadowing polyp in the gallbladder lumen (Fig. 13.1).

Diagnosis Gallbladder polyp

Differential Diagnosis • •

Adherent gallstone Biliary sludge

Discussion Background Gallbladder polyps can be benign or malignant. The most common type of gallbladder polyp is a cholesterol polyp, which is a benign condition. Other benign causes of polyps include inflammatory polyps, leiomyoma, fibroma, hemangioma, hamartoma, lipoma, and granular cell neoplasm. Adenoma of gallbladder, which is a premalignant condition, may also present as a polyp. The risk of malignancy correlates with the size of the adenoma, with more chances of lesions with size > 1.2 to 1.5

47

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cm being malignant. Malignant polyps seen in the gallbladder include adenocarcinoma, squamous cell carcinoma, anaplastic carcinoma, and angiosarcoma.

Clinical Findings Patients are usually asymptomatic unless associated conditions, such as gallstones, make the condition symptomatic.

Complications • •

Detachment of polyp with obstruction of cystic duct Malignant transformation of adenomatous polyp

Etiology Cholesterol polyps are thought to arise from direct cholesterol deposit from serum cholesterol or bile. They are formed of foamy histiocytes containing cholesterols covered by a single layer of columnar epithelium. Usually cholesterol polyps are associated with cholesterolosis.

Imaging Findings • • •



Ultrasound shows a well-defined, nonshadowing, soft tissue solid structure along the wall, not moving with changes in patient position. Computed tomography (CT) and magnetic resonance imaging (MRI) show contrast enhancement characteristics of the polyp. A benign polyp shows contrast enhancement similar to the gallbladder wall. Lesions showing excessive enhancement warrant further investigation because this type of lesion can be malignant (Fig. 13.2). Imaging findings that should arouse suspicion for malignancy include rapid increase in size, gallbladder wall thickening with changes in surrounding tissues, and intense contrast enhancement.

Treatment •

Polyps that are < 5 mm need no follow-up or treatment. Polyps 5 to 10 mm in size require follow-up every 6 to 12 months. Symptomatic polyps, polyps > 10 mm, and polyps with atypical imaging features need aggressive evaluation and treatment to rule out malignancy.

Prognosis •

The prognosis for gallbladder polyps is excellent with < 1% lesions being malignant. In malignant polyps, the prognosis depends on the stage of disease.

PE ARL



Small hyperchoic lesions that are fixed to the gallbladder wall and do not layer with gravity.

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A

B

Fig. 13.2 (A) Ultrasound image of the gallblad-

C

der in an 18-year-old Caucasian man showing a large hyperechoic soft tissue structure filling the gallbladder lumen. (B) On a Doppler study, the gallbladder lumen showed extensive vascularity. (C) Axial contrast-enhanced CT image in the same patient shows a heterogeneous intensely enhancing structure filling the gallbladder lumen. This structure was found to be a hamartomatous polyp on histopathologic correlation.

PITFALL



It may be difficult to distinguish polyps from adherent stones.

Suggested Readings Csendes A, Burgos AM, Csendes P, Smok G, Rojas J. Late follow-up of polypoid lesions of the gallbladder smaller than 10 mm. Ann Surg 2001;234(5):657–660 Sugiyama M, Xie XY, Atomi Y, Saito M. Differential diagnosis of small polypoid lesions of the gallbladder: the value of endoscopic ultrasonography. Ann Surg 1999;229(4):498–504

CASE 14 Clinical Presentation A middle-aged patient complains of nonspecific abdominal pain.

Fig. 14.1 Axial contrast-enhanced CT image of the gallbladder shows thick, dense, circumferential calcification within the wall of the gallbladder without an associated enhancing mass lesion.

Radiologic Findings An axial contrast-enhanced computed tomography (CT) image of the gallbladder shows thick, dense, circumferential calcification within the wall of the gallbladder without an associated enhancing mass lesion (Fig. 14.1).

Diagnosis Porcelain gallbladder

Differential Diagnosis • • •

Large gallstone Gallbladder carcinoma Emphysematous cholecystitis on ultrasound

Discussion Background Porcelain gallbladder is a rare, usually asymptomatic condition. It is important to diagnose this condition because of the incidence (0–5%) of coexisting adenocarcinoma associated with this condition. It is found in 0.6 to 0.8% of patients with cholecystectomy. It is most commonly seen in the 6th decade of life and mostly in women. Porcelain gallbladder is associated with gallstones in 90 to 95% of cases.

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51

Clinical Findings Patients are usually asymptomatic; however, they may present with symptoms of biliary colic due to 90 to 95% association of this condition with gallstones.

Complications •

Carcinoma (adenocarcinoma or, rarely, squamous or adenosquamous cell carcinoma)

Etiology Chronic inflammation of the gallbladder is supposed to be an etiologic factor. Other factors suggested are impaction of a gallstone in the neck of the gallbladder, causing occlusion of the cystic duct, and cystic artery occlusion, leading to ischemia and calcification of the gallbladder.

Imaging Findings • • •

Two types of gallbladder wall calcifications can be found: continuous calcification in the muscular layer and focal calcifications in the wall of the gallbladder (Fig. 14.2). Plain radiograph shows curvilinear wall calcification in the right upper quadrant. Noncontrast CT clearly shows the wall calcification. Contrast-enhanced examination is useful to assess an associated abnormally enhancing soft tissue mass lesion that can be seen in associated malignancy.

Treatment •

Prophylactic cholecystectomy is the treatment of choice because of the high incidence of association with malignancies.

Prognosis •

The prognosis is good for patients with early detection of the disease. For a delayed diagnosis, the prognosis is bad due to the development of carcinoma.

Fig. 14.2 Axial contrast-enhanced CT image of the gallbladder shows focal discontinuous calcifications within the wall of the gallbladder without an associated enhancing mass lesion.

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PE ARL



Curvilinear, thick, and circumferential calcification of the gallbladder wall is representative of this condition.

PITFALL



Large gallstones, if multiple, can mimic this condition.

Suggested Readings Ashur H, Siegal B, Oland Y, Adam YG. Calcified gallbladder (porcelain gallbladder). Arch Surg 1978; 113(5):594–596 Berk RN, Armbuster TG, Saltzstein SL. Carcinoma in the porcelain gallbladder. Radiology 1973;106(1): 29–31 Oschner SF, Carrera GM. Calcification of the gallbladder (“porcelain gallbladder”). AJR Am J Roentgenol 1963;89:847–853

CASE 15 Clinical Presentation A 45-year-old Caucasian woman presents with recurrent right upper quadrant pain made worse after having fatty food.

Fig. 15.1 Axial contrast-enhanced CT image shows an annular area of narrowing in the gallbladder with dumbbell-shaped compartmentalization. There are associated outpouchings in the gallbladder wall and thickening.

Radiologic Findings An axial contrast-enhanced computed tomography (CT) image shows an annular area of narrowing in the gallbladder with dumbbell-shaped compartmentalization. There are associated outpouchings in the gallbladder wall and thickening (Fig. 15.1).

Diagnosis Adenomyomatosis of gallbladder

Differential Diagnosis • •

Chronic cholecystitis Gallbladder carcinoma

Discussion Background Adenomyomatosis is found in 3% of the cholecystectomy specimens and is associated with thickening of the gallbladder wall with the presence of intramural diverticuli, which may contain bile, biliary sludge, or cholesterol crystals. Adenomyomatosis may be associated with cholesterolosis in some cases.

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Clinical Findings Most patients are asymptomatic; however, some patients present with vague abdominal pain, biliary colic, dyspepsia, bloating, and intolerance to fatty foods. Very rarely patients with adenomyomatosis present with fever and jaundice.

Complications There are no known complications.

Etiology The etiology is unknown; however, it is thought to be due to increased intraluminal pressure. Histologically, adenomyomatosis appears as hyperplastic mucosa of the gallbladder with diverticuli, crypts, or sinus tracts (termed Rokitansky-Aschoff sinuses) extending through the muscular layer.

Imaging Findings •

• •







There are three forms of adenomyomatosis: diffuse/generalized, annular/segmental, and localized. The diffuse form involves the entire gallbladder; the segmental form involves the proximal, middle, or distal third of the gallbladder in a circular/annular fashion; and the localized form involves only part of the gallbladder, most commonly the fundus of the gallbladder. Depending on the type of involvement, imaging appearances vary. Ultrasound is the most commonly used modality for assessment of the gallbladder. It shows the thickened wall of the gallbladder (< 3 mm) with multiple anechoic cystic areas within the wall. The appearance of the Rokitansky-Aschoff sinuses depends on the contents of the gallbladder, with cholesterol crystals producing reverberation artifacts. The segmental or annular form of adenomyomatosis involves the gallbladder in a circumferential fashion and apparent stricture, resulting in a dumbbell-shaped gallbladder with compartmentalization. The localized form of adenomyomatosis results in the appearance of a sessile fundal mass with a central anechoic cystic area with central umbilication (Fig. 15.2). CT and magnetic resonance imaging (MRI) are helpful in differentiating adenomyomatosis from carcinoma. On contrast-enhanced images, normal mucosal enhancement can be differentiated from the marked enhancement of gallbladder carcinoma. On magnetic resonance cholangiopancreatography (MRCP), generalized adenomyomatosis gives a “pearl necklace” sign due to the presence of bile within the Rokitansky-Aschoff sinuses.

Treatment •

Adenomyomatosis alone in an asymptomatic patient can be left alone safely because it is a nonneoplastic condition. If symptomatic and associated with gallstones, cholecystectomy is the treatment of choice.

Prognosis •

The prognosis for adenomyomatosis is good. When patients are symptomatic and do not have gallstones, cholecystectomy may not always alleviate the symptoms because adenomyomatosis may not always be the cause of symptoms.

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B

A

Fig. 15.2 (A) Ultrasound image of the gallbladder shows focal thickening of the fundus of the gallbladder. (B) Contrastenhanced axial CT image in the same patient shows focal thickening of the gallbladder fundus with central nonenhancing hypodensity.

PE ARL



The “pearl necklace” sign on MRCP.

PITFALL



Adenomyomatosis may be difficult to differentiate from focal early tumors.

Suggested Readings Berk RN, van der Vegt JH, Lichtenstein JE. The hyperplastic cholecystoses: cholesterolosis and adenomyomatosis. Radiology 1983;146:593–601 Raghavendra BN, Subramanyam BR, Balthazar EJ, Horii SC, Megibow AJ, Hilton S. Sonography of adenomyomatosis of the gallbladder: radiologic-pathologic correlation. Radiology 1983;146:747–752

CASE 16 Clinical Presentation A young man complains of right upper quadrant pain and jaundice.

B

A

Fig. 16.1 (A) Axial contrast-enhanced CT image shows a dilated common bile duct with a filling defect. (B) Endoscopic retrograde cholangiopancreatography performed subsequently shows multiple linear filling defects with dilatation of the common bile duct.

Radiologic Findings An axial contrast-enhanced computed tomography (CT) image shows a dilated common bile duct with a filling defect. Endoscopic retrograde cholangiopancreatography (ERCP) performed subsequently shows multiple linear filling defects with dilatation of the common bile duct (Fig. 16.1).

Diagnosis Biliary ascariasis

Differential Diagnosis • • •

Biliary stones Biliary hemorrhage Biliary metastases

Discussion Background Infestation with Ascaris lumbricoides (roundworm) is one of the most common helminthic infestations and is highly endemic in developing tropical and subtropical countries.

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57

Clinical Findings Clinical disease is mostly restricted to subjects with heavy worm loads. The manifestations of ascariasis vary and include constitutional symptoms, particularly pulmonary and gastrointestinal complaints. Hepatobiliary and pancreatic ascariasis can cause distinct clinical presentations: biliary colic, acalculous cholecystitis, acute cholangitis, acute pancreatitis, and hepatic abscess.

Complications • • • • • •

Mainly seen due to mechanical obstruction of the bile and pancreatic ducts Biliary colic Acalculous cholecystitis Acute cholangitis Acute pancreatitis Hepatic abscess

Etiology Infection with A. lumbricoides follows ingestion of embryonated eggs. After ingestion, the shells of the embryonated eggs are dissolved by the gastric juice, and the embryos emerge in the duodenum as rhabdoid larvae. The larvae migrate to the cecum and penetrate the surface epithelium of the mucosa. They then enter the veins of the portal system and are carried to the liver. In the liver, larvae move freely in the sinusoids. Some may subsequently pass via the hepatic veins to the heart and lungs. Some larvae may enter the lymphatic system of bowel and are carried via the thoracic duct to the lungs. The larvae break through the capillary wall and enter the alveolar space and the bronchial tree. They ascend the tracheobronchial tree and larynx to the hypopharynx, where they are swallowed. On reaching the small intestine, the larvae attain sexual maturity in 2 to 3 months. The normal habitat for the adult worm is the jejunum. The time from the larval infection to maturity of adult worms is usually 4 months. Ascariasis of the gallbladder, unlike that of the bile duct, is a rare entity. Adult worms live mainly in the jejunum. Their radiologic appearances in the bowel are well known. From there they can move up into the main biliary tract, reaching the intrahepatic ducts and the gallbladder. If they are trapped in the ducts and die, they form a nidus of stones. The high glucoronidase activity of worms and of Escherichia coli deconjugates biliribin and helps to form pigment stones.

Imaging Findings •

Ultrasound has been advocated as a quick and relatively inexpensive modality for suspected biliary ascariasis. The reported sonographic appearances of roundworm are ⴰ Stripe sign: A single, long linear or curved echogenic nonshadowing structure without an inner tube, located within the common bile duct or gallbladder ⴰ Inner-tube sign: A thick, long, linear or curved nonshadowing echogenic stripe containing either a central anechoic tube or a tubular structure with amorphous fragments inside the gallbladder or common bile duct ⴰ Spaghetti sign: Multiple, long, linear, overlapping echogenic structures due to coiling of a single worm or several worms in the common bile duct

58 •





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Other sonographic appearances that have been described in patients with biliary ascariasis include dilatation of the bile duct, gallbladder distension with the edematous wall, and the presence of echogenic sludge within the gallbladder. On CT, the worms will appear as linear areas of increased density associated with dilatation of the biliary ducts and secondary complications, if present. Similarly, on magnetic resonance imaging (MRI), the worms would appear as linear areas of filling defects within high-signal intensity bile on a T2-weighted sequence. ERCP, in addition to providing a diagnostic test, offers a therapeutic option, as it is possible to extract the worm via the papilla.

Treatment •

• •

Several drugs are effective in the treatment of ascariasis. Pyrantel pamoate (a single dose of 11 mg/kg orally, with a maximum dose of 1.0 g), mebendazole (100 mg orally 2 times per day for 3 days), and albendazole (a single dose of 400 mg orally) are drugs of first choice. Treatment with an antihelminthic agent is usually effective in mild cases, and the prognosis is excellent. Endoscopy is successful in the treatment of Ascaris infestation resistant to medical therapy. More severe infection may cause significant morbidity and require surgical intervention. Surgery is important in the management of infestations complicated by biliary or pancreatic strictures and stones or worms in the gallbladder.

Prognosis •

Once treated, the prognosis is usually good.

PE ARL



Roundworm is seen as a linear intraductal filling defect in common bile duct.

PITFALL



When complicated by infection, it may be difficult to make the diagnosis.

Suggested Readings Kamath PS, Joseph DC, Chandran R, et al. Biliary ascariasis: ultrasonography, endoscopic retrograde cholangiopancreatography, and biliary drainage. Gastroenterology. 1986;91:730–732 Khuroo MS, Zargar SA, Mahajan R, et al. Sonographic appearances in biliary ascariasis. Gastroenterology 1987;93:267–272 Schulman A, Loxton AJ, Heydenrych JJ, Abdurahman KE. Sonography diagnosis of biliary ascariasis. AJR Am J Roentgenol 1982;139:485–489

CASE 17 Clinical Presentation A middle-aged woman complains of right upper quadrant pain and jaundice.

A

B

C

D

Fig. 17.1 (A–C) Axial and coronal contrast-enhanced CT images show nodular soft tissue masses in the gallbladder with extraluminal extension of the masses. There are associated ascites and biliary ductal dilatation. (D) Percutaneous image-guided biopsy confirmed the diagnosis of gallbladder adenocarcinoma.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) image shows nodular soft tissue masses in the gallbladder with extraluminal extension of the masses. There are associated ascites and biliary ductal dilatation (Fig. 17.1).

Diagnosis Gallbladder carcinoma

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Differential Diagnosis • • • • •

Chronic cholecystitis Adenomyomatosis Xanthogranulomatous cholecystitis Gallbladder metastases Hepatoma

Discussion Background Gallbladder carcinoma, a highly lethal condition, is the most common type of biliary cancer.

Clinical Findings Most common clinical findings include right upper quadrant pain, weight loss, jaundice, and vomiting. Gallbladder carcinoma is seen more commonly in women. The most common pathologic type is adenocarcinoma (90%), with squamous or anaplastic being less common (10%).

Complications • • • •

Local spread to liver and adjacent organs Lymphatic spread to regional lymph nodes Intraperitoneal spread Perineural invasion

Etiology Risk factors include postmenopausal status, cigarette smoking, gallstones (seen in > 65% of cases of gallbladder carcinoma), porcelain gallbladder (5–60% later develop gallbladder carcinoma), ulcerative colitis, and primary sclerosing cholangitis. The presence of a choledochal cyst, anomalous junction of the pancreaticobiliary ducts, and low insertion of the cystic duct are also associated with a higher incidence.

Imaging Findings There are three common imaging appearances for gallbladder carcinoma: • • •

Mass replacing the gallbladder (most common type of imaging presentation) Focal or diffuse wall thickening Polypoid mass

Ultrasound is useful for detecting the primary tumor as well as adjacent liver invasion. CT and magnetic resonance imaging are more useful for evaluating the extent of the disease, such as direct extension to the liver, periportal and peripancreatic lymphadenopathy, extension to the biliary tree (resulting in biliary obstruction), and hematogenous metastases.

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Treatment •

Cholecystectomy for lesions confined to the gallbladder, with more extensive surgical dissection reserved for advanced disease.

Prognosis •

Very poor prognosis, as most patients present with late disease.

PE ARL



Think gallbladder tumor if a large or ill-defined mass is seen centered in the gallbladder fossa.

PITFALL



The presence of calcification and chronic inflammation makes early detection difficult.

Suggested Readings Levy AD, Murakata LA, Rohrmann CA Jr. Gallbladder carcinoma: radiologic-pathologic correlation. Radiographics 2001;21(2):295–314; questionnaire, 549–555 Mekeel KL, Hemming AW. Surgical management of gallbladder carcinoma: a review. J Gastrointest Surg 2007;11(9):1188–1193

CASE 18 Clinical Presentation A 52-year-old Asian woman complains of vague abdominal pain.

A

B

C

D

Fig. 18.1 (A–D) Axial and coronal contrast-enhanced CT images show mild prominence of the extra- and intrahepatic bile duct. The dilated duct leads to a hypodense dilated distal choledochocele within the duodenum (arrow). 10.1055/978-1-58890-656-4c018

Radiologic Findings Axial and coronal contrast-enhanced computed tomography (CT) image shows mild prominence of the extra- and intrahepatic bile duct. The dilated duct leads to a hypodense dilated distal end within the duodenum (Fig. 18.1).

Diagnosis Choledochocele (type III choledochal cyst; Table 18.1)

Table 18.1 Types of Choledochal Cysts Type

Description

Occurrence (%)

I II III IV V

Solitary extrahepatic cyst Extrahepatic supraduodenal diverticulum Intraduodenal diverticulum (choledochocele) Extrahepatic and intrahepatic dilatation Multiple intrahepatic cysts (Caroli disease)

50 to 70 1 to 3 1 to 4 15 to 33 10–15 mm), irregular thickening of the duct walls, a solid protruding mass in the dilated ducts, and attenuating or calcified intraluminal contents (Fig. 24.2). MRCP can very accurately depict the extent and location of pancreatic duct involvement as well as all the other features of IPMN (Fig. 24.3).

Treatment •

IPMNs have a potential malignancy, but the accurate and precise diagnosis of these tumors at thin-section CT or MRCP has changed the clinical approach. Small IPMNs in asymptomatic patients do not always require surgical removal, but they are followed by periodic imaging surveillance to ensure stability.

Fig. 24.3 Three-dimensional magnetic resonance cholangiopancreatography image shows a T2 hyperintense lesion (arrow) in the region of the head and uncinate process of the pancreas with close association to the main pancreatic duct.

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Prognosis •

Even IPMNs found to be malignant at histologic evaluation can successfully be resected. The prognosis is generally favorable when compared with ductal adenocarcinomas and cystoadenocarcinomas.

PE ARL



IPMNs have specific radiologic features, the most important being the communication with the main pancreatic duct and the hypodense contents due to the presence of mucinous secretion. These findings, together with the absence of peripheral calcifications (typical of mucinous cystoadenomas), are helpful in determining management of these lesions.

PITFALL



IPMNs can be misinterpreted as benign cystic pancreatic lesions in the absence of identification of the communication with the main duct; this can lead to erroneous clinical management.

Suggested Readings Kim YH, Saini S, Sahani DV, Hahn PF, Mueller PR, Auh YH. Imaging diagnosis of cystic pancreatic lesions: pseudocyst versus nonpseudocyst. Radiographics 2005;25(3):671–685 Klimstra DS. Cystic, mucin-producing neoplasms of the pancreas: the distinguishing features of mucinous cystic neoplasms and intraductal papillary mucinous neoplasms. Semin Diagn Pathol 2005;22(4):318–329 Morana G, Guarise A. Cystic tumors of the pancreas. Cancer Imaging 2006;6:60–71 Pilleul F, Rochette A, Partensky C, Scoazec JY, Bernard P, Valette PJ. Preoperative evaluation of intraductal papillary mucinous tumors performed by pancreatic magnetic resonance imaging and correlated with surgical and histopathologic findings. J Magn Reson Imaging 2005;21(3):237–244 Procacci C, Graziani R, Bicego E, et al. Intraductal mucin-producing tumors of the pancreas: imaging findings. Radiology 1996;198:249–257 Sahani DV, Kadavigere R, Blake M, Fernandez-del Castillo C, Lauwers GY, Hahn PF. Intraductal papillary mucinous neoplasm of pancreas: multi-detector row CT with 2D curved reformations—correlation with MRCP. Radiology 2006;238:560–569 Sahani DV, Kadavigere R, Saokar A, Fernandez-del Castillo C, Brugge WR, Hahn PF. Cystic pancreatic lesions: a simple imaging-based classification system for guiding management. Radiographics 2005;25(6):1471–1484 Sohn TA, Yeo CJ, Cameron JL, et al. An updated experience intraductal papillary mucinous neoplasms of the pancreas. Ann Surg 2004;239(6):788–799 Taouli B, Vilgrain V, Vullierme MP, et al. Intraductal papillary mucinous tumors of the pancreas: helical CT with histopathologic correlation. Radiology 2000;217:757–764

CASE 25 Clinical Presentation A 38-year-old woman presents with abdominal pain and epigastric tenderness.

A

B

C

D

Fig. 25.1 (A–D) Images from a contrast-enhanced abdominal CT scan show a large, lobulated, well-defined, hypodense, finely septated mass associated with the pancreatic head and body.

Radiologic Findings Abdominal contrast-enhanced computed tomography (CT) scans (Fig. 25.1) show a large, lobulated, hypodense lesion with multiple thin septations, centered in the upper abdomen, intimately associated with the pancreas. The superior mesenteric artery and vein and the portal vein are patent.

Diagnosis Pancreatic lymphangioma

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Differential Diagnosis • • • • • • • •

Pseudocyst Pancreatic cystic neoplasms: mucinous cystic neoplasms, intraductal papillary mucinous neoplasia (IPMN) Rare pancreatic cystic neoplasms: solid pseudopapillary tumor, acinar cell cystoadenocarcinoma, hemangioma, paraganglioma Solid pancreatic lesion with cystic degeneration: pancreatic adenocarcinoma, cystic islet cell tumor Metastasis Cystic teratoma True epithelial cyst (associated with von Hippel-Lindau disease, autosomal dominant polycystic kidney disease, cystic fibrosis) Lymphocele (if patients have recently undergone surgery)

Discussion Background Lymphangiomas are rare, benign tumors more common in childhood. They are more frequently located in the neck and axillary region but have been described in other sites of the body. In the abdomen, for instance, lymphangiomas usually occur in the mesentery and retroperitoneum; pancreatic involvement is very rare and more commonly described in women.

Clinical Findings These lesions are usually asymptomatic and the finding incidental. A distended abdomen has been noticed on physical examination in cases of very large lesions.

Complications Complications depend on the size and location of these tumors; anemia, hemorrhage, infection, torsion, and rupture have been reported.

Etiology Lymphangiomas are congenital tumors due to lymphatic system malformation and consequent blockage of lymphatic flow. The formation of a lymphatic mass in the pancreas can be related to the abnormal development of the lymphatic system in the dorsal mesoduodenum during the 2nd or 3rd month of gestation.

Imaging Findings •



At contrast-enhanced CT, pancreatic lymphangiomas present as cystic, hypodense, thin-walled, predominantly nonenhancing lesions, usually appearing lobulated and well defined; they do not show any involvement of vascular structures or any communication with pancreatic ducts. The thin walls and septations may show faint enhancement. At magnetic resonance imaging, lymphangiomas are usually nonenhancing T1 hypointense, T2 hyperintense lesions with septations.

III PANCREAS

85

Treatment •

Surgical removal is mandatory in cases of life-threatening complications; as soon as lymphangiomas are proven, radiologic follow-up is suggested, as recurrence is possible.

Prognosis •

These tumors have a good prognosis in the absence of major complications.

PE ARL



Phleboliths are rarely seen in lymphangiomas.

PITFALL



Pancreatic lymphangiomas must be distinguished from malignant neoplasms, such as IPMN and mucinous cystadenoma.

Suggested Readings Brugge WR, Lauwers GY, Sahani DV, Fernandez-del Castillo C, Warshaw AL. Cystic neoplasms of the pancreas. N Engl J Med 2004;351(12):1218–1226 de Lima JE Jr, Javitt MC, Mathur SC. Residents’ teaching files: mucinous cystic neoplasm of the pancreas. Radiographics 1999;19(3):807–811 Demos TC, Posniak HV, Harmath C, Olson MC, Aranha G. Cystic lesions of the pancreas. AJR Am J Roentgenol 2002;179(6):1375–1388 Hayashi J, Yamashita T, Kakegawa T, Ogata M, Nakashima O. A case of cystic lymphangioma of the pancreas. J Gastroenterol 1994;29(3):372–376 Igarashi A, Maru OY, Ito T, et al. Huge cystic lymphangioma of the pancreas: report of a case. Surg Today 2001;31(8):743–746 Kalra MK, Maher MM, Mueller PR, Saini S. State-of-the-art imaging of pancreatic neoplasms. Br J Radiol 2003;76(912):857–865 Kim YH, Saini S, Sahani DV, Hahn PF, Mueller PR, Auh YH. Imaging diagnosis of cystic pancreatic lesions: pseudocyst versus nonpseudocyst. Radiographics 2005;25(3):671–685 Koenig TR, Loyer EM, Whitman GJ, Raymond AK, Charnsangave JC. Cystic lymphangioma of the pancreas. AJR Am J Roentgenol 2001;177:1090 Sahani DV, Kadavigere R, Saokar A, Fernandez-del Castillo C, Brugge WR, Hahn PF. Cystic pancreatic lesions: a simple imaging-based classification system for guiding management. Radiographics 2005;25(6):1471–1484

CASE 26 Clinical Presentation A 68-year-old man presents with vomiting and epigastric pain.

B

A

Fig. 26.1 (A–C) Images from a contrast-enhanced abdominal CT scan reveal massive fluid collections extending in the abdomen along the anterior aspect of the liver, in the mesentery, and in the anterior pararenal fasciae. The pancreatic parenchyma shows no enhancement and is almost completely replaced by ill-defined fluid collections. Diffuse mesenteric and peripancreatic fat stranding consistent with inflammatory changes is also noted.

C

Radiologic Findings Abdominal contrast-enhanced computed tomography (CT) scan (Fig. 26.1) shows diffuse inflammatory changes in the peripancreatic region, seen as peripancreatic and mesenteric fat stranding, extensive peripancreatic and perihepatic fluid collection, and absence of enhancement within the pancreatic head, neck, and body.

Diagnosis Acute necrotizing pancreatitis

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Differential Diagnosis Acute pancreatitis coexisting with one of the following: • • •

Pancreatic cystic neoplasms Metastasis Cystic teratoma

Discussion Background Necrotizing pancreatitis is a life-threatening complication of pancreatic tissue inflammation. Patients are at high risk of sepsis, multiorgan failure, and death. Prompt diagnosis and therapy are therefore mandatory. Three different types of necrosis have been described: (1) interstitial, the most common and usually related to alcohol abuse, cholelithiasis, and metabolic disorders; (2) ductal (rare cause, associated with circulatory failure); and (3) acinar (due to infectious agents).

Clinical Findings Clinical findings include abdominal epigastric pain and tenderness, vomiting, and more dramatic symptoms, such as shock, pulmonary failure, renal insufficiency, and gastrointestinal bleeding. Turner and Cullen signs are physical examination stigmata of severe pancreatitis with superimposed hemorrhage, but they are very rarely observed at clinical examination.

Complications Complications are frequent and can be life threatening. Multiorgan system failure, infection (pancreatic abscess), pseudocyst rupture, venous thrombosis, fistula formation (enterocutaneous after surgical procedures, entero-entero, enterovascular), and bowel obstruction.

Etiology Cholelithiasis and alcohol abuse account for most cases in developed countries. Pancreatitis has also been noticed as a possible complication of endoscopic retrograde cholangiopancreatography (ERCP). Autoimmune as well as inflammatory etiology has been described. Patients with pancreas divisum are known to be prone to pancreatitis due to the variant pancreatic ductal drainage. Less common causes include hyperlipidemia, hypercalcemia, hyperparathyroidism, and drugs (azathioprine, thiazides, sulfonamides).

Imaging Findings CT has gained importance in the diagnosis of pancreatitis, as it can depict and quantify the extent of pancreatic tissue damage, and consequently predict patients’ outcome. Pancreatic necrosis has been defined at CT as focal or diffuse areas of nonenhanced pancreatic parenchyma. The extent of necrosis is related to the presence of fluid collections and therefore to the development of complications. CT findings in pancreatitis may include abnormal pancreatic appearance, focal or diffuse enlargement of the pancreas, pancreatic abnormalities, peripancreatic inflammation, one or more peripancreatic fluid collections, and/or gas in or adjacent to the pancreas.

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Treatment •

If amenable, surgical débridement or CT-guided drainage of fluid collections is recommended to avoid risk of superinfection (abscess) or rupture.

Prognosis •

The prognosis is related to the extent of pancreatic necrosis.

PE ARL



CT can promptly detect pancreatitis complications, such as necrosis and superinfection of fluid collections, and is a useful tool in planning percutaneous draining procedures.

PITFALL



One must be careful to assess for the extent of pancreatic tissue damage and complications, including vascular complications such as splenic vein thrombosis and pseudoaneurysm formation.

Suggested Readings Balthazar EJ. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology 2002;223:603–613 Balthazar EJ. Complications of acute pancreatitis: clinical and CT evaluation. Radiol Clin North Am 2002;40:1211–1227 Balthazar EJ, Ranson JH, Naidich DP, Megibow AJ, Caccavale R, Cooper MM. Acute pancreatitis: prognostic value of CT. Radiology 1985;156:767–772 Calculli L, Pezzilli R, Casadei R, Fiscaletti M, Gavelli G. Imaging techniques for acute necrotizing pancreatitis: multidetector computed tomography. JOP 2006;7(1):104–109 Kim YH, Saini S, Sahani DV, Hahn PF, Mueller PR, Auh YH. Imaging diagnosis of cystic pancreatic lesions: pseudocyst versus nonpseudocyst. Radiographics 2005;25(3):671–685 Kloppel G. Acute pancreatitis. Semin Diagn Pathol 2004;21(4):221–226 Sahani DV, Kadavigere R, Saokar A, Fernandez-del Castillo C, Brugge WR, Hahn PF. Cystic pancreatic lesions: a simple imaging-based classification system for guiding management. Radiographics 2005;25(6):1471–1484

CASE 27 Clinical Presentation A 65-year-old man presents with epigastric pain.

A

B

C

D

Fig. 27.1 (A–D) Contrast-enhanced axial images from an abdominal CT scan show the pancreatic parenchyma replaced by a low-density fluid collection. The collection is well defined and has mildly enhancing walls. Gas is seen within the collection (arrow). The portal and splenic veins are patent.

Radiologic Findings Abdominal contrast-enhanced computed tomography (CT) scan (Fig. 27.1) shows a hypodense fluid collection replacing most of the pancreatic parenchyma and exerting mass effect on the posterior margin of the stomach. Gas is seen within this fluid collection. The portal and splenic veins are patent.

Diagnosis Pancreatic abscess

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Differential Diagnosis •

Postsurgical abscess, abscess secondary to gastric or bowel perforation

Discussion Background Pancreatic abscesses are a life-threatening complication of acute pancreatitis and are usually delayed in presentation. They are usually the result of superinfection of necrotic pancreatic parenchyma and/ or peripancreatic fluid collections. Enteric bacteria are the most common pathogens.

Clinical Findings Pancreatic abscesses are delayed in presentation, usually seen > 4 weeks after a bout of acute pancreatitis.

Complications Clinical findings include sepsis with a high mortality rate if not promptly treated. Obstruction of the hollow viscera and biliary system is possible.

Etiology The most frequently isolated pathogens in pancreatic abscesses are enteric organisms, through translocation through the gut. The most common bacteria are Escherichia coli, Klebsiella pneumoniae, Enterococcus faecalis, Staphylococcus aureus, Pseudomonas aeruginosa, Proteus mirabilis, and Streptococcus species.

Imaging Findings A pancreatic abscess is characterized by the presence of gas within an intrapancreatic fluid collection in a patient known to have a history of pancreatitis. Infected necrosis is distinguished by the absence of pus.

Treatment •

Percutaneous image-guided drainage or surgical drainage and débridement are required.

Prognosis •

Without drainage, the prognosis is poor, with nearly 100% mortality.

PE ARL



CT can promptly detect pancreatitis complications, especially superinfection of necrotic parenchyma or fluid collections, and is a useful tool in planning percutaneous and surgical draining procedures.

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PITFALL



The delayed presentation of pancreatic abscess formation may be clinically confusing. Therefore, if a patient presents with sepsis and has a recent history of acute pancreatitis, pancreatic abscess formation must be considered.

Suggested Readings Balthazar EJ. Acute pancreatitis: assessment of severity with clinical and CT evaluation. Radiology 2002;223:603–613 Balthazar EJ. Complications of acute pancreatitis: clinical and CT evaluation. Radiol Clin North Am 2002;40:1211–1227 Balthazar EJ, Ranson JH, Naidich DP, Megibow AJ, Caccavale R, Cooper MM. Acute pancreatitis: prognostic value of CT. Radiology 1985;156:767–772 Kim YH, Saini S, Sahani D, Hahn PF, Mueller PR, Auh YH. Imaging diagnosis of cystic pancreatic lesions: pseudocyst versus nonpseudocyst. Radiographics 2005;25(3):671–685 Sahani DV, Kadavigere R, Saokar A, Fernandez-del Castillo C, Brugge WR, Hahn PF. Cystic pancreatic lesions: a simple imaging-based classification system for guiding management. Radiographics 2005;25(6):1471–1484

CASE 28 Clinical Presentation A 46-year-old man presents with abdominal pain and weight loss.

B

A

Fig. 28.1 (A,B) Axial contrast-enhanced axial abdominal CT scan reveals mild swelling and enlargement of the pancreatic parenchyma with irregular dilatation of the main pancreatic duct (white arrow). The parenchyma shows loss of the normal lobulated contour. There is also a rind of soft tissue seen surrounding the parenchyma (black arrow).

Radiologic Findings Abdominal contrast-enhanced computed tomography (CT) scan (Fig. 28.1) shows moderate diffuse enlargement and swelling of the pancreatic parenchyma; the main pancreatic duct is tortuous and mildly dilated. No calcifications, intraductal stones, peripancreatic fluid collections, mesenteric fat stranding, or lymphoadenopathy are present.

Diagnosis Autoimmune pancreatitis

Differential Diagnosis • •

Chronic inflammatory pancreatitis Pancreatic solid neoplasms if focal

Discussion Background Many cases of pancreatitis previously labeled as idiopathic have recently been classified as autoimmune pancreatitis. Even though its prevalence and incidence are still not well documented, autoimmune pancreatitis shows a strong predominance in men age 60 and older. Association with other autoimmune diseases, such as primary sclerosing cholangitis, Sjögren syndrome, diabetes mellitus,

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autoimmune hepatitis, sialadenitis, retroperitoneal fibrosis, various kidney disorders, and hypothyroidism, has been described.

Clinical Findings Clinical findings include vague abdominal pain, weight loss, and jaundice; sometimes steatorrhea and hyperglycemia have been identified. Patients have been documented to have elevated immunoglobulin class G (IgG) levels, hypergammaglobulinemia, and autoantibodies.

Complications Narrowing of the distal common bile duct can cause dilatation of both intra- and extrahepatic biliary ducts and subsequent jaundice.

Etiology Recent studies have suggested that the pathogenesis of this disease is related to an autoimmune reaction against carbonic anhydrase type II and lactoferrin. Further investigations are required.

Imaging Findings Imaging findings are most important to promptly recognize autoimmune pancreatitis, as laboratory data and pathologic examination can be nonspecific. Diffuse or focal (less frequent) swelling and enlargement of pancreatic parenchyma, loss of typical fatty marbling, multifocal narrowing of the main pancreatic duct, tapering of the distal common bile duct, and narrowing of peripancreatic vessels (main portal vein, superior mesenteric artery, splenic vein, left renal vein) have been described as the most common imaging features of autoimmune pancreatitis at CT. Mild inflammatory changes confined to the peripancreatic fat without involvement of the mesentery have been described. Delayed scans usually show mild pancreatic enhancement compared with arterial phase images. Lack of lymphoadenopathy, calcifications, and pseudocyst or fluid collections can be helpful in achieving the correct diagnosis.

Treatment •

Steroids have proven to be effective even though dosage and duration of therapy are still not well standardized.

Prognosis •

Autoimmune pancreatitis is a benign entity: morphologic and functional changes are usually reversible if steroids are promptly administered to patients.

PE ARL



The presence of pancreatic enlargement with loss of parenchymal fatty marbling and a surrounding thin rind of increased attenuation confined to the peripancreatic fat, the absence of typical chronic inflammatory changes, such as calcifications and intraductal stones, and the prominence of the main pancreatic duct are helpful in distinguishing this condition.

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PITFALL



Focal enlargement of the pancreatic head and uncinate process can be mistaken for pancreatic cancer and therefore leads to unnecessary surgical treatment.

Suggested Readings Adsay NV, Basturk O, Thirabanjasak D. Diagnostic features and differential diagnosis of autoimmune pancreatitis. Semin Diagn Pathol 2005;22(4):309–317 Irie H, Honda H, Baba S, et al. Autoimmune pancreatitis: CT and MR characteristics. AJR Am J Roentgenol 1998;170:1323–1327 Kamisawa T, Chen PY, Tu Y, et al. MRCP and MRI findings in 9 patients with autoimmune pancreatitis. World J Gastroenterol 2006;12(18):2919–2922 Kim KP, Kim MH, Song MH, Lee SS, Seo DW, Lee SK. Autoimmune chronic pancreatitis. Am J Gastroenterol 2004;99:1605–1616 Sahani DV, Kalva SP, Farrell F, et al. Autoimmune pancreatitis: imaging features. Radiology 2004;233:345–352 Yang DH, Kim KW, Kim TK, et al. Autoimmune pancreatitis: radiologic findings in 20 patients. Abdom Imaging 2006;31(1):94–102

CASE 29 Clinical Presentation A young woman presents to the emergency room with abdominal pain after sustaining blunt abdominal trauma in a motor vehicle accident.

Fig. 29.1 Axial contrast-enhanced CT image shows a highdensity hematoma (arrow) dissecting the pancreatic body. The stranding in the anterior abdominal wall is consistent with a soft tissue contusion.

Radiologic Findings An axial abdominal contrast-enhanced computed tomography (CT) scan image (Fig. 29.1) shows a high-density hematoma in the region of the pancreatic body. The stranding in the anterior abdominal wall is consistent with a soft tissue contusion.

Diagnosis Pancreatic transection

Differential Diagnosis •

None in the proper clinical setting

Discussion Background The pancreas is not as commonly involved in abdominal blunt trauma as the liver or spleen, but its injuries even if overlooked at an early CT scan can subsequently lead to life-threatening complications, especially in the setting of pancreatic duct rupture.

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Clinical Findings Patients usually present with diffuse abdominal pain and tenderness and abdominal wall ecchymoses over the epigastrium. Laboratory findings such as hyperamylasemia or increased serum lipase level are nonspecific. Clinical findings do not show a correlation with the grade of pancreatic injuries; therefore, imaging is mandatory to evaluate the patient’s outcome.

Etiology Pancreatic transection is due to compression of the pancreatic parenchyma against the vertebral column.

Complications Vascular injuries can be seen in the acute setting, especially when transection has occurred in the head of the pancreas. Delayed mortality and morbidity are related to pancreatic duct disruption; abscess, pseudocyst, fistulas, and pancreatitis represent the most life-threatening complications due to this condition.

Imaging Findings At CT, diffuse enlargement of pancreatic parenchyma is the most common finding, as well as hyperdense fluid collection in the lesser sac consistent with hemorrhage. Transection if easily identified presents as a hypodense fracture line through the parenchyma; it is most frequently found in the body of the pancreas. Careful attention must be paid in evaluating the pancreatic duct, and magnetic resonance imaging and endoscopic cholangiopancreatography are very useful in this respect.

Treatment •

Uncomplicated pancreatic injuries are treated conservatively. If pancreatic duct disruption is present, endoscopic and/or surgical treatment is recommended.

Prognosis •

Prognosis relies on the prompt identification of complications (vascular or neighboring organ injuries, pancreatic duct disruption).

PE ARL



Pancreatic transection is almost always associated with other organ injuries usually involving the stomach, duodenum, liver, or spleen.

PITFALL



The involvement of the pancreatic duct can be overlooked or missed in early scans, and specific imaging of the assessment of the pancreatic duct is strongly recommended.

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Suggested Readings Bradley EL, Young PR Jr, Chang MC, et al. Diagnosis and initial management of blunt pancreatic trauma: guidelines from a multiinstitutional review. Ann Surg 1998;227(6):861–869 Brestas PS, Karakiklas D, Gardelis J, Tsouroulas M, Drossos C. Sequential CT evaluation of isolated non-penetrating pancreatic trauma. JOP 2006;7(1):51–55 Gupta A, Stuhlfaut JW, Fleming KW, Lucey BC, Soto JA. Blunt trauma of the pancreas and biliary tract: a multimodality imaging approach to diagnosis. Radiographics 2004;24:1381–1395 Lopez P, LeBlang S, Popkin CA , Byers PM. Blunt duodenal and pancreatic trauma. J Trauma 2002;53(6):1195 Wong YC, Wang LJ, Lin BC, Chen CJ, Lim KE, Chen RJ. CT grading of blunt pancreatic injuries: prediction of ductal disruption and surgical correlation. J Comput Assist Tomogr 1997;21:246–250

CASE 30 Clinical Presentation A 75-year-old man with a history of multiple myeloma presents with abdominal pain.

B

A

Fig. 30.1 (A,B) Axial contrast-enhanced CT image of the abdomen shows a round, well-defined mass in the pancreatic head and body (arrow) extending to the third portion of the duodenum. The splenic vein is encased by the pancreatic mass and can be appreciated only in its proximal part.

Radiologic Findings Contrast-enhanced computed tomography (CT) images of the pancreas (Fig. 30.1) show a large mass centered in the pancreas and causing extrinsic compression of the duodenum; the splenic vein appears to be obliterated in the region of the mass. The tail of the pancreas is spared and shows no atrophy or pancreatic duct dilatation.

Diagnosis Extramedullary plasmacytoma

Differential Diagnosis Pancreatic mass: • • •

Pancreatic neoplasm (ductal adenocarcinoma, neuroendocrine tumor) Lymphoma Metastasis

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Discussion Background Multiple myeloma is a hematological malignancy characterized by clonal proliferation of plasma cells; this disease mostly affects bones, but extramedullary plasmacytomas have been noticed in almost every site of the body and described as soft tissue masses, especially in the gastrointestinal tract.

Clinical Findings Symptoms may be nonspecific, such as back and abdominal pain, fatigue, and weight loss. Laboratory findings may include hypercalcemia, an elevated erythrocyte sedimentation rate, and hyperamylasemia.

Complications In the advanced stage, multiple myeloma may be associated with recurrent infections, multiple pathologic bony fractures, neurologic symptoms, and renal failure.

Etiology There are genetic and environmental causes, as well as a common association with monoclonal gammopathy of unknown significance.

Imaging Findings Imaging findings are usually nonspecific. The pancreas is not a common site of extramedullary involvement, as plasmacytomas are more frequently seen in hematopoietic tissues, such as the liver, spleen, and abdominal lymph nodes (reticuloendothelial system). At CT, they usually present as either hypodense or mildly peripherally enhancing masses. Jaundice associated with pancreatic and bile duct dilatation has been described when plasmacytomas are located in the head of the pancreas. Large tumors may show necrosis and infiltration or encasement of adjacent structures.

Treatment •

Possible treatment options include radiation therapy, chemotherapy, and autologous bone marrow transplantation.

Prognosis •

New treatments have definitely improved the survival rate. Prognosis for extramedullary plasmacytoma is better than that for bone plasmacytoma.

PE ARL



When a pancreatic mass is seen in a patient with a history of multiple myeloma, an extramedullary plasmacytoma should be considered in the differential diagnosis.

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PITFALL



Because pancreatic involvement is not very common, extramedullary plasmacytomas can be misunderstood for pancreatic adenocarcinoma, leading to unnecessary surgical procedures. Patients’ clinical history should always be carefully considered.

Suggested Readings Balliu E, Casas JD, Barluenga E, Guash I. Multifocal involvement of the pancreas in multiple myeloma: sonographic, CT and MR imaging findings. AJR Am J Roentgenol 2003;180(2):545–546 Davidson BS, Lee JE, Dodd LG, Dimopoulos MA, Evans DB. Extramedullary plasmacytoma of the pancreas. Am J Clin Oncol 1993;16(4):363–368 Hiller N, Goiten O, Ashkenazi YJ. Plasmacytoma of the pancreas. Isr Med Assoc J 2004;6(11):704– 705 Kazama T, Ng CS, Giralt SA. Multiphasic CT and MRI appearance of extramedullary multiple myeloma involving the stomach, pancreas and bladder. Clin Imaging 2005;29(4):263–265 Monill J, Pernas J, Montserrat E, et al. CT features of abdominal plasma cell neoplasms. Eur Radiol 2005;15(8):1705–1712 Olson MC, Kalbhen CL, Posniak HV. Pancreatic plasmacytomas in a patient with multiple myeloma: CT and ultrasound findings. Abdom Imaging 1993;18(4):323–324 Paakko E, Autio R, Lahde S. Plasmacytoma of the pancreas: CT and MRI appearance. Rofo 1998;169(6):673–675

CASE 31 Clinical Presentation A 63-year-old woman complains of epigastric discomfort.

B

A

Fig. 31.1 (A) Axial postcontrast CT image shows a well-defined low-density lesion with fine septations in the body of the pancreas. (B) Axial T2-weighted image in the same patient shows a well-defined hyperintense mass lesion within the body of the pancreas with a central scar (arrow).

Radiologic Findings Postcontrast axial computed tomography (CT) and magnetic resonance (MR) (Fig. 31.1) images of the pancreas show a well-defined cystic lesion in the body of the pancreas with enhancing thin septation and a central scar.

Diagnosis Microcystic adenoma (serous cystadenoma) of the pancreas

Differential Diagnosis • • • • • • •

Mucinous cystic neoplasm Neuroendocrine tumor Intraductal papillary mucinous tumor Pseudocyst Pancreatic abscess Adenocarcinoma Lymphangioma

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Discussion Background The pseudocyst is the most common cystic lesion of the pancreas and accounts for 80 to 85% of pancreatic cysts. Other cystic lesions of the pancreas include serous (microcystic) cystadenoma, mucinous cystic neoplasm, intraductal papillary mucinous neoplasm, solid (or cystic) and papillary epithelial neoplasm, complicated pseudocyst, and pancreatic abscess. Microcystic adenoma usually presents as a microcystic neoplasm and much less commonly as an oligocystic or macrocystic adenoma. Oligocystic serous adenomas are more commonly found in the head of the pancreas, have lesser septal enhancement, and have lobulated contours. Microcystic adenoma is associated with von Hippel-Lindau disease.

Clinical Findings Typical presentation is a female patient > age 60 with nonspecific abdominal symptoms. Other symptoms include epigastric pain and weight loss.

Complications Complications can include obstructive jaundice due to mass effect on the biliary tree, pancreatitis, and, rarely, malignant transformation. Large lesions may cause symptoms due to mass effect on adjacent structures.

Etiology The etiology is unclear; however, obesity and von Hippel-Lindau syndrome are associated with increased risk.

Imaging Findings •





The ultrasound appearance of the tumor depends on the size of the cyst that it contains. The presence of microcysts in the tumor gives a diffuse hyperechoic appearance. However, if the cysts are larger in size, a hypoechoic cystic mass with a honeycomb appearance may be seen with or without a central stellate calcified scar. The typical CT appearance of microcystic adenoma is a cystic pancreatic lesion measuring 2 to 12 cm with no zonal predominance and deforming the pancreatic contour (lobulated appearance). The lesion can be well or poorly defined and may be of fluid, solid, or mixed attenuation. The internal architecture of a lesion may not always be appreciable because of the presence of numerous microcysts or solid components. There are usually more than six cysts < 2 cm in size. Classically, a microcystic adenoma will have a multiloculated honeycomb appearance with avidly enhancing thin septations and occasionally a central stellate scar, which may have calcifications. Main pancreatic ductal dilatation and pancreatic atrophy are unusual with microcystic adenoma. The MRI appearance is that of a well-defined, noninvasive, multiloculated cystic lesion, hypointense on T1-weighted imaging and hyperintense with central septa or scars on T2-weighted imaging. Intense septal enhancement is usually seen, sometimes with delayed enhancement of the central scar. T1 hyperintensity indicates hemorrhage within the lesion.

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Treatment •

Imaging surveillance with careful observation to ensure stability is the treatment of choice in asymptomatic patients. Surgical treatment is recommended in symptomatic patients.

Prognosis •

Prognosis of microcystic adenoma is excellent because of negligible risk of malignancy.

PE ARL



A cystic pancreatic lesion with small cysts, a central scar showing delayed enhancement, and calcification is strongly suggestive of a microcystic adenoma.

PITFALL



Macrocystic or noncystic variants without a central scar and variable enhancement cannot be accurately categorized by imaging and mandate endoscopic or percutaneous biopsy. The presence of glycogen and the absence of mucin within the cyst fluid are typical for this lesion.

Suggested Readings Buetow PC, Rao P, Thompson LD. From the archives of the AFIP. Mucinous cystic neoplasms of the pancreas: radiologic-pathologic correlation. Radiographics 1998;18:433–449 Demos TC, Posniak HV, Harmath C, Olson MC, Aranha G. Cystic lesions of the pancreas. AJR Am J Roentgenol 2002;179:1375–1388 Kim YH, Saini S, Sahani D, Hahn PF, Mueller PR, Auh YH. Imaging diagnosis of cystic pancreatic lesions: pseudocyst versus nonpseudocyst. Radiographics 2005;25:671–685

CASE 32 Clinical Presentation A 75-year-old man presents with mild abdominal pain, loss of appetite, and weight loss in the last few months.

B

A

Fig. 32.1 (A–C) Axial contrast-enhanced CT images show a large, enhancing mass (arrow) within the body of the pancreas. The distal pancreatic parenchyma appears markedly atrophic with a dilated main pancreatic duct (curved arrow). The mass encases a portion of the celiac artery (dotted arrow) but spares the mesenteric artery. No calcifications are noted. There is no local lymphoadenopathy.

C

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images (Fig. 32.1) show a hypodense, peripherally enhancing mass within the body of the pancreas associated with marked pancreatic ductal dilatation and atrophy of the pancreas proximal to the mass. Massive peripancreatic vessel encasement is seen.

Diagnosis Ductal adenocarcinoma of the pancreatic head

Differential Diagnosis • • • • •

Ductal cell origin tumors: giant cell carcinoma, adenosquamous carcinoma, microadenocarcinoma Endocrine tumors: gastrinoma, insulinoma Autoimmune pancreatitis Pseudocyst (necrotic degeneration) Metastasis

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Discussion Background Ductal pancreatic adenocarcinomas are the fifth leading cause of death in Western countries, representing almost 75 to 85% of nonendocrine pancreatic malignancies. These tumors, more frequently located in the head of the pancreas (60–70% of cases), usually affect elderly men in their 7th or 8th decade.

Clinical Findings Presenting symptoms are extremely variable and related to the location and size of the tumor. Patients can experience abdominal pain, fatigue, loss of appetite, weight loss, nausea, vomiting, and jaundice, the latter usually noticed in the case of extensive tumors of the pancreatic head. Laboratory findings often include elevated carbohydrate antigen (CA) 19-9.

Complications Tumors of the pancreatic head can cause common bile duct obstruction and therefore jaundice; patients with metastatic disease can present paraneoplastic syndromes such as Trousseau syndrome, characterized by recurrent superficial thrombophlebitis.

Etiology Recent studies have shown that patients with a family history of pancreatic cancer, diabetes, and Peutz-Jeghers syndrome are at higher risk to develop these tumors, but the etiology still remains unknown. Other factors, such as cigarette smoking, high-protein and high-fat diets, and exposure to industrial carcinogens, have been implicated as possible causative agents of pancreatic cancer.

Imaging Findings Multidector CT has greatly improved the detection of pancreatic malignancies, as it allows acquisition of multiple phases of contrast enhancement (arterial, parenchymal, and delayed), multiplanar reconstructions, and two- and three-dimensional angiographic evaluation of the splanchnic vessels. Ductal adenocarcinomas usually present as focal solid, hypoattenuating (hypovascular) lesions, mostly arising from the pancreatic head; sometimes they are associated with an overall increase in pancreatic size, but this finding is more typically found in chronic or autoimmune pancreatitis. In the advanced stage, these tumors can cause chronic biliary duct dilatation as well as obstruction and dilatation of the main pancreatic duct with consequent pancreatic atrophy. Angiographic reconstructions are imperative to assess the extent of ductal adenocarcinomas around the splanchnic vessels. Vascular invasion (contiguity tumor-to-vessel > 50%) of the peripancreatic vessels (celiac trunk, superior mesenteric artery) is the most important criterion of surgical unresectability, followed by the presence of peritumoral lymph node enlargement, metastases (most commonly identified in the liver), and ascites (this finding almost always associated with peritoneal carcinomatosis).

Treatment •

Pancreatic ductal adenocarcinomas are frequently diagnosed at advanced stages, so that only a very small percentage of patients are eligible for curative surgical resection.

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Prognosis •

Prognosis is extremely poor; the medial survival rate after surgery is only 14 to 18 months. A mildly improved survival rate is seen only in those patients with neoplasms < 2 cm.

PE ARL



Loss of the typical fatty interstices that characterize the normal pancreatic glandular CT appearance, as well as morphologic abnormalities associated with pancreatic duct dilatation in patients with no previous history of pancreatitis, is highly suspicious of pancreatic malignancy.

PITFALL



Ductal adenocarcinomas can be misinterpreted as focal areas of chronic or autoimmune pancreatitis. The clinical history of patients should be carefully considered.

Suggested Readings Balci NC, Semelka RC. Radiologic diagnosis and staging of pancreatic ductal adenocarcinoma. Eur J Radiol 2001;38(2):105–112 Ichikawa T, Haradome H, Hachiya J, et al. Pancreatic ductal adenocarcinoma: preoperative assessment with helical CT versus dynamic MR imaging. Radiology 1997;202:655–662 Mergo PJ, Helmberger TK, Buetow PC, Helmberger RC, Ros PR. Pancreatic neoplasms: MR imaging and pathologic correlation. Radiographics 1997;17:281–301 Miller FH, Rini NJ, Keppke AL. MRI of adenocarcinoma of the pancreas. AJR Am J Roentgenol 2006;187(4):W365–W374 Prokesh RW, Schima W, Chow LC, Jeffrey RB. Multidetector CT of pancreatic adenocarcinoma: diagnostic advances and therapeutic relevance. Eur Radiol 2003;13(9):2147–2154 Vargas R, Nino-Murcia M, Trueblood W, Jeffrey RB Jr. MDCT in pancreatic adenocarcinoma: prediction of vascular invasion and resectability using a multiphasic technique with curved planar reformations. AJR Am J Roentgenol 2004;182:419–425

CASE 33 Clinical Presentation A 53-year-old woman presents with mild abdominal pain, diaphoresis, and palpitations.

B

A

Fig. 33.1 (A) Axial contrast-enhanced CT image shows a small arterially enhancing lesion in the tail of the pancreas (arrow). (B) The lesion is also seen on an early arterial phase gadolinium-enhanced MRI. (C) The patient underwent intraoperative ultrasound prior to resection, which confirmed the lesion.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images (Fig. 33.1) show a small arterially enhancing lesion in the tail of the pancreas. The lesion is also seen on an early arterial-phase gadolinium-enhanced magnetic resonance (MR) image. Intraoperative ultrasound confirmed the lesion prior to resection.

Diagnosis Islet cell tumor of the pancreas (insulinoma)

Differential Diagnosis • •

Metastasis (hypervascular) Vascular malformations

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Discussion Background Islet cell tumors or endocrine neoplasms of the pancreas represent only 2% of pancreatic malignancies and are more often seen in women in their 3rd to 5th decade. These lesions can be associated with genetic syndromes such as multiple endocrine neoplasia (MEN) type 1, von Hippel-Lindau disease, neurofibromatosis 1, and tuberous sclerosis. The main feature of these neoplasms is their ability to produce and secrete one or more hormones according to their specific site of origin (beta cells producing insulin, alpha cells producing glucagon, delta cells producing somatostatin, etc.); the secretion of these substances into the blood sometimes leads to clinically recognizable syndromes. Some of these tumors, even though hormonally active, are not able to cause symptoms and can be incidentally discovered by imaging. The most frequent islet cell tumors are insulinoma and gastrinoma, followed by glucagonoma, VIPoma, and somatostatinoma.

Clinical Findings Patients can be asymptomatic (in cases of nonfunctioning tumors) or present extremely variable symptoms according to the specific hormones released into the bloodstream. Insulinoma, the most common of these endocrine tumors, presents with the so-called Whipple triad: spontaneous hypoglycemia with blood sugar levels < 50 mg/100 mL, central nervous system or vasomotor symptoms, and relief of symptoms by oral or intravenous administration of glucose. These patients can experience diaphoresis, tachycardia, and palpitations due to catecholamine release.

Complications Islet cell tumors can cause symptoms due to mass effect when they grow to a considerable size; these patients can present abdominal pain and discomfort or jaundice for biliary duct compression.

Imaging Findings Immunohistochemical staining alone is not able to distinguish between malignant and benign lesions; therefore, imaging, especially multidetector CT, plays a primary role in the diagnosis and staging of islet cell neoplasms. Other techniques, such as gadolinium-enhanced MRI, somatostatin receptor imaging, and endoscopic ultrasound, also seem useful. Islet cell neoplasms usually appear hypervascular compared with the enhancing pancreatic parenchyma and are best recognized in the arterial phase; their size can vary from a few millimeters (in case of lesions causing recognizable endocrinopathy) to several centimeters: these are larger lesions (> 5 cm), albeit not able to produce clinical symptoms. The size is a major predictor of malignant behavior; in fact, larger tumors are more aggressive and prone to metastasize than smaller ones. Insulinoma can arise anywhere within the pancreatic parenchyma, whereas other endocrine neoplasms show either slightly different or extrapancreatic locations (gastrinoma is typically located in a triangle-shaped area bordered by the confluence of the common and cystic bile duct superiorly, the pancreatic body and neck medially, and the second and third portion of the duodenum inferiorly; glucagonoma can be extrapancreatic or occur in the body or tail of the pancreas; VIPoma is usually intrapancreatic; and somatostatinoma can be found both in the pancreas and in the duodenum).

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Treatment •

Surgical resection is the most curative treatment: small tumors can be endoscopically removed; larger tumors, located in the head of the pancreas, usually require Whipple surgery.

Prognosis •

Prognosis is good; a complete surgical removal allows a long-term survival. The recurrence rate is extremely high for these tumors, but resection can improve the chances of survival.

PE ARL



Three-dimensional reconstruction can perfectly depict peripancreatic vessels and therefore helps radiologists to distinguish between vascular pseudoaneurysms or aneurysms and hypervascular pancreatic islet cell tumors.

PITFALL



Endocrine pancreatic tumors are not always hypervascular and hyperattenuating compared with normal pancreatic parenchyma.

Suggested Readings Buetow PC, Miller DL, Parrino TV, Buck JL. Islet cell tumors of the pancreas: clinical, radiologic, and pathologic correlation in diagnosis and localization. Radiographics 1997;17(2):453–472; quiz 472A– 472B Chung EM, Travis MD, Conran RM. From the archives of the AFIP: pancreatic tumors in children: radiologic-pathologic correlation. Radiographics 2006;26:1211–1238 Horton KM, Hruban RH, Yeo C, Fishman EK. Multi-detector row CT of pancreatic islet cell tumors. Radiographics 2006;26:453–464 Ichikawa T, Peterson MS, Federle MP, et al. Islet cell tumor of the pancreas: biphasic CT versus MR imaging in tumor detection. Radiology 2000;216:163–171 Noone TC, Hosey J, Firat Z, Semelka RC. Imaging and localization of islet-cell tumours of the pancreas on CT and MRI. Best Pract Res Clin Endocrinol Metab 2005;19:195–211 Thoeni RF, Mueller-Lisse UG, Chan R, Do NK, Shyn PB. Detection of small, functional islet cell tumors in the pancreas: selection of MR imaging sequences for optimal sensitivity. Radiology 2000;214:483–490

CASE 34 Clinical Presentation A 70-year-old man presents with epigastric pain 1 year after left nephrectomy for renal cell carcinoma.

Fig. 34.1 Axial contrast-enhanced image in the early arterial phase of enhancement in this patient with left nephrectomy shows a well-defined enhancing hypervascular lesion in the body of the pancreas (arrow).

Radiologic Findings A well-defined homogeneously enhancing hypervascular lesion is seen in the body of the pancreas anteriorly. Diffuse fatty atrophy of the pancreas is present. Note the surgical clips in the left renal fossa at the location of the left renal vascular pedicle consistent with a past history of nephrectomy for renal cell carcinoma (Fig. 34.1).

Diagnosis Metastatic renal cell carcinoma to the pancreas

Differential Diagnosis • •

Metastases from known primary Primary pancreatic neoplasms, such as neuroendocrine tumor

Discussion Background Pancreatic metastases are usually incidentally detected tumors on follow-up studies for primary malignancy and are seen in patients with malignancies of the lung, breast, kidney, bowel, and thyroid, as well as in the setting of melanoma, hepatocellular carcinoma, and osteosarcoma. Identifying and characterizing the lesion as a pancreatic metastasis are crucial to proper oncologic management and the determination of prognosis.

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Clinical Findings Symptoms, if present, are usually nonspecific.

Complications Complications include pancreatic ductal obstruction with or without resultant pancreatitis or obstructive jaundice.

Etiology Metastases to the pancreas are due to hematogenous spread or direct local invasion.

Imaging Findings •



Pancreatic metastases can have three patterns on imaging: solitary mass lesion, multiple mass lesions, or diffuse pancreatic enlargement without a recognizable mass. The imaging appearance of the metastatic lesion depends on the primary malignancy. The cross-sectional imaging appearance of metastases varies; masses can be solid with enhancement, nonenhancing necrotic masses, multicystic tumors, or purely cystic lesions. Pancreatic ductal enlargement depends on the location of the metastatic focus. Those within or compressing the pancreatic duct lead to obstructive dilatation. Renal cell carcinoma and bronchogenic carcinoma metastases to the pancreas usually show intense enhancement, which can be best appreciated on arterial phase images on cross-sectional imaging and angiography. The magnetic resonance appearance of pancreatic metastases also depends on the primary tumor; however, pancreatic metastases are usually hypointense on T1-weighted and relatively hyperintense on T2-weighted imaging. Rarely, pancreatic metastases can rupture spontaneously, leading to hemoperitoneum and ascites.

Prognosis •

Prognosis in patients with pancreatic metastases is poor. The survival rate of patients with pancreatic metastases is 4.4% for 3 years and 2.7% at 5 years.

PE ARL



Metastatic disease to the pancreas must be considered in the setting of a new pancreatic mass in a patient with a history of prior malignancy. Multiple pancreatic masses is a pattern not seen in primary pancreatic malignancy and should make one suspicious of metastatic disease; similarly, the presence of a pancreatic mass and the presence of metastases to the skeleton or adrenal glands, locations that are atypical for metastases from a pancreatic primary, should provoke the search for another primary malignancy.

PITFALL



The imaging appearance of pancreatic metastases is nonspecific and can be confused with various benign and malignant mass lesions of the pancreas.

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Suggested Readings Chao K, Hurley J, Neerhut G, Kiroff G. Multiple pancreatic metastases from renal cell carcinoma. ANZ J Surg 2002;72:312–313 Kalra MK, Maher MM, Mueller PR, Saini S. State-of-the-art imaging of pancreatic neoplasms. Br J Radiol 2003;76:857–865 Klein KA, Stephens DH, Welch TJ. CT characteristics of metastatic disease of the pancreas. Radiographics 1998;18:369–378 Scatarige JC, Horton KM, Sheth S, Fishman EK. Pancreatic parenchymal metastases: observations on helical CT. AJR Am J Roentgenol 2001;176:695–699

CASE 35 Clinical Presentation A 70-year-old man presents with abdominal pain and weight loss in the last few months.

B

A

Fig. 35.1 (A) An axial contrast-enhanced CT image of the abdomen demonstrates a large, encapsulated, rounded mass localized in the head and neck of the pancreas. The mass is extremely heterogeneous, as it contains both areas of fluid and soft tissue attenuation; a thin capsule is observed and presents mild enhancement as well as the peripheral solid intratumoral components. The pancreatic parenchyma is otherwise unremarkable, and no sign of pancreatic duct dilatation is documented. (B) Axial image through the liver in the same patient shows a well-demarcated lesion in the left hepatic lobe of the liver with attenuation characteristics similar to the primary pancreatic lesion. This was found to represent a solitary metastasis on surgical biopsy.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images of the upper abdomen (Fig. 35.1) show a large, well-defined, round pancreatic mass centered within the head and neck; the lesion has areas of low and high attenuation. A similar appearing focal lesion is also seen in the liver.

Diagnosis Solid papillary epithelial neoplasm (SPEN)

Differential Diagnosis • • • • • •

Pancreatic cystic neoplasms: serous cystoadenoma, mucinous cystic neoplasms Rare pancreatic cystic neoplasms: acinar cell cystoadenocarcinoma, hemangioma, paraganglioma Solid pancreatic lesion with cystic degeneration: pancreatic adenocarcinoma, nonfunctioning cystic islet cell tumor (insulinoma, glucagonoma, gastrinoma) Calcified hemorrhagic pseudocyst Pancreatoblastoma Metastases

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Discussion Background Solid papillary epithelial neoplasm is an uncommon benign/low-malignant potential pancreatic tumor mostly occurring in young women in their 2nd to 4th decade and usually located within the pancreatic tail. At pathologic examination, SPEN has been described as a large, encapsulated mass containing a mixture of solid, cystic, and hemorrhagic components; in particular, a well-defined capsule and intratumoral hemorrhage are very important features to differentiate SPEN from other, more common pancreatic tumors (adenocarcinoma, islet cell tumors, etc.). It is important to recognize this pathologic entity because it is a low-grade malignancy and therefore potentially curable with surgical resection.

Clinical Findings SPEN may be incidentally discovered at cross-sectional imaging in asymptomatic patients.

Complications Hepatic (as seen in this patient) and peritoneal extension may occur in middle-aged or older patients.

Etiology The etiology is still controversial. Some authors suggest that SPENs may have an endocrine origin, as they have often been documented in association with pregnancy, polycystic ovary syndrome, and Sertoli cell tumors; moreover, their high prevalence in women may reflect a hormonal influence. Other authors claim that SPENs arise from pluripotent stem cells or acinar cells or ductal cells. The immunohistochemical positive staining for vimentin and alpha1-antitrypsin suggests both a neuroendocrine and an acinar–ductal cell differentiation.

Imaging Findings • •





CT plays an important role in the evaluation of pancreatic SPENs, as it demonstrates their most important pathologic features. Magnetic resonance imaging (MRI) is as well performed, but if compared with CT, it provides a more accurate characterization of the hemorrhagic foci and cystic degeneration areas commonly described in these tumors. With CT, SPEN appears as a large, heterogeneously enhancing, and encapsulated mass localized anywhere within the pancreatic parenchyma (some studies report a slightly higher predominance in the tail). Despite its tendency to grow up to several centimeters (16–20 cm), this neoplasm commonly displaces the surrounding structures rather than invading them. Calcifications either linear or punctate represent a rare finding and are more often described peripherally. MRI typically demonstrates a large lesion with heterogeneous signal intensity (low or high on both T1- and T2-weighted images); areas of high signal intensity on T1-weighted and low signal intensity on T2-weighted images are helpful to differentiate blood products from solid components. The fibrous capsule is well delineated and appears hypointense on T2-weighted images. Gadolinium-enhanced dynamic MRI usually shows an early, peripheral enhancement of the solid components with progressive fill-in.

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Treatment •

Surgical resection is usually curative, as SPENs have low malignant potential.

Prognosis •

Prognosis is favorable. SPENs are very unlikely to recur or progress after surgical intervention, although in older patients the incidence of tumor progression tends to be higher.

PE ARL



The presence of a fibrous capsule together with intratumoral hemorrhage in a large pancreatic lesion is highly suspicious for SPEN.

PITFALL



SPENs can sometimes present atypical features that may mimic those of other pancreatic malignancies, including  Absence of cystic degeneration areas (the tumor may resemble a solid lesion, e.g., ductal cell carcinomas)  Extracapsular invasion (more often described in older patients, due to higher potential for malignancy)  Dense calcification: prominent peripheral curvilinear calcifications (central, eggshell calcifications have also been reported)  Male patients: rarely seen, but SPEN should be considered in the differential diagnosis if the findings are typical.

Suggested Readings Buetow PC, Buck JL, Pantongrag-Brown L, Beck KG, Ros PR, Adair CF. Solid and papillary epithelial neoplasm of the pancreas: imaging-pathologic correlation on 56 cases. Radiology 1996;199:707–711 Buetow PC, Rao P, Thompson LD. From the Archives of the AFIP. Mucinous cystic neoplasms of the pancreas: radiologic-pathologic correlation. Radiographics 1998;18:433–449 Cantisani V, Mortele KJ, Levy A, et al. MR imaging features of solid pseudopapillary tumor of the pancreas in adult and pediatric patients. AJR Am J Roentgenol 2003;181(2):395–401 Choi JY, Kim MJ, Kim JH, et al. Solid pseudopapillary tumor of the pancreas: typical and atypical manifestations. AJR Am J Roentgenol 2006;187(2):W178–W186 D’Onofrio M, Malago R, Vecchiato F, et al. Contrast-enhanced ultrasonography of small solid pseudopapillary tumors of the pancreas: enhancement pattern and pathologic correlation of 2 cases. J Ultrasound Med 2005;24(6):849–854 Kim YH, Saini S, Sahani DV, Hahn PF, Mueller PR, Auh YH. Imaging diagnosis of cystic pancreatic lesions: pseudocyst versus nonpseudocyst. Radiographics 2005;25(3):671–685 Mergo PJ, Helmberger TK, Buetow PC, Helmberger RC, Ros PR. Pancreatic neoplasms: MR imaging and pathologic correlation. Radiographics 1997;17:281–301 Morana G, Guarise A. Cystic tumors of the pancreas. Cancer Imaging 2006;6:60–71 Ohtomo K, Furui S, Onoue M, et al. Solid and papillary epithelial neoplasm of the pancreas: MR imaging and pathologic correlation. Radiology 1992;184:567–570

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Sahani DV, Kadavigere R, Saokar A, Fernandez-del Castillo C, Brugge WR, Hahn PF. Cystic pancreatic lesions: a simple imaging-based classification system for guiding management. Radiographics 2005;25(6):1471–1484 Washington K. Solid-pseudopapillary tumor of the pancreas: challenges presented by an unusual pancreatic neoplasm. Ann Surg Oncol 2002;9:3–4

CASE 36 Clinical Presentation A 58-year-old Caucasian woman presented with a history of epigastric discomfort, anorexia, and weight loss over 3 to 4 months and recent-onset jaundice.

Fig. 36.1 Axial contrast-enhanced CT image of the pancreas shows a well-defined fluid density, multicystic mass lesion in the body and tail of the pancreas with thick enhancing nodular wall, septum, and mural excrescences.

Radiologic Findings An axial contrast-enhanced computed tomography (CT) image of the pancreas shows a well-defined fluid density, multicystic lesion in the body and tail of the pancreas with thick, enhancing nodular wall, septum, and mural excrescences (Fig. 36.1).

Diagnosis Pancreatic mucinous cystadenocarcinoma

Differential Diagnosis • • • • • • • • •

Microcystic tumor Pseudocyst Lymphangioma Complex cyst Abscess Dermoid Neurofibroma Hydatid cyst Tuberculosis

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Discussion Background Mucinous cystadenocarcinomas are the most common cystic neoplasms seen in the pancreas and account for 50% of all pancreatic cystic neoplasms.

Clinical Findings Mucinous cystadenocarcinomas are most commonly seen in women 50 to 60 years old. Symptoms are palpable epigastric mass lesion, epigastric discomfort with or without pain, weight loss, jaundice, early satiety, and fullness of the stomach. Laboratory studies show high levels of carcinoembryonic antigen, which correlates well with the degree of malignancy of the tumor.

Complications • • • • •

Pancreatitis Invasion of adjacent organs and vascular structures Gastrointestinal bleeds Biliary ductal blockade with jaundice and secondary complications Hemorrhage within the lesion

Etiology The exact etiology remains unknown; however, diabetes, smoking, chronic pancreatitis, and a family history are considered risk factors for pancreatic malignancies.

Imaging Findings • •





Mucinous cystadenomas and cystadenocarcinomas are most commonly seen in the body and tail of the pancreas. The tumor size positively correlates with the potential for malignancy. Transabdominal and endoscopic ultrasound shows the cystic nature of the lesion with multiple septa, mural nodules, debris, and peripheral calcifications. On CT, tumors are fluid density, rounded lesions with lobulated outlines that can be better appreciated in elderly patients because of associated pancreatic atrophy. Multiple large cysts (usually fewer than six) 2 to 20 mm in size in the presence of enhancing thick walls, mural nodules, and peripheral curvilinear calcifications (10–15%), with the mass in the body and/or tail of the pancreas, are suggestive of the diagnosis. On T1-weighted imaging, the tumor is seen as hypo- or hyperintense (depending on the protein content of the mucin); on T2-weighted imaging, it is seen as hyperintense. The internal architecture of the tumors, pancreatic and common biliary ductal obstruction, and dilatation can be better appreciated on magnetic resonance imaging and magnetic resonance cholangiopancreatography. On 18F-fluorodeoxyglucose positron emission tomography (FDG PET), avid uptake of FDG is strongly suggestive of a malignant lesion. Occasionally, the tumor invades the adjacent organs and presents with secondary complications related to the involved organ (e.g., splenic rupture in the case of splenic involvement by the lesion). Cyst fluid carcinoembryonic antigen and carbohydrate antigen (CA) 19–9 measurements obtained by endoscopic ultrasound-guided aspiration have the highest sensitivity and specificity for diagnosis.

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Treatment •

Surgical resection is the treatment of choice for localized disease. Nonsurgical treatment options are of limited efficacy and can be used in inoperable cases with limited success.

Prognosis •

Prognosis is good for completely resected benign tumors and malignant tumors without invasion, detected at an earlier stage. In patients with invasive unresectable malignant tumors, the prognosis is the same and as worse as that of pancreatic adenocarcinomas.

PE ARL



A round, lobulated lesion in the body and/or tail of the pancreas with multiple large cysts (usually fewer than six) 2 to 20 mm in size, as well as thick, enhancing walls and septa, mural nodules, and peripheral curvilinear calcifications.

PITFALL



Smaller lesions with atypical appearances are difficult to distinguish from microcystic neoplasms, and the diagnosis largely depends on biopsy.

Suggested Readings Buetow PC, Rao P, Thompson LDR. From the Archives of the AFIP. Mucinous cystic neoplasms of the pancreas: radiologic-pathologic correlation. Radiographics 1998;18:433–449 Sakorafas GH, Sarr MG. Cystic neoplasms of the pancreas; what a clinician should know. Cancer Treat Rev 2005;31:507–535 Scott J, Martin I, Redhead D, Hammond P, Garden OJ. Mucinous cystic neoplasms of the pancreas: imaging features and diagnostic difficulties. Clin Radiol 2000;55:187–192 Wu H, Cheng NS, Zhang YG, Luo HZ, Yan LN, Li J. Improved early diagnosis of cystadenocarcinoma of the pancreas. Hepatobiliary Pancreat Dis Int 2007;6:87–91

CASE 37 Clinical Presentation A 70-year-old Caucasian man presents with 2 months’ history of fullness of the stomach, 6 lb (2.7 kg) weight loss, and recent yellowish discoloration of the eyes and skin.

B

A

Fig. 37.1 (A) Axial contrast-enhanced CT image shows a subtle hypoattenuating lesion (arrows) in the head of the pancreas with no significant common duct dilatation. The portal vein is patent. (B) Axial 18F-fluorodeoxyglucose positron emission tomography (FDG PET) image in the same patient shows FDG uptake within the lesion.

Radiologic Findings An ill-defined hypoattenuating mass is seen in the head of the pancreas (Fig. 37.1) without proximal common bile duct dilatation. There is very little mass effect due to the lesion. A corresponding positron emission tomography (PET) image in the same location shows 18F-fluorodeoxyglucose (FDG) avidity of the lesion.

Diagnosis Primary pancreatic lymphoma (non-Hodgkin type)

Differential Diagnosis • • • •

Adenocarcinoma Metastases Pancreatic cystadenoma Pancreatitis

Discussion Background Pancreatic lymphoma accounts for < 0.5 to 1.0% of cases of total pancreatic neoplasms. With the increasing population of people with human immunodeficiency virus (HIV), it is becoming increasingly common.

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Clinical Findings • • • • • • • • • •

Right hypochondriac or epigastric pain Weight loss Jaundice Epigastric mass without superficial palpable lymph nodes Nausea, vomiting Night sweats, fever, chills Gastrointestinal bleeding Fullness of the stomach Early satiety Anorexia

Complications • • •

Common biliary duct obstruction Secondary acute pancreatitis due to pancreatic ductal obstruction Regional lymph nodal involvement

Etiology Etiologic factors are unknown; however, risk factors for the development of non-Hodgkin lymphoma are old age, Epstein-Barr virus infection, autoimmune disorders, HIV infection, posttransplant patient on immunosuppressants, and exposure to pesticides, fertilizers, or solvents.

Imaging Findings •





Ultrasound may show a large homogeneous, hypoechoic mass without calcifications causing biliary and mild pancreatic ductal dilatation. Endoscopic ultrasound is more sensitive than transabdominal ultrasound and may show peripancreatic and periaortic isoechoic lymph nodes. Computed tomography (CT) is the imaging modality of choice and usually shows a large (usually 7–8 cm), well-defined or ill-defined infiltrating, mildly or nonenhancing homogeneous mass in the pancreatic head without calcifications or necrosis, with peripancreatic or regional lymphadenopathy. Involvement of the surrounding organs (liver and spleen) is very unusual even in large-sized mass lesions. The invasion and occlusion of adjacent vascular structures are less common than in adenocarcinoma. Common biliary duct narrowing and occlusion is common; however, dilatation of the Wirsung duct is rare as compared with adenocarcinoma. Lymph node involvement below the level of the renal veins is an important finding to differentiate lymphoma from adenocarcinoma. On T1-weighted imaging, primary pancreatic lymphoma appears as a homogeneous, mildly enhancing hypointense mass lesion. On T2-weighted imaging, it appears as a slightly heterogeneous hypoto isointense mass lesion with signal intensity greater than the rest of the pancreatic tissue.

Treatment •

Chemotherapy is the treatment of choice. CHOP chemotherapy (cyclophosphamide, doxorubicin, vincristine, and prednisone) and rituximab (anti-CD20 chimeric monoclonal antibody) are well accepted. Radiotherapy is used as an adjunct to chemotherapy. The role of surgery is controver-

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sial. Endoscopic stent placement in the common biliary duct achieves rapid symptomatic relief in patients with a ductal obstruction.

Prognosis •

The prognosis is better than that for adenocarcinoma. Using multiple treatment options, cure rates are 25 to 35%.

PE ARL



Mass seen as a bulky, homogenous, and noncalcified lesion in the head of the pancreas without much dilatation of the pancreatic duct.

PITFALL



Early-stage disease with a smaller tumor can be confused with adenocarcinoma.

Suggested Readings Merkle EM, Bender GN, Brambs HJ. Imaging findings in pancreatic lymphoma: differential aspects. AJR Am J Roentgenol 2000;174:671–675 Mulkeen AL, Yoo PS, Cha C. Less common neoplasms of the pancreas. World J Gastroenterol 2006; 12(20):3180–3185

CASE 38 Clinical Presentation A 35-year-old woman presents with nonspecific abdominal pain.

B

A

Fig. 38.1 (A) Axial noncontrast CT image shows an exophytic lesion arising from the tail of the pancreas (arrow) with eccentric calcification. (B) The lesion shows early arterial enhancement and continues to stay enhanced on the (C) portal venous-phase image.

C

Radiologic Findings Axial noncontrast computed tomography (CT) image (Fig. 38.1A) shows an exophytic lesion arising from the tail of the pancreas with eccentric calcification. The lesion shows early arterial and sustained enhancement on the contrast-enhanced series (Fig. 38.1B,C).

Diagnosis Nonfunctioning neuroendocrine tumor of the pancreas

Differential Diagnosis • • • •

Ductal adenocarcinoma Mucinous cystic tumor of the pancreas Metastasis Solid papillary epithelial neoplasm (SPEN)

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Discussion Background Nonfunctioning neuroendocrine tumors of the pancreas are rare slow-growing tumors with a more indolent natural history compared with pancreatic adenocarcinoma. They constitute the majority of islet cell tumors of the pancreas and may account for up to 60% of all neuroendocrine tumors of the pancreas. Ninety percent of nonfunctioning tumors are malignant at presentation. Patients with nonfunctioning tumors do not have any symptoms from excessive hormone secretion by the tumor because the tumor does not release any hormones into the blood.

Clinical Findings These tumors have a histologic appearance of islet cell tumors but do not produce any symptoms because they do not release excessive amounts of hormones. Because of this, they can grow silently for a long time before they are discovered. They are almost always very large, ranging in size from 3 to 24 cm in diameter. Malignant nonfunctioning tumors often present like adenocarcinoma. Preoperative accurate differentiation between endocrine and exocrine pancreatic tumor is very important because endocrine tumors reveal more indolent behavior, a higher resectability, a better response to chemotherapy, and a better prognosis compared with adenocarcinomas. They can produce pain, jaundice, or variceal bleeding.

Complications More than 50% of all nonfunctioning islet cell tumors are malignant. At the time of diagnosis, the tumors are typically large and easily localized by CT scanning or magnetic resonance imaging (MRI). Patients with nonfunctioning islet cell tumors can live with metastases for many years and can have a 5-year survival of ~45%.

Etiology Increased risk factors include cigarette smoking, diabetes, chronic pancreatitis, and a high-fat diet.

Imaging Findings Nonfunctioning tumors are usually manifested as large, well-defined masses with moderate to strong enhancement without invasion of adjacent vessels. The typical imaging characteristics of these lesions are hypervascularity and calcifications. The enhancement pattern may be typical of hyperattenuation on arterial and portal phases. Morphologically, nonfunctioning large tumors are less likely to encase adjacent vascular structures and rarely show central necrosis. Imaging findings that are useful in the differentiation of endocrine tumors from ductal adenocarcinomas include the presence of calcification, lack of vascular encasement, lack of ductal obstruction, less common central necrosis and cystic degeneration, and lack of desmoplastic reaction. Calcifications can be seen in ~20% cases and are discrete, nodular, or shell-like. Calcification is more common in malignant than in benign neoplasms. Imaging findings that are suggestive of malignancy in the nonfunctioning neuroendocrine tumor include necrosis, invasion of retroperitoneal structures, and discrete nodular calcification. The liver and lymph nodes are the most common sites for metastasis. Like the primary tumor, liver metastases tend to demonstrate increased enhancement relative to normal hepatic parenchyma or uniform ring enhancement.

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Treatment •

Surgical resection is the most curative treatment.

Prognosis •

The prognosis is good; complete surgical removal allows long-term survival.

PE ARL



These tumors are diagnosed by the presence of calcification, lack of vascular encasement, lack of ductal obstruction, and lack of desmoplastic reaction. Findings that are suggestive of malignancy include necrosis, invasion of retroperitoneal structures, and discrete nodular calcification.

PITFALL



These tumors when large and with local and regional metastases may be difficult to differentiate from other solid pancreatic masses with or without pancreatic ductal dilatation.

Suggested Readings Pereira PL, Wiskirchen J. Morphological and functional investigations of neuroendocrine tumors of the pancreas. Eur Radiol 2003;13:2133–2146 Kotoulas C, Panayiotides J, Antiochos C, Sambaziotis D, Papadopoulos G, Karameris A. Huge non-functioning pancreatic cystic neuroendocrine tumour: a case report. Eur J Surg Oncol 1998;24:74–76 Madura JA, Cummings OW, Wiebke EA, Broadie TA, Goulet RL Jr, Howard TJ. Nonfunctioning islet cell tumors of the pancreas: a difficult diagnosis but one worth the effort. Am Surg 1997;63:573–577; discussion 577–578

CASE 39 Clinical Presentation A 48-year-old man presents with severe epigastric pain, nausea, vomiting, and diarrhea.

A

B

C

D

E

F

Fig. 39.1 (A–F) Axial and coronal contrast-enhanced CT images show pancreatic calcification along with dilatation of the pancreatic duct. There is a multiloculated lesion seen in the anatomical plane between the pancreatic head and duodenum (pancreaticoduodenal groove). Postcholecystectomy clips are noted.

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Radiologic Findings Axial and coronal contrast-enhanced computed tomography (CT) images show pancreatic calcification along with dilatation of the pancreatic duct. There is a multiloculated lesion seen in the anatomical plane between the pancreatic head and the duodenum (pancreaticoduodenal groove). Postcholecystectomy clips are noted (Fig. 39.1).

Diagnosis Groove pancreatitis

Differential Diagnosis • • • •

Pancreatic adenocarcinoma Pseudocyst Primary duodenal neoplasm Periampullary neoplasm

Discussion Background Groove pancreatitis is a form of chronic segmental pancreatitis affecting the groove in the region of the pancreatic head, duodenum, and common bile duct. In 1982, Stolte et al coined the term groove pancreatitis and described it as a special form of segmental pancreatitis characterized by fibrous scars of the anatomical space between the dorsocranial part of the head of the pancreas, the duodenum, and the common bile duct.

Clinical Findings Groove pancreatitis is often diagnosed in 40- to 50-year-old men suffering from alcohol abuse. The patients usually present with postprandial abdominal pain and, subsequently, impaired motility, stenosis of the duodenum, and postprandial vomiting, often leading to significant weight loss. Blood tests often show a slight elevation of serum pancreatic enzymes and occasionally serum hepatic enzymes.

Complications Secondary obstruction of the common bile duct with jaundice

Etiology The pathogenesis of groove pancreatitis remains unclear, although several factors, such as peptic ulcers, gastric resection, true duodenal wall cysts, and pancreatic heterotopia in the duodenal wall, may be related to this condition. Becker et al classified it into a pure form and a segmental form. The pure form of groove pancreatitis involves the groove only, with the pancreatic parenchyma and main pancreatic duct preserved. The segmental form of groove pancreatitis involves both the groove and the pancreatic head with main pancreatic duct stenosis. Groove pancreatitis and cystic dystrophy of the duodenal wall are the same entity. In both cases there is inflammation of the pancreatic tis-

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sue in the groove, which leads to chronic obstructive pancreatitis; the former may be a solid aspect that poses problems in differential diagnosis with pancreatic carcinoma, and the latter a macrocystic aspect (as was seen in this patient).

Imaging Findings •



On contrast-enhanced CT or magnetic resonance imaging (MRI), soft tissue–attenuation material with delayed enhancement is noted between the pancreatic head and the adjacent duodenum. In addition, this condition shows smooth stenosis of the bile duct and main pancreatic duct on endoscopic retrograde cholangiopancreatography, duodenal luminal narrowing at upper gastrointestinal series, and a platelike mass in this region at ultrasonography, CT, and MRI. The distinction between fibrous scar in groove pancreatitis and scirrhous adenocarcinoma of pancreatic cancer is difficult on CT and MRI. Cystic dystrophy of the duodenal wall is seen as the presence of cystic lesions in the thickened wall of the second portion of the duodenum. On magnetic resonance cholangiopancreatography, the intrapancreatic portion of the bile duct in patients with groove pancreatitis has a long, smooth, narrowed configuration, in contrast to the abrupt, circumscribed, irregular ductal stenosis or complete ductal obstruction seen in patients with pancreatic carcinoma.

Treatment •

The surgical treatment of choice is a pancreaticoduodenectomy using the Whipple procedure or a pylorus-preserving pancreaticoduodenectomy.

Prognosis •

Prognosis is generally good if treated promptly.

PE ARL



A complex mass when located in the pancreaticoduodenal groove with no significant biliary ductal dilatation keeps groove pancreatitis in the differential.

PITFALL



It may be difficult to differentiate groove pancreatitis from primary scirrhous adenocarcinoma of the pancreas.

Suggested Readings Procaccci C, Graziani R, Zamboni G, et al. Cystic dystrophy of the duodenal wall: radiologic findings. Radiology 1997;205:741–747 Stolte M, Weiss W, Volkholz H, et al. A special form of segmental pancreatitis: groove pancreatitis. Hepatogastroenterology 1982;29:198–208

CASE 40 Clinical Presentation An 81-year-old man presents with a history of bloating and epigastric pain.

B

A

Fig. 40.1 (A–C) Axial contrast-enhanced images in the pancreatic phase of CT shows a large enhancing lesion in the head of the pancreas (arrow). There was no intrahepatic ductal dilatation. The portal vein and the superior mesenteric artery were patent and not involved.

C

Radiologic Findings Axial contrast-enhanced images in the pancreatic phase of computed tomography (CT) show a large enhancing lesion in the head of the pancreas (Fig. 40.1). There was no intrahepatic ductal dilatation. The portal vein and the superior mesenteric artery were patent and not involved.

Diagnosis Acinar cell carcinoma of the pancreas

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Differential Diagnosis • • • • •

Neuroendocrine tumor of the pancreas Pancreatic lymphoma Pancreatoblastoma Ductal adenocarcinoma Metastases

Discussion Background Acinar cell carcinomas are solid epithelial exocrine tumors of the pancreas that account for only 1% of all pancreatic tumors. They may mimic the histologic appearance of the more common but less aggressive low-grade neuroendocrine tumors and solid pseudopapillary tumors or the more ominous ductal adenocarcinomas and pancreatoblastomas.

Clinical Findings Clinical findings include nonspecific gastrointestinal symptoms; the initial presentation may be similar to that of ductal adenocarcinoma of the pancreas. Patients (up to 15%) can also present with widespread subcutaneous fat necrosis, polyarthritis, and eosinophilia (Schmid’s triad) due to increased circulating lipase secreted by the tumor.

Complications The most common site of metastases is the liver. Extra-abdominal metastases are rare.

Etiology Acinar cell carcinomas occur more commonly in men and show a peak incidence in the 7th decade. These tumors are lower grade than ductal carcinomas, although they are usually advanced at presentation. Acinar cell carcinomas can involve the head or tail of the pancreas. They are usually well circumscribed, partly encapsulated, pink to tan, homogeneous fleshy masses, averaging 11 cm in greatest diameter, occasionally demonstrating extensive hemorrhage and necrosis.

Imaging Findings On CT and magnetic resonance imaging (MRI), > 90% of acinar cell tumors are well marginated with clearly defined margins. They are either partially or completely exophytic with very little desmoplastic reaction. On CT, acinar cell tumors are hypodense with occasional calcifications, a central necrotic area, and a well-defined, enhancing wall. They may demonstrate early enhancement. These tumors are slightly hypointense on T1-weighted MRI and hyperintense on T2-weighted images. They demonstrate poor enhancement after gadolinium injection due to relative hypovascularity compared with pancreatic parenchyma.

Treatment •

Resection is the treatment of choice, with or without chemoradiation therapy, and metastases may be present at the time of diagnosis.

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Prognosis •

Acinar cell carcinomas are aggressive tumors, and most patients die of their cancer within a mean of 18 months after diagnosis and a 5-year survival of 5.9%; however, the overall survival rate is better than that for pancreatic ductal adenocarcinoma. Younger patients (< 60 years old) and patients with tumors < 10 cm tend to have longer survival rates than patients > 60 years or with larger tumors. Patients who present with symptoms of elevated lipase do much worse (mean survival 8.8 months).

PE ARL



Suspect acinar cell carcinoma if there is a large exophytic, well-marginated pancreatic lesion.

PITFALL



It may be difficult to differentiate acinar cell carcinoma of the pancreas from a neuroendocrine tumor.

Suggested Readings Hartman GG, Hongyu N, Pickleman J. Acinar cell carcinoma of the pancreas. Arch Pathol Lab Med 2001;125:1127–1128 Mergo PJ, Helmberger TK, Buetow PC, Helmberger RC, Ros PR. Pancreatic neoplasms: MR imaging and pathologic correlation. Radiographics 1997;17:281–301

IV Spleen CASE 41 Clinical Presentation A 44-year-old man presents with abdominal discomfort.

A

B

C

D

Fig. 41.1 (A) Axial T2-weighted image in a young man shows a well-defined hypointense lesion in the tail of the pancreas (arrow) with signal characteristics similar to the spleen. (B) Axial T1-weighted gradient echo in-phase image in the same patient shows a well-defined hypointense lesion in the tail of the pancreas (arrow), isointense to the spleen. (C) Axial T1-weighted gradient echo out-of-phase image in the same patient shows no drop of signal in the pancreatic tail lesion (arrow). (D) Axial postcontrast fat-saturated T1-weighted image in the same patient shows the homogeneously enhancing, isointense lesion in the tail of the pancreas (arrow), isointense to the spleen.

Radiologic Findings Axial magnetic resonance (MR) images of the pancreas show the presence of a focal lesion in the tail of the pancreas that has signal characteristics similar to that of the spleen on T1- and T2-weighted images (Fig. 41.1).

Diagnosis Accessory spleen in the pancreatic tail

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Differential Diagnosis • • • • • •

Pancreatic primary neoplasm Metastases Thrombosed aneurysm Hematoma Complex pseudocyst Abscess

Discussion Background Accessory spleen is the presence of splenic tissue in an ectopic location. It is also referred to as splenule, splenunculus, and supernumerary spleen. The incidence of accessory spleen is ~30% in autopsy studies and 16% in imaging studies. The reported incidence of intrapancreatic ectopic spleen is one in six cases of total accessory spleen cases. It is important to differentiate accessory spleen from other lesions to obviate invasive procedures.

Clinical Findings Patients may be asymptomatic or have pain in the left upper abdomen.

Complications • • • • • •

Enlargement after splenectomy Torsion Spontaneous hemorrhage Abscess Primary tumors Metastases

Etiology Failure of fusion of the splenic anlage, located in the dorsal mesogastrium, during the 5th week of fetal life leads to the formation of an accessory spleen.

Imaging Findings •





The most common locations for an accessory spleen are adjacent to the splenic hilum and in the pancreatic tail. It also can be found in perirenal locations, in other parts of the abdominal cavity, and, very rarely, in the scrotum. The most important imaging criteria for identifying and characterizing the lesion are a soft tissue structure with well-defined margins; size < 2 cm; a rounded, ovoid, or triangular shape; homogeneous contrast enhancement; and typical location of the lesion with imaging characteristics similar to splenic tissue. On computed tomography (CT) and MRI, an accessory spleen appears as a rounded, solid, soft tissue lesion with contrast enhancement characteristics similar to the spleen.

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On MRI, an accessory spleen appears hyperintense to the surrounding pancreas on T2-weighted imaging and iso- to hypointense to the surrounding pancreas on T1-weighted imaging. Superparamagnetic enhanced iron oxide contrast-enhanced MRI can be used as the ectopic splenic tissue and will show contrast uptake similar to the normal spleen, with little or no uptake in the pancreas. Radionuclide imaging is more specific in identifying and characterizing the lesion. Scintigraphy is currently the most specific imaging technique for the diagnosis of accessory spleen, however, at the cost of impaired anatomical resolution. Technetium 99m sulfur colloid scans and radiolabeled heat-damaged red blood cells and indium 111-labeled autologous platelets are the radiotracers used for radionuclide imaging of an accessory spleen.

Treatment •

No treatment is required in asymptomatic cases. Biopsy and surgical removal, if required, are recommended in symptomatic cases in which the accessory spleen causes secondary complications due to its location and functional activity and cases where the accessory spleen cannot be differentiated from other lesions of the pancreas.

Prognosis •

The prognosis is excellent in uncomplicated cases where splenic reticuloendothelial function does not interfere with the patient’s primary disease condition. The prognosis is not bad in patients where splenic function has an effect on the primary hematological disorder (in which case, surgical removal of the accessory splenic tissue can be done without serious complications).

PE ARL



Accessory spleen is seen as a soft tissue density structure in typical location with imaging characteristics similar to that of the spleen.

PITFALL



In patients with primary malignancies and other pancreatic diseases, it may not always be possible to differentiate spleen from primary malignancies and metastases. Partial averaging of the accessory spleen < 1 cm in size can lead to a hypodense appearance of the accessory spleen in the pancreatic tail, making it more difficult to differentiate it from other conditions.

Suggested Readings Kim SH, Lee JM, Lee JY, Han JK, Choi BI. Contrast-enhanced sonography of intrapancreatic accessory spleen in six patients. AJR Am J Roentgenol 2007;188:422–428 Mortelé KJ, Mortelé B, Silverman SG. CT features of the accessory spleen. AJR Am J Roentgenol 2004;183:1653–1657

CASE 42 Clinical Presentation A 34-year-old woman complains of nonspecific abdominal pain.

Fig. 42.1 Axial contrast-enhanced CT image shows an enhancing exophytic splenic lesion (arrow) arising from the inferior pole of the spleen.

Radiologic Findings An axial contrast-enhanced computed tomography (CT) image (Fig. 42.1) demonstrates a well-defined exophytic lesion arising from the inferior pole of the splenic parenchyma and shows homogeneous enhancement after contrast administration.

Diagnosis Hemangioma of the spleen

Differential Diagnosis • •

Predominantly solid splenic lesions: hamartomas, lymphoma, metastasis, angiosarcoma, inflammatory pseudotumors, littoral cell angioma Predominantly cystic lesions: cyst, abscess, lymphangioma

Discussion Background Hemangiomas represent the most common primary benign neoplasms of the spleen, being recognized in 0.3 to 14.0% of cases at autopsy. These lesions, which tend to be slightly more common in men, result from the proliferation of splenic vascular channels with endothelial lining and may undergo several changes, including fibrosis, hemorrhage, and necrosis; they usually tend to grow slowly, so that symptoms and complications, although unusual, manifest in late adulthood. The term hemangiomatosis refers to the presence of multiple hemangiomas within the splenic parenchyma; this condition may be part of a systemic angiomatosis as described in Klippel-Trénaunay-Weber, Turner, Kasabach-Merritt, and Beckwith-Wiedemann syndromes.

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Clinical Findings Clinical presentation mostly relies on the size of the hemangiomas. Some patients may experience abdominal pain and fullness over the left upper quadrant, whereas most may be completely asymptomatic.

Complications Spontaneous splenic rupture represents the most common complication and is usually related to large lesions. Hypersplenism with anemia, thrombocytopenia, and coagulopathy (Kasabach-Merritt syndrome) has been documented with large hemangiomas. Malignant transformation has been reported to occur, though rarely. Hemangiomatosis may be associated with either portal hypertension or coagulopathy.

Etiology Hemangiomas are considered congenital lesions arising from the endothelium of splenic sinusoids. The etiology, though, is still uncertain.

Imaging Findings Hemangiomas are often found incidentally at radiologic examinations; they may be either solid or partially cystic and contain calcifications either centrally or peripherally. Sonographic findings reflect the wide spectrum of solid and cystic changes identified at histology: hemangiomas may be either hyperechoic (solid components) or complex (both solid and cystic components); cystic spaces may appear anechoic or demonstrate echogenic debris corresponding to areas of hemorrhage or necrosis. On nonenhanced CT, hemangiomas are usually seen as hypodense, round, usually well-defined lesions with thin or eggshell-like calcifications. After injection of contrast, these lesions may demonstrate progressive filling from the periphery to the center, although not as often as hepatic hemangiomas. On magnetic resonance imaging (MRI) (Fig. 42.2), hemangiomas typically appear hypointense relative to the spleen on T1-weighted images and hyperintense on T2-weighted images. Larger hemangiomas may demonstrate variable signal intensity on T1-weighted images owing to the presence of foci of infarction, thrombosis, or hemorrhage. After contrast administration, they may show early centripetal filling and diffuse uniform enhancement at delayed imaging.

Treatment •

Splenectomy is recommended only if rupture is likely to occur or in cases of large hemangiomas associated with severe coagulopathy; otherwise, no treatment is required.

Prognosis •

The prognosis is usually favorable, as hemangiomas are benign lesions unlikely to undergo malignant changes; the risk of spontaneous splenic rupture is related to the size of these lesions (the larger the lesions, the higher the risk).

PE ARL



The enhancement pattern (early centripetal and delayed uniform filling) is pathognomonic of hemangiomas.

IV SPLEEN

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A

B

C

D

Fig. 42.2 Axial MR images in the same patient as Fig. 42.1. (A) T1-weighted image shows an ill-defined focal splenic lesion that is isointense to the spleen. (B) On an axial T2-weighted fat-suppressed image, the lesion appears hyperintense. (C–E) Dynamic MR images after gadopentetate dimeglumine intravenous administration: the splenic lesion demonstrates early centripetal filling of contrast material and diffuse uniform enhancement on delayed images. This enhancement pattern is typical for hemangiomas.

PITFALL



Some hemangiomas may be relatively avascular or show slow, partial filling after the administration of contrast material.

Suggested Readings Abbott RM, Levy AD, Aguilera NS, Gorospe L, Thompson WM. From the Archives of the AFIP. Primary vascular neoplasms of the spleen: radiologic-pathologic correlation. Radiographics 2004;24: 1137–1163

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Elsayes KM, Narra VR, Mukundan G, Lewis JS Jr, Menias CO, Heiken JP. MR imaging of the spleen: spectrum of abnormalities. Radiographics 2005;25:967–982 Luna A, Ribes R, Caro P, Luna L, Aumente E, Ros PR. MRI of focal splenic lesions without and with dynamic gadolinium enhancement. AJR Am J Roentgenol 2006;186:1533–1547 Rabushka LS, Kawashima A, Fishman EK. Imaging of the spleen: CT with supplemental MR examination. Radiographics 1994;14:307–332 Ramani M, Reinhold C, Semelka RC, et al. Splenic hemangiomas and hamartomas: MR imaging characteristics of 28 lesions. Radiology 1997;202:166–172

CASE 43 Clinical Presentation A 63-year-old man complains of fatigue, general malaise, and weight loss.

B

A

Fig. 43.1 (A,B) Axial contrast-enhanced CT images of the abdomen show multiple small, hypodense nodular lesions scattered within a normal-sized spleen. No lesions are seen in the liver. There is no evidence of abnormal lymphadenopathy or fluid collection.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images of the abdomen (Fig. 43.1) demonstrate multiple small, hypodense lesions within the splenic parenchyma.

Diagnosis Splenic sarcoidosis

Differential Diagnosis • • • •

Lymphoma Metastases Infection Littoral cell angiomas

Discussion Background Sarcoidosis is a multisystemic granulomatous disease usually occurring in young to middle-aged adults with a slightly higher prevalence in women. The incidence is extremely variable worldwide according to distinct racial and geographic predilections; in the United States, most of the cases have been described in African Americans, whereas outside the United States, Swedes and Danes appear

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to be more affected. Japan accounts for most of the cases encountered in Eastern countries. Although sarcoidosis mostly affects pulmonary parenchyma and mediastinal lymph nodes (> 90% of patients), every other organ system can be involved, including the liver and spleen, skin, central nervous system, genitourinary system, muscles, and bone. The diagnosis of sarcoidosis relies on both clinical and radiologic findings subsequently confirmed at histology (noncaseating granulomas with epithelioid and multinucleated giant cells).

Clinical Findings Patients may be either asymptomatic (~50%) or present with nonspecific symptoms, including fatigue, malaise, weight loss, and low-grade fever. Laboratory tests often demonstrate an increased level of angiotensin-converting enzyme (ACE), elevated erythrocyte sedimentation rate, anemia, leukopenia, and eosinophilia. Hypercalciuria and/or hypercalcemia have been reported in up to 30% of cases.

Complications Splenic dysfunction in sarcoidosis is rarely documented.

Etiology Infectious agents, drugs, genetic factors, and autoimmunity have all been considered potential causes of sarcoidosis, but the etiology of this disease remains unclear. Several authors suggest that the exposure to specific environmental agents in genetically predisposed patients may trigger an exaggerated cellular immune response leading to granuloma formation.

Imaging Findings • •



Imaging plays a major role in management, as radiographic evidence of sarcoidosis may be present even in the absence of clinical or laboratory abnormalities. The most common CT findings are splenomegaly without imaging evidence of focal lesions, multiple hypodense lesions resulting from the coalescence of microscopic granulomata, and diffuse parenchymal inhomogeneity; the latter finding is probably due to the presence of multiple lesions too small to be distinguished at imaging (sarcoid granulomas are typically < 2 mm). Abdominal lymphadenopathy frequently accompanies splenic nodules. At magnetic resonance imaging (MRI), focal lesions of splenic sarcoidosis appear hypointense in all sequences, although they may be better appreciated on T2-weighted fat-suppressed images. After intravenous gadolinium administration, these lesions generally present minimal and delayed enhancement.

Treatment •

Asymptomatic patients with isolated hepatosplenic sarcoidosis do not require treatment. On the contrary, corticosteroids are considered the treatment of first choice in cases of multisystemic involvement; patients with aggressive disease or frequent recurrence may be unresponsive to this therapy and therefore may benefit from other medications, including methotrexate, azathioprine, and cyclophosphamide. Newer therapeutic strategies include the use of monoclonal antibodies and tumor necrosis factor.

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Prognosis •

The prognosis is favorable; patients with isolated splenic lesions usually do not need treatment.

PE ARL



Differential diagnosis should always include lymphoma, metastatic disease, and infection, as these disorders commonly present with splenic low-attenuation nodular lesions. Lymphomas, in particular, should be carefully considered, as they can cause similar symptoms and be associated with lymphadenopathy and splenomegaly.

PITFALL



Splenic lesions may be too small to be recognized at imaging (false-negative studies).

Suggested Readings Elsayes KM, Narra VR, Mukundan G, Lewis JS Jr, Menias CO, Heiken JP. MR imaging of the spleen: spectrum of abnormalities. Radiographics 2005;25:967–982 Freeman JL, Jafri SZ, Roberts JL, Mezwa DG, Shirkhoda A. CT of congenital and acquired abnormalities of the spleen. Radiographics 1993;13:597–610 Koyama T, Ueda H, Togashi K, Umeoka S, Kataoka M, Nagai S. Radiologic manifestations of sarcoidosis in various organs. Radiographics 2004;24:87–104 Warshauer DM, Dumbleton SA, Molina PL, Yankaskas BC, Parker LA, Woosley JT. Abdominal CT findings in sarcoidosis: radiologic and clinical correlation. Radiology 1994;192:93–98 Warshauer DM, Molina PL, Hamman SM, et al. Nodular sarcoidosis of the liver and spleen: analysis of 32 cases. Radiology 1995;195:757–762

CASE 44 Clinical Presentation A 30-year-old woman complains of abdominal pain.

A

B

C

D

Fig. 44.1 (A–E) Contrast-enhanced CT study shows the

E

absence of the spleen in the left upper quadrant. The spleen is present inferior to the liver with a torsed pedicle seen as a whirl-like appearance of splenic vessels and surrounding fat noted at the splenic hilum (D).

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Radiologic Findings Axial contrast-enhanced computed tomography (CT) images of the abdomen (Fig. 44.1) reveal the absence of the spleen in the left upper quadrant. The spleen is seen inferior to the liver in the right lower quadrant.

Diagnosis Wandering spleen

Differential Diagnosis •

Malrotation

Discussion Background This clinical entity usually presents between the ages of 20 and 40 years and is most commonly seen in women; most are of reproductive age at the time. Children make up one third of all cases, and 30% of them are younger than 10 years of age. This condition can be acquired or congenital. The acquired form is usually seen in multiparous women, attributed to hormonal changes during pregnancy that cause laxity of the ligaments normally attached to the spleen. In the congenital form, there is failure of normal development of the dorsal mesogastrium when the lesser sac is formed. The attachments of the dorsal mesentery to the posterior peritoneum and diaphragm are faulty. Suspensory ligaments of the spleen are not formed or are only partially formed. The length of its vascular pedicle determines the mobility of the spleen in the absence of some or all of these ligaments.

Clinical Findings Clinical presentations of wandering spleen are variable, and patients may present with an asymptomatic abdominal mass, intermittent abdominal pain, or acute abdomen. The nature of the pain reflects the degree of vascular occlusion and ischemia to the splenic pedicle. Acute torsion may precipitate fever, vomiting, and acute abdominal pain; recurrent, chronic torsion and detorsion may present as intermittent colicky pain or vague abdominal discomfort. Acute pancreatitis may be associated because of the incorporation of the tail of the pancreas in the spleen’s vascular pedicle. Gastric compression or distention also may occur.

Complications Complications include acute pain, torsion, splenic infarction and gangrene, splenic abscess, splenic trauma, variceal hemorrhage, gastric outlet obstruction, and pancreatitis.

Etiology Wandering spleen may be congenital or acquired.

Imaging Findings CT is the best modality to diagnose wandering spleen and delineates other anatomical relationships of the spleen. In addition, the tail of the pancreas, as well as other normal or abnormal intra-abdominal structures, can be evaluated. CT findings of wandering spleen include the absence of the spleen

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B

A

Fig. 44.2 (A,B) Contrast-enhanced CT study shows a torsed spleen with infarct (arrow). (C) Note the whorled appearance of the splenic vessels at the hilum (arrow).

C

in the left upper quadrant and a soft tissue mass resembling the spleen elsewhere in the abdomen (Fig. 44.1). If significant torsion of the splenic pedicle occurs, the torsed pedicle is seen as a “whirllike” appearance of splenic vessels and surrounding fat, usually noted at the splenic hilum (Fig. 44.2). Occasionally, ascites or necrosis of the pancreatic tail can be seen. If torsion is chronic, a thick pseudocapsule is evident. The spleen is not enhanced by intravenous contrast medium if torsion has occurred and blood supply is lost. Arteriography allows definitive evaluation of the splenic vasculature and signs of left-sided portal hypertension, if present. Several different radiologic modalities exist to diagnose a wandering spleen.

Treatment •

Definitive treatment for wandering spleen is surgical because nonoperative treatment is associated with a complication rate as high as 65%. Splenopexy with splenic salvage is now the procedure of choice in children. If the spleen appears infarcted, a splenectomy should be performed instead. Splenopexy is a reasonable option when the spleen appears viable after detorsion and the splenic vein is not thrombosed.

Prognosis •

The prognosis is favorable when the condition is diagnosed and appropriate treatment is instituted.

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PE ARL



Consider the diagnosis of wandering spleen when the organ is absent in the left upper quadrant and is present inferior to the liver.

Suggested Readings Allen KB, Gay BB Jr, Skandalakis JE. Wandering spleen: anatomic and radiologic considerations. South Med J 1992;85:976–984 Desai DC, Hebra A, Davidoff AM, Schnaufer L. Wandering spleen: a challenging diagnosis. South Med J 1997;90:439–443 Duperier T, Schmidt H, Davies R. Wandering spleen: an unusual presentation of abdominal pain. Contemp Surg 2001;57:520–524 Gayer G, Zissin R, Apter S, Atar E, Portnoy O, Itzchak Y. CT findings in congenital anomalies of the spleen. BJR Br J Radiol 2001;74:767–772 Nemcek AA Jr, Miller FH, Fitzgerald SW. Acute torsion of a wandering spleen diagnosis by CT and duplex Doppler and color flow sonography. AJR Am J Roentgenol 1991;157:307–309 Raissaki M, Prassopoulos P, Daskalogiannaki M, Magkanas E, Gourtsoyiannis N. Acute abdomen due to torsion of wandering spleen: CT diagnosis. Eur Radiol 1998;8:1409–1412 Swischuk LE, Williams JB, John SD. Torsion of wandering spleen: the whorled appearance of the splenic pedicle on CT. Pediatr Radiol 1993;23:476–477

CASE 45 Clinical Presentation A 61-year-old woman with a previous history of endometrial carcinoma and elastofibroma of the shoulder complains of upper abdominal pain. She underwent splenectomy following her initial evaluation.

B

A

Fig. 45.1 (A–C) Axial contrast-enhanced CT images of the abdomen show an enhancing, exophytic lesion adjacent to the splenic hilum.

C

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images of the abdomen (Fig. 45.1) show a heterogeneously enhancing, exophytic lesion adjacent to the splenic hilum.

Diagnosis Inflammatory splenic pseudotumor

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Differential Diagnosis • • • •

Hemangioma Hematoma Lymphoma Metastases

Discussion Background Inflammatory pseudotumor (IPT) is an ill-defined benign entity of unknown origin presenting as a masslike lesion with inflammation and mesenchymal repair. It is composed of plasma cells, lymphocytes, foreign body giant cells, histiocytes, foam cells, and numerous vascular elements. This lesion has been observed in tissues of the respiratory tract, gastrointestinal tract, orbit, soft tissues, lymph nodes, and other organs, with splenic occurrence of IPT being extremely rare. It is frequently misdiagnosed clinically and radiologically as a malignant neoplasm.

Clinical Findings There are no specific clinical symptoms for this condition.

Complications There are no known complications.

Etiology Although no specific etiologic factor has been found conclusively, several hypotheses have been suggested. Matsubayashi et al suggested that the rupture of splenic hemangioma may result in IPT, whereas other authors have postulated that the etiology and pathogenesis may be due to ineffective antibiotic therapy, a specific unidentified infectious agent, the granulomatous inflammation process and disturbance of the blood supply, autoimmune disorders, or an abnormality of lipid metabolism.

Imaging Findings • •





Sonography can demonstrate IPT as a hypoechoic lesion in the spleen, not typical of a cyst, or shows a large, partially calcified, well-defined echogenic mass. Nonenhanced CT demonstrates a rounded mass with low attenuation values with or without partial calcification. Enhanced CT demonstrates a slightly heterogeneous mass in the spleen with minimal enhancement (Fig. 45.1). On magnetic resonance imaging (MRI), the lesion appears isointense on T1-weighted images and with either increased or decreased signal intensity on T2-weighted images with respect to the surrounding normal spleen. Although sonography, CT scan, and MRI may aid in the identification of space-occupying lesions of the spleen, these techniques do not permit a definitive diagnosis.

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Treatment •

Although the condition is benign, imaging does not allow accurate differentiation from malignant splenic conditions. Hence these patients may have a splenectomy for definitive diagnosis.

Prognosis •

The prognosis is favorable when the condition is diagnosed.

PE ARL



This is a rare lesion with no specific imaging features.

Suggested Readings Chen HD, Huang YS, Chai CY, Huang TJ. Inflammatory pseudotumor of the spleen: a case report. Kaohsiung J Med Sci 2001;17:441–443 Cotelingam JD, Jaffe ES. Inflammatory pseudotumor of the spleen. Am J Surg Pathol 1984;8:375–380 Franquet T, Montes M, Aizcorbe M, Barberena J, Ruiz de Azua Y, Cobo F. Inflammatory pseudotumor of the spleen: ultrasound and computed tomographic findings. Gastrointest Radiol 1989;14:181–183 Wiernik PH, Rader M, Becker NH, Morris SF. Inflammatory pseudotumor of the spleen. Cancer 1990;66:597–600

CASE 46 Clinical Presentation A 25-year-old patient presents with sickle cell disease.

B

A

Fig. 46.1 (A–C) Noncontrast CT scans of the upper abdomen show a partially calcified small spleen.

Radiologic Findings Noncontrast axial computed tomography (CT) scan shows a calcified small spleen (Fig. 46.1).

Diagnosis Autosplenectomy from sickle cell disease

Differential Diagnosis • •

Hemosiderosis Thorotrast accumulation

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Discussion Background Sickle cell disease is a common hereditary disorder caused by a hemoglobinopathy. The disease affects multiple organ systems in the body, and the spleen is a common site of involvement. Sickle cell disease encompasses several entities: sickle cell anemia (SS), sickle cell–hemoglobin C (SC) disease, and sickle cell–␤-thalassemia. Hemoglobin S is a result of the single gene substitution of a valine for a glutamic acid in the sixth amino acid position of the ␤-globin chain. This produces a hemoglobin tetramer that has low solubility in conditions of deoxygenation. The symptoms of sickle cell disease are caused by the particular properties of hemoglobin S. In conditions of low oxygenation, the sickle hemoglobin forms rigid polymers that cause the red blood cells to deform into sickle shapes. This malformed hemoglobin causes vasoocclusion in small vessels and results in slowed blood flow in larger vessels. Severe, chronic hemolytic disease, as well as various manifestations of vasoocclusive disease, characterizes sickle cell disease.

Clinical Findings Sickle cell disease can be diagnosed in newborns as well as in children and adults with hemoglobin electrophoresis, isoelectric focusing, or deoxyribonucleic acid (DNA) analysis. It is diagnosed when electrophoresis shows hemoglobin with an intermediate mobility, between those of hemoglobin A and hemoglobin A2. In the homozygous form of the disease, the spleen is destroyed in the 1st decade of life, with painful vasoocclusive-infarctive crisis, and becomes small, fibrotic, and even calcified in virtually all adult patients (autosplenectomy).

Complications Secondary infections are rare.

Etiology Autosplenectomy or end-stage spleen is typically seen in patients with homozygous sickle cell disease. During the early phase of the disease, microinfarctions of the spleen occur secondary to venoocclusive disease. This leads to perivascular fibrosis with resulting decrease in the size of the spleen, along with hemosiderin and calcium deposition.

Imaging Findings Although the calcification can be seen on plain films, this finding is best seen with CT. The typical CT finding is a small, calcified, nonfunctioning spleen. The two main differential conditions that may mimic calcified small spleen, hemosiderosis and Thorotrast accumulation, also involve the liver.

Treatment •

No specific treatment is needed for this radiographic finding.

Prognosis •

Patients with abdominal findings of sickle cell disease are susceptible to disease-related prognoses.

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PE ARL



A small, calcified spleen seen on imaging is suggestive of autosplenectomy in a patient with sickle cell disease.

PITFALL



Autosplenectomy from sickle cell disease can be confused with hemosiderosis or Thorotrast deposition.

Suggested Readings Beutler E. The sickle cell diseases and related disorders. In: Williams WS, Beutler E, Erslev AS, et al, eds. Hematology. New York: McGraw-Hill; 1991:613–614 Levin TL, Berdon WE, Haller JO, et al. Intrasplenic masses of “preserved” functioning splenic tissue in sickle cell disease: correlation of imaging findings (CT, ultrasound, MRI, and nuclear scintigraphy). Pediatr Radiol 1996;26:646–649 Magid D, Fishman EK, Charache S, Siegelman SS. Abdominal pain in sickle cell disease: the role of CT. Radiology 1987;163:325–328 Wagner GM, Vichnsky EP, Lande WM, et al. Sickling syndromes and unstable hemoglobin disease. In: Petz LD, Garratty G, eds. Hereditary Haemolytic Anemias. New York: Churchill Livingstone; 1989: 198–221

CASE 47 Clinical Presentation A 60-year-old man complains of vague abdominal pain.

A

B

Fig. 47.1 (A–C) Noncontrast CT scan of the upper abdomen shows a small, dense spleen, along with small, dense lymph nodes in the upper abdomen.

C

Radiologic Findings Noncontrast axial computed tomography (CT) scan shows a small, dense spleen (Fig. 47.1), along with focal specks of hyperdensity in the upper abdominal lymph nodes and liver.

Diagnosis Thorotrast accumulation in the liver, spleen, and lymph nodes

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Differential Diagnosis • •

Hemosiderosis Autosplenectomy seen in sickle cell disease

Discussion Background Thorotrast was a colloidal suspension of thorium dioxide that was used until the 1950s as an intravascular contrast agent. Following administration, the agent is retained by the reticuloendothelial system and is therefore found in the liver, spleen, lymph nodes, and bone marrow years after it is administered. Thorotrast is no longer used because thorium is an alpha emitter and has a very long half-life (400 years), making it extremely carcinogenic.

Clinical Findings No specific clinical findings are seen with Thorotrast deposition. This condition is incidentally detected by imaging.

Complications Increased risk of hepatic and splenic angiosarcoma, cholangiocarcinoma, and hepatoma

Etiology Thorotrast particles were 3 to 10 μm in size and were phagocytized by the reticuloendothelial system cells in the liver, spleen, lymph nodes, and bone marrow. The liver absorbed 70% of the injected dose and the spleen 20%, the remaining dose shared between the bone marrow and the lymph nodes. The average latency from exposure to the development of liver cancer was 26 years.

Imaging Findings The radiographic pattern differed from the immediate distribution of Thorotrast. CT scans obtained years after Thorotrast administration predominantly show distribution in the spleen and lymph nodes. The spleen is small in size owing to pulp fibrosis. The lymph nodes and spleen appear very dense on noncontrast CT images.

Treatment •

No specific treatment is needed for this radiographic finding.

Prognosis •

The dismal prognosis in patients with Thorotrast-induced hepatosplenic neoplasms is related in part to the advanced stage of the disease found at the time of detection.

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Pe a r l



A small, dense spleen, along with punctate high-density abdominal lymph nodes, should raise a suspicion of prior Thorotrast administration.

Pitfa l l



Thorotrast accumulation can be confused with hemosiderosis or autosplenectomy in sickle cell disease.

Suggested Readings Andersson M, Vyberg M, Visfeldt J, Carstensen B, Storm HH. Primary liver tumors among Danish patients exposed to Thorotrast. Radiat Res 1994;137(2):262–273 Isner JM, Sazama KJ, Roberts WC. Vascular complications of thorium dioxide. Am J Med 1978;64(6):1069–1074 Kato I, Kido C. Increased risk of death in Thorotrast-exposed patients during the late follow-up period. Jpn J Cancer Res 1987;78(11):1187–1192 Velasquez G, Ward CF, Bohrer SP. Thorium dioxide: still around. South Med J 1985;78(6):743–745

CASE 48 Clinical Presentation A 40-year-old man presents with abdominal pain and a single episode of an upper gastrointestinal (GI) bleed.

B

A

Fig. 48.1 (A) Contrast-enhanced axial CT image shows the presence of a splenic arteriovenous fistula (arrow). (B) Note the dilated upper abdominal venous varices (arrows).

Radiologic Findings Contrast-enhanced axial computed tomography (CT) scans (Fig. 48.1) show an enlarged spleen with an arteriovenous (AV) fistula and early opacification of the splenic vein. Note the enlarged collateral veins in the upper abdomen.

Diagnosis Splenic AV fistula with features of portal hypertension

Differential Diagnosis •

None; the differential is in the etiology of a splenic AV fistula.

Discussion Background Splenic arteriovenous fistula (SAVF) is rare and usually presents with features of established portal hypertension.

Clinical Findings These patients can have an asymptomatic abdominal bruit or may present with symptoms of portal hypertension.

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Complications Complications are portal hypertension leading to variceal bleeding, mesenteric ischemia, and congestive heart failure.

Etiology SAVF can be congenital or acquired. It is thought that the fistula arises from the rupture of a preexisting splenic artery aneurysm into the splenic vein due to high intra-abdominal pressure. Congenital fistulas can occur with splenic artery aneurysms and are seen in patients with Osler-Weber-Rendu disease and Ehlers-Danlos syndrome. Acquired fistulas are secondary to trauma, splenic biopsy, and splenic aneurysmal rupture or are, rarely, spontaneous. Portal hypertension in SAVF is secondary to hyperdynamic circulation and is associated with a hepatopetal flow. These patients manifest with varices, splenomegaly, ascites, and diarrhea.

Imaging Findings SAVF should be suspected in patients with presinusoidal portal hypertension with a hepatopetal flow. Doppler study, angiography, and magnetic resonance angiography are useful in establishing the diagnosis. Early opacification of the portal vein in the arterial phase of dynamic CT offers a clue to the diagnosis. Multiple varices are seen in the upper abdomen.

Treatment •

Angioembolization of low-flow fistulas with Gelfoam/steel coils and high-flow fistulas with balloons should be the primary treatment option. The role of surgery is limited to fistulas that are not amenable to embolization and fistulas near the splenic hilum, when splenectomy is an easier option.

Prognosis •

The prognosis is good if therapy results in the cessation of fistulous communication between the splenic artery and vein.

PE ARL



Suspect SAVF in patients with portal hypertension and no demonstrable liver disease.

PITFALL



SAVF may be difficult to detect if an early phase CT is not performed.

Suggested Readings McClary RD, Finelli DS, Croker B, Davis GL. Portal hypertension secondary to a spontaneous splenic arteriovenous fistula: case report and review of the literature. Am J Gastroenterol 1986;81:572–575 Stanley JC, Wakefield TW, Graham LM, Whitehouse WM Jr, Zelenock GB, Lindenauer SM. Clinical importance and management of splanchnic artery aneurysms. J Vasc Surg 1986;3:836–840

CASE 49 Clinical Presentation A 55-year-old woman presents with abdominal pain, low-grade fever, and weight loss.

A

B

Fig. 49.1 (A–C) Axial contrast-enhanced CT images show multiple, well-defined, low-density focal lesions in the spleen. Also seen are thickening of the stomach wall, enlarged retroperitoneal abdominal lymph nodes, and a left pleural effusion.

C

Radiologic Findings Contrast-enhanced axial computed tomography (CT) scans show multiple low-density lesions in the spleen, along with diffuse thickening of the stomach, left pleural effusion, and enlarged abdominal lymph nodes (Fig. 49.1).

Diagnosis Secondary involvement of the spleen in lymphoma

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Differential Diagnosis • • • • •

Splenic metastases Splenic abscesses Spleen primary tumor Splenic infarcts Sarcoidosis

Discussion Background Lymphoma is the most common malignant tumor involving the spleen. Splenic involvement can be primary (without evidence of nodal disease) or secondary from disseminated disease. Although lymphomatous involvement can be the cause of splenomegaly, splenic size is not a reliable clinical and imaging indicator of the presence or absence of disease.

Clinical Findings Patients usually present with systemic clinical findings seen with lymphoma, such as fever, weight loss, night sweats, and malaise.

Complications • • •

Splenomegaly Splenic rupture Splenic infarcts

Etiology Splenic lymphoma is common in both Hodgkin disease (seen in 40–60%) and non-Hodgkin lymphoma (seen in 70%), but it may be difficult to detect by imaging techniques because the disease may manifest as diffuse infiltration rather than discrete nodules. Splenic enlargement alone is not a good indicator of lymphomatous involvement.

Imaging Findings •



On CT scans, lymphomatous involvement can be seen as one of the following patterns: diffuse infiltration and enlargement, homogeneous enlargement, multiple focal lesions of varying size (as seen in this case), or a single large hypodense lesion. Accompanying changes of lymphoma will also be seen in the abdomen. Detecting lymphomatous involvement of the spleen with positron emission tomography imaging depends on identifying increased glucose metabolism by tumor cells and hence will show multiple hypermetabolic foci.

Treatment •

Chemotherapy, radiation, or surgery in isolated patients.

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Prognosis •

The early stage has a good prognosis.

PE ARL



Splenic enlargement is not always seen with lymphomatous involvement. The disease may present as diffuse infiltration, making it difficult to detect by conventional imaging techniques.

PITFALL



It may be difficult to distinguish secondary involvement of the spleen in lymphoma from other splenic neoplastic conditions.

Suggested Readings Hahn PF, Weissleder R, Stark DD, Saini S, Elizondo G, Ferrucci JT. MR imaging of focal splenic tumors. AJR Am J Roentgenol 1988;150(4):823–827 Urban BA, Fishman EK. Helical CT of the spleen. AJR Am J Roentgenol 1998;170:997–1003

CASE 50 Clinical Presentation A 42-year-old man with known aortic valve endocarditis presents with left upper abdominal pain and low-grade fever.

B

A

Fig. 50.1 (A–C) Axial contrast-enhanced CT images show multiple, well-defined, wedge-shaped areas of low attenuation in the spleen and left kidney associated with a left pleural effusion.

C

Radiologic Findings Contrast-enhanced axial computed tomography (CT) scans show multiple wedge-shaped areas of low attenuation seen in the spleen and the left kidney, along with a small left pleural effusion (Fig. 50.1).

Diagnosis Septic emboli causing infarcts in the spleen and left kidney

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Differential Diagnosis • • •

Splenic abscess Splenic neoplasm Splenic laceration

Discussion Background Splenic infarcts can be segmental or global, involving the entire organ, and may result from arterial or venous compromise. They are most commonly associated with hematologic disorders, but they can also result from embolization in the setting of a left atrial or ventricular mural thrombus formed as a result of various etiologies.

Clinical Findings Patients commonly present with left upper quadrant pain and fever. About half show anemia and leukocytosis.

Complications Infarcts can be global, affecting the entire organ. Infected emboli may result in secondary infection and abscess formation. Sympathetic pleural effusions are seen on the left side.

Etiology • • • • •

Embolic Hematologic Splenic vascular disease Anatomical variants, such as splenic torsion and wandering spleen Miscellaneous causes, such as pancreatic disease and collagen vascular disease

Imaging Findings On contrast-enhanced CT images, splenic infarcts are seen as wedge-shaped or rounded areas of low attenuation. If the entire organ is affected, there is a global lack of enhancement. In cases of embolization, associated infarcts can be seen in other visceral organs, such as the kidneys or liver.

Treatment •

If patients are asymptomatic, no treatment is necessary. In the case of global ischemia and if the patient is symptomatic with complications, a splenectomy may be needed.

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Prognosis •

The prognosis varies with the severity of the disease and the treatment.

PE ARL



Wedge-shaped areas of low attenuation in the spleen and other parenchymal organs require a work-up for the sources of the emboli.

PITFALL



If the infarcts are not wedge-shaped, these lesions can mimic a splenic abscess or tumor.

Suggested Readings Balthazar EJ, Hilton S, Naidich D, Megibow A, Levine R. CT of splenic and perisplenic abnormalities in septic patients. AJR Am J Roentgenol 1985;144:53–56 Haft JI, Altieri J, Smith LG, Herskowitz M. Computed tomography of the abdomen in the diagnosis of splenic emboli. Arch Intern Med 1988;148:193–197

CASE 51 Clinical Presentation A 35-year-old man presents with vague abdominal pain.

A

B

C

D

Fig. 51.1 (A–D) Contrast-enhanced axial CT scans show multiple homogeneously enhancing nodules in the left upper quadrant and the right abdomen (arrow). Note the absence of the spleen, the patient was involved in a motor vehicle accident as a teenager and had undergone a splenectomy.

Radiologic Findings Contrast-enhanced axial computed tomography (CT) scans shows multiple homogeneously enhancing nodules in the abdomen (Fig. 51.1). Note the absence of the spleen; the patient was involved in a motor vehicle accident as a teenager and had undergone a splenectomy.

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Diagnosis Splenosis

Differential Diagnosis • •

Multiple accessory spleen Polysplenia

Discussion Background Splenosis, or heterotopic autotransplantation of splenic tissue, is a common sequel to traumatic or surgical injury to the splenic capsule with intraperitoneal seeding of splenic pulp. Thirty to 70% of posttraumatic splenectomy cases are reported to have splenosis. Intra-abdominal splenosis can occur anywhere in the peritoneal cavity, with the most frequent sites being the serosal surfaces of the small intestine, greater omentum, parietal peritoneum, large intestine, mesentery, and undersurface of the diaphragm. Each accessory spleen has its own hilum, capsule, and splenic arterial supply.

Clinical Findings Splenosis is usually asymptomatic and is an incidental finding, sometimes mimicking renal or adrenal tumors, metastases, lymphoma, and endometriosis. Occasionally, patients present with vague abdominal pain, dyspareunia, torsion, intestinal obstruction, or rupture.

Complications None

Etiology Splenosis is usually seen following surgical removal of the spleen after traumatic splenic injury.

Imaging Findings •

• • •

On ultrasound, focal areas of splenosis are seen as well-defined hypoechoic areas within the abdominal cavity, usually with a hyperechoic rim. A sonographic differentiating feature from accessory spleens is the presence of multiple vessels penetrating the dense pseudocapsule on color or power Doppler, together with the absence of a vascular hilum. On CT, splenosis manifests as variably shaped, multiple, homogeneous soft tissue masses that are slightly hypodense to liver on contrast-enhanced scans scattered throughout the abdomen. On magnetic resonance imaging, the lesions are T1 hypointense to liver and T2 hyperintense to liver. Of all imaging modalities, scintigraphic imaging is the most specific. Technetium 99m heat-damaged red cell scan is most sensitive and specific, particularly for splenectomized patients, as 90% of damaged red cells are trapped in the spleen, whereas only 10% of the sulfur colloid is taken up by splenic tissue.

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Treatment •

None

Prognosis •

Good

PE ARL



Consider this diagnosis if the patient has a history of splenectomy.

PITFALL



Focal areas of splenosis, when large, can mimic tumors in the abdomen and pelvis.

Suggested Readings Buchbinder JH, Lipkoff CJ. Multiple peritoneal splenic implants following abdominal injury. Surgery 1939;6:927–934 Lindell RG, Brown JM, Lindgren RD. Splenosis: CT demonstration of heterotopic autotransplantation of splenic tissue. J Comput Assist Tomogr 1982;6:1184–1187 Mandelson DS, Cohen BA, Armas RD. CT appearance of splenosis. J Comput Assist Tomogr 1982;6:1188– 1190

V

Kidneys and Ureters

CASE 52 Clinical Presentation A 31-year-old man presents with hypertension.

Fig. 52.1 Axial image from a contrast-enhanced CT scan of the abdomen demonstrates numerous cysts within the liver and kidneys. Most of the cysts are simple in appearance.

Radiologic Findings Axial image from a contrast-enhanced computed tomography (CT) scan of the abdomen (Fig. 52.1) demonstrates numerous cysts within the liver and kidneys. Most of the cysts are simple in appearance.

Diagnosis Autosomal dominant polycystic kidney disease (ADPKD)

Differential Diagnosis • • •

Acquired cystic disease Tuberous sclerosis Von Hippel-Lindau disease

Discussion Background ADPKD is one of the more common autosomal dominant inheritable diseases and is a common cause of renal failure.

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Clinical Findings Patients with the disease are typically asymptomatic, but they may have a family history of renal disease. The disease is often diagnosed in young patients after the 3rd decade of life. Patients may present with abdominal pain and/or hypertension or with symptoms related to cyst rupture. The diagnosis is often unsuspected and may be detected as an incidental finding. Renal failure develops in nearly all patients over time.

Complications The cysts can be complicated by infection or hemorrhage. In addition, these patients are at increased risk of renal stone formation and can present with pain secondary to urinary tract obstruction. Cysts may also rupture and cause acute pain or retroperitoneal hemorrhage. Approximately 10% of patients die following the rupture of an associated intracranial berry aneurysm.

Etiology The disease is thought to be related to defective polycystins that appear to contribute to cyst formation by affecting epithelial cell maturation, resulting in the development of cysts of different sizes in the cortex and medulla. The gene defect is located on chromosome arm 16p in 90% of patients and is related to spontaneous mutation in 10% of patients.

Imaging Findings •

• • •



Typical imaging findings include bilateral renal enlargement with innumerable cysts in both kidneys. Hepatic cysts are present in up to 70% of cases, pancreatic cysts in 9%, and intracranial aneurysms in 20%. On intravenous urography, a “Swiss cheese” nephrogram, with nephrographic parenchymal defects relating to the cysts, may be seen. On ultrasound, uncomplicated cysts are anechoic with increased through-transmission and an imperceptible wall. Hemorrhagic cysts may have internal echoes and septations. CT scanning shows uncomplicated cysts as well-circumscribed fluid attenuation lesions (< 10–15 Hounsfield units) with no detectable enhancement. If cysts become hemorrhagic, their native density will increase. Mural calcifications are commonly seen. Uncomplicated cysts are T1 hypointense and T2 hyperintense on MRI (Fig. 52.2) with a thin wall and no enhancement. Hemorrhagic cysts may vary in signal intensity depending on the age of the blood products. Most commonly, hemorrhagic cysts are T1 and T2 hyperintense.

Treatment •

ADPKD is a progressive disease with no known treatment. Complications such as hypertension are treated medically. Large cysts causing clinical symptoms may be percutaneously aspirated and sclerosed using CT or ultrasound guidance. Patients eventually require dialysis and renal transplantation. Approximately 10% of patients on renal dialysis have ADPKD.

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Fig. 52.2 Coronal single-shot fast spin-echo T2-weighted image of the abdomen shows bilaterally enlarged kidneys with multiple T2 hyperintense cysts. Note the accompanying multiple hyperintense cysts within the liver.

Prognosis •

Most patients develop renal failure by age 60.

PE ARL



ADPKD is associated with the presence of intracranial aneurysms in 20%.

PITFALL



Infection or hemorrhage within the cysts can create a complex appearance; however, there is no increase in the risk of renal cell carcinoma unless the patient is also on dialysis.

Suggested Readings Gupta S, Seith A, Dhiman RK, et al. CT of liver cysts in patients with autosomal dominant polycystic kidney disease. Acta Radiol 1999;40:444–448 Gupta S, Seith A, Sud K, et al. CT in the evaluation of complicated autosomal dominant polycystic kidney disease. Acta Radiol 2000;4:280–284 Mosetti MA, Leonardou P, Motohara T, et al. Autosomal dominant polycystic kidney disease: MR imaging evaluation using current techniques. J Magn Reson Imaging 2003;18:210–215

CASE 53 Clinical Presentation Patient underwent ultrasound exam for nonspecific abdominal pain; incidental finding.

B

A

Fig. 53.1 (A,B) Ultrasound images show a single large echogenic lesion (arrow) arising from the lower pole of the right kidney with internal color Doppler flow. (C) Contrastenhanced coronal CT image from the same patient demonstrates a predominantly fat-containing vascular mass in the lower pole of the right kidney (arrow).

Radiologic Findings A sagittal ultrasound image demonstrates a large echogenic lesion in the lower pole of the right kidney (Fig. 53.1A) with internal color Doppler flow (Fig. 53.1B). Contrast-enhanced coronal computed tomography (CT) images from the same patient demonstrate a predominantly fat-containing vascular mass in the lower pole of the right kidney corresponding to the lesion seen on ultrasound (Fig. 53.1C).

Diagnosis Renal angiomyolipoma (AML)

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Differential Diagnosis On ultrasound: • • • • •

Renal cell carcinoma Oncocytoma Renal metastasis Retroperitoneal sarcoma Renal lymphoma On CT:

• •

None as long as the lesion demonstrates typical uniform distribution of fat Variants of AML where the muscular or vascular components predominate are difficult to differentiate from renal cell carcinoma.

Discussion Background In adults, AML is the most common benign tumor of the kidney with mesenchymal components. Pathologically, it is composed of three elements: adipose tissue, abnormal blood vessels, and smooth muscle. Typically, the fat component predominates. Twenty percent of cases of AML are associated with tuberous sclerosis, and 80% of patients with tuberous sclerosis have AMLs.

Clinical Findings Most AMLs are asymptomatic and are found incidentally at imaging. Less commonly, patients may present with pain, bleeding, and/or a palpable mass.

Complications The most common complication associated with a renal AML is hemorrhage, usually seen with tumors > 4 cm.

Etiology AML is a benign tumor that develops spontaneously and occurs as an isolated, incidental finding in the majority of patients.

Imaging Findings •



CT is the best imaging modality for the evaluation of an AML and can provide a definitive diagnosis in the majority of cases. Nonenhanced CT demonstrates a well-delineated renal cortical mass of predominantly fat density. However, up to 5% of renal AMLs have no detectable fat on CT. Occasionally, AMLs grow to become quite large. Contrast-enhanced CT may demonstrate variable enhancement of the tumor. On ultrasound, AMLs are markedly hyperechoic relative to the normal kidney. However, this is a nonspecific finding, as up to a third of renal cell carcinomas < 3 cm in size may appear hyperechoic.

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• •

171

On magnetic resonance imaging, AMLs are T1 hyperintense and demonstrate signal loss on fat suppression sequences. As with CT, contrast enhancement is variable. Angiography shows a highly vascular lesion with multiple pseudoaneurysms.

Treatment •

AMLs < 4 cm in diameter are usually managed conservatively, and imaging surveillance can be used to assess for increase in size. Surgical resection may be recommended for tumors > 4 cm because of the increased risk of rupture and hemorrhage. Tumor embolization may be performed preoperatively to minimize intraoperative hemorrhage or to treat acute bleeding.

Prognosis •

AMLs are benign lesions. Large tumors may bleed and can lead to massive hemorrhage.

PE ARL S

• •

There is a risk of rupture and hemorrhage with AMLs > 4 cm. The presence of multiple, bilateral AMLs suggests the diagnosis of tuberous sclerosis.

PITFALL



Approximately 5% of AMLs are fat poor, making characterization and differentiation from renal cell carcinoma difficult.

Suggested Readings Federle MP, Jeffrey RB, Desser TS. Diagnostic Imaging: Abdomen. Vol. 3. Salt Lake City, UT: Amirsys; 2004:88–91. Wagner BJ, Wong-You-Cheong JJ, Davis CJ Jr. Adult renal hamartomas. Radiographics 1997;17(1): 155–169

CASE 54 Clinical Presentation A 72-year-old man presents with a 1-month history of left lower quadrant pain.

A

B

Fig. 54.1 (A,B) Axial and coronal images from a contrastenhanced CT demonstrate an exophytic, well-circumscribed enhancing mass (arrows) in the upper pole of the left kidney, which was (C) biopsied under CT guidance.

C

Radiologic Findings Axial and coronal images from a contrast-enhanced computed tomography (CT) scan demonstrate an exophytic, well-circumscribed enhancing mass in the upper pole of the left kidney (Fig. 54.1A,B), which was biopsied under CT guidance (Fig. 54.1C).

Diagnosis Lipid-poor angiomyolipoma

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Differential Diagnosis • • •

Renal cell carcinoma (RCC) Oncocytoma Metastases

Discussion Background Angiomyolipoma, also referred to as a renal hamartoma, is a benign tumor composed predominantly of fat, smooth muscle, and blood vessels. Necrosis and calcification are rare. The vast majority arise from the renal cortex.

Clinical Findings Most patients are asymptomatic, and the lesions are usually discovered incidentally.

Complications Lesions > 4 cm in diameter may present with flank pain or hematuria.

Etiology Approximately 80% of all lesions occur sporadically and are seen most often in middle-aged women. They are usually small, solitary tumors. Approximately 20% of cases are associated with tuberous sclerosis. In this subset of patients, angiomyolipomas may be of a larger size and often tend to be multiple and bilateral.

Imaging Findings •

• •

On CT, angiomyolipomas usually demonstrate the presence of fatty tissue; however, intratumoral fat is not visualized in ~5% of lesions. Contrast enhancement is variable and is dependent on the relative amounts of fat, soft tissue, and vascular components. On ultrasound, most angiomyolipomas are well circumscribed and predominantly hyperechoic. On magnetic resonance imaging, predominantly fatty angiomyolipomas appear hyperintense on T1-weighted imaging with signal loss on fat suppression sequences. In- and out-of-phase gradient echo imaging will show signal dropout on out-of-phase imaging.

Treatment •

Selective embolization or elective resection of large lesions should be considered.

Prognosis •

These are benign lesions. Lesions > 4 cm in diameter may bleed, sometimes causing massive hemorrhage.

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PE ARL



Most angiomyolipomas are predominantly fat-containing masses with a diagnostic appearance at CT.

PITFALL



Although a definitive diagnosis can usually be made using CT, ~5% of angiomyolipomas appear as solid masses containing little or no fat, making differentiation from RCC difficult. Percutaneous biopsy of these lesions should be considered.

Suggested Readings Jinzaki M, Tanimoto A, Narimatsu Y, et al. Angiomyolipoma: imaging findings in lesions with minimal fat. Radiology 1997;205:497–502 Pereira JM, Sirlin CB, Pinto PS, Casola G. CT and MR imaging of extrahepatic fatty masses of the abdomen and pelvis: techniques, diagnosis, differential diagnosis, and pitfalls. Radiographics 2005;25: 69–85 Wagner BJ, Wong-You-Cheong JJ, Davis CJ Jr. Adult renal hamartomas. Radiographics 1997;17: 155–169

CASE 55 Clinical History A 21-year-old patient presents with recurrent urinary tract infections.

Radiologic Findings Contrast-enhanced axial computed tomography (CT) images demonstrate an atrophic right kidney (Fig. 55.1A) with renal cortical scarring and dilatation of the right renal pelvis. Sequential images from a voiding cystourethrogram (VCUG) demonstrate contrast opacification of the urinary bladder, the right ureter, and the right renal collecting system (Fig. 55.1B). There is dilatation of the right renal pelvis and ballooning of the renal calyces.

Diagnosis Atrophic right kidney secondary to reflux nephropathy

Differential Diagnosis • • •

Atrophic kidney from renal infarction Renal infection, congenitally Atrophic kidney

Discussion Background Vesicoureteral reflux (VUR) is defined as the retrograde flow of urine from the urinary bladder toward the kidney. Although VUR is classically described as a disorder affecting children, structural changes within the kidney are often detected in adulthood.

Clinical Findings The most common clinical presentation of VUR is urinary tract infection.

Complications Patients with severe long-standing reflux disease may develop recurrent pyelonephritis, hypertension, renal insufficiency, renal scarring, and atrophy.

Etiology VUR is thought to result from an abnormally angulated insertion of the ureter into the urinary bladder. The disorder often resolves spontaneously at puberty, possibly because of changes in the ureteral angulation with growth. Other causes of VUR are periureteral (Hutch) diverticula, bladder outlet obstruction (most commonly related to posterior urethral valves in male patients), ureterocele, and neurogenic bladder.

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Fig. 55.1 (A) Contrast-enhanced axial CT images dem-

A

B

onstrate an atrophic right kidney with renal cortical scarring and dilatation of the right renal pelvis. (B) Sequential images from a voiding cystourethrogram demonstrate contrast opacification of the urinary bladder, the right ureter, and the right renal collecting system. There is dilatation of the right renal pelvis and ballooning of the renal calyces.

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Imaging Findings •



VCUG and radionuclear cystourethrography are the imaging tests of choice for the diagnosis, grading, and follow-up of VUR. It is the preferred imaging technique for the initial diagnosis of reflux, given its ability to demonstrate anatomical details of the urinary tract. On VCUG, VUR is best seen on the oblique images of the urinary bladder just prior to voiding. Contrast is seen coursing retrogradely into the ureter and possibly into the renal collecting system. Expansion and distortion of the renal calyces may be seen. On cross-sectional imaging, dilatation of the renal pelvis and calyces, focal renal parenchymal thinning, and irregularity of the renal cortex may be seen.

Treatment •

VUR resolves spontaneously by puberty in most patients. More severe reflux may require surgical correction with reimplantation of an abnormally inserted ureter or correction of a ureterocele, Hutch diverticulum, or posterior urethral valve.

Prognosis •

Prognosis is generally excellent in patients with low-grade reflux. Chronic high-grade reflux may lead to pyelonephritis, hypertension, and renal insufficiency.

PE ARL



Reflux nephropathy is a cause of a unilateral small, irregular kidney.

PITFALL



VUR can be seen in the setting of duplicated collecting systems, especially involving the lower pole moiety. Evaluation of a patient with reflux nephropathy should include assessment for ureteral duplication.

Suggested Readings Berrocal T, Lopez-Pereira P, Arjonilla A, Gutierrez J. Anomalies of the distal ureter, bladder, and urethra in children: embryologic, radiologic, and pathologic features. Radiographics 2002;22(5):1139–1164 Fernbach SK, Feinstein KA, Schmidt MB. Pediatric voiding cystourethrography: a pictorial guide. Radiographics 2000;20(1):155–168; discussion 168–171

CASE 56 Clinical Presentation A patient with a known abdominal aortic aneurysm and recent cardiac catheterization presents with new-onset right flank pain.

Fig. 56.1 Contrast-enhanced axial CT image shows a lack of enhancement in a geographic wedge-shaped area of the right kidney. The left kidney enhances normally. An infrarenal aortic aneurysm is also seen.

Radiologic Findings Contrast-enhanced axial computed tomography (CT) image shows a lack of enhancement in a geographic wedge-shaped area of the right kidney (Fig. 56.1). The left kidney enhances normally. An infrarenal aortic aneurysm is also seen.

Diagnosis Renal infarct following angiographic catheter manipulation in the setting of an abdominal aortic aneurysm

Differential Diagnosis • • • •

Pyelonephritis Abscess Lymphoma Infiltrating renal mass

Discussion Background Renal infarction has a variety of causes. It most commonly occurs in patients with a history of thromboembolic disease.

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Clinical Findings Patients may present with nausea/vomiting, flank pain, abdominal pain, back pain, fever, or hematuria and usually give a history of thromboembolic disease. Elevated creatinine and white blood cell count may be seen. Markedly elevated serum lactate dehydrogenase, in the appropriate clinical setting, is strongly suggestive of renal infarction.

Complications Renal functional impairment and renal atrophy may occur.

Etiology Embolic risk factors include atrial fibrillation, left ventricular thrombus in patients with a myocardial infarction, rheumatic heart disease, prosthetic valves, and infectious endocarditis. Thrombotic risk factors include underlying atherosclerosis, vasculitides, and aortic and renal aneurysms. Trauma, renal artery dissection, hypertension, sickle cell disease, and renal vein thrombosis can also cause renal infarction.

Imaging Findings •





On CT, imaging findings depend on the size and etiology of the infarct. Single or multiple wedgeshaped, cortically based areas of lack of enhancement may be seen when small arterial branches are occluded. A global infarct is described when there is hypoattenuation of at least 50% of the kidney, when a large branch of the renal artery is occluded. A cortical rim sign, described as a 1 to 3 mm rim of enhancement overlying an infarct, is seen in ~50% of cases (Fig. 56.2). This occurs because the subcapsular area is perfused by small capsular arterial branches, which are usually preserved. Ultrasound findings include focally increased echogenicity of the infarcted portion. Color-flow Doppler can be useful in the diagnosis of renal artery thrombosis and may demonstrate the absence of an intrarenal arterial signal, a tardus parvus waveform in an incomplete occlusion, or collateral supply. On nuclear imaging, a photopenic area corresponding to the infarct is seen.

Fig. 56.2 Contrast-enhanced axial CT image shows a global lack of enhancement of the left kidney with a cortical rim sign. The right kidney enhances normally.

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Treatment •

Treatment options include anticoagulation, intra-arterial thrombolytic therapy, and surgical revascularization.

Prognosis •

Prognosis depends on the size of the infarct and underlying etiology.

PE ARL



Renal infarcts usually appear as multifocal, wedge-shaped areas of lack of enhancement on contrast CT. A cortical rim sign is identified in ~50% of cases.

PITFALL



When infarcts are small, they may be mistaken for focal renal lesions or infection.

Suggested Readings Domanovits H, Paulis M, Nikfardjam M, et al. Acute renal infarction: clinical characteristics of 17 patients. Medicine (Baltimore) 1999;78(6):386–394 Suzer O, Shirkhoda A, Jafri SZ, Madrazo BL, Bis KG, Mastromatteo JF. CT features of renal infarction. Eur J Radiol 2002;44(1):59–64 Wong WS, Moss AA, Federle MP, Cochran ST, London SS. Renal infarction: CT diagnosis and correlation between CT findings and etiologies. Radiology 1984;150:201–205

CASE 57 Clinical Presentation A 60-year-old man presents with right-sided abdominal pain, fever, and an elevated white blood cell count.

B

A

Fig. 57.1 (A,B) Contrast-enhanced CT images show an enlarged right kidney with linear areas of low attenuation and associated perinephric stranding. The left kidney is of normal size and demonstrates normal enhancement.

Radiologic Findings Contrast-enhanced computed tomography (CT) images show an enlarged right kidney with linear areas of low attenuation (Fig. 57.1). There is right-sided perinephric stranding. The left kidney is of normal size and demonstrates normal enhancement.

Diagnosis Pyelonephritis of the right kidney

Differential Diagnosis • • • • •

Renal infarct Renal vein thrombosis Radiation nephritis Lymphoma Medullary sponge kidney

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Discussion Background Pyelonephritis is an infection of the kidney and usually occurs secondary to ascending infection from the urinary bladder. It is more common in women than in men. Risk factors include personal or family history of urinary tract infections, stress incontinence, diabetes, and other immunocompromised states.

Clinical Findings Patients typically present with dysuria, urgency, and frequency. Other symptoms include fever, chills, nausea/vomiting, flank pain, and abdominal pain. Physical examination may reveal costovertebral angle tenderness.

Complications Complications include abscess formation, emphysematous pyelonephritis, chronic renal damage leading to renal failure and hypertension, sepsis, and renal papillary necrosis.

Etiology The most common pathogen is Escherichia coli. Other pathogens include Staphylococcus saprophyticus, Enterococcus, Klebsiella, Proteus, and Pseudomonas.

Imaging Findings • •

Pyelonephritis is often a clinical diagnosis. Imaging may be performed to evaluate for complications. Findings on CT include enlargement of the kidney, perinephric inflammatory stranding, and wedge-shaped, linear, or patchy areas of low attenuation in the renal cortex.

Treatment •

Antibiotic therapy is the treatment of choice.

Prognosis •

Early diagnosis and appropriate treatment lead to a good prognosis. Immunocompromised patients, the elderly, and those with diabetes are at risk for complications.

PE ARL



A striated nephrogram is a nonspecific sign on contrast studies; however, in the appropriate clinical setting, it may be diagnostic of acute pyelonephritis.

PITFALL



Patients with diabetes are at increased risk for serious complications due to pyelonephritis. Infants and children who have had pyelonephritis should be evaluated for urinary tract abnormalities.

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Suggested Readings Majd M, Nussbaum Blask AR, Markle BM, et al. Acute pyelonephritis: comparison of diagnosis with 99mTc-DMSA, SPECT, spiral CT, MR imaging, and power Doppler US in an experimental pig model. Radiology 2001;218:101–108. Scholes D, Hooton TM, Roberts PL, Gupta K, Stapleton AE, Stamm WE. Risk factors associated with acute pyelonephritis in healthy women. Ann Intern Med 2005;142(1):20–27

CASE 58 Clinical Presentation Incidental finding in a 26-year-old patient complaining of vague abdominal pain.

A

Fig. 58.1 (A,B) Ultrasound scans reveal a well-circumscribed, heterogeneous mass in the upper pole of the left kidney with a central linear region of decreased echogenicity. (continued)

B

Radiologic Findings Ultrasound examination reveals a well-circumscribed, heterogeneous mass in the upper pole of the left kidney with a central linear region of decreased echogenicity (Fig. 58.1A,B). The contrastenhanced axial image demonstrates a solid, heterogeneously enhancing mass in the medial interpolar

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D

C

Fig. 58.1 (continued) (C) Contrast-enhanced axial image demonstrates a solid, heterogeneously enhancing mass in the medial interpolar region of the left kidney with an enhancement pattern similar to normal adjacent renal parenchyma. There is a central, nonenhancing portion within the mass. No fat is seen within the lesion. (D) Axial gradient echo T1weighted image obtained in the arterial phase after gadolinium injection shows a well-demarcated arterially enhancing lesion with a central scar.

region of the left kidney with an enhancement pattern similar to normal adjacent renal parenchyma. There is a central, nonenhancing portion within the mass. No fat is seen within the lesion (Fig. 58.1C). An axial gradient echo T1-weighted image obtained in the arterial phase after gadolinium injection shows a well-demarcated arterially enhancing lesion with a central scar (Fig. 58.1D).

Diagnosis Oncocytoma

Differential Diagnosis • • •

Renal cell carcinoma (RCC) Metastases Angiomyolipoma

Discussion Background Oncocytomas are benign renal tumors that compose ~5% of all renal neoplasms. They are diagnosed most frequently in the 6th to 7th decade of life and are seen more frequently in men than in women. Approximately 3% are bilateral, and ~5% are multicentric.

Clinical Findings Oncocytomas are usually detected incidentally, and patients are usually asymptomatic.

Complications Patients may present with hematuria, a palpable mass, or flank pain.

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Etiology These are benign neoplasms comprising tubular epithelium arising from the intercalated cells of the collecting duct. Pathologic specimens demonstrate a well-circumscribed, tannish brown tumor with a predominantly gelatinous center.

Imaging Findings •







On computed tomography (CT), these lesions are usually of similar density to normal renal parenchyma on nonenhanced studies. Postcontrast, they usually enhance homogeneously and less avidly than the adjacent renal parenchyma. In approximately one third of cases, they may demonstrate a central, stellate, hypoattenuating scar. Necrosis, hemorrhage, and calcification are rarely seen. On magnetic resonance imaging (MRI), oncocytomas are usually iso- to hypointense on T1weighted imaging and iso- to slightly hypointense on T2-weighted imaging. Heterogeneous enhancement is demonstrated on postgadolinium sequences. The central scar, if present, is of low-signal intensity relative to the mass on both T1 and T2 sequences and does not enhance postcontrast. On ultrasound, oncocytomas appear as well-circumscribed, iso- to hypoechoic masses. When present, the central scar is echogenic. Central, radiating vessels may be demonstrated with color Doppler. On angiography, approximately one half of cases will demonstrate a “spoke-wheel” pattern of enhancement.

Treatment •

Surgical resection

Prognosis •

These are benign lesions.

PE ARL



A central scar is seen in approximately one third of cases.

PITFALL



Differentiation from RCC is difficult, as there is considerable overlap in the imaging appearances of both lesions. Biopsy of RCC may demonstrate oncocytic elements and cannot therefore be relied upon to distinguish between RCC and oncocytoma. The central scar is a nonspecific sign and cannot be reliably differentiated from an area of central necrosis, which is often seen in RCC.

Suggested Readings Laperriere J, Lafortune M. Case of the day: General. Oncocytoma of the right kidney. Radiographics 1990;10(6):1105–1107 Dyer RB, Chen MY, Zagoria RJ. Classic signs in uroradiology. Radiographics 2004;24:S247–S280

CASE 59 Clinical Presentation A 56-year-old woman with a history of kidney stones presents with persistent left flank pain. A diagnostic noncontrast computed tomography (CT) scan performed several months earlier showed no evidence of nephrolithiasis and/or renal masses.

Fig. 59.1 Single composite image comprising a noncontrast axial image, contrast-enhanced axial and coronal images in portal venous phase, and an axial image in the delayed phase following contrast administration. Noncontrast-enhanced CT demonstrates no discrete focal lesion. In the portal venous phase following contrast enhancement, there is a well-circumscribed mass in the left kidney (arrow), which is hypodense to the surrounding parenchyma. The lesion continues to be visible on the delayed phase (arrow).

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Radiologic Findings A single composite image comprises a noncontrast axial image, contrast-enhanced axial and coronal images in the portal venous phase, and an axial image in the delayed phase following contrast administration (Fig. 59.1). Noncontrast-enhanced CT demonstrates no discrete focal lesion. In the portal venous phase following contrast enhancement, there is a well-circumscribed mass in the left kidney, which is hypodense to the surrounding parenchyma. The lesion continues to be visible on the delayed phase.

Diagnosis Metanephric adenoma

Differential Diagnosis • • • •

Renal cell carcinoma Oncocytoma Lymphoma Focal pyelonephritis

Discussion Background Metanephric adenoma is a rare, benign renal tumor. It is also known as nephrogenic adenofibroma and embryonal adenoma. There is a slight female predominance with a wide age range at presentation. The tumor develops from remnants of metanephric blastema and is histologically similar to a Wilms tumor. There is no association with metastases or recurrence.

Clinical Findings Patients are usually asymptomatic, and the lesion is usually discovered incidentally. Patients can, however, present with flank pain, hematuria, a palpable mass, or hypertension.

Complications Hypercalcemia and polycythemia have been described in association with metanephric adenoma.

Etiology Metanephric adenomas arise from remnant metanephric blastema during embryonic development.

Imaging Findings •



Imaging findings on CT are variable and nonspecific. On unenhanced CT, metanephric adenoma presents as a well-defined mass of iso- or increased attenuation relative to the adjacent renal parenchyma. Septa or calcifications are rarely seen. Mild enhancement may be demonstrated postcontrast administration. The ultrasound appearance is also variable. These tumors can demonstrate both decreased and increased echogenicity, sometimes with increased through-transmission. Doppler interrogation shows a hypovascular mass.

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T1-weighted magnetic resonance (MR) images demonstrate a hypointense mass, which is slightly hyperintense on T2-weighted MR images.

Treatment •

These tumors may be treated with local surgical resection with sparing of adjacent renal tissue.

Prognosis •

These are benign lesions with no association with metastasis or recurrence.

PE ARL



Metanephric adenomas are rare, benign, well-circumscribed masses with an excellent prognosis.

PITFALL



Metanephric adenomas have nonspecific imaging features. Adequate tissue sampling is necessary to differentiate this tumor from a renal cell carcinoma or Wilms tumor.

Suggested Readings Fielding JR, Visweswaran A, Silverman SG, Granter SR, Renshaw AA. CT and ultrasound features of metanephric adenoma in adults with pathologic correlation. J Comput Assist Tomogr 1999;23(3):441– 444. Lowe LH, Isuani BH, Heller RM, et al. Pediatric renal masses: Wilms tumor and beyond. Radiographics 2000;20:1585–1603 Patankar T, Punekar S. Metanephric adenoma in a solitary kidney. Br J Radiol 1999;72:80–81

CASE 60 Clinical Presentation A patient who is on chronic lithium therapy for bipolar disorder presents with renal functional impairment.

B

A

Fig. 60.1 (A,B) Select postcontrast CT images demonstrate numerous small, low-attenuation lesions distributed throughout both kidneys.

Radiologic Findings Select postcontrast computed tomography (CT) images demonstrate numerous small, low-attenuation lesions distributed throughout both kidneys (Fig. 60.1).

Diagnosis Renal changes from lithium toxicity

Differential Diagnosis • • • •

Autosomal dominant polycystic kidney disease (ADPKD) Acquired cystic disease secondary to chronic renal failure or long-term dialysis Glomerulocystic kidney disease Medullary cystic disease

Discussion Background Nephrotoxicity is a well-recognized side effect of lithium treatment. Chronic lithium administration can lead to nephrogenic diabetes insipidus and chronic tubulointerstitial nephropathy (CTIN). Histologic features of CTIN include interstitial fibrosis, tubular atrophy, dilatation, and cyst formation. Tubular cysts have been detected in the renal biopsy specimens of up to 62% of patients with biopsy-proven lithium-related CTIN.

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Clinical Findings Up to 87% of patients with lithium nephrotoxicity have clinical evidence of nephrogenic diabetes insipidus and complain of polyuria and polydipsia. Thirty-three percent of patients have hypertension.

Complications The withdrawal of lithium therapy does not lead to a reversal of renal dysfunction in all patients, and progression to end-stage renal disease (ESRD) can occur.

Etiology Direct damage to the tubular cells by lithium is thought to be the cause of lithium-induced nephrotoxicity.

Imaging Findings • •

CT imaging demonstrates multiple small, low-attenuation cysts separated by normal-enhancing renal tissue, distributed throughout the renal parenchyma bilaterally. Magnetic resonance imaging (MRI) demonstrates multiple small cysts measuring 1 to 2 mm in diameter, uniformly distributed throughout both kidneys. They are homogeneously bright on T2weighted images. The kidneys are not enlarged, as may be seen in ADPKD.

Prognosis •

Lithium-induced CTIN can lead to chronic renal insufficiency and in some cases ESRD. Renal dysfunction may progress despite discontinuation of lithium. Serum creatinine at the time of diagnosis of renal insufficiency may be a predictor of ESRD.

PE ARL



The finding of multiple, bilateral, 1 to 2 mm renal cysts on imaging studies of patients on longterm lithium therapy is characteristic of lithium nephrotoxicity.

PITFALL



If the appropriate history is not elucidated, the imaging appearance can be mistaken for other disease entities.

Suggested Readings Farres MT, Ronco P, Saadoun D, et al. Chronic lithium nephropathy: MR imaging for diagnosis. Radiology 2003;229(2):570–574 Markowitz GS, Radhakrishnan J, Kambham N, Valeri AM, Hines WH, D’Agati VD. Lithium nephrotoxicity: a progressive combined glomerular and tubulointerstitial nephropathy. J Am Soc Nephrol 2000;11(8):1439–1448

CASE 61 Clinical Presentation Incidental finding on an abdominal computed tomography (CT) scan.

A

B

C

D

Fig. 61.1 (A–D) Select postcontrast CT images demonstrate multiple low-attenuation cysts throughout the right kidney, with intervening enhancing septations or renal parenchyma. No mural calcification or nodules are seen. The left kidney and other visualized abdominal viscera appear normal.

Radiologic Findings Select computed tomography (CT) postcontrast images demonstrate multiple low-attenuation cysts throughout the right kidney, with intervening enhancing septations or renal parenchyma (Fig. 61.1). No mural calcification or nodules are seen. The left kidney and other visualized abdominal viscera appear normal.

Diagnosis Localized cystic disease of the kidney

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Differential Diagnosis • • • • •

Unilateral autosomal dominant polycystic kidney disease (ADPKD) Multilocular cystic nephroma Cystic Wilms tumor Cystic renal cell carcinoma (RCC) Multicystic dysplastic kidney

Discussion Background Localized cystic disease of the kidney is a rare, benign condition that presents more commonly in men than in women, with a mean age at diagnosis of 50 years. It is characterized by the presence of multiple renal cysts of varying sizes separated by normal renal parenchyma. The cysts may be distributed throughout the kidney or confined to a localized portion of the kidney.

Clinical Findings The condition is often detected incidentally. Patients may present with a palpable flank mass, abdominal pain, or hematuria.

Complications There is no association with renal functional impairment. Although it is a benign condition that usually does not require surgical intervention, some patients may obtain relief from flank pain with aspiration or deroofing of a dominant cyst.

Etiology The etiology is unknown. There appears to be no genetic predisposition to the condition. There are no associated lesions in the contralateral kidney or within other viscera.

Imaging Findings •



Ultrasound may demonstrate multiple simple cystic masses separated by normal renal parenchyma. Attenuated renal tissue may give the appearance of multiple septations of varying thickness, similar to a complex cystic mass. Contrast CT demonstrates multiple low-attenuation, nonenhancing simple cysts of varying sizes presenting either involving the entire kidney or confined to a single area of the kidney. The cysts are separated by normal-enhancing renal tissue. When this tissue is attenuated between multiple large cysts, the appearance may resemble that of a complex cystic mass with multiple septations. Mural calcification may de demonstrated. There may be evidence of high-attenuation fluid, consistent with hemorrhagic fluid, within some cysts. The cysts are localized to one kidney; the contralateral kidney is normal.

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Multiple cystic masses that are predominantly of high signal on T2-weighted images and separated by normal renal parenchyma are identified on magnetic resonance imaging. The intervening renal parenchyma enhances following the administration of gadolinium.

Prognosis •

This is a benign condition.

PE ARL



Imaging findings at presentation and follow-up can allow this benign condition to be differentiated from other renal cystic lesions with poorer prognosis that may require surgical intervention, such as cystic RCC and ADPKD.

PITFALL



ADPKD may initially present with unilateral disease, particularly in children; therefore, careful examination of other abdominal viscera and a family history should be obtained when the diagnosis of localized cystic disease is suspected.

Suggested Readings Hwang DY, Ahn C, Lee JG, et al. Unilateral renal cystic disease in adults. Nephrol Dial Transplant 1999;14(8):1999–2003 Review Slywotzky CM, Bosniak MA . Localized cystic disease of the kidney. AJR Am J Roentgenol 2001;176(4):843–849

CASE 62 Clinical Presentation A 45-year-old woman complains of right flank pain and hematuria.

B

A

Fig. 62.1 (A–C) Delayed postcontrast CT images show a heterogeneous mass arising from the renal parenchyma and herniating into the renal pelvis. No calcification or hemorrhage is identified.

Radiologic Findings Delayed postcontrast computed tomography (CT) images reveal a heterogeneous mass arising from the renal parenchyma and herniating into the renal pelvis (Fig. 62.1). No calcification or hemorrhage is identified.

Diagnosis Multilocular cystic nephroma (MLCN)

Differential Diagnosis • • • •

Cystic renal cell carcinoma Transitional cell carcinoma Cystic partially differentiated nephroblastoma Wilms tumor

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C

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Discussion Background MLCN is a rare, benign, nonfamilial renal tumor. A biphasic age and sex distribution at presentation has been observed. Approximately two thirds of cases are detected in boys younger than 4 years of age; the remaining one third of cases occur predominantly in female patients, with a peak in middle age. Pathology reveals a well-defined, encapsulated, cystic mass composed of multiple locules separated by thin septations. The locules may contain serous fluid, myxomatous material, or hemorrhage. Herniation of the mass into the renal pelvis is commonly observed.

Clinical Findings Patients may present with abdominal or flank pain, hematuria, hypertension, or urinary tract infection. Children most commonly present with a palpable abdominal mass.

Complications Malignant transformation does not occur. Herniation of the mass into the renal pelvis may lead to hematuria or to obstruction of the collecting system, resulting in urinary tract infection.

Etiology The etiology is unknown.

Imaging Findings • •



The typical appearance on ultrasound is that of an anechoic mass containing numerous thin septations; however, the appearance may vary according to the size and composition of the locules. On CT, the mass has the appearance of a complex cystic lesion. The attenuation value of individual locules is variable, depending on the contents. The locules do not enhance, as the mass is not in communication with the renal collecting system; however enhancement of the septations may be seen. Mural calcification also may be seen. On magnetic resonance imaging, the signal intensity observed within locules varies according to locule contents. The capsule and septations are of low signal intensity on T2-weighted imaging, and the septations enhance following contrast administration. No contrast is identified within individual locules.

Prognosis •

MLCN is a benign entity, and surgical resection is curative.

PE ARL



Herniation of the mass into the renal pelvis is commonly observed.

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PITFALL



MLCN is a cystic mass; however, with imaging it may appear to contain solid elements when in fact it contains several small cysts with high-density hemorrhagic or proteinaceous material.

Suggested Readings Hopkins JK, Giles HW Jr, Wyatt-Ashmead J, Bigler SA. Best cases from the AFIP: cystic nephroma. Radiographics 2004;24(2):589–593 Madewell JE, Goldman SM, Davis CJ Jr, Hartman DS, Feigin DS, Lichtenstein JE. Multilocular cystic nephroma: a radiographic-pathologic correlation of 58 patients. Radiology 1983;146(2):309–321

CASE 63 Clinical Presentation Routine follow-up study in an asymptomatic patient with known von Hippel-Lindau disease.

B

A

Fig. 63.1 (A) Postcontrast CT image shows bilateral renal cysts. There is a large cyst within the right kidney with thick enhancing septations (arrowhead). Note the multiple pancreatic cysts (arrow). (B) Axial image shows a mixed solid and cystic lesion in the left kidney (arrowhead), along with an enhancing nodule in the chord (arrow). (C) An additional complex cyst with enhancing septation is seen in the right kidney (arrowhead), along with a small enhancing lesion in the left kidney (arrowhead).

C

Radiologic Findings Postcontrast computed tomography (CT) images demonstrate bilateral multiple low-attenuation renal cysts, some of which show enhancing nodules or septations or have solid components (Fig. 63.1). There is also an enhancing lesion within the spinal cord, as well as multiple cysts seen in the pancreatic head.

Diagnosis Von Hippel-Lindau disease

Differential Diagnosis • • •

Autosomal dominant polycystic kidney disease Tuberous sclerosis Acquired cystic disease of dialysis

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Discussion Background Von Hippel-Lindau disease is a rare familial syndrome that is inherited as an autosomal dominant disorder. It is characterized by a predisposition to renal, pancreatic, hepatic, splenic, epididymal, and broad ligament cysts; renal cell carcinoma (RCC); pheochromocytoma; pancreatic islet cell tumors; pancreatic cystadenomas; endolymphatic sac tumors; and hemangioblastomas of the retina, brain, and spinal cord. Renal cysts occur in up to 75% of patients, and ~50% of patients develop renal cell carcinoma, with bilateral and multiple tumors occurring in 65 and 85% of these patients, respectively.

Clinical Findings The presenting symptoms of von Hippel-Lindau disease depend on the organs involved. Regular screening studies lead to the detection of several asymptomatic lesions. Renal cysts and RCC may cause flank pain. RCC also may present with hematuria or as a palpable abdominal mass.

Complications RCC may develop as a de novo solid lesion or arise from a complex cystic lesion. Metastatic disease is common at the time of diagnosis. RCC is the cause of death in ~50% of patients with von HippelLindau disease.

Etiology Von Hippel-Lindau disease is inherited in an autosomal dominant inheritance pattern. The related tumor suppressor gene has been localized to the short arm of chromosome 3.

Imaging Findings • •



Renal ultrasound may demonstrate multiple bilateral simple anechoic cysts of varying sizes. Complex cystic lesions and solid renal tumors may be detected. Contrast CT will demonstrate multiple, nonenhancing simple renal cysts. RCC may appear as a complex cystic mass with thick septations and enhancing nodules or as a solid, heterogeneous, poorly enhancing mass. Simple renal cysts are bright on T2-weighted images. RCC is best detected using T1 fat-saturated postcontrast sequences.

Prognosis •

The median life expectancy of patients with von Hippel-Lindau disease is 49 years. RCC is the cause of death in up to 50% of patients.

PE ARL



Regular imaging of the abdomen and central nervous system is recommended in patients with von Hippel-Lindau disease to screen for RCC, pancreatic tumors, pheochromocytoma, and hemangioblastomas. RCCs are often multiple and bilateral.

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PITFALL



Early detection of RCC allows for treatment options, such as nephron-sparing surgery and radiofrequency ablation. However, tumors are often multiple and bilateral, and tumor recurrence posttreatment is common; therefore, continued regular renal imaging is necessary.

Suggested Readings Choyke PL, Glenn GM, Walther MM, Patronas NJ, Linehan WM, von Zbar B. Hippel-Lindau disease: genetic, clinical, and imaging features. Radiology 1995;194(3):629–642 Hes FJ, Feldberg MA. Von Hippel-Lindau disease: strategies in early detection (renal-, adrenal-, pancreatic masses). Eur Radiol 1999;9(4):598–610 Taouli B, Ghouadni M, Correas JM, et al. Spectrum of abdominal imaging findings in von HippelLindau disease. AJR Am J Roentgenol 2003;181(4):1049–1054

CASE 64 Clinical Presentation A 62-year-old patient complains of right flank pain.

A

B

Fig. 64.1 (A) Noncontrast CT image shows an inferior vena cava filter in place. There is an exophytic low-attenuating lesion arising from the right kidney, with thickening seen along the right lateral wall. (B) Following the administration of contrast, there is an enhancing nodule (arrow) seen within the lesion. In addition, there are ill-defined septations and thickening of the left lateral wall.

Radiologic Findings Noncontrast computed tomography (CT) image shows an inferior vena cava filter in place. There is an exophytic low-attenuating lesion arising from the right kidney, with thickening seen along the right lateral wall (Fig. 64.1A). Following the administration of contrast, there is an enhancing nodule seen within the lesion (Fig. 64.1B). In addition, there are ill-defined septations and thickening of the left lateral wall.

Diagnosis Cystic renal cell carcinoma (RCC)

Differential Diagnosis • • • •

Renal abscess Complex inflammatory or infected renal cyst Cystic metastases Solid RCC with cystic degeneration

Discussion Background RCCs account for 85% of all renal malignancies. They are usually solid, but up to 20% can be cystic.

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Clinical Findings Most cystic RCCs are incidentally discovered, as patients are usually asymptomatic. Occasionally, a patient may complain of flank pain and may even have hematuria.

Complications Cystic tumors usually have a slower growth rate, have a more favorable pathologic stage and lower histologic grade, and thus have a better prognosis.

Imaging Findings Up to 8% of renal cysts do not meet the strict criteria for a simple cyst or cystic neoplasm and are therefore indeterminate. Features that may arouse suspicion for malignancy are • • • • •

Calcification (although a small amount of calcification in the wall or septa may be benign) Abnormal density (a change of > 10 Hounsfield units before and after contrast studies suggests vascularity) Septations (if thin and smooth, these can be considered benign; signs of malignancy include irregularity and thickness > 1 mm) Nodularity (solid tissue within the cyst wall indicates malignancy) Wall thickening (the wall of a simple cyst is imperceptible)

Treatment •

Surgical resection.

Prognosis •

The prognosis is good if the cystic renal cancers are identified early and are surgically resected.

PE ARL



When confronted with low-attenuating cystic renal lesions, use the Bosniak criteria to characterize the lesions (Table 64.1).

Table 64.1 The Bosniak Classification System Classification

Imaging Features

Management

I

Simple benign cyst measuring water density; no enhancement seen on intravenous contrast Benign cyst with few hairline thin septa; fine calcification may be present in the wall or septa. Uniformly high-attenuating lesions < 3 cm are sharply marginated and show no enhancement Lesions are indeterminate (multilocular) cystic masses that have thickened irregular walls or septa in which enhancement can be seen Marginal irregularity; enhancing solid component

Nonsurgical

II

III IV

Nonsurgical

Renal sparing surgery Radical nephrectomy

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PITFALL



It may be difficult to differentiate a renal abscess or inflammatory cysts from cystic RCCs.

Suggested Readings Benjaminov O, Atri M, O’Malley M, Lobo K, Tomlinson G. Enhancing component on CT to predict malignancy in cystic renal masses and interobserver agreement of different CT features. AJR Am J Roentgenol 2006;186:665–672 Israel GM, Hindman N, Bosniak MA. Evaluation of cystic renal masses: comparison of CT and MR imaging by using the Bosniak classification system. Radiology 2004;231:365–371

CASE 65 Clinical Presentation A 78-year-old diabetic man presents with a spiking fever and flank pain.

Fig. 65.1 Axial contrast-enhanced CT image in a diabetic patient with a history of urinary tract infection shows an ill-defined, hypodense corticomedullary renal abscess.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) image shows an ill-defined, hypodense left renal lesion with thick walls (Fig. 65.1).

Diagnosis Renal abscess

Differential Diagnosis • • • • • • • •

Lymphoma Complicated cyst Renal cell carcinoma Hydatid cyst Renal infarct Metastases Calyceal diverticulum Focal xanthogranulomatous pyelonephritis

Discussion Background A renal abscess is an uncommon renal condition. It can be cortical or corticomedullary, depending on the route of infection. When left untreated, a renal abscess can lead to significant mortality and morbidity. With the use of image-guided intervention techniques and antibiotics, mortality and morbidity due to renal abscess are significantly reduced.

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Clinical Findings • • • • • • •

Fever Chills Malaise Fatigue Pain in the abdomen and/or flanks Septic shock Costovertebral angle tenderness

Complications • • • •

Septicemia Renal scarring leading to obstruction of the collecting system with secondary complications (e.g., ureteropelvic obstruction) Rupture of the abscess into the perinephric space and subsequent perinephric abscess formation Complications related to drainage procedures (e.g., hemorrhage) that can be life threatening, septicemia, pleural puncture leading to empyema

Etiology Bacterial spread by a hematogenous route (e.g., in subacute bacterial endocarditis and intravenous drug abuse) leads to a renal cortical abscess, whereas an ascending infection from the collecting system (in patients with urinary tract anomalies, infection, urinary tract obstruction due to any of the causes, or vesicoureteric reflux) leads to a corticomedullary abscess. Causative organisms in corticomedullary abscesses are most commonly Escherichia coli, Proteus, Klebsiella, Enterobacter, and Serratia species. Staphylococcus aureus accounts for 90% of the cases of cortical abscess. Corticomedullary abscess is most commonly seen in diabetic patients with poorly controlled blood sugar levels with or without obstruction of the urinary tract. Emphysematous pyelonephritis is a distinct type of necrotizing renal infection with higher rates of mortality, is most commonly seen in diabetic patients, and is caused by anaerobic microorganisms.

Imaging Findings •



Contrast-enhanced CT scan is the imaging modality of choice. Imaging features of abscess are heterogeneously enhancing lesions with cortical bulge, thick and irregular enhancing walls, and multiple low-density areas, with or without septations. Peripheral lesions are more commonly associated with stranding of perinephric fat. Ultrasound is useful for diagnosis, imaging-guided drainage, and follow-up study. It can be used to perform bedside examination and does not involve ionizing radiation, which is an important concern in young and pregnant patients. However, functional information about the kidneys, perinephric tissue pathologies, and lesion enhancement characteristics cannot be studied. Ultrasound shows a welldefined, thick-walled cystic lesion with multiple internal echoes and mobile debris. A fluid debris level is commonly seen. The presence of air detected by the presence of hyperechoic specks with dirty shadowing, in cases with no prior instrumentation, indicates emphysematous infection.

Treatment •

Intravenous antibiotics with percutaneous image-guided drainage are the treatment of choice. Open surgery is required in complicated cases.

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Prognosis •

The prognosis is excellent in patients with an anatomically normal urinary tract and localized disease without comorbid conditions. In patients with extrarenal spread of abscess and emphysematous pyelonephritis, the prognosis is worse with higher mortality. A poor prognosis is seen in elderly patients with poorly controlled diabetes, lethargy, and elevated serum blood urea nitrogen levels.

PE ARL



A low-density multiseptated renal lesion in a patient with fever should raise concern for a renal abscess.

PITFALL



A renal abscess may mimic a malignancy on imaging and should be in the differential in the right clinical setting.

Suggested Readings Kawashima A, Sandler CM, Goldman SM. Imaging in acute renal infection. BJU Int 2000;86(Suppl 1):70–79 Yen DH, Hu SC, Tsai J, et al. Renal abscess: early diagnosis and treatment. Am J Emerg Med 1999;17: 192–197

CASE 66 Clinical Presentation A 67-year-old man presents with hematuria.

A

B

Fig. 66.1 (A) Axial contrast-enhanced CT image shows a well-defined, exophytic, intensely enhancing solid lesion from the anterior cortex of the right kidney. (B) CT image of the pelvis in the same patient shows a large, round, heterogeneously enhancing soft tissue mass lesion in the anterosuperior iliac spine on the left side, causing bone destruction.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) image shows a well-defined, exophytic, intensely enhancing solid lesion arising from the anterior cortex of the right kidney. There are associated bony metastases in the left ilium (Fig. 66.1).

Diagnosis Renal cell carcinoma (RCC)

Differential Diagnosis • • •

Oncocytoma Angiomyolipoma Metastases

Discussion Background RCC is the most common lethal urologic malignancy. It accounts for 95% of cases of renal tumors. With the growing popularity of imaging studies, the prevalence of RCC has increased, with more than half of the cases being detected coincidentally on the imaging studies done for nonrenal indications. Clear cell is the most common and most aggressive histologic type of RCC. RCC is cystic in 10 to 15% of the total cases of RCC.

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Clinical Findings Most patients are asymptomatic, with the renal lesion detected incidentally on radiologic examination done for other causes. Presenting clinical features can be hematuria, pain in the abdomen or flanks, abdominal mass, weight loss, anorexia, night sweats, fever, or symptoms from distant metastatic disease. Bilateral RCCs can be seen in von Hippel-Lindau disease, tuberous sclerosis, familial RCCs, and acquired renal cystic disease.

Complications • • • • •

Metastatic disease Hemorrhage Renal function abnormalities Paraneoplastic syndromes Anemia/polycythemia

Etiology The exact causes of RCC are unknown; however, know risk factors are cigarette smoking; obesity; hypertension; long-term analgesic use; exposure to petroleum products, solvents, asbestos, and cokeoven emissions; dialysis-related renal cystic disease; tuberous sclerosis; von Hippel-Lindau disease; and lymphoma.

Imaging Findings •





Contrast-enhanced dynamic CT is the modality of choice for the initial evaluation of RCC. The nephrographic phase (25–70 s after the beginning of contrast injection) of dynamic contrastenhanced CT is most important for localization and characterization of renal masses and metastatic lesions. RCC appears as a heterogeneously and intensely enhancing (> 12 Hounsfield units [HU]), solid, solitary, exophytic mass lesion with or without calcifications (11%), causing a bulge in the renal contour. Smaller tumors are more homogeneous, whereas larger tumors appear more heterogeneous because of the presence of necrosis and hemorrhage. Tumor extension or tumor thrombus can be seen inside the renal vein and inferior vena cava. The presence of color flow on Doppler imaging, flow voids on magnetic resonance imaging (MRI), and heterogeneous contrast enhancement on CT or MRI are definitive signs of tumor thrombosis. The presence of enlarged lymph node metastases in RCC is associated with a poor prognosis. On MRI, RCC appears iso- to hypointense on T1-weighted imaging, and iso- to hyperintense with or without hypointense areas (due to necrosis, hemorrhage, and calcifications) on T2-weighted imaging. Dynamic contrast-enhanced MRI is used for assessing tumor vascularity and the response of the tumor to various therapies. Various subtypes of RCC have typical imaging features that can suggest a histologic diagnosis of the tumor. On CT, clear cell RCC and collecting duct RCC appear as well-defined, heterogeneously enhancing mass lesions with areas of necrosis and calcifications (10%). Intense contrast enhancement of > 84 HU during the corticomedullary phase and > 44 HU in the excretory phase is characteristic of the clear cell histologic type. Both clear cell and collecting duct RCCs are aggressive

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renal neoplasms. Papillary and chromophobe RCCs are other less common and less aggressive subtypes of RCC. Papillary RCC appears homogeneous and shows mild to moderate enhancement on imaging. Hemorrhage, necrosis, and calcifications can be seen in larger tumors. Bilateralism and multicentricity are more common in von Hippel-Lindau disease, hereditary RCCs, and papillary RCCs than any other histologic subtypes.

Treatment •

The gold standard treatment for localized early-stage disease is radical nephrectomy with removal of all contents of the Gerota fascia and adjacent adrenal gland. Partial nephrectomy with nephronsparing surgery is considered in patients with a unilateral functioning kidney and patients with bilateral RCCs. Cytoreductive surgery followed by immunotherapy is recommended for later stage disease. Immunotherapy with cytokines is the main treatment for advanced stages of disease. Image-guided radiofrequency ablation of the lesion is a recent development and is currently used in patients with inoperable disease and peripherally located RCCs.

Prognosis •



The prognosis is good in patients with localized disease; the 10-year survival rate is > 72% in patients treated with partial nephrectomy, with a recurrence rate of 3%. Recurrence is less common (2%) in patients treated with radical nephrectomy than with partial nephrectomy. The prognosis for advanced metastatic disease is poor. In patients with metastatic RCC, the 2-year survival rate is 15 to 20%.

PE ARL



A solid enhancing renal lesion should be considered RCC unless proven otherwise.

PITFALL S

• • •



The presence of fat in the lesion can lead to the erroneous diagnosis of angiomyolipoma. However, if calcifications are present, it points toward RCC. A spoke-wheel pattern of enhancement can be seen in oncocytoma as well as papillary RCC. The presence of filling defects in the inferior vena cava or other vascular structures should be confirmed on the delayed venous phase of contrast enhancement to prevent the erroneous diagnosis of thrombosis. Perinephric fat stranding is not always indicative of the extension of tumor beyond the renal capsule and can be caused by other associated inflammatory conditions.

Suggested Readings Drucker BJ. Renal cell carcinoma: current status and future prospects. Cancer Treat Rev 2005;31: 536–545

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Kim KA, Choi JW, Park CM, et al. Unusual renal cell carcinomas: a pictorial essay. Abdom Imaging 2006;31:154–163 Prasad SR, Humphrey PA, Catena JR. Common and uncommon histologic subtypes of renal cell carcinoma: imaging spectrum with pathologic correlation. Radiographics 2006;26:1795–1810 Sheth S, Scatarige JC, Horton KM, Corl FM, Fishman EK. Current concepts in the diagnosis and management of renal cell carcinoma: role of multidetector CT and three-dimensional CT. Radiographics 2001;21:S237–S254

CASE 67 Clinical Presentation A 59-year-old woman with a known primary history of adenocarcinoma of the lung presents with flank pain.

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Fig. 67.1 (A) Contrast-enhanced image in a 59-year-old patient shows the presence of an enhancing right hilar adenocarcinoma. (B) A more inferior abdominal axial image shows the presence of a low-density metastatic liver lesion along with a low-density left renal lesion (arrow). (C) An additional low-density lesion is seen in the right kidney (arrow).

Radiologic Findings Axial computed tomography (CT) image of the chest shows the patient’s known primary right lung cancer (Fig. 67.1A). Abdominal images show hypoattenuating hepatic metastases as well as bilateral low-density renal lesions (Fig. 67.1B,C).

Diagnosis Renal metastases from primary lung adenocarcinoma

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Differential Diagnosis • • • • •

Renal cell carcinoma Renal lymphoma Renal abscess Oncocytoma Angiomyolipoma

Discussion Background Metastases to the kidney are very rare. Among nonlymphomatous malignancies, lung cancer is the most common primary tumor metastasizing to the kidney. A high index of suspicion in known cases of primary tumor and histopathologic examination of the renal lesion are important for differentiating metastatic lesions from renal primaries. Based on imaging alone, metastatic lesions are indistinguishable from renal cell carcinoma. Forty percent of cases of renal metastases of lung cancer are bilateral, and up to 10% of patients have associated renal cell carcinoma. Renal metastases are associated with metastases in other major organs in 90% of cases. A prior histopathologic correlation in patients with suspected metastases obviates the need for the surgical removal of the renal mass.

Clinical Findings • • • • •

Asymptomatic Flank pain Hematuria Abnormal renal function tests Symptoms due to metastases to other organs

Complications •

Hematuria

Etiology Hematogenous spread from know primary pulmonary and other malignancies

Imaging Findings • • •

Ultrasound shows an iso- to hyperechoic rounded lesion in the kidney with hypoechoic necrotic contents. CT is the investigation of choice for imaging renal metastases. Bilateral, small, multicentric, intensely enhancing lesions with a necrotic center are the characteristic imaging findings. Based on imaging criteria alone, metastases cannot be differentiated from renal cell carcinoma; however, knowledge of the primary malignancy with a high index of suspicion can suggest the diagnosis.

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Treatment •

The primary form of treatment of the primary tumor is chemoradiation, depending on the type of tumor. Radiofrequency ablation of renal lesions can be done as a palliative measure.

Prognosis •

The association of renal metastases with inoperable lesions and metastases in other organs puts the patient at a higher stage of malignancy and is associated with a poorer prognosis than for patients without metastases. The finding of renal metastases puts the patient at a very high risk of having metastases at other sites. The prognosis in patients with metastatic lung cancer treated with chemotherapy is better than for untreated patients.

PE ARL



Bilateral, intensely enhancing renal masses in a patient with known primary tumor.

PITFALL



Renal metastases cannot be differentiated from renal cell carcinoma based on imaging alone.

Suggested Readings Choyke PL, White EM, Zeman RK, Jaffe MH, Clark LR. Renal metastases: clinicopathologic and radiologic correlation. Radiology 1987;162:359–363

CASE 68 Clinical Presentation A 76-year-old woman presents with a low-grade fever and weight loss.

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Fig. 68.1 (A–C) Contrast-enhanced axial CT images of the abdomen demonstrate a soft tissue mass in the perirenal space involving the right kidney and associated with thickening of Gerota fascia. There is extension of the mass into the renal sinus with encasement of the renal artery. There is also destruction of the adjacent vertebral body.

C

Radiologic Findings Contrast-enhanced axial computed tomography (CT) images of the abdomen demonstrate a soft tissue mass in the perirenal space involving the right kidney and associated with thickening of Gerota fascia. There is extension of the mass into the renal sinus with encasement of the renal artery. There is also destruction of the adjacent vertebral body (Fig. 68.1).

Diagnosis Non-Hodgkin lymphoma (NHL) involving the kidney

Differential Diagnosis • •

Retroperitoneal sarcoma Metastasis to the perinephric space

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• •

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Perinephric hematoma Extramedullary hematopoiesis

Discussion Background Extranodal spread of lymphoma to the genitourinary system and kidneys is very common and has been reported in approximately one third of cases in autopsy studies. Renal involvement usually occurs in the setting of widespread NHL. Primary renal lymphoma isolated to the renal parenchyma without systemic disease is uncommon, accounting for < 1% of cases of extranodal lymphoma.

Clinical Findings The majority of the cases are clinically asymptomatic and may undergo radiologic evaluation due to elevated blood urea nitrogen and creatinine levels. The patients, however, may present with nonspecific signs and symptoms of flank pain, weight loss, hematuria, or palpable mass. Patients with primary lymphoma are usually middle aged or older.

Complications In the absence of an appropriate diagnosis and treatment, the prognosis for renal lymphoma is poor, and morbidity and mortality are secondary to progressive renal failure.

Etiology Most commonly, renal lymphoma occurs in the setting of widespread intermediate- or high-grade B-cell NHL, either through hematogenous spread or via direct extension from the retroperitoneum. In primary renal lymphoma, the tumor may originate in the lymphatic tissue of the renal capsule or the perinephric fat and secondarily invade the parenchyma. In the setting of chronic inflammation, the tumor may arise from deposited lymphocytes.

Imaging Findings • •



The imaging modality of choice is CT, which shows the lymphomatous tumors as hypovascular masses with poor enhancement characteristics. Magnetic resonance imaging is the optimal modality in patients with renal insufficiency demonstrating hypointensity on T1-weighted images and slightly hypointense to isointensity on T2weighted images. Most commonly, renal lymphoma presents with multiple parenchymal lesions, followed by direct extension from large retroperitoneal masses. Solitary lesions may occur in 10 to 25% of patients. Isolated perinephric lymphoma is unusual and occurs in < 10% of cases. Occasionally, renal lymphoma presents with nephromegaly without distortion of the normal shape of the kidneys. Uncommonly, lymphoma preferentially affects the renal sinus.

Treatment •

The treatment for renal lymphoma is systemic chemotherapy. Surgery is not indicated, but biopsy may be necessary to differentiate it from primary renal cell carcinoma and metastasis to the kidneys.

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Prognosis •

Patients usually respond well to systemic chemotherapy without residual tumor in the kidneys.

PE ARL



Lymphomatous involvement of the kidneys may present with a variety of clinical and radiologic findings. Primary extranodal NHL of the kidney is an uncommon presentation of lymphoma.

PITFALL



A delay in the diagnosis and treatment of renal lymphoma may create serious risks for the patient, especially if the lymphoma is confined to the kidneys. Failure to correctly distinguish renal lymphoma from other lesions in the kidneys may cause serious damage, requiring nephrectomy.

Suggested Readings Sheth S, Ali S, Fishman E. Imaging of renal lymphoma: patterns of disease with pathologic correlation. Radiographics 2006;26:1151–1168 Shirkhoda A. Kidney, lymphoma. eMedicine Web site. Available at: http://www.emedicine.com/radio/ topic373.htm. Accessed August 21, 2007

CASE 69 Clinical Presentation A 65-year-old man complains of a dull back pain.

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Fig. 69.1 (A,B) Axial contrast-enhanced CT images show diffuse bilateral soft tissue infiltration of the perirenal space extending into the renal hilum with evidence of hydronephrosis. There is also plaquelike thickening surrounding the aorta and the medial aspect of the inferior vena cava.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images show diffuse bilateral soft tissue infiltration of the perirenal space extending into the renal hilum with evidence of hydronephrosis. There is also plaquelike thickening surrounding the aorta and the medial aspect of the inferior vena cava (IVC) (Fig. 69.1).

Diagnosis Retroperitoneal fibrosis (RPF)

Differential Diagnosis • • •

Retroperitoneal malignancies Retroperitoneal lymphoma Retroperitoneal hemorrhage, infection, amyloidosis

Discussion Background RPF is a relatively uncommon clinical entity, predominantly affecting men in their 4th to 6th decade. This disorder is characterized by the development of extensive fibrosis occurring throughout the retroperitoneum, ultimately leading to encasement and entrapment of retroperitoneal structures.

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RPF usually begins at the level of the fourth and fifth lumbar vertebrae and subsequently spreads cephalad, encasing the aorta, IVC, and ureters.

Clinical Findings Clinical findings are usually vague and nonspecific; patients most commonly experience a dull, poorly localized pain in the back or lower abdomen. Other symptoms include fever, lower extremity and scrotal edema due to lymphatic obstruction, fatigue, general malaise, anorexia, and weight loss. Laboratory test abnormalities include elevated erythrocyte sedimentation rate and C-reactive protein, polyclonal hypergammaglobulinemia, and increased urea and creatinine levels.

Complications Ureteric entrapment by fibrotic tissue may lead to progressive renal failure in cases of delayed diagnosis. Obstructive uropathy may lead to an increase in serum renin levels and therefore to hypertension. Other complications include small or large bowel obstruction, spinal cord compression, peripheral edema, and deep venous thrombosis.

Etiology Idiopathic retroperitoneal fibrosis, also known as Ormond disease, roughly accounts for almost 70% of cases. Recent studies have suggested that this disorder results from an immunologic response to antigens leaking into the retroperitoneum from atherosclerotic plaques in the aorta or common iliac vessels. The remaining one third of cases are ascribed to drugs, such as methysergide, methyldopa, and ␤-blockers; retroperitoneal hemorrhage; urine extravasation; surgery; radiation therapy; infection; abdominal aortic aneurysms; and desmoplastic response to tumors, including sarcomas, lymphomas, and carcinomas of the kidney, colon, breast, and uterine cervix.

Imaging Findings •





The imaging diagnosis of RPF was previously obtained with intravenous urography, to demonstrate the medial deviation and smooth extrinsic compression of the ureters at the level of the lower lumbar spine and associated hydronephrosis. However, these findings are nonspecific, as they may be observed with ureteral tumors or periureteral adenopathy. At ultrasound, RPF appears as a well-defined, hypoechoic retroperitoneal plaque, although this technique is typically performed to monitor the response to treatment by demonstrating the presence or absence of hydronephrosis. CT and magnetic resonance imaging (MRI) are both extremely useful in assessing the extent of the fibrotic process. At CT, RPF appears as a plaque with the same attenuation of the adjacent muscle centered in the retroperitoneum around the aorta and IVC and extending to the ureters (Fig. 69.2). The enhancement of the plaque varies according to the stage of development of the fibrotic process and therefore correlates with the degree of inflammation; the immature plaque (more peripherally located) is vascular and enhances to a greater degree, whereas in late stages, the plaque is almost nonenhancing. MRI demonstrates low signal intensity on T1-weighted images and variable signal intensity on T2-weighted images: high signal on T2 is associated with fluid content and hypercellularity (acute inflammation), whereas low signal is observed in chronic inflammation corresponding to fibrotic tissue.

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Fig. 69.2 Axial contrast-enhanced CT image in a different patient shows soft tissue infiltration surrounding the aorta, inferior vena cava, and ureters bilaterally. Also seen are bilateral ureteral stents.

Treatment •

Corticosteroids represent the mainstay of RPF treatment; if patients do not respond to corticosteroids, antiestrogen (tamoxifen) and immunosuppressive therapy (azathioprine, cyclophosphamide, and cyclosporin) may be attempted.

Prognosis •

The prognosis is usually favorable in patients without impaired renal function, with a 90% longterm success rate. Patients with RPF associated with retroperitoneal malignancies usually have a dismal prognosis, with a mean survival of 3 to 6 months.

PE ARL



RPF is associated with medial displacement of the ureters, whereas retroperitoneal malignancies and lymphadenopathy typically cause lateral displacement. In the primary form (Ormond disease), the fibrosis typically spares the posterior wall of the aorta.

PITFALL



Atypical RPF (multifocal appearance with sparing of the aorta, IVC, and ureters) may mimic retroperitoneal malignancies.

Suggested Readings Das CJ, Sharma R, Jain TP, Rai V, Chumber S, Das AK. Unusual appearance of retroperitoneal fibrosis simulating a tumour. Br J Radiol 2006;79(946):137–139 Geoghegan T, Byrne AT, Benfayed W, McAuley G, Torreggiani WC. Imaging and intervention of retroperitoneal fibrosis. Australas Radiol 2007;51(1):26–34 Vaglio A, Salvarani C, Buzio C. Retroperitoneal fibrosis. Lancet 2006;367(9506):241–251

VI

Adrenal Glands

CASE 70 Clinical Presentation A 52-year-old woman complaining of nonspecific abdominal pain.

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A

Fig. 70.1 (A) Ultrasound image shows the complex left suprarenal lesion containing multiple septations and mixed hypoand hyperechoic debris. (B) Axial contrast-enhanced CT image in the same patient shows a large well-defined, thick-walled, complex cystic lesion with hyperdense heterogeneous contents.

Radiologic Findings Axial computed tomography (CT) and ultrasound images of a left adrenal mass show a large welldefined, thick-walled, complex cystic lesion with heterogeneous contents (Fig. 70.1).

Diagnosis Left adrenal cyst

Differential Diagnosis • • • • •

Adenoma Parasitic (hydatid) cyst Cystic pheochromocytoma Cystic adrenal carcinoma Pseudocyst of pancreas, exophytic renal cyst, cystic schwannoma, or cystic adenomatoid tumor mimicking an adrenal cystic lesion

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Discussion Background Adrenal cystic lesions are more commonly seen in women. It is important to distinguish adrenal cysts from adenoma because adenoma is treated conservatively, whereas adrenal cysts may need surgical intervention if imaging appearances suggest the possibility of complications.

Clinical Findings Clinical features depend on the type of adrenal cystic lesion. In cases of simple cyst and pseudocyst, patients are usually asymptomatic until the cysts become larger. Cystic pheochromocytoma presents with persistent hypertension and its sequel-like hypertensive crisis, hypertensive retinopathy, and encephalopathy. Hydatid cysts usually have daughter cysts within the parent cyst and hepatic cysts at presentation.

Complications •

Hemorrhage

Etiology Four types of cysts are recognized on the basis of pathologic classification: endothelial, epithelial, parasitic, and posttraumatic pseudocysts.

Imaging Findings • • •

Ultrasound and magnetic resonance imaging (MRI) can effectively distinguish between adenoma and cysts. MRI can provide additional tissue information and enhancement characteristics of the lesion. Adrenal cysts typically are hypointense on T1-weighted and hyperintense on T2-weighted images. On CT, adrenal cysts are seen as water-density lesions with a thin wall (< 3 mm), with or without septal (Fig. 70.2) or mural (Fig. 70.3) calcifications. A thick wall > 5 mm, heterogeneous appearance, and stippled central or thick peripheral calcifications are the features of the cysts

Fig. 70.2 Axial contrast-enhanced CT image of a right adrenal epithelial cyst in a 57-year-old woman shows a welldefined, rounded cystic lesion with a thin wall having rimlike calcification and fluid attenuation.

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Fig. 70.3 Axial contrast-enhanced CT image of a left adrenal cystic lesion shows a mural nodular calcification in a simple epithelial cyst.

Fig. 70.4 Axial contrast-enhanced CT image of a right adrenal pseudocyst shows a fluid–fluid layer (arrow) and hyperdense blood in the dependent portion of the cyst.

complicated by chronic hemorrhage. Hemorrhage within the cyst can also be suggested by the presence of hyperdense contents within the lesion with fluid–fluid levels (Fig. 70.4). Rimlike mural calcification is the most common type found in adrenal cysts; other types of calcification found are nodular and septal. Adrenal pseudocysts usually tend to be more unilocular and have rimlike mural calcification. Adrenal endothelial cysts usually are multilocular and have septal calcification. Large thick-walled, enhancing, heterogeneous lesions should always be viewed with suspicion for adrenal carcinoma.

Treatment •

Uncomplicated benign lesions are usually managed conservatively. Complicated lesions, hyperfunctioning lesions, and lesions with features suspicious of malignancy require more aggressive surgical management. Indeterminate lesions can be managed with percutaneous needle aspiration of conservative treatment, depending on the patient’s clinical status.

Prognosis •

The prognosis depends on the etiology of the cystic lesion. In general, the prognosis is excellent for uncomplicated benign cystic lesions. The prognosis for malignant lesions depends on the stage of malignancy.

PE ARL



MRI can be useful in differentiating adrenal pseudocysts from adenomas.

PITFALL



Despite their characteristic appearance, adrenal cysts may be difficult to differentiate from neoplastic lesions.

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Suggested Readings McLoughlin RF, Bilbey JH. Tumors of the adrenal gland: findings on CT and MR imaging. AJR Am J Roentgenol 1994;163:1413–1418 Rozenblit A, Morehouse HT, Amis ES Jr. Cystic adrenal lesions: CT features. Radiology 1996;201: 541–548 Sroujieh AS, Farah CR, Haddad M, Ahu-Khalaf MM. Adrenal cyst: diagnosis and management. Br J Urol 1990;65:570–575

CASE 71 Clinical Presentation A 41-year-old man presents with right inguinal pain.

Fig. 71.1 Axial contrast-enhanced CT image through the upper abdomen shows a well-defined hypodense, nonenhancing right adrenal mass lesion with fat density.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) image through the upper abdomen shows a small nonenhancing right adrenal mass lesion with central fat density (Fig. 71.1).

Diagnosis Myelolipoma

Differential Diagnosis •

Retroperitoneal lipoma or liposarcoma

Discussion Background Myelolipoma is a benign lesion found in adrenal and extra-adrenal sites that contains mature fat and marrow elements. Extra-adrenal sites of myelolipoma are the retroperitoneum, presacral region, perirenal locations, liver, and mediastinum.

Clinical Findings Myelolipoma is usually asymptomatic and is an incidental finding on imaging studies done for other indications.

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Complications • • •

Spontaneous hemorrhage Rupture following trauma Pressure on adjacent organs causing complications

Etiology Myelolipoma is presumed to arise from metaplasia of the reticuloendothelial cells of blood capillaries as a result of tissue response to stressful stimuli.

Imaging Findings • • •

Imaging features depend on the amount of fatty and marrow elements present within the lesion. On ultrasound, myelolipoma appears as a hyperechoic adrenal lesion with some hypoechoic components, depending on the amount of the hematopoietic component present within the lesion. On CT and magnetic resonance imaging (MRI), the diagnosis depends on the demonstration of macroscopic fat within the lesion (Fig. 71.2). CT shows hypodense fat with an enhancing com-

A

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C

D

Fig. 71.2 (A) Contrast-enhanced axial CT image through the upper abdomen in a patient with liver cirrhosis shows a large well-defined, heterogeneous right adrenal mass lesion with variable contrast enhancement and fat density. (B) Axial T1weighted gradient echo sequence image in the same patient show areas of high signal intensity corresponding to macroscopic fat. (C) Axial T1-weighted image with fat saturation shows a drop in the signal corresponding to areas of macroscopic fat. (D) Axial contrast-enhanced T1-weighted image in the same patient shows variable heterogeneous enhancement.

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ponent of hematopoietic marrow elements. On T1-weighted images, the lesion appears hyperintense with signal loss on fat saturation. On T2-weighted images, myelolipomas show intermediate signal intensity. In myelolipomas with predominant marrow elements, the diagnosis can be difficult because the imaging appearance can simulate other tumors of the adrenal glands, and biopsy may be necessary to establish the diagnosis.

Treatment •

Unless symptomatic, myelolipomas can be left alone. Myelolipomas can cause symptoms because of hemorrhagic complications or pressure on adjacent tissues.

Prognosis •

The prognosis for uncomplicated myelolipomas is very good. Myelolipomas are almost never reported to have malignant potential.

PE ARL



Adrenal lesion containing macroscopic fat

PITFALL



Very large tumors can be confused with lipoma or liposarcoma (distinguishing features are invasion of the adjacent organs, heterogeneous appearance of the tumor, and varying degrees of enhancement).

Suggested Readings Elsayes KM, Mukundan G, Narra VR. Adrenal masses: MR imaging features with pathologic correlation. Radiographics 2004;24:S73–S86 Otal P, Escourrou G, Mazerolles C, et al. Imaging features of uncommon adrenal masses with histopathologic correlation. Radiographics 1999;19:569–581 Rao P, Kenney PJ, Wagner BJ, Davidson AJ. Imaging and pathologic features of myelolipoma. Radiographics 1997;17:1373–1385

CASE 72 Clinical Presentation A 41-year-old woman presents with a history of persistent hypertension.

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D

Fig. 72.1 (A) Axial T1-weighted image shows a well-defined right adrenal nodule (arrow) isointense to muscle. (B) Axial T2-weighted image shows the lesion to have homogeneous high signal intensity. (C) Axial postcontrast image shows homogeneous enhancement within the lesion. (D) I 123 MIBG SPECT scan shows a high uptake in the right adrenal region.

Radiologic Findings Magnetic resonance (MR) images of the right adrenal gland show a small hypointense lesion on the T1-weighted sequence that is hyperintense on the T2-weighted image and shows homogeneous intense enhancement on the postcontrast image. The lesion is uniformly hot on I 123 thyroid, MIBG (iobenguane/m-iodobenzylguanidine) single-photon emission computed tomography (SPECT) scan (Fig. 72.1).

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Diagnosis Pheochromocytoma

Differential Diagnosis • • •

Adenoma Carcinoma Metastases

Discussion Background Paraganglioma, when present in the adrenal medullary location, is referred to as pheochromocytoma. When extra-adrenal, these tumors have more malignant potential and are commonly referred to as paragangliomas or chemodectomas. The most common extra-adrenal sites of paragangliomas are the organ of Zuckerkandl (which is the confluence of neural tissue just below the aortic bifurcation), sympathetic chain, and urinary bladder. Pheochromocytoma usually follows the rule of 10 (10% incidence of being extra-adrenal, malignant, bilateral, familial, and not associated with hypertension). Pheochromocytomas are also associated with multiple endocrine neoplasia (MEN) types 2A and B, von Hippel-Lindau disease, neurofibromatosis 1, cerebellar hemangioblastoma, Sturge-Weber syndrome, tuberous sclerosis, Carney triad, and familial pheochromocytoma.

Clinical Findings Clinical findings include persistent or paroxysmal hypertension, hypertensive crisis, tachycardia, palpitations, flushing, headache, tremors, nausea, anxiety, feeling of impending doom, abdominal pain, constipation, and orthostatic hypotension. Elevated 24-hour excretion of urinary catecholamine metabolites—vanillylmandelic acid and total metanephrines or free catecholamines (norepinephrine and epinephrine)—is diagnostic of pheochromocytoma. Clinically, asymptomatic pheochromocytomas tend to be larger in size than functioning pheochromocytomas.

Complications • • • • •

Cardiac arrhythmias, pheochromocytoma crisis, hypertensive crisis (provoked by anesthesia, systemic intravenous iodinated contrast, selective angiography, and surgical interventions) Hemorrhage within the tumor Hypertensive encephalopathy, hypertensive retinopathy, transient thyrotoxicosis, hypercalcemia Metastases to the axial skeleton, liver, lungs, and lymph nodes Cerebral infarction secondary to cardiac arrhythmias leading to thromboembolic phenomena

Etiology Pheochromocytoma is an adrenal medullary paraganglioma, which is derived from chromaffin cells and secretes catecholamines.

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Fig. 72.2 Axial postcontrast CT image of the pelvis in a 48-year-old man with a history of familial paraganglioma shows a large well-defined, intensely enhancing mass anterior to the aortic bifurcation. Postoperatively, this lesion was confirmed to be an organ or Zuckerkandl paraganglioma.

Imaging Findings •





Typical pheochromocytomas on CT appear as well-defined, unilateral, homogeneous iso- to hypodense adrenal masses with CT value >10 Hounsfield units with negative pixels and without any calcifications (95%) showing intense contrast enhancement with < 50% washout. They may be homogeneous or heterogeneous, solid or cystic complex masses or may show calcification. Extraadrenal lesions may show imaging features similar to that seen in adrenal lesions (Fig. 72.2). On T1-weighted MR images, pheochromocytomas are usually isointense to muscle and hypointense to liver. T2-weighted MRI is particularly useful to screen for extra-adrenal pheochromocytomas because of their bright appearance or the so-called lightbulb sign on T2-weighted imaging. T2-weighted imaging helps to differentiate pheochromocytoma from adrenal carcinomas. On chemical shift imaging with MRI, a pheochromocytoma does not turn dark on out-of-phase imaging due to the lack of fat within the lesion. Chemical shift imaging is very helpful in ruling out adrenal adenomas. The lesions show brisk homogeneous enhancement following the administration of gadolinium. Radioscintigraphy can be with I 131 MIBG and indium (In) 111 octreotide. It has more specificity than CT and MRI but less sensitivity. When both I 131 MIBG and In 111 octreotide are used together, sensitivity of the study can be increased. Radioscintigraphy can be less sensitive in cases of tumors with necrotic tissue. The combination of MRI and MIBG scintigraphy has up to 100% sensitivity and positive predictive value.

Treatment •

Surgical resection is the treatment of choice for localized disease. For malignant, metastatic, and unresectable disease, surgery, chemotherapy, and radiation are alternative options.

Prognosis • •

For benign, resectable, localized disease, the prognosis is excellent after resection. Extra-adrenal pheochromocytoma has more malignant potential and is associated with a poorer prognosis.

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PE ARL



Adrenal lesion showing T2 hypersensitivity (lightbulb bright) and arterial enhancement.

PITFALL



Cystic lesions in the adrenal can be cystic pheochromocytomas and should be evaluated further if clinical data support the diagnosis of pheochromocytoma.

Suggested Readings Blake MA, Kalra MK, Maher MM, et al. Pheochromocytoma: an imaging chameleon. Radiographics 2004;24:S87–S99 Goldstein DS, Eisenhofer G, Flynn JA, Wand G, Pacak K. Diagnosis and localization of pheochromocytoma. Hypertension 2004;43:907–910 Lee TH, Slywotzky CM, Lavelle MT, Garcia RA. Best cases from the AFIP: cystic pheochromocytoma. Radiographics 2002;22:935–940

CASE 73 Clinical Presentation A 75-year-old man on anticoagulant treatment presents with easily bleeding gums and abdominal discomfort.

Fig. 73.1 Noncontrast axial CT image through the left adrenal gland shows a rounded left adrenal mass (arrow) that is hyperdense on CT with a density of 55 to 60 HU.

Radiologic Findings A small hyperdense lesion is seen in the left adrenal gland (Fig. 73.1).

Diagnosis Adrenal hemorrhage

Differential Diagnosis • •

Hemorrhage within an adrenal neoplasm or cyst Neuroblastoma

Discussion Background Adrenal hemorrhage is a rare condition that usually occurs in response to stressful stimuli, such as infection, septicemia, blunt abdominal trauma, hypotensive shock, burns, neonatal asphyxia, coagulopathies with different causes, and inferior vena caval or renal venous thrombosis. Unilateral right adrenal involvement is most common.

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Clinical Findings Neonates with a history of asphyxia and/or septicemia can present with an abdominal mass, hypotension, hemodynamic shock, anemia, and jaundice and, rarely, with scrotal hematoma. In adults with coagulopathies, blunt trauma, and septicemia, adrenal hemorrhage is detected as an incidental finding on a work-up for internal concealed bleeds.

Complications • • • •

Shock Prolonged physiologic jaundice Renal vein thrombosis Infection of liquefied hematoma may result in abscess formation.

Etiology The complex and delicate vasculature of the adrenals makes them susceptible to hemorrhage in response to a variety of stimuli. The adrenal vasculature contains high levels of catecholamines that act on the vascular smooth muscles, leading to sudden alterations in the blood flow in the venous system and making them prone to thrombosis. The right adrenal vein is shorter, which makes it more susceptible to hemorrhage because of pressure changes in the inferior vena cava. Adrenal neoplasms, which can present with hemorrhage, are adrenal pseudocyst, myelolipoma, pheochromocytoma, adenoma, carcinoma, metastatic bronchogenic carcinoma, angiosarcoma, and melanoma. Hemorrhage within the adrenal cysts is reported to occur in cases of Beckwith-Wiedemann syndrome.

Imaging Findings • •

On ultrasound, acute blood appears hyperechoic and later becomes heterogeneous in subacute stages, finally becoming hypoechoic with cystic change. CT shows hyperdense (55 to 70 Hounsfield units [HU]) acute hemorrhage and becomes hypodense as the hemorrhage starts evolving into a cystic mass before shrinking. The lesions can be bilateral (Fig. 73.2). Calcifications within the adrenal hemorrhage are seen as early as 2 weeks in neonates. The pattern of calcifications is usually of the punctate or eggshell variety, which can also be seen in Wolman disease.

Fig. 73.2 Axial noncontrast CT image in a different patient with systemic coagulopathy shows bilateral hyperdense adrenal masses with a density of 55 to 60 HU.

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A hematoma without any underlying malignancy usually shows no contrast enhancement; if it does, the possibility of underlying malignancy should be considered. Magnetic resonance imaging (MRI) shows changes according to the age of the bleed and appears iso- to hypointense on T1-weighted imaging and markedly hypointense on T2-weighted imaging in the first 7 days. The bleed starts to become hyperintense on T1- and T2-weighted imaging in the 2nd week until the end of the 7th week and appears hypointense on both T1- and T2weighted imaging after 8 weeks. Associated renal vein thrombosis can be well seen on MRI.

Treatment • •

Uncomplicated adrenal hemorrhage can be left alone without any treatment. Ultrasound- or CTguided drainage can be done in cases of liquefied infected bleeds. Supportive treatment is begun for hemodynamic shock, along with treatment of the primary cause.

Prognosis •

The prognosis depends on the underlying cause of adrenal hemorrhage. Mortality is usually due to the condition predisposing to adrenal hemorrhage.

PE ARL



High-density lesion within the adrenal glands with acute presentation; suspect hemorrhage.

PITFALL



Adrenal hemorrhage can make it difficult to rule out an underlying neoplastic condition.

Suggested Readings Kawashima A, Sandler CM, Ernst RD, et al. Imaging of nontraumatic hemorrhage of the adrenal gland. Radiographics 1999;19:949–963

CASE 74 Clinical Presentation A 70-year-old man with a history of right nephrectomy for renal cell carcinoma comes for restaging of a malignancy.

A

B

C

D

Fig. 74.1 (A) Axial noncontrast CT image in a 70-year-old man with a history of nephrectomy for renal cell carcinoma shows a well-defined, isodense left adrenal mass lesion (arrow). (B) Axial fat-saturated T2-weighted image in the same patient shows the lesion to be hyperintense. (C) On T1-weighted out-of-phase gradient echo imaging, the lesion shows no drop in signal intensity. (D) Axial contrast-enhanced T1-weighted imaging in the same patient shows intense enhancement of the lesion on an early arterial phase scan.

Radiologic Findings Axial computed tomography (CT) and magnetic resonance (MR) images show a left adrenal mass that appears isointense on T1-weighted imaging, moderately hyperintense on T2-weighted imaging, does not show a drop in signal intensity on out-of-phase spoiled gradient echo images, and shows intense enhancement on contrast administration (Fig. 74.1).

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Diagnosis Metastatic renal cell carcinoma to the left adrenal gland

Differential Diagnosis • • •

Pheochromocytoma Adenoma Adrenal carcinoma

Discussion Background Adrenal metastases are common in the setting of malignancies, with most common malignancies metastasizing to the adrenals being lung, melanoma, breast, genitourinary, and gastrointestinal.

Clinical Findings Most cases of adrenal metastases are asymptomatic; patients may present with adrenal hormone deficiency symptoms in cases with bilateral adrenal disease.

Complications • • •

Hemorrhage Necrosis Invasion of the adjacent organs and vascular structures

Etiology The most common primary malignancies metastasizing to the adrenals are lung, melanoma, breast, genitourinary, and gastrointestinal.

Imaging Findings • •





On ultrasound, adrenal metastases appear as solid hypoechoic, heterogeneous lesions. These lesions are usually found on staging CTs or MRIs. On CT, calcifications are less common in metastatic disease than other primary adrenal lesions; however, they may be seen with colorectal metastases. Adrenal metastatic mass lesions complicated by hemorrhage are usually secondary to metastatic bronchogenic carcinoma. The lesions can be bilateral (Fig. 74.2). On CT and MR imaging, most metastases are usually hypovascular, with the exception of metastatic renal cell carcinoma and other vascular metastases. On MR imaging, metastases usually appear hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging except melanoma metastases, which appear hyperintense on T1-weighted imaging (renal cell cancer metastases can also appear iso- to hyperintense on T1-weighted imaging). Positron emission tomography has higher sensitivity for the detection of adrenal metastases; however, false-negative results can be seen in metastases with hemorrhagic or necrotic metastases, small-sized metastases < 10 mm, and pulmonary bronchoalveolar carcinoma and carcinoid metastases.

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Fig. 74.2 Axial contrast-enhanced CT image in a 45-yearold woman with non-small cell lung carcinoma shows bilateral hypodense nonenhancing adrenal metastases. On the left side, an adrenal metastasis appears larger and has invaded the kidney.

Treatment •

Radiofrequency ablation of the adrenal metastases has shown good results in controlling local disease and is currently used in palliative treatment for smaller lesions.

Prognosis •

The prognosis in a patient with stage 4 disease with distant adrenal metastases is always poor.

PE ARL



A solid adrenal lesion in a patient with a known primary malignancy

PITFALL



An adrenal metastasis may be difficult to differentiate from a primary adrenal neoplasm.

Suggested Readings Dunnick NR, Korobkin M. Imaging of adrenal incidentalomas: current status. AJR Am J Roentgenol 2002;179:559–568 Pena CS, Boland GWL, Hahn PF, Lee MJ, Mueller PR. Characterization of indeterminate (lipid-poor) adrenal masses: use of washout characteristics at contrast-enhanced CT. Radiology 2000;217: 798–802

CASE 75 Clinical Presentation A 40-year-old man presents with a recent-onset cough.

A

Fig. 75.1 (A) Contrast-enhanced axial CT image shows a well-defined rounded, lobulated, heterogeneously enhancing left adrenal mass. (B) Coronal reformatted CT image shows multiple enlarged hypodense celiac and mediastinal lymph nodes with a large heterogeneously enhancing left adrenal mass.

Radiologic Findings Computed tomography (CT) scanning reveals a heterogeneously enhancing rounded left adrenal mass with extensive mediastinal and celiac lymphadenopathy (Fig. 75.1).

Diagnosis Adrenocortical carcinoma

Differential Diagnosis • • •

Lymphoma Metastatic disease Renal cell carcinoma

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Discussion Background Adrenocortical carcinoma is a rare malignancy of the adrenocortical tissue, with an incidence of 1 to 2 per million population. It is mostly found in adults, with the median age at diagnosis being 44 years. In 70% of diagnosed cases, tumor invades into adjacent tissues by the time of diagnosis.

Clinical Findings In 60 to 80% of cases, patients show clinical features of functional activity of the tumor (adrenocorticotropic hormone [ACTH]–independent Cushing or Conn syndrome). In men, almost all feminizing tumors of the adrenal glands are malignant. In the remaining cases, clinical features depend on the organ involved by local spread or metastases. Adrenal carcinoma is known to be associated with Beckwith-Wiedemann syndrome, Li-Fraumeni syndrome, Gardner syndrome, multiple endocrine neoplasia syndrome type 1, familial adenomatous polyposis syndrome, and sarcoma, breast, lung, and adrenal (SBLA) carcinoma.

Complications •

Invasion of the adjacent organs

Etiology Adrenocortical carcinoma, as the name implies, is a malignancy arising from the adrenocortical tissue.

Imaging Findings • • •

On imaging, these lesions are typically large in size (> 4 cm) and show heterogeneity, calcifications, and invasion of adjacent organs. On CT, heterogeneity of the lesion is due to necrosis and/or hemorrhage. The nonnecrotic component of the lesion usually appears hyperdense compared with the rest of the tumor density. On T1-weighted imaging, adrenal carcinoma appears heterogeneous and may show foci of high signal intensity due to the presence of methemoglobin. On T2-weighted imaging, it appears heterogeneous with areas of high signal intensity due to necrotic foci within the tumor. On contrast administration, the tumor shows variable enhancement, and the heterogeneous appearance of the lesion can be better appreciated.

Treatment •

Surgical resection of the tumor is the treatment of choice. Complete curative resection of the tumor is the treatment of choice for tumors confined to the adrenal glands. In patients with metastatic disease, palliative resection of the primary tumor and metastases is one of the treatment options.

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Prognosis •

The completeness of the resection and the stage at diagnosis are the two most important prognostic factors, with a 40% 5-year survival rate in patients with surgical resection. Patients without any local spread or lymphatic metastases have a better prognosis.

PE ARL



Large heterogeneous adrenal mass with areas of necrosis, hemorrhage, and calcification with invasion of adjacent organs.

PITFALL



A very large adrenal carcinoma can be confused with lesions of adjacent organs, such as the liver, kidneys, inferior vena cava, or lymphoma. Magnetic resonance imaging helps with better visualization of soft tissue planes.

Suggested Readings Elsayes KM, Mukundan G, Narra VR. Adrenal masses: MR imaging features with pathologic correlation. Radiographics 2004;24:S73–S86 Glazer GM, Woolsey EJ, Borrello J, et al. Adrenal tissue characterization using MR imaging. Radiology 1986;158:73–79 Mayo-Smith WW, Dupuy DE. Adrenal neoplasms: CT-guided radiofrequency ablation—preliminary results. Radiology 2004;231:225–230

CASE 76 Clinical Presentation A 20-year-old woman presents with abdominal pain.

Fig. 76.1 Left adrenal ganglioneuroma in a 20-year-old woman. (A,B) Axial and coronal enhanced CT scans demonstrate a well-defined oval mass in the left adrenal gland. (C) The mass appears heterogeneous and contains small central punctate calcifications (arrow).

A

B

C

Radiologic Findings A large mass is seen arising from the left adrenal gland with heterogeneous enhancement and calcification (Fig. 76.1).

Diagnosis Adrenal ganglioneuroma

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Differential Diagnosis • • • • •

Adrenocortical carcinoma Metastatic disease Adrenal adenoma Pheochromocytoma Lymphoma

Discussion Background Adrenal ganglioneuroma is a benign neoplasm originating from the sympathetic ganglia or adrenal medulla.

Clinical Findings Adrenal ganglioneuromas are usually asymptomatic, but if they are large, they can lead to palpation of an abdominal mass or abdominal fullness.

Complications Hormonally active forms have been reported; the secretion of catecholamines, vasoactive intestinal polypeptide, or androgenic hormones explains such symptoms as hypertension, diarrhea, and virilization.

Etiology These benign neoplasms are commonly seen in the 20-to-60-year-old age group. It is seen in the retroperitoneum in 30 to 50% of cases and in the posterior mediastinum in 39 to 43% of cases.

Imaging Findings • • •



Ganglioneuromas appear as well-defined oval, crescentic, or lobulated masses by imaging. They tend to encase major blood vessels but do not invade. The ultrasound appearance is nonspecific, with the mass demonstrating a heterogeneous solid structure. Computed tomography (CT) clearly demonstrates the tumor; the relationship to the vessels is best shown with helical acquisition. CT is useful for detecting calcifications, which are present in 2.4 to 40.0% of cases. Areas of low attenuation that do not enhance are common. Enhancement is usually poor. The lesion is hypointense on T1-weighted imaging and hyperintense on T2-weighted imaging. There is delayed, heterogeneous enhancement seen with dynamic magnetic resonance imaging.

Treatment •

Surgical resection is the definitive treatment.

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Prognosis •

The prognosis is excellent, and recurrence is rare after surgical resection.

PE ARL



Well-defined adrenal mass that encases rather than displaces vessels.

PITFALL



It may be difficult to differentiate adrenal ganglioneuromas from other primary adrenal neoplasms.

Suggested Readings Ichikawa T, Koyama A, Fujimoto H, et al. Retroperitoneal ganglioneuroma extending across the midline: MR features. Clin Imaging 1993;17:19–21 Ichikawa T, Ohtomo K, Araki T, et al. Ganglioneuroma: CT and MR features. Br J Radiol 1996;69: 114–121 Moriwaki Y, Miyake M, Yamamoto T, et al. Retroperitoneal ganglioneuroma: a case report and review of the Japanese literature. Intern Med 1992;31:82–85

VII GI Tract, Peritoneal Cavity, and Retroperitoneum CASE 77 Clinical Presentation Dysphagia.

Fig. 77.1 Barium esophagram shows smooth,

Fig. 77.2 Magnetic resonance angiography image shows the origin (arrow) and course of the aberrant right subclavian artery toward the contralateral side.

linear indentation producing a mild filling defect (arrow) over the posterior wall of the esophagus, causing partial obstruction with mild dilatation of the proximal esophagus.

Radiologic Findings Barium esophagram shows a smooth, linear indentation with regular margins over the posterior wall of the middle third of the esophagus with mild proximal dilatation of the cervical esophagus (Fig. 77.1). Magnetic resonance angiography (MRA) images (Figs. 77.2, 77.3) show an aberrant right subclavian artery (ARSA) arising from the left aortic arch, causing an impression in the posterior wall of the esophagus.

Diagnosis Aberrant right subclavian artery

Differential Diagnosis • • •

Double aortic arch Esophageal spasm Extrinsic compression of the esophagus from nonesophageal tumors (retrosternal extension of the thyroid) or lymphadenopathy

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Fig. 77.3 Magnetic resonance angiography image shows the retroesophageal course of the aberrant right subclavian artery (arrow).

Discussion Background The origin of the subclavian artery from the proximal descending aorta is referred to as an aberrant subclavian artery. A left aortic arch with an ARSA is the most common congenital anomaly of the aortic arch; the second most common variant is a right-sided aortic arch with an aberrant left subclavian artery (ALSA). The left ligamentum arteriosum can form a vascular ring, causing tracheal compression, and is associated more commonly with ALSA and right aortic arch. Kommerell diverticulum is a bulbous dilatation at the origin of the subclavian artery measuring more than double the diameter of the distal part of the artery. It is more commonly associated with a right aortic arch and an ALSA. A midline descending aorta is in an abnormal location anterior to the vertebral bodies and is associated with a right aortic arch with ALSA. Both ARSA and ALSA run posterior to the esophagus. Levels of tracheal compression are different for both variants.

Clinical Findings ARSA presents in adults with dysphagia more commonly than airway symptoms. ALSA presents with breathing difficulties due to the airway compression and dysphagia in children. Older patients can present with shoulder pain, neck pain, or thromboembolic disease of the extremities.

Complications Complications include esophageal obstruction, tracheal compression, thromboembolic disease, and, rarely, arterioesophageal fistula.

Etiology Embryologically, the subclavian artery is derived from the seventh intersegmental artery; a developmental anomaly leads to aberrant subclavian arteries.

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Imaging Findings • •



Barium esophagram shows smooth indentation over the posterior wall of the middle third of the esophagus. Angiography, computed tomography scan, and MRA can all be used to show the subclavian artery crossing posterior to the esophagus. Additional information about the presence, size, and complications of Kommerell diverticulum can be obtained on cross-sectional studies. Esophagoscopy shows a pulsatile extrinsic compression of the esophagus.

Treatment •

Surgical intervention is considered in symptomatic patients and patients with complicated disease. Surgical resection and reanastomosis with revascularization of the vertebral and subclavian arteries are available options.

Prognosis •

The prognosis depends on the presentation of disease. Generally, the prognosis is good in uncomplicated patients without debility in whom surgical treatment is successful without life-threatening complications. Subclavian steal syndrome can be a possible complication in surgically treated patients.

PE ARL



Aberrant subclavian arteries should be considered in the presence of a smooth, linear indentation over the posterior wall of the esophagus.

PITFALL



Posterior indentation over the esophageal wall is also caused by double aortic arch, benign or malignant tumors of the esophagus, nonesophageal tumors such as thyroid neoplasms with retrosternal extension, and vertebral spurs.

Suggested Readings Berrocal T, Torres I, Gutiérrez J, Prieto C, del Hoyo ML, Lamas M. Congenital anomalies of the upper gastrointestinal tract. Radiographics 1999;19:855–872 Donnelly LF, Fleck RJ, Pacharn P, Ziegler MA, Fricke BL, Cotton RT. Aberrant subclavian arteries: crosssectional imaging findings in infants and children referred for evaluation of extrinsic airway compression. AJR Am J Roentgenol 2002;178:1269–1274 Lowe GM, Donaldson JS, Backer CL. Vascular rings: 10-year review of imaging. Radiographics 1991; 11:637–646

CASE 78 Clinical Presentation A 63-year-old man complains of epigastric pain, chronic fatigue, and weight loss.

B

A

Fig. 78.1 (A,B) Contrast-enhanced CT images demonstrate circumferential thickening of the gastric antrum with associated gastric distention and lymphadenopathy.

Radiologic Findings Contrast-enhanced computed tomography (CT) images (Fig. 78.1) demonstrate circumferential thickening of the gastric antrum with associated gastric distention and lymphadenopathy.

Diagnosis Gastric mucosa-associated lymphoid tissue (MALT) lymphoma

Differential Diagnosis • • •

Gastritis/gastric ulcer Gastric metastases Gastric carcinoma

Discussion Background The stomach represents the most common primary site of extranodal lymphomas in the gastrointestinal (GI) tract (65–75%), although these tumors account for only 2 to 5% of gastric primary malignancies. However, the relative frequency of gastric lymphoma, unlike that of carcinoma, has increased as

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a result of the acquired immunodeficiency syndrome (AIDS) epidemic. Lymphomas typically occur in patients ages 50 to 60 years and show no evidence of sex predilection. Chronic gastritis caused by Helicobacter pylori plays a major role in the development of lymphoid tissue (MALT), which is thought to be the precursor of gastric MALT lymphomas. At histology, MALT lymphomas can be classified into two types: low-grade (50–72% of cases) and high-grade, which probably results from the transformation of low-grade lymphomas.

Clinical Findings Clinical presentation is usually nonspecific. Patients may experience symptoms mimicking gastritis or peptic ulcer disease, such as epigastric pain and dyspepsia. Other symptoms, such as low-grade fever, chronic fatigue, weight loss, and anemia, have been reported.

Complications Patients may experience GI bleeding due to tumor ulceration or obstruction. Rarely, perforation may occur.

Etiology The etiology is still controversial. Several studies have demonstrated the high frequency of H. pylori infection in patients affected by gastric lymphoma; furthermore, some of these neoplasms may regress after the eradication of H. pylori. Several cytogenetic abnormalities have been demonstrated, the most common being trisomy 3 and 11:18 translocation.

Imaging Findings •





Double-contrast upper GI examination demonstrates a wide spectrum of radiologic findings, especially in cases of low-grade lymphomas: multiple erosions and ulcers either shallow or deep associated with converging thickened gastric folds represent the most common finding in both low- and high-grade tumors. Gastric lymphomas, particularly high-grade lymphomas, may appear as large masses with or without ulcers. Other fluoroscopic imaging findings include round or oval mucosal nodules of variable size and prominent areae gastricae. However, differentiation of MALT lymphomas from gastritis or gastric adenocarcinoma is extremely challenging by imaging despite the presence of these typical findings. Multidetector CT has been increasingly performed for the detection of primary gastric malignancies because of its multiplanar capabilities; appropriate distention of the gastric lumen (oral administration of water prior to scanning) is recommended to improve the assessment of the gastric mucosa. The typical CT patterns of gastric lymphomas include diffuse thickening of the wall (> 50% involved), segmented thickening, and a localized polypoid mass. These tumors commonly extend through the pyloric region into the duodenum, whereas gastric carcinoma tends to spread to the gastroesophageal junction. Patients with gastric lymphomas, unlike those with carcinomas, often present with multiple, bulky lymph nodes usually extending below the renal hilum. Another major key point in the differential diagnosis is the degree of the wall thickening, which is more prominent in lymphomas (average value 5 cm). The enhancement pattern of lymphomas is usually variable and therefore nonspecific for the diagnosis of these tumors.

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Treatment •



Eradication of H. pylori represents the first line of therapy according to the central role played by this bacterium in the pathogenesis of lymphomas. Either chemotherapy or monoclonal antibody therapy (rituximab: anti-CD20 monoclonal antibody) is used in case of failure of antibiotic treatment or in those neoplasms not associated with H. pylori infection. Surgery has a limited role due to the efficacy of medical treatment.

Prognosis •

The prognosis depends on the histologic grade; low-grade lymphomas have a favorable prognosis, as they may even regress after antibiotic therapy.

PE ARL



Marked gastric wall thickening, especially when associated with bulky lymphadenopathy, should place lymphoma high in the differential diagnosis.

PITFALL



Gastric lymphomas may present overlapping radiologic findings with chronic gastritis (ulcers, erosions, and fold thickening) and gastric adenocarcinoma (bulky intraluminal masses). Underdistention of the stomach at CT may simulate wall thickening.

Suggested Readings Al-Akwaa AM, Siddiqui N, Al-Mofleh IA . Primary gastric lymphoma. World J Gastroenterol 2004;10(1):5–11 An SK, Han JK, Kim YH, et al. Gastric mucosa-associated lymphoid tissue lymphoma: spectrum of findings at double-contrast gastrointestinal examination with pathologic correlation. Radiographics 2001;21:1491–1504 Ba-Ssalamah A, Prokop M, Uffmann M, Pokieser P, Teleky B, Lechner G. Dedicated multidetector CT of the stomach: spectrum of diseases. Radiographics 2003;23:625–644 Buy JN, Moss AA. Computed tomography of gastric lymphoma. AJR Am J Roentgenol 1982;138: 859–865 Cho KC, Baker SR, Alterman DD, Fusco JM, Cho S. Transpyloric spread of gastric tumors: comparison of adenocarcinoma and lymphoma. AJR Am J Roentgenol 1996;167:467–469 Cohen SM, Petryk M, Varma M, Kozuch PS, Ames ED, Grossbard ML. Non-Hodgkin’s lymphoma of mucosa-associated lymphoid tissue. Oncologist 2006;11(10):1100–1117 Fishman EK, Kuhlman JE, Jones RJ. CT of lymphoma: spectrum of disease. Radiographics 1991;11: 647–669 Fishman EK, Urban BA , Hruban RH. CT of the stomach: spectrum of disease. Radiographics 1996;16:1035–1054 Kim JH, Eun HW, Goo DE, Shim CS, Auh YH. Imaging of various gastric lesions with 2D MPR and CT gastrography performed with multidetector CT. Radiographics 2006;26:1101–1116

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Kim YH, Lim HK, Han JK, et al. Low-grade gastric mucosa-associated lymphoid tissue lymphoma: correlation of radiographic and pathologic findings. Radiology 1999;212:241–248 Levine MS, Pantongrag-Brown L, Aguilera NS, Buck JL, Buetow PC. Non-Hodgkin lymphoma of the stomach: a cause of linitis plastica. Radiology 1996;201:375–378 Park SH, Han JK, Kim TK, et al. Unusual gastric tumors: radiologic-pathologic correlation. Radiographics 1999;19:1435–1446 Smith C, Kubicka RA, Thomas CR Jr. Non-Hodgkin lymphoma of the gastrointestinal tract. Radiographics 1992;12:887–899 Yoo CC, Levine MS, Furth EE, et al. Gastric mucosa-associated lymphoid tissue lymphoma: radiographic findings in six patients. Radiology 1998;208:239–243

CASE 79 Clinical Presentation A 28-year-old man complains of epigastric pain, anorexia, and weight loss.

A

B

Fig. 79.1 (A,B) Axial contrast-enhanced CT images of the abdomen show mild enhancement and diffuse increased thickness of the gastric walls; these findings are suspicious for gastric neoplasm, although an inflammatory process cannot be excluded. Multiple hypodense cystic lesions are seen in the liver and both kidneys.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images of the abdomen (Fig. 79.1) demonstrate mild and diffuse thickening of the gastric walls. The images from the upper gastrointestinal (GI) series (Fig. 79.2) demonstrate abnormal and persistent narrowing of the distal stomach.

Diagnosis Gastric adenocarcinoma

Differential Diagnosis • • • • • •

Gastric metastases Gastritis Gastric mucosa-associated lymphoid tissue lymphoma Gastric Crohn disease Caustic ingestion Gastric tuberculosis

Discussion Background Gastric carcinoma is a deadly disease, with decreasing incidence in the past 50 years in North America and Western Europe owing to the earlier identification at imaging and endoscopy. Currently, the incidence of gastric carcinoma is extremely variable worldwide, with the highest number of cases

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B

A

Fig. 79.2 (A,B) Upper gastrointestinal series images (double-contrast barium examination) demonstrate an abnormally narrowed and nondistensible gastric outlet suspicious for gastric malignancy. No discrete ulceration is identified.

in Japan, China, Russia, and Eastern Europe (> 30 cases per 100,000); men are usually 2 times more commonly affected than women, with a peak incidence in those ages of 50 to 70 years. Different histologic types have been described: adenocarcinomas (intestinal and diffuse types) account for almost 95% of cases, and lymphomas, leiomyosarcomas, carcinoids, and sarcomas for the remaining 5%. Adenocarcinomas have been classified into four different subtypes: papillary, tubular, mucinous, and signet ring. Almost 30% of gastric malignancies arise from the antrum, 30% from the body, and 40% from the fundus and cardia region.

Clinical Findings Clinical presentation mostly depends on the disease stage; patients may be asymptomatic (early stage) or may present with epigastric pain, anorexia, weight loss, nausea, vomiting, and upper GI bleeding (hematemesis, melena, occult blood in stools).

Complications In advanced stages, liver metastases may cause hepatomegaly and jaundice; less common sites for metastases include the lung, adrenal glands, and kidneys. Pelvic masses can result from ovarian metastases (Krukenberg tumors).

Etiology Several dietary and environmental factors have been identified: dietary nitrates, certain foods (salted fish and meat, smoked foods), hypochlorhydria resulting from drugs or previous surgery, cigarette smoking, and Helicobacter pylori infection. In particular, patients with H. pylori gastritis are 3 to 6 times more likely to develop gastric cancer. Other precancerous conditions include Ménétrier disease, adenomatous gastric polyps, partial gastrectomy, and pernicious anemia.

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Imaging Findings • • •



Endoscopy is currently considered the diagnostic procedure of first choice in patients with suspected gastric malignancies. Barium studies, either with single or double contrast, have been performed extensively for the detection of gastric tumors, although their overall sensitivity is somewhat lower than endoscopy. Conventional CT has been limited generally to the identification of lymph nodes (N) and distant metastases (M). The recent introduction of multidetector CT, with its thin-slice collimation and its multiplanar capabilities, has dramatically improved the detection of primary gastric malignancies (T); moreover, the water-filling method allows a detailed visualization of the gastric wall and therefore of intramural invasion. Early gastric neoplasms may present as polypoid (protruding in the lumen), superficial (associated only with irregularity of gastric folds), and excavated (malignant ulcer) features. Advanced tumors cause thickening of the walls (> 1 cm at CT), diffuse rigidity, and narrowing of the stomach (linitis plastica) and may be associated with perigastric fat stranding. Mucin-producing gastric tumors show features including multiple calcifications and a predominantly low-attenuation value corresponding to the mucin pool located within the thickened middle and outer layer. CT is also useful in defining the N stage: the TNM classification system is based on the number of regional nodes involved in the perigastric group and around the celiac axis. Gastric cancer initially tends to spread to local lymph nodes (gastrohepatic and gastrocolic lymph nodes) and then to regional lymph nodes located in the porta hepatis, hepatoduodenal ligament, and peripancreatic region. Distant lymph nodes (found in the mesentery or retroperitoneum) are usually considered as distant metastases. Ascites represent a common finding in patients with diffuse peritoneal carcinomatosis. High spatial resolution magnetic resonance imaging, used in in vitro experimental studies, is a promising imaging modality for the assessment of the depth of gastric tumor invasion because of its accuracy in depicting the layers of the gastric wall.

Treatment •



Complete resection of the tumor and adjacent lymph nodes is considered the only curative treatment, although a surgical procedure may be associated with several late complications, including dumping syndrome, vitamin B12 deficiency, and reflux esophagitis; some selected neoplasms may benefit from endoscopic mucosal resection. Chemotherapy is administered in patients with systemic metastatic disease.

Prognosis •

Gastric cancer presents a dismal prognosis, with overall 5-year survival rates < 20%; however, early gastric cancers are potentially curable, with a mean 5-year survival rate of almost 90%. Hence prompt diagnosis of these tumors is mandatory.

PE ARL



Distention of the gastric lumen with a negative contrast medium (water, air) may improve the detection of small superficial gastric lesions.

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PITFALL S

Different pitfalls may be identified at CT, including • • • •

Depth of tumor invasion may not be accurately assessed with CT. Underdistention of the stomach may simulate wall thickening. A normal gastroesophageal junction may be misinterpreted as a tumor. Enlargement of lymph nodes may be related to inflammatory causes.

Suggested Readings Ba-Ssalamah A, Prokop M, Uffmann M, Pokieser P, Teleky B, Lechner G. Dedicated multidetector CT of the stomach: spectrum of diseases. Radiographics 2003;23:625–644 Chen CY, Hsu JS, Wu DC, et al. Gastric cancer: preoperative local staging with 3D multi-detector row CT—correlation with surgical and histopathologic results. Radiology 2007;242:472–482 Hori S, Tsuda K, Murayama S, Matsushita M, Yukawa K, Kozuka T. CT of gastric carcinoma: preliminary results with a new scanning technique. Radiographics 1992;12:257–268 Kim JH, Eun HW, Goo DE, Shim CS, Auh YH. Imaging of various gastric lesions with 2D MPR and CT gastrography performed with multidetector CT. Radiographics 2006;26:1101–1116 Lim JS, Yun MJ, Kim MJ, et al. CT and PET in stomach cancer: preoperative staging and monitoring of response to therapy. Radiographics 2006;26:143–156 Park MS, Yu JS, Kim MJ, et al. Mucinous versus nonmucinous gastric carcinoma: differentiation with helical CT. Radiology 2002;223:540–546 Shaw PC, van Romunde LK, Griffioen G, Janssens AR, Kreuning J, Eilers GA. Peptic ulcer and gastric carcinoma: diagnosis with biphasic radiography compared with fiberoptic endoscopy. Radiology 1987;163:39–42 Shimizu K, Ito K, Matsunaga N, Shimizu A, Kawakami Y. Diagnosis of gastric cancer with MDCT using the water-filling method and multiplanar reconstruction: CT–histologic correlation. AJR Am J Roentgenol 2005;185:1152–1158 Shindoh N, Nakagawa T, Ozaki Y, Kyogoku S, Sumi Y, Katayama H. Overlooked gastric carcinoma: pitfalls in upper gastrointestinal radiology. Radiology 2000;217:409–414 Sohn KM, Lee JM, Lee SY, Ahn BY, Park SM, Kim KM. Comparing MR imaging and CT in the staging of gastric carcinoma. AJR Am J Roentgenol 2000;174:1551–1557 Urban BA, Fishman EK, Hruban RH. Helicobacter pylori gastritis mimicking gastric carcinoma at CT evaluation. Radiology 1991;179:689–691 Yamada I, Saito N, Takeshita K, et al. Early gastric carcinoma: evaluation with high-spatial-resolution MR imaging in vitro. Radiology 2001;220:115–121

CASE 80 Clinical Presentation A 77-year-old man presents with abdominal pain.

Fig. 80.1 Contrast-enhanced CT scan shows a lobulated, heterogeneously enhancing mass arising from the proximal stomach (arrow).

Radiologic Findings An abdominal computed tomography (CT) scan (Fig. 80.1) shows a large, lobulated, heterogeneously enhancing mass arising from the proximal stomach.

Diagnosis Gastrointestinal stromal tumor (GIST)

Differential Diagnosis • • • •

Gastric adenocarcinoma Leiomyoma/leiomyosarcoma Schwannoma/neurofibroma Metastasis

Discussion Background GISTs are the most common mesenchymal tumors arising from the gastrointestinal (GI) tract wall. Nevertheless, they are uncommon, accounting for only 1 to 3% of all GI neoplasms, and usually affect patients > 50 years of age without any gender predilection. These tumors are also reported to occur in 10 to 25% of patients affected by neurofibromatosis 1. Previously mistaken for smooth muscle and neural tumors, GISTs show distinctive genetic and histologic features. They can occur anywhere from the rectum to the esophagus, the stomach being the most common site of origin; they can also be located in the mesentery, omentum, and retroperitoneum.

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Clinical Findings The clinical presentation relies on the location, size, and pattern of growth of the tumor and is mainly characterized by abdominal pain or distention, anemia or melena, or bowel obstruction.

Complications Malignant GIST can be aggressive and spread to the liver, retroperitoneum, and mesentery, and less frequently to the bones, lungs, and lymph nodes. Intraluminal GISTs can cause bowel obstruction.

Etiology GISTs have distinctive immunohistochemical properties, the most important being the expression of KIT (CD117), a tyrosine kinase growth factor receptor, which promotes the growth of mesenchymal neoplastic cells.

Imaging Findings Although tumor expression of the KIT receptor is needed for a definitive diagnosis of GIST, imaging, especially CT, has proved to be instrumental. GISTs are usually seen as exophytic, heterogeneously enhancing, rarely calcified masses arising from the GI tract wall. Most of them, especially larger ones, show heterogeneous density due to the presence of intratumoral necrosis (Fig. 80.2), hemorrhagic foci, and cystic degeneration.

Treatment • •

Surgical removal is recommended, but despite complete resection, the recurrence rate is high, especially in the setting of less well differentiated lesions. New drugs targeting the growth factor receptor KIT appear promising, but so far they have been used only for unresectable tumors.

Prognosis •

Recent advancements in therapy have increased the average survival rate, especially in malignant nonmetastatic GISTs.

Fig. 80.2 Contrast-enhanced CT in a different patient shows a large heterogeneous mass arising from the stomach. Multiple hepatic cysts are present.

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PE ARL



Differential diagnosis of gastrointestinal lesions should always include GISTs, especially in the setting of an exophytic, necrotic-appearing mass associated with the hollow viscera.

PITFALL



GIST can be difficult to distinguish from other mesenchymal malignancies, such as soft tissue tumors (e.g., leiomyosarcoma) and neural cell tumors.

Suggested Readings Burkill GJ, Badran M, Al-Muderis O, et al. Malignant gastrointestinal stromal tumor: distribution, imaging features, and pattern of metastatic spread. Radiology 2003;226:527–532 Da Ronch T, Modesto A, Bazocchi M. Gastrointestinal stromal tumour: spiral computed tomography features and pathologic correlation. Radiol Med (Torino) 2006;111(5):661–673 Lee CM, Chen HC, Leung TK, Chen YY. Gastrointestinal stromal tumor: computed tomographic features. World J Gastroenterol 2004;10(16):2417–2418 Levy AD, Patel N, Abbott RM, Dow N, Miettinen M, Sobin LH. Gastrointestinal stromal tumors in patients with neurofibromatosis: imaging features with clinicopathologic correlation. Am J Roentgenol 2004;183(6):1629–1636 Levy AD, Remotti HE, Thompson WM, Sobin LH, Miettinen M. Gastrointestinal stromal tumors: radiologic features with pathologic correlation. Radiographics 2003;23:283–304 Logrono R, Bhanot P, Chava C, Cao L, Waxman I, Bhutani MS. Imaging, morphologic, and immunohistochemical correlation in gastrointestinal stromal tumors. Cancer 2006;108(4):257–266 Sandrasegaran K, Rajesh A, Rydberg J, Rushing DA, Akisik FM, Henley JD. Gastrointestinal stromal tumors: clinical, radiologic, and pathologic features. AJR Am J Roentgenol 2005;184(3):803–811

CASE 81 Clinical Presentation A middle-aged man presents for evaluation of long-standing dysphagia with episodic periods of more intense discomfort.

A

B

Fig. 81.1 (A) Contrast-enhanced axial CT image demonstrates a large hiatal hernia. The distal esophagus is midline, and the gastroesophageal (GE) junction as well as a portion of the stomach is located within the intrathoracic hernia. (B) Overhead radiograph and (C) spot fluoroscopic image from an upper gastrointestinal series show a large hiatal hernia. The radiograph illustrates that the “concave” greater curvature of the gastric body is located cephalad to the “convex” lesser curvature, the GE junction and pylorus. The GE junction and pylorus maintain their normal relationship.

C

Radiologic Findings Contrast-enhanced axial computed tomography (CT) image demonstrates a large hiatal hernia (Fig. 81.1A). The distal esophagus is midline, and the gastroesophageal (GE) junction as well as a portion of the stomach is located within the intrathoracic hernia. An overhead radiograph and spot fluoroscopic image (Fig. 81.1B,C) from an upper gastrointestinal (GI) series show a large hiatal hernia. The radiograph

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illustrates that the “concave” greater curvature of the gastric body is located cephalad to the “convex” lesser curvature, the GE junction and pylorus. The GE junction and pylorus maintain their normal relationship, which excludes a mesenteroaxial gastric volvulus. There is no gastric outlet obstruction.

Diagnosis Organoaxial gastric volvulus in a large hiatal hernia

Differential Diagnosis • • •

Sliding hiatal hernia Paraesophageal hernia Large intra-abdominal mass with superior displacement of the stomach

Discussion Background Gastric volvulus represents abnormal torsion of the stomach, usually > 180 degrees. If the greater curvature rotates superior to the lesser curvature along the long axis of the stomach, this is termed an organoaxial volvulus and accounts for ~60% of gastric volvulus cases. If the antrum and pylorus rotate anterosuperior to the fundus and GE junction, this is termed a mesenteroaxial volvulus, representing ~30% of volvulus cases. The volvulus is also classified with respect to the diaphragm: supradiaphragmatic (two thirds) or subdiaphragmatic/intraperitoneal (one third).

Clinical Findings In cases of chronic volvulus, patients typically present with nonspecific abdominal complaints, including vague abdominal or chest pain, early satiety or fullness, dysphagia, or dyspnea. Chronic volvulus may be noted incidentally on chest radiographs or an upper GI series or esophagram. Acute volvulus demonstrates more dramatic presentations, including severe pain, an inability to ingest liquids or solids or pass an enteric tube, gastric outlet obstruction, and peritonitis when there is gastric ischemia or perforation. Purportedly diagnostic of acute obstructing volvulus, the classic Borchardt triad describes severe constant chest or epigastric pain, nausea with inability to vomit, and difficulty passing a nasogastric tube.

Complications Organoaxial volvulus can be complicated by strangulation in ~5 to 20% of cases secondary to twisting of the left gastric artery and occlusion of venous drainage. Ischemia in mesenteroaxial volvulus is rare. Any type of gastric volvulus can be associated with gastric outlet obstruction. Obstruction with strangulation is usually seen only in cases of acute volvulus. Mortality ranges from < 10% for chronic cases to > 40% for acute volvulus.

Etiology Organoaxial volvulus is usually seen in adults and is associated with a diaphragmatic defect in > 50% of cases, including hiatal hernia, paraesophageal hernia, eventration, and diaphragmatic rupture. This defect allows for abnormal movement of the gastric body into the thorax with resultant organoaxial volvulus. In this way, the majority of organoaxial volvulus cases also represent the supradiaphragmatic variety.

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In comparison, mesenteroaxial volvuli are overwhelmingly subdiaphragmatic and most often seen in children. Thought to be due to abnormal laxity of the suspensory ligaments of the stomach, mesenteroaxial volvulus can also be associated with a “wandering” ectopic spleen.

Imaging Findings •





Plain radiographic findings of organoaxial volvulus are usually nonspecific with respect to the stomach itself. Radiography alone may reveal a mediastinal density or air–fluid level consistent with the frequently associated hiatal or paraesophageal hernia. The upper GI series is the gold standard for volvulus diagnosis. In the setting of organoaxial volvulus, the greater curvature rotates superior to the lesser curvature along the long axis of the stomach. The GE junction may be intrathoracic or below the diaphragm depending on the type of herniation. In mesenteroaxial volvulus, the antrum and pylorus rotate anterosuperior to the fundus with a twisting around the short axis of the stomach. Cross-sectional imaging with CT and magnetic resonance (MR) clearly demonstrates the hiatal or paraesophageal hernia with the intrathoracic stomach. Often, the “twisting” component of the volvulus will be overlooked on axial images only; a swirling of mesenteric vessels may be noted. Multiplanar MR and three-dimensional reformations for CT have improved the characterization of volvulus type with these modalities.

Treatment • •

Acute gastric volvulus is initially treated with attempted nasogastric tube decompression. Surgical repair is indicated for all cases of volvulus and involves untwisting of the volvulus, return of the stomach to a subdiaphragmatic position, gastropexy in an anatomical position, and repair of any predisposing diaphragmatic defect. Surgical access may be via thoracotomy, laparotomy, or peritoneal laparoscopy. Chronic volvulus can be treated electively, whereas acute cases with obstruction, incarceration, or strangulation require immediate repair. Uncomplicated subdiaphragmatic chronic gastric volvulus cases without diaphragmatic defect can be treated with endoscopic decompression and gastropexy, reserving surgery for endoscopic failure.

Prognosis •

Following successful repair with gastropexy, the risk of recurrent gastric volvulus is low and is related to failure of gastropexy and adequacy of repair of any known diaphragmatic defect.

PE ARL



Acute gastric volvulus is a surgical emergency because of the moderate risk of ischemic strangulation and gastric outlet obstruction and requires repair of both the gastric torsion and any diaphragmatic defect.

PITFALL S



Chronic volvulus can be intermittent, and the upper GI series may only demonstrate hiatal or paraesophageal hernia during an asymptomatic period.

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The volvulus component of an intrathoracic stomach can be overlooked with axial MR or CT imaging alone. Consider multiplanar imaging or reformations.

Suggested Readings Abbara S, Kalan MM, Lewicki AM. Intrathoracic stomach revisited. AJR Am J Roentgenol 2003;181:403– 414 Godshall D, Mossallam U, Rosenbaum R. Gastric volvulus: case report and review of the literature. J Emerg Med 1999;17:837–840 Green J. Gastric volvulus. Available at: http://www.emedicine.com/radio/topic296.htm. Accessed August 22, 2007 Levine MS, Rubesin SE, Laufer I. Double Contrast Gastrointestinal Radiology. 3rd ed. Philadelphia: WB Saunders; 2000:248–258

CASE 82 Clinical Presentation A 42-year-old man presents with postprandial epigastric discomfort.

Fig. 82.1 Ultrasound image shows a well-defined cystic structure with a gut signature in continuity with the lateral duodenal wall and the lumen of the vertical part of the duodenum. The lumen and the wall of the lesion are contiguous with the lateral wall of the second part of the duodenum.

Radiologic Findings Upper abdominal ultrasound shows a well-demarcated hypoechoic structure (Fig. 82.1) in close proximity to the second portion of the duodenum. The structure has a gut signature on ultrasound with alternating hyper- and hypoechoic layers in the wall.

Diagnosis Duodenal diverticulum arising from the lateral wall of the duodenum

Differential Diagnosis • • • •

Postbulbar duodenal ulcer Pancreatic pseudocyst Cystic pancreatic tumor Duodenal duplication

Discussion Background The duodenum is the second most common site for diverticula formation after the large bowel. The incidence of duodenal diverticula is 5 to 15% on barium examinations, 20 to 25% at autopsy. The peak incidence of duodenal diverticula is found in the 5th to 6th decades of life. They typically arise

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from the medial wall of the second and third parts of the duodenum within 2 cm of the ampulla of Vater. Intraluminal duodenal diverticula are rare. Diverticula arising from the lateral wall tend to be larger in size and are less common. Diverticula can also be classified as primary or secondary (due to postbulbar ulcer).

Clinical Findings • • • • • •

Asymptomatic Abdominal discomfort Pain in the epigastric or umbilical region Central abdominal pain radiating to the back Jaundice in the case of compression of the biliary tree Pain and fever in cases of diverticulitis

Complications • • • • • • • • • •

Diverticulitis Perforation Pancreatitis secondary to perforation Bleeding Obstructive jaundice due to compression of the biliary channels Cholangitis Failure of endoscopic retrograde cholangiopancreatography if the common bile duct drains into the diverticula Increased incidence of cholelithiasis Neoplastic change Bezoar formation

Etiology Primary diverticula are thought to arise because of the presence of a weakened wall in the duodenum at the vessel’s entry site, biliary ductal entry sites, muscular weakness in the wall, or heterotopic pancreatic tissue.

Imaging Findings •





On an upper gastrointestinal series with barium, the diverticula are seen as typical outpouchings arising from the duodenum without any distortion of mucosal folds, which changes their configuration with time (Fig. 82.2). Delayed retention of barium in the diverticula is a diagnostic finding. Intraluminal diverticula appear as intraluminal projections of barium-filled linear structures with surrounding lucency, giving a typical “wind sock” appearance. Ultrasound demonstrates a clear fluid- or food-containing structure with the presence of gas in the nondependent portion of the lesion. The wall of the duodenal diverticula typically shows the multilayered gut signature on ultrasound. Use of real-time ultrasound imaging helps, and diverticula can be better demonstrated after the ingestion of large quantities of fluids. CT shows gas-containing diverticula (Fig. 82.3). In cases where gas is absent, diverticula can be confused with cystic neoplasms, pseudocysts, or abscess. In such cases, repeat scans may demonstrate the presence of gas within the structure.

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Fig. 82.2 Upper gastrointestinal series image in a different patient shows the presence of diverticula arising from the medial wall of the second and third parts of the duodenum (arrows).



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Fig. 82.3 Axial contrast-enhanced CT image in a 63-yearold man shows the presence of a gas-filled diverticulum arising from the lateral wall of the third part of the duodenum (arrow).

T2-weighted magnetic resonance images show a hyperintense fluid-containing structure and hypointense gas within the nondependent portion of the lesion.

Treatment •

Conservative treatment is preferred in asymptomatic primary duodenal diverticular disease without any complications. The patient can be advised to adopt a position that favors diverticular emptying. Surgical treatment in symptomatic primary diverticular disease is undertaken only in patients with complications and persistent symptoms despite conservative management. In patients with secondary disease because of an ulcer, the treatment of the ulcer by medications and surgery is recommended.

Prognosis •

The prognosis for primary duodenal diverticular disease is excellent with lesser incidence of complications. In patients with secondary diverticula due to a postbulbar ulcer who are treated, the prognosis is good; however, the rates of complications are higher.

PE ARL



The presence of gas and continuity with the duodenum help to differentiate duodenal diverticula from other pathologies.

PITFALL



Duodenal diverticula filled with fluid can be mistaken for cystic neoplasms from the head of the pancreas, in which case barium examination should be considered.

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Suggested Readings Jayaraman MV, Mayo-Smith WW, Movson JS, Dupuy DE, Wallach MT. CT of the duodenum: an overlooked segment gets its due. Radiographics 2001;21:S147–S160 Macari M, Lazarus D, Israel G, Megibow A. Duodenal diverticula mimicking cystic neoplasms of the pancreas: CT and MR imaging findings in seven patients. AJR Am J Roentgenol 2003;180:195–199

CASE 83 Clinical Presentation A 57-year-old man presents with abdominal pain and discomfort. Physical examination reveals a palpable mass in the anterior abdominal wall, in the midabdomen.

A

B

Fig. 83.1 (A,B) Axial CT image show small bowel loops herniating through the abdominal wall and surrounded by a rim of soft tissue density with stranding, consistent with mild inflammation. There is mild distention of the small bowel proximally to the herniated loops.

Radiologic Findings Axial computed tomography (CT) images (Figs. 83.1) show small bowel loops herniating through the abdominal wall and surrounded by a rim of soft tissue density with stranding, consistent with mild inflammation. There is mild distention of the small bowel proximally to the herniated loops.

Diagnosis Abdominal wall hernia

Differential Diagnosis • • • • • •

Abdominal wall tumors (desmoid, lymphoma, hemangiomas, lipoma, metastases, etc.) Rectus sheath hematomas (posttraumatic, associated with coagulopathy) Enlarged lymph nodes (infections, lymphomas, etc.) Enlarged, prominent vessels (as seen in cirrhotic patients with portal venous shunts) Undescended testis Abdominal wall endometriosis

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Fig. 83.2 An axial contrast-enhanced CT image through the pelvis demonstrates a direct left inguinal hernia. Small bowel loops are present along the left spermatic cord. Neither inflammatory changes nor signs of strangulation are present.

Fig. 83.3 Axial contrast-enhanced CT image shows a left ventral hernia containing small bowel loops and mesentery.

Discussion Background A hernia is commonly defined as the protrusion of any viscus from its proper cavity into a saclike structure formed by the same membrane with which the cavity is usually lined. Different types of hernias have been described according to their anatomical distribution, the most frequent in both men and women being inguinal hernias (direct Fig. 83.2 and indirect). Others include • •



Femoral hernia: occurs medial to the femoral vein and posterior to the inguinal ligament; commonly right-sided Ventral hernia: ⴰ Midline defects: umbilical, paraumbilical, epigastric, and hypogastric hernias. Umbilical is the most common type, usually occurring in women (risk factors: obesity, multiple pregnancies, ascites, intra-abdominal masses) ⴰ Lateral defects—spigelian hernia (Fig. 83.3): occurs along the lateral aspect of the rectus muscle through the hiatus semilunaris Posterior defects—lumbar hernia: occurs either through defects in the superior (Grynfeltt) (Fig. 83.4) or inferior (Petit) lumbar triangle

B

A

Fig. 83.4 (A,B) Lumbar hernia of Grynfellt seen on CT (arrow). Note that this hernia contains a portion of Gerota fascia. The contents of these hernias can be confused with a lipomatous tumor.

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Fig. 83.5 Axial CT image of the pelvis shows a herniated bowel loop in the left obturator fossa (arrow).

• •

Obturator hernia: occurs through the obturator foramen, usually in elderly multiparous women (Fig. 83.5) Incisional hernia: represents a delayed complication of abdominal surgery

Abdominal wall hernias are very common, with more than 500,000 operations performed in the United States every year. Unfortunately, surgical repair is associated with a high rate of complications (up to 20%), such as recurrence, fluid collections, and infection of prosthetic materials. The clinical diagnosis may be difficult in cases of obesity or abdominal scarring from a previous surgery; hence imaging plays a central role in recognizing this pathologic entity and decreasing the morbidity associated with complications.

Clinical Findings Clinical presentation depends on the anatomical location and severity of abdominal hernias. Patient presentation can range from vague abdominal tenderness and discomfort with a palpable abnormality to a bowel obstruction.

Complications Major complications include strangulation (Fig. 83.6) and incarceration (Figs. 83.1), both leading to bowel obstruction or perforation in case of missed or delayed diagnosis. Incarceration refers to those hernias that cannot be manually reduced because of progressive narrowing of the neck of the hernia sac. Strangulation refers to ischemia of the protruded organ due to impaired blood supply. Other, less frequent complications include herniation of other organs, either solid (liver, kidneys) or nonsolid (stomach, bladder).

Fig. 83.6 Axial contrast-enhanced CT image shows a ventral hernia in the left lower quadrant, which contains a loop of descending colon. There is a small amount of fluid in the hernia sac. The bowel within the colon demonstrates mild wall thickening. The colon distal to the hernia is underdistended. These findings are consistent with strangulation.

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Etiology Most abdominal hernias are seen in adults and are related to an acquired weakness of the muscular abdominal wall. Abdominal trauma (iatrogenic or high-impact blunt trauma) may cause different types of hernias by disrupting the abdominal wall musculature. Pediatric hernias are less frequent and commonly described in the groin as a consequence of a patent processus vaginalis. The formation of hernias in the abdominal wall is promoted by any condition that increases intra-abdominal pressure: obesity, coughing, chronic lung disease, straining during defecation or voiding, heavy lifting, and ascites.

Imaging Findings •



Currently, multidetector CT has become a major diagnostic tool for the evaluation and characterization of abdominal wall hernias, as it provides very accurate anatomical details for surgical planning by means of its multiplanar reconstruction capabilities. Supine acquisition is usually performed after intravenous administration of contrast material (to evaluate vascular supply). Either positive or negative oral contrast material may be used to improve bowel loop visualization. Postural maneuvers (prone or lateral decubitus) or maneuvers aimed to increase abdominal pressure (Valsalva) may be useful in case of subtle hernias. CT is also very helpful in detecting early signs of complications, such as incarceration, strangulation, and bowel obstruction.

Treatment •

Surgical treatment is usually advised even in asymptomatic patients to avoid complications. Different procedures may be performed, such as laparoscopic suture and mesh repair, which currently is the standard surgical technique for abdominal wall hernias. Recurrence represents the most common complication after hernia repair, usually occurring 2 to 3 years after the surgical procedure. Other complications may be the result of mesh infection or mesh shrinkage.

Prognosis •

The prognosis is favorable in cases of prompt diagnosis and surgical repair, although the recurrence rate is very high (~50% of patients may require a second operation).

PE ARL



Valsalva maneuver, increasing abdominal pressure, may be useful to detect subtle or unknown hernias at imaging.

PITFALL



Imaging is unable to always distinguish between an uncomplicated reducible hernia and an incarcerated hernia, which may lead to different management.

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Suggested Readings Aguirre DA, Casola G, Sirlin C. MDCT Findings. AJR Am J Roentgenol 2004;183:681–690 Aguirre DA, Santosa AC, Casola G, Sirlin CB. Abdominal wall hernias: imaging features, complications, and diagnostic pitfalls at multi-detector row CT. Radiographics 2005;25:1501–1520 Crespi G, Giannetta E, Mariani F, Floris F, Pretolesi F, Marino P. Imaging of early postoperative complications after polypropylene mesh repair of inguinal hernia. Radiol Med (Torino) 2004;108(1–2): 107–115 Di Mugno M, Runfola M, Magalini S, Sermoneta D, Gui D. Rippled mesh: a CT sign of abdominal wall ePTFE prosthesis infection. G Chir 2006;27(10):384–387 Emby DJ, Aoun G. CT technique for suspected anterior abdominal wall hernia. AJR Am J Roentgenol 2003;181:431–433 Emby DJ, Aoun G. Valsalva’s maneuver in abdominal wall hernia imaging. AJR Am J Roentgenol 2005;185:1081–1082 Gossios K, Zikou A, Vazakas P, et al. Value of CT after laparoscopic repair of postsurgical ventral hernia. Abdom Imaging 2003;28(1):99–102 Harrison LA, Keesling CA, Martin NL, Lee KR, Wetzel LH. Abdominal wall hernias: review of herniography and correlation with cross-sectional imaging. Radiographics 1995;15:315–332 Lee GH, Cohen AJ. CT imaging of abdominal hernias. AJR Am J Roentgenol 1993;161:1209–1213 Miller PA, Mezwa DG, Feczko PJ, Jafri ZH, Madrazo BL. Imaging of abdominal hernias. Radiographics 1995;15:333–347 Zafar HM, Levine MS, Rubesin SE, Laufer I. Anterior abdominal wall hernias: findings in barium studies. Radiographics 2006;26:691–699 Zarvan NP, Lee FT Jr, Yandow DR, Unger JS. Abdominal hernias: CT findings. AJR Am J Roentgenol 1995;164:1391–1395

CASE 84 Clinical Presentation A 75-year-old man presents with severe, poorly localized abdominal pain and diarrhea.

B

A

Fig. 84.1 (A,B) Axial and (C) coronal CT images show diffuse bowel wall thickening of the descending colon extending from the splenic flexure with pericolonic fat stranding and loss of the normal haustral pattern. The affected segment of colon has a typical targeted appearance with mild enhancement of the mucosal layer.

C

Radiologic Findings Axial and coronal computed tomography (CT) images (Fig. 84.1) show diffuse bowel wall thickening of the descending colon extending from the splenic flexure with pericolonic fat stranding and loss of the normal haustral pattern. The affected segment of colon has a typical targeted appearance with mild enhancement of the mucosal layer.

Diagnosis Acute mesenteric ischemia

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Differential Diagnosis • • • •

Inflammatory bowel disease (Crohn disease, ulcerative colitis) Infectious colitis Pseudomembranous colitis Neutropenic colitis (typhlitis)

Discussion Background Mesenteric ischemia is a rare pathologic disorder (0.1% of emergency room admissions) predominantly affecting the older population of both genders (> 60 years), although it may occur in younger patients with predisposing risk factors. The prevalence of this condition is growing with the increase in average life expectancy. Three arteries provide the blood supply to the bowel: the celiac trunk, the superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA). A decrease in blood flow can cause ischemia and subsequent reperfusion cell damage, leading to intestinal necrosis. Mesenteric ischemia may be acute or chronic, arterial or venous, diffuse or focal (watershed areas in the transverse colon near the splenic flexure or in the sigmoid colon are extremely vulnerable in cases of hypovolemia). Different etiologies, clinical presentations, and imaging findings have been identified for each of these pathologic entities.

Clinical Findings Patients with acute mesenteric ischemia usually present severe abdominal pain, diarrhea, nausea, and vomiting. Patients affected by chronic ischemia commonly experience postprandial abdominal pain (intestinal angina), weight loss, and food avoidance. Laboratory tests may reveal leukocytosis and an elevated serum lactate level (usually a late finding).

Complications Ischemia causes tissue necrosis, which in turn may lead to bowel perforation and subsequent peritonitis.

Etiology Major causes of acute mesenteric ischemia include •

• • •

Arterial embolism (SMA most commonly affected), accounting for almost one third of the total cases (atrial fibrillation, valvular disease, and ventricular aneurysm are the most important predisposing factors) Arterial thrombosis: responsible for ~20 to 30% of cases, usually associated with preexisting atherosclerosis of at least two intestinal vessels Nonocclusive mesenteric vasoconstriction: prolonged hypoperfusion secondary to cardiogenic shock or heart failure, sepsis, cocaine abuse, digitalis, and so on Mesenteric and portal venous thrombosis: mostly described in patients with portal hypertension, hypercoagulable state (oral contraceptive use), intra-abdominal sepsis, pancreatitis, and recent abdominal surgery

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Aortic dissection Complicated bowel obstruction or overdistention

Chronic mesenteric ischemia mostly results from severe atherosclerotic disease of two or more intestinal vessels. Other causes are fibromuscular dysplasia, median arcuate ligament syndrome (i.e., extrinsic compression of the celiac trunk by the median arcuate ligament that connects the left and right crura of the diaphragm), granulomatous vasculitis (in particular, Takayasu arteritis) and connective tissue diseases such as Ehlers-Danlos syndrome.

Imaging Findings Currently, catheter-directed angiography remains the gold standard for the assessment of mesenteric ischemia, as it directly demonstrates the presence of thrombi or emboli (filling defects) within the vessels. However, CT angiography (CTA) has become a key imaging technique for the evaluation of mesenteric ischemia, as it provides high spatial resolution of the mesenteric vessels and additional information about the condition of the hollow viscera. Moreover, three-dimensional (3D) datasets ease surgical and interventional planning because they allow multiplanar reconstructions of the diseased vessels. Contrast-enhanced 3D magnetic resonance angiography (MRA) is also widely used, especially in children. The recent understanding of the relationship between renal insufficiency and nephrogenic systemic fibrosis has made MRA a less attractive modality in patients with impaired renal function. Accurate CT imaging requires biphasic acquisition during the arterial and portal phases after the intravenous administration of contrast material to demonstrate the patency of mesenteric arteries and veins. Unenhanced images may add valuable information, as they help to delineate vascular calcifications, intramural hemorrhage, or hyperattenuating intravascular clotting. Positive or negative oral contrast material can be administered to distend bowel loops. CT findings of mesenteric ischemia are varied. The most important include •

• • • •

Bowel thickening: the most common but least specific feature of bowel ischemia (it may be observed in inflammatory bowel disease, infectious colitis, etc.); mostly related to intramural edema, hemorrhage, or superinfection (This finding is not always predictive of poor outcome because transmural ischemia usually results in thinning of the bowel wall.) Dilatation: related to interruption of peristalsis in the injured bowel; common findings in case of transmural extent of infarction Abnormal wall enhancement Mesenteric fat stranding and fluid collections (the latter mostly seen in acute ischemia) Pneumatosis or portomesenteric gas

Treatment • • •

• •

Acute mesenteric ischemia requires immediate surgical treatment before irreversible damage occurs to the bowel. Embolectomy with resection of the nonviable intestine represents the standard surgical procedure for emboli. Bypass grafting or endoarterectomy is usually performed in case of in situ thrombosis. Intra-arterial infusion of papaverine (30–50 mg/h) is the mainstay of treatment for nonocclusive mesenteric ischemia. Chronic mesenteric ischemia may be treated with endovascular techniques (intra-arterial catheter-directed thrombolysis, angioplasty, stent placement). Mesenteric venous thrombosis is treated with anticoagulation. Patients with signs of peritonitis need prompt surgical intervention regardless of the etiology.

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Prognosis •

The prognosis is poor, with the mortality rate ranging from 60 to 100%. Patients with severe atherosclerosis of mesenteric vessels may benefit from endovascular stent placement or angioplasty to prevent acute ischemia.

PE ARL



It is imperative for the radiologist to include the mesenteric arteries and veins in their search pattern, especially in the presence of colitis.

PITFALL



CT findings in bowel ischemia may be extremely varied and nonspecific.

Suggested Readings Bradbury MS, Kavanagh PV, Bechtold RE, et al. Mesenteric venous thrombosis: diagnosis and noninvasive imaging. Radiographics 2002;22:527–541 Chang RW, Chang JB, Longo WE. Update in management of mesenteric ischemia. World J Gastroenterol 2006;12(20):3243–3247 Horton KM, Fishman EK. Multi-detector row CT of mesenteric ischemia: can it be done? Radiographics 2001;21:1463–1473 Horton KM, Fishman EK. Volume-rendered 3D CT of the mesenteric vasculature: normal anatomy, anatomic variants, and pathologic conditions. Radiographics 2002;22:161–172 Kirkpatrick ID, Kroeker MA, Greenberg HM. Biphasic CT with mesenteric CT angiography in the evaluation of acute mesenteric ischemia: initial experience. Radiology 2003;229:91–98 Klein HM, Lensing R, Klosterhalfen B, Tons C, Gunther RW. Diagnostic imaging of mesenteric infarction. Radiology 1995;197:79–82 Landis MS, Rajan DK, Simons ME, et al. Percutaneous management of chronic mesenteric ischemia: outcomes after intervention. J Vasc Interv Radiol 2005;16:1319–1325 Rha SE, Ha HK, Lee SH, et al. CT and MR imaging findings of bowel ischemia from various primary causes. Radiographics 2000;20:29–42 Shih MC, Angle JF, Leung DA, et al. CTA and MRA in mesenteric ischemia: 2. Normal findings and complications after surgical and endovascular treatment. AJR Am J Roentgenol 2007;188:462–471 Shih MC, Hagspiel KD. CTA and MRA in mesenteric ischemia: 1. Role in diagnosis and differential diagnosis. AJR Am J Roentgenol 2007;188:452–461 Sreenarasimhaiah J. Diagnosis and management of intestinal ischaemic disorders. BMJ 2003; 326(7403):1372–1376 Taourel PG, Deneuville M, Pradel JA, Regent D, Bruel JM. Acute mesenteric ischemia: diagnosis with contrast-enhanced CT. Radiology 1996;199:632–636 Wiesner W, Khurana B, Jib H, Ros PR. CT of acute bowel ischemia. Radiology 2003;226:635–650

CASE 85 Clinical Presentation A 42-year-old man presents with abdominal cramps, fever, and diarrhea.

A

B

Fig. 85.1 (A) An axial contrast-enhanced CT image shows severe bowel wall thickening and enhancement of the ascending colon. (B) Inferior axial scan shows prominent lymph nodes scattered in the mesenteric fat, likely reactive. This finding may favor the infectious etiology of colitis. (C) Axial image through the pelvis shows involvement of the distal large bowel with prominent mesocolic vasculature.

C

Radiologic Findings Axial computed tomography (CT) images (Fig. 85.1) of the abdomen obtained after the administration of intravenous contrast show severe bowel wall thickening and pericolonic fat stranding involving the majority of the ascending and the entire transverse colon. Scattered mesenteric lymph nodes are noted.

Diagnosis Infectious colitis

Differential Diagnosis • • • • • •

Pseudomembranous colitis Crohn disease Ulcerative colitis Ischemic colitis Radiation colitis Typhlitis

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Discussion Background Infectious colitis is caused by a variety of infectious agents and is described in both immunocompetent and immunocompromised or hospitalized patients. The lesions seen in these patients may be either superficial (similar to ulcerative colitis) or transmural (as in Crohn disease), diffuse (cytomegalovirus and Escherichia coli), predominantly right-sided (as seen in colitis caused by Yersinia, Salmonella, amebiasis, and tuberculosis), or mostly left-sided (schistosomiasis, shigellosis, herpes, gonorrhea, syphilis, and lymphogranuloma venereum). Stool analysis, blood culture, and endoscopic biopsy are required for the diagnosis, as there is a considerable overlap in the CT appearance of these colitides.

Clinical Findings Clinical presentation is extremely variable according to the different etiologies. Patients may be either asymptomatic or present with abdominal pain and cramping, nausea, fever, diarrhea, and even dysentery.

Complications Transmural involvement may cause perforation and subsequent peritonitis. Toxic megacolon represents an uncommon complication of infectious colitis and is more commonly described in pseudomembranous colitis, cytomegalovirus colitis, and amebiasis.

Etiology Different agents may cause infectious colitis, including •

• • •

Bacteria: Salmonella typhi, E. coli (enterohemorrhagic, enteroinvasive), Shigella, Campylobacter, Yersinia, gonococcus, and Chlamydia trachomatis (rectal lymphogranuloma venereum). Mycobacterium tuberculosis may be involved in patients with pulmonary tuberculosis or after ingestion of contaminated milk products. Virus: cytomegalovirus causing a rare form of colitis, typically seen in immunocompromised patients Parasites: Entamoeba histolytica is the most common cause of parasitic colitis. Other agents are Strongyloides stercoralis, Trichuris trichiura, and Schistosoma. Pseudomembranous colitis is a particular form of infection occurring 1 to 6 weeks after the administration of broad-spectrum antibiotic therapy (clindamycin, lincomycin, tetracycline, and ampicillin; chemotherapeutic agents may also be responsible). The resulting alteration of normal microflora favors the colonic overgrowth of toxin-producing Clostridium difficile.

Imaging Findings CT findings in infectious colitis are extremely nonspecific and mainly consist of the typical inflammatory changes also described in inflammatory bowel disease and ischemic colitis. Common features include •

Bowel wall thickening, a sensitive but nonspecific finding; in pseudomembranous colitis, the average thickness of the colonic wall is 15 mm with preserved haustra (accordion sign due to the presence of contrast between the thickened bowel folds)

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Pericolonic fat stranding Fluid collections (ascites is more commonly observed in acute colitides, particularly in pseudomembranous colitis and cytomegalovirus colitis)

Treatment •

Blood culture and stool analysis must be performed to identify the infectious etiology. Surgery is required only in case of complications (perforation, toxic megacolon).

Prognosis •

The prognosis is usually favorable if patients are given an appropriate antimicrobial therapy.

PE ARL



Careful history taking, including inquiry regarding recent travel or antibiotic therapy, can be important in the evaluation of patients with suspected infectious colitides.

PITFALL



Imaging features of different infectious colitides and other inflammatory processes in the hollow viscera demonstrate considerable overlap, which makes a precise etiology difficult to ascertain by imaging alone.

Suggested Readings Ahualli J. The target sign: bowel wall. Radiology 2005;234:549–550 Ash L, Baker ME, O’Malley CM Jr, Gordon SM, Delaney CP, Obuchowski NA. Colonic abnormalities on CT in adult hospitalized patients with Clostridium difficile colitis: prevalence and significance of findings. AJR Am J Roentgenol 2006;186:1393–1400 Desai RK, Tagliabue JR, Wegryn SA, Einstein DM. CT evaluation of wall thickening in the alimentary tract. Radiographics 1991;11:771–784 Horton KM, Corl FM, Fishman EK. CT evaluation of the colon: inflammatory disease. Radiographics 2000;20:399–418 Miller FH, Ma JJ, Scholz FJ. Imaging features of enterohemorrhagic Escherichia coli colitis. AJR Am J Roentgenol 2001;177:619–623 Murray JG, Evans SJ, Jeffrey PB, Halvorsen RA Jr. Cytomegalovirus colitis in AIDS: CT features. AJR Am J Roentgenol 1995;165:67–71 Nakamura S, Iida M, Tominaga M, Yao T, Hirata N, Fujishima M. Salmonella colitis: assessment with double-contrast barium enema examination in seven patients. Radiology 1992;184:537–540 Philpotts LE, Heiken JP, Westcott MA, Gore RM. Colitis: use of CT findings in differential diagnosis. Radiology 1994;190:445–449 Thoeni RF, Cello JP. CT imaging of colitis. Radiology 2006;240:623–638 Wittenberg J, Harisinghani MG, Jhaveri K, Varghese J, Mueller PR. Algorithmic approach to CT diagnosis of the abnormal bowel wall. Radiographics 2002;22:1093–1109

CASE 86 Clinical Presentation A 24-year-old man presents with right lower quadrant pain, fever, and nausea.

B

A

Fig. 86.1 (A,B) Axial contrast-enhanced CT images demonstrate appendiceal enlargement and wall thickening (arrow) with stranding in the periappendicular fat (mesoappendix). (C) Coronal reformatted image shows the thickened appendix along with periappendiceal inflammatory changes.

C

Radiologic Findings Axial and coronal contrast-enhanced computed tomography (CT) images (Fig. 86.1) demonstrate appendiceal enlargement and wall thickening with mild stranding in the periappendicular fat (mesoappendix). A calcified appendicolith is noticed within the appendix. These findings are consistent with acute appendicitis.

Diagnosis Acute appendicitis

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Differential Diagnosis • • • • •

Cecal diverticulitis Inflammatory bowel disease (Crohn disease and ulcerative colitis) Mucocele (abnormal accumulation of mucus within the appendix) Adenocarcinoma, cystadenocarcinoma Carcinoid

Discussion Background Appendicitis represents the most common cause of right lower quadrant pain, usually occurring in young patients of both genders with a slightly higher male predominance. This disease requires prompt surgical treatment to avoid complications; for this reason, radiologists should be able to recognize this entity as promptly as possible.

Clinical Findings Appendicitis usually presents with right lower quadrant pain and tenderness, fever, anorexia, nausea, and vomiting. However, the clinical presentation can be protean and mimic other pathologies. The variable position of the appendix, the degree of inflammation, and the timing of onset can all contribute to a difficult clinical diagnosis. Laboratory tests typically show a leukocytosis with left shift.

Complications Lumen distention may lead to perforation of the appendix with consequent spillage of pus into the peritoneal cavity. Once perforation has occurred, appendicitis may progress to abscess formation. Less frequent complications are hepatic abscess and small bowel obstruction.

Etiology Appendicitis is mostly the result of luminal obstruction by means of appendicoliths (calcified fecal material usually located at the appendiceal orifice) or lymphoid hyperplasia; other less common causes are parasitic infestation (Ascaris and Strongyloides species), tumors, and foreign bodies. Appendiceal obstruction results in the accumulation of fluid, luminal distention, venous engorgement, and bacterial invasion leading to inflammation. Perforation may occur whenever the diagnosis is delayed.

Imaging Findings •



CT represents the most sensitive imaging technique to evaluate appendicitis and its complications, although ultrasound has been shown to be a reliable tool as well and should be performed as initial imaging test in pediatric patients and should be considered in women of childbearing age. Magnetic resonance imaging may be used in early pregnancy. At CT, the normal appendix appears as a small, tubular, commonly air-filled structure usually located at the ileocecal valve or posterior to the cecum (a retrocecal appendix has been described in ~65% of patients); its length usually varies from a few centimeters to 20 cm. An abnormal appendix, as seen in acute appendicitis, is dilated (> 6 mm in diameter) and distended by fluid or debris; its walls appear mildly enhancing and thickened. Other imaging findings are periap-

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pendicular inflammatory fat stranding, asymmetrical cecal wall thickening, and lymphadenopathy in the mesoappendix. Calcified appendicoliths may be seen within the appendix in 25 to 40% of cases. The use of oral contrast material at CT is well established, as it can helpful to show the partial filling of the diseased appendix. When rectally administered, the contrast media depict an arrowhead-shaped area due to focal thickening of the cecal wall at the os of the appendix. This finding, called the arrowhead sign, is specific for appendicitis. CT is also useful in assessing the presence of complications; an abscess appears as a pericecal fluid collection surrounded by inflammatory changes, whereas perforation is seen as small pockets of periappendicular free air or, less commonly, as pneumoperitoneum.

Treatment • •

Surgical management is recommended as soon as possible to avoid complications, such as perforation and abscess formation. If an abscess is present, management may include image-guided percutaneous catheter drainage and an interval appendectomy.

Prognosis •

The prognosis is usually favorable if appendicitis is promptly recognized. Any delay in the diagnosis may increase the mortality/morbidity rate. Therefore, cross-sectional imaging plays a central role in patient management.

PE ARL



The presence of an appendicolith within the lumen of the appendix associated with periappendicular inflammatory changes is highly suspicious for appendicitis.

PITFALL



Periappendicular/pericecal inflammatory changes (fat stranding, lymphadenopathy, fluid collections) without evidence of appendiceal abnormalities are not diagnostic for appendicitis, as they have been described in inflammatory bowel disease and cecal diverticulitis.

Suggested Readings Callahan MJ, Rodriguez DP, Taylor GA. CT of appendicitis in children. Radiology 2002;224:325–332 Horton KM, Corl FM, Fishman EK. CT evaluation of the colon: inflammatory disease. Radiographics 2000;20:399–418 Kaiser S, Frenckner B, Jorulf HK. Suspected appendicitis in children: US and CT—a prospective randomized study. Radiology 2002;223:633–638 Oto A, Ernst RD, Shah R, et al. Right-lower-quadrant pain and suspected appendicitis in pregnant women: evaluation with MR imaging—initial experience. Radiology 2005;234:445–451 Rao PM, Rhea JT, Novelline RA . Distal appendicitis: CT appearance and diagnosis. Radiology 1997;204:709–712

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Rao PM, Rhea JT, Novelline RA, et al. Helical CT technique for the diagnosis of appendicitis: prospective evaluation of a focused appendix. Radiology 1997;202:139–144 Rao PM, Wittenberg J, McDowell RK, Rhea JT, Novelline RA. Appendicitis: use of arrowhead sign for diagnosis at CT. Radiology 1997;202:363–366 Sivit CJ, Applegate KE, Berlin SC. Evaluation of suspected appendicitis in children and young adults: helical CT. Radiology 2000;216(2):430–433 Tamburrini S, Brunetti A, Brown M, et al. CT appearance of the normal appendix in adults. Eur Radiol 2005;15(10):2096–2103

CASE 87 Clinical Presentation A 45-year-old man with chronic abdominal symptoms presents with abdominal pain, diarrhea, and weight loss.

Fig. 87.1 An axial CT image shows mild enhancement and thickening of terminal ileal (arrow) and cecum walls at the ileocecal junction with mild peri-inflammatory fat stranding.

Fig. 87.2 An axial CT image shows moderate, irregular wall thickening of the terminal ileum (arrow). The walls of inflamed bowel loops have a stratified appearance and present mild enhancement after intravenous administration of contrast medium. There is prominence of mesenteric vessels surrounding the inflamed bowel.

Radiologic Findings Axial and coronal computed tomography (CT) images (Figs. 87.1, 87.2, and 87.3) of the abdomen obtained after oral administration of negative contrast material show diffuse, irregular wall thickening of distal small bowel loops mostly affecting the terminal ileum. There is moderate prominence of the fat surrounding the diseased bowel loops. The ileocecal junction appears affected as well, with mild cecal wall thickening.

Diagnosis Crohn disease (regional enteritis/terminal ileitis/granulomatous ileocolitis)

Differential Diagnosis • • • •

Infectious enterocolitis, including tuberculosis Eosinophilic enteritis Radiation enteritis Behçet disease

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Fig. 87.3 Coronal CT image of the abdomen. Again, notice the findings previously described at the terminal ileum and cecum with irregular wall thickening. Other jejunal bowel loops located in the upper mesogastrium appear clustered and affected by inflammatory changes.

• • • •

Ulcerative colitis Diverticulitis Acute appendicitis, which can be mimicked by acute ileitis Carcinoma or lymphoma

Discussion Background Crohn disease is a chronic granulomatous inflammatory condition of unknown etiology, occurring in multiple discontiguous sites of the gastrointestinal tract. Lesions may occur anywhere from the mouth to the anus but are mostly encountered in the small bowel, especially the terminal ileum (in 80%), colon (in 70%), and, less commonly, duodenum (in 20%). The small and large bowels are frequently both involved. Incidence is higher among Caucasians in their 2nd to 3rd decade, and women are slightly more affected than men. The most typical pathologic feature is the involvement of all layers of the diseased bowel. In early stages, the submucosal layer is affected by hyperplasia of lymphoid tissue and lymphedema; as the disease progresses, the inflammation extends transmurally, and mucosal aphthous lesions develop. At advanced stages, ulcers tend to become deeper, leading to sinus tracts and fistulas. Scarring and fibrosis are the final results of this inflammatory process. Despite the presence of these typical features, Crohn disease cannot always be distinguished from ulcerative colitis (~20% of patients present indeterminate findings).

Clinical Findings Clinical presentation is extremely varied, depending on the acuity of onset, anatomical location, and extent of the disease. Most patients experience abdominal pain and discomfort (more commonly right-sided), vomiting, fever, diarrhea, anorexia, and weight loss. Bloody diarrhea is not typical of Crohn disease. Laboratory tests may reveal anemia, leukocytosis in active disease, and abnormal serum chemical analysis (hypoalbuminemia, hypokalemia, hypocalcemia). Extraintestinal manifestations include gallstones and kidney stones, arthritis, iritis, episcleritis, and sclerosing cholangitis.

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Complications Major complications are toxic megacolon, perforation, obstruction (due to stricturing), abscess formation, and fistulas (enterovesical, enteroenteric, enteromesenteric, enterocutaneous, rectovaginal, and perianal). Surgical therapy may be needed, although generally conservative medical therapy is attempted as first-line therapy. Diarrhea prevents nutrient absorption and hence may cause malnutrition. Patients with Crohn disease have an increased risk of developing colorectal cancer and lymphoma compared with the general population.

Etiology The etiology remains uncertain. Several studies suggest that autoimmune, infectious, and genetic factors may all be involved. Poor diet, tobacco use, and oral contraceptive use have also been cited as potential causative factors. Other studies focus on the presence of mesenteric vascular alterations (damage to submucosal blood vessels), thus defining Crohn disease as a granulomatous vasculitis.

Imaging Findings Conventional imaging modalities (barium enema, small bowel series, and enteroclysis studies), as well as ultrasonography and cross-sectional imaging techniques (CT and magnetic resonance [MR]), have been used for the evaluation of Crohn disease. Both CT and MRI present some advantages, including the ability to demonstrate the extent of inflammation within bowel walls and in the surrounding fat; multiplanar capabilities are useful in the assessment of complications and fistulas. Intravenous (IV) contrast media are advocated in the assessment of patients with Crohn disease, and intraluminal contrast media, either ingested or administered by means of a nasojejunal catheter (enteroclysis), are helpful in the assessment of the mucosa and the search for strictures and fistulas. The most important findings of Crohn disease are • • • • • • • • •

Asymmetric/eccentric bowel wall thickening (> 4–5 mm) Stratified appearance of the affected bowel loops (target or double-halo sign) with the inner and outer layers surrounding a hypodense middle layer Prominent enhancement of the diseased walls after IV injection of a contrast medium Luminal narrowing and prestenotic dilatation Fibrofatty proliferation (creeping fat) surrounding the inflamed bowel loops Comb sign (dilatation, tortuosity, and prominence of the mesenteric vasa recta due to hypervascularity of the affected mesentery) Abscess and phlegmons occurring in the mesentery, abdominal wall, psoas muscles, and perianal region Fistulas and sinus tracts (better demonstrated with positive oral contrast) Mesenteric lymphadenopathy (3–8 mm; if >10 mm, suspect carcinoma or lymphoma)

Capsule endoscopy represents a promising noninvasive diagnostic tool for the study of small bowel disease and may be very useful in the detection of early lesions in patients with Crohn disease. However, this modality is contraindicated in the setting of strictures.

Treatment •

Medical treatments aim to inhibit the inflammatory process, control infections, and avoid malnutrition. Four different classes of drugs are therefore administered to fulfill these goals: corticosteroids, aminosalicylates, antibiotics, and immunomodulators.

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Surgical treatment is required when medical therapy has proved inadequate to control the disease.

Prognosis •

The prognosis depends on the anatomical site and extent of the disease. The recurrence rate is high even in patients responding to medical therapy; moreover, ~50% of patients require surgical treatment. Quality of life is affected by long-term medical treatment (e.g., corticosteroids causing osteoporosis, osteomyelitis, or increasing susceptibility to infections).

PE ARL



Crohn disease has a bimodal distribution in terms of age at presentation, with the majority of patients presenting in the 2nd to 3rd decade and a small cohort presenting in the 7th to 8th decade.

PITFALL



Positive oral contrast (high attenuation) may hide mural enhancement or obscure small early lesions. Negative oral contrast (low attenuation) may not be able to easily demonstrate fistulas or extramural fluid collection, such as an abscess.

Suggested Readings Desai RK, Tagliabue JR, Wegryn SA, Einstein DM. CT evaluation of wall thickening in the alimentary tract. Radiographics 1991;11:771–784 Furukawa A, Saotome T, Yamasaki M, et al. Cross-sectional imaging in Crohn disease. Radiographics 2004;24:689–702 Hara AK, Leighton JA, Sharma VK, Heigh RI, Fleischer DE. Imaging of small bowel disease: comparison of capsule endoscopy, standard endoscopy, barium examination, and CT. Radiographics 2005;25: 697–711 Horton KM, Corl FM, Fishman EK. CT evaluation of the colon: inflammatory disease. Radiographics 2000;20:399–418 Koh DM, Miao Y, Chinn RJ, et al. MR imaging evaluation of the activity of Crohn’s disease. AJR Am J Roentgenol 2001;177:1325–1332 Madureira AJ. The comb sign. Radiology 2004;230:783–784 Paulsen SR, Huprich JE, Fletcher JG, et al. CT enterography as a diagnostic tool in evaluating small bowel disorders: review of clinical experience with over 700 cases. Radiographics 2006;26:641–657 Prassopoulos P, Papanikolaou N, Grammatikakis J, Rousomoustakaki M, Maris T, Gourtsoyiannis N. MR enteroclysis imaging of Crohn disease. Radiographics 2001;21:S161–S172 Sailer J, Peloschek P, Schober E, et al. Diagnostic value of CT enteroclysis compared with conventional enteroclysis in patients with Crohn’s disease. AJR Am J Roentgenol 2005;185:1575–1581 Wills JS, Lobis IF, Denstman FJ. Crohn disease: state of the art. Radiology 1997;202:597–610 Wold PB, Fletcher JG, Johnson CD, Sandborn WJ. Assessment of small bowel Crohn disease: noninvasive peroral CT enterography compared with other imaging methods and endoscopy—feasibility study. Radiology 2003;229:275–281

CASE 88 Clinical Presentation A 54-year-old man presents with abdominal pain, vomiting, and rectal bleeding.

B

A

Fig. 88.1 (A–C) Axial CT images obtained after administration of an oral positive-contrast medium show the typical bowel-within-bowel configuration of intussusception. A polypoidlike lesion (arrow) is noticed within the affected bowel loops and may be consistent with a tumor acting as a lead point. There is no sign of bowel obstruction, as the oral positive-contrast material is seen beyond the involved loops as well as in the colon. No peri-inflammatory changes are noticed in the surrounding mesenteric fat.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images (Fig. 88.1) show an intussuscepted small bowel loop within the left midabdomen with a polypoid-appearing lead point. Contrast is seen beyond this loop and in the colon.

Diagnosis Intussusception

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C

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Differential Diagnosis • •

Polypoid neoplasms (benign or malignant) Inverted Meckel diverticulum

Discussion Background Intussusception is the invagination of a bowel loop with its mesentery (intussusceptum) into the lumen of a contiguous loop (intussuscipiens). This abnormality mostly occurs in infants (40% at an age of 6–7 months) but also in adults (5%), accounting for 1% of all bowel obstructions. Intussusceptions may affect almost any part of the small and large bowel, so that different types have been described: ileocolic, ileoileocolic (together they account for 90% of cases in childhood), ileoileal, and colocolic. Intussusceptions may be further classified as idiopathic or nonidiopathic if a causative lead point is present.

Clinical Findings Pediatric patients usually present with colicky abdominal pain, vomiting, and the typical red “currant jelly” stools (i.e., stools mixed with blood and mucus), although most infants have only stools positive for occult blood. Physical examination may reveal a mass upon palpation of the abdomen. Fever is rarely a presenting symptom and may be the result of a complication, such as sepsis. Adults present with nonspecific complaints similar to symptoms of bowel obstruction.

Complications If not promptly resolved, intussusception may result in obstruction or perforation of the affected loops as soon as the compression of the mesenteric fold of the intussusceptum leads to venous engorgement, ischemia, and necrosis. Intussusceptions may also recur (10% of cases), especially within 48 hours after radiologic reduction.

Etiology Almost 90% of all pediatric intussusceptions present no lead point; these idiopathic cases may be related to hypertrophy of lymphoid tissues secondary to viral infection. Other predisposing factors are cystic fibrosis and recent upper respiratory infections. In the remaining 10% of cases, a mechanical lead point can be identified: Meckel diverticulum, intestinal polyps (Peutz-Jeghers syndrome, juvenile polyposis, etc.), blunt abdominal trauma, intestinal lymphosarcoma, foreign bodies, hemangiomas, cysts, and Henoch-Schönlein purpura (small bowel hematomas) represent the most common causative agents. In adults almost all symptomatic intussusceptions are due to an underlying disease (e.g., lipoma, adenomatous polyps, metastases, lymphoma, adenocarcinoma, and postoperative adhesion) acting as a lead point. An increasing number of idiopathic intussusceptions (no evidence of a lead point) have been identified at cross-sectional imaging, CT, and in the absence of symptoms or mechanical obstruction and are felt to be physiologic.

Imaging Findings •

Abdominal plain films (both supine and prone views) may be normal, may show a soft tissue mass with an abnormal intestinal gas pattern, or may have features suggestive of bowel obstruction.

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The typical ultrasound finding of intussusceptions is the target or doughnut sign on transverse sections due to the presence of a central hyperechoic area surrounded by a hypoechoic edematous bowel loop; on longitudinal sections, this abnormality displays a pseudokidney or reniform appearance. The same findings may be described at CT, but this imaging technique better depicts the surrounding inflammatory changes, the complications related to this abnormality, as well as the underlying causes. Small bowel intussusceptions without a lead point are more common than intussusceptions with a lead point and usually appear shorter and smaller in diameter. Most large bowel intussusceptions (50%) have a lead point, such as adenocarcinoma, lymphoma, metastases, lipoma, and adenomatous polyps. CT can identify the underlying lesions but may not be able to characterize them.

Treatment •



In children, surgery must be performed in case of perforation, peritonitis, or hypovolemic shock. If patients are clinically stable, reduction by means of barium or air with fluoroscopic guidance may be successfully performed. Ultrasound has been increasingly acknowledged as an alternative method for the reduction of childhood intussusception because of its high success rate (80%) and its avoidance of radiation exposure. In adults, surgical removal of the underlying cause is required to solve intussusceptions.

Prognosis •

The outcome is favorable if the intussusception is promptly recognized and properly treated. The recurrence rate after barium enema reduction or ultrasound-guided reduction is 6 to 10%, with half of the cases occurring within 48 hours.

PE ARL



The presence of a bowel-within-bowel configuration with or without the typical inflammatory changes due to the compression of the mesenteric fold and vessels is pathognomonic of intussusception.

PITFALL



Increasingly seen physiologic intussusceptions on cross-sectional imaging can lead to unnecessary imaging and patient concern.

Suggested Readings Bisset GS III, Kirks DR. Intussusception in infants and children: diagnosis and therapy. Radiology 1988;168(1):141–145 Boudiaf M, Soyer P, Terem C, Pelage JP, Maissiat E, Rymer R. CT evaluation of small bowel obstruction. Radiographics 2001;21:613–624 Bramis J, Griniatsos J, Papaconstantinou I, et al. Emergency helical CT scan in acute abdomen: a case of intestinal intussusception. Ulus Travma Acil Cerrahi Derg. 2006;12(2):155–158 Cois A, Pisanu A, Pilloni L, Uccheddu A. Intussusception of the appendix by mucinous cystadenoma: report of a case with an unusual clinical presentation. Chir Ital 2006;58(1):101–104

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Del Pozo G, Albillos JC, Tejedor D, et al. Intussusception in children: current concepts in diagnosis and enema reduction. Radiographics 1999;19:299–319 Kim YH, Blake MA, Harisinghani MG, et al. Adult intestinal intussusception: CT appearances and identification of a causative lead point. Radiographics 2006;26:733–744 Khong PL, Peh WC, Lam CH, et al. Ultrasound-guided hydrostatic reduction of childhood intussusception: technique and demonstration. Radiographics 2000;20:E1 Luzier J, Verhey P, Dobos N. Preoperative CT diagnosis of appendiceal intussusception. AJR Am J Roentgenol 2006;187(3):W325–W326 Nakayama Y, Fukushima M, Sakai M, et al. Intramural hematoma of the cecum as the lead point of intussusception in an elderly patient with hemophilia A: report of a case. Surg Today 2006;36(6): 563–565 Sargent MA, Babyn P, Alton DJ. Plain abdominal radiography in suspected intussusception: a reassessment. Pediatr Radiol 1994;24(1):17–20

CASE 89 Clinical Presentation A 72-year-old man presents with diffuse abdominal pain.

A

B

Fig. 89.1 (A) Axial CT image shows gas in the portal vein branches (peripherally located, as opposed to central gas in the pneumobilia) and free gas under the anterior abdominal wall. (B) Lower axial CT image in the same patient shows curvilinear gas collections in the wall of the distended bowel loops.

Radiologic Findings Axial computed tomography (CT) images in a patient with massive bowel ischemia show the presence of hypodense curvilinear gas lucencies in the bowel wall and portal vein branches (Fig. 89.1).

Diagnosis Bowel pneumatosis with portal venous gas

Differential Diagnosis • • • • •

Pneumatosis cystoids intestinalis Bowel perforation Bowel ischemia Intestinal obstruction Postoperative bowel

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Discussion Background The presence of gas within the bowel wall is termed pneumatosis intestinalis. Recognition of pneumatosis intestinalis in symptomatic patients is important because it may be the only finding of an underlying pathology, which may not be always obvious on imaging. Pneumatosis intestinalis can be primary (idiopathic) or secondary (due to underlying causes).

Clinical Findings • • • • • • •

Asymptomatic Sudden onset of abdominal pain Bloody diarrhea Abdominal distention Vomiting Back pain Obstipation

Complications • • • •

Hemodynamic shock Functional intestinal obstruction Peritonitis Pneumoperitoneum

Etiology • • • • • • • • • • • • • • • •

Mucosal disruption from any cause Chronic obstructive pulmonary disease (causes primary form) Bowel ischemia Bowel perforation Postoperative bowel Necrotizing enterocolitis Caustic and corrosive ingestion Intestinal obstruction Inflammatory bowel disease Celiac sprue Whipple disease Connective tissue disorders Inflammatory or infectious enterocolitis Chemotherapy, cancer, and bone marrow transplantation Immunosuppression due to any cause Idiopathic

Imaging Findings •

Plain radiographs can reveal the presence of pneumatosis and portomesenteric gas. CT clearly demonstrates pneumatosis in all cases with or without an underlying cause (Figs. 89.2, 89.3).

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Fig. 89.2 Axial noncontrast CT image in a 45-year-old man

Fig. 89.3 Axial noncontrast CT image in a

with a subacute small intestinal obstruction shows the presence of pneumatosis.

32-year-old-man with vague abdominal pain shows the presence of pneumatosis and retroperitoneal gas in the right hemiabdomen.







The presence of liner or cystic gas collections in the nondependent portion of the bowel wall is the hallmark of this condition. Multiple vesicles < 1 cm are more commonly seen in primary pneumatosis, whereas liner gas collections within the bowel wall are characteristic of the secondary and more severe form. The presence of free fluid, portomesenteric gas, bowel wall thickening, and fat stranding should prompt an extensive search for the underlying cause in otherwise symptomatic patients and necessitates contrast CT examination to rule out bowel ischemia. Patients with bowel ischemia also have multiple dilated intestinal loops because of associated paralytic ileus and edema of the bowel wall, which appears thickened with lesser mucosal enhancement. The presence of a transition point between dilated and nondilated bowel loops suggests an intestinal obstruction.

Treatment •

The primary form of bowel pneumatosis does not need any treatment unless it is associated with complications. The treatment of any underlying abnormality resolves pneumatosis in patients with the secondary form.

Prognosis •

The prognosis is excellent for primary pneumatosis cystoids intestinalis. Secondary pneumatosis with the presence of portomesenteric gas is associated with a grave prognosis and higher mortality rates.

PE ARL



The presence of pneumatosis and associated findings in symptomatic patients can suggest the diagnosis.

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PITFALL



The underlying condition leading to pneumatosis intestinalis may not always be apparent on imaging.

Suggested Readings Kernagis LY, Levine MS, Jacobs JE. Pneumatosis intestinalis in patients with ischemia: correlation of CT findings with viability of the bowel. AJR Am J Roentgenol 2003;180(3):733–736 St Peter SD, Abbas MA, Kelly KA. The spectrum of pneumatosis intestinalis. Arch Surg 2003;138(1): 68–75 Wiesner W, Khurana B, Ji H, Ros PR. CT of acute bowel ischemia. Radiology 2003;226(3):635–650

CASE 90 Clinical Presentation A 72-year-old woman presents with abdominal distention, fullness, and pain in the right iliac fossa.

B

A

Fig. 90.1 (A) Axial contrast-enhanced CT image shows the presence of a cystic lesion with thick walls in the right iliac fossa with surrounding fat stranding and free fluid. (B) Axial contrast-enhanced CT image of the liver in the same patient shows scalloping of the liver margins and ascites with peritoneal thickening.

Radiologic Findings Contrast computed tomography (CT) images show the presence of a cystic lesion in the right lower quadrant with ascites and scalloping of the liver margins (Fig. 90.1).

Diagnosis Malignant mucocele of the appendix with pseudomyxoma peritonei

Differential Diagnosis • • • • • • • • •

Abscess Normal fluid-filled ileal loop Tuberculous ascites Peritoneal metastases Malignant ascites Ovarian cystic lesions Bowel perforation Peritoneal mesothelioma Meckel diverticulitis with perforation

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Discussion Background Mucocele of the appendix is the accumulation of mucus with luminal distention of the appendix. The reported incidence is 0.2 to 0.5% of appendectomies. It can be benign or malignant. The benign variety results from occlusion of the appendiceal luminal opening into the cecum from a phlebolith or impacted feces. A malignant mucocele results from mucin-secreting adenocarcinoma of the appendix. Either a benign or a malignant mucocele can result in the development of pseudomyxoma peritonei on rupture.

Clinical Findings • • • • •

Chronic pain in the abdomen Abdominal distention Mass in the right iliac fossa Intermittent colicky pain due to intussusception Vomiting

Complications • • • •

Rupture of the mucocele Development of pseudomyxoma peritonei Intestinal obstruction Intussusception

Etiology •

Obliteration of appendiceal lumen from any cause

Imaging Findings •





On ultrasound, the mucocele may appear as a thin-walled cystic mass in the right iliac fossa, attached to the cecum, filled with diffuse internal echoes in the dependent portion with or without septa and polypoidal luminal projections, and with posterior acoustic enhancement. The presence of a solid mass within the nondependent portions of the lesion indicates the possibility of adenocarcinoma. Similar findings are seen with CT, with the mucocele appearing as a low-attenuating structure in the right lower abdomen. Calcifications within an unruptured mucocele can be curvilinear or plaquelike and can be appreciated on plain radiographs of the abdomen (Fig. 90.2). The size of the lesion varies, with lesions measuring up to 15 cm reported in the literature. A ruptured mucocele shows fluid-density ascites with internal echoes and fixed bowel loops. In patients with the development of pseudomyxoma peritonei, diffuse coarse internal echoes within the ascitic fluid can be seen with scattered calcifications and scalloping on the peritoneal surfaces of the abdominal organs. Multiple solid translucent globules of uniform size that calcify in the course of time and shift with movement are pathognomonic of the myxoglobulosis variant of a mucocele. The presence of mucinous nodules within the remnant umbilical vein is a feature that helps to differentiate pseudomyxoma peritonei from ascites.

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Fig. 90.2 Axial contrast-enhanced CT image in a different patient reveals a cystic lesion with thick walls in the right iliac fossa. The lesion shows the presence of calcifications in its wall.

Treatment •



Surgical resection of the appendix is the treatment of choice for an unruptured mucocele of the appendix. In patients with a ruptured mucocele with the development of pseudomyxoma peritonei, wide peritoneal stripping is done for cytoreductive surgery, followed by heated intraoperative intraperitoneal chemotherapy with mitomycin C, doxorubicin, and fluorouracil (5-FU). Systemic chemotherapeutic agents can be used in resistant disease and recurrent disease.

Prognosis •

Patients with an unruptured mucocele of the appendix have an excellent prognosis. Patients with pseudomyxoma peritonei and mucinous adenocarcinoma have a worse prognosis with treatmentresistant disease, higher mortality, and posttreatment complications.

PE ARL S

• •

A cystic oblong mass in the right iliac fossa should include mucocele in the differential. Scalloping of the peritoneal surfaces of abdominal organs represents pseudomyxoma peritonei.

PITFALL



Imaging cannot always differentiate between benign and malignant causes of mucocele of the appendix and pseudomyxoma peritonei.

Suggested Readings Dachman AH, Lichtenstein JE, Friedman AC. Mucocele of the appendix and pseudomyxoma peritonei. AJR Am J Roentgenol 1985;144:923–929 Madwed D, Mindelzun R, Jeffrey RB Jr. Mucocele of the appendix: imaging findings. AJR Am J Roentgenol 1992;159:69–72 Sasaki K, Ishida H, Komatsuda T. Appendiceal mucocele: sonographic findings. Abdom Imaging 2003;28:15–18

CASE 91 Clinical Presentation A 74-year-old man presents with lower abdominal pain and discomfort associated with a recent change in bowel habits.

Fig. 91.1 An axial contrast-enhanced CT image shows diffuse diverticulosis, most significant in the sigmoid colon, with evidence of related mild muscular hypertrophy. No pericolonic inflammatory changes are noticed.

Radiologic Findings An axial contrast-enhanced computed tomography (CT) image (Fig. 91.1) shows diffuse diverticulosis, most significant in the sigmoid colon, with evidence of related mild muscular hypertrophy. No pericolonic inflammatory changes are noticed.

Diagnosis Diverticulosis

Differential Diagnosis • • •

Inflammatory bowel disease (Crohn disease and ulcerative colitis) Colonic carcinoma Small bowel diverticulosis

Discussion Background Diverticula are outpouchings of the intestinal walls, involving either all the layers (true diverticula) or just the mucosal and submucosal layers (false diverticula). Diverticular disease has been described anywhere in the gastrointestinal (GI) tract but is most frequently present in the sigmoid colon (95–98%) due to the higher segmental intraluminal pressures. These diverticula usually form through weaker points of the colonic walls, which represent the natural openings for the vasa recta and other nutrient vessels.

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B

A

Fig. 91.2 (A,B) Axial contrast-enhanced CT images show diffuse bowel wall thickening of the sigmoid colon with surrounding inflammatory mesenteric fat stranding. These findings are consistent with severe diverticulitis.

Clinical Findings Diverticulosis is a common, usually asymptomatic condition. Patients with multiple diverticula may present with different symptoms according to their location; clinical presentation most frequently includes left lower abdominal pain, nausea, and changes in bowel habits, including diarrhea, constipation, and tenesmus.

Complications Major complications include GI bleeding (melena, hematochezia) and diverticulitis due to occlusion of the neck of a diverticulum by stool, inflammation, or ingested material, causing subsequent microperforation of a diverticulum and associated pericolic inflammation (Fig. 91.2). Inflammation may resolve or progress, causing abscess formation, fistulas (to local structures, e.g., the bladder, uterus, or vagina), abdominal obstruction, or free perforation.

Etiology Diverticulosis is related to the low-fiber/high-fat diet typical of industrialized countries leading to abnormal peristalsis, intestinal dyskinesia, and increased intraluminal pressures. Its incidence increases with age; in fact, colonic diverticular disease is uncommon in people younger than 40 years. Genetics may play a predisposing role, as left-sided diverticula are usually described in Caucasian populations, whereas right-sided diverticula are typically seen in persons of Asian descent.

Imaging Findings • •

Water-soluble contrast enemas represent a safe but somewhat outmoded imaging study for diverticulosis. On CT, diverticula appear as multiple, air-filled outpouchings of the intestinal walls ranging in size from 2 to 3 mm to 2 cm (giant diverticula have been reported but are rare) and usually located in the sigmoid colon; the affected intestinal segment may have thickened walls due to muscular hypertrophy. CT is also useful to evaluate the complications of diverticular disease, such as acute diverticulitis (wall thickening and pericolic fat stranding), abscesses (fluid collections with peripheral enhancing rims), and perforation (extraluminal free air). Colovesicular fistulas are suggested by the presence of gas in the bladder or focal bladder wall thickening in close proximity to the affected segment of the bowel with loss of dividing fat planes.

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Treatment •

Conservative treatment is advised in cases of asymptomatic diverticula. Surgery is suggested after repeated bouts of acute diverticulitis and may be required in case of fistulas, obstruction, and sepsis.

Prognosis •

The prognosis is usually favorable, barring severe complications.

PE ARL



Diverticulitis may be present even though diverticula are not radiographically evident.

PITFALL



Diverticulitis and a perforated colon cancer may have overlapping imaging findings; therefore, gastroenterology consultation is usually performed by the referring physician for endoscopy to exclude the possibility of malignancy.

Suggested Readings Chintapalli KN, Esola CC, Chopra S, Ghiatas AA, Dodd GD III. Pericolic mesenteric lymph nodes: an aid in distinguishing diverticulitis from cancer of the colon. AJR Am J Roentgenol 1997;169:1253–1255 Horton KM, Corl FM, Fishman EK. CT evaluation of the colon: inflammatory disease. Radiographics 2000;20:399–418 Jarrett TW, Vaughan ED Jr. Accuracy of computerized tomography in the diagnosis of colovesical fistula secondary to diverticular disease. J Urol 1995;153:44–46 Padidar AM, Jeffrey RB Jr, Mindelzun RE, Dolph JF. Differentiating sigmoid diverticulitis from carcinoma on CT scans: mesenteric inflammation suggest diverticulitis. AJR Am J Roentgenol 1994;163:81–83 Silva AC, Wellnitz CV, Hara AK. Three-dimensional virtual dissection at CT colonography: unraveling the colon to search for lesions. Radiographics 2006;26:1669–1686 Thomas S, Peel RL, Evans LE, Haarer KA. Best cases from the AFIP: giant colonic diverticulum. Radiographics 2006;26:1869–1872 Zaidi E, Daly B. CT and clinical features of acute diverticulitis in an urban U.S. population: rising frequency in young, obese adults. AJR Am J Roentgenol 2006;187:689–694

CASE 92 Clinical Presentation A 70-year-old patient presents with constipation and hematochezia.

Fig. 92.1 Axial contrast-enhanced CT image of the sigmoid colon shows an enhancing “apple core” lesion causing short segment narrowing (arrow).

Fig. 92.2 Axial CT image of the upper abdomen in the same patient shows a peripherally enhancing hypodense hepatic metastasis in the liver (arrow). Also seen are perihepatic malignant ascites.

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images through the pelvis show an enhancing “apple core” lesion causing short segment narrowing in the sigmoid colon (Figs. 92.1, 92.2). Figure 92.2 shows a hypodense peripherally enhancing hepatic metastasis in the same patient, along with malignant perihepatic ascites.

Diagnosis Adenocarcinoma sigmoid colon with hepatic metastasis

Differential Diagnosis • • • •

Colitis Diverticulitis Inflammatory fibrous polyp Benign stricture due to inflammatory bowel disease or ischemia or smooth muscle hypertrophy from chronic diverticulosis

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Discussion Background Colorectal cancers are the second most common cause of cancer-related deaths in the United States and Europe. The sigmoid colon is the second most common site of colonic malignancy following the rectum.

Clinical Findings Symptoms include abdominal pain and distention, constipation, change in bowel habits, weight loss, melena, hematochezia, and symptoms related to disseminated metastatic disease. Findings on clinical and laboratory examination include a palpable abdominal or rectal mass, heme-positive stool, iron deficiency anemia, abnormal liver function tests, and raised carcinoembryonic antigen (CEA) levels.

Complications Complications include intestinal obstruction, perforation, metastatic disease, fistula formation, secondary infection leading to abscess formation, local invasion, and intussusceptions.

Etiology Risk factors for colorectal carcinoma include advanced age (> 50 years), personal and/or family history of colorectal adenomatous polyps or cancers or polyposis syndromes, hereditary nonpolyposis colorectal cancer (HNPCC, or Lynch syndrome), inflammatory bowel disease, low-fiber/high-fat diet from animal sources, physical inactivity, smoking, and heavy use of alcohol.

Imaging Findings •





Annular and semiannular lesions tend to be more common than polypoidal and carpet (plaquelike) lesions. They also tend to have extraserosal extension and lymph node metastases more commonly than polypoidal lesions. Focal and irregular bowel wall thickening with luminal narrowing giving the appearance of an apple core lesion is a typical appearance of sigmoid colonic carcinoma. Radiologic criteria for polypoidal lesion being malignant are irregular outline, broad base, size > 1 to 2 cm in diameter, retraction at the base of the polyp, and significant growth between two separate examinations. Pericolonic and mesenteric fat stranding and higher attenuation of fat adjacent to the lesion suggest extraserosal spread of malignancy or surrounding inflammatory changes. The mesentery should be assessed for lymphadenopathy. Carpet lesions in colon cancer present as asymmetric nodular wall thickening. The liver is the most common organ involved in metastatic disease. Other usual sites of metastases are the lungs, bones, and brain. Hepatic metastases are most commonly hypodense, best visualized in the portal venous phase. Metastases from mucinous colon cancers can be cystic and calcified. Widespread peritoneal carcinomatosis is more frequently seen with mucinous cancers.

Treatment •

Treatment depends on the stage of malignancy. In early stages without serosal involvement and mesenteric lymphadenopathy, the typical treatment is surgical resection. Chemotherapy is considered for patients with more advanced disease. Adjuvant radiation therapy is useful for the

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treatment of tumor with spread to adjacent organs. Surgical resection of hepatic metastases is performed in some patients.

Prognosis •

The survival rate depends on the initial presentation of the tumor. More than 90% of patients with early-stage disease have a 5-year survival rate, whereas < 5% of those with metastatic disease do.

PE ARL



A discrete intraluminal soft tissue mass and irregular bowel wall thickening with luminal narrowing in the setting of mesenteric lymphadenopathy favor the diagnosis of carcinoma.

PITFALL



Colonic mucosal lesions are not well seen on cross-sectional imaging, and inadequate bowel preparation or distention for CT colonography can make early colon cancers difficult to identify. There is also imaging overlap between colon cancer and other conditions, such as diverticulosis and diverticulitis.

Suggested Readings Horton KM, Abrams RA, Fishman EK. Spiral CT of colon cancer: imaging features and role in management. Radiographics 2000;20:419–430 Jang HJ, Lim HK, Park CK, Kim SH, Park JM, Choi YL. Segmental wall thickening in the colonic loop distal to colonic carcinoma at CT: importance and histopathologic correlation. Radiology 2000;216(3): 712–717 Skucas J, Spataro RF, Cannucciari DP. The radiographic features of small colon cancers. Radiology 1982;143:335–340

CASE 93 Clinical Presentation A 69-year-old man presents with abdominal pain and gastrointestinal (GI) bleeding.

A

B

Fig. 93.1 (A–C) CT colonoscopy with insufflated carbon dioxide in the colon. Axial CT images of the pelvis show a small isodense lesion protruding in the wall of the sigmoid colon, consistent with a sessile polyp (arrow).

C

Radiologic Findings Axial images from computed tomography (CT) colonography show a small isodense protruding lesion arising from the wall of the sigmoid colon (Fig. 93.1).

Diagnosis Sigmoid colonic polyp

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Differential Diagnosis • • • • • • •

Colonic adenocarcinoma Inverted diverticulum Carcinoid Metastases Lipoma Leiomyoma Foreign bodies

Discussion Background Polyps are protruding intraluminal lesions arising from the epithelial lining of the GI tract, mostly affecting the sigmoid colon and rectum. These lesions more commonly occur in elderly men, but they have also been noticed in younger patients affected by familial inherited polyposis syndromes such as Gardner/familial adenomatous polyposis syndrome and Turcot syndrome (adenomatous polyps), Peutz-Jeghers and Cowden syndromes (hamartomatous polyps), and juvenile polyposis syndrome (inflammatory polyps). At hystologic analysis, polyps are divided into inflammatory, hamartomatous, and adenomatous, the latter being the only premalignant type. Morphology and size are the most reliable features for predicting malignant degeneration.

Clinical Findings Clinical presentation mainly relies on the size and location of the polyps; patients can be asymptomatic or present with changes in bowel habits, GI bleeding or mucous rectal discharge, and hypokalemia (hypersecretory syndrome usually described in villose adenomatous polyps).

Complications Prompt detection of adenomatous polyps is mandatory, as these lesions are known to be a precursor of colonic cancer, one of the leading causes of cancer death in the United States.

Etiology Hyperplastic inflammatory polyps are focal nonneoplastic proliferations of colonic epithelium. Adenomatous polyps are premalignant; the sequence of morphologic, molecular, and genetic steps that lead to malignant transformation is known as the adenoma-to-carcinoma sequence.

Imaging Findings •



At barium enema, polyps are described as filling defects arising from the colonic walls; however, this technique has revealed low sensitivity to detect polyps < 1 cm and has been overwhelmed by the introduction of colonoscopy as well as of CT and magnetic resonance (MR) colonography. CT colonography can depict the colonic wall in a manner similar to that seen with optical endoscopy; current software allows for the creation of two- and three-dimensional reformatted images, improving both the sensitivity and the specificity of this technique. Research is ongoing to establish

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the best way to prepare patients for CT colonography; some experts advocate a traditional bowel preparation akin to what is done for optical colonoscopy, with contrast and postprocessing subtraction techniques used to assess the mucosa. The overall experience with MR colonoscopy is still limited. Although these imaging studies have proved to be very promising, optical colonoscopy remains the most reliable technique for the detection of polyps.

Treatment •

Endoscopic removal is advised to prevent malignant transformation of adenomatous polyps.

Prognosis •

The prognosis is favorable if these premalignant lesions are promptly recognized and removed.

PE ARL



Polyps ≥ 1 cm in size should be referred for biopsy.

PITFALL



The presence of fecal masses and insufficient colonic distention may be potential problems in the identification of colonic polyps.

Suggested Readings Geenen RWF, Hussain SM, Cademartiri F, Poley J-W, Siersema PD, Krestin GP. CT and MR colonography: scanning techniques, postprocessing, and emphasis on polyp detection. Radiographics 2004 24:18e Hara AK, Johnson CD, Reed JE, et al. Detection of colorectal polyps with CT colonography: initial assessment of sensitivity and specificity. Radiology 1997;205:59–65 Macari M, Bini EJ, Jacobs SL, Lange N, Lui YW. Filling defects at CT colonography: pseudo- and diminutive lesions (the good), polyps (the bad), flat lesions, masses, and carcinomas (the ugly). Radiographics 2003;23:1073–1091 Macari M, Bini EJ, Jacobs SL, et al. Colorectal polyps and cancers in asymptomatic average-risk patients: evaluation with CT colonography. Radiology 2004;230:629–636 Thompson WM, Foster WL, Paulson EK, et al. Rocky causes of errors in polyp detection at air-contrast barium enema examination. Radiology 2006;239:139–148

CASE 94 Clinical Presentation A 45-year-old man presents with abdominal cramps and rectal bleeding.

A

B

Fig. 94.1 (A–C) Axial CT images of the abdomen show mild diffuse wall thickening of the ascending colon with surrounding peri-inflammatory changes. Multiple small lymph nodes are noticed. The thickened wall presents a typical stratified appearance with negative attenuation (fatty halo sign) of the middle layer and mild hyperdensity of the inner and outer layer. No fluid collections are seen. (continued)

C

Radiologic Findings Axial and coronal computed tomography (CT) images of the abdomen obtained after administration of positive oral contrast medium (Fig. 94.1) show diffuse wall thickening of the entire large bowel. The mesentery presents mild fat stranding with multiple small lymphadenopathies mostly located in the right quadrant close to the ascending colon. There are no fluid collections.

Diagnosis Ulcerative colitis

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D

E

Fig. 94.1 (continued) (D,E) Coronal CT images of the abdomen show the typical foreshortened, narrowed, and ahaustral appearance of the affected colon in ulcerative colitis. All the segments of the large bowel are similarly involved. Note the involvement of the terminal ileum (backwash ileitis).

Differential Diagnosis • • • • • • •

Crohn disease Infectious colitis Ischemic colitis in elderly patients Radiation colitis Pseudomembranous colitis Colon adenocarcinoma Rectal cancer

Discussion Background Ulcerative colitis is a chronic idiopathic inflammatory disease, affecting the entire large bowel but primarily the rectum (95%). It has a worldwide distribution but is most common in North America, northern Europe, and Australia. Its incidence is higher among Caucasians, with a first peak at the age of 15 to 25 and a second at 55 to 65, although it may present at any age. Women are more affected than men. The inflammatory process in ulcerative colitis typically starts from the rectum, then spreads from the distal to the proximal colon (no skip areas), sometimes also involving the terminal ileum (this is more commonly seen in patients with pancolonic ulcerative colitis). The main pathologic feature of ulcerative colitis is the limited involvement of the mucosal and submucosal layers of the diseased bowel loops. Although ulcerative colitis presents typical clinical, histologic, and

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radiologic features, it cannot always be distinguished from other bowel inflammatory diseases, such as infectious colitis and Crohn disease (5–10% of patients may demonstrate Crohn-like findings).

Clinical Findings Most patients present abdominal pain, persistent diarrhea, urgency of defecation, tenesmus, fever, anorexia, and weight loss. Rectal bleeding and bloody diarrhea are characteristic features of ulcerative colitis. Laboratory tests may reveal anemia, thrombocytosis, and abnormal serum chemical analysis (hypoalbuminemia, hypokalemia, hypomagnesemia). Extracolonic manifestations are arthritis, synovitis, ankylosing spondylitis, uveitis, episcleritis, erythema nodosum, pyoderma gangrenosum, and sclerosing cholangitis.

Complications Toxic megacolon is an episode of fulminant transmural colitis leading to neurogenic loss of motor tone and progressive colonic dilatation (> 6 cm; transverse colon is usually the most commonly involved segments). It represents the most life-threatening complication of ulcerative colitis, as patients are usually septic and need to be hospitalized. Other complications are strictures and bowel obstruction. Several studies have demonstrated that colorectal cancer is a prime risk factor for mortality in patients with ulcerative colitis; the risk correlates with the extent of the inflammatory process, the duration of disease, and the presence of colorectal mucosal dysplasia, a well-known premalignant condition.

Etiology The etiology of ulcerative colitis is unknown, although several studies suggest that environmental and genetic factors may be involved; in fact, a more common occurrence has been described within members of the same family as well as within northern areas of North America and Europe. Some studies have shown that smoking is protective against developing ulcerative colitis; this relationship is reversed in Crohn disease.

Imaging Findings CT has become a major diagnostic tool for the evaluation of ulcerative colitis because of its ability to demonstrate mucosal lesions, peribowel inflammatory changes, intraperitoneal complications (abscess, fistulas), and lymphadenopathy. It also can be easily performed in the setting of acute colitis (i.e., toxic megacolon) when bowel perforation is suspected. The most important imaging findings of ulcerative colitis are • •

• • •

Symmetric continuous wall thickening (average thickness is less than in Crohn disease) Stratified appearance of the affected bowel loops (target or halo sign) with an inner (mucosa) and outer (muscularis propria) layer surrounding a hypodense middle layer (submucosa) (the attenuation of this intermediate layer is usually negative in ulcerative colitis) Prominent enhancement of the diseased walls after intravenous injection of contrast medium best seen in the enteric phase (the intensity of enhancement correlates with the degree of inflammation) Strictures either benign (fibrosis) or malignant (“apple core” or plaquelike lesions are suspicious for malignancy) Fat proliferation surrounding the diseased bowel loops

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Treatment • •

Pharmacotherapy aims to reduce and control the inflammatory process but is not curative. Elective surgery may be performed in case of medical therapy failure, drug-related side effects, or presence of colonic dysplasia or malignancy. Emergency colectomy may be required in the setting of fulminant colitis unresponsive to medical therapy.

Prognosis •

Ulcerative colitis is characterized by periodic remissions and exacerbations, which may be controlled by medical therapy. Colectomy is curative. Long-term morbidity results from side effects of drugs (especially steroids).

PE ARL S

• • •

Ulcerative colitis almost always affects the rectum (95%), then extends from the distal to the proximal colon (no skip areas). Wall thickening is symmetric and less prominent than that seen in Crohn disease. Careful surveillance is needed for malignancy (risk is 5–30 times higher than the general population).

PITFALL



Patients may present overlapping radiologic signs of inflammatory bowel disease, so that it may not be possible to differentiate ulcerative colitis from Crohn disease.

Suggested Readings Desai RK, Tagliabue JR, Wegryn SA, Einstein DM. CT evaluation of wall thickening in the alimentary tract. Radiographics 1991;11:771–784 Freeny PC. Crohn’s disease and ulcerative colitis: evaluation with double-contrast barium examination and endoscopy. Postgrad Med 1986;80(3):139–146, 149, 152–156 Giardiello FM, Bayless TM. Colorectal cancer and ulcerative colitis. Radiology 1996;199:28–30 Horton KM, Corl FM, Fishman EK. CT evaluation of the colon: inflammatory disease. Radiographics 2000;20:399–418 Kelvin FM, Oddson TA, Rice RP, Garbutt JT, Bradenham BP. Double contrast barium enema in Crohn’s disease and ulcerative colitis. AJR Am J Roentgenol 1978;131(2):207–213 Paulsen SR, Huprich JE, Fletcher JG, et al. CT enterography as a diagnostic tool in evaluating small bowel disorders: review of clinical experience with over 700 cases. Radiographics 2006;26:641–657 Philpotts LE, Heiken JP, Westcott MA, Gore RM. Colitis: use of CT findings in differential diagnosis. Radiology 1994;190:445–449 Roggeveen MJ, Tismenetsky M, Shapiro R. Best cases from the AFIP: ulcerative colitis. Radiographics 2006;26:947–951 Thoeni RF, Cello JP. CT imaging of colitis. Radiology 2006;240:623–638

CASE 95 Clinical Presentation A 64-year-old man complains of bloody diarrhea.

Fig. 95.1 Axial T2-weighted MRI image of the pelvis shows ill-defined circumferential thickening of the rectum due to a low signal intensity tumor (arrow). There is extension of the tumor into the perirectal fat (arrowhead), making it a T3 disease, as well as an adjacent metastatic lymph node (curved arrow).

Radiologic Findings Axial T2-weighted magnetic resonance (MR) image of the pelvis shows ill-defined circumferential thickening of the rectum. There is soft tissue extension into the perirectal fat as well as an adjacent lymph node (Fig. 95.1).

Diagnosis Rectal adenocarcinoma with perirectal extension of tumor

Differential Diagnosis • •

Rectal lymphoma Rectal metastases (rare)

Discussion Background Colorectal carcinoma is the second most common cancer in the United States. Approximately one third of these cancers occur in the rectum. Ninety-eight percent of rectal cancers are adenocarcinomas, and they usually arise from adenomatous polyps. The Duke system and the TNM (tumor-nodes-metastasis) system use the depth of tumor penetration of the bowel wall and the presence of lymph node involvement and metastases to stage the disease. Accurate staging with preoperative imaging allows the most appropriate treatment option

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to be selected. Patients with T1 disease are usually treated with local resection, those with T2 or T3 disease are usually treated with total mesorectal excision, and those with T4 disease may be suitable for preoperative chemoradiation in an attempt to downsize the tumor prior to surgery.

Clinical Findings Patients may present with a change in bowel habit, blood or mucus per rectum, tenesmus, weight loss, and abdominal discomfort.

Complications Complications are bowel obstruction and perforation. Rectal carcinoma most commonly metastasizes to the liver, lungs, and adrenals.

Etiology Risk factors include a high-fat/low-fiber diet, a family history of colorectal carcinoma, a personal history of colorectal carcinoma or colonic polyps, smoking, alcohol, diabetes, inflammatory bowel disease, familial adenomatous polyposis, and hereditary nonpolyposis colorectal cancer (HNPCC). Rectal carcinoma is more common in men than women and most commonly occurs after age 50.

Imaging Findings •





Endoluminal ultrasound clearly delineates the layers of the wall of the rectum and can accurately determine the T stage of the tumor in ~85% of cases. It may also demonstrate enlarged lymph nodes in the adjacent mesorectal fat and invasion of adjacent pelvic organs. Computed tomography (CT) cannot clearly demonstrate the layers of the bowel wall and has a sensitivity of only 79% for detection of extension of the tumor through the bowel wall with adjacent tissue invasion. It is also poor at detecting involved adjacent lymph nodes. CT is helpful in the detection of distant metastases. MRI may be performed using an endorectal coil or a surface phased array coil. Both techniques allow clear delineation of the layers of the rectal wall; however, surface phased array coils provide a wider field of view and a clearer depiction of the mesorectal fat and fascia. MRI is reported to have an accuracy of T staging of ~86%. Multiplanar imaging is performed, and particular attention is paid to the distance of the tumor from the mesorectal fascia. On T2-weighted images, the tumor is of intermediate signal intensity, relative to the adjacent perirectal fat and rectal wall.

Prognosis •

The prognosis depends on the stage of the disease at diagnosis, with a 5-year survival rate of ~72% with T1 and T2 disease and 7% with T4 disease.

PE ARL



Contrast-enhanced T1 imaging has not been shown to improve diagnostic accuracy, and highresolution T2-weighted imaging is generally sufficient for diagnosis.

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PITFALL



Endoluminal ultrasound, CT, and MRI are poor at detecting regional nodal disease; this is partly because there are no agreed size criteria for involved lymph nodes. New MRI contrast ultra-small particle ion–based contrast agents may improve the characterization of regional lymph nodes.

Suggested Readings Bipat S, Glas AS, Slors FJ, Zwinderman AH, Bossuyt PM, Stoker J. Rectal cancer: local staging and assessment of lymph node involvement with endoluminal US, CT, and MR imaging—a meta-analysis. Radiology 2004;232:773–783 Heneghan JP, Salem RR, Lange RC, Taylor KJ, Hammers LW. Transrectal sonography in staging rectal carcinoma: the role of gray-scale, color-flow, and Doppler imaging analysis. AJR Am J Roentgenol 1997;169:1247–1252 Iafrate F, Laghi A, Paolantonio P, et al. Preoperative staging of rectal cancer with MR imaging: correlation with surgical and histopathologic findings. Radiographics 2006;26:701–714

CASE 96 Clinical Presentation A 52-year-old man complains of vague abdominal pain and weight loss.

A

B

Fig. 96.1 Contrast-enhanced axial CT images show circumferential thickening of the sigmoid colon (white arrow) associated with adjacent pericolic lymph nodes (black arrow). There are no signs of bowel obstruction.

Radiologic Findings Contrast-enhanced axial computed tomography (CT) images show circumferential thickening of the sigmoid colon associated with adjacent pericolic lymph nodes. There are no signs of bowel obstruction (Fig. 96.1).

Diagnosis Lymphoma of the sigmoid colon

Differential Diagnosis • • • •

Adenocarcinoma of the sigmoid Metastases Infection and inflammatory bowel disease (less likely) Focal bowel ischemia (less likely)

Discussion Background Most primary gastrointestinal (GI) tract lymphomas are non-Hodgkin lymphomas (NHLs). They are seen more frequently in the stomach and small bowel than in the colon. They occur more commonly in men than in women, with a median age at diagnosis of 55 years. Primary colonic lymphoma is

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rare, accounting for 4% of cases of extranodal NHL and < 1% of all colonic malignancies. The cecum and rectum are the most common sites of involvement.

Clinical Findings Patients with primary colonic lymphoma usually present with nonspecific GI symptoms, such as changes in bowel habit, abdominal pain, blood per rectum, and weight loss.

Complications Complications include bowel wall perforation or ulceration, which can lead to massive intra-abdominal hemorrhage. Intussusception is a complication of cecal lymphoma. Colonic obstruction rarely occurs.

Etiology Risk factors for the development of primary colonic lymphoma are immunosuppression, human immunodeficiency virus (HIV) infection, and inflammatory bowel disease.

Imaging Findings •



Barium enema in primary lymphoma of the cecum may demonstrate a bulky polypoid mass. Double-contrast imaging in cases of primary lymphoma of other areas of the colon may demonstrate an infiltrating mass, seen as an annular lesion, with some luminal narrowing. The mucosa may be smooth or demonstrate ulceration with thickening of the folds. Cavitation of the mass may be seen. Segmental narrowing of the colon secondary to a circumferential soft tissue mass may be seen with CT imaging. The mass may appear bulky and may demonstrate cavitation. Regional lymph node enlargement may be demonstrated.

Prognosis •

Primary colonic lymphoma has a poorer prognosis than other forms of GI NHL, with a 5-year survival rate postsurgical resection and adjuvant chemotherapy of 27 to 55%. The prognosis depends on the depth of the wall invasion and the presence of involved lymph nodes or disseminated disease.

PE ARL



Although lymphoma may lead to significant luminal narrowing of a bowel segment, obstruction is rare because lymphoma infiltration leads to weakening of the muscularis propria and does not elicit a desmoplastic reaction.

PITFALL



Patients in whom there is colonic involvement as part of generalized NHL may have imaging findings that differ from those of primary colonic lymphoma. Multiple small, smooth submucosal nodules involving a focal segment or distributed throughout the colon are generally seen.

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Suggested Readings Doolabh N, Anthony T, Simmang C, et al. Primary colonic lymphoma. J Surg Oncol 2000;74(4): 257–262 Ghai S, Pattison J, Ghai S, et al. Primary gastrointestinal lymphoma: spectrum of imaging findings with pathologic correlation. Radiographics 2007;27:1371–1388 Levine MS, Rubesin SE, Pantongrag-Brown L, Buck JL, Herlinger H. Non-Hodgkin’s lymphoma of the gastrointestinal tract: radiographic findings. AJR Am J Roentgenol 1997;168(1):165–172

CASE 97 Clinical Presentation A 45-year-old Armenian man presents with 2 days of severe left upper abdominal pain and fever. He has had similar episodes every few months since childhood. Sometimes these episodes are associated with nausea and vomiting, but there is no associated diarrhea. The episodes usually last a few days and are self-limited. His past medical history is otherwise significant for remote appendectomy and small bowel obstruction with exploratory laparotomy and lysis of adhesions.

A

Fig. 97.1 (A) Axial and coronal CT at the time of initial presentation shows pericolonic and perienteric soft tissue inflammatory stranding in the left upper abdomen. (B) CT performed 2 months later shows mesenteric vascular engorgement, omental and mesenteric edema, and fluid in the left paracolic gutter. (continued)

B

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Fig. 97.1 (continued) (C) A third CT scan performed 2 months after the second scan shows right nephromegaly and new asymmetric right perirenal fat stranding; a 4 mm distal right ureteral stone was diagnosed (not shown). Notice the absence of inflammatory changes in the peritoneal cavity.

C

Radiologic Findings Axial and coronal computed tomography (CT) scans at the time of initial presentation (Fig. 97.1A) show pericolonic and perienteric soft tissue inflammatory stranding in the left upper abdomen. CT performed 2 months later (Fig. 97.1B) shows mesenteric vascular engorgement, omental and mesenteric edema, and fluid in the left paracolic gutter. A third CT scan performed 2 months after the second (Fig. 97.1C) image shows right nephromegaly and new asymmetric right perirenal fat stranding; a 4 mm distal right ureteral stone was diagnosed (not shown). Notice the absence of inflammatory changes in the peritoneal cavity.

Diagnosis Acute abdominal attack in familial Mediterranean fever

Differential Diagnosis • • • • • • • • •

Enterocolitis Infectious colitis Inflammatory colitis Ischemic colitis Acute appendicitis Small bowel obstruction Cholecystitis Renal colic Spontaneous bacterial peritonitis

Discussion Background Familial Mediterranean fever (FMF) is an autosomal recessive disease prevalent in ethnic groups originating in the Mediterranean area, mainly in Sephardic Jews, Arabs, Turks, and Armenians. The diagnosis of FMF is usually clinical because there are no specific imaging or laboratory tests, other than a molecular genetic test that is not widely available. It is usually a diagnosis of exclusion.

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Clinical Findings FMF represents repeated, self-limited episodes of fever and inflammation of synovial and serous surfaces, mainly of the peritoneum and joints. In 90% of cases, the first attack occurs before age 20. Patients usually experience no symptoms between attacks. An acute abdominal attack usually presents with severe, diffuse abdominal pain, rigidity, and fever, a clinical setting commonly defined as an “acute abdomen.”

Complications Complications of repeated abdominal attacks in patients with FMF include adhesive small bowel obstruction secondary to repeated peritonitis and previous exploratory laparotomies. The dreaded complication of repeated attacks of FMF is the development of amyloidosis, which is responsible for increased morbidity and eventual mortality of some patients. The prevalence of amyloidosis has been reported as high as 60% in certain populations with FMF, such as Turks.

Imaging Findings •

Imaging findings on computed tomography (CT) are engorged mesenteric vessels, thick mesenteric folds, and mesenteric and retroperitoneal lymphadenopathy. Ascites is a frequent finding. Changes related to focal peritonitis may be visible. Some patients may demonstrate splenomegaly. If there has been an adhesive small bowel obstruction, dilated small bowel loops will be visible on imaging.

Treatment •

Treatment includes conservative therapy to relieve pain and inflammation and intravenous hydration. Colchicine may be used on a daily basis as a preventive therapy. In the past, patients underwent exploratory laparotomy to exclude surgical emergencies, such as acute appendicitis and adhesive small bowel obstruction, although the era of cross-sectional imaging and the consideration of the possibility of this disease process in the proper setting may help prevent unnecessary surgery.

PE ARL



Radiologists should be familiar with CT findings of peritoneal irritation in patients with FMF during an acute attack and may suggest this clinical diagnosis in the proper clinical setting in patients who have not been previously diagnosed.

PITFALL



During clinical evaluation, it may be difficult to differentiate an attack of FMF from other acute abdominal conditions necessitating interventions, such as acute appendicitis and small bowel obstruction or, as in this case, urolithiasis. In these circumstances, imaging studies are useful for directing management. One would not want to assume that a patient’s presentation with an acute abdomen is due to the known FMF, as patients with FMF are also susceptible to the remainder of the spectrum of causes of abdominal pain.

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Suggested Readings Ishak GE, Khoury NJ, Birjawi GA, et al. Imaging findings of familial Mediterranean fever. Clin Imaging 2006;30:153–159 Matzner Y. Biologic and clinical advances in familial Mediterranean fever. Crit Rev Oncol Hematol 1995;18:197–205 Meyerhoff J. Familial Mediterranean fever. emedicine.com/med/TOPIC1410.HTM. Accessed August 29, 2007 Zissin R, Rathaus V, Gayer G, Shapiro-Feinberg M, Hertz M. CT findings in patients with familial Mediterranean fever during an acute abdominal attack. Br J Radiol 2003;76:22–25

CASE 98 Clinical Presentation A 59-year-old woman with a history of breast cancer presents with a complaint of abdominal pain and weight loss.

A

B

Fig. 98.1 (A,B) Upper gastrointestinal (GI) study shows a lobulated filling defect in the duodenal bulb (arrow). There is no wall irregularity. (C) CT scan performed in the same patient shows multiple rim-enhancing lesions in the liver, likely representing metastasis with central areas of necrosis. There is an enhancing mass in the antrum of the stomach (arrow). Given the appearance on the upper GI series and the CT appearance, the primary lesion is likely a pedunculated lesion arising from the antrum and herniating into the duodenal bulb.

C

Radiologic Findings Upper gastrointestinal (GI) study shows a lobulated filling defect in the duodenal bulb. Computed tomography (CT) scan performed in the same patient shows multiple rim-enhancing lesions in the liver, likely representing metastasis with central areas of necrosis. There is an enhancing mass in the antrum of the stomach (Fig. 98.1).

Diagnosis Pedunculated gastric carcinoid, type III (sporadic subtype)

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Differential Diagnosis • • • • •

Adenocarcinoma of the gastric antrum Lymphoma GI stromal tumor (GIST) Metastatic disease Giant pedunculated hyperplastic polyp

Discussion Background Carcinoids are relatively uncommon neoplasms, of which ~9% occur in the stomach. Gastric carcinoids are relatively less common than other gastric neoplasms, representing ~1.8% of all gastric malignancies. Three subtypes of enterochromaffin-like cell (ECL) carcinoids are recognized in the stomach. Type I is associated with autoimmune chronic atrophic gastritis, type II is associated with Zollinger-Ellison syndrome (ZES) and can be seen in patients with multiple endocrine neoplasia (MEN) type 1, and type III occurs sporadically. Type I is the most common in the stomach. Non-ECL gastric carcinoids are rare.

Clinical Findings Type I carcinoids are more frequent in women, with an average age of 60. They are found incidentally during endoscopy performed for dyspepsia or anemia related to chronic gastritis. Patients generally do not present with symptoms directly related to the carcinoid tumor. Type II carcinoids present equally in both genders, with a mean age of 50. Their pathogenesis is related to elevated levels of gastrin-stimulating ECL hyperplasia. In the setting of MEN type 1, multiple carcinoids can develop. Given that carcinoids are rarely seen in patients with isolated ZES, it is postulated that altered tumor suppression in MEN type 1 contributes to carcinoid tumor formation. Type III carcinoids occur more commonly in men, with an average age of 55. They are seen more commonly in the gastric body and fundus. They often demonstrate aggressive features, and metastatic spread is present in 50 to 70% of cases.

Complications In the absence of hepatic metastasis, carcinoid syndrome does not occur.

Imaging Findings •



Gastric carcinoids associated with chronic atrophic gastritis and ZES/MEN type 1 often present as multiple, well-marginated, variably sized (1–2 cm) mural masses located in the gastric body and fundus. Hypersecretions of gastric fluids may cause flocculations of barium and poor gastric mucosal coating. Type II carcinoids may present as numerous nodules with a diffusely thickened gastric wall. There may be multiple erosions and ulcers. On CT, numerous nodular mucosal and mural masses may be present. Gastric distention with neutral contrast media and scanning in the arterial and portal venous phase of contrast enhancement may maximize detection of the primary gastric lesion and possible hepatic metastasis. Differential considerations for type I and II include entities that produce multiple polypoid masses, as seen in familial adenomatous polyposis, Peutz-Jeghers syndrome, Cronkhite-Canada syndrome, Cowden disease, and multiple hyperplastic polyps; Kaposi sarcoma; and metastasis.

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Type III gastric carcinoids often present as large (> 2 cm) solitary mural masses in the body or fundus. They may be ulcerated. Given the malignant potential, patients should be screened for perigastric adenopathy as well as hepatic metastasis. Somatostatin-receptor scintigraphy is the study of choice in the management of patients with carcinoid tumors. Indium In 111 pentetreotide is the most commonly used agent, often to localize the primary tumor or stage the disease. Positron emission tomography has not been shown to be effective due to slow tumor growth and low cellular turnover.

Treatment and Prognosis • •



Type I gastric carcinoids are generally benign. Patients can be treated conservatively with endoscopic follow-up or partial gastric resection. Metastasis occurs in < 2% of patients. Type II gastric carcinoids are the least common and are prone to lymphatic metastasis. Tumorrelated deaths and carcinoid syndrome are rare. Treatment is not uniform. Gastrectomy, polypectomy, and treatment with somatostatin analogues have been reported. Type III is the most aggressive subtype, with a poor prognosis and ~20% survival in 5 years. In the absence of hepatic metastasis, total gastrectomy with en bloc resection of lymph nodes is recommended. Chemotherapy and antitumoral therapies are recommended when hepatic metastases are present.

PE ARL AND PITFALL



GI carcinoids have a diverse spectrum of clinical, pathologic, and radiologic appearances based on their origin within the GI tract.

Suggested Readings Binstock AJ, Johnson CD, Stephens DH, Lloyd RV, Fletcher JG. Carcinoid tumors of the stomach: a clinical and radiographic study. AJR Am J Roentgenol 2001;176:947–951 Halpert RD. Gastrointestinal imaging: the requisites. 3rd ed. St. Louis: CV Mosby; 2006 Levy AD, Sobin LH. From the archives of the AFIP. Gastrointestinal carcinoids: imaging features with clinicopathologic comparison. Radiographics 2007;27:237–257

CASE 99 Clinical Presentation Nonspecific abdominal pain

B

A

Fig. 99.1 Upper gastrointestinal series shows an outpouching (arrow) arising from the gastric fundus.

Radiologic Findings Upper gastrointestinal (GI) series shows an outpouching arising from the gastric fundus (Fig. 99.1).

Diagnosis Gastric fundal diverticulum

Differential Diagnosis • • •

Cystic adrenal, renal, or pancreatic lesions Necrotic lesions or abscess in cases where air–fluid levels are present Duplication cysts

Discussion Background Fundal diverticula are the most common gastric diverticula arising from the cardiofundic region. They are congenital and usually seen on the posterior wall of the stomach. These are true diverticula and contain all layers of the stomach wall; they are variable in size, ranging from 1 to 10 cm.

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Fig. 99.2 Axial CT image of the upper abdomen shows a contrast-filled fundal diverticulum (arrow).

Clinical Findings Patients are often asymptomatic. Some patients may present with intermittent pain, worse when supine.

Complications Usually these are asymptomatic; however, cases of bleeding and ulcerations exist. Patients may present with pain and abdominal discomfort. If diverticula are large, impaired emptying may occur. Additionally, the condition may lead to excessive work-up due to misinterpretation of a diverticulum as an adrenal mass.

Imaging Findings • •

Lateral view of a barium swallow and upper GI studies may demonstrate an outpouching on the posterior aspect of the gastric cardia, with a characteristic finding of a fundal diverticulum. Computed tomography may show a collection of contrast material arising from the posterior aspect of the gastric fundus. It usually projects in the retroperitoneal cavity. Occasionally, when poorly opacified with oral contrast, a fundal diverticulum may mimic an adrenal mass and is considered in the differential for an adrenal pseudomass (Fig. 99.2).

Treatment and Prognosis •

Treatment is conservative and expectant.

PE ARL



Classic appearance on barium studies

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PITFALL



When poorly filled with oral contrast or if collapsed, gastric fundal diverticula may mimic adrenal lesions.

Suggested Readings Bothen NF, Eklof O. Diverticula and duplications (enterogenous cysts) of the stomach and duodenum. Am J Roentgenol Radium Ther Nucl Med 1966;96:375–381 Halpert RD. Gastrointestinal Imaging: The Requisites. 3rd ed. St. Louis: CV Mosby; 2006 Schwartz AN, Goiney RC, Graney DO. Gastric diverticulum simulating an adrenal mass: CT appearance and embryogenesis. AJR Am J Roentgenol 1986;146:553–554

CASE 100 Clinical Presentation A middle-aged man with a recent history of a high-speed motor vehicle accident who underwent emergent open reduction and internal fixation of pelvic fractures presents months later with pelvic pain and fevers.

A

B

C

D

Fig. 100.1 (A) Supine abdominal radiograph shows screw and plate fixations of the patient’s pelvic fractures. Partially obscured by the orthopedic hardware is a radiodense ribbon at the level of the pubis (arrow). (B–D) Contrast-enhanced CT images show a right pelvic abscess collection (arrow) in the right obturator space that demonstrates an enhancing rind around a spongiform gas collection with mass effect on the rectum. (D) The radiodense ribbon is best seen on bone windows and is within the collection (curved arrow).

Radiologic Findings Supine abdominal radiograph shows screw and plate fixations of the patient’s pelvic fractures (Fig. 100.1A). Partially obscured by the orthopedic hardware is a radiodense ribbon at the level of the pubis. Contrast-enhanced computed tomography (CT) images show a right pelvic abscess collection in the right obturator space that demonstrates an enhancing rind around a spongiform gas collection with mass effect on the rectum. The radiodense ribbon is best seen on bone windows and is within the collection (Fig. 100.1B–D).

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Diagnosis Gossypiboma (textiloma or retained surgical sponge)

Differential Diagnosis Abscess as a complication of • • • • • •

Acute appendicitis Acute diverticulitis Surgery Perforated tumor or stercoral ulcer Tumor Hematoma

Discussion Background Laparotomy sponges are used to pack the exposed laparotomy wound to absorb hemorrhage and other body fluids and to help with hemostasis. The most common retained foreign body after surgery is the cotton laparotomy pad, a rectangular sponge with an integrated radiopaque tag, as is seen in this case. A retained surgical sponge is known as a gossypiboma, from the Latin gossypium for “cotton” and the Swahili boma for “place of concealment.” Retention of surgical swabs or sponges occurs in 1 in 100 to 5000 operations in the United States and is an important cause of malpractice claims.

Clinical Findings A retained sponge may be asymptomatic or may present with evidence of sepsis and abscess formation or gastrointestinal symptoms, such as bowel obstruction. Symptoms may present acutely or in a delayed manner.

Complications A retained sponge can lead to an aseptic granuloma with a surrounding fibrinous response that may be asymptomatic or to a more morbid exudative response with complications, such as abscess formation and sepsis, intraperitoneal adhesions, and fistula formation. Extrusion into the hollow viscera has been reported.

Etiology Despite careful attention by surgical teams, sponges are, on occasion, left in the abdomen and pelvis. A normal sponge count does not exclude the presence of a retained sponge.

Imaging Findings • •

Linear, spongiform, or whirl-like radiolucencies reflect gas trapped in the folds of the retained fabric on radiographs or CT; the body of the sponge itself is usually not detected. Many surgical sponges or swabs are labeled with radiopaque markers that will make them easier to detect. Tags, as in this case, may appear crenulated when inside the patient. Calcifications may form in chronic collections around surgical sponges.

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On contrast-enhanced CT, there is usually dense rim enhancement surrounding a low-density or complex mass in a patient with a history of surgery. On ultrasound, retained sponges are nonspecific in appearance and may be seen as complex collections or as echogenic and densely shadowing masses even in the absence of retained gas or calcifications. On magnetic resonance imaging, retained sponges have a variable appearance but usually resemble a soft tissue mass with a well-defined T1 and T2 hypointense enhancing capsule. They have a low-signal internal whorled appearance on T2 sequences.

Treatment •

Exploratory laparotomy and removal of the retained surgical sponge are indicated. Complications of retained sponges require appropriate management.

PE ARL S





Radiologists should be careful to investigate the presence of a surgical sponge on imaging, because too frequently sponges are inadvertently left inside patients. In addition, radiologists should be familiar with the imaging appearance of sponges used at their institutions. Radiopaque tags on retained sponges are often most easily seen on scout radiographs for CT scans due to beam hardening artifacts on the axial images.

PITFALL S

• •

On occasion sponges are intentionally left in a patient when a second-look operation is planned. Absorbable hemostatic sponges can mimic the appearance of an abscess.

Suggested Readings Hunter TB, Taljanovic MS. Medical devices of the abdomen and pelvis. Radiographics 2005;25: 503–523 Kim CK, Park BK, Ha H. Gossypiboma in abdomen and pelvis: MRI findings in four patients. AJR Am J Roentgenol 2007;189:814–817 Kokubo T, Itai Y, Ohtomo K, Yoshikawa K, Iio M, Atomi Y. Retained surgical sponges: CT and US appearance. Radiology 1987;165:415–418 O’Connor AR, Coakley FV, Meng MV, Eberhardt S. Retained surgical sponges in the abdomen and pelvis. AJR Am J Roentgenol 2003;180:481–489

CASE 101 Clinical Presentation A middle-aged patient complains of a palpable abdominal wall mass.

Fig. 101.1 Axial noncontrast CT image through the pelvis demonstrates a defect in the anterior abdominal wall, just lateral to the semilunar line. The sigmoid colon is seen herniating through this defect (arrow).

Radiologic Findings Axial noncontrast computed tomography (CT) image through the pelvis demonstrates a defect in the anterior abdominal wall, just lateral to the semilunar line. The sigmoid colon is seen herniating through this defect (Fig. 101.1).

Diagnosis Spigelian hernia

Differential Diagnosis Incisional hernia

Discussion Background Spigelian hernias are ventral hernias that occur at the intersection of the semilunar line and semicircular line. The lateral edge of the rectus muscles forms the semilunar line; the semicircular line is the point inferior to which only the transversalis fascia is posterior to the rectus abdominalis muscle.

Clinical Findings Spigelian hernias are well described in the literature but occur rarely. They can be difficult to diagnose clinically because the herniated contents can remain between the layers of muscle and fascia of the anterior abdominal wall.

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Complications Incarceration leading to infarction can occur.

Etiology The lack of a posterior sheath in this location creates an area of relative weakness.

Treatment • •

Surgical repair of the fascial defect is required once the diagnosis is made, as up to 20% will be incarcerated at diagnosis. Repair does not require prosthetic mesh, although it is being used by some now performing laparoscopic repair.

Prognosis •

Surgical repair has a good prognosis.

PE ARL



The location of this hernia is classic for spigelian hernias.

Suggested Readings Harrison L, Keesling CA, Martin NL, Lee KR, Wetzel LH. Abdominal wall hernias: review of herniography and correlation with cross-sectional imaging. Radiographics 1995;15:315–332 Palanivelu C, Vijaykumar M, Jani KV, Rajan PS, Maheshkumaar GS, Rajapandian S. Laparoscopic transabdominal preperitoneal repair of spigelian hernias. JSLS Journal of the Society of Laparoendoscopic Surgeons 2006;10:193–198

CASE 102 Clinical Presentation A 42-year-old woman presents with abdominal pain and fever 10 days after laparoscopic cholecystectomy for severe gangrenous cholecystitis with a gallbladder full of stones.

B

A

Fig. 102.1 (A–C) Axial CT images with oral and intravenous contrast demonstrate cholecystectomy clips. Caudal images show a subhepatic fluid collection with rim enhancement (arrow) and surrounding fat stranding containing four radiopaque gallstones (curved arrow).

C

Radiologic Findings Axial computed tomography (CT) images with oral and intravenous contrast demonstrate a subhepatic fluid collection with rim enhancement and surrounding fat stranding containing four radiopaque gallstones (Fig. 102.1).

Diagnosis Subhepatic abscess secondary to dropped gallstones

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Differential Diagnosis • • • •

Simple abscess Tumor Hematoma Biloma

Discussion Background Spillage of gallstones during laparoscopic cholecystectomy occurs in ~4 to 50% of cases. Complications from dropped stones are very rare and occur in only ~0.08 to 0.30% of patients.

Clinical Findings Clinical presentation is usually related to signs and symptoms of abdominal pain and infection. Patients may present as soon as 1 month to as long as 20 years after laparoscopic cholecystectomy.

Complications Complications of laparoscopic cholecystectomy include bile duct injury and bile and/or gallstone spillage. Late infections and abscess formation are uncommon complications of dropped gallstones.

Etiology Spillage of gallstones may occur during the dissection of the gallbladder from the liver bed or during extraction of the gallbladder from the abdominal wall port sites. A combination of multiple gallstones and infected bile increases the incidence of abscess formation.

Imaging Findings •



Cross-sectional imaging, including ultrasound, CT, and magnetic resonance, demonstrate an abscess collection containing gallstones or stone fragments generally confined to the subhepatic space or the retroperitoneum below the subhepatic space. Unusual locations have been reported, including the right thorax, the subphrenic space, the abdominal wall, and the site of incisional hernias.

Treatment •

Treatment consists of percutaneous drainage of the abscess followed by removal of the gallstones. If complete evacuation of all gallstones cannot be obtained with minimally invasive procedures, laparotomy may be necessary.

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Prognosis •

With complete evacuation of all of the gallstones after abscess drainage, the prognosis is excellent. Any retained stones can be a nidus for recurrent infection.

PE ARL S





A high index of suspicion is paramount in the correct diagnosis of spilled gallstone abscess. Radiologists should consider this diagnosis in patients with intra-abdominal abscess and a remote history of laparoscopic cholecystectomy. Identification of radiopaque stones within the abscess cavity on CT is diagnostic of this condition.

PITFALL



Failure to recognize radiopaque dropped gallstones in the abscess collection may lead to misdiagnosis of a simple abscess or tumor, which may lead to delay or inadequate treatment.

Suggested Readings Horton M, Florence MG. Unusual abscess patterns following dropped gallstones during laparoscopic cholecystectomy. Am J Surg 1998;175:375–379 Morrin MM, Kruskal JB, Hochman MG, Saldinger PF, Kane RA. Radiologic features of complications arising from dropped gallstones in laparoscopic cholecystectomy. AJR Am J Roentgenol 2000;174: 1441–1445 Rice DC, Memon MA, Jamison RL, et al. Long-term consequences of intraoperative spillage of bile and gallstones during laparoscopic cholecystectomy. J Gastrointest Surg 1997;1:85–90 Sathesh-Kumar T, Saklani AP, Vinayagam R, Blackett RL. Spilled gallstone during laparoscopic cholecystectomy: a review of the literature. Postgrad Med J 2004;80:77–79 Treotola SO, Lillemoe KD, Malloy PC, Osterman FA. Percutaneous removal of “dropped” gallstones after laparoscopic cholecystectomy. Radiology 1993;188:419–421

CASE 103 Clinical Presentation A 73-year-old woman presents with abdominal discomfort and flank pain.

Fig. 103.1 Coronal reformatted contrast-enhanced CT image show a heterogeneous, ill-defined mass in the left perinephric region surrounding the left kidney. The lesion shows areas of fat density and foci of calcifications adjacent to the left kidney.

Radiologic Findings Coronal reformatted, contrast-enhanced computed tomography (CT) image shows a heterogeneous, ill-defined mass in the left perinephric region surrounding the left kidney. The lesion shows areas of fat density and foci of calcifications adjacent to the left kidney (Fig. 103.1).

Diagnosis Dedifferentiated retroperitoneal liposarcoma

Differential Diagnosis • • • • •

Malignant fibrous histiocytoma Retroperitoneal lymphoma Metastases Retroperitoneal dermoid Infection (rare)

Discussion Background Liposarcoma is the second most common type of soft tissue sarcoma in adults and is most commonly seen in the 5th decade of life.

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Clinical Findings • • • • •

Abdominal fullness Flank pain Vomiting Abnormal renal function tests in patients with renal invasion Hematuria

Complications • •

Invasion of adjacent organs, mainly kidneys Metastases (very rare)

Etiology Unknown

Imaging Findings •

• •



On imaging, a retroperitoneal, large, ill-defined, heterogeneous, fat-containing mass with involvement of adjacent organs and bridging across the fascial planes is seen. Tumors are almost always large in size at presentation, and patients usually present with nonspecific symptoms. CT may show calcifications that are commonly nodular in configuration. Involvement of adjacent organs, mesenteric vessels, and renal vessels is common and should be carefully assessed at imaging. Contiguity with an adjacent organ remains an important issue for complete assessment because tumors tend to invade adjacent organs without any direct evidence of involvement on imaging. The presence of fat on CT and magnetic resonance imaging (MRI) helps in diagnosing the condition; however, macroscopic fat is not always present in liposarcomas (Fig. 103.2).

Fig. 103.2 Axial contrast-enhanced CT image in a different patient shows a hypoattenuating lesion with a thick enhancing capsule. The lesion is posterior to the kidney, compressing and displacing the kidney anteriorly. Because no discrete focus of macroscopic fat was seen, it was difficult to diagnose this lesion as liposarcoma; however, the lesion was found to be dedifferentiated liposarcoma on surgical pathology.

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Treatment •

Surgical resection of the tumor is the treatment of choice in patients without metastases. Contiguity with the kidneys necessitates nephrectomy in addition to resection of the primary neoplasm.

Prognosis •

The prognosis is worse in patients with renal involvement and vascular encasement of the aorta and/or inferior vena cava. However, in patients with surgically resectable liposarcoma without adjacent organ involvement, the prognosis remains excellent after treatment, although long-term follow-up imaging is important to detect recurrence.

PE ARL



Large, ill-defined, heterogeneous, fat-density retroperitoneal lesion

PITFALL



Lesions that do not demonstrate macroscopic fat on MRI and fat density on CT cannot be differentiated from other retroperitoneal sarcomatous lesions, necessitating a biopsy.

Suggested Readings Gupta AK, Cohan RH, Francis IR, Sondak VK, Korobkin M. CT of recurrent retroperitoneal sarcomas. AJR Am J Roentgenol 2000;174:1025–1030 Nishino M, Hayakawa K, Minami M, et al. CT and MR imaging findings with anatomic and pathologic diagnostic clues. Radiographics 2003;23:45–57

CASE 104 Clinical Presentation A 91-year-old man presents with abdominal pain and nausea.

A

B

C

D

Fig. 104.1 (A) Axial CT image of the abdomen shows multiple contrast-filled, dilated small bowel loops and a small mesenteric mass (arrow) with a surrounding desmoplastic reaction and an adherent small bowel loop, which demonstrates a circumferentially thickened wall and a narrowed lumen. (B–D) MR images of the abdomen in the same patient demonstrate the small mesenteric mass that is isointense to muscle on T1 and T2; linear bands radiate from the mass and cause retraction of the adjacent small bowel mesentery.

Radiologic Findings Computed tomography (CT) scan of the abdomen performed at the time of presentation demonstrates multiple dilated small bowel loops and a small mesenteric mass with a surrounding desmoplastic reaction and an adherent small bowel loop, which demonstrates a circumferentially thickened wall and a narrowed lumen. Magnetic resonance imaging (MRI) of the abdomen in the same patient demonstrates the small mesenteric mass is isointense to muscle on T1 and T2; linear bands radiate from the mass and cause retraction of the adjacent small bowel mesentery (Fig. 104.1).

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Diagnosis Small bowel carcinoid with mesenteric metastases

Differential Diagnosis • • • • • •

Primary mesenteric desmoid tumor Sclerosing mesenteritis (fibrosing mesenteritis) Metastatic disease from pancreatic, gastric, or colon cancer Other primary gastrointestinal (GI) malignancy (e.g., adenocarcinoma or GI stromal tumor) Lymphoma Endometriotic implant (in a woman)

Discussion Background Carcinoid tumors arise from neuroendocrine cells anywhere in the body but most frequently occur in the GI tract or bronchopulmonary system. They have variable potential for malignancy, and 20% of patients have metastases at the time of diagnosis. Metastatic disease occurs in 30 to 50% of all patients and may occur at any time, from diagnosis up to 20 years after presentation. The most frequent sites of metastatic disease from a carcinoid arising from the midgut are the liver and mesenteric lymph nodes. Midgut carcinoid tumors most often spread to the mesentery by direct extension, but they also occur by invasion of local lymphatic vessels. The primary intestinal carcinoid is often small and difficult to detect on CT, whereas a dominant mesenteric mass may be discovered first.

Clinical Findings and Complications Many patients are asymptomatic at the time of presentation. Other patients may present with nonspecific abdominal pain, a palpable abdominal mass, diarrhea, small bowel obstruction, or GI bleeding. Patients with liver metastases may experience carcinoid syndrome with episodic flushing, wheezing, and diarrhea. Elevated levels of serotonin or 5-hydroxytryptophan are found in the blood, and 5-hydroxyindoleacetic acid (5-HIAA) levels are elevated in the urine.

Etiology Neuroendocrine tumor arising from the enterochromaffin or Kulchitsky cells

Imaging Findings • •



On CT, mesenteric metastases appear as ill-defined enhancing soft tissue masses. Seventy percent of mesenteric metastases contain calcifications (Fig. 104.2). Low-attenuating, nonenhancing foci within the soft tissue mass may represent tumor necrosis and can produce a rimlike pattern of enhancement on CT and MRI. Linear, “fingerlike” radiating bands may be seen in the mesenteric fat with adjacent tethering of the small bowel. This represents a mesenteric desmoplastic reaction secondary to fibrosis and mesenteric ischemia caused by the release of serotonin by the tumor (Fig. 104.3). CT angiography reveals tethering, encasement, or occlusion of mesenteric vessels.

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Fig. 104.2 Axial contrast-enhanced CT image shows a

Fig. 104.3 Coronal reformatted CT image shows a

soft tissue mesenteric mass (arrow) with calcifications. Surrounding desmoplastic reaction is seen.

soft tissue mesenteric mass (arrow). There is accompanying desmoplastic reaction in the mesentery and small bowel ischemic changes.

• • •

MRI demonstrates a mesenteric mass that is T1 and T2 isointense to muscle with hypointense desmoplastic stranding. Mesenteric metastases are strongly positive on octreotide scintigraphy. A fluoroscopic examination or CT enteroclysis may show target lesions from ulceration of a submucosal tumor, thickening of mucosal folds, and tethering of small bowel loops.

Treatment •

A distal small bowel carcinoid with mesenteric metastases may be treated by surgical resection of bowel and mesentery often with a hemicolectomy. Proximal small bowel tumors are treated with pancreaticoduodenectomy. Many palliative options are also available, including cytotoxic agents, somatostatin analogues, and chemoembolization of liver metastases.

Prognosis •

Carcinoid tumors are relatively slow-growing neoplasms. Even in the presence of metastatic disease, patients may survive many years. The overall 5-year survival rate for all patients with a carcinoid tumor is ~70 to 80%.

PE ARL



Consider carcinoid with mesenteric metastases for any soft tissue mass arising within the small bowel mesentery with calcifications or a desmoplastic reaction.

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Mesenteric carcinoid metastases may present as a large, dominant mesenteric mass, and a primary tumor is often difficult to identify at CT. A close examination of the small bowel mucosa is recommended to evaluate for the presence of a small primary carcinoid tumor. Retractile mesenteritis cannot be distinguished from a carcinoid tumor or lymphoma by imaging alone, and biochemical analysis or histologic sampling is required to make the distinction.

Suggested Readings Levy A, Sobin L. From the archives of the AFIP. Gastrointestinal carcinoids: imaging features with clinicopathologic comparison. Radiographics 2007;27:237–257 Scarsbrook A, Ganeshan A, Statham J, et al. Anatomic and functional imaging of metastatic carcinoid tumors. Radiographics 2007;27:455–477 Sheth S, Horton K, Garland M, Fishman E. Mesenteric neoplasms: CT appearances of primary and secondary tumors and differential diagnosis. Radiographics 2003;23:457–473

CASE 105 Clinical Presentation A 28-year-old man presents with a relatively short history of constipation and urinary problems.

B

A

D C

E

F

Fig. 105.1 (A,B) Axial contrast-enhanced CT images demonstrate a large low-attenuation mass with coarse central calcifications located anterior to the urinary bladder. A subtle cortical defect is present in the left pubic symphysis where the mass abuts it (arrow). (C,D) Axial T1-weighted MR images demonstrate a large T1 hypointense mass causing mass effect on the urinary bladder. (E) The mass is heterogeneously bright on an axial T2 sequence and (F) demonstrates heterogeneous, predominantly peripheral enhancement on the fat-suppressed T1 postcontrast image.

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Radiologic Findings An axial contrast-enhanced computed tomography (CT) scan (Fig. 105.1A,B) demonstrates a large low-attenuation mass with coarse central calcifications located anterior to the urinary bladder. A subtle cortical defect is present in the left pubic symphysis where the mass abuts it. Axial T1-weighted magnetic resonance (MR) images (Fig. 105.1C,D) demonstrate a large T1 hypointense mass causing mass effect on the urinary bladder. The mass is heterogeneously bright on an axial T2 sequence and demonstrates heterogeneous, predominantly peripheral enhancement on the fat-suppressed T1 postcontrast image (Fig. 105.1E,F).

Diagnosis Juxtacortical chondrosarcoma mimicking a pelvic visceral mass

Differential Diagnosis •





Sarcoma  Malignant fibrous histiocytoma  Poorly differentiated liposarcoma  Leiomyosarcoma Bladder tumor  Urachal adenocarcinoma (mucinous type)  Rhabdomyosarcoma  Pheochromocytoma  Leiomyomas  Hemangioma Periosteal osteosarcoma and other tumors of bony origin

Discussion Background Chondrosarcoma is the third most common primary malignant bone tumor. About 4% of chondrosarcomas are juxtacortical chondrosarcomas that arise on the surface of bone and occur in adults in the 3rd to 4th decade. Because of a lack of symptoms, these lesions may be very large at the time of diagnosis and may mimic a soft tissue mass. They generally contain a chondroid matrix and metaplastic ossification.

Clinical Findings Patients present with nonspecific symptoms and signs and most commonly have a painless, palpable mass that is slow growing. Symptoms may be due to mass effect on adjacent organs.

Etiology Chondrosarcomas may occur primarily or result from malignant degeneration of osteochondromas or enchondromas.

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Imaging Findings • • •

The most suggestive radiographic finding of chondrosarcomas is a lytic lesion with chondroid matrix and mineralization in the form of rings and arcs. Aggressive features such as endosteal scalloping, cortical destruction, and soft tissue extension are best evaluated by CT scanning. Chondrosarcomas have high water content and therefore appear as low attenuation on CT and demonstrate high signal intensity on T2-weighted images on MRI. Enhancement is seen in the septa, with a ring and arc pattern.

Treatment •

Treatment is surgical and depends on the histologic grade of the tumor. An aggressive, wide surgical excision is necessary for high-grade tumors to prevent local recurrence and metastasis. Radiation and chemotherapy are used as adjunctive treatment for higher grade chondrosarcomas.

Prognosis •

The overall 5-year survival rates for chondrosarcoma are 90 to 94% (grade 1), 61 to 81% (grade 2), and 43 to 44% (grade 3). Dedifferentiated chondrosarcomas have the worst prognosis.

PE ARL



The presence of a chondroid matrix with mineralization in rings and arcs is highly suggestive of a chondrosarcoma.

PITFALL



Juxtacortical chondrosarcomas may mimic a soft tissue mass because they occur on the surface of bones and are usually very large at the time of diagnosis. Although malignant, chondrosarcomas may be well circumscribed and appear benign.

Suggested Readings Murphey MD, Walker EA, Wilson AJ, Kransdorf MJ, Temple HT, Gannon FH. From the archives of the AFIP. Imaging of primary chondrosarcoma: radiologic-pathologic correlation. Radiographics 2003;23:1245–1278 Varma DG, Ayala AG, Carrasco CH, Guo SQ, Kumar R, Edeiken J. Chondrosarcoma: MR imaging with pathologic correlation. Radiographics 1992;12:687–704

CASE 106 Clinical Presentation A 34-year-old man is evaluated for chest pain.

B

A

Fig. 106.1 (A–C) Axial CT images show a lobulated, lowattenuation mass, inferior to the body and tail of the pancreas without enhancement.

C

Radiologic Findings Axial computed tomography (CT) images reveal a lobulated, low-attenuation mass, inferior to the body and tail of the pancreas without enhancement (Fig. 106.1).

Diagnosis Retroperitoneal lymphangioma

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Differential Diagnosis • • • • •

Enteric duplication cyst Enteric cyst Mesothelial cyst Pancreatic pseudocyst Cystic leiomyoma or leiomyosarcoma

Discussion Background Approximately 95% of lymphangiomas are found in the neck and axilla. Other locations include the retroperitoneum, mesentery, omentum, mediastinum, and bone. Retroperitoneal lymphangiomas represent 1% of retroperitoneal neoplasms. They tend to grow and insinuate between organs.

Clinical Findings Retroperitoneal lymphangiomas are usually found in infancy because of symptoms, but they may be found as asymptomatic lesions in adults. Symptoms when present vary but can include a palpable mass, fever, nausea, and pain.

Complications • • •

Hemorrhage Infection Displacement of the kidneys

Etiology Lymphangiomas are congenital lesions that develop when there is a failure in the formation of normal connections within the lymphatic system.

Imaging Findings • • •

On ultrasound, lymphangiomas appear as anechoic, well-defined lesions with increased throughtransmission. Internal septa can be seen. On CT, lymphangiomas appear as multiloculated lesions with Hounsfield units ranging from near water to near fat, depending on their composition. On magnetic resonance imaging, they tend be isointense to slightly hypointense to muscle on T1-weighted images and appear hyperintense to fat on T2-weighted images.

Treatment •

Surgical excision

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Prognosis •

Complete surgical excision has a lower recurrence rate than aspiration or injection of a sclerosing agent.

PE ARL



Lymphangiomas can cross from one retroperitoneal compartment to another.

PITFALL



Lymphangiomas can measure near water density to near fat density.

Suggested Readings Davidson AJ, Hartman DS. Lymphangioma of the retroperitoneum: CT and sonographic characteristics. Radiology 1990;175:507–510 Mar CR, Pushpanathan C, Price D, Cramer B. Best cases from the AFIP: omental lymphagioma with a small bowel volvulus. Radiographics 2003;23:847–851 Yang DM, Jung DH, Kim H, et al. Retroperitoneal cystic masses: CT, clinical and pathologic findings and literature review. Radiographics 2004;24:1353–1365

CASE 107 Clinical Presentation A 46-year-old woman presents with a history of retroperitoneal liposarcoma status postresection.

A

B

Fig. 107.1 (A) Axial and (B) coronal contrast-enhanced CT images show a rounded, relatively homogeneous mass that measures water density by Hounsfield units in the retroperitoneal region adjacent to the left psoas muscle (arrow).

Radiologic Findings Axial and coronal contrast-enhanced computed tomography (CT) images show a rounded, relatively homogeneous mass that measures water density by Hounsfield units in the retroperitoneal region adjacent to the left psoas muscle (Fig. 107.1).

Diagnosis Metastatic liposarcoma with pseudocystic sign

Differential Diagnosis • • • • •

Seroma Retroperitoneal lymphocele Abdominal abscess Necrotic solid tumor Lymphangioma

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Discussion Background Liposarcoma is a malignancy of adipose cells. It is the most common primary retroperitoneal tumor and the second most common soft tissue sarcoma in adults. Liposarcomas make up 95% of all fatty retroperitoneal tumors. They are usually seen in patients ages 40 to 60 years and occur more commonly in men than in women.

Clinical Findings and Complications Liposarcomas are usually asymptomatic until they become large. Patients may present with abdominal pain due to impingement of neighboring structures by an enlarging mass. The tumor may come to attention if the patient has an episode of trauma in the region of the mass. Other symptoms are painful swelling, decreased motion, numbness, and weight loss.

Etiology There is no well-established causative factor, although trauma has been implicated. Rarely, liposarcomas arise from lipomas.

Imaging Findings •







Both CT and magnetic resonance imaging (MRI) can be useful for imaging liposarcomas. CT is better at assessing cortical bone erosion and tumor mineralization, whereas MRI is more effective at depicting the fatty nature of the tumor. Liposarcomas that are a mixture of fat and soft tissue can appear to be water density on CT due to volume averaging, commonly referred to as the pseudocystic pattern. Well-differentiated liposarcomas have a well-defined or lobulated border and are composed mainly of adipose tissue. Well-differentiated liposarcomas may show faint enhancement after intravenous contrast administration. As the grade of malignancy increases, contrast enhancement becomes more intense and heterogeneous. The noncontrast appearance of myxoid liposarcomas may be homogeneous or mildly heterogeneous. However, postcontrast, myxoid liposarcomas demonstrate moderate to marked heterogeneous enhancement. Pleomorphic liposarcomas are markedly heterogeneous both before and after contrast administration. Risk assessment can be done based on 18F-fluorodeoxyglucose positron emission tomography imaging for liposarcomas by determining the pretherapy standardized uptake values of the tumor. A maximum standardized uptake value of > 3.6 was found to be associated with significantly reduced disease-free survival.

Treatment •

A wide and deep surgical excision with radiation and/or chemotherapy for high-grade tumors should be performed. Liposarcoma is the most radiosensitive sarcoma (32% 5-year survival). Use of chemotherapy, however, remains experimental.

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Prognosis •

The well-differentiated type and most myxoid types have favorable prognoses, with 100 and 88% 5-year survival rates, respectively. They do, however, tend to recur even if completely excised. Poorly differentiated types have a poor prognosis, with a 5-year survival rate of ~50%.

PE ARL



The amount of lipomatous tissue in the tumor can help differentiate between well-differentiated and higher grade liposarcomas.

PITFALL



Liposarcomas that are a mixture of fat and soft tissue can appear to be water density on CT due to volume averaging.

Suggested Readings Pereira JM, Sirlin CB, Pinto PS, Casola G. CT and MR imaging of extrahepatic fatty masses of the abdomen and pelvis: techniques, diagnosis, differential diagnosis, and pitfalls. Radiographics 2005;25: 69–85 Sung MS, Kang HS, Suh JS, et al. Myxoid liposarcoma: appearance at MR imaging with histologic correlation. Radiographics 2000;20:1007–1019

CASE 108 Clinical Presentation A 60-year-old woman presents with abdominal discomfort.

Fig. 108.1 Axial CT image with oral and intravenous contrast demonstrates a hazy appearance to the mesentery with small mesenteric lymph nodes.

Radiologic Findings Axial computed tomography (CT) image with oral and intravenous contrast (Fig. 108.1) demonstrates a hazy appearance to the mesentery with small mesenteric lymph nodes.

Diagnosis Misty mesentery

Differential Diagnosis • • • • • •

Mesenteric panniculitis Malignancy, specifically non-Hodgkin lymphoma Inflammation due to processes such as inflammatory bowel disease and pancreatitis Infection Mesenteric edema/lymphedema Trauma and hemorrhage

Discussion Background The term misty mesentery refers to increased CT attenuation of the mesenteric fat caused by infiltration with fluid, inflammatory cells, tumor, or fibrosis.

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Clinical Findings Clinical findings may be nonspecific or secondary to the underlying condition. Findings may be incidental in an asymptomatic patient imaged for other reasons.

Etiology The increased CT attenuation may be the result of infiltration of the mesenteric fat by a variety of causes, depending on the underlying condition. Causes include fluid such as mesenteric edema due to hypoalbuminemic states, cirrhosis, inferior vena cava obstruction, Budd-Chiari syndrome, or lymphatic obstruction; hemorrhage; or inflammatory cells as in mesenteric panniculitis, tumor cells, and fibrosis.

Imaging Findings •

Misty mesentery refers to nonspecific increased CT attenuation of the mesenteric fat.

Treatment •

Close follow-up with CT is recommended to search for occult malignancy. Follow-up examinations may demonstrate resolution of the inflammatory condition. In cases of persistent misty mesentery with unknown cause, biopsy may be necessary for definitive diagnosis.

Prognosis •

The prognosis depends on the underlying condition.

PE ARL



Misty mesentery refers to increased CT attenuation of the mesenteric fat and is a nonspecific finding that may occur in a variety of clinical situations.

PITFALL



Failure to recognize misty mesentery on CT may lead to a delay in diagnosis and treatment of infiltrating neoplastic conditions.

Suggested Readings Horton KM, Lawler LP, Fishman EK. CT findings in sclerosing mesenteritis (panniculitis): spectrum of disease. Radiographics 2003;23:1561–1567 Mindelzun RE, Jeffrey RB, Lane MJ, Silverman PM. The misty mesentery on CT: differential diagnosis. AJR Am J Roentgenol 1996;167:61–65 Seo BK, Ha HK, Kim AY, et al. Segmental misty mesentery: analysis of CT features and primary causes. Radiology 2003;226:86–94 Sheth S, Horton KM, Garland MR, Fishman EK. CT appearance of primary and secondary tumors and differential diagnosis. Radiographics 2003;23:457–473

CASE 10 9 Clinical Presentation A middle-aged woman presents with abdominal pain and vomiting.

B

A

Fig. 109.1 (A–C) Axial and coronal contrast-enhanced CT scans show dilation of the small bowel, indicative of a mechanical obstruction. The obstruction is proximal to the herniated bowel loop, seen along the anterolateral pelvic wall between the pectineal and obturator externus muscles (arrows).

Radiologic Findings Axial and coronal contrast-enhanced computed tomography (CT) scans show dilation of the small bowel, indicative of a mechanical obstruction. The obstruction is proximal to the herniated bowel loop, seen along the anterolateral pelvic wall between the pectineal and obturator externus muscles (Fig. 109.1).

Diagnosis Small bowel obstruction secondary to obturator hernia

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C

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Differential Diagnosis Other causes of small bowel obstruction

Discussion Background Obturator hernias occur when the peritoneal sac and its contents protrude through the obturator canal. The hernia sac protrudes between the obturator externus and the pectineus muscle. These hernias may also be found between the superior and medial fasciculi of the obturator externus muscle or the external and internal obturator muscles.

Clinical Findings Obturator hernias are uncommon and difficult to diagnose. They typically occur in elderly, emaciated women with a history of prior pregnancies and in obese women who have undergone significant weight loss. Because this hernia is located deep within the abdominal wall musculature, a palpable inguinal mass is uncommon. Most patients complain of vague groin or abdominal pain, weight loss, or recurrent episodes of small bowel obstruction. Compression of the obturator nerve by the hernia sac produces the characteristic Howship-Romberg sign, in which compression of the obturator nerve results in pain along the ipsilateral medial thigh to the knee worsened by adduction, extension, or internal rotation of the thigh. On physical examination, the hernia sac may present as a tender, palpable mass if incarcerated. Obturator hernias are 6 times more common in women than men and are more often found on the right side. Other predisposing factors are chronic cough, chronic constipation, and ascites.

Complications Because these hernias are difficult to diagnose, appropriate surgical treatment is often delayed, and incarcerated bowel is common. Early diagnosis is important because of the advanced age and often debilitated condition of the affected population, with significant morbidity and mortality associated with this type of hernia.

Etiology This type of condition is an acquired defect in the obturator membrane that results in herniation of the peritoneal sac and its contents through the obturator canal.

Imaging Findings •

• •

Plain or barium-enhanced radiographs show a complete or partial small bowel obstruction and may demonstrate a fixed loop of bowel containing gas or contrast adjacent to the obturator canal or superior pubic ramus. CT scan shows the presence of a hernia sac protruding through the obturator foramen with extension between the pectineal and obturator muscles. These hernias most often contain a loop of ileum but may also contain other bowel loops, omentum, bladder, appendix, uterus, or adnexal tissue.

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Treatment •

Prompt surgical treatment is indicated to avoid bowel incarceration. The majority of patients require resection of strangulated small bowel.

Prognosis •

Obturator hernias have the highest reported mortality rate of all abdominal wall hernias, ranging from 12 to 70%.

PE ARL S

• • • •

Obturator hernias are most commonly found in multiparous, emaciated elderly women or in obese women with a significant weight loss. Obturator hernias should be considered in all elderly, debilitated women with small bowel obstructions and no history of prior abdominal surgery. The hernia sac most commonly protrudes between the obturator externus and the pectineus muscle. The Howship-Romberg sign occurs because of compression of the obturator nerve by the hernia sac, resulting in pain along the ipsilateral medial thigh to the knee worsened by adduction, extension, or internal rotation of the thigh.

PITFALL S

• •

The signs and symptoms of an obturator hernia are nonspecific, resulting in delayed preoperative diagnosis. Obturator hernias have the highest mortality rate of all abdominal wall hernias because of delayed diagnosis and resultant incarcerated small bowel.

Suggested Readings Aguirre DA, Santosa AC, Casola G, Sirlin CB. Abdominal wall hernias: imaging features, complications, and diagnostic pitfalls at multi-detector row CT. Radiographics 2005;25:1501–1520 Harrison LA, Keesling CA, Martin NL, Lee KR, Wetzel LH. Abdominal wall hernias: review of herniography and correlation with cross-sectional imaging. Radiographics 1995;15:315–332 Miller PA, Mezwa DG, Feczko PJ, Jafri ZH, Madrazo BL. Imaging of abdominal hernias. Radiographics 1995;15:333–347

CASE 110 Clinical Presentation A 48-year-old man complains of abdominal pain, severe bladder pressure, and pain with coughing for 2 years.

A

B

C

D

Fig. 110.1 (A–D) Axial and sagittal images of the abdomen and pelvis show a large, low-attenuating mass in the right lower quadrant of the abdomen extending into the pelvis with internal septations.

Radiologic Findings There is a large, low-attenuating mass in the right lower quadrant of the abdomen extending into the pelvis with internal septations (Fig. 110.1).

Diagnosis Multilocular mesothelial (peritoneal) inclusion cyst

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Differential Diagnosis • • • • •

Lymphangioma Ovarian cystadenoma/cystadenocarcinoma Cystic carcinoma Mesenteric-omental cyst Visceral cysts

Discussion Background Multiloculated mesothelial (peritoneal) inclusion cysts, or multicystic mesothelioma of the peritoneum, is a nonneoplastic proliferation of mesothelial cells lining the peritoneum, omentum, and abdominal and pelvic viscera with a predilection for surfaces of the pelvis. They usually occur in young to middle-aged women.

Clinical Findings Most patients are premenopausal women who present with pelvic or abdominal pain.

Etiology Multiloculated mesothelial (peritoneal) inclusion cysts usually develop in the setting of fluid secretion from active ovaries. The formation of cysts is facilitated by the presence of peritoneal adhesions, which accumulate fluid and cause reactive proliferation of mesothelial cells.

Imaging Findings •

Cross-sectional imaging demonstrates multilocular thin-walled cysts containing watery secretions. Internal septations may show enhancement on contrast-enhanced computed tomography or magnetic resonance imaging.

Treatment • • • •

Treatment is achieved by total surgical excision. Oral contraceptive treatment may be useful in suppressing fluid secretion from the ovaries. Radiation and chemotherapy are not effective. In rare cases, laparoscopic or open surgical excision of adhesions may be necessary.

Prognosis •

With surgical excision, the rate of recurrence is 30 to 50%.

PE ARL



Multilocular mesothelial (peritoneal) inclusion cysts are formed by the accumulation of peritoneal fluid inside peritoneal adhesions, which usually occur in premenopausal women. They may mimic cystic neoplasms, especially those of the ovaries. Preoperative diagnosis should be considered in the appropriate clinical setting.

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Suggested Readings Hoffer FA, Kozakewich H, Colodny A, Goldstein DP. Peritoneal inclusion cysts: ovarian fluid in peritoneal adhesions. Radiology 1988;169:189–191 Jain KA. Pictorial essay: imaging of peritoneal inclusion cysts. AJR Am J Roentgenol 2000;174: 1559–1563 Wong WL, Johns TA, Herlihy WG, Martin HL. Best cases from the AFIP: multicystic mesothelioma. Radiographics 2004;24:247–250

CASE 111 Clinical Presentation An 84-year-old woman presents with diarrhea and leukocytosis.

A

B

C

D

Fig. 111.1 (A–D) Axial and coronal images from a contrast-enhanced CT show an enlarged appendix filled with soft tissue density material and concentric calcifications. There is no significant soft tissue stranding in the surrounding mesentery. Additionally, there are coarse, rounded calcifications within the lymph nodes adjacent to the appendix.

Radiologic Findings Axial and coronal images from a contrast-enhanced computed tomography (CT) scan show an enlarged appendix filled with soft tissue density material and concentric calcifications. There is no significant soft tissue stranding in the surrounding mesentery. Additionally, there are coarse, rounded calcifications within the lymph nodes adjacent to the appendix (Fig. 111.1).

Diagnosis Porcelain appendix secondary to an appendiceal mucocele

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Differential Diagnosis •

• • •

Mucocele of the appendix  Nonneoplastic occlusion of the appendix (e.g., appendicolith)  Benign neoplasm (e.g., mucinous cystadenoma)  Malignant neoplasm (e.g., mucinous cystadenocarcinoma) Chronic tubercular or pyogenic abscess Porcelain gallbladder Degenerated leiomyoma

Discussion Background Epithelial neoplasms of the appendix are less common than carcinoid tumors. Most epithelial neoplasms occur in middle-aged or older adults and tend to be mucinous rather than nonmucinous, unlike the epithelial tumors elsewhere in the colon. The term mucocele refers to an appendix that has filled with mucinous material either due to an obstruction from a nonneoplastic cause or a benign or malignant mucinous tumor of the appendix. When curvilinear calcifications form around the mucocele, it is referred to as a porcelain appendix.

Clinical Findings Appendiceal mucoceles from benign neoplasms are generally asymptomatic and may be found incidentally on physical examination as a palpable mass or by an imaging study. Symptomatic patients may present with acute appendicitis, intussusception, torsion, or right ureteral obstruction.

Complications Appendiceal mucoceles may become superinfected and present with appendicitis. Rupture of a benign or malignant mucocele results in accumulation of gelatinous material in the peritoneal cavity and is called pseudomyxoma peritonei. In the case of a benign mucocele, only a localized collection develops. However, rupture of a malignant mucocele results in diffuse pseudomyxoma peritonei with proliferation of malignant cells and spread of gelatinous material throughout the peritoneal cavity.

Imaging Findings • • •

The diagnosis of a porcelain appendix may be suggested by an abdominal radiograph when a soft tissue mass with curvilinear calcifications is seen in the right lower quadrant. A contrast enema will show a smooth impression on the medial aspect of the cecum. CT scans may be useful in identifying the cause of the porcelain appendix as well as in assessing for complications, such as superinfection and the development of pseudomyxoma peritonei.

Treatment • • •

Treatment is surgical excision to eliminate malignant potential and prevent complications. Because of the risk of rupture and peritoneal extension, a laparoscopic approach is not recommended. Appendectomy is sufficient for cystadenomas when the appendiceal base is intact, but cecal resection is recommended for cystadenomas with a large base. Cystadenocarcinomas require a hemicolectomy.

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Prognosis •

Patients with a simple or benign neoplastic mucocele have a 5-year survival rate of 91 to 100%. However, patients with diffuse pseudomyxoma peritonei have an unrelenting course with a 5-year survival rate of only ~65%.

PE ARL



When curvilinear calcifications are seen in the region of the appendix on an abdominal radiograph, a porcelain appendix should be considered.

PITFALL



Excessive manipulation of the appendiceal mucocele should be avoided during colonoscopy or surgery to prevent rupture and development of pseudomyxoma peritonei.

Suggested Readings Persaud T, Swan N, Torreggiani WC. Giant mucinous cystadenoma of the appendix. Radiographics 2007;27:553–557 Pickhardt PJ, Levy AD, Rohrmann CA Jr, Kende AI. Primary neoplasms of the appendix: radiologic spectrum of disease with pathologic correlation. Radiographics 2003;23:645–662

CASE 112 Clinical Presentation A 55-year-old woman presents with a 2-month history of abdominal discomfort, anorexia, and frequent bowel movements after being treated for rectal carcinoma.

B

A

Fig. 112.1 (A,B) Axial images from a contrast CT scan show thickening pelvic small bowel loops with loss of normal folds. (C) Small bowel barium series demonstrates deep ulcers in the small bowel, mucosal edema, and strictures.

C

Radiologic Findings Axial images from a contrast-enhanced computed tomography (CT) scan show thickening pelvic small bowel loops with loss of normal folds. A small bowel barium series demonstrates deep ulcers in the small bowel, mucosal edema, and strictures (Fig. 112.1).

Diagnosis Radiation enteritis

Differential Diagnosis • •

Bacterial enteritis Inflammatory bowel disease

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Discussion Background Portions of the gastrointestinal tract that are in the field of external beam radiation can be affected acutely or chronically. The small bowel is the most radiosensitive abdominal organ. Within the small bowel, the ileum is the most commonly affected portion, as it is the least mobile segment. Factors affecting the development of radiation enteritis include small body size, prior surgery or inflammatory conditions causing adhesions, hypertension, diabetes, and combination chemotherapy.

Clinical Findings Hyperemia, edema, and inflammation of the submucosa are seen acutely. The subacute phase, defined as 2 to 12 months postradiation, demonstrates partial tissue regeneration and also arteriolar obliteration. Progressive fibrosis of the bowel wall marks the late stage, which can also include adhesion and fistula formation. The development of radiation enteritis is related to the radiation dose.

Complications • • •

Diarrhea Malabsorption Abnormal peristalsis

Etiology Related to radiation treatment of adjacent organs

Imaging Findings • •

Barium studies performed during the acute and subacute stages can show thumbprinting and nodular filling defects. Chronic-stage radiation enteritis can show wall thickening, strictures, adhesions, and fistulas.

Treatment • •

Typically, medical treatment of diarrheal symptoms and dietary adjustment suffice. Up to 10% of patients who have had 5000 rad of radiation require surgical intervention to treat the complications of radiation enteritis.

Prognosis •

Acute radiation enteritis symptoms usually resolve over 2 to 3 weeks, whereas chronic radiation enteritis symptoms may persist.

PE ARL



History of prior radiation, with distinct demarcation of abnormality (edge of the radiation field).

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PITFALL



May be difficult to differentiate from inflammatory bowel disease and ischemic colitis.

Suggested Readings Capps GW, Fulcher AS, Szucs RA, Turner MA. Imaging findings of radiation-induced changes in the abdomen. Radiographics 1997;17:l455–l473 Brant WE, Helms CA. The Brant and Helms Solution: Fundamentals of Diagnostic Radiology. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 1990

CASE 113 Clinical Presentation A 35-year-old woman with a past history of Hodgkin lymphoma presents with right-sided abdominal pain.

A

B

Fig. 113.1 (A) A noncontrast CT scan shows a large, asymmetrically dumbbell-shaped mass arising from a right neural foramen at a superior lumbar level. The mass measures soft tissue attenuation and causes widening of the right neural foramen. (B–E) On MRI, the mass is homogeneously hypointense to muscle on T1, predominantly hyperintense on T2, and demonstrates intense, heterogeneous enhancement after the administration of gadolinium. Coronal imaging confirms that the mass arises from a neural foramen and superiorly displaces the right kidney. (continued)

C

Radiologic Findings A noncontrast computed tomography (CT) scan shows a large, asymmetrically dumbbell-shaped mass arising from a right neural foramen at a superior lumbar level. The mass measures soft tissue attenuation and causes widening of the right neural foramen. On magnetic resonance imaging (MRI), the mass is homogeneously hypointense to muscle on T1, predominantly hyperintense on T2, and demonstrates intense, heterogeneous enhancement after the administration of gadolinium. Coronal imaging confirms that the mass arises from a neural foramen and superiorly displaces the right kidney (Fig. 113.1).

Diagnosis Retroperitoneal schwannoma (also known as a neurilemoma or neurinoma)

Differential Diagnosis •

Neurofibroma

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D

E

Fig. 113.1 (continued)

• • • • •

Lateral meningocele Paraspinal abscess Sympathetic ganglion tumor (ganglioneuroma) Metastasis or recurrence of lymphoma Soft tissue sarcoma

Discussion Background Schwannomas are benign tumors arising from peripheral nerves. They may occur anywhere in the body but are most often found along spinal or sympathetic nerve roots in the head or neck and flexor surfaces of the upper and lower extremities. The posterior mediastinum and retroperitoneum are other common locations. Schwannomas are usually < 5 cm in size; however, retroperitoneal schwannomas are often larger at presentation, as they grow slowly over a long period of time before detection. The majority of spinal nerve root schwannomas are intradural extramedullary lesions and are most commonly found in the thoracic spine.

Clinical Findings Schwannomas occur in young to middle-aged adults. Most tumors are asymptomatic and may be found incidentally. They are usually solitary, slow-growing entities with benign features. The presence of multiple schwannomas may be seen with neurofibromatosis 2 (NF2). Schwannomatosis is a condition in which patients demonstrate multiple schwannomas without additional clinical features of NF2.

Complications Large spinal nerve root schwannomas may cause neurologic symptoms, such as radicular pain and parasthesias.

Etiology A schwannoma is a benign neurogenic tumor arising from peripheral nerve sheaths.

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Imaging Findings •





On CT imaging, schwannomas are well-circumscribed, rounded masses associated with a peripheral nerve. They may demonstrate cystic degeneration, hemorrhage, or, less commonly, calcification. In spinal nerve root schwannomas, the neural foramen and interpedicular distance may be widened and the pedicle thinned. Large lesions may be seen to expand the central canal. MRI characteristics of schwannomas depend on the type of tissue that they contain. Schwannomas containing myxoid tissue will appear hyperintense on T2, whereas those containing cellular tissue will appear hypointense on both T1- and T2-weighted images. Those schwannomas with solid fibrous tissue will enhance on contrast-enhanced CT and MRI. Inadequate blood supply to the center of a schwannoma will result in degeneration, resulting in the target sign, in which lesions demonstrate a T2 hypointense center with a hyperintense rim. The fascicular sign also may be seen, reflecting the presence of fascicular bundles within a peripheral nerve sheath tumor.

Treatment •

Complete surgical resection of the schwannoma and the involved peripheral nerve root is recommended.

Prognosis • •

Schwannomas are slow-growing tumors, and malignant degeneration is uncommon. Recurrence is rare in patients with solitary lesions; however, new lesions may develop in patients with NF2.

PE ARL S

• •

A well-circumscribed, dumbbell-shaped mass that expands the neural foramen and demonstrates enhancement is highly suspicious for a schwannoma. The majority of spinal schwannomas are solitary lesions. Multiple lesions occur with NF2.

PITFALL S

• •

If NF2 is suspected, the entire neuraxis should be scanned to rule out the presence of additional lesions. It is not possible to distinguish a schwannoma from a neurofibroma by imaging characteristics.

Suggested Readings Beaman FD, Kransdorf MJ, Menke DM. Schwannoma: radiologic-pathologic correlation. Radiographics 2004;24:1477–1481 Nishino M, Hayakawa K, Minami M, Yamamoto A, Ueda H, Takasu K. Primary retroperitoneal neoplasms: CT and MR imaging findings with anatomic and pathologic diagnostic clues. Radiographics 2003;23:45–57 Rha SE, Byun JY, Jung SE, Chun HJ, Lee HG, Lee JM. Neurogenic tumors in the abdomen: tumor types and imaging characteristics. Radiographics 2003;23:29–43

CASE 114 Clinical Presentation An 80-year-old man presents with abdominal pain, distention, and vomiting.

Fig. 114.1 (A) Axial and (B) coronal CT images show multiple dilated loops of the small bowel/jejunum filled with contrast. There is an oval-shaped mixed density bezoar in a loop of distal jejunum (arrows) distal to which the loops of the small bowel are decompressed.

A

B

Radiologic Findings Axial and coronal computed tomography (CT) images show multiple dilated loops of the small bowel/ jejunum filled with contrast. There is an oval-shaped mixed density lesion in a loop of distal jejunum to which the loops of the small bowel are decompressed (Fig. 114.1).

Diagnosis Mechanical small bowel obstruction secondary to phytobezoar

Differential Diagnosis Other foreign bodies, such as ingested packets of illegal drugs or gallstones

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Discussion Background Bezoars of the small bowel are uncommon, but they usually result from ingestion of a significant amount of high-fiber vegetables or fruits. In recent years, there has been an increased incidence of phytobezoars in patients who have undergone gastric outlet surgery to treat gastroduodenal peptic ulcer disease.

Clinical Findings Patients often present with abdominal pain, nausea, and vomiting. Complete bowel obstruction at the level of the jejunum or proximal ileum is the most common clinical presentation.

Complications Perforation and abscess formation

Imaging Findings •

CT findings include an intraluminal mass outlined by fluid contained in the small bowel. There is a heterogeneous and mottled appearance of the mass secondary to pockets of air contained in the interstices. This may appear similar to small bowel fecalization seen in cases of severe small bowel obstruction.

Treatment and Prognosis •

Acute, complete, and high-grade obstruction requires immediate surgery. Partial obstruction can be managed conservatively. Strangulation constitutes an emergency, given the risk of ischemia.

Suggested Readings Boudiaf M, Soyer P, Terem C, Pelage JP, Maissiat E, Rymer R. CT evaluation of small bowel obstruction. Radiographics 2001;21:613–624 Furukawa A, Yamasaki M, Furuichi K, et al. Helical CT in the diagnosis of small bowel obstruction. Radiographics 2001;21:341–355

CASE 115 Clinical Presentation A 30-year-old man presents with a 1-day history of emesis and diarrhea.

A

B

Fig. 115.1 (A–C) Axial, (D,E) coronal, and (F,G) sagittal images of the abdomen and pelvis show a tubular structure arising from the distal small bowel (arrows) filled with gas and particulate material. There is accompanying soft tissue stranding seen surrounding this structure.

C

Radiologic Findings Axial, coronal, and sagittal images of the abdomen and pelvis show a tubular structure arising from the distal small bowel filled with gas and particulate material. There is accompanying soft tissue stranding seen surrounding this structure (Fig. 115.1).

Diagnosis Perforated Meckel diverticulum

Differential Diagnosis • • •

Acute appendicitis Crohn disease Ileal diverticulitis

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E

F

G

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Fig. 115.1 (continued)

• •

Foreign body perforation Perforated neoplasm

Discussion Background Meckel diverticulum is the most common congenital abnormality of the gastrointestinal tract seen with a slight male predominance. The rule of 2s in Meckel diverticulum is 2% prevalence, 2 feet from the ileocolic valve, and 2 inches in length.

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Clinical Findings Patients who present with Meckel diverticulitis are most often clinically suspected of having acute appendicitis and may present with symptoms suggestive of acute appendicitis.

Complications The total lifetime complication rate of a Meckel diverticulum is ~4%. Complications include •



• • • •

Bowel obstruction (35%)  Especially in adults  Secondary to omphalomesenteric band, internal hernia, or volvulus through or around vitelline duct remnants Hemorrhage (32%)  Especially in children  Secondary to heterotopic gastric mucosa Diverticulitis (22%) Umbilical fistula (10%) Littre hernia: Meckel diverticulum entrapped in an inguinal hernia Neoplasms

Etiology A Meckel diverticulum represents a true diverticulum that contains all three layers of the intestinal wall and arises from the antimesenteric border of the small bowel. This diverticulum forms as a result of incomplete closure of the intestinal end of the omphalomesenteric duct, which connects the primitive midgut to the yolk sac during embryonic development.

Imaging Findings • •



Patients with Meckel diverticulum may be imaged with nuclear medicine techniques as well as by computed tomography (CT) scans. Nuclear medicine pertechnetate “Meckel’s” scan is an accurate technique that yields positive results only in the presence of ectopic gastric mucosa and has an overall diagnostic accuracy of 90% in these patients. This test is most useful in children and has a positive predictive value of only 60% in the adult population. A Meckel diverticulum may be shown at small bowel follow-through examination; however, sensitivity for visualizing the diverticulum is increased by performing enteroclysis. The CT appearance of the inflamed diverticulum varies considerably. The diverticulum may appear as a blind-ending pouch that contains fluid and air or particulate material with absence of oral contrast material. The inflamed diverticula may also show mural enhancement.

Treatment •

Definitive treatment of a complication, such as a bleeding Meckel diverticulum, is the excision of the diverticulum along with the adjacent ileal segment.

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Prognosis •

Generally good if promptly identified and treated

PE ARL



Tubular structure arising from distal small bowel: suspect Meckel diverticulum

PITFALL



May be difficult to identify if not inflamed

Suggested Readings Gardner-Thorpe J, Hardwick RH, Carroll NR, Gibbs P, Jamieson NV, Praseedom RK. Adult duodenal intussusception associated with congenital malrotation. World J Gastroenterol 2007;13:3892–3894 Wasike R, Saidi H. Perforated Meckel’s diverticulitis presenting as a mesenteric abscess: case report. East Afr Med J 2006;83:580–584

CASE 116 Clinical Presentation A teenage boy presents with recurrent upper abdominal pain for several days after beginning a new exercise routine.

B

A

Fig. 116.1 (A,B) Contrast-enhanced axial CT images demonstrate a well-circumscribed fatty lesion anterior to the stomach (arrows). The lesion shows central fat density with internal wisps of soft tissue density and surrounding inflammatory soft tissue stranding.

Radiologic Findings Contrast-enhanced axial computed tomography (CT) images demonstrate a well-circumscribed fatty lesion anterior to the stomach. The lesion shows central fat density with internal wisps of soft tissue density and surrounding inflammatory soft tissue stranding. The absence of adjacent gastric wall thickening is a pertinent negative finding (Fig. 116.1).

Diagnosis Focal omental infarction

Differential Diagnosis • • • • •

Mesenteric lipodystrophy (a subset of sclerosing mesenteritis) Acute epiploic appendagitis (EA) Acute diverticulitis Fat necrosis associated with pancreatitis Liposarcoma

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Discussion Background The greater omentum, which is composed of a double layer of peritoneum, originates from the greater curvature of the stomach and extends anteroinferiorly to drape over the transverse colon. It has a variable length of 15 to 36 cm. “Omental infarct” actually represents only a segmental infarction of the greater omentum; infarction of the entire omentum has not been reported. Following an insult, the classic pathologic findings of infarction develop, including vascular congestion or thrombosis, tissue necrosis, inflammatory cell aggregation, and hemorrhage. The majority of omental infarction occurs in the right aspect of the omentum.

Clinical Findings Approximately 85% of cases occur in adults and 15% in the pediatric population. Most patients present with acute abdominal pain. Classically, there is focal tenderness, and the pain localizes to the right abdomen (upper or lower quadrant). Because of this localization, the presentation can mimic appendicitis, ulcer disease, or cholecystitis. Elevation of the white blood cell count or fever is unusual.

Complications Serious complications of omental infarct are rare. However, the inflammatory response may heal with resultant intraperitoneal adhesions, which can secondarily cause bowel obstructions. Reactive ascites is not common in omental infarction; however, superinfection and abscess formation have been reported.

Etiology Omental infarct likely represents the sequelae of multiple etiologies. These etiologies lead to decreased perfusion to the omentum. Physical torsion or direct trauma of the omentum can cause stenosis or kinking of the arterial supply or venous drainage of the omentum. Anomalous or congenitally stenosed arterial supply has also been suggested. Kinking of the veins has also been hypothesized due to increased intra-abdominal pressure. The most frequent etiology may be thrombosis of the omental draining veins whether from a hypercoagulable state or direct injury with resultant venous congestion and infarct. Predisposing clinical factors include abdominal trauma or surgery, obesity, strenuous activity (a form of trauma), congestive heart failure, and digitalis use.

Imaging Findings •

Acute nonspecific and focal right abdominal pain is overwhelmingly evaluated with CT or, in the pediatric age group, also with ultrasound. The omental infarction appears as a fatty lesion in the anterior peritoneum. As in the case depicted, it has both internal and surrounding soft tissue density inflammatory stranding. Because the omentum arises from the stomach and is intimately

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associated with the peritoneal portions of the colon, the infarct often appears to be involving the serosa of the colon or stomach. Although reactive thickening of the adjacent bowel has been reported, it is atypical. If the omental infarct occurs in a region of colon containing a diverticulum, definitive differentiation of these two entities by imaging may not be possible. Diverticulitis is statistically more common in the descending and sigmoid colon, whereas omental infarcts are traditionally seen anterior to the transverse and ascending colon. EA also presents as an inflammatory fatty mass intimately associated with the colonic wall. The characteristic central hyperdense focus of EA may be a helpful discriminating factor, as it is not seen with infarcts. Omental infarcts can be quite large in size, 10 cm or more in maximal diameter, whereas it is unusual for EA to present with > 5 cm of inflammatory change. A true distinction between EA and omental infarct may not be clinically relevant because management is with expectant pain treatment for both.

Treatment •



The mainstay is symptomatic treatment of the patient’s pain, usually with nonsteroidal antiinflammatory medications. Antibiotics are not routinely administered. Some pediatric surgeons advocate laparoscopic resection of the inflammatory mass for quicker pain relief, although this recommendation is not universal. If, as mentioned above, the omental infarct occurs in the location of adjacent diverticulosis and differentiation from diverticulitis is not possible, appropriate antibiotic coverage may be indicated.

Prognosis • •

The complications listed above are generally rare; therefore, prognosis for this benign entity is excellent. Most patients’ symptoms resolve without further problems or recurrence. Dedicated follow-up imaging is not needed when the initial clinical and imaging presentation is classic. If imaging is done for other reasons, the infarct may show healing with a small resultant mixed fatty-fibrous focus and/or dystrophic calcification.

PE ARL S AND PITFALL S

• •

Focal omental infarction is a benign process that, on clinical presentation, can mimic acute appendicitis, cholecystitis, or diverticulitis. CT imaging is usually diagnostic and obviates surgical intervention, as complications are rare. When the omental infarct occurs in the setting of diverticulosis, antibiotic therapy and follow-up imaging may be prudent to avoid false-negative diagnosis of diverticulitis, a mimic of omental infarction.

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Suggested Readings Grattan-Smith JD, Blews DE, Brand T. Omental infarction in pediatric patients: sonographic and CT findings. AJR Am J Roentgenol 2002;178:1537–1539 Pickhardt PJ, Bhalla S. Unusual nonneoplastic peritoneal and subperitoneal conditions: CT findings. Radiographics 2005;25:719–730 Singh AK, Gervais DA, Hahn PF, Sagar P, Mueller PR, Novelline RA. Acute epiploic appendagitis and its mimics. Radiographics 2005;25:1521–1534 Sompayrac SW, Mindelzun RE, Silverman PM, Sze R. The greater omentum. AJR Am J Roentgenol 1997;168:683–687

CASE 117 Clinical Presentation A 30-year-old woman complains of abdominal swelling.

A

B

C

D

Fig. 117.1 (A) Contrast-enhanced axial image shows a moderately enhancing homogeneous lesion in the muscular compartment of the anterior abdominal wall. (B) Noncontrast axial T1-weighted image shows a well-defined midline anterior abdominal wall lesion isointense to muscles in the muscular compartment. (C) Axial T2-weighted image shows a welldefined midline anterior abdominal wall lesion isointense to muscles. (D) Contrast-enhanced coronal T1-weighted image shows an avidly enhancing, well-defined, midline anterior abdominal wall lesion.

Radiologic Findings Postcontrast computed tomography (CT) scan and pre- and postcontrast magnetic resonance imaging (MRI) show a well-defined homogeneously enhancing lesion in the anterior abdominal wall musculature in the midline that is isodense and isointense to muscles (Fig. 117.1).

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Diagnosis Anterior abdominal wall desmoid tumor (aggressive fibromatosis)

Differential Diagnosis • • • • • • •

Malignant soft tissue sarcoma Benign myositis ossificans Arteriovenous malformation Extranodal lymphoma Fibrosarcoma Malignant fibrous histiocytoma Metastatic deposits (usually lung carcinoma)

Discussion Background Desmoid tumor is a benign neoplasm, composed of spindle cells, that arises in musculotendinous tissues (anterior abdominal wall and shoulder musculature most commonly). It commonly affects postpartum women, is locally aggressive, and does not metastasize to distant organs, which is why it is termed benign. In children, desmoid tumors occur in association with familial adenomatous polyposis (FAP) syndrome in 10 to 15% of patients. In Gardner syndrome, desmoid tumors occur with gastrointestinal polyps, which are premalignant multiple osteomas, epidermoid cysts, and other soft tissue tumors. Desmoid tumors in association with FAP occur more frequently in the areas of prior surgery. Intra-abdominal desmoid tumors tend to be more aggressive than superficial ones and grow larger in size by the time of clinical presentation.

Clinical Findings A painless lump in the anterior abdominal wall is the classic presenting symptom in cases of abdominal wall desmoids. The clinical presentation of an intra-abdominal desmoid depends on the degree of invasion of the surrounding viscera. Presenting symptoms include changes in bowel habits, pain, and rectal bleeding.

Complications The invasion of surrounding organs as a result of the locally aggressive nature of desmoid tumors leads to intestinal obstruction, neurovascular deficit, and bleeding. The invasion of surrounding neurovascular structures also makes surgical resection of the tumor more difficult.

Etiology The etiology of desmoid tumors is unknown. Possible causes include surgical trauma and endocrine factors (because they are more commonly seen in postpartum women and tend to regress during menopause and with oral contraceptive use).

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Imaging Findings • • •

Ultrasound shows a homogeneous hypoechoic, rounded, lobulated lesion in the muscle plane elevating the fascia covering it. CT shows a homogeneously enhancing mass iso- to hypodense to the muscle. MRI shows a homogeneous avidly enhancing iso- to hyperintense mass on T1-weighted images and hyperintense and heterogeneous on T2-weighted and short T1 inversion recovery images. Hypointense bands seen on all sequences are characteristic of desmoid tumors.

Treatment •

The treatment of choice for a desmoid tumor is surgical excision with normal margins. Radiotherapy, tamoxifen, and interferon-␣ are other treatment options; they are thought to reduce the rate of recurrence and are important in cases with neurovascular invasion by the tumor.

Prognosis •

The recurrence rate after surgical resection is 25 to 65%, higher in young patients. Desmoid tumors reach a “plateau phase,” after which they cease to grow. In such cases, a less aggressive therapeutic approach is advisable.

PE ARL



The location of the lesion on MRI is suggestive of this diagnosis.

PITFALL



Although MRI findings are characteristic, they are not specific for desmoid tumor. Biopsy confirmation is frequently necessary for confirmation of the diagnosis.

Suggested Readings Desmoid Tumor Research Foundation Web site. Available at: http://www.dtrf.org. Accessed September 2, 2007 Ferenc T, Sygut J, Kopczynski J, et al. Aggressive fibromatosis (desmoid tumors): definition, occurrence, pathology, diagnostic problems, clinical behavior, genetic background. Pol J Pathol 2006;57(1):5–15 Mitchell G, Thomas JM, Harmer CL. Aggressive fibromatosis: evidence for a stable phase. Sarcoma 1998;2:149–154 Lee JC, Thomas JM, Phillips S, Fisher C, Moskovic E. Aggressive fibromatosis: MRI features with pathologic correlation. AJR Am J Roentgenol 2006;186(1):247–254

CASE 118 Clinical Presentation A 73-year-old woman presents with abdominal discomfort and flank pain.

Fig. 118.1 Coronal reformatted contrast-enhanced CT image shows a heterogeneous, ill-defined mass in the left perinephric region surrounding the left kidney. The lesion shows areas of fat density and foci of calcifications adjacent to the left kidney.

Radiologic Findings Coronal reformatted contrast-enhanced computed tomography (CT) image shows a heterogeneous, ill-defined mass in the left perinephric region surrounding the left kidney. The lesion shows areas of fat density and foci of calcifications adjacent to the left kidney (Fig. 118.1).

Diagnosis Dedifferentiated retroperitoneal liposarcoma

Differential Diagnosis • • • • •

Malignant fibrous histiocytoma Retroperitoneal lymphoma Metastases Retroperitoneal dermoid Infection (rare)

Discussion Background Liposarcoma is the second most common type of soft tissue sarcoma in adults and is most commonly seen in the 5th decade of life.

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Clinical Findings • • • • •

Abdominal fullness Flank pain Vomiting Abnormal renal function tests in patients with renal invasion Hematuria

Complications • •

Invasion of adjacent organs, mainly kidneys Metastases (very rare)

Etiology Unknown

Imaging Findings •

• •



Seen on imaging is a retroperitoneal large, ill-defined, heterogeneous fat-containing mass with involvement of adjacent organs and bridging across the fascial planes. Tumors are almost always large in size at presentation, and patients usually present with nonspecific symptoms. CT may show calcifications that are commonly nodular in configuration. The involvement of adjacent organs, mesenteric vessels, and renal vessels is common and should be carefully assessed at imaging. Contiguity with an adjacent organ remains an important issue for complete assessment because tumor tends to invade adjacent organs without any direct evidence of involvement on imaging. The presence of fat on CT and magnetic resonance imaging (MRI) helps in diagnosing the condition; however, macroscopic fat is not always present in liposarcomas (Fig. 118.2).

Treatment • •

Surgical resection of the tumor is the treatment of choice in patients without metastases. Contiguity with kidneys necessitates nephrectomy in addition to resection of the primary neoplasm.

Fig. 118.2 Axial contrast-enhanced CT image in a different patient shows a hypoattenuating lesion with a thick enhancing capsule. The lesion is posterior to the kidney, compressing and displacing the kidney anteriorly. Because no discrete focus of macroscopic fat was seen, it was difficult to diagnose this lesion as liposarcoma; however, the lesion was found to be dedifferentiated liposarcoma on surgical pathology.

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Prognosis •

The prognosis is worse in patients with renal involvement and vascular encasement of the aorta and/or inferior vena cava. However, in patients with surgically resectable liposarcoma without adjacent organ involvement, the prognosis remains excellent after treatment, although long-term follow-up imaging is important to detect recurrence.

PE ARL



Large retroperitoneal mass, which is ill-defined, heterogeneous, and has fat density.

PITFALL



Lesions that do not demonstrate macroscopic fat on MRI and fat density on CT cannot be differentiated from other retroperitoneal sarcomatous lesions, necessitating biopsy.

Suggested Readings Gupta AK, Cohan RH, Francis IR, Sondak VK, Korobkin M. CT of recurrent retroperitoneal sarcomas. AJR Am J Roentgenol 2000;174:1025–1030 Nishino M, Hayakawa K, Minami M, et al. CT and MR imaging findings with anatomic and pathologic diagnostic clues. Radiographics 2003;23:45–57

CASE 119 Clinical Presentation A 64-year-old woman presents with vague abdominal pain.

A

B

Fig. 119.1 (A) Axial contrast-enhanced CT image shows retroperitoneal fat and stranding passing through an abdominal wall defect (arrows) in the left flank. (B,C) There is soft tissue density from fat necrosis (arrow) seen within the herniated fat.

C

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images show retroperitoneal fat and stranding passing through an abdominal wall defect in the left flank. There is soft tissue density seen within the herniated fat (Fig. 119.1).

Diagnosis Lumbar hernia of Grynfeltt through the superior lumbar triangle

Differential Diagnosis • •

Lipoma Inferior lumbar hernia (Petit hernia)

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Discussion Background Grynfeltt is a hernia through the superior lumbar (Grynfeltt) triangle. Inferior and superior lumbar hernias may be congenital (20%) or acquired (80%). Congenital hernias are discovered in infancy and are due to defects in the musculoskeletal system. Acquired lumbar hernias can be primary or secondary. Primary lumbar hernias (55% of all lumbar hernias) are spontaneous, without a causal factor, such as surgery, infection, or trauma. Risk factors for primary lumbar hernias are age, extremes of body habitus, quick weight loss, chronic disease, muscular atrophy, chronic bronchitis, wound infection, postoperative sepsis, and strenuous physical activity. Herniation through the superior lumbar triangle, also known as the Grynfellt triangle, is more common. The superior lumbar triangle is defined by the quadratus lumborum muscle medially, the 12th rib superiorly, and the internal oblique muscle laterally. The floor of the triangle is the transversalis fascia and the aponeurosis of the transversalis muscle of the abdomen. The roof of the triangle is the external oblique and latissimus dorsi muscles.

Clinical Findings Lumbar hernias may contain the small or large bowel, mesentery, omentum, stomach, ovary, spleen, or kidney. Patients with lumbar hernias can present with a variety of symptoms, including a posterolateral mass, back pain, bowel obstruction (if contents contain bowel), and urinary obstruction (if contents are renal).

Complications • • •

Bowel herniation and strangulation Abscess formation Herniation of retroperitoneal structures

Imaging Findings •



Typically present on the left, superior lumbar hernias are best seen on CT when containing retroperitoneal structures or bowel. They may present as protrusions of structures through the posterior abdominal wall into the subcutaneous tissues. Stranding of the fat may reflect strangulation of the blood supply of the herniated structures, requiring surgical repair.

Treatment and Prognosis •

Lumbar hernias will gradually enlarge and lead to symptoms ranging from low back pain to bowel strangulation with significant associated morbidity. About 25% of lumbar hernias have incarcerated bowel. All lumbar hernias require surgical repair.

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Suggested Readings Aguirre DA, Casola G, Sirlin C. Abdominal wall hernias: MDCT findings. AJR Am J Roentgenol 2004;183:681–690 Killeen KL, Girard S, DeMeo JH, Shanmuganathan K, Mirvis SE. Using CT to diagnose traumatic lumbar hernia. AJR Am J Roentgenol 2000;174:1413–1415

VIII Bladder CASE 120 Clinical Presentation A 65-year-old man presents with suprapubic pain.

Fig. 120.1 Noncontrast axial CT image in the supine position demonstrates a calcified round stone in the dependent location of the bladder.

Fig. 120.2 Postcontrast image in the same patient obtained in the prone position demonstrates a change in the position of this stone, which is freely mobile within the bladder lumen.

Radiologic Findings Noncontrast axial computed tomography (CT) image in the supine position demonstrates a calcified round stone in the dependent portion of the bladder (Fig. 120.1). Additional postcontrast imaging obtained in the prone position demonstrates a change in the position of this stone, which is freely mobile within the bladder lumen (Fig. 120.2).

Diagnosis Bladder stone

Differential Diagnosis • •

Bladder tumor Blood clot

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Discussion Background Most urinary bladder calculi develop primarily within the bladder, but some may initially form within the kidneys and subsequently pass into the bladder, where additional deposition of crystals may cause the stones to grow. The most common types of stones in adults are composed of calcium oxalate or calcium phosphate. Vesical calculi may be single or multiple, especially in the presence of bladder diverticula. Vesical calculi can be small or large enough to occupy the entire bladder. They span the spectrum from being soft to extremely hard and from having smooth-faceted surfaces to jagged spiculated surfaces.

Clinical Findings Patients with bladder calculi may be completely asymptomatic. More commonly, however, patients report suprapubic pain, dysuria, intermittency, nocturia, frequency, hesitancy, and gross hematuria.

Complications Complications include recurrent infections, acute urinary retention, suprapubic pain, and significant gross hematuria.

Etiology Bladder outlet obstruction remains the most common factor leading to the development of bladder calculi in adults. Also, patients who have urinary stasis and develop urinary infections have a tendency to form bladder stones. Foreign bodies in the bladder may act as nidus for stone formation.

Imaging Findings • •

• • • •

Bladder stones may be visualized with radiography, excretory urography, ultrasound, and CT. On radiography, bladder stones vary from very dense to radiolucent and should lie in the midline of the bladder lumen with the patient supine. Bladder stones identified on plain film not lying in the midline may lie within a bladder diverticulum. Depending on their composition, bladder stones may be completely obscured on excretory urography or seen as filling defects. Ultrasound demonstrates bladder stones as echogenic foci with acoustic shadowing even if they are radiolucent. CT shows all bladder calculi as highly dense regardless of their composition. Imaging the patient in the prone and supine position is a highly specific method, as it demonstrates the mobility of the stones.

Treatment •

The only potentially effective medical treatment for bladder calculi is urinary alkalinization for the dissolution of uric acid stones. Small bladder stones can be removed by cystoscopy. Larger stones must be crushed using lithotripsy, and very large stones are removed surgically.

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Fig. 120.3 Postcontrast image in the same location as Fig. 120.2 fails to show the stone due to improper window level and width setting. PE ARL



The presence of a calcified mobile mass in the bladder is diagnostic of a bladder stone (Fig. 120.2).

PITFALL



The presence of dense contrast material in the bladder or improper window level and width when visualizing the contrast-filled bladder can sometimes obscure visualization of the calculus (Fig. 120.3).

Suggested Readings Dunnick RN. The urinary bladder. In: Dunnick RN, Amis SE, Sandler CM, Newhouse CM, eds. Textbook of Uroradiology. 4th ed. Philadelphia: Lippincott Williams & Wilkins, 352–393

CASE 121 Clinical Presentation A 72-year-old diabetic woman presents with a 3-day history of abdominal pain and dysuria.

B

A

Fig. 121.1 (A–C) Axial noncontrast CT images through the AQ3 pelvis demonstrate gas within the wall of the urinary bladder. Gas is also present within the lumen of the bladder.

C

Radiologic Findings Axial noncontrast computed tomography (CT) images through the pelvis demonstrate gas within the wall of the urinary bladder (Fig. 121.1). Gas is also present within the lumen of the bladder.

Diagnosis Emphysematous cystitis

Differential Diagnosis • •

Gas in the bladder wall:  None Gas in the lumen of the bladder:  Recent instrumentation  Bladder fistula (vesicovaginal, colovesical, enterovesical)  Trauma

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Discussion Background Emphysematous cystitis represents a rare form of acute inflammation of the bladder mucosa and underlying musculature. Underlying poorly controlled diabetes mellitus is present in over half of the reported cases, with women being affected twice as often as men. Other predisposing conditions are neuropathic bladder, immunosupression, and chronic in-dwelling urinary catheters. A contributing factor is bladder outlet obstruction. The gas, a mixture of carbon dioxide and hydrogen, is initially formed in the bladder wall, which may then rupture into the bladder lumen.

Clinical Findings Dysuria, increased urinary frequency, and hematuria are common. The presence of pneumaturia is a rare although more specific finding.

Etiology Most often the infection is caused by Escherichia coli, although other bacterial pathogens, including Clostridium and fungal species, are occasionally identified.

Imaging Findings • •

Conventional radiography characteristically shows curvilinear or mottled areas of radiolucency conforming to the wall of the urinary bladder separate from more posterior rectal gas. CT is a highly sensitive modality that allows detection of intraluminal or intramural gas.

Treatment •

Treatment for emphysematous cystitis involves broad-spectrum antimicrobial therapy, satisfactory urinary drainage, and control of hyperglycemia.

Prognosis •

Emphysematous cystitis almost always responds rapidly to appropriate antibiotic therapy and control of underlying diabetes. It does not progress to a chronic condition.

PE ARL



Gas within the bladder wall is pathognomonic of infection with gas-forming organisms.

PITFALL



Gas in the lumen of the bladder can sometimes mimic intramural gas. Careful attention should be paid to the presence of gas in the dependent portions of the bladder wall, as this is a very specific sign of emphysematous cystitis.

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Suggested Readings Grayson DE, Abbott RM, Levy AD, Sherman PM. Emphysematous infections of the abdomen and pelvis: a pictorial review. Radiographics 2002;22:543–561

CASE 122 Clinical Presentation A 53-year-old man, an immigrant from the Middle East, presents with hematuria.

Fig. 122.1 Noncontrast image through the pelvis demonstrates diffuse circumferential calcification (arrow) in the wall of the bladder.

Fig. 122.2 Noncontrast image through the lower abdomen demonstrates circumferential calcification (arrows) in the wall of the ureters.

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Fig. 122.3 (A) The circumferential wall calcification is difficult to see following contrast administration. (B) There is accompanying mild dilatation of the ureters and left hydronephrosis.

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Radiologic Findings Noncontrast images through the pelvis demonstrate diffuse circumferential calcification in the wall of the bladder and both ureters (Figs. 122.1 and 122.2). There is mild dilatation of the ureters and left hydronephrosis (Fig. 122.3), but urinary bladder volume is preserved.

Diagnosis Schistosomiasis

Differential Diagnosis • • • • •

Tuberculosis Radiation cystitis Cytoxan cystitis Amyloidosis Squamous cell carcinoma of the bladder

Discussion Background Schistosomiasis is one of the most common parasitic infections in the world and is seen in Africa and the Middle East, but is most prevalent in the Nile Valley. The disease typically involves the bladder. The infected snails release cercariae into the water, which penetrate human skin and enter systemic circulation, becoming schistosomula. They eventually reach the vesical venous plexus, where their eggs produce a severe granulomatous reaction.

Clinical Findings Patients typically present with hematuria due to cystitis and urethritis. In the initial stages, the bladder mucosa is edematous and hemorrhagic. In advanced disease, the bladder becomes fibrotic with a reduced volume and calcified wall.

Complications The most serious complication of urinary tract schistosomiasis is increased incidence of squamous cell carcinoma of the bladder. Other complications are urolithiasis, ascending urinary tract infection, vesicoureteral reflux, urethral and ureteral stricture with subsequent hydronephrosis, and renal failure.

Etiology Schistosoma haematobium

Imaging Findings •

Calcifications in the wall of the bladder can be identified on plain radiographs; however, computed tomography (CT) better delineates the extent of these calcifications. Calcification of the distal ureter may be seen but is rarely present without bladder involvement. Ureteral strictures can be found as the disease progresses. The ureterovesical junction may be partially obstructed by the changes in the bladder wall, resulting in ureteral dilatation.

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Treatment •

Treatment of urinary tract schistosomiasis involves mainly two drugs: praziquantel and metrifonate. The diagnosis is made by the microscopic identification of eggs in the urine or by bladder wall biopsy.

Prognosis •

If treated early, the prognosis is very good, and complete recovery is expected.

PE ARL



Although there are other causes of bladder calcification, none are as common or as dramatic as schistosomiasis. A bladder tumor should be suspected when follow-up studies show an absence of wall calcification in areas that were previously calcified.

PITFALL



CT obtained with intravenous contrast may obscure the presence of bladder calcifications (Fig. 122.3).

Suggested Readings Dunnick, RN. Urinary bladder. In: Dunnick RN, Amis SE, Sandler CM, Newhouse JH. Textbook of Uroradiology. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 352–393

CASE 123 Clinical Presentation A 77-year-old man presents with right scrotal swelling and urinary retention.

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Fig. 123.1 (A–F) Axial noncontrast CT images of the pelvis show herniation of the urinary bladder into the right inguinal canal with nearly the entirety of the bladder herniated into the scrotum.

Radiologic Findings Axial and coronal noncontrast computed tomography (CT) images show herniation of the urinary bladder into the right inguinal canal with nearly the entirety of the bladder herniated into the scrotum (Fig. 123.1).

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Diagnosis Urinary bladder hernia

Differential Diagnosis •

Cystocele

Discussion Background One to 3% of all inguinal hernias involve the urinary bladder. Most bladder hernias involve the inguinal and femoral canals, although herniation through ischiorectal, obturator, and other abdominal wall defects has also been described. Herniation of the bladder can be within a true hernia sac; however, bladder herniation is most commonly paraperitoneal in location, with the bladder remaining extraperitoneal and medial to a true inguinal hernia sac.

Clinical Findings Most bladder hernias are asymptomatic and discovered incidentally. Patients may sometimes present with swelling in the inguinal region or scrotum that increases as the urinary bladder fills. Patients may experience nonspecific symptoms, such as dysuria, frequency, urgency, and nocturia; those individuals with large hernias may experience two-stage micturition, with manual compression of the herniated bladder needed to complete voiding.

Complications Complications of bladder herniation can lead to upper tract obstruction. Bladder strangulation, infarction, and perforation can also occur. Urinary calculi and tumors have been described within bladder hernias. Damage to the herniated urinary bladder has been described as a complication of herniorrhaphy.

Etiology A variety of factors can contribute to the development of bladder hernias. Among these are the presence of urinary outlet obstruction causing chronic bladder distention often in the setting of prostatism, loss of bladder tone with weakness of supporting structures, obesity, and the presence of space-occupying pelvic lesions.

Imaging Findings • •

Bladder herniation can usually be seen when the bladder is filled with contrast medium during excretory urography or retrograde cystography. CT and magnetic resonance imaging (MRI) will demonstrate pointing of the bladder toward the side of the hernia. With larger hernias, one is able to follow the bladder down into the inguinal or femoral canal. Even in the absence of contrast medium in the herniated bladder, identification of its wall surrounding unopacified urine can suggest the diagnosis. CT and MRI can demonstrate the relationship of the hernia to the inferior epigastric vessels, thus classifying the lesion as direct or indirect according to its position (medial or lateral, respectively) in relation to the vascular landmarks.

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Diagnostic criteria for ultrasound are the presence of a fluid-filled sac in the groin or scrotum that can be followed to join the intra-abdominal portion of the bladder, a beaked appearance of its cranial aspect, and changes in volume after micturition.

Treatment •

Herniorrhaphy is recommended for patients with bladder hernias due to potential complications if the hernia is left untreated.

PITFALL



Retrograde cystography is usually considered the best technique to image a bladder hernia. However, with this examination the lesion can become visible only during voiding, when increased intravesical pressure allows the contrast medium to enter or, as an alternative explanation, if herniation occurs only during the voiding phase. Herniation is best demonstrated on upright views.

Suggested Readings Bacigalupo EL, Michele Bertolotto M, Barbiera F, et al. Imaging of urinary bladder hernias. AJR Am J Roentgenol 2005;184:546–551 Reed Dunnick. Urinary bladder. In: Dunnick RN, Amis SE, Sandler CM, Newhouse JH (eds.) Textbook of Uroradiology. 4th ed. Philadelphia: Lippincott Williams & Wilkins: 352–393

CASE 124 Clinical Presentation A 46-year-old woman presents with hematuria.

Fig. 124.1 Delayed contrast-enhanced axial CT image through the bladder demonstrates a smooth, fat-containing polypoid mass (arrow) arising from the posterior bladder wall.

Radiologic Findings Delayed contrast-enhanced axial computed tomography (CT) image through the bladder demonstrates a smooth, fat-containing polypoid mass arising from the posterior bladder wall (Fig. 124.1).

Diagnosis Lipoma of the urinary bladder

Differential Diagnosis On cystography and intravenous (IV) urography: • • • • •

Transitional cell carcinoma Leiomyoma Hemangioma Paraganglioma Neurofibroma On magnetic resonance imaging (MRI) and CT: no differential diagnosis, findings are pathognomonic.

Discussion Background Bladder lipoma is a benign bladder tumor containing well-encapsulated fatty tissue within the submucosa of the bladder wall. To date, very few cases of bladder lipoma have been reported.

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Clinical Findings Patients with bladder lipoma are usually asymptomatic or have symptoms related to urinary infection. Microhematuria can also occur.

Complications Hematuria has been described due to ulceration of overlying mucosa.

Etiology Unknown

Imaging Findings • •

On IV urography and cystography, a bladder lipoma is seen as a nonspecific filling defect in the bladder wall that cannot be differentiated from other bladder tumors. Imaging with CT and MRI demonstrates macroscopic fat within this lesion, which is diagnostic of bladder lipoma.

Treatment •

If symptomatic, bladder lipoma can be removed cystoscopically.

Prognosis •

Malignant degeneration or local recurrence of bladder lipoma has not been reported.

PE ARL



Tumor containing macroscopic fat in the bladder wall is diagnostic of a lipoma.

PITFALL



Very few lesions can mimic a bladder lipoma, and the presence of fat in a submucosal lesion is virtually pathognomonic of this entity.

Suggested Readings Eggener SE, Hairston J, Rubenstein JN, Gonzalez CM. Bladder lipoma. J Urol 2001;166(4):1395 Lang EK. Symptomatic bladder lipomas. J Urol 2005;174(1):313 Meraj S, Narasimhan G, Gerber E, Nagler HM. Bladder wall lipoma. Urology 2002;60(1):164

CASE 125 Clinical Presentation A 59-year-old man presents with painless gross hematuria.

Fig. 125.1 Noncontrast CT image through the pelvis shows a polypoid lesion (arrow) arising from the left posterior wall of the bladder.

Radiologic Findings Noncontrast computed tomography (CT) image through the pelvis shows a polypoid lesion arising from the left posterior wall of the bladder (Fig. 125.1).

Diagnosis Transitional cell carcinoma of the bladder

Differential Diagnosis • • • • • • • • •

Primary bladder cancer Malignant mesenchymal tumors (leiomyosarcoma, rhabdomyosarcoma) Benign mesenchymal tumors (leiomyoma, paraganglioma, papilloma) Blood clot Prostatic enlargement Infection (tuberculosis, schistosomiasis) Hematoma Lymphoma Metastatic disease

Discussion Background Bladder cancer is ranked as the fourth most common malignancy in the United States. Transitional cell carcinoma accounts for 90% of cases and has a propensity to be multicentric with synchronous and metachronous bladder and upper tract tumors. Multicentric bladder tumors occur in 30 to 40%

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Fig. 125.2 Contrast-enhanced CT image of the pelvis shows multiple enhancing lesions (arrows) arising from the lateral bladder wall.

of cases (Fig. 125.2). Upper tract tumors occur in 3 to 5% of bladder tumor cases and are seen most frequently when multiple bladder lesions are present.

Clinical Findings Gross hematuria is the most common presenting sign, although microscopic hematuria may be detected at urinalysis. Patients may also experience voiding symptoms, such as frequency and dysuria, or pelvic pain and pressure.

Complications The morbidity of untreated bladder cancer includes hematuria, dysuria, urinary symptoms, urinary retention, incontinence, ureteral obstruction, and pelvic pain.

Etiology There is a well-established association between transitional cell carcinoma and chemical carcinogens. Smoking also represents a major risk factor. Less common malignancies of the urinary bladder, such as squamous cell carcinoma and adenocarcinoma, occur in the setting of chronic bladder infection and irritation.

Imaging Findings •



The imaging work-up for gross hematuria and suspected urothelial tumors has shifted from excretory urography to cross-sectional modalities, with CT as the primary imaging modality for cancer of the urinary bladder. Optimally, rapid scanning is performed in the nephrographic phase before excreted intravenous contrast material reaches the bladder. Thus, the enhancing tumor can be visualized against a background of low-attenuation urine within the bladder (Fig. 125.3). On delayed scanning, the lesion appears as a mural nodule or nodular thickening of the bladder wall against a background of high-attenuation contrast material within the bladder (Fig. 125.4). The mass may appear as asymmetric wall thickening of the opacified bladder (Fig. 125.5). Five percent of transitional cell carcinomas contain calcifications.

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Fig. 125.3 Contrast-enhanced CT image of the pelvis shows a nodular enhancing mass (arrow) arising from a bladder diverticulum. The enhanced mass is seen against a background of unopacified urine.

• •

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Fig. 125.4 Multicenteric bladder cancer. Multiple nodules are seen against a background of opacified urine. There is a high-density calcification (arrow) present in one of the nodular tumors.

Cross-sectional imaging modalities add the ability to screen for lymphatic or disseminated metastasis (Fig. 125.6). The presence of hydronephrosis is important to note, as this finding represents a poor prognostic sign.

Treatment •



Superficial tumors are treated with cystoscopic resection followed by close urologic monitoring for recurrences. Radical cystectomy and urinary diversion are reserved for invasive cancer. In the appropriate clinical setting, bladder sparing surgery can be performed. Systemic chemotherapy is used for local recurrence after surgery or to palliate metastatic disease.

Fig. 125.5 Contrast-enhanced CT image of the pelvis shows asymmetric thickening and enhancement of the left bladder wall (arrow).

Fig. 125.6 Contrast-enhanced CT shows a diffuse bladder wall tumor in a collapsed bladder. An enhancing metastatic lymph node (arrow) is seen along the right pelvic side wall.

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Prognosis •

The pathologic stage is the most important predictor of survival. Superficial bladder cancer has a good prognosis, with 5-year survival rates of 82 to 100%. The 5-year survival rate decreases with increasing stage; patients in the T4 stage have a 0 to 22% survival rate at 5 years.

PITFALL



Enhancement, density, and nondependent location of a bladder mass help differentiate it from a calculus, blood clot, or foreign body.

Suggested Readings Kundra V, Silverman PM. Imaging in the diagnosis, staging, and follow-up of cancer of the urinary bladder. AJR Am J Roentgenol 2003;180:1045–1054 Wong-You-Cheong JJ, Woodward PJ, Manning MA, Sesterhenn IA. Neoplasms of the urinary bladder: radiologic-pathologic correlation. Radiographics 2006;26:553–580

CASE 126 Clinical Presentation A 47-year-old asymptomatic woman

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Fig. 126.1 (A–E) Sequential axial contrast-enhanced CT images through the pelvis show a midline, well-defined soft tissue mass overlying the anterosuperior aspect of the bladder containing low-density areas and scattered punctate calcifications (arrow).

Radiologic Findings Axial contrast-enhanced computed tomography (CT) images through the pelvis demonstrate a midline, well-defined soft tissue mass overlying the anterosuperior aspect of the bladder containing low-density areas and scattered punctate calcifications (Fig. 126.1).

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Diagnosis Urachal adenocarcinoma

Differential Diagnosis • • •

Infected urachal remnant Urothelial tumors of the bladder dome Rare benign urachal neoplasms (adenomas, fibromas, fibroadenomas, fibromyomas, and hamartomas)

Discussion Background The urachus is a midline tubular structure that extends upward from the anterior dome of the bladder toward the umbilicus. Urachal remnant diseases include urachal diverticulum, urachal sinus, urachal cyst, and urachal carcinoma. Malignant urachal neoplasms are rare, representing < 0.5% of all bladder cancers. Although the normal urachus is most commonly lined by the transitional epithelium, urachal carcinoma predominantly manifests as adenocarcinoma (90% of cases). Urachal carcinoma most commonly presents as a midline juxtavesical mass.

Clinical Findings Urachal tumors are typically silent because of their extraperitoneal location; consequently, the majority of patients exhibit advanced disease such as local invasion or metastases at presentation. Patients can sometimes present with hematuria.

Complications Extravesical spread of the tumor is very common. There is bladder wall invasion in 92% and metastatic disease in 48% of cases.

Etiology Although the etiology remains unknown, urachal cysts have an increased prevalence of carcinoma after puberty.

Imaging Findings •



CT is the best modality to depict urachal carcinoma. At CT, urachal carcinoma may be solid, cystic, or a combination of the two (Fig. 126.1). Ninety percent of urachal carcinomas arise in the juxtavesical portion of the urachus and extend superiorly toward the umbilicus and inferiorly through the bladder wall. Urachal carcinoma can be intraluminal, but the bulk of tumor is outside the bladder in 90% of cases, which allows distinction from typical bladder masses. Calcification occurs in 50 to 70% of cases and may be punctate, stippled, or curvilinear and peripheral. Lowattenuation components are seen in 60% of cases, reflecting the mucin content. At magnetic resonance imaging, the location of urachal carcinoma is best demonstrated on sagittal images. On T2-weighted images, focal areas of high signal intensity from mucin are highly suggestive. The solid portions of the tumor are isointense to soft tissue on T1-weighted images and enhance with intravenous contrast material.

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Ultrasound may show a soft tissue lesion in the anterior abdominal wall with echogenic calcifications; cystic mucin-containing portions of the tumor demonstrate internal echoes.

Treatment • •

Treatment for localized bladder dome urachal cancer includes surgery to remove the cancer and the bladder, in whole or in part. Many experts advocate the use of radiation therapy because the most common area of recurrence is at or near the bladder dome.

Prognosis •

The prognosis in urachal adenocarcinoma is related to the stage and degree of differentiation, although it is generally poor because the tumor arises in a clinically silent area and is discovered only after it has become locally advanced or has extended into adjacent organs. Local invasion and systemic metastases result in a low 5-year survival rate of 6.5 to 15.0%.

PE ARL



A midline supravesical mass with calcifications is considered pathognomonic for urachal carcinoma.

PITFALL



Urachal carcinomas may be confused with primary tumors of the bladder dome; unlike vesical tumors, however, urachal tumors are centered in the perivesical space toward the umbilicus.

Suggested Readings Wong-You-Cheong JJ, Woodward PJ, Manning MA, Sesterhenn IA. Neoplasms of the urinary bladder: radiologic-pathologic correlation. Radiographics 2006;26:553–580 Yu JS, Kim KW, Lee HJ, Lee YJ, Yoon CS, Kim MJ. Urachal remnant diseases: spectrum of CT and US findings. Radiographics 2001;21:451–461

CASE 127 Clinical Presentation An elderly woman with a prior history of diverticulitis complains of pneumaturia and passing foul-smelling urine.

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Fig. 127.1 Contrast-enhanced (A–C) axial and (D) coronal images show the presence of gas and fecal material (Fig. 127.1B, arrow) within the lumen of the urinary bladder. (D) A fistula between the bladder and the sigmoid colon (Fig. 127.1D, arrow) can be seen.

Radiologic Findings Contrast-enhanced axial and coronal computed tomography (CT) images show the presence of gas within the lumen of the urinary bladder. There if fecal material within the bladder. A fistula between the bladder and the sigmoid colon is seen on the coronal image (Fig. 127.1).

Diagnosis Colovesical fistula secondary to a prior episode of diverticulitis

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Differential Diagnosis Other etiologies for fistula are • • • • •

Pelvic malignancy Inflammatory bowel disease Radiation therapy Trauma Instrumentation

Discussion Background Complications of diverticulitis include abscess formation, bleeding, fistula formation, perforation, and bowel obstruction. Colovesical fistula commonly involves the rectosigmoid.

Clinical Findings The patient may present with nonspecific symptoms of cystitis. Pneumaturia and fecaluria are the most common symptoms that are specific to this condition. Additional symptoms are urinary tract infection, abdominal pain, and fever.

Complications Persistent urinary tract infection

Etiology Diverticulitis is the most common cause of colovesical fistula, followed by colon cancer. Crohn disease is the most common cause of enterovesical fistula. Other causes are radiation therapy (seen 12–18 months after therapy), trauma, surgery, and granulomatous disease.

Imaging Findings •





CT scanning of the abdomen and pelvis is the most sensitive test for detecting a colovesical fistula. It should be included as part of the initial evaluation of patients with suspected colovesical fistulas. The presence of gas and/or fecal material within the bladder associated with bladder wall thickening is indicative of colovesical fistula. There is accompanying thickening of the adjacent colon. Reformatted images can show the fistula between the colon and the bladder. If there is difficulty in visualizing the fistula, CT cystography can be used to show the communication.

Treatment •

Treatment depends on the etiology and general condition of the patient. Because a colovesical fistula seldom closes spontaneously, surgical repair is necessary.

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PE ARL



Gas and fecal material in the bladder suggest the presence of a colovesical fistula.

PITFALL



If the fistula is small, it may be difficult to demonstrate without a CT cystogram.

Suggested Readings Jarrett TW, Vaughan ED. Accuracy of computerized tomography in the diagnosis of colovesical fistula secondary to diverticular disease. J Urol 1995;153(1):44–46

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CASE 128 Clinical Presentation A 36-year-old woman presents with a history of postvoid dribbling and dysuria.

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Fig. 128.1 MRI of the pelvis. (A) Sagittal T2-weighted image of the pelvis shows a teardrop-shaped T2 hyperintense diverticulum (arrow) arising from the urethra and present anterior to the vagina (note the tampon in the vagina). (B) Axial T2-weighted image shows the T2 hyperintense diverticulum anterior to the vagina. (C) Axial T1-weighted gradient echo image shows the diverticulum to be T1 bright with dark signal from the vaginal tampon.

Radiologic Findings Magnetic resonance imaging (MRI) of the pelvis with a vaginal tampon in place shows a smoothly contoured lesion that is hyperintense on T1- and T2-weighted images. The sagittal T2-weighted sequence best demonstrates a teardrop configuration extending from the posterior aspect of the distal urethra (Fig. 128.1).

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Diagnosis Urethral diverticulum

Differential Diagnosis • • • • •

Gartner duct cyst Müllerian duct cyst Vaginal epithelial inclusion cyst Skene gland abscess Ectopic ureterocele

Discussion Background Urethral diverticula are defined as a localized saccular outpouchings of the urethra with mass effect on the anterior vaginal wall. These diverticula may be single or multiple, unilocular or septated. Urethral diverticula may have either a narrow or wide neck and are usually located posterolateral to the urethra.

Clinical Findings Patients present with stress incontinence or irritative voiding symptoms, such as urinary frequency, urgency, and dysuria. Recurrent urinary tract infections occur in ~40% of patients, whereas ~25% report postvoid dribbling. Approximately 10% report dyspareunia. Other, less frequent presentations include hematuria and a palpable anterior vaginal wall mass.

Complications • •

Female urethral diverticula may be complicated by infection, the formation of calculi, bladder outlet obstruction, and malignancy. Infection may be acute or chronic and may result in abscess formation.

Etiology Female urethral diverticula are felt to be acquired diverticula arising from dilated and infected periurethral glands, resulting in pseudodiverticulum formation.

Imaging Findings • •



The diagnosis can be made with several imaging modalities, including voiding cystourethrography, double-balloon urethrography, or cross-sectional imaging, as well as urethroscopy. MRI is the most sensitive technique in the detection of urethral diverticula, particularly in the diagnosis of narrow-neck, noncommunicating diverticula. On T1-weighted images, the typical urethral diverticulum appears as a focal urethral enlargement anterior to the vagina with homogeneous low-signal intensity. On T2-weighted images, the diverticulum appears hyperintense. Transvaginal ultrasound has also been used for identifying urethral diverticula in women, but this modality is limited in distinguishing urethral diverticula from paravaginal cysts. Urethral diverticula may surround the urethra (“saddlebag” diverticula). Mass effect exerted on the bladder

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base from diverticula arising in the proximal urethra can create an imaging appearance similar to that seen in elderly men with enlarged prostate glands; this finding is referred to as the “female prostate” sign.

Treatment •

Surgical diverticulectomy is the treatment of choice.

Prognosis •

With appropriate surgical management, cure rates are high, and recurrences are rare.

PE ARL S

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Fluid-filled outpouching of the urethra with mass effect on the anterior vaginal wall is consistent with a urethral diverticulum. Gartner duct cyst is usually located more superiorly in the anterolateral vaginal wall.

PITFALL



Urethral diverticula may sometimes demonstrate elevated T1 signal intensity that may be due to its proteinaceous content.

Suggested Readings Kawashima A, Sandler CM, Wasserman NF, LeRoy AJ, King BF, Goldman MS. Imaging of urethral disease: a pictorial review. Radiographics 2004;24:S195–S216 Kim B, Hricak H, Tanagho EA. Diagnosis of urethral diverticula in women: value of MR imaging. AJR Am J Roentgenol 1993;161:809–815

CASE 129 Clinical Presentation A 53-year-old woman presents with pelvic pain.

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Fig. 129.1 (A) Transvaginal ultrasound image shows an enlarged uterus with heterogeneous echotexture of the myometrium. (B) Sagittal T2-weighted image of the pelvis shows focal thickening of the junctional zone (arrow). There are T2 hyperintense foci seen in the thickened junctional zone. (C) Coronal T2-weighted image of the pelvis shows a similar finding as the sagittal image (arrow).

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Radiologic Findings Transvaginal ultrasound image shows an enlarged uterus with heterogeneous echotexture of the myometrium. Axial and sagittal magnetic resonance (MR) T2-weighted images show a diffusely enlarged uterus with thickening of the junctional zone; small, scattered T2 hyperintense foci are seen within the myometrium (Fig. 129.1A).

Diagnosis Adenomyosis

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Differential Diagnosis • • • • •

Uterine leiomyoma Endometrial carcinoma Adenomatoid tumor of the uterus Metastases Uterine sarcoma

Discussion Background Adenomyosis is a common gynecologic disorder, typically occurring in premenopausal multiparous women and characterized at histology by the presence of heterotopic endometrial glands and stroma within the myometrium with compensatory smooth muscle hyperplasia. The ectopic endometrial tissue usually consists of basalis-type cells that are scarcely responsive to hormonal stimuli.

Clinical Findings Patients usually present with pelvic pain, dysmenorrhea, and abnormal uterine bleeding, although these symptoms are nonspecific and may be seen in other gynecologic disorders, such as leiomyoma, uterine malignancies, and dysfunctional uterine bleeding. In some cases, adenomyosis is associated with infertility.

Complications Adenocarcinomas may arise from adenomyosis, but this finding is extremely rare.

Etiology The etiology is under debate but still unknown. Recent studies demonstrate the central role of tamoxifen, a nonsteroidal antiestrogen agent routinely administered for the treatment of estrogen-sensitive breast cancer.

Imaging Findings •

Ultrasound is considered the initial imaging technique for the evaluation of adenomyosis; a transvaginal approach performed with dedicated transducers significantly improves the sensitivity and specificity of this modality. Ultrasound findings include (Figs. 129.1B and 129.1C) (1) abnormal myometrial echogenicity with hypoechoic areas (smooth muscle hyperplasia) and multiple foci of echogenicity (islands of endometrial tissue), (2) myometrial cysts corresponding to cystic dilatation of endometrial glands (this appearance is predominant in cases of cystic adenomyosis), (3) linear echogenic lesions corresponding to heterotopic endometrium extending into the myometrium (this feature may be misinterpreted as a pseudowidening of the endometrium), (4) poor definition of the endomyometrial junction, (5) asymmetric thickening of the myometrium without mass effect on the endometrium, and (6) a penetrating pattern of color Doppler flow (rather than the draping pattern seen with leiomyomata).

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MRI is a highly accurate noninvasive imaging technique for the diagnosis of adenomyosis and is also helpful in differentiating this disorder from other gynecologic conditions. Uterine anatomy is best depicted with T2-weighted images, but T1-weighted images are helpful in localizing hemorrhagic foci; gadolinium contrast need not be routinely administered but may be used to exclude other mimicking lesions. Typical MRI findings include (1) irregular, either diffuse or focal widening of the junctional zone that histologically corresponds to smooth muscle cell hyperplasia (despite the considerable variation in thickness of the inner myometrium in the normal female population, widening > 12 mm is considered highly suspicious for adenomyosis) and (2) multiple T2 hyperintense foci (linear or focal) located within the myometrium and corresponding to the islands of ectopic endometrial tissue and cystic dilatation of glands. These lesions may undergo cyclic changes according to the menstrual period and appear T1 hyperintense in the presence of hemorrhage.

Treatment •



Currently, patients may benefit from different therapeutic options according to their age and symptoms. Conservative therapy (administration of gonadotropin-releasing hormone agonists) may be able to control symptoms by inducing a hypoestrogenic state, although adenomyosis is less responsive to hormonal therapy than endometriosis. Recently, uterine artery embolization has been performed as an alternative treatment to surgery, although its efficacy is not well established. Hysterectomy is an option in severe cases of adenomyosis.

Prognosis •

The prognosis is favorable with the current therapeutic options. The risk of malignant transformation is almost negligible.

PE ARL



The presence of T2 hyperintense foci embedded in a thickened junctional zone is highly suspicious for adenomyosis.

PITFALL S

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MRI should not be performed during the menstrual phase to avoid the physiologic thickening of the junctional zone. Other conditions may mimic adenomyosis, including transient myometrial contractions and leiomyomas.

Suggested Readings Atri M, Reinhold C, Mehio AR. Adenomyosis: US features with histologic correlation in an in vitro study. Radiology 2000;215(3):783–790 Bennett GL, Slywotzky CM, Giovanniello G. Gynecologic causes of acute pelvic pain: spectrum of CT findings. Radiographics 2002;22:785–801

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Byun JY, Kim SE, Choi BG, et al. Diffuse and focal adenomyosis: MR imaging findings. Radiographics 1999;19:S161–S170 Del Frate C, Girometti R, Pittino M, Del Frate G, Bazzocchi M, Zuiani C. Deep retroperitoneal pelvic endometriosis: MR imaging appearance with laparoscopic correlation. Radiographics 2006;26(6): 1705–1718 Imaoka I, Wada A, Matsuo M, Yoshida M, Kitagaki H, Sugimura K. MR imaging of disorders associated with female infertility: use in diagnosis, treatment, and management. Radiographics 2003;23: 1401–1421 Kim MD, Kim S, Kim NK, et al. Long-term results of uterine artery embolization for symptomatic adenomyosis. AJR Am J Roentgenol 2007;188:176–181 Kitamura Y, Allison SJ, Jha RC, Spies JB, Flick PA, Ascher SM. MRI of adenomyosis: changes with uterine artery embolization. AJR Am J Roentgenol 2006;186:855–864 Kuligowska E, Deeds L III, Lu K III. Pelvic pain: overlooked and underdiagnosed gynecologic conditions. Radiographics 2005;25:3–20 Reinhold C, McCarthy S, Bret PM, et al. Diffuse adenomyosis: comparison of endovaginal US and MR imaging with histopathologic correlation. Radiology 1996;199:151–158 Tamai K, Togashi K, Ito T, et al. MR imaging findings of adenomyosis: correlation with histopathologic features and diagnostic pitfalls. Radiographics 2005;25:21–40 Utsunomiya D, Notsute S, Hayashida Y, et al. Endometrial carcinoma in adenomyosis: assessment of myometrial invasion on T2-weighted spin-echo and gadolinium-enhanced T1-weighted images. AJR Am J Roentgenol 2004;182:399–404 Williams PL, Laifer-Narin SL, Ragavendra N. US of abnormal uterine bleeding. Radiographics 2003;23:703–718

CASE 130 Clinical Presentation A 28-year-old woman presents with pelvic pain and dyspareunia.

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C

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Fig. 130.1 (A–C) Axial, sagittal, and coronal T2-weighted images of the pelvis show a well-defined T2 hyperintense lesion (arrows) located within the wall of the left vaginal fornix. (D) T1-weighted axial image after intravenous gadolinium administration shows mild peripheral rim enhancement in the lesion (arrow).

Radiologic Findings Axial, sagittal, and coronal T2-weighted images of the pelvis (Fig. 130.1A,B,C) show a well-defined T2 hyperintense lesion located within the wall of the left vaginal fornix; after intravenous gadolinium administration, the lesion shows mild peripheral rim enhancement (Fig. 130.1D).

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Diagnosis Gartner duct cyst

Differential Diagnosis • • • • •

Urethral diverticula Skene cyst Duplication cyst Endometriotic implants Bartholin gland cyst

Discussion Background Gartner duct cysts derive from the vestigial remnant of the vaginal portion of the mesonephric (wolffian) duct; in the case of incomplete involution, cysts may develop due to secretion by persistent glandular tissue. Remnants of the mesonephric duct may be found in one fourth of women, although the cysts are rarely described (1–2%). Gartner cysts are typically paravaginal and located within the anterolateral aspect of the proximal third of the vagina.

Clinical Findings Gartner duct cysts may be incidentally discovered at imaging in a completely asymptomatic patient or be associated with pelvic pain and dyspareunia.

Complications Larger Gartner cysts may complicate vaginal delivery or cause urethral or even ureteral obstruction. Common association with renal or urogenital malformations has been reported, including HerlynWerner-Wunderlich syndrome (ipsilateral renal agenesis). Infrequently, ectopic ureters have been documented to communicate with Gartner cysts, causing continuous urinary incontinence.

Etiology Gartner duct cysts develop when the vaginal portion of the mesonephric duct fails to regress during the second trimester of gestation.

Imaging Findings •

• •

Magnetic resonance imaging (MRI) is a very accurate imaging technique for the evaluation and characterization of female pelvis abnormalities. Gartner duct cysts are well documented within the anterolateral wall of the proximal vagina and typically present high signal intensity on T2weighted images and variable signal intensity on T1-weighted images according to their content (hyperintense if proteinaceous or hemorrhagic, hypointense if containing simple fluid). Thickening of the wall and peripheral enhancement after intravenous gadolinium administration have been reported in cases of infection. Ultrasound may be performed to detect cystic anomalies of the female pelvis, but MRI is more accurate at establishing anatomical relationships.

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Treatment •

Surgical treatment is recommended in symptomatic patients.

Prognosis •

The prognosis is favorable.

PE ARL



The differential diagnosis should include urethral diverticula, Bartholin gland cysts, and Skene cysts. Urethral diverticula are usually midline in location. Bartholin cysts (female homologue of the male Cowper gland) are typically located below the pubic symphysis in the posterolateral wall of the lower vagina. Skene cysts lie lateral to the external urethral meatus.

PITFALL



There is imaging overlap between the above-mentioned entities, which can make diagnosis difficult.

Suggested Readings Berrocal T, López-Pereira P, Arjonilla A, Gutiérrez J. Anomalies of the distal ureter, bladder, and urethra in children: embryologic, radiologic, and pathologic features. Radiographics 2002;22:1139–1164 Garel L, Dubois J, Grignon A, Filiatrault D, Van Vliet G. US of the pediatric female pelvis: a clinical perspective. Radiographics 2001;21:1393–1407 Gilsanz V, Cleveland RH, Reid BS. Duplication of the müllerian ducts and genitourinary malformations: 2. Analysis of malformations. Radiology 1982;144:797–801 Hagspiel KD. Giant Gartner duct cyst: magnetic resonance imaging findings. Abdom Imaging 1995;20(6):566–568 Hahn WY, Israel GM, Lee VS. MRI of female urethral and periurethral disorders. AJR Am J Roentgenol 2004;182:677–682 Prasad SR, Menias CO, Narra VR, et al. Cross-sectional imaging of the female urethra: technique and results. Radiographics 2005;25:749–761 Sherer DM, Abulafia O. Transvaginal ultrasonographic depiction of a Gartner duct cyst. J Ultrasound Med 2001;20(11):1253–1255 Siegelman ES, Outwater EK, Banner MP, Ramchandani P, Anderson TL, Schnall MD. High-resolution MR imaging of the vagina. Radiographics 1997;17:1183–1203 Vanhoutte JJ. Ureteral ectopia into a Wolffian duct remnant (Gartner’s duct or cysts) presenting as a urethral diverticulum in two girls. Am J Roentgenol Radium Ther Nucl Med 1970;110:540–545 Wepfer JF, Boex RM. Mesonephric duct remnants (Gartner’s duct). AJR Am J Roentgenol 1978;131: 499–500

CASE 131 Clinical Presentation A 34-year-old woman presents with severe pelvic pain and a history of dysmenorrhea.

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Fig. 131.1 (A,B) Sagittal and coronal MR T2-weighted images demonstrate a large, heterogeneous, low signal intensity myometrial mass (arrow) displacing the endometrial stripe, most consistent with a uterine leiomyoma. (C) The lesion shows homogeneous early enhancement on a sagittal MR image obtained after the intravenous administration of gadolinium.

C

Radiologic Findings Sagittal and coronal magnetic resonance (MR) T2-weighted images (Fig. 131.1A,B) demonstrate a large, heterogeneous fundal mass displacing the endometrial stripe, most consistent with a uterine leiomyoma. The lesion shows homogeneous early enhancement on a sagittal MR image obtained after the intravenous (IV) administration of gadolinium (Fig. 131.1C).

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Diagnosis Leiomyoma

Differential Diagnosis • • • • •

Adenomyosis Uterine leiomyosarcoma Solid adnexal masses Metastases Focal uterine contractions

Discussion Background Uterine leiomyomas, also called fibroids or myomas, represent the most common gynecologic tumor, occurring in ~20 to 30% of women in their 2nd to 3rd decades. They arise from smooth muscle cells of the myometrium and contain variable amounts of fibrous tissue; some of these lesions have a high rate of growth resulting in different types of degeneration, such as hyaline, myxoid, and hemorrhagic (red) degeneration. These histopathologic features are responsible for the variable appearance of leiomyomas at imaging but are unrelated to clinical symptoms. The location of these lesions within the uterus deeply affects clinical presentation; according to their location within the uterus, leiomyomas are classified as submucosal, intramural, or subserosal. Submucosal leiomyomas are the least common (only 5%) but the most commonly symptomatic, causing dysmenorrhea, menorrhagia, and infertility. Intramural and subserosal leiomyomas are usually asymptomatic, but they may be associated with menorrhagia and menstrual irregularities; moreover, some subserosal leiomyomas may become pedunculated and grow laterally within the folds of broad ligament (intraligamentous leiomyomas), resembling ovarian masses at imaging. Uterine leiomyomas may also have unusual patterns of growth and extent outside the uterus, as seen in parasitic leiomyomas (which incorporate an extrauterine blood supply and can become separated from the uterus), IV leiomyomatosis, intraperitoneal leiomyomatosis, and benign metastatic leiomyomas.

Clinical Findings Clinical presentation varies according to the size, location, and number of leiomyomas. Patients commonly present pelvic pain (usually during menstruation), menorrhagia (chronic loss of blood may cause severe anemia), and infertility. Other symptoms include urinary frequency and urgency resulting from pressure on the bladder or constipation and difficult defecation from pressure on the colon.

Complications Sarcomatous transformation may occur but is rare; uterine leiomyosarcomas usually tend to arise independently. Subserosal pedunculated leiomyomas may cause ovarian torsion.

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Fig. 131.2 Transvaginal ultrasound shows a large leiomyoma with echotexture similar to the myometrium, outlined by caliper markers and with > 50% projection into the endometrial canal.

Fig. 131.3 Transvaginal ultrasound shows a large intramural leiomyoma with heterogeneous echotexture.

Etiology The etiology is uncertain, but several studies suggest that estrogen and progesterone play a central role in the development of these lesions; in fact, leiomyomas may enlarge with oral contraceptive use, during pregnancy, and in perimenopausal women undergoing hormonal replacement therapy or decrease in size after menopause. A genetic predisposition has also been demonstrated.

Imaging Findings •



Ultrasound is the imaging modality of choice for the diagnosis of leiomyomas. The most common appearance on ultrasound is that of a well-circumscribed, solid, variably hypoechoic mass (Figs. 131.2 and 131.3). Leiomyomas also present a different degree of echogenicity resulting from degenerative changes and may appear heterogeneous, hyperechoic, or partially anechoic (necrosis, cystic degeneration). Isoechoic lesions have been described with their only sign at ultrasound being a bulge in the endometrial contour. MRI is currently acknowledged as the most accurate imaging modality for the evaluation and characterization of leiomyomas. Nondegenerated leiomyomas typically appear as well-circumscribed

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lesions, homogeneously hypointense on T1- and T2-weighted images, but signal intensity may vary according to the histology. Highly cellular lesions with no or little fibrous tissue usually have higher signal intensity and may have mild enhancement after IV administration of contrast. Degenerative changes frequently occurring within these lesions lead to a considerable variation in MRI appearance:   Hyaline or calcific degeneration shows as low signal intensity on T2-weighted images (findings similar to those of nondegenerated leiomyomas).  Cystic degeneration shows as high signal on T2-weighted images without enhancement.  Myxoid degeneration shows as very high signal on T2-weighted images with minimal enhancement.  Red degeneration (necrotic infarction) shows as either peripheral or diffuse high signal on T1-weighted images related to the presence of blood products and variable signal with or without a low signal intensity rim on T2-weighted images. Some leiomyomas may have a high signal intensity peripheral rim on T2-weighted images corresponding to a pseudocapsule of lymphatics, vessels, and edema.

Treatment •



Most leiomyomas (~80%) are asymptomatic. Hysterectomy (either open or laparoscopic) is reserved for symptomatic women who have completed childbearing, whereas myomectomy (and preservation of the uterus) is performed in patients with a positive history of miscarriages or chronic anemia for hypermenorrhea. Uterine artery embolization represents a promising method of treating symptomatic lesions, especially in case of uncontrollable bleeding. Administration of gonadotropin-releasing hormone (both estrogen and progesterone receptors are present in leiomyomas) is not recommended because of the risk of osteoporosis, but it may be useful preoperatively to reduce tumor size and vascularity (thus minimizing intraoperative blood loss).

Prognosis •

Patient outcome is favorable with the current therapeutic options. The risk of sarcomatous transformation is negligible. Chronic loss of blood resulting in anemia and infertility represent the most worrisome complications.

Pe a r l



Rapid enlargement of a previously diagnosed leiomyoma in a postmenopausal woman is suspicious for sarcomatous degeneration.

Pitfa l l s





Other gynecologic conditions may present similar findings at cross-sectional imaging, including  Adenomyosis: leiomyomas usually appear as capsulated, well-circumscribed lesions, whereas adenomyomas (focal form of adenomyosis) are commonly ill defined and scarcely marginated.  Solid adnexal masses: some ovarian neoplasms, such as ovarian fibromas and Brenner tumors (both containing a variable amount of fibrous tissue), have an appearance similar to that of leiomyomas.  Uterine contractions: present low signal intensity on T2-weighted images but are transient.

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Suggested Readings Abramson S, Gilkeson RC, Goldstein JD, Woodard PK, Eisenberg R, Abramson N. Benign metastasizing leiomyoma: clinical, imaging, and pathologic correlation. AJR Am J Roentgenol 2001;176:1409–1413 Bennett GL, Slywotzky CM, Giovanniello G. Gynecologic causes of acute pelvic pain: spectrum of CT findings. Radiographics 2002;22:785–801 Casillas J, Joseph RC, Guerra JJ Jr. CT appearance of uterine leiomyomas. Radiographics 1990;10:999– 1007 Cohen DT, Oliva E, Hahn PF, Fuller AF Jr, Lee SI. Uterine smooth-muscle tumors with unusual growth patterns: imaging with pathologic correlation. AJR Am J Roentgenol 2007;188:246–255 DeSouza NM, Williams AD. Uterine arterial embolization for leiomyomas: perfusion and volume changes at MR imaging and relation to clinical outcome. Radiology 2002;222:367–374 Imaoka I, Wada A, Matsuo M, Yoshida M, Kitagaki H, Sugimura K. MR imaging of disorders associated with female infertility: use in diagnosis, treatment, and management. Radiographics 2003;23: 1401–1421 Katsumori T, Nakajima K, Tokuhiro M. Gadolinium-enhanced MR imaging in the evaluation of uterine fibroids treated with uterine artery embolization. AJR Am J Roentgenol 2001;177:303–307 Kido A, Togashi K, Koyama T, Yamaoka T, Fujiwara T, Fujii S. Diffusely enlarged uterus: evaluation with MR imaging. Radiographics 2003;23:1423–1439 Murase E, Siegelman ES, Outwater EK, Perez-Jaffe LA, Tureck RW. Uterine leiomyomas: histopathologic features, MR imaging findings, differential diagnosis, and treatment. Radiographics 1999;19: 1179–1197 Pelage J-P, Cazejust J, Pluot E, et al. Uterine fibroid vascularization and clinical relevance to uterine fibroid embolization. Radiographics 2005;25:S99–S117 Razavi MK, Hwang G, Jahed A , Modanloo S, Chen B. Abdominal myomectomy versus uterine fibroid embolization in the treatment of symptomatic uterine leiomyomas. AJR Am J Roentgenol 2003;180:1571–1575 Ueda H, Togashi K, Konishi I, et al. Unusual appearances of uterine leiomyomas: MR imaging findings and their histopathologic backgrounds. Radiographics 1999;19:S131–S155 Weinreb JC, Barkoff ND, Megibow A, Demopoulos R. The value of MR imaging in distinguishing leiomyomas from other solid pelvic masses when sonography is indeterminate. AJR Am J Roentgenol 1990;154:295–299 Williams PL, Laifer-Narin SL, Ragavendra N. US of abnormal uterine bleeding. Radiographics 2003;23:703–718

CASE 132 Clinical Presentation A 32-year-old woman presents with abdominal tenderness and fever.

B

A

Fig. 132.1 (A,B) Contrast-enhanced axial CT images of the pelvis demonstrate a heterogeneously enhancing area associated with mild fat stranding in the left adnexal region with an associated oval-shaped fluid density structure (arrow). There is free fluid in the pelvis.

Radiologic Findings Contrast-enhanced axial computed tomography (CT) images of the pelvis (Fig. 132.1) demonstrate a heterogeneously enhancing area associated with mild fat stranding in the left adnexal region with an associated oval-shaped fluid density structure. There is free fluid in the pelvis.

Diagnosis Pelvic inflammatory disease with tubo-ovarian abscess

Differential Diagnosis • • • • • •

Ovarian torsion Endometrioma/endometriosis Ectopic pregnancy Ovarian malignancies Appendicitis Diverticulitis

Discussion Background Pelvic inflammatory disease (PID) represents a common and potentially life-threatening disease among women of childbearing age, mostly occurring in their 2nd to 3rd decade (peak incidence: 20–24 years). This condition typically results from ascending infection of the female genital tract

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and is typically caused by Neisseria gonorrhoeae or Chlamydia trachomatis, although 40% of cases are associated with polymicrobial agents. PID usually begins with a cervicitis that subsequently extends to the endometrium and fallopian tubes; the infection may spread via tubal spillage to the peritoneum, leading to a local peritonitis. Tubo-ovarian abscess is the result of postinflammatory fusion of an infected fallopian tube and ovary (tubo-ovarian complex).

Clinical Findings Clinical diagnosis is often inaccurate, as patients may experience multiple nonspecific symptoms, including abdominal and pelvic pain, high fever, nausea, vomiting, vaginal discharge, uterine bleeding, dysuria, dyspareunia, and adnexal or cervical tenderness. Conversely, ~35% of patients with PID have no noticeable symptoms. Laboratory findings are suggestive of infection such as leukocytosis, elevated erythrocyte sedimentation rate, and elevated C-reactive protein.

Complications PID often results in damage to the fallopian tubes, scarring, and obstruction, leading to long-term complications such as infertility, ectopic pregnancy (sixfold higher risk), and chronic pelvic pain. Tubo-ovarian abscess is a common late complication occurring in almost one third of PID patients (young women have a higher risk than postmenopausal women).

Etiology PID results from ascending venereal infection, as described above. Young age, multiple sexual partners, low socioeconomic status, and douching have been identified as risk factors for PID. Intrauterine devices can predispose to a nonvenereal infection with Actinomyces israelii. Other potential causative agents are facultative anaerobes of the endogenous vaginal and perineal flora, including Gardnerella vaginalis, Streptococcus agalactiae, Peptostreptococcus species, Bacteroides species (other than B. fragilis), genital Mycoplasma and Ureaplasma species, and coliforms. Nongenital bacteria, such as Haemophilus influenzae and H. parainfluenzae, may also cause, albeit less commonly, some PID cases. In underdeveloped countries, Mycobacterium tuberculosis and some Schistosoma species may cause granulomatous salpingitis, subsequently evolving into PID.

Imaging Findings •

Ultrasound is the preferred imaging modality for the evaluation of PID and its complications, although almost one third of symptomatic patients may have a normal examination. Several imaging findings have been described for PID according to the site and extent of the infection. In endometritis, the inflamed uterus is usually enlarged and may have an endometrial canal that is indistinct or distended by fluid. In salpingitis, the fallopian tubes are distended by fluid (hydrosalpinx or pyosalpinx; Fig. 132.2) and may have increased wall thickness; acute salpingitis may progress to tubo-ovarian abscess usually described as either a solid, cystic, or heterogeneous mass located in the adnexal region and commonly associated with fluid collections (Fig. 132.3). In severe infection, the tubo-ovarian complex may become almost unrecognizable with irregular septations and fluid–debris levels. In these cases, CT and magnetic resonance imaging are used to help differentiate this condition from ovarian malignancies. At CT, tubo-ovarian abscesses appear as fluid-filled, tubular, thick-walled masses; septations, air bubbles, periadnexal fat stranding, and thickening of the uterosacral ligaments have been described as associated findings. Fibrosis and adhesions are commonly seen in end-stage, chronic disease.

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Fig. 132.2 (A,B) Axial MR T2-weighted images of the pelvis show bilateral tubular structures completely distended and filled by fluid; these findings suggest the presence of bilateral hydrosalpinx.

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C

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Fig. 132.3 (A–C) Coronal and sagittal MR T2-weighted images demonstrate a dilated cystic structure separated from the ovary with evidence of fluid level and complex debris; these findings are consistent with tubo-ovarian abscess. The uterus is enlarged with multiple fibroids.

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Treatment • •

PID is usually treated with analgesics and oral broad-spectrum antibiotics for both aerobes and anaerobes. In patients presenting with tubo-ovarian abscess, surgery or interventional radiology may be required in cases of suspected abscess rupture or failure of medical treatment.

Prognosis •

PID should be promptly identified and treated to avoid long-term complications.

PE ARL



Because the imaging findings are usually nonspecific, the clinical presentation is very important, and PID should be considered in the presence of infectious signs and symptoms.

PITFALL



Imaging examination may be normal in patients with PID. Abnormal, fluid-distended tubes may resemble bowel loops or dilated pelvic veins. Doppler sonography may be helpful in these circumstances. Severe cases of tubo-ovarian abscess may be difficult to differentiate from ovarian malignancies by imaging alone, and the patient’s clinical history should always be considered.

Suggested Readings Bennett GL, Slywotzky CM, Giovanniello G. Gynecologic causes of acute pelvic pain: spectrum of CT findings. Radiographics 2002;22:785–801 Birnbaum BA, Jeffrey RB Jr. CT and sonographic evaluation of acute right lower quadrant abdominal pain. AJR Am J Roentgenol 1998;170:361–371 Kaakaji Y, Nghiem HV, Nodell C, Winter TC. Sonography of obstetric and gynecologic emergencies: 2. Gynecologic emergencies. AJR Am J Roentgenol 2000;174:651–656 Kim SH, Kim SH, Yang DM, Kim KA. Unusual causes of tubo-ovarian abscess: CT and MR imaging findings. Radiographics 2004;24:1575–1589 McCormack WM. Pelvic inflammatory disease. N Engl J Med 1994;330(2):115–119 Sam JW, Jacobs JE, Birnbaum BA. Spectrum of CT findings in acute pyogenic pelvic inflammatory disease. Radiographics 2002;22:1327–1334 Tukeva TA, Aronen HJ, Karjalainen PT, Molander P, Paavonen T, Paavonen J. MR imaging in pelvic inflammatory disease: comparison with laparoscopy and US. Radiology 1999;210:209–216 Varghese JC, O’Neill MJ, Gervais DA, Boland GW, Mueller PR. Transvaginal catheter drainage of tuboovarian abscess using the trocar method: technique and literature review. AJR Am J Roentgenol 2001;177:139–144 Wilbur AC, Aizenstein RI, Napp TE. CT findings in tubo-ovarian abscess. AJR Am J Roentgenol 1992;158:575–579

CASE 133 Clinical Presentation A 27-year-old woman presents with secondary amenorrhea, hirsutism, and obesity.

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Fig. 133.1 (A,B) Transvaginal ultrasound images demonstrate enlargement of the ovaries with multiple, small, peripherally located hypoechoic follicles and slightly increased echogenicity of the central stroma.

Radiologic Findings Transvaginal ultrasound images (Fig. 133.1) demonstrate enlargement of the ovaries with multiple, small, peripherally located hypoechoic follicles and slightly increased echogenicity of the central stroma.

Diagnosis Polycystic ovary syndrome (POS)

Differential Diagnosis • • •

Functional ovarian cysts (follicular or corpus luteum cyst) Multifollicular ovaries (related to other endocrinologic disorders) Ovarian hyperstimulation syndrome (associated with increased human chorionic gonadotropin serum level as seen in gestation trophoblastic disease)

Discussion Background Polycystic ovary syndrome, also known as Stein-Leventhal syndrome, is one of the most common endocrine disorders occurring in women of reproductive age (4–12%). This condition is characterized by chronic anovulation, presumably associated with hypothalamic pituitary dysfunction, which leads to abnormalities in the metabolism of both estrogen and androgens. At pathology, the ovaries are enlarged and sclerotic, with multiple atretic peripherally located follicles and a thickened external capsule due to hyperplasia of the theca stromal cells.

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Clinical Findings Patients typically present with infertility, menstrual abnormalities such as oligomenorrhea (menstrual bleeding occurring at longer interval) or secondary amenorrhea (absence of menses for more than 6 consecutive months), dysfunctional vaginal bleeding, hirsutism, and obesity. Minor findings are sleep apnea, acanthosis nigricans (dark, pigmented skin on elbows, knuckles, and skinfolds), acne, and androgenic alopecia. Laboratory findings usually include increased luteinizing hormone (LH) levels and LH/follicle-stimulating hormone (FSH) ratio (> 2), as well as high serum concentration of androgenic hormones, such as testosterone, androstenedione, and dehydroepiandrosterone sulfate.

Complications POS may be associated with peripheral insulin resistance and hyperinsulinemia leading to diabetes mellitus type 2 (10% of POS patients) and glucose intolerance (30–40%). Hyperinsulinemia is also responsible for dyslipidemia and elevated levels of plasminogen activator inhibitor-1 (PAI-1), both increasing the risk of intravascular thrombosis.

Etiology Hypothalamic pituitary dysfunction results in increased production of LH, which in turn increases androgen production; peripheral aromatization of androgen into estrogen depresses secretion of FSH, thereby affecting the development of ovarian follicles and leading to chronic anovulation. Peripheral conversion of estrogen typically occurs in fat tissues, thus explaining the common correlation between POS and obesity.

Imaging Findings •



Currently, ultrasound is considered the imaging modality of choice for the evaluation of POS because of its convenience and cost-effectiveness. Diagnostic criteria of POS have been evolving in the last few years, the most specific being increased echogenicity of the central stroma (stromal brightness), increased follicularity (10 or more), and small size of the follicles (2–8 mm). Bilateral enlargement and peripheral distribution of follicles are considered less strong predictive factors. Magnetic resonance imaging (MRI) can be a valuable alternative to ultrasound imaging because of its excellent soft tissue contrast and ability to differentiate benign from malignant lesions. Although imaging criteria for POS are still not well established, MR findings typically include the following (Fig. 133.2): ⴰ Bilateral enlargement of the ovaries ⴰ Prominent central stroma, hypointense on T2-weighted images (not specific but an important feature to differentiate POS from other multicystic ovarian lesions) ⴰ Multiple peripherally located follicles uniform in size (typically < 1 cm) and appearance (high signal intensity on T2-weighted images)

Treatment •

Medical treatment is usually preferred and aims to manage all the disorders associated with POS, including menstrual irregularities (oral contraceptives) and hirsutism (oral contraceptive and antiandrogens, e.g., spironolactone). Metformin, an antidiabetic drug, is administered to improve insulin resistance and decrease hyperinsulinemia. Patients are also encouraged to diet and exercise to reduce weight.

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Fig. 133.2 (A,B) Axial and coronal MR T2-weighted images show multiple, small, peripherally located T2 hyperintense follicles within both of the ovaries. These findings in the appropriate clinical setting represent changes with polycystic ovary syndrome.



Surgical treatment includes different procedures (electrocautery, laser drilling, and multiple biopsies for damaged ovarian cortex and stroma) but is less frequently performed since the introduction of ovulation-inducing medications.

Prognosis •

Patients with POS have an increased risk for the development of cardiovascular disease, diabetes mellitus type 2, and endometrial carcinoma due to the chronic estrogenic stimulation of the endometrium.

PE ARL



The diagnosis is based on clinical and endocrinologic findings rather than imaging findings.

PITFALL



Ovaries may be morphologically normal in one third of the patients with clinical and endocrinologic evidence of POS. Conversely, multicystic ovaries have been described in patients with other disorders, including anorexia nervosa, virilizing neoplasms of the ovary or adrenal gland, and hypothyroidism. Premenarchal girls may have multiple ovarian follicles.

Suggested Readings Atiomo WU, Pearson S, Shaw S, Archibald P, Dubbins P. Ultrasound criteria in the diagnosis of polycystic ovary syndrome. Ultrasound Med Biol 2000;26:977–980 Erdem CZ, Bayar U, Erdem LO, Barut A, Gundogdu S, Kaya E. Polycystic ovary syndrome: dynamic contrast-enhanced ovary MR imaging. Eur J Radiol 2004;51(1):48–53 Imaoka I, Wada A, Matsuo M, Yoshida M, Kitagaki H, Sugimura K. MR imaging of disorders associated with female infertility: use in diagnosis, treatment, and management. Radiographics 2003;23: 1401–1421

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Kimura I, Togashi K, Kawakami S, et al. Polycystic ovaries: implications of diagnosis with MR imaging. Radiology 1996;201:549–552 Lakhani K, Seifalian AM, Atiomo WU, Hardiman P. Polycystic ovaries. Br J Radiol 2002;75(889):9–16 Maubon A, Courtieu C, Vivens F, et al. Magnetic resonance imaging of normal and polycystic ovaries: preliminary results. Ann N Y Acad Sci 1993;687:224–229 Pache TD, Wladimiroff JW, Hop WC, Fauser BC. How to discriminate between normal and polycystic ovaries: transvaginal US study. Radiology 1992;183:421–423 Pan HA, Wu MH, Cheng YC, Li CH, Chang FM. Quantification of Doppler signal in polycystic ovary syndrome using three-dimensional power Doppler ultrasonography: a possible new marker for diagnosis. Hum Reprod 2002;17(1):201–206 Saksouk FA, Johnson SC. Recognition of the ovaries and ovarian origin of pelvic masses with CT. Radiographics 2004;24:S133–S146 Tamai K, Koyama T, Saga T, et al. MR features of physiologic and benign conditions of the ovary. Eur Radiol 2006;16(12):2700–2711

CASE 134 Clinical Presentation A 27-year-old woman presents with vaginal bleeding. Laboratory test reveal increased levels of ␤-human chorionic gonadotropin (HCG).

A

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Fig. 134.1 (A–C) Transvaginal ultrasound images show a large intrauterine echogenic solid mass extending through the myometrium and containing multiple hypoechoic cystic spaces. These sonographic features are suggestive of gestational trophoblastic disease. Color Doppler sonography demonstrates increased vascularity within the intrauterine mass, a typical finding in gestational trophoblastic disease.

C

Radiologic Findings Transvaginal ultrasound images (Fig. 134.1) demonstrate a hypervascular complex intrauterine mass containing many small cysts, extending from the internal os through the fundal endometrium, posterior myometrium, and possibly to or through the posterior serosa.

Diagnosis Gestational trophoblastic disease (GTD)

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Differential Diagnosis • • • •

Incomplete abortion/retained products of conception Endometrial neoplasm Leiomyoma with degeneration Ectopic pregnancy

Discussion Background The term gestational trophoblastic disease covers a spectrum of diseases arising from placental trophoblastic tissue after normal or abnormal fertilization. The most common forms of GTD are complete hydatidiform mole (~80% of cases), invasive mole (chorioadenoma destruens), and choriocarcinoma. Partial hydatidiform moles and placental site trophoblastic tumors are less frequently described. Hydatidiform moles can occur at any age, but they are usually reported in pregnant women in their teens or in their 4th to 5th decades (older patients are more likely to have malignant forms). Several epidemiologic studies have documented broad geographic variations in the prevalence of GTD; higher frequencies have been observed in Asia and Latin America, whereas North America and Europe tend to have a lower incidence.

Clinical Findings Patients with hydatidiform mole may experience abnormal vaginal bleeding during the first trimester of pregnancy, vaginal discharge of hydropic trophoblastic villi, and severe prolonged hyperemesis gravidarum. Physical examination may reveal a disproportionately enlarged uterus for the estimated gestational age and enlarged ovaries, as well the presence of theca lutein cysts. Increased levels of ␤-HCG are associated with all forms of GTD.

Complications Choriocarcinomas, the malignant form of GTD, can metastasize to the lungs, brain, lower genital tract, liver, kidneys, and gastrointestinal tract, causing hematuria, hemoptysis, abdominal pain, and neurologic symptoms. Villous trophoblastic tissue may escape from the uterus into the venous outflow, causing signs and symptoms of acute pulmonary embolism (dyspnea, hemoptysis). Hyperthyroidism may occur as a consequence of the thyroid-stimulating properties of ␤-HCG.

Etiology Different predisposing factors have been identified, including maternal age, previous history of molar pregnancy, and maternal blood group (women with type A blood appear to be at higher risk of developing choriocarcinomas). Cytogenetic studies have demonstrated that most of the complete hydatidiform moles present a diploid karyotype 46,XX resulting from the fertilization of an empty ovum

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by two haploid spermatozoa or one haploid spermatozoon that duplicates its chromosomes (the maternal chromosomes are absent); no fetal parts can be identified in this form. Partial hydatidiform moles have a triploid (69,XXY) or even tetraploid (92,XXXY) karyotype resulting from the fertilization of a normal egg with two different spermatozoa, one carrying an X, the other a Y chromosome; fetal parts may be present in partial moles, as the embryo survives for several weeks.

Imaging Findings • •

• •

Ultrasound represents the imaging modality of choice for the evaluation of suspected GTD in patients with abnormally increased titer of ␤-HCG. Second-trimester hydatidiform moles have a classic sonographic appearance (snowstorm pattern or cluster of grapes appearance with alternating cystic and solid areas within the endometrial cavity) resulting from the hydropic enlargement of chorionic villi (Fig. 134.2). However, during the first trimester, molar pregnancies may mimic other gynecologic disorders, such as incomplete abortion, anembryonic gestation, and endometrial proliferative disease. Sometimes moles appear as echogenic masses filling the endometrial cavity without the typical vesicular pattern (as chorionic villi are probably too small to be observed). Focal myometrial thinning is suspicious for myometrial invasion in patients with invasive mole and choriocarcinoma. Malignant GTD is also suggested by the presence of irregular, multiple hypoechoic areas corresponding to hemorrhagic or necrotic foci. Doppler sonography may be helpful in GTD diagnosis, as these tumors are extremely vascular and demonstrate a very high diastolic blood flow. Computed tomography and magnetic resonance imaging (MRI) are usually performed to exclude the presence of molar tissue outside the uterus (distant metastases to the lungs, brain, and liver). At MRI, hydatidiform moles have low-intermediate signal on T1-weighted images and high signal intensity on T2-weighted images, reflecting the vesicular nature of the tumors; T1-weighted images help to detect hemorrhagic or necrotic foci. Invasive mole and choriocarcinomas appear as heterogeneous, variably enhancing masses typically distorting junctional zone anatomy.

Treatment •



Surgery (evacuation of the uterus and suction curettage) is recommended in case of complete hydatidiform mole, whereas both invasive mole and choriocarcinomas are treated with chemotherapeutic agents. Beta-HCG titers are continuously monitored after surgery and chemotherapy.

Fig. 134.2 Transvaginal ultrasound image of the uterus shows increased echogenicity of the placenta, along with multiple small cystic areas.

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Prognosis • •

The prognosis is usually favorable in patients with hydatidiform mole, although 15% may develop invasive moles or choriocarcinomas. Chemotherapy is extremely effective in cases of choriocarcinoma, resulting in up to 100% cure or remission.

PE ARL



Sonographic findings should always be evaluated according to clinical and laboratory data (especially ␤-HCG titers).

PITFALL



During the first trimester of pregnancy, hydatidiform moles may not demonstrate the typical snowstorm pattern and may mimic other gynecologic conditions.

Suggested Readings Allen SD, Lim AK, Seckl MJ, Blunt DM, Mitchell AW. Radiology of gestational trophoblastic neoplasia. Clin Radiol 2006;61(4):301–313 Altieri A, Franceschi S, Ferlay J, Smith J, La Vecchia C. Epidemiology and aetiology of gestational trophoblastic diseases. Lancet Oncol 2003;4(11):670–678 Atri M, Leduc C, Gillett P, et al. Role of endovaginal sonography in the diagnosis and management of ectopic pregnancy. Radiographics 1996;16:755–775 Barton JW, McCarthy SM, Kohorn EI, Scoutt LM, Lange RC. Pelvic MR imaging findings in gestational trophoblastic disease, incomplete abortion, and ectopic pregnancy: are they specific? Radiology 1993;186:163–168 Desai RK, Desberg AL. Diagnosis of gestational trophoblastic disease: value of endovaginal color flow Doppler sonography. AJR Am J Roentgenol 1991;157:787–788 Dohke M, Watanabe Y, Okumura A, et al. Comprehensive MR imaging of acute gynecologic diseases. Radiographics 2000;20:1551–1566 Green CL, Angtuaco TL, Shah HR, Parmley TH. Gestational trophoblastic disease: a spectrum of radiologic diagnosis. Radiographics 1996;16:1371–1384 Jain KA. Gestational trophoblastic disease: pictorial review. Ultrasound Q 2005;21(4):245–253 Nalaboff KM, Pellerito JS, Ben-Levi E. Imaging the endometrium: disease and normal variants. Radiographics 2001;21(6):1409–1424 Vitellas KM, Bennett WF, Bova JG. Case 2: placental site trophoblastic tumor. AJR Am J Roentgenol 2000;175:898–900 Wagner BJ, Woodward PJ, Dickey GE. From the archives of the AFIP. Gestational trophoblastic disease: radiologic-pathologic correlation. Radiographics 1996;16:131–148 Williams PL, Laifer-Narin SL, Ragavendra N. US of abnormal uterine bleeding. Radiographics 2003;23:703–718

CASE 135 Clinical Presentation A 31-year-old woman presents with severe pelvic pain and a history of dysmenorrhea.

A

B

Fig. 135.1 Axial MR T1-weighted images (A) with and (B) without fat saturation demonstrate bilateral T1 hyperintense ovarian lesions, which show relative hypointensity on (C) an axial T2-weighted image consistent with multiple endometriomas.

C

Radiologic Findings Axial magnetic resonance (MR) T1-weighted images with and without fat saturation (Fig. 135.1) demonstrate bilateral T1 hyperintense ovarian lesions, which show relative hypointensity on an axial T2-weighted image consistent with multiple endometriomas.

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Diagnosis Endometrioma (chocolate cyst)

Differential Diagnosis • • • • •

Hemorrhagic cysts Hemorrhagic corpus luteum Dermoid Mucinous cystic adnexal neoplasms (especially if containing hemorrhagic components) Ectopic pregnancy

Discussion Background Endometriosis is a gynecologic disorder, typically occurring in women of childbearing age (mean age 25–29 years), defined by the presence of ectopic endometrial tissue mostly located in the ovaries (endometrioma), fallopian tubes, cervix, vagina, uterosacral or broad ligaments, and cul-de-sac of Douglas. The term adenomyosis refers to the presence of endometrial tissue within the myometrium, but it is considered a distinct clinical entity according to the different symptoms, pathophysiology, and epidemiology. The gastrointestinal (GI) tract represents the most common extrapelvic site of endometriosis, but endometriosis has been reported in the abdominal wall (including laparoscopic scars), bladder, kidneys, spleen, gallbladder, nasal mucosa, pleura, lung parenchyma, and central nervous system. These lesions vary in size, ranging from microscopic implants to large lesions. The main risk factors for endometriosis are positive familiar history, hypermenorrhea, early age of menarche, and delayed childbearing.

Clinical Findings Patients may be completely asymptomatic or present with infertility (30–50% of cases), severe pelvic pain, dysmenorrhea, dyspareunia, and dyschezia (pain during defecation). Other symptoms are dependent on the site of disease and may include cyclic hemoptysis and catamenial pneumothorax if the chest is involved, for example, or urinary urgency, hematuria, and frequent urination in case of bladder involvement. Seizures, cyclic headaches, and subarachnoid hemorrhages have been described with central nervous system lesions.

Complications Endometriosis implants in the GI tract may cause rectal bleeding, constipation, and obstruction. Hydronephrosis and ureteral obstruction have been described as well. Some patients may present with signs mimicking an acute abdomen in case of sudden rupture of ovarian endometriomas. Malignant degeneration is described but is rare (< 1% of cases).

Etiology The etiology remains unclear. The metastatic theory suggests that endometriosis results from retrograde menstruation with seeding of endometrial tissue through the fallopian tubes into the peritoneal cavity; metastatic spread of endometrial cells may also take place via lymphatic channels or the

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bloodstream. The metaplastic theory suggests that peritoneal cells may differentiate into endometrial cells according to their common origin from coelomic wall epithelium. Currently, researchers are investigating the role of growth factors and immunity in the development of endometriosis.

Imaging Findings • •





Imaging plays a central role in the identification of endometriosis, although small peritoneal foci may not be detected. Ultrasound is mostly used to evaluate endometriomas with either a transabdominal or a transvaginal approach. These lesions usually appear homogeneous in echogenicity and are round, variably hypoechoic, often bilateral, and either unilocular or multilocular with thin or thick internal septa and wall nodularity. Anechoic endometriomas resembling a functional ovarian cyst have been described rarely. Currently MRI is the most specific technique for the assessment of endometriosis, as it is able to characterize endometriomas as well as small peritoneal endometriotic foci. The MRI protocol should include T1- and T2-weighted images as well as fat-suppressed T1-weighted images to narrow the differential diagnosis and to allow for the detection of extraovarian endometriosis. Administration of gadolinium is usually not required for the characterization of endometriosis because these lesions demonstrate nonspecific and extremely variable enhancement. MRI findings may vary according to the different concentration and age of blood products; the most common features are ⴰ Low signal on T2-weighted images (shading) resulting from cyclic bleeding and subsequent chronic accumulation of blood products (high concentration of protein and iron), although endometriomas may also demonstrate high or intermediate signal ⴰ Typically high signal on T1-weighted images (these represent the most reliable findings for the diagnosis of endometriomas regardless of their appearance on T2-weighted images) Despite some technical limitations, MRI is becoming a useful imaging tool for the assessment of deep subperitoneal endometriosis. These deep pelvic endometriotic implants present variable signal at MRI but often have a T1- and T2-weighted hypointense appearance due to associated fibrosis. Laparoscopy is currently more commonly used for the diagnosis or confirmation and staging of endometriosis.

Treatment •



Medical treatment aims to control pelvic pain with anti-inflammatory drugs and hormonal agents, such as gonadotropin-releasing hormone agonists, contraceptive pills, and progestational drugs; unfortunately, the recurrence rate of symptoms is high after therapy cessation. Conservative laparoscopic treatment is performed to relieve symptoms and maintain reproductive function (lysis of adhesions); total abdominal hysterectomy with bilateral salpingo-oophorectomy is commonly performed in women with intractable pain.

Prognosis •

Mortality is negligible, but life quality is considerably affected because of recurrent pelvic pain and infertility.

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PE ARL



An ovarian lesion presenting high signal on T1-weighted images and shading of signal on T2weighted images is highly suggestive of endometriomas.

PITFALL



Hemorrhagic ovarian cysts or hemorrhagic corpus luteum may demonstrate similar features, as can some hemorrhagic tumors. The patient’s history should always be carefully considered; resolution of hemorrhagic lesion on a follow-up examination allows radiologists to rule out endometriosis.

Suggested Readings Bazot M, Darai E, Hourani R, et al. Deep pelvic endometriosis: MR imaging for diagnosis and prediction of extension of disease. Radiology 2004;232:379–389 Bennett GL, Slywotzky CM, Giovanniello G. Gynecologic causes of acute pelvic pain: spectrum of CT findings. Radiographics 2002;22:785–801 Bhatt S, Kocakoc E, Dogra VS. Endometriosis: sonographic spectrum. Ultrasound Q 2006;22(4):273–280 Carbognin G, Girardi V, Pinali L, Raffaelli R, Bergamini V, Pozzi Mucelli R. Assessment of pelvic endometriosis: correlation of US and MRI with laparoscopic findings. Radiol Med (Torino) 2006;111(5):687–701 Del Frate C, Girometti R, Pittino M, Del Frate G, Bazzocchi M, Zuiani C. Deep retroperitoneal pelvic endometriosis: MR imaging appearance with laparoscopic correlation. Radiographics 2006;26(6):1705–1718 Gougoutas CA, Siegelman ES, Hunt J, Outwater EK. Pelvic endometriosis: various manifestations and MR imaging findings. AJR Am J Roentgenol 2000;175:353–358 Hensen JH, Van Breda Vriesman AC, Puylaert JB. Abdominal wall endometriosis: clinical presentation and imaging features with emphasis on sonography. AJR Am J Roentgenol 2006;186:616–620 Imaoka I, Wada A, Matsuo M, Yoshida M, Kitagaki H, Sugimura K. MR imaging of disorders associated with female infertility: use in diagnosis, treatment, and management. Radiographics 2003;23:1401–1421 Kuligowska E, Deeds L III, Lu K III. Pelvic pain: overlooked and underdiagnosed gynecologic conditions. Radiographics 2005;25:3–20 Lee YR, Choi YW, Jeon SC, Paik SS, Kang JH. On the AJR viewbox. Pleuropulmonary endometriosis: CT-pathologic correlation. AJR Am J Roentgenol 2006;186:1800–1801 Woodward PJ, Sohaey R, Mezzetti TP Jr. Endometriosis: radiologic-pathologic correlation. Radiographics 2001;21:193–216

CASE 136 Clinical Presentation A 26-year-old woman presents with vaginal bleeding. She has a history of multiple miscarriages.

B

A

Fig. 136.1 (A) Axial MR T2-weighted image demonstrates two uterine horns with a single cervix. Uterine zonal anatomy appears otherwise normal. A rounded T2 hyperintense focus is visualized within the cervix consistent with a nabothian cyst. (B) Axial MR T1-weighted fat-suppressed image obtained after the administration of intravenous gadolinium shows normal enhancement of the uterus.

Radiologic Findings An axial magnetic resonance (MR) T2-weighted image (Fig. 136.1) demonstrates two uterine horns with a single cervix. The uterine zonal anatomy appears otherwise normal. A rounded T2 hyperintense focus is visualized within the cervix consistent with a nabothian cyst. An axial MR T1-weighted fat-suppressed image obtained after the administration of intravenous gadolinium shows normal enhancement of the uterus.

Diagnosis Bicornuate uterus

Differential Diagnosis • • •

Arcuate uterus Septate uterus Uterus didelphys

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Discussion Background Uterovaginal (müllerian) anomalies result from alterations in the development or fusion of müllerian ducts and are associated with a high incidence of infertility, spontaneous abortion, fetal intrauterine growth retardation, preterm labor, and retained placenta; for this reason, most of these abnormalities are discovered in young adulthood or during pregnancy. The incidence is roughly estimated to range between 0.1 and 0.5% in the female population. Müllerian duct anomalies are commonly categorized into four classes according to embryology: •







Class I: dysgenesis—agenesis or hypoplasia of müllerian duct derivatives (uterus, cervix, and upper part of the vagina), as in Mayer-Rokitansky-Kuster-Hauser syndrome (agenesis of the uterus and proximal part of the vagina) Class II: disorders of vertical fusion—failure of fusion of the descending müllerian duct with the ascending sinovaginal bulb (this group includes cervical agenesis/dysgenesis and obstructive or nonobstructive transverse vaginal septa) Class III: disorders of lateral fusion—failure of fusion of the paired müllerian ducts (uterus didelphys and bicornuate uterus) and failure of resorption of the midline septum (septate uterus); a subclassification differentiates asymmetric obstructive forms (unicornuate uterus with obstructed horn, unilaterally obstructed double uterus, and unilateral vaginal obstruction) from symmetric nonobstructive forms (unicornuate, bicornuate, septate, didelphys, and diethylstilbestrol [DES]– related uteri) Class IV: unusual configurations and combined anomalies

Prompt identification of these anomalies is mandatory for the appropriate treatment of infertility and related symptoms.

Clinical Findings Uterovaginal anomalies may be suspected in a newborn/infant as a palpable abdominal mass (obstructed system: mucocolpos), in an adolescent girl presenting with delayed menarche, or in a woman of childbearing age being evaluated for infertility or repeated pregnancy loss. Patients with obstructed or partially obstructed müllerian systems may present with abdominal pain, hematosalpinx, hematocolpos, and endometriosis.

Complications As previously stated, müllerian anomalies are associated with infertility and an increased rate of spontaneous abortions. Genitourinary tract abnormalities, such as renal ectopia and agenesis, are also frequently described in these patients.

Etiology See embryologic classification.

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Imaging Findings •

• •

Ultrasound is usually the first examination performed for suspected abnormalities of the female genital system, but it cannot routinely delineate the external fundal contour, which is needed to distinguish between a bicornuate and septate uterus. Three-dimensional sonographic techniques can be used to assess the uterine anatomy in a multiplanar format, but they are not available in all medical centers. MRI is an excellent imaging modality for the diagnosis and characterization of female genital system abnormalities. Different parameters can be evaluated to properly classify these alterations: uterine size, external fundal contour, intercornual distance, uterine zonal anatomy, and the presence of vaginal or uterine septa. Recent advances in MRI (use of endovaginal or pelvic phased-array coils) provide a better assessment of female pelvic abnormalities. The most common findings on MRI according to the American Fertility Society classification of müllerian duct anomalies are ⴰ Dysgenesis: a hypoplastic uterus presents a small size, reduced intercornual distance (< 2 cm), and a poorly differentiated junctional zone on T2-weighted images. Mayer-Rokitanski-KusterHauser syndrome is a severe example of dysgenesis. ⴰ Unicornuate uterus: banana-shaped, usually laterally deviated uterus with one fallopian tube resulting from the agenesis of one müllerian duct; normal zonal anatomy on T2-weighted sequences ⴰ Uterus didelphys: resulting from complete failure of fusion of müllerian ducts; two separated uterine horns or bodies form, each one with its own cervix. Normal zonal anatomy is observed on T2-weighted images. Transverse and longitudinal vaginal septa are common. ⴰ Bicornuate uterus: due to partial fusion of the müllerian ducts, two uterine bodies with one cervix are formed. MRI features are intercornual distance > 4 cm and concavity of the fundal contour with a fundal cleft > 1 cm in depth. Arcuate uterus (Fig. 136.2) is the mildest form of bicornuate uterus and presents a convex or flat fundal contour. ⴰ Septate uterus (Fig. 136.3): failure of resorption of the septum. At MRI, a usually flat fundal contour and normal intercornual distance are seen; the septum may be either muscular (intermediate intensity signal on T2-weighted images) or fibrotic (low intensity signal on T2-weighted images), and the septation can be complete (if it reaches the internal os) or partial.

Fig. 136.2 Axial T2-weighted image shows a configuration of the uterine cavity most consistent with an arcuate uterus. No septum is appreciated. The endometrial canal is otherwise normal in appearance.

Fig. 136.3 Axial T2-weighted image demonstrates two uterine horns partially separated by a T2 low intensity signal midline septum; the external fundal contour is flat, and the intercornual distance is normal. These findings are consistent with a septated uterus.

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DES uterus: T-shaped or hypoplastic uterus; this condition is related to intrauterine exposure of female fetuses to DES.

Treatment •

Surgical treatment is performed according to the anomalies found at MRI. Didelphys and bicornuate uteri usually do not require surgery. Arcuate uterus is usually asymptomatic. Patients with a septate uterus may benefit from hysteroscopic metroplasty to improve fertility.

Prognosis •

The prognosis is generally favorable once the underlying anomaly is recognized.

PE ARL



Once a müullerian anomaly is identified, careful assessment should be performed of the urinary tract, as renal agenesis and ectopia are associated.

PITFALL S

• • •

Ultrasound may fail to distinguish between a bicornuate and a septate uterus (the latter may benefit from surgery). MRI should be recommended to assess uterine abnormalities. Hysterosalpingography can demonstrate two cornua but fails to assess the uterine fundus and therefore cannot be used to completely evaluate müullerian anomalies.

Suggested Readings Carrington BM, Hricak H, Nuruddin RN, et al. Müllerian duct anomalies: MR imaging evaluation. Radiology 1990;176(3):715–720 Fielding JR. MR imaging of müullerian anomalies: impact on therapy. AJR Am J Roentgenol 1996;167:1491–1495 Imaoka I, Wada A, Matsuo M, Yoshida M, Kitagaki H, Sugimura K. MR imaging of disorders associated with female infertility: use in diagnosis, treatment, and management. Radiographics 2003;23:1401–1421 Oppelt P, von Have M, Paulsen M, et al. Female genital malformations and their associated abnormalities. Fertil Steril 2007;87(2):335–342 Pellerito JS, McCarthy SM, Doyle MB, et al. Diagnosis of uterine anomalies: relative accuracy of MR imaging, endovaginal sonography, and hysterosalpingography. Radiology 1992;183(3):795–800 Raga F, Bonilla-Musoles F, Blanes J, Osborne NG. Congenital müullerian anomalies: diagnostic accuracy of three- dimensional ultrasound. Fertil Steril 1996;65(3):523–528 Saleem SN. MR imaging diagnosis of uterovaginal anomalies: current state of the art. Radiographics 2003;23:e13 Troiano RN, McCarthy SM. Müllerian duct anomalies: imaging and clinical issues. Radiology 2004;233:19–34 Woodward PJ, Wagner BJ, Farley TE. MR imaging in the evaluation of female infertility. Radiographics 1993;13:293–310

CASE 137 Clinical Presentation A 26-year-old woman presents with acute, severe pelvic pain, nausea, and vomiting.

A

B

Fig. 137.1 (A) Axial contrast-enhanced CT image demonstrates a heterogeneous, well-defined lesion centered in the midpelvis with a predominantly fat content and a fluid–fat level consistent with a dermoid; the right ovary is in close proximity to this lesion and appears ill-defined and edematous when compared with the contralateral side. These findings are highly suspicious for ovarian torsion. (B) Coronal CT image of the pelvis better emphasizes the size and location of the dermoid, as well as the edema and fluid collection surrounding the affected right ovary.

Radiologic Findings Axial and coronal computed tomography (CT) images of the abdomen obtained after administration of contrast (Fig. 137.1) show a heterogeneous density mass in the midpelvis, with mixed fat and soft tissue density. Adjacent and to the right of this mass there is an ill-defined soft tissue density, likely representing an edematous and enlarged right ovary. The left ovary appears otherwise normal.

Diagnosis Adnexal torsion secondary to ovarian dermoid

Differential Diagnosis • •

Adnexal solid masses Metastases

Discussion Background Ovarian torsion is an uncommon but significant cause of lower abdominal pain, occurring at any age but mostly in the early reproductive years. Its incidence is slightly higher in developed countries as a consequence of ovarian stimulation for infertility, although other causative factors should be considered. This condition is caused by the torsion of the ovary and/or fallopian tube around the vascular

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pedicle, resulting in vascular compromise; a delayed diagnosis may lead to infarction of the ovary. Prompt identification of ovarian torsion at imaging is therefore mandatory for radiologists.

Clinical Findings Clinical presentation is often nonspecific. Patients experience severe acute abdominal pain, usually over the involved side and radiating to the back and pelvis, as well as nausea, vomiting, and fever.

Complications If not promptly recognized, torsion may result in ovary infarction and possibly subsequent infection and peritonitis.

Etiology Different causes have been described according to the patient’s age, although benign ovarian tumors (e.g., dermoid cysts, fibromas, fibrothecomas, and cystoadenomas) represent the most common predisposing factor at any age: • • • • •

Young prepubertal women: developmental anomalies such as long fallopian tubes or absent mesosalpinx Women of childbearing age: functional cysts (follicular cysts, corpora albicans cysts), hemorrhagic cysts, endometriomas, and polycystic ovarian disease (Stein-Leventhal syndrome) Pregnancy: multiple follicles in enlarged ovaries as a result of induction of ovulation for infertility, corpus luteum cyst enlarging the ovary, and greater laxity of the tissues adjoining the adnexa Postmenopausal women: solid adnexal neoplasms (malignant lesions are less likely to cause torsion than benign ones, as they tend to fix the ovary to the surrounding structures) Adhesions resulting from previous pelvic surgery may increase the risk of ovarian torsion, independent of age.

Imaging Findings • • •

• •



Ultrasound represents the imaging modality of choice for the evaluation of suspected ovarian torsion. Unilateral ovarian enlargement (resulting from impaired lymphatic/venous drainage and edema) represents the most common sonographic feature. Color Doppler sonography can be used to demonstrate the lack of perfusion within the diseased ovary and thereby predict the viability of adnexal structures, but its role is not well established. In fact, pulsed Doppler shows limited specificity (e.g., normal arterial flow in proven adnexal torsion) probably because of a dual ovarian blood supply (ovarian artery and ovarian arterial branches of uterine artery) or venous thrombosis (occurring before arterial thrombosis). CT and magnetic resonance imaging are very useful imaging tools for diagnosing ovarian torsion. The most common findings are fallopian tube thickening (diameter > 10 mm); smooth, eccentric wall thickening due to edematous wall congestion; ascites, typically observed in the cul-de-sac (may be associated with adnexal hemorrhagic infarction); and uterine deviation to the side of the affected ovary. Less common findings are hemorrhage either within the thickened tube or the ovary and hemoperitoneum. Administration of intravenous contrast may be helpful in diagnosing ovarian torsion by demonstrating the lack of enhancement in the diseased adnexa.

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Treatment •

Salpingo-oophorectomy is limited to severe vascular compromise with necrotic infarction or peritonitis; currently, conservative treatment is preferred and performed laparoscopically to untwist the affected ovary and fix it (oophoropexy). Triplication of the utero-ovarian ligament is reserved for young patients with excessively long ligaments resulting in recurrent episodes of torsion.

Prognosis •

A delayed diagnosis may lead to severe complications, including infection and peritonitis, that may require surgical intervention.

PE ARL



Adnexal torsion should be suspected when an ovarian mass is noticed in the appropriate clinical setting.

PITFALL



Hemorrhagic cysts, endometriomas, and corpus luteum cysts may mimic an ovarian torsion. The patient’s clinical history should be carefully considered.

Suggested Readings Albayram F, Hamper UM. Ovarian and adnexal torsion: spectrum of sonographic findings with pathologic correlation. J Ultrasound Med 2001;20(10):1083–1089 Birchard KR, Brown MA, Hyslop WB, Firat Z, Semelka RC. MRI of acute abdominal and pelvic pain in pregnant patients. AJR Am J Roentgenol 2005;184(2):452–458 Ghossain MA, Hachem K, Buy JN, et al. Adnexal torsion: magnetic resonance findings in the viable adnexa with emphasis on stromal ovarian appearance. J Magn Reson Imaging 2004;20(3):451–462 Kimura I, Togashi K, Kawakami S, Takakura K, Mori T, Konishi J. Ovarian torsion: CT and MR imaging appearances. Radiology 1994;190(2):337–341 Lee EJ, Kwon HC, Joo HJ. Diagnosis of ovarian torsion with color Doppler sonography: depiction of twisted vascular pedicle. J Ultrasound Med 1998;17(2):83–89 Madrazo BL, Cordes JF, Cacciarelli AA. Ultrasound case of the day: right adnexal torsion. Radiographics 1992;12:201–202 Outwater EK, Dunton CJ. Imaging of the ovary and adnexa: clinical issues and applications of MR imaging. Radiology 1995;194(1):1–18 Pretorius ES, Outwater EK, Hunt JL, Siegelman ES. Magnetic resonance imaging of the ovary. Top Magn Reson Imaging 2001;12(2):131–146 Rha SE, Byun JY, Jung SE, et al. CT and MR imaging features of adnexal torsion. Radiographics 2002;22:283–294 Van Kerkhove F, Cannie M, Op de Beeck K, et al. Ovarian torsion in a premenarcheal girl: MRI findings. Abdom Imaging 2007;32(3):424–427 Warner MA, Fleischer AC, Edell SL, et al. Uterine adnexal torsion: sonographic findings. Radiology 1985;154:773–775

CASE 138 Clinical Presentation A 76-year-old woman presents with lower abdominal pain, weight loss, and changes in bowel habits.

A

B

Fig. 138.1 (A,B) Axial MR T2-weighted images demonstrate a large, cystic mass centered in the pelvis with multiple, small, solid papillary projections present along the walls of the lesion.

Radiologic Findings Axial magnetic resonance (MR) T2-weighted images (Fig. 138.1) demonstrate a large, cystic mass centered in the pelvis with multiple, small, solid papillary projections present along the walls of the lesion.

Diagnosis Ovarian mucinous cystoadenocarcinoma

Differential Diagnosis • • • • • •

Benign ovarian neoplasms (mucinous or serous cystoadenoma) Germ cell and sex cord–stromal malignancies Mucinous cystoadenocarcinoma of the appendix Metastases Hemorrhagic ovarian cyst Endometrioma

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Discussion Background Ovarian cancer represents the deadliest gynecologic malignancy and the fifth leading cause of death worldwide from cancer in the female population; most of the cases (90%) are sporadic and occur in postmenopausal women (more often in their 6th to 7th decades), with a small percentage (1–5%) described in younger patients with a family history of ovarian cancer. This neoplasm is extremely insidious, as it causes minimal or no symptoms in its early stages; thus, the diagnosis is often delayed. Ovarian tumors may be grouped according to their cellular origin into three major categories: •

• •

Epithelial tumors (arising from surface epithelium and mesothelium): serous or mucinous cystoadenoma or cystoadenocarcinoma, endometrioid carcinoma, clear cell carcinoma, and Brenner tumor Germ cell tumors: dysgerminoma, embryonal cell cancer, teratoma, and choriocarcinoma Sex cord–stromal tumors: granulosa cell tumor, Sertoli-Leydig cell tumor, thecoma, and fibroma

Among malignant neoplasms, the epithelial type is the most common (85% of cases) in the postmenopausal population; conversely, malignant germ cell tumors represent more than two thirds of ovarian malignancies affecting younger patients (< 20 years of age).

Clinical Findings Symptoms are usually minimal or nonspecific. In advanced stages, patients may experience abdominal pain, weight loss, changes in bowel habits, abdominal distention, or bowel obstruction. Cancer antigen 125 (CA 125) may be either increased or within normal limits (> 50% of cases); 85% of patients younger than 50 years with elevated CA 125 have benign disease, such as pelvic inflammatory disease, endometriosis, fibroids, or early pregnancy.

Complications In advanced stages, ovarian carcinoma is commonly associated with extensive ascites and/or pleural effusion (Meigs syndrome). Mucin-producing tumors spread in the peritoneal cavity and may fill with gelatinous material. This condition, known as pseudomyxoma peritonei, can lead to severe bowel obstruction. Some patients may present with hydronephrosis related to extrinsic compression of the ureters.

Etiology The etiology is unknown, although different factors have been identified as important for the development of ovarian cancer. According to the ovulation hypothesis, the risk of cancer is directly related to the number of ovulatory cycles; therefore, all of the conditions suppressing ovulation play a protective role, including multiparity, a history of breastfeeding, and the use of oral contraceptives. Nulliparity, early menarche, and late menopause all represent predisposing factors. A small but significant percentage of ovarian cancer is hereditary and occurs in younger, premenopausal women. Two different hereditary syndromes have been described: breast/ovarian syndrome, genetically linked to

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mutations of BRCA1 and BRCA2 tumor suppressor genes; and Lynch II syndrome, characterized by early onset colorectal carcinoma, endometrial carcinoma, upper gastrointestinal tract cancer, and, to a lesser extent, ovarian carcinoma.

Imaging Findings •

• • •

• • • • •

Staging represents the most important prognostic factor of ovarian carcinoma and is usually performed laparoscopically before surgery. Two main classification systems exist: the tumor-nodesmetastasis (TNM) system and the more commonly used International Federation of Gynecology and Obstetrics (FIGO) system based on surgical findings: ⴰ Stage I: limited to one ovary ± ascites (IC) ⴰ Stage II: involving one or both ovaries with pelvic extension (fallopian tubes, uterus: IIA; rectum, bladder, peritoneum: IIB) ± ascites (IIC) ⴰ Stage III: extrapelvic extension (retroperitoneal lymph node metastases, peritoneal implants outside the pelvis) ⴰ Stage IV: distant metastases The main purposes of imaging are to detect distant metastases, preventing the risk of understaging, and to demonstrate disease that may complicate surgical removal. Ultrasound is usually the primary imaging modality for the evaluation of adnexal masses, although it cannot be used for staging. Findings suggestive of malignancy include increased ovarian size (especially in postmenopausal women), cystic lesions > 5 cm with irregular wall thickening, internal thick septations (> 2 mm), and solid components. Calcifications are rare and usually linear in mucinous tumors, psammomatous in serous ones. CT is currently performed for staging ovarian carcinomas, although it may fail to detect peritoneal metastases < 1 cm. Administration of oral contrast medium is usually recommended to better differentiate bowel from serosal neoplastic implants and cystic ovarian masses. Peritoneal metastases may appear as focal soft tissue masses along the peritoneum and the hemidiaphragms or as nodular thickening or spiculation of the bowel wall. MRI can be performed for staging purposes but is definitely more sensitive than both computed tomography and ultrasound for the characterization of adnexal masses. Cystoadenocarcinomas present different signal intensity on T1- and T2-weighted images according to their different content (cystic or solid) and demonstrate marked enhancement of the tumor wall and septa.

Treatment •

Cytoreductive debulking surgery is the cornerstone of treatment for ovarian carcinoma: this surgical procedure aims to remove the primary adnexal mass as well as the serosal and omental implants. An optimal debulking represents the most important prognostic indicator for a patient’s survival, as it considerably improves the response to chemotherapy. Patients with initially unresectable disease may benefit from neoadjuvant chemotherapy before debulking surgery.

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Prognosis •

The prognosis is related to the stage of the disease at diagnosis. Overall, patients’ outcome is poor, with a 50% 5-year survival rate.

PE ARL



In patients with a previous history of ovarian carcinoma, the presence of abdominal ascites is highly suspicious for recurrence.

PITFALL



Differentiating borderline (low-malignant potential) lesions or benign lesions may sometimes be very challenging for the radiologist at both ultrasound and MRI. Clinical history should be carefully considered.

Suggested Readings Brown DL, Doubilet PM, Miller FH, et al. Benign and malignant ovarian masses: selection of the most discriminating gray-scale and Doppler sonographic features. Radiology 1998;208:103–110 Coakley FV, Choi PH, Gougoutas CA, et al. Peritoneal metastases: detection with spiral CT in patients with ovarian cancer. Radiology 2002;223:495–499 Forstner R, Hricak H, Occhipinti KA, Powell CB, Frankel SD, Stern JL. Ovarian cancer: staging with CT and MR imaging. Radiology 1995;197:619–626 Jung SE, Lee JM, Rha SE, Byun JY, Jung JI, Hahn ST. CT and MR imaging of ovarian tumors with emphasis on differential diagnosis. Radiographics 2002;22:1305–1325 Kawamoto S, Urban BA, Fishman EK. CT of epithelial ovarian tumors. Radiographics 1999;19:S85–S102 Kinkel K, Hricak H, Lu Y, Tsuda K, Filly RA. US characterization of ovarian masses: a meta-analysis. Radiology 2000;217:803–811 Kurtz AB, Tsimikas JV, Tempany CM, et al. Diagnosis and staging of ovarian cancer: comparative values of Doppler and conventional US, CT, and MR imaging correlated with surgery and histopathologic analysis—report of the Radiology Diagnostic Oncology Group. Radiology 1999;212:19–27 Lee SI. Imaging evaluation of adnexal masses: self-assessment module. AJR Am J Roentgenol 2006;187(3):S457–S459 Saksouk FA, Johnson SC. Recognition of the ovaries and ovarian origin of pelvic masses with CT. Radiographics 2004;24:S133–S146 Tanaka YO, Tsunoda H, Kitagawa Y, Ueno T, Yoshikawa H, Saida Y. Functioning ovarian tumors: direct and indirect findings at MR imaging. Radiographics 2004;24:S147–S166 Wagner BJ, Buck JL, Seidman JD, McCabe KM. From the archives of the AFIP. Ovarian epithelial neoplasms: radiologic-pathologic correlation. Radiographics 1994;14:1351–1376 Woodward PJ, Hosseinzadeh K, Saenger JS. From the archives of the AFIP: radiologic staging of ovarian carcinoma with pathologic correlation. Radiographics 2004;24:225–246

CASE 139 Clinical Presentation A 65-year-old woman presents with vaginal bleeding.

A

B

Fig. 139.1 (A) Sagittal T2-weighted image demonstrates a solid mass with low-intermediate signal intensity within the endometrial cavity. The mass extends inferiorly, with infiltration of the cervical stroma, and invades the myometrium superiorly. (B) Sagittal gadolinium-enhanced image shows a relative lack of enhancement of the tumor compared with the myometrium.

Radiologic Findings Sagittal T2-weighted images (Fig. 139.1) demonstrate a solid mass with low-intermediate signal intensity within the endometrial cavity. The mass extends inferiorly, with infiltration of the cervical stroma, and invades the myometrium superiorly.

Diagnosis Endometrial adenocarcinoma

Differential Diagnosis • • • •

Endometrial hyperplasia Endometrial polyp Endometrial sarcoma Cervical cancer

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Discussion Background Endometrial carcinoma is the most common gynecologic malignancy in the United States but only the eighth leading cause of death from cancer in the female population, as it is usually detected at an early stage. This neoplasm mostly affects perimenopausal and postmenopausal women in their 5th to 6th decades, whereas it is uncommonly seen in patients younger than 40 years (< 5%). Nearly 80% of endometrial neoplasms are adenocarcinomas, but other histologic subtypes have been described, including adenosquamous, clear cell, and papillary serous carcinomas. Sarcomas are considerably rarer than adenocarcinomas, but they are associated with a poorer prognosis. Adenocarcinomas may arise from adenomatous hyperplasia of the endometrium (higher risk of progression in cases of cellular atypia); this condition results from the overgrowth of uterine endometrium in postmenopausal women treated with exogenous estrogen or affected by estrogenproducing ovarian neoplasms. Endometrial adenocarcinomas have also been shown to arise from endometrial polyps (~10% are malignant in postmenopausal women); these lesions are usually discovered by accident, although some of them may be associated with vaginal bleeding.

Clinical Findings The most common symptom observed in up to 90% of patients is postmenopausal vaginal spotting or bleeding. Other presenting symptoms are purulent vaginal discharge, pain, weight loss, and changes in bladder and bowel habits, however, these are symptoms of advanced disease.

Complications In advanced stages, patients may present with distant metastases, typically to the liver, lung, and brain.

Etiology Different risk factors have been identified, including obesity, nulliparity, late menopause, exogenous unopposed estrogen therapy, use of tamoxifen (estrogenic stimulation of the uterus), diabetes, hypertension, high dietary fat consumption, and pelvic radiation therapy (the latter associated with increased risk of carcinosarcomas).

Imaging Findings •



Cross-sectional imaging, especially magnetic resonance imaging (MRI), plays a key role in the diagnosis and staging of endometrial carcinomas; in fact, the assessment of the disease stage (evaluation of the depth of myometrial involvement and identification of lymph node metastases) is very important for patients’ management. The staging classification is defined as follows: ⴰ Stage I: IA—limited to the endometrium; IB—invasion of less than one half of the myometrium; IC—invasion of one half or more than one half of the myometrium ⴰ Stage II: IIA—endocervical glandular involvement only; IIB—cervical stromal invasion

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Stage III: IIIA—invasion of serosa and/or adnexa and/or positive peritoneal cytology; IIIB— vaginal metastases; IIIC—metastases to pelvic and/or para-aortic lymph nodes ⴰ Stage IV: IVA—invasion of bladder and/or bowel mucosa: IVB—distant metastases, including intra-abdominal metastases and/or inguinal lymph nodes At MRI, the signal intensity of endometrial neoplasms may be similar to normal endometrial tissue. After the administration of contrast, they demonstrate variable enhancement patterns but are usually lower signal intensity than normal inner myometrium. Disruption or discontinuity of the junctional zone suggests myometrial invasion. Ultrasound is also performed for the evaluation of endometrial neoplasms, as it provides excellent visualization of the endometrial stripe (linear hyperechoic appearance). Most authors agree to consider 8 mm as the threshold value of thickness in postmenopausal women, although the normal endometrium may measure up to 12 mm in those women being treated with unopposed estrogen therapy. A thickness of 4 mm or less is generally associated with endometrial atrophy. Ultrasound may also be useful to assess the depth of myometrial invasion, typically described as obliteration of the hypoechoic inner myometrium.

Treatment •

• •

Surgery alone represents the mainstay of treatment for most endometrial malignancies in the early stages (management for stage I patients is total abdominal hysterectomy and bilateral salpingooophorectomy). Nonsurgical therapies, such as radiation therapy, chemotherapy, and hormonal therapy, have been used mostly to treat recurrences and metastatic disease. Radiation therapy is the first choice for the treatment of early-stage endometrial neoplasms in patients who are considered poor surgical candidates.

Prognosis •

The prognosis depends on the depth of myometrial invasion and the presence of lymph node metastases, but it is generally favorable, as almost 80% of cases are detected in the early stages.

PE ARL



Hormonal therapies should always be investigated before scanning postmenopausal women; patients using sequential hormones should be studied at either the beginning or the end of the hormone cycle to evaluate the endometrium at its thinnest. Women treated with unopposed estrogen therapy (higher risk to develop cancers) have a thicker endometrial stripe; in case of sudden changes in thickness or bleeding, a biopsy is recommended.

PITFALL



Gross evaluation of myometrial invasion, a critical finding for endometrial carcinoma staging and patients’ outcome, becomes less reliable with increasing tumor dimension.

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Suggested Readings Atri M, Nazarnia S, Aldis AE, Reinhold C, Bret PM, Kintzen G. Transvaginal US appearance of endometrial abnormalities. Radiographics 1994;14:483–492 Davis PC, O’Neill MJ, Yoder IC, Lee SI, Mueller PR. Sonohysterographic findings of endometrial and subendometrial conditions. Radiographics 2002;22:803–816 DelMaschio A, Vanzulli A, Sironi S, et al. Estimating the depth of myometrial involvement by endometrial carcinoma: efficacy of transvaginal sonography vs MR imaging. AJR Am J Roentgenol 1993;160:533–538 Hann LE, Giess CS, Bach AM, Tao Y, Baum HJ, Barakat RR. Endometrial thickness in tamoxifen-treated patients: correlation with clinical and pathologic findings. AJR Am J Roentgenol 1997;168:657–661 Hulka CA, Hall DA, McCarthy K, Simeone JF. Endometrial polyps, hyperplasia, and carcinoma in postmenopausal women: differentiation with endovaginal sonography. Radiology 1994;191:755–758 Lee EJ, Byun JY, Kim BS, Koong SE, Shinn KS. Staging of early endometrial carcinoma: assessment with T2-weighted and gadolinium-enhanced T1-weighted MR imaging. Radiographics 1999;19:937–947 Levine D, Gosink BB, Johnson LA. Change in endometrial thickness in postmenopausal women undergoing hormone replacement therapy. Radiology 1995;197:603–608 Manfredi R, Mirk P, Maresca G, et al. Local-regional staging of endometrial carcinoma: role of MR imaging in surgical planning. Radiology 2004;231:372–378 Nalaboff KM, Pellerito JS, Ben-Levi E. Imaging the endometrium: disease and normal variants. Radiographics 2001;21(6):1409–1424 Posniak HV, Olson MC, Dudiak CM, et al. MR imaging of uterine carcinoma: correlation with clinical and pathologic findings. Radiographics 1990;10:15–27 Rockall AG, Meroni R, Sohaib SA, et al. Evaluation of endometrial carcinoma on magnetic resonance imaging. Int J Gynecol Cancer 2007;17(1):188–196 Takahashi S, Murakami T, Narumi Y, et al. Preoperative staging of endometrial carcinoma: diagnostic effect of T2-weighted fast spin-echo MR imaging. Radiology 1998;206:539–547 Williams PL, Laifer-Narin SL, Ragavendra N. US of abnormal uterine bleeding. Radiographics 2003;23:703–718

CASE 140 Clinical Presentation A 56-year-old woman presents with abnormal postmenopausal vaginal bleeding.

B

A

Fig. 140.1 (A) Sagittal MR T2-weighted image shows a low-intermediate signal intensity mass (arrow) located in the cervix, extending both superiorly to the uterine cavity and inferiorly to the upper third of the vagina. (B,C) Axial MR T2weighted images demonstrate disruption of the T2 hypointense fibrous stromal ring (arrow) of the parametrium. This finding is suggestive of parametrial invasion (stage IIB).

C

Radiologic Findings Sagittal and axial magnetic resonance (MR) T2-weighted images (Fig. 140.1) demonstrate a mildly T2 hyperintense mass centered in the cervix. There is evidence of parametrial invasion on the left.

Diagnosis Cervical carcinoma

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Differential Diagnosis • • • • • •

Endocervical polyp Metastases (typically from endometrial carcinomas) Cervical leiomyoma Cervicitis Endometrial carcinoma Complex nabothian cysts

Discussion Background Cervical cancer represents the third most common gynecologic malignancy in the United States and the most common gynecologic neoplasm in women age < 45 years worldwide. The incidence has been decreasing in the last few years because of the growing use of screening programs, but it is still high in economically disadvantaged countries. Most cervical neoplasms (90%) are squamous cell carcinomas (SCCs); adenocarcinomas account for the remaining 10% of cases, with different hystopathologic subtypes identified for both of these tumors. SCCs usually spread to the lower uterine segment, vagina, and paracervical spaces along the broad and uterosacral ligament; in advanced stages, progressive involvement of the bladder, rectum, pelvic lymph nodes, and pelvic side wall is common. Radiologic staging plays a central role in patients’ management, as it affects both treatment and outcome.

Clinical Findings Clinical presentation is correlated strongly with the cervical cancer stage; patients may be asymptomatic (typically in the early stages) or may present with abnormal vaginal bleeding (irregular menses, hypermenorrhea, or painless metrorrhagia) or abnormal vaginal discharge (watery, mucoid, or purulent). Abdominal and pelvic pain, along with rectal or urinary symptoms, usually occurs in advanced stages.

Complications Advanced carcinomas may progress through the parametrium to involve the pelvic side wall and ureters, leading to hydronephrosis, pyelonephritis, and renal failure. In some patients the sciatic plexus may be involved, with consequent lumbar pain.

Etiology Human papilloma virus (types 13, 16, 18, 31, 33, and 35) is widely acknowledged as the most important causative agent of cervical carcinomas, although it cannot account for all the mutations recognized at the molecular level. Several risk factors have been identified, including low socioeconomic status, race (incidence is slightly higher in African-American women than in Caucasians), multiple sexual partners, young age at first pregnancy, and multiparity. Currently, the Papanicolaou smear (Pap test) represents a valuable screening tool for the early identification of cervical carcinomas and is recommended annually.

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Imaging Findings •



• •



Cervical carcinoma is staged according to the International Federation of Gynecology and Obstetrics (FIGO) system based on pelvic physical examination, intravenous urography, and radiologic evaluation of the chest and bones. Major categories of the FIGO classification system are ⴰ Stage 0: carcinoma in situ ⴰ Stage I: tumor confined to the uterus ⴰ Stage II: tumor extends beyond the uterus but not to the pelvic wall or the lower third of the vagina; IIA: no parametrial invasion; IIB: parametrial invasion (critical for exclusion from surgical treatment) ⴰ Stage III: tumor extends to the pelvic wall or the lower third of the vagina or causes hydronephrosis or a nonfunctioning kidney ⴰ Stage IVA: tumor extends beyond the true pelvis or invades the mucosa of the bladder or rectum; IVB: distant metastases MRI has been increasingly performed for the evaluation of cervical carcinoma because of its excellent visualization of the female pelvis; moreover, MRI staging obviates the use of invasive procedures (cystoscopy or proctoscopy) and reliably identifies tumor volume and lymph node involvement (critical prognostic factors). The tumor typically appears as a T2 hyperintense mass centered in the cervix, either extending into the vagina or invading the lower myometrium (stage I); preservation of the T2 hypointense rim of the fibrous cervical stroma represents a reliable finding to rule out tumor invasion beyond to the cervix (stage II). MRI is also superior to other imaging techniques for the evaluation of parametrial invasion, which is the most crucial point in preoperative staging: disruption of the T2 hypointense fibrous stromal ring is consistent with parametrial invasion (stage IIB), which would contraindicate surgical therapy. Dynamic gadolinium-enhanced imaging may be useful to detect a small tumor. Ultrasound plays a minor role in cervical carcinoma staging because of its inability to visualize lymph nodes and disseminated metastases; nonetheless, it usually represents the initial imaging modality for patients presenting with typical symptoms. Because cervical masses may appear isoechoic with normal cervical tissue, the enlargement of the cervix may be the only sign of cancer. Fluid within the uterine cavity may result from lesions obstructing the endocervical canal. Tumor-infiltrated parametrium is replaced by parenchymatous tissue, with the sonographic appearance identical to that of the primary cancer.

Treatment •



Treatment varies according to the preoperative stage. Carcinomas in situ (stage 0) or microinvasive cancer can be managed with superficial ablative techniques, including laser conization, laser vaporization, and cryotherapy. Surgery is recommended for patients with stage IA/B (tumor confined to the uterus) and stage IIA (tumor extends beyond the uterus with involvement of the proximal vagina). Patients with stage IIB or higher are treated with radiation therapy. Differentiation between stages IIA and IIB is critical for treatment planning.

Prognosis • •

The prognosis relies on the early detection (screening programs) and prompt treatment of the tumor. Invasive cervical cancer remains a major cause of death in the female population worldwide.

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PE ARL



Establishing the preservation of the T2 hypointense ring of fibrous cervical stroma is crucial to determining whether or not the patient is a surgical candidate.

PITFALL



Ultrasound can miss isoechoic cervical carcinomas.

Suggested Readings Kim SH, Choi BI, Lee HP, et al. Uterine cervical carcinoma: comparison of CT and MR findings. Radiology 1990;175:45–51 Milestone BN, Schnall MD, Lenkinski RE, Kressel HY. Cervical carcinoma: MR imaging with an endorectal surface coil. Radiology 1991;180:91–95 Nicolet V, Carignan L, Bourdon F, Prosmanne O. MR imaging of cervical carcinoma: a practical staging approach. Radiographics 2000;20:1539–1549 Okamoto Y, Tanaka YO, Nishida M, Tsunoda H, Yoshikawa H, Itai Y. MR imaging of the uterine cervix: imaging-pathologic correlation. Radiographics 2003;23:425–445 Pannu HK, Corl FM, Fishman EK. CT evaluation of cervical cancer: spectrum of disease. Radiographics 2001;21:1155–1168 Scheidler J, Heuck AF. Imaging of cancer of the cervix. Radiol Clin North Am 2002;40(3):577–590 Sironi S, De Cobelli F, Scarfone G, et al. Carcinoma of the cervix: value of plain and gadoliniumenhanced MR imaging in assessing degree of invasiveness. Radiology 1993;188:797–801 Subak LL, Hricak H, Powell CB, et al. Cervical carcinoma: computed tomography and magnetic resonance imaging for preoperative staging. Obstet Gynecol 1995;86(1):43–50 Tsuda K, Murakami T, Kurachi H, et al. MR imaging of cervical carcinoma: comparison among T2weighted, dynamic, and postcontrast T1-weighted images with histopathological correlation. Abdom Imaging 1997;22(1):103–107 Yamashita Y, Takahashi M, Sawada T, Miyazaki K, Okamura H. Carcinoma of the cervix: dynamic MR imaging. Radiology 1992;182:643–648

CASE 141 Clinical Presentation Computed tomography (CT) scans of the chest, abdomen, and pelvis were obtained in a 73-yearold woman as part of a staging work-up for a recently diagnosed lung cancer.

A

B

Fig. 141.1 Contrast-enhanced CT scans reveal (A) a large right ovarian mass with macroscopic fat (arrows), soft tissue components, and (B) a focus of calcification (arrow).

Radiologic Findings Contrast-enhanced CT reveals a large right ovarian mass with macroscopic fat, soft tissue components, and a focus of calcification (Fig. 141.1).

Diagnosis Mature cystic teratoma (dermoid cyst)

Differential Diagnosis • •

Lipoma in pelvis Liposarcoma

Discussion Background Ovarian teratomas are the most common germ cell neoplasm and are subdivided into mature cystic teratomas (dermoid cysts), immature teratomas, and monodermal teratomas (i.e., struma ovarii and carcinoid tumors). Mature cystic teratomas are the most prevalent subtype.

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Clinical Findings Mature cystic teratomas are usually asymptomatic and discovered incidentally during pelvic sonography. Nonspecific symptoms, such as abdominal pain, occur in a minority of cases. Immature teratomas usually are seen in younger patients (usually the first 2 decades) and are more commonly symptomatic.

Complications Ovarian torsion is the most common complication of mature cystic teratomas. This can be seen in up to 15% of cases and is more common in larger lesions.

Imaging Findings •



Mature cystic teratomas with classic findings can be diagnosed with ultrasound. However, they can have a variety of sonographic appearances and, at times, the sonographic diagnosis is challenging. Typical sonographic appearances are an echogenic mass with sound attenuation, a cystic lesion containing a densely echogenic plug (dermoid plug or Rokitansky nodule), a fat–fluid level, and a mass with multiple, thin, echogenic bands (dot–dash pattern), which is thought to represent hair within a cyst (Fig. 141.2). The diagnosis can be confirmed with CT or magnetic resonance imaging (MRI) in difficult cases. On CT, fat attenuation within a cyst is diagnostic. On MRI, frequency-selective fat saturation is used to demonstrate macroscopic fat (Fig. 141.3). An enlarging soft tissue component noted within the lesion or arising from the lesion and invading adjacent structures suggests malignant transformation. Immature teratomas differ from mature cystic teratomas in that they usually contain a large and irregular solid component.

Treatment •



In general, the treatment for mature cystic teratomas is surgical resection. Premenopausal women with small lesions, especially those who desire pregnancy, can be followed without surgery. Larger tumors are usually excised due to risk of torsion. Elderly patients with comorbidities and high surgical risk can be managed expectantly.

Fig. 141.2 A right ovarian mass with echogenic dots and thin bands, likely corresponding to hair, within a pathologically confirmed mature cystic teratoma.

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B

A

Fig. 141.3 (A) T2-weighted, (B) T1-weighted, and (C) T1weighted with fat saturation images reveal a right ovarian mass with high T2 signal and high T1 signal, with corresponding low signal on fat saturation image, consistent with macroscopic fat within mature cystic teratomas.

PE ARL



Macroscopic fat within an ovarian cystic lesion seen on CT or MRI is diagnostic.

PITFALL



Hemorrhage into an ovarian cyst or endometrioma can mimic a mature teratoma on ultrasound. Teratomas also can be confused with shadowing gas-filled bowel, given the ability of fat to cause acoustic shadowing.

Suggested Readings Caspi B, Appelman Z, Rabinerson D, Zalel Y, Tulandi T, Shoham Z. The growth pattern of ovarian dermoid cysts: a prospective study in premenopausal and postmenopausal women. Fertil Steril 1997;68(3):501–505 Outwater EK, Siegelman ES, Hunt JL. Ovarian teratomas: tumor types and imaging characteristics. Radiographics 2001;21:475–490

C

CASE 142 Clinical Presentation A 67-year-old woman presents with subacute abdominal pain, constipation, and increased abdominal girth.

A

B

Fig. 142.1 (A) Sagittal T2-weighted image reveals a bulky, lobulated mass centered in the uterine cervix with intermediate signal. (B,C) Transverse T1-weighted images show the mass with homogeneous low signal, which demonstrates moderate, fairly uniform enhancement.

C

Radiologic Findings A sagittal T2-weighted image (Fig. 142.1A) reveals a bulky, lobulated mass centered in the uterine cervix with intermediate signal. Transverse T1-weighted images (Fig. 142.1B,C) show the mass with homogeneous low signal, which demonstrates moderate, fairly uniform enhancement.

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Diagnosis Cervical lymphoma (large B-cell, follicular type)

Differential Diagnosis • • •

Cervical carcinoma Sarcoma of the cervix or uterus Metastatic disease

Discussion Background Cervical lymphoma is a rare disease, accounting for < 1% of cervical malignancies. Cervical involvement in the context of multiorgan disease is more common than primary cervical lymphoma. Primary malignant lymphoma of the genital tract accounts for only 1% of extranodal lymphomas.

Clinical Findings Patients typically present with abnormal vaginal bleeding, similar to patients with squamous cell carcinoma of the cervix. Patients may also experience urinary symptoms, constipation, or a palpable mass. A bulky cervix is discovered on pelvic examination.

Complications Cervical lymphoma can be difficult to diagnose. A diagnosis can be suggested based on imaging; however, the imaging findings are nonspecific. Additional sites of disease can be a clue to the diagnosis. Cervical cytology can be normal in the setting of cervical lymphoma, as the malignancy arises within the stroma as opposed to the mucosa. Therefore, a deep cervical biopsy may be needed to establish the diagnosis. It is important to establish a diagnosis of cervical lymphoma because the treatment plan differs from that of more common cervical cancers.

Imaging Findings •



Assessment and staging of a cervical mass is best performed with pelvic magnetic resonance imaging (MRI). Cervical lymphoma typically appears as a large mass centered in the uterine cervix with lobulated contours. Cervical lymphoma is usually homogeneous in signal intensity without evidence of significant necrosis and demonstrates moderate, diffuse enhancement. These imaging features can help in distinguishing lymphoma from other large cervical/uterine masses (i.e., cervical carcinoma, endometrial carcinoma, and degenerating leiomyomas), which tend to be more heterogeneous in appearance. Lymphoma can extensively involve the uterus and can spread locally into the vagina and parametrium. Lymphadenopathy can be seen both within and outside the pelvis. Findings on computed tomography (CT) are similar to MRI (a large, lobulated, homogeneous cervical mass), although MRI is superior in the evaluation of the local extent of disease. CT is equivalent to MRI with respect to identifying enlarged lymph nodes within the abdomen and pelvis. CT is better than MRI for the assessment of disease in the chest.

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Cervical lymphoma can be seen on ultrasound as a nonspecific large mass centered in the cervix. Ultrasound is not adequate for evaluating the local extent of disease or for staging.

Treatment •

The treatment of cervical lymphoma is not entirely standardized and may depend on several factors, such as age, extent of disease, functional status of the patient, and desire for fertility. Treatment can include some combination of chemotherapy, radiation, and surgery. The preferred treatment of patients with advanced disease is combined chemotherapy and radiation. Young women who wish to retain their fertility can be treated with combination chemotherapy alone. Patients with cervical lymphoma tend have a good prognosis.

Suggested Readings Chan JK, Loizzi V, Magistris A, et al. Clinicopathologic features of six cases of primary cervical lymphoma. Am J Obstet Gynecol 2005;193(3):866–872 Thyagarajan MS, Dobson MJ, Biswas A. Appearance of uterine cervical lymphoma on MRI: a case report and review of the literature. Br J Radiol 2004;77:512–515

CASE 143 Clinical Presentation A 21-year-old man presents with an absent left testicle.

B

A

Fig. 143.1 (A–C) T1- and T2-weighted MRI images reveal the presence of an ovoid mass adjacent to the left external iliac vessels. The mass is hypointense on the T1weighted image and hyperintense on the T2-weighted image (arrows).

C

Radiologic Findings T1- and T2-weighted magnetic resonance (MR) images (Fig. 143.1) reveal the presence of an ovoid mass adjacent to the left external iliac vessels. The mass is hypointense on the T1-weighted image and hyperintense on the T2-weighted image.

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Diagnosis Undescended testis (cryptorchidism)

Differential Diagnosis • • •

Enlarged external iliac lymph node Aneurysm of the left external iliac artery Soft tissue mesenchymal tumor

Discussion Background Cryptorchidism means “hidden or obscure testis” and generally refers to an undescended or maldescended testis. Although 4% of newborns have undescended testes, the incidence falls to 0.8% by 3 months, as the testis may spontaneously descend after birth.

Clinical Findings The most common sign is an absent testis in the scrotal sac. Infertility can result from impaired function of the cryptorchid testis.

Complications There is increased risk of malignant neoplasm in the cryptorchid testis. The increased risk is also present in the contralateral testis. Orchidopexy is not protective against subsequent testis cancer. Testicular tumors after previously successful orchidopexy most frequently are nonseminomatous germ cell tumors; abdominal testes may develop seminomas. The increased incidence of nonseminomatous tumors after orchidopexy has been postulated to be due to ischemic atrophy and secondary hypogonadism.

Etiology The multifactorial mechanism resulting in the interruption of the embryologic process of testicular descent is (1) differential body growth relative to the spermatic cord/gubernaculum; (2) increased abdominal pressure; (3) hormonal factors, including testosterone, müllerian inhibiting substance, and extrinsic estrogen; (4) development/maturation of the epididymis; and (5) gubernacular attachment. These patients may have associated abnormalities, such as renal agenesis, renal ectopia, prune belly syndrome, epispadias, wolffian duct anomalies (including seminal vesicle cysts), and ectopic ureter.

Imaging Findings • • •

Radiologic studies to localize the testis are currently of very little value. Ultrasonography is associated with high false-negative rates in the evaluation of a nonpalpable testis. However, it may show the undescended testis in the inguinal canal. MRI and computed tomography (CT) may show the presence of an intra-abdominal testis. Oral and intravenous contrasts are recommended to differentiate bowel loops.

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Ultrasound of the upper urinary tracts has been investigated because of the embryologic association of the ureteric bud and the wolffian duct, but the yield of significant urinary pathology is no greater than the incidence of anomalies found in the general population. There are four types of cryptorchid testes: ⴰ Retractile: moves intermittently between the groin and the scrotal base ⴰ Canalicular: present between the internal and external inguinal rings ⴰ Abdominal: present proximal to the internal ring ⴰ Ectopic: remote from the normal pathway of descent

Treatment •

Orchiopexy before age 2; surgical removal postpuberty

Prognosis •

The prognosis is generally good if the condition is detected and orchiopexy is performed early in life.

PE ARL



Soft tissue mass in the pelvis along the expected testicular course of descent in a young male patient

PITFALL



An undescended testis may be difficult to detect by imaging if it is small and atrophic.

Suggested Readings Docimo SG. The results of surgical therapy for cryptorchidism: a literature review and analysis. J Urol 1995;154(3):1148–1152 Shadbolt CL, Heinze SB, Dietrich RB. Imaging of groin masses: inguinal anatomy and pathologic conditions revisited. Radiographics 2001;21:261–271

CASE 14 4 Clinical Presentation A 26-year-old man complains of dull pain in the right scrotum.

B

A

C

D

Fig. 144.1 (A,B) Ultrasound images of the right testicle show an ill-defined, hypoechoic area with no increased Doppler flow. (C,D) Sagittal and axial T2-weighted images show an ill-defined, hypointense area within a hyperintense normal testis. (continued)

Radiologic Findings Ultrasound of the right testis shows an ill-defined, hypoechoic area with no increase in Doppler flow. T2-weighted magnetic resonance imaging (MRI) shows an ill-defined, hypointense area in the right testis, which shows a lack of enhancement on the postgadolinium-enhanced T1-weighted image (Fig. 144.1).

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Fig. 144.1 (continued) (E) On a postgadoliniumenhanced T1-weighted image, there is a focal area that shows a lack of normal enhancement.

E

Diagnosis Segmental testicular infarct

Differential Diagnosis • • • •

Focal testicular tumor Granulomatous orchitis Lymphoma Metastases

Discussion Background Segmental testicular infarction is rare and usually diagnosed after orchiectomy.

Clinical Findings Patients usually complain of ill-defined scrotal pain. Unlike testicular torsion, which can cause sharp, acute pain, testicular infarct usually causes dull pain.

Complications Although no direct complications arise from the condition, it can be commonly mistaken for a focal tumor and may lead to surgical exploration, as was the case in this patient.

Etiology Segmental infarct of the testicle is relatively rare and has been reported in patients at risk for small vessel ischemic disease, such as those with underlying vasculitis, sickle cell disease, and hypercoagulable states. It may also be an uncommon complication of epididymo-orchitis, scrotal trauma, and inguinal hernia repair.

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Imaging Findings •

• •

At ultrasound, the infarct appears as a wedge-shaped or geographic area of low echogenicity with its vertex directed toward the testicular mediastinum. It may, however, be ill defined and mimic a focal tumor. On MRI, the focal area of infarction is hypointense on T1- and T2-weighted images unless there is hemorrhage in the area of infarction, in which case there are T1 hyperintense areas. One finding that has been found to be specific for segmental infarct is the presence of a surrounding markedly enhanced rim on postgadolinium-enhanced images (seen in > 90% of the patients).

Treatment • •

No specific treatment is needed, provided the correct diagnosis is made. The primary etiologic factor needs to be corrected.

Prognosis •

Generally, the prognosis is good if the condition is correctly diagnosed.

PE ARL



An ill-defined, hypointense area on MRI with an enhancing rim in the patient at risk should raise suspicion of this uncommon entity.

PITFALL



Segmental testicular infarct is difficult to differentiate from focal neoplasm.

Suggested Readings Chin SC, Wu CJ, Chen A, Hsiao HS. Segmental hemorrhagic infarction of testis associated with epididymitis. J Clin Ultrasound 1998;26:326–328 Sriprasad S, Kooiman GG, Muir GH, Sidhu PS. Acute segmental testicular infarction: differentiation from tumour using high frequency colour Doppler ultrasound. Br J Radiol 2001;74:965–967

CASE 145 Clinical Presentation A 31-year-old male patient complains of ill-defined abdominal pain.

A

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Fig. 145.1 (A–C) Contrast-enhanced axial and coronal images show bulky retroperitoneal adenopathy. (continued)

C

Radiologic Findings Contrast-enhanced computed tomography (CT) images (Fig. 145.1) show bulky retroperitoneal adenopathy centered at the level of the renal hila. Subsequent ultrasound images of the left testis shows a well-defined, hypoechoic, intratesticular mass with increased Doppler flow.

Diagnosis Left malignant germ cell tumor of the testis with metastatic bulky retroperitoneal adenopathy

Differential Diagnosis •

Testicular hematoma

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D

E

Fig. 145.1 (continued) (D,E) Ultrasound images of the left testicle show a well-defined, hypoechoic seminoma with increased Doppler flow.

• • •

Testicular lymphoma Focal segmental infarct Epidermoid cyst

Discussion Background Ninety-five percent of primary testicular tumors are germ cell tumors, of which seminoma is the most common histologic subtype. Other histologic subtypes are embryonal cell carcinoma, teratoma, teratocarcinoma, and choriocarcinoma. Testicular cancer is the most common cancer in men ages 15 to 34. Seminomas are rare before age 10 and after age 60.

Clinical Findings Young male patients present with a palpable testicular mass. Dull, chronic pain is seen in ~20% of patients.

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Complications The tumors can metastasize to retroperitoneal lymph nodes and if allowed to progress can cause distant metastases in the lungs and other parenchymal organs.

Etiology Testicular tumors are associated with cryptorchidism, previous contralateral tumor, microlithiasis, and a family history of cancer.

Imaging Findings •

• •

On ultrasound, a testicular tumor presents as a focal, hypoechoic, and homogeneous intratesticular mass. Seminomas are less likely to demonstrate calcification or cystic areas. The other histologic subtypes are poorly defined and may show cystic areas and calcification. On magnetic resonance imaging, seminomas are usually homogeneous in appearance and hypointense on T2-weighted images. CT scans are helpful in detecting retroperitoneal spread of malignancy to lymph nodes. Nodes in the typical drainage area, even if < 1 cm, should be considered suspicious.

Treatment • •

Orchiectomy for tumors is confined to the testis. If after radical orchiectomy is performed and the tumor is identified as a nonseminomatous germ cell tumor, clinical and/or surgical staging is mandatory with retroperitoneal node dissection.

Prognosis •

Generally, the prognosis is good if the condition is adequately treated.

PE ARL



If retroperitoneal adenopathy is seen in a young male patient, always scan the testis to exclude a primary testicular tumor.

PITFALL



In patients > age 50, other testicular conditions may mimic seminomas.

Suggested Readings Dogra VS, Gottlieb RH, Oka M, Rubens DJ. Sonography of the scrotum. Radiology 2003;227:18–36 Kim W, Rosen MA, Langer JE, Banner MP, Siegelman ES, Ramchandani P. US–MR imaging correlation in pathologic conditions of the scrotum. Radiographics 2007;27:1239–1253 Woodward PJ, Sohaey R, O’Donoghue MJ, Green DE. Tumors and tumorlike lesions of the testis: radiologic-pathologic correlation. Radiographics 2002;22:189–216

CASE 146 Clinical Presentation A 33-year-old man complains of a 2-month history of a nontender left testicular mass.

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C

D

Fig. 146.1 (A–E) Ultrasound images of the left scrotum

E

show a normal-appearing left testis with a heterogeneous, predominantly hypoechoic left extratesticular mass with some Doppler flow.

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Radiologic Findings Ultrasound images of the left scrotum show a normal-appearing left testis with a heterogeneous, predominantly hypoechoic left extratesticular mass with some Doppler flow (Fig. 146.1).

Diagnosis Left extratesticular adenomatoid tumor

Differential Diagnosis • • • • •

Scrotal lipoma Epididymitis Epididymal cystadenoma Scrotal hematoma Inguinal hernia with bowel loops in the scrotum

Discussion Background Adenomatoid tumors are benign, solid, extratesticular neoplasms of mesothelial origin; they account for ~30% of all paratesticular tumors. These tumors usually arise from the epididymis, but they may arise from the testicular tunica or the spermatic cord. They are typically unilateral and are seen on the left side.

Clinical Findings Adenomatoid tumors are usually seen as incidental findings in young male patients; they may present as a painless lump in the testis.

Complications The lesion is benign and, depending on where they arise from, may mimic primary testicular tumors.

Etiology No known association

Imaging Findings • •

On ultrasound, adenomatoid tumors are seen as well-defined, extratesticular masses with heterogeneous echotexture. There may be Doppler flow seen. Magnetic resonance imaging may be useful in identifying the extratesticular location of this tumor, as the tumor shows enhancement that is different from normal testicular parenchyma.

Treatment •

Surgical resection is curative.

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Prognosis •

The prognosis is generally good.

PE ARL



Most common extratesticular tumor

PITFALL



If adenomatoid tumors arise from the tunica, they may mimic intratesticular cancers.

Suggested Readings Kim W, Rosen MA, Langer JE, Banner MP, Siegelman ES, Ramchandani P. US MR imaging correlation in pathologic conditions of the scrotum. Radiographics 2007;27:1239–1253 Woodward PJ, Sohaey R, O’Donoghue MJ, Green DE. Tumors and tumorlike lesions of the testis: radiologic-pathologic correlation. Radiographics 2002;22:189–216

CASE 147 Clinical Presentation A 65-year-old man with a known history of lymphoma presents with a painless enlargement of his right testis.

B

A

Fig. 147.1 (A–C) Ultrasound images of the right scrotum show an enlarged right testicle with an ill-defined hypoechoic lesion involving the testicular parenchyma and associated with increased Doppler flow.

Radiologic Findings Ultrasound images of the right scrotum (Fig. 147.1) show an enlarged right testicle with an ill-defined hypoechoic lesion involving the testicular parenchyma and associated with increased Doppler flow.

Diagnosis Testicular lymphoma

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C

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Differential Diagnosis • • • • • • •

Testicular hematoma Sarcoidosis Tuberculosis Orchitis Segmental infarct of the testis Testicular metastases Seminoma

Discussion Background Testicular lymphoma constitutes 1 to 9% of all testicular tumors and is the most common tumor in men between the ages of 60 and 80. Bilateral involvement is rare.

Clinical Findings Testicular lymphoma is usually seen in patients with a known history of lymphoma. Patients usually present with a painless swelling of the testis. They can present with painful testicular swelling or with systemic symptoms, such as weight loss, night sweats, anorexia, fever, and weakness.

Complications Testicular lymphoma is locally aggressive and can infiltrate the epididymis, spermatic cord, or scrotal skin.

Etiology Testicular lymphoma may be the primary manifestation of malignant lymphoma, or it may occur during the clinical course of a patient with established lymphoma. Secondary involvement of the testis in patients with lymphoma is far more common than primary testicular lymphoma. Although predisposing causes for the development of testicular lymphoma remain unclear, various reports have implicated prior trauma, chronic orchitis, cryptorchidism, and filariasis of the spermatic cord as potential risk factors. Immunosuppressed patients are at increased risk for developing testicular lymphoma. Most testicular lymphomas are diffuse large B-cell lymphomas, which are high-grade neoplasms.

Imaging Findings • • •

The imaging features of testicular lymphoma reflect its infiltrative characteristics. At ultrasound, the normally homogeneous echogenic testis is replaced focally or diffusely with hypoechoic vascular lymphomatous tissue. Lymphoma typically demonstrates increased intralesional blood flow regardless of the size of the tumor. The condition typically infiltrates the epididymis, which then becomes enlarged and hypoechoic.

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Treatment •

Although treatment is evolving, mainstay treatment includes orchiectomy and systemic chemotherapy. Prophylactic irradiation of the scrotum and administration of intrathecal methotrexate are usually offered to patients who experience complete remission to prevent recurrence in the contralateral testis and central nervous system.

Prognosis • •

Testicular lymphoma carries a worse prognosis than its nodal counterpart, with a 5-year survival rate of ~12% and a median survival time of < 12 months. Factors that have been linked to more favorable outcomes are younger patient age, localized disease, smaller tumor size, lower histologic tumor grade, and a lack of epididymal or spermatic cord involvement.

PE ARL



Hypoechoic vascular intratesticular lesion in a patient > age 60: suspect lymphoma

PITFALL



Because the disease is infiltrative, it may be difficult to differentiate from other systemic illnesses that can localize to the testis.

Suggested Readings Ferry J, Harris N, Young R, et al. Malignant lymphoma of the testis, epididymis, and spermatic cord. Am J Surg Pathol 1994;18:376–390 Zicherman JM, Weissman D, Gribbin C, Epstein R. Best cases from the AFIP: primary diffuse large B-cell lymphoma of the epididymis and testis. Radiographics 2005;25:243–248

CASE 148 Clinical Presentation A 35-year-old man complains of testicular pain.

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Fig. 148.1 (A–D) Ultrasound evaluation of the testicles shows bilateral normal-sized testicles with heterogenous echotexture. There are multiple small calcifications measuring ~1 mm diffusely throughout both testicles. In addition, there are focal well-defined, hypoechoic germ cell neoplasms seen in the left testis (arrows).

Radiologic Findings Ultrasound evaluation of the testicles shows bilateral normal-sized testicles with heterogeneous echotexture. There are multiple small calcifications measuring ~1 mm diffusely scattered throughout both testicles (Fig. 148.1). In addition, there are focal well-defined, hypoechoic lesions seen in the left testis.

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Diagnosis Testicular microlithiasis with multifocal seminoma in the left testis

Differential Diagnosis The ultrasound appearance of microlithiasis is diagnostic.

Discussion Background Testicular microlithiasis is an uncommon condition in which calcifications are present within the lumen of seminiferous tubules.

Clinical Findings It is usually an incidental finding and is asymptomatic.

Complications There is a high association between testicular microlithiasis and testicular germ cell tumors.

Etiology Testicular microlithiasis has been associated with several conditions, including cryptorchid testes, testicular atrophy, infertility, Klinefelter syndrome, male pseudohermaphroditism, Down syndrome, pulmonary alveolar microlithiasis, acquired immunodeficiency syndrome, and intratubular germ cell neoplasia.

Imaging Findings • •



Sonography demonstrates innumerable small, hyperechoic foci diffusely scattered throughout the testicular parenchyma that rarely shadow and occasionally show a comet tail appearance. A generally accepted definition of testicular microlithiasis is the presence of five or more microliths in either or both testes on at least one image. Bilateral involvement may occur. The absence of acoustic shadowing in the vast majority of cases distinguishes testicular microlithiasis from other forms of intratesticular calcification. The pattern may range from a few scattered foci to widespread parenchymal involvement. Testicular microlithiasis is not detected with magnetic resonance imaging (MRI), but MRI may be helpful if there is concern for a coexisting mass.

Treatment •

Although the condition itself does not warrant any therapy, the presence of germ cell tumors requires treatment as warranted by the staging of the tumor.

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Prognosis •

The clinical significance of testicular microlithiasis arises from an increased risk of testicular malignancy. Most investigators believe there is an association between testicular microlithiasis and testicular neoplasia and thus follow up affected individuals with scrotal sonography to ensure that a testicular neoplasm does not develop. The recommended follow-up is semiannual or annual testicular sonography.

PE ARL



Multiple hyperechoic foci within the testis that rarely shadow

PITFALL



Diligent scanning may be needed to detect the small germ cell tumor in this condition.

Suggested Readings Heinemann V, Frey U, Linke J, Dieckmann KP. Testicular microlithiasis: one case and four points to note. Scand J Urol Nephrol 2003;37:515–518 Miller FN, Sidhu PS. Does testicular microlithiasis matter? A review. Clin Radiol 2002;57:883–890

CASE 14 9 Clinical Presentation A 37-year-old man complains of left scrotal swelling, pain, and low-grade fever.

A

B

C

D

Fig. 149.1 (A–D) Ultrasound evaluation of the testicles shows an ill-defined heterogeneous, predominantly hypoechoic lesion arising from the left epididymis and extending into the left testis.

Radiologic Findings Ultrasound evaluation of the testicles shows an ill-defined heterogeneous, predominantly hypoechoic lesion arising from the left epididymis and extending into the left testis (Fig. 149.1).

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Diagnosis Tuberculous epididymo-orchitis

Differential Diagnosis • • • • • •

Primary testicular tumor Lymphoma Metastases Sarcoid Hematoma Scrotal hernia

Discussion Background Tuberculous infection of the scrotum is rare and occurs in ~7% of patients with tuberculosis. The infection results from retrograde extension from the prostate and seminal vesicles as well as from hematogenous spread. Infection usually affects the epididymis first, but if the initial therapy is not appropriate, testicular involvement may follow.

Clinical Findings Men ages 20 to 50 are affected most commonly. Clinically, patients usually present with a painless or slightly painful scrotal mass.

Complications The infection is usually confined if diagnosed and treated. However, systemic spread can lead to psoas abscesses and tuberculous spread to parenchymal organs.

Etiology Tuberculosis epididymitis usually starts in the tail of the epididymis. Tuberculosis orchitis usually occurs as a result of contiguous extension from the epididymis. Isolated tuberculosis orchitis from hematogenous spread without epididymal involvement is rare.

Imaging Findings •



Tuberculous epididymitis can be seen as a diffusely enlarged, hypoechoic epididymis or nodularappearing heterogeneous epididymis. The heterogeneity of the epididymis is thought to be caused by various pathologic stages of the disease, which include caseation necrosis, the presence of granulomas, and fibrosis. An accompanying hydrocele with septation can also be seen. Gray-scale sonographic patterns of the associated tuberculosis orchitis include diffusely enlarged, predominantly hypoechoic testis; diffusely enlarged, homogeneously hypoechoic testis; and nodular enlarged, heterogeneously hypoechoic testis. Multiple small hypoechoic nodules in the enlarged testis (miliary type) may also be seen with orchitis.

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Treatment •

Adequate antituberculous treatment needs to be instituted as soon as the diagnosis is made.

Prognosis •

The prognosis is good if the condition is treated promptly.

PE ARL AND PITFALL



The diagnosis may be difficult if the condition is not clinically suspected.

Suggested Readings Chung JJ, Kim MJ, Lee T, Yoo HS, Lee JT. Sonographic findings in tuberculous epididymitis and epididymo-orchitis. J Clin Ultrasound 1997;25:390–394 Muttarak M, Peh WC, Lojanapiwat B, Chaiwun B. Tuberculous epididymitis and epididymo-orchitis: sonographic appearances. AJR Am J Roentgenol 2001;176:1459–1466

CASE 150 Clinical Presentation A 65-year-old man with an elevated prostate-specific antigen (PSA) level complains of hesitancy in urination.

B

A

Fig. 150.1 (A) Axial T2-weighted endorectal image of the prostate shows a low signal intensity tumor (arrow) on the right. Note the nodular extracapsular extension (curved arrow). (B) Sagittal T2-weighted endorectal image of the prostate shows extension of a low signal intensity tumor (arrow) into the right seminal vesicle.

Radiologic Findings T2-weighted endorectal magnetic resonance (MR) images show a loss of normal high signal in the right peripheral zone of the prostate gland, with T2 dark signal extending into the right seminal vesicle (Fig. 150.1).

Diagnosis Prostate carcinoma with extracapsular and seminal vesicle extension

Differential Diagnosis • •

Benign prostatic hyperplasia Granulomatous prostatitis

Discussion Background Prostate cancer has the highest incidence of any noncutaneous cancer in the United States and is among the leading causes of cancer death in American men. The prevalence of seminal vesicle invasion (SVI) in surgical series performed in the past 10 years is 5 to 23%. Preoperative identification

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of SVI is an important factor for staging and prognosis and may modify treatment selection and treatment planning.

Clinical Findings Most patients with prostate cancer present with symptoms related to urination. They may be asymptomatic as well.

Complications Complications can be local and related to glandular enlargement, bladder outlet obstruction, and hydronephrosis. Distant spread can lead to adenopathy and bony metastases.

Etiology There is no known etiology for prostate cancer. Advancing age, hormonal influence, and environmental and genetic factors play a role. The cancer is seen in men > age 40 and is more common in African-American men.

Imaging Findings •

MRI is the mainstay for diagnosis and local staging. T2-weighted images allow tumor detection, and the tumor appears as a focal area of local signal within high signal intensity of the peripheral zone of the gland. The tumor is most often located in the peripheral zone. Extracapsular extension is suggested by obliteration or blunting of the rectoprostatic angle, nodular extension of tumor outside the gland, asymmetry of the neurovascular bundle, and focal bulge. MRI may also identify enlarged pelvic lymph nodes and pelvic bony metastases.

Treatment • •

The recommended treatment is radical resection of tumor confined to the gland. Radiation therapy is done if there is tumor with extracapsular extension but no distant spread. Hormonal therapy is administered for distant metastases.

Prognosis •

The prognosis is good if the condition is detected early and appropriate therapy is instituted.

PE ARL AND PITFALL



Focal granulomatous prostatitis can mimic carcinoma within the gland.

Suggested Readings Hricak H, White S, Vigneron D, et al. Carcinoma of the prostate gland: MR imaging with pelvic phasedarray coils versus integrated endorectal-pelvic phased-array coils. Radiology 1994;193:703–709 Ikonen S, Karkkainen P, Kivisaari L, et al. Magnetic resonance imaging of clinically localized prostatic cancer. J Urol 1998;159:915–919

CASE 151 Clinical Presentation A 30-year-old man presents with acute, painful swelling of the penis following vaginal intercourse.

A

B

Fig. 151.1 (A) Axial T2-weighted MR image shows focal discontinuity in the tunica albuginea (arrow). (B) Coronal T2-weighted MR image shows the transverse tear of the corpus cavernosum (arrow) and penile hematoma.

Radiologic Findings T2-weighted magnetic resonance (MR) images show focal discontinuity in the tunica albuginea associated with a transverse tear of the corpus cavernosum and penile hematoma (Fig. 151.1).

Diagnosis Penile fracture

Differential Diagnosis Imaging findings when present with a history are diagnostic of this condition.

Discussion Background Penile fracture constitutes a rare urologic emergency and is defined as rupture of a corpus cavernosum and its surrounding fibroelastic sheath, the tunica albuginea.

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Clinical Findings Patients complain of an audible crack, a sudden onset of pain, and an immediate loss of erection, accompanied by rapid swelling, widespread ecchymosis, and deviation toward the side opposite the injury. The fracture usually occurs unilaterally in the distal two thirds of the penis and typically involves less than one half of the cavernosal circumferences.

Complications Urethral injury may occur along with penile fracture and will result in hematuria or dysuria.

Etiology The tunica albuginea thins during erection and is susceptible to injury. Sudden, direct force acting on the dorsum of the penis can often lead to fracture. In most cases, a tear occurs in only one of the corpora cavernosa and its surrounding tunica albuginea. However, the corpus spongiosum and the urethra can also be involved.

Imaging Findings •

MRI is the mainstay for diagnosis. The tear is seen as a focal area of discontinuity in the lowsignal tunica. The tear within the corpora is considered transversely oriented when its transverse dimension exceeds its longitudinal dimension; otherwise, it is considered to be longitudinally oriented. Accompanying penile hematoma is seen as high signal on T1-weighted images.

Treatment •

Although penile fracture can be treated conservatively, recent studies have demonstrated the clear advantage of early surgical intervention.

Prognosis • •

The prognosis is good if appropriate therapy is instituted. Early surgical intervention can prevent late complications, such as fibrous plaque formation and angulation, thereby reducing the time of convalescence.

PE ARL AND PITFALL



MRI is needed to fully evaluate the extent of the abnormality.

Suggested Readings Rahmouni A, Hoznek A, Duron A, et al. Magnetic resonance imaging of penile rupture: aid to diagnosis. J Urol 1995;153:1927–1928 Ruckle HC, Hadley HR, Lui PD. Fracture of penis: diagnosis and management. Urology 1992;40:33–35

CASE 152 Clinical Presentation A 68-year-old man with known prostate cancer presents with penile pain and intermittent priapism.

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A

C

Fig. 152.1 (A–C) Postgadolinium T1-weighted images of the penis show multiple focal lesions (arrows) within the corpora cavernosa.

Radiologic Findings Postgadolinium T1-weighted images of the penis show multiple focal lesions within the corpora cavernosa (Fig. 152.1).

Diagnosis Penile metastases from primary prostate cancer

Differential Diagnosis • • •

Multiple primary neoplasms Tuberculosis Nonspecific inflammatory lesions

Discussion Background Penile metastases are rare and usually secondary to other genitourinary primary tumors.

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Clinical Findings Metastatic spread to the penis may be associated with penile pain, penile mass, or priapism.

Complications The penis has a rich and complex vascular circulation interconnected to the pelvic organs. Despite this, metastases to the penis are rare, representing a late manifestation of systemic disease.

Etiology There are multiple routes of dissemination of the malignant cells from the primary neoplasm to the penis. The chief mechanism is direct extension to the base of the penis, corpora cavernosa, and crura via retrograde venous flow, which can be associated with lesions over the shaft of the penis. Retrograde lymphatic extension and arterial emboli have also been described as potential pathways of seeding the penis. Dissemination of tumor emboli following instrumentation of the urethra involved by the tumor and paradoxical spread via a patent foramen ovale have also been suggested. The most common primary tumors to spread to the penile shaft are bladder and prostate, followed by renal and rectosigmoid. Less common are the nonpelvic organs, such as the lung, pancreas, nasopharynx, larynx, and bone.

Imaging Findings •

Magnetic resonance imaging, when performed, will show multiple nodules within the penile shaft. These usually appear as focal areas of abnormality against a backdrop of richly enhancing corpora.

Treatment •

Penile metastases are a late manifestation of most primary tumors; thus, therapeutic options are limited. Penectomy, tumor excision, hormonal treatment, chemotherapy, radiation teletherapy, immunotherapy, and hyperthermia have been used to treat secondary penile carcinoma with limited success.

Prognosis •

Penile metastases have a very poor prognosis—survival rates range from 1 to 24 months.

PE ARL AND PITFALL



If a metastasis is solitary, it may be difficult to differentiate it from primary neoplastic processes.

Suggested Readings Griffin JH, Wheeler JS, Olson M, Melian E. Prostate carcinoma metastatic to penis: magnetic resonance imaging and brachytherapy. J Urol 1996;155:1701–1702 Mugharbil ZH, Childs C, Tannenbaum M, Schapira H. Carcinoma of prostate metastatic to penis. Urology 1985;25:314–315

CASE 153 Clinical Presentation A 66-year-old man presents with a left scrotal mass on routine physical examination.

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A

Fig. 153.1 (A) Scrotal ultrasound reveals a 1.9 ⫻ 1.3 cm cyst within the left epididymal head likely corresponding to the palpable abnormality. Tubular and branching cystic structures are identified within the (B) left and (C) right mediastinum testes.

C

Radiologic Findings Scrotal ultrasound reveals a 1.9 ⫻ 1.3 cm cyst within the left epididymal head, most likely corresponding to the palpable abnormality. Tubular and branching cystic structures are identified within the left and right mediastinum testes (Fig. 153.1).

Diagnosis Tubular ectasia of the rete testes. Alternative names are dilatation, cystic dilatation, cystic ectasia, and seminiferous tubular ectasia of the rete testes.

Differential Diagnosis • •

Intratesticular varicocele Cystic testicular neoplasm

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Discussion Background The rete testis is located in the mediastinum testis, which is an invagination of the tunica albuginea and is located in the posterior aspect of the testis. The vasculature of the testis enters and exits through the mediastinum. The rete testis is composed of multiple sperm-containing tubular structures, which are formed at the confluence of the seminiferous tubules. The rete testis is connected to the efferent ducts, which lead to the epididymis. Tubular ectasia of the rete testis is characterized by dilatation of the rete testis within the mediastinum of the testis.

Clinical Findings Tubular ectasia of the rete testis is usually asymptomatic and is discovered incidentally in up to 10% of scrotal ultrasounds. A benign condition, it tends to occur in men > age 55. Tubular ectasias are commonly associated with spermatoceles/epididymal cysts (46–100%).

Etiology There is evidence that tubular ectasia is associated with obstruction at the epididymal level. Fortysix to 100% of patients with this entity have an associated spermatocele/epididymal cyst. Ten to 55% of patients with tubular ectasia have a history suggesting ductal obstruction, such as vasectomy, ipsilateral hernia repair, or epididymitis.

Imaging Findings •

Tubular ectasia of the rete testis is characterized by multiple cystic, tubular, and branching anechoic structures within the mediastinum testis without associated color Doppler flow. The individual cystic structures vary in size (~3–15 mm) and can increase in size with time. No solid components should be seen. Tubular ectasia is frequently bilateral.

Treatment •

No treatment or follow-up imaging is needed.

PE ARL



It is the location of cystic dilatation in or adjacent to the mediastinum testis in conjunction with the presence of epididymal cysts that is characteristic of tubular ectasia. Malignant cystic testicular neoplasms have associated soft tissue and can occur anywhere in the testicular parenchyma.

PITFALL



Testicular neoplasms can rarely cause obstruction of spermatic ducts. In the setting of tubular ectasia of the rete testis, exclusion of a solid mass is necessary.

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Suggested Readings Burrus JK, Lockhart ME, Kenney PJ, Kolettis PN. Cystic ectasia of the rete testis: clinical and radiographic features. J Urol 2002;168(4 Pt 1):1436–1438 Colangelo SM, Fried K, Hyacinthe LM, Fracchia JA. Tubular ectasia of the rete testis: an ultrasound diagnosis. Urology 1995;45(3):532–534 Dogra V, Gottlieb RH, Oka M, Rubens D. Sonography of the scrotum. Radiology 2003;227:18–36 Gooding GA, Leonhardt W, Stein R. Testicular cysts: US findings. Radiology 1987;163:537–538 Rouvière O, Bouvier R, Pangaud C, Jeune C, Dawahra M, Lyonnet D. Tubular ectasia of the rete testis: a potential pitfall in scrotal imaging. Eur Radiol 1999;9(9):1862–1868

CASE 154 Clinical Presentation A 58-year-old man with recently diagnosed prostate cancer and a remote history of trauma to the left side of the body following a high-speed motor vehicle accident presents for a staging computed tomography (CT) examination.

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C

D

Fig. 154.1 (A,B) Delayed contrast-enhanced CT scans reveal an enlarged prostate with a prominent median lobe projecting into the bladder. A lobulated soft tissue pelvic mass is seen along the left pelvic side wall (arrow). This was felt to represent a nodal mass, and patient was referred for MRI. (C) Coronal contrast-enhanced T1-weighted image reveals enlarged and tortuous enhancing vessels within the left pelvis. (D) Volume-rendered MR image demonstrates an abnormal tangle of vessels within the left pelvis supplied by an enlarged left internal iliac artery.

Radiologic Findings Delayed contrast-enhanced CT scans (Fig. 154.1A,B) reveal an enlarged prostate with a prominent median lobe projecting into the bladder. A lobulated soft tissue pelvic mass is seen along the left pelvic side wall. This was felt to represent a nodal mass, and the patient was referred for magnetic resonance imaging (MRI). Coronal contrast-enhanced T1-weighted image (Fig. 154.1C) reveals

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enlarged and tortuous enhancing vessels within the left pelvis. Volume-rendered MR image (Fig. 154.1D) demonstrates an abnormal tangle of vessels within the left pelvis supplied by an enlarged left internal iliac artery.

Diagnosis Pelvic arteriovenous malformation (AVM)

Differential Diagnosis On noncontrast examination, this lesion can mimic enlarged lymph nodes.

Discussion Background An AVM is a type of vascular malformation characterized by an abnormal collection of arteries and veins. AVMs are most commonly found in the central nervous system, lungs, or extremities. Pelvic AVMs are rare.

Clinical Findings Pelvic AVMs can be clinically silent and discovered incidentally, as in this case. They can also present with hemorrhage, pain, and mass effect.

Complications Pelvic AVMs can result in spontaneous hemorrhage or hemorrhage as a complication of trauma. They can also complicate routine surgical procedures; there are reports in the literature of severe hemorrhage from clinically occult pelvic AVMs following transurethral resection of the prostate. Iliac vein thrombosis and ureteral obstruction have been reported as complications of pelvic AVMs.

Etiology The etiology of pelvic AVMs is somewhat controversial. In general, AVMs are thought to be congenital in nature. However, the detection of pelvic AVMs in patients who have a history of pelvic surgery or trauma provides evidence that some of these lesions may be acquired.

Imaging Findings •

• • •

Pelvic AVMs are traditionally evaluated with conventional angiography. They are characterized by an abnormal collection of vessels (the nidus) and tend to be supplied and drained by enlarged and tortuous arteries and veins, respectively. Flow dynamics are well-evaluated with conventional angiography. Noninvasive evaluation of pelvic AVMs can be obtained with MRI. Exposure to radiation and iodinated contrast makes CT a less desirable means for evaluation.

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Treatment •

Depending on the size and symptomatology, pelvic AVMs can be treated conservatively and followed with imaging. The mainstay of invasive treatment of pelvic AVMs is transcatheter embolization with or without subsequent surgical excision. Complications to this form of treatment are potential ischemia of the buttock, colon, or femoral/sciatic nerve. Other complications are those inherent to arterial puncture and contrast reactions.

PE ARL



Pelvic AVMs consist of a nidus with feeding arteries and draining veins.

PITFALL



Transcatheter embolization carries the risk of nontarget embolization or ischemia.

Suggested Readings Chikamatsu E, Nagashima T, Mizukami Y, Ikuta K, Sakurai T. Pelvic arteriovenous malformation with iliac vein thrombosis: a case report. J Cardiovasc Surg (Torino) 2001;42(1):115–118 Díaz Candamio MJ, Lee VS, Rofsky NM, Krinsky GA, Weinreb JC. Pelvic atreriovenous malformations: gadolinium-enhanced three-dimensional MR angiography findings. Eur Radiol 2000;10(8):1257–1260 Jacobowitz GR, Rosen RJ, Rockman CB, et al. Transcatheter embolization of complex pelvic vascular malformations: results and long-term follow-up. J Vasc Surg 2001;33(1):51–55 Kelly J, Alvarez RD, Roland PY. Arteriovenous malformation presenting as a complex pelvic mass with ureteral obstruction: a case report. J Reprod Med 1998;43(10):916–918 Touyama H, Hatano T, Ogawa Y. Massive prostatic bleeding after transurethral resection of the prostate in a patient with a congenital pelvic arteriovenous malformation. J Urol 1998;160(5):1803

CASE 155 Clinical Presentation A 66-year-old Caucasian man presents with painless irreducible scrotal swelling progressively increasing in size.

A

B

C

D

Fig. 155.1 (A) Coronal contrast-enhanced CT image shows a large, well-defined, fat-containing, and heterogeneously enhancing lesion with cystic and soft tissue contents in the scrotal sac. (B) Axial contrast-enhanced CT image in the same patient shows a large, well-defined, fat-containing, and heterogeneously enhancing lesion with cystic and soft tissue contents in the scrotal sac. (C) Axial image at a higher slice location shows fat density (arrow) contents within the inguinal canal, causing its expansion and displacement of the vascular structures anteriorly. (D) Axial image at a higher slice location in the pelvis shows heterogeneous intraperitoneal accumulation of the fat density structure with enhancing foci anterolateral to the urinary bladder in the left inguinal region (arrow). (continued)

Radiologic Findings Computed tomography (CT) and magnetic resonance (MR) images show a large, well-defined, fatcontaining, and heterogeneously enhancing lesion with cystic and soft tissue contents in the scrotal sac extending into the peritoneal cavity through the inguinal canal (Fig. 155.1).

Diagnosis Dedifferentiated spermatic cord liposarcoma

Differential Diagnosis • •

Lipoma Incarcerated hernia

498

IX PELVIS

E

F

499

G

Fig. 155.1 (continued) (E) Coronal T2-weighted image in the same patient shows a large, well-defined, heterogeneous lesion with fatty, cystic, and soft tissue components. (F) Sagittal T2-weighted image in the same patient shows extension of the lesion in the inguinal canal. (G) Axial contrast-enhanced fat-saturated T1-weighted image in the same patient demonstrates saturation of the fatty component within the lesion.

• •

Scrotal hemorrhage Angiomyolipoma

Discussion Background Malignant testicular lesions outnumber benign scrotal lesions by a large difference, which is why testicular lesions are always considered malignant unless proven otherwise. Extratesticular masses that are cystic are almost always benign. Most extratesticular solid lesions are benign, with lipoma being the most common tumor. Malignant tumors account for 3% of the extratesticular scrotal solid masses. Sarcoma is the most common malignant lesion of the spermatic cord, with primary undifferentiated being the most common type of tumor. Rhabdomyosarcoma is the most common malignant spermatic cord tumor in children. Liposarcoma accounts for 3 to 7% of spermatic cord neoplasms. The most common age group involved is 50 to 80 years.

Clinical Findings • • •

Painless, irreducible inguinoscrotal swelling progressively increasing in size over months to years Scrotal heaviness Rapid progression of the size of the inguinal swelling

Complications • •

Local recurrence after surgical resection Very rarely metastases

Etiology The exact etiology remains unknown. Liposarcomas are believed to arise from the mesenchymal cells. Malignant transformation of the lipomatous cells is a less accepted hypothesis.

500

TEACHING ATLAS OF ABDOMINAL IMAGING

Imaging Findings • •





Ultrasound usually shows a homogeneously hyperechogenic or echogenic lesion separate from the testis. CT reveals a typically negative density fat lesion with irregular margins and minimal heterogeneity. Extension of the lesion into the abdomen may not always be evident; however, it can be suspected in patients with focal accumulation of fat in the intraperitoneal region adjacent to the inguinal ring. MRI provides better soft tissue delineation and is a more sensitive technique to detect the extension of the tumor. Late recurrence of the tumor can occur, and follow-up studies are indicated in affected patients. Metastatic work-up of the patient may not be necessary because metastases are very rare in patients with spermatic cord liposarcoma.

Treatment •



The primary treatment involves wide local surgical excision of the tumor with high inguinal orchidectomy with or without hemiscrotectomy, depending on scrotal skin involvement and lymph nodal dissection. If, on postoperative pathologic studies, the tumor is found to involve resected margins, the patient is given adjuvant therapy in the form of radiochemotherapy (Adriamycin, ifosfamide, + radiation therapy). Adjuvant therapy is also considered in patients with recurrence of the tumor and in patients with lymphatic invasion.

Prognosis •



Local recurrence is common and occurs in 50% patients after surgical resection. It can be significantly reduced by achieving surgical resection with clean margins and postoperative adjuvant radiochemotherapy. The prognosis is good in treated patients, with survival rates > 50% at 15 years.

PE ARL



Fat-containing inguinoscrotal mass.

PITFALL



At times inguinoscrotal liposarcoma is difficult to distinguish from incarcerated hernia and lipoma.

Suggested Readings Hornick JL, Bosenberg MW, Mentzel T, McMenamin ME, Oliveira AM, Fletcher CDM. Pleomorphic liposarcoma: clinicopathologic analysis of 57 cases. Am J Surg Pathol 2004;28:1257–1267 Woodward PJ, Schwab CM, Sesterhenn IA. From the archives of the AFIP: extratesticular scrotal masses:radiologic-pathologic correlation. Radiographics 2003;23:215–240 Schwartz SL, Swierzewski SJ 3rd, Sondak VK, Grossman HB. Liposarcoma of the spermatic cord: report of 6 cases and review of the literature. J Urol 1995;153:154–157

X   Appendixes

Appendix 1  64-Slice Protocol for Routine Abdomen and Pelvic CT Scan Indications Abdominal pain, altered bowel habit, inflammatory bowel disease, unexplained weight loss, anemia, known or suspected bowel tumor

Oral Contrast Three doses of Gastrografin for emergency room and inpatients; Volumen for outpatients

IV Contrast • • • •

370 mg I/mL  < 135 lb: 65 cc  136 to 200 lb: 95 cc  > 200 lb: 120 cc Saline: 40 cc Rate of injection: 3 cc/s IV: 20 gauge

Technical Details See Table 10.1. Table 10.1   64-Slice Protocol for Routine Abdomen and Pelvic CT Scan Series 1: Abdomen/Pelvis

Smart Prep HU Mon. delay ROI level ROI location ISD Diagnostic delay Series auto transfer DMPR Mode Time Thickness Pitch Speed Interval Gantry tilt SFOV kV Auto mA



Min Max

55 50 Midliver Liver 5 3s OFF ON Helical 0.5 0.625 1.375 55 0.625 0 Large 120 150 550–800

Recon 2: Series auto transfer Thickness Interval DFOV

ON 2.5 2.5 Skin to skin

Reformats: Coronals Thickness Interval DFOV Window

501

3 3 Skin to skin Abdomen

502

APPENDIX 1

Table 10.1

(continued)

Noise index

28 32 35

DFOV ALG

< 135 lb 136–200 lb > 200 lb Skin to skin Standard

Series 2: Delays for Lesions: Liver or Renals Mode Series auto transfer DMPR Time Thickness Pitch Speed Interval Gantry tilt SFOV kV Auto mA Noise index

DFOV ALG

Min Max 10 12.5 15

Helical ON OFF 0.5 5 1.375 55 5 0 Large 120 150 550–800 < 135 lb 136–200 lb > 200 lb Skin to skin Standard

Abbreviations: ALG, algorithm; DFOV, display field of view; DMPR, direct multiplanar reformat; HU, Hounsfield units; ISD, interscan delay; mon., monitoring delay; ROI, region of interest; SFOV, scan field of view.

APPENDIX 2 64-SLICE PROTOCOL FOR DUAL-PHASE LIVER CT SCAN Indications Known or suspected case of hepatocellular carcinoma. Characterizations of a known or suspected liver lesion: abnormal liver function tests, focal mass on portal venous phase computed tomography (CT) or ultrasound that needs evaluation; known or suspected cholangiocarcinoma evaluation; hypervascular metastases detection from primaries, such as renal cell carcinoma, sarcoma/neuroendocrine, or tumor/carcinoid.

Oral Contrast Three doses of Gastrografin

IV Contrast •

• • •

370 mg I/mL  < 135 lb: 65 cc  136 to 200 lb: 95 cc  > 200 lb: 120 cc Saline: 40 cc Rate of injection: 4 to 5 cc/s IV: 18 gauge

Technical Details See Table 10.2. Table 10.2 64-Slice Protocol for Dual-Phase Liver CT Scan Series 1: Abdomen/Pelvis Smart Prep HU Mon. delay ROI level ROI location Diagnostic delay ISD

150 12 Midliver Aorta 12 s 3

Group 1: Arterial Liver Location Series auto transfer DMPR Mode Time Detector

Recon 2: Liver only OFF ON Helical 0.5; increase if mA table is at maximum 40

503

Thickness Interval DFOV ALG Auto transfer

2.5 2.5 Skin to skin Std ON

504

APPENDIX 2

Table 10.2

(continued)

Thickness Pitch Speed Interval Gantry tilt SFOV kV Auto mA

Min Max

Noise index 28 32 35 DFOV ALG

0.625 1.375 55 0.625 0 Large 120 150 550–800 for larger patients pt. weight Up to 135 lb 136–200 lb 200 lb and over Skin to skin Standard

Reformats: Coronals Thickness Interval window DFOV

Group 2: PV Abdomen/Pelvis

Retro Recon:

Location Delay Series auto transfer

Dome of liver through SP 55 s from start of injection OFF

DMPR Mode Time Detector Thickness Pitch Speed Interval Gantry tilt SFOV kV auto mA

ON Helical 0.5; increase for larger patients 40 0.625 1.375 55 0.625 0 Large 120 150 550–800 pt. weight Up to 135 lb 136 to 200 lb 200 lb and over Skin to skin Standard

Min Max

Noise index 28 32 35 DFOV ALG

Series 2: Delayed Scans; through Lesions Only Location Series auto transfer DMPR Mode Time Detector Thickness Pitch Speed Interval Gantry tilt SFOV

3 3 Abd Skin to skin

Lesions only ON OFF Helical 0.5; increase for larger patients 40 5 1.375 55 5 0 Large

Thickness Interval ALG DFOV Auto transfer

2.5 2.5 Std Skin to skin ON

Reformats: Thickness Interval window DFOV

Coronal 3 3 Abd Skin to skin

APPENDIX 2 kV Auto mA

Min Max

Noise index 10 12.5 15 DFOV ALG

505

120 150 550–800 pt. weight Up to 135 lb 136–200 lb 200 lb and over Skin to skin Standard

Abbreviations: ALG, algorithm; DFOV, display field of view; DMPR, direct multiplanar reformat; HU, Hounsfield units; ISD, interscan delay; mon., monitoring delay; PV, portal-venous; ROI, region of interest; SFOV, scan field of view; SP, symphysis pubis.

APPENDIX 3

64-SLICE CT PROTOCOL FOR EVALUATION OF HEMATURIA

Indications Gross of microscopic hematuria; suspected mass in urinary collecting system

Oral Contrast 3 cups of water

IV Contrast • • • • •

Noncontrast followed by contrast 370 mg I/mL 40 cc first injection/80 cc second injection Rate of injection: 3 cc/s IV: 20 gauge

Technical Details See Table 10.3. Table 10.3 64-Slice CT Protocol for Evaluation of Hematuria Series 1: Abdomen/Pelvis I Series auto transfer Location Mode Time DMPR Thickness Pitch Speed Rotation time Interval Gantry tilt SFOV kV Auto mA Min Max Noise index DFOV ALG

ON Top of the kidneys to SP Helical 0.5; increase if mA table is at maximum OFF 5 1.375 55 0.5 5 0 Large 120 On 150 550 to maximum of scanner 20 Skin to skin Standard

Retro Recon: Thickness 1.25 Interval 0.625 ALG Soft Do NOT send series Reformats: Coronal Thickness Interval Window

3 3 Abd

• Inject 40 cc of contrast. Next, hang a 250 mL bag of saline to gravity drip into the patient; wait until all of the saline is in. Put patient back on the table in the prone position. SCOUT first, then inject 80 cc contrast at 3 cc/s with a 100 s delay.

506

APPENDIX 3

507

Series 2: Prone Abdomen/Pelvis Prep delay Location Series auto transfer DMPR Mode Time DMPR Thickness Pitch Speed Interval Gantry tilt SFOV kV Auto mA

Noise index

100 s

Min Max 28 32 35

DFOV ALG

Prone Top of the kidneys to SP OFF ON Helical 0.5; increase if mA table is at maximum ON 0.625 1.375 55 0.625 0 Large 120 ON 150 550 to maximum of scanner < 135 lb 136–200 lb > 200 lb Skin to skin Standard

Prospective Recon 2: Series auto transfer ALG Thickness Interval DFOV

ON Std 2.5 2.5 Skin to skin

Reformats: Coronals Thickness Interval Window DFOV

3 3 Abd Skin to skin

Series 3: Delays if Needed Location Series auto transfer DMPR Mode Time DMPR Thickness Pitch Speed Interval Gantry tilt SFOV kV Auto mA Noise index

DFOV ALG kV Auto mA

Min Max 28 32 35

Min Max

Noise index 10 12.5 15 DFOV ALG

Through ureters not visualized on series 2 OFF ON Helical 0.5; increase if mA table is at maximum ON 5 1.375 55 5 0 Large 120 150 550 to maximum of scanner < 135 lb 136–200 lb > 200 lb Skin to skin Standard 120 150 550–800 pt. weight Up to 135 lb 136–200 lb 200 lb and over Skin to skin Standard

Abbreviations: ALG, algorithm; DFOV, display field of view; DMPR, direct multiplanar reformat; SFOV, scan field of view; SP, symphysis pubis.

APPENDIX 4 64-SLICE PROTOCOL FOR PANCREATIC CT SCAN Indications Presurgical staging of a known pancreatic solid or cystic mass

Oral Contrast Water

IV Contrast •

• • •

370 mg I/mL  < 135 lb: 65 cc  136 to 200 lb: 95 cc  > 200 lb: 120 cc Saline: 40 cc Rate of injection: 5 cc/s IV: 18 gauge

Technical Details See Table 10.4. Table 10.4

64-Slice Protocol for Pancreatic CT Scan

Series 1: Abdomen-Only Pancreas Locator Series auto transfer DMPR Location Mode Time Thickness Pitch Speed Interval Gantry tilt SFOV kV Auto mA Noise index DFOV ALG

Min Max

ON OFF Dome of liver to crest Helical 0.5 5 1.375 55 5 0 Large 120 150 550–800 15 Skin to skin Standard

508

APPENDIX 4

509

Series 2: Abdomen Arterial Phase Prep group delay DMPR Series auto transfer Mode Time Thickness Pitch Speed Rotation time Interval Gantry tilt SFOV kV Auto mA Noise index

Min Max 28 32 35

DFOV ALG

50 s ON ON Helical 0.5; increase if mA table is at maximum 0.625 1.375 55 0.5 0.625 0 Large 140 150 700 (maximum of the scanner) < 135 lb 136–200 lb > 200 lb Skin to skin Standard

Series 3: Venous Phase, Abdomen Only Prep delay Series auto transfer Mode Rotation time Time DMPR Thickness Pitch Speed Rotation time Interval Gantry tilt SFOV kV Auto mA Noise index

DFOV ALG

Min Max 28 32 35

35 s ON Helical 0.5 0.5 ON 0.625 1.375 55 0.5 0.625 0 Large 120 150 550 < 135 lb 136–200 lb > 200 lb Skin to skin Std

Prospective Recon 2: Series auto transfer Thickness Interval ALG DFOV

ON 2.5 2.5 Std Skin to skin

Reformats: Coronals Thickness Interval ALG DFOV

3 3 Std 28

Prospective Recon 2: Series auto transfer Thickness Interval ALG DFOV

ON 2.5 2.5 Std Skin to skin

Reformats: Coronals Thickness Interval Window DFOV

3 3 Std Skin to skin

NO DELAYED SERIES Abbreviations: ALG, algorithm; DFOV, display field of view; DMPR, direct multiplanar reformat; SFOV, scan field of view.

APPENDIX 5

64-SLICE CT PROTOCOL FOR EVALUATION OF ADRENAL MASS

Indications Evaluation of adrenal lesion

Oral Contrast Water

IV Contrast •

• • •

370 mg I/mL  < 135 lb: 65 cc  136 to 200 lb: 95 cc  > 200 lb: 120 cc Saline: 40 cc Rate of injection: 3 cc/s IV: 20 gauge

Technical Details See Table 10.5. Table 10.5 64-Slice CT Protocol for Evaluation of Adrenal Mass Series 1: I—Adrenals Only Location Series auto transfer Mode Time DMPR Thickness Pitch Speed Interval Gantry tilt SFOV kV Auto mA Min Max Noise index DFOV ALG

T10–L2 ON Helical 0.5 OFF 2.5 1.375 55 2.5 0 Large 120 ON 150 500–700 for larger patients 20 Skin to skin Standard

510

APPENDIX 5

511

Series 2: Dual Energy, I—Adrenals Only, 5 to 10 Slices Location Series auto transfer Mode Time DMPR Thickness Pitch Speed Interval Gantry tilt SFOV kV Auto mA Min Max Noise index DFOV ALG

Adrenals only plan from series 1 images ON Helical 0.5 OFF 2.5 1.375 55 2.5 0 Large 80 ON 150 500 20 Skin to skin Standard

Series 3: Through the Adrenals Only, T10–L2 Prep delay Mode Time Series auto transfer DMPR Thickness Pitch Speed Rotation time Interval Gantry tilt SFOV kV Auto mA

Noise Index

DFOV ALG

Min Max 28 32 35

100 s Helical 0.5 ON On 0.625 1.375 55 0.5 0.625 0 Large 120 ON 150 550–700 for larger patients < 135 lb 136–200 lb > 200 lb Skin to skin Standard

Series 4: 10-Minute Delays through the Adrenals Only Location Mode Series auto transfer Time DMPR Thickness Pitch Speed Rotation time

Adrenals only, T10–L2 Helical ON 0.5 OFF 2.5 1.375 55 0.5

Prospective Recon 2: Thickness Interval DFOV ALG Series transfer

2.5 2.5 Skin to skin Std ON

Reformats: Coronals Thickness Interval Window Series Transfer

3 3 Abd ON

512

APPENDIX 5

Table 10.5

(continued)

Interval Gantry tilt SFOV kV Auto mA Min Max Noise index DFOV ALG

2.5 0 Large 120 ON 150 550–700 for larger patients 20 Skin to skin Standard

Abbreviations: ALG, algorithm; DFOV, display field of view; DMPR, direct multiplanar reformat; SFOV, scan field of view.

INDEX

Note: Page numbers followed by f and t represent figures and tables respectively. A Abdominal testis, 467 Abdominal wall desmoid tumor of, 376–378, 376f hernias of, 265–269, 265f–267f Aberrant left subclavian artery (ALSA), 244 Aberrant right subclavian artery (ARSA), 243–245, 243f, 244f Ablation techniques. See also Radiofrequency ablation (RFA) for calcified hepatic metastases, 36 for cervical carcinoma, 457 ABPKD (autosomal dominant polycystic kidney disease), 166–168, 166f, 168f Abscess(es) hepatic pyogenic, 18–20, 18f pancreatic, 89–91, 89f renal, 204–206, 204f retained surgical sponge and, 326 subhepatic, 330–332, 330f tubo-ovarian, inflammatory pelvic disease with, 424–427, 424f, 426f Accessory spleen, 132–134, 132f ACE (angiotensin-converting enzyme), in splenic sarcoidosis, 140 Acinar cell carcinoma of pancreas, 129–131, 129f Acute abdominal attack, in familial Mediterranean fever, 315–317, 315f Acute appendicitis, 277–279, 277f Acute mesenteric ischemia, 270–273, 270f Adenocarcinoma ductal, of pancreatic head, 104–106, 104f endometrial, 451–453, 451f gallbladder, diagnostic technique for, 59, 59f gastric, 250–253, 250f, 251f ovarian mucinous cystic, 447–450, 447f porcelain gallbladder and, 50 rectal, 308f, 309–311 sigmoid colon, 299–301, 299f urachal, 403–405, 403f Adenoma, 5–8, 5f–7f hepatic, 9–13, 9f–12f multiple, 10, 10f metanephric, 187–189, 187f microcystic, of pancreas, 101–103, 101f Adenomatoid tumor, extratesticular, 474–476, 474f Adenomatosis liver transplantation for, 12 multiple adenomas in, 10

513

Adenomyomatosis of gallbladder, 53–55, 53f, 55f Adenomyosis, 412–414, 412f endometriosis and, 437 leiomyoma and, 422 Adnexal masses, solid, 422 Adnexal torsion, from ovarian dermoid, 444–446, 444f Adrenal glands carcinoma of, 237–239, 237f cyst of, 220–222, 220f–222f ganglioneuroma of, 240–242, 240f hemorrhage from, 231–233, 231f, 232f metastatic renal cell carcinoma and, 234, 234f myelolipoma of, 224–226, 224f, 225f pheochromocytoma of, 227–230, 227f, 228f, 229f Adrenocortical carcinoma, 237–239, 237f Age, in ovarian dermoid etiology, 445 Albendazole therapy, in hydatid disease, 16 Alcohol abuse acute necrotizing pancreatitis and, 87 groove pancreatitis and, 127 ALSA (aberrant left subclavian artery), 244 American Fertility Society, Müllerian duct anomaly classification, 441 imaging findings, 442–443 Aminosalicylate therapy, in Crohn disease, 283 AML (angiomyolipoma), renal. See Angiomyolipoma, renal Aneurysm, abdominal aortic, 178–180, 178f, 179f Angioembolization, for splenic AV fistula, 156 Angiography. See also Computed tomography angiography (CTA); Magnetic resonance angiography (MRA) aberrant right subclavian artery, 245 acute mesenteric ischemia, 272 hepatic hemangioma, 2 oncocytoma, 186 renal angiomyolipoma, 171 Angiomatosis, hemangioma of spleen and, 135 Angiomyolipoma, renal, 169–171, 169f lipid poor, 172–174, 172f Angiotensin-converting enzyme (ACE), in splenic sarcoidosis, 140 Antibiotic therapy for Crohn disease, 283 for hepatic pyogenic abscess, 19

514

INDEX

Antibiotic therapy (continued) for inflammatory disease with tubo-ovarian abscess, 427 for primary sclerosing cholangitis, 73 for pyelonephritis, 182 for renal abscess, 205 Antiestrogen therapy, for retroperitoneal fibrosis, 219 Anti-inflammatory therapy for endometrioma, 438 for focal omental infraction, 374 Aortic aneurysm, abdominal, 178–180, 178f, 179f Appendectomy, 358 Appendicitis, 277–279, 277f Appendicoliths, 278 Appendix, malignant mucocele of, 293–295, 293f, 295f “Apple core” lesion, in colorectal cancer, 299, 307 Arcuate uterus, 442, 442f ARSA (aberrant right subclavian artery), 243–245, 243f, 244f Arterial embolization for hepatic adenoma, 12 for hepatic hemangioma, 2 for hepatic venous malformation, 23 for hepatocellular carcinoma, 40 Arterial phase computed tomographic imaging, in hepatocellular carcinoma, 38, 38f, 39, 40f Arteriography, wandering spleen, 144 Arteriovenous (AV) fistula, spleen with, 155–156, 155f Arteriovenous malformation (AVM), pelvic, 495–497, 495f Ascariasis biliary, 56–58, 56f of gallbladder, 57 Ascaris lumbricoides infestation, biliary tract, 56–58, 56f Autoimmune pancreatitis, 92–94, 92f Autosomal dominant polycystic kidney disease (ABPKD), 166–168, 166f, 168f Autosplenectomy, 149–151, 149f AV (arteriovenous) fistula, spleen with, 155–156, 155f AVM (arteriovenous malformation), pelvic, 495–497, 495f B Bacterial spread, renal abscess and, 205 Barium studies aberrant right subclavian artery, 243, 243f, 245 gastric adenocarcinoma, 252 gastric fundal diverticulum, 322f, 323 lymphoma of sigmoid colon, 313 radiation enteritis, 360, 360f, 361 small bowel obstruction, 352

“Beaded” appearance, in primary sclerosing cholangitis, 72 Beckwith-Wiedemann syndrome, splenic hemangioma in, 135 Bezoar, small bowel obstruction secondary to, 366–367, 366f Bicornuate uterus, 440–443, 440f, 442f Bile duct Ascaris infection of, 56–58, 56f injury to, bile leak from, 74–76, 74f Bile leak, 74–76, 74f Biliary ascariasis, 56–58, 56f Biliary tree obstruction hepatic hemangioma and, 2 hepatic metastatic disease and, 32–34, 32f Biloma, 75 percutaneous drainage of, 76 Biopsy accessory spleen, 134 liver, in primary sclerosing cholangitis, 72 percutaneous image-guided in gallbladder carcinoma diagnosis, 59, 59f in lipid-poor angiomyolipoma, 172, 172f Bladder. See Urinary bladder entries Blood supply, to liver, 21 Bone marrow transplantation, for extramedullary plasmacytoma, 99 BOPTA (gadolinium benzyloxypropionictetraacetate), in focal nodular hyperplasia imaging, 7f Bosniak classification, renal cell carcinoma, 202t Bowel pneumatosis with portal venous gas, 289–292, 289f, 291f Breast cancer, calcified hepatic metastases in, 35–37, 35f Breast/ovarian syndrome, 448–449 Budd-Chiari syndrome, 23 “Bull’s eye” sign, 69 C Calcification(s) adrenal cyst, 221, 221f–222f, 222 adrenal ganglioneuroma, 240, 240f bladder stones and, 385, 385f, 386, 387f in cystic renal cell carcinoma, 202 gallbladder wall, in porcelain gallbladder, 51, 51f in groove pancreatitis, 126f, 127 in hepatic metastatic disease, 35–37, 35f mature cystic teratoma, 459, 459f mucocele of appendix, 294, 295f nonfunctioning neuroendocrine tumors of pancreas, 123f, 124 retained surgical sponge and, 326 retroperitoneal liposarcoma, 333f, 334, 379, 379f, 380 in schistosomiasis of urinary bladder and ureters, 391, 391f, 392 splenic, 149, 149f, 150 in testicular microlithiasis, 480, 480f, 481

INDEX

in transitional cell carcinoma of urinary bladder, 400, 401f Calculi, urinary bladder, 385–387, 385f, 387f Canalicular testis, 467 Capsule endoscopy, in Crohn disease, 283 Carbohydrate antigen, in pancreatic mucinous cystadenocarcinoma, 118 Carcinoembryonic antigen (CEA) in hepatic metastatic disease, 33 pancreatic mucinous cystadenocarcinoma and, 118 Carcinoids classification, 320–321 gastric pedunculated, 319–321, 319f small bowel, with mesenteric metastases, 336–339, 336f, 338f Carcinoma. See also Adenocarcinoma adrenocortical, 237–239, 237f breast, calcified hepatic metastases in, 35–37, 35f cervical, 455–458, 455f colorectal, 299–301, 299f gallbladder, 59–61, 59f hepatocellular, 38–41, 38f, 40f pancreatic. See Pancreatic cancer prostate. See Prostate cancer renal cell. See Renal cell carcinoma transitional cell, of urinary bladder, 399–402, 399f–402f Caroli disease, 64 Carpet lesions, colorectal, radiologic criteria for, 300 CEA. See Carcinoembryonic antigen (CEA) Central dot sign, 64 Cervix carcinoma of, 455–458, 455f lymphoma of, 462–464, 462f Chemoradiation therapy for acinar cell carcinoma of pancreas, 130 for dedifferentiated spermatic cord liposarcoma, 500 for renal metastases, 213 Chemotherapy for appendiceal mucocele, 295 for gastrointestinal tract lesions adenocarcinoma in sigmoid colon, 300 gastric adenocarcinoma, 252 gastric MALT lymphoma, 248 juxtacortical chondrosarcoma, 342 metastatic liposarcoma, 347 for hepatic lesions for calcified hepatic metastases, 36 lymphoma, 30 metastatic disease, 33 for non-Hodgkin lymphoma involving kidney, 216 for pancreatic lesions extramedullary plasmacytoma, 99 lymphoma, 121 for pelvic lesions

515

cervical lymphoma, 464 endometrial adenocarcinoma, 453 in gestational trophoblastic disease, 434 ovarian mucinous cystoadenocarcinoma, 449 for urinary bladder transitional cell carcinoma, 401 Childhood, pancreatic lymphangioma in, 84 Chocolate cyst (endometrioma), 436–439, 436f Cholangiocarcinoma classification of, 26 hilar, 26 intrahepatic, 25–28, 25f risk in primary sclerosing cholangitis, 72 Cholangitis, primary sclerosing, 71–73, 71f Cholecystectomy for acute acalculous cholecystitis, 45 for gallbladder carcinoma, 61 in Mirizzi syndrome, 67 prophylactic, for porcelain gallbladder, 51 Cholecystitis acute acalculous, 42–46, 42f, 44f–45f gangrenous, 43, 44, 44f Choledochal cysts, 62, 62f Choledochocele, 62–64, 62f, 64f Choledocholithiasis, 68–70, 68f Cholelithiasis, acute necrotizing pancreatitis and, 87 Cholesterol polyp, 47, 48 Chondrosarcoma, dedifferentiated juxtacortical, 340–342, 340f CHOP chemotherapy, for primary pancreatic lymphoma, 121 Choriocarcinoma, in gestational trophoblastic disease, 433 Chronic tubulointerstitial nephropathy (CTIN), lithium-induced, 190, 191 Coagulation therapy, for hepatocellular carcinoma, 39 Colchicine therapy, in familial Mediterranean fever, 317 Colectomy, in ulcerative colitis, 307 Colitis infectious, 274–276, 274f pseudomembranous, 275 ulcerative, 305–308, 305f Colonoscopy, sigmoid colon polyp and, 302, 302f, 303–304 Color Doppler sonography, ovarian dermoid, 445 Colorectal carcinoma, 299–301, 299f, 309–311, 309f Colovesical fistula, 406–408, 406f Common bile duct ascariasis in, 56–58, 56f stones in, 68–70, 68f Common hepatic duct obstruction (Mirizzi syndrome), 65–67, 65f, 67f Computed tomography (CT) aberrant right subclavian artery, 245 accessory spleen in pancreatic tail, 133

516

INDEX

Computed tomography (CT) (continued) arterial phase, in hepatocellular carcinoma, 38, 38f, 39, 40f cervical lymphoma, 463 contrast-enhanced. See Contrast-enhanced computed tomographic imaging cryptorchidism, 466 gastric carcinoid, 319, 319f, 320 in gestational trophoblastic disease diagnosis, 434 mesenteric fat, 349–350, 349f metanephric adenoma, 187f, 188 multidetector. See Multidetector computed tomography (MDCT) noncontrast. See Noncontrast computed tomographic imaging in ovarian mucinous cystoadenocarcinoma, 447, 447f, 449 postcontrast. See Postcontrast computed tomographic imaging rectal adenocarcinoma, 309, 309f, 310 sigmoid colon polyp, 302–304, 302f thin section, intraductal papillary mucinous neoplasia, 80, 81 Computed tomography angiography (CTA) in acute mesenteric ischemia, 272 in retroperitoneal lymphangioma, 343, 343f, 344 in small bowel carcinoid, 337 Computer tomography (CT)-guided drainage in acute necrotizing pancreatitis, 88 in adrenal hemorrhage, 233 of pancreatic abscess, 88 Contrast enema. See also Barium studies in diverticulosis, 297 porcelain appendix, 358 Contrast-enhanced computed tomographic imaging adrenal gland lesions adrenocortical carcinoma, 237, 237f, 238 cyst, 220, 220f, 221, 221f–222f ganglioneuroma, 240, 240f metastatic renal cell carcinoma and, 234, 234f, 235, 236f myelolipoma, 224, 224f, 225f, 335 gallbladder and bile duct lesions acute acalculous cholecystitis, 42, 42f, 44, 44f, 45f adenomyomatosis, 53, 53f, 54, 55f biliary ascariasis, 56, 56f, 58 carcinoma, 59, 59f choledochocele, 62, 62f choledocholithiasis, 68, 68f, 69 in Mirizzi syndrome, 65, 65f, 66, 67f polyp, 48, 49f porcelain gallbladder, 50, 50f, 51f primary sclerosing cholangitis, 71, 71f gastrointestinal tract lesions adenocarcinoma in sigmoid colon, 299, 299t

bowel pneumatosis with portal venous gas, 289, 289f, 291, 291f in Crohn disease, 281, 281f, 282f, 283 desmoid tumor of anterior abdominal wall, 376, 376f, 378 diverticulosis, 296, 296f, 297, 297f duodenal diverticulum, 262, 263f in familial Mediterranean fever, 315f–316f, 316, 317 focal omental infarction, 372, 372f, 373–374 gastric adenocarcinoma, 250, 250f, 252 gastric fundal diverticulum, 323, 323f gastric MALT lymphoma, 246, 246f, 247 gossypiboma, 325, 325f, 326–327 infectious colitis, 274, 274f, 275–276 intussusception, 285, 285f, 287 juxtacortical chondrosarcoma, 340f, 341, 342 lymphoma in sigmoid colon, 312, 312f, 313 metastatic liposarcoma, 346, 346f, 347 organoaxial gastric volvulus in hiatal hernia, 257, 257f, 259 perforated Meckel diverticulum, 368, 368f, 370 radiation enteritis, 360–362, 360f retroperitoneal liposarcoma, dedifferentiated, 333f, 334 small bowel carcinoid, 336, 336f, 337, 338f small bowel obstruction, 351, 351f, 352, 366, 366f, 367 spigelian hernia, 328, 328f stromal tumor, 254, 254f, 255, 255f subhepatic abscess, 330, 330f, 331 ulcerative colitis, 305, 305f, 306f, 307 hepatic lesions adenoma, 10f, 11f focal nodular hyperplasia, 5f hemangioma, 1f in hydatid disease, 14, 14f, 15 intrahepatic cholangiocarcinoma, 25, 25f, 27 lymphoma, 29, 29f, 30 metastasis from primary pancreatic cancer, 32, 32f, 33 pyogenic abscess, 18, 18f, 19 venous malformations, 21, 21f, 23 pancreatic lesions abscess, 89, 89f acinar cell carcinoma, 129, 129f, 130 acute necrotizing pancreatitis, 86, 86f, 87 autoimmune pancreatitis, 92, 92f, 93 ductal adenocarcinoma of pancreatic head, 104, 104f, 105 extramedullary plasmacytoma, 98, 98f, 99 groove pancreatitis, 126f, 127, 128 islet cell tumor, 107, 107f, 108 lymphangioma, 83, 83f, 84 lymphoma, 120, 120f, 121 metastases, from renal cell carcinoma, 110, 110f

INDEX

mucinous cystadenocarcinoma, 117, 117f, 118 nonfunctioning neuroendocrine tumor, 123, 123f solid papillary epithelial neoplasm, 113, 113f, 114 transection, 95, 95f, 96 pelvic lesions arteriovenous malformation, 495, 495f, 496 inflammatory disease with tubo-ovarian abscess, 424, 424f, 425 malignant germ cell tumor of testis, 471, 472f, 473 in mature cystic teratoma, 459, 459f, 460 ovarian dermoid, 444, 444f, 445 spermatic cord liposarcoma, dedifferentiated, 498f, 500 peritoneal lesions abdominal wall hernias, 265–267, 265f–267f acute appendicitis, 277, 277f, 278–279 acute mesenteric ischemia, 270, 270f, 272 mucocele of appendix, 293, 293f multilocular mesothelial inclusion cyst, 354, 354f, 355 porcelain appendix, 357, 357f, 358 renal lesions abscess, 204, 204f angiomyolipoma, 169, 169f, 170, 172, 172f, 173 atrophic kidney, 175, 176f in autosomal dominant polycystic kidney disease, 166, 166f, 167 infarct, 178, 178f, 179, 179f metanephric adenoma, 187f, 188 metastases, 211, 211f, 212 non-Hodgkin lymphoma, 214, 214f, 215 oncocytoma, 185, 185f, 186 in pyelonephritis, 181, 181f, 182 renal cell carcinoma, 207, 207f, 208 retroperitoneal fibrosis, 217, 217f, 218, 219f retroperitoneal lesions liposarcoma, dedifferentiated, 333, 333f, 379, 379f, 380, 380f lumbar hernia of Grynfellt, 382, 382f, 383 metastatic liposarcoma, 346, 346f, 347 splenic lesions arteriovenous fistula, 155, 155f hemangioma, 135, 135f, 137 infarcts, 160, 160f, 161 inflammatory pseudotumor, 146, 146f lymphoma, 157, 157f, 158 in sarcoidosis, 139, 139f, 140 in splenosis, 163, 163f, 164 wandering spleen, 142f, 143–144, 144f urinary bladder lesions in colovesical fistula, 406, 406f emphysematous cystitis, 388, 388f, 389 lipoma, 397, 397f, 398 transitional cell carcinoma, 399–400, 400f–401f

517

urachal adenocarcinoma, 403, 403f, 404 Cortical rim sign, 179 Corticosteroid therapy in Crohn disease, 283 for retroperitoneal fibrosis, 219 for splenic sarcoidosis, 140 Crohn disease, 281–284, 281f, 282f Cryptorchidism, 465–467, 465f CTIN (chronic tubulointerstitial nephropathy), lithium-induced, 190, 191 Cystadenocarcinoma hemicolectomy for, 358 pancreatic mucinous, 117–119, 117f Cystectomy, in transitional cell carcinoma of urinary bladder, 401 Cystic disease, localized renal, 192–194, 192f Cystic pheochromocytoma, adrenal, 221 Cystic teratoma, mature, 459–461, 459f–461f Cystitis, emphysematous, 388–389, 388f Cystoadenocarcinoma, ovarian mucinous, 447–450, 447f Cystography in colovesical fistula, 407 in urinary bladder lipoma, 398 Cyst(s) adrenal, 220–222, 220f, 221f–222f chocolate (endometrioma), 436–439, 436f dermoid. See Dermoids Gartner duct, 416–418, 416f hydatic. See Hydatid cysts inclusion, multilocular mesothelial, 354–356, 354f Cytoreductive surgery for ovarian mucinous cystoadenocarcinoma, 449 for renal cell carcinoma, 209 D Dedifferentiated chondrosarcoma, juxtacortical, 340–342, 340f Dedifferentiated liposarcoma retroperitoneal, 333–335, 333f, 334f, 379–381, 379f, 380f spermatic cord, 498–500, 498f Degenerative changes, in leiomyoma, 422 Dermoids, 459–461, 459f–461f ovarian, adnexal torsion from, 444–446, 444f DES uterus, 443 Desmoid tumor, anterior abdominal wall, 376–378, 376f Diverticula duodenal, 261–263, 261f, 263f gastric fundal, 322–324, 322f, 323f Meckel, perforated, 368–371, 368f, 369f urethral, 409–411, 409f Diverticulectomy, for urethral diverticulum, 411 Diverticulitis colovesical fistula and, 406–408, 406f Meckel, 370

518

INDEX

Diverticulosis, 296–298, 296f, 297f Doppler sonography extratesticular adenomatoid tumor, 474f, 475 gallbladder polyp, 49f in gestational trophoblastic disease diagnosis, 434 malignant germ cell tumor of testis, 471, 472f ovarian dermoid, 445 testicular lymphoma, 477, 477f tubular ectasia of rete testis, 493 Double-balloon urethrography, urethral diverticulum, 410 Double-contrast studies gastric adenocarcinoma, 251f, 252 gastric MALT lymphoma, 247 lymphoma of sigmoid colon, 313 Drainage CT-guided. See Computer tomography (CT)guided drainage percutaneous. See Percutaneous drainage Duct of Santorini, 77, 77f Ductal adenocarcinoma of pancreatic head, 104–106, 104f Duodenal bulb, filling defect in, 319, 319f Duodenal diverticulum, 261–263, 261f, 263f Dysgenesis, uterine, 442 E EA (epiploic appendagitis), imaging appearance of, 374 Echinococcosis, 15 Echinococcus infection, hydatid disease and, 14–17, 14f Ectopic spleen, intrapancreatic, 133 imaging techniques and, 134 Ectopic testis, 467 Ehlers-Danlos syndrome, splenic AV fistula in, 156 Embolectomy, in acute mesenteric ischemia, 272 Embolization selective, for lipid-poor angiomyolipoma, 173 transcatheter, for pelvic arteriovenous malformation, 497 uterine artery. See Uterine artery embolization Emphysematous cystitis, 388–389, 388f Endoluminal ultrasound, rectal adenocarcinoma, 309, 309f, 310 Endometrial adenocarcinoma, 451–453, 451f Endometrioma, 436–439, 436f Endometriosis, 437 Endometritis, 425 Endoscopic retrograde cholangiopancreatography (ERCP) in acute acalculous cholecystitis, 45 acute necrotizing pancreatitis as complication of, 87 bile leak secondary to bile duct injury, 74, 74f, 75

in biliary ascariasis, 58 choledochal cysts, 64, 64f in Mirizzi syndrome, 65, 65f, 66 in pancreas divisum, 78 primary sclerosing cholangitis, 71, 71f, 72 Endoscopic therapy in biliary ascariasis, 58 in choledocholithiasis, 70 in primary sclerosing cholangitis, 73 Endoscopy, in gastric adenocarcinoma diagnosis, 252 Enteritis, radiation-induced, 360–362, 360f Epididymo-orchitis, tuberculous, 483–485, 483f Epiploic appendagitis (EA), imaging appearance of, 374 Epithelial tumors, ovarian, 448 ERCP. See Endoscopic retrograde cholangiopancreatography (ERCP) Escherichia coli infection, hepatic pyogenic abscess and, 19 Esophagoscopy, aberrant right subclavian artery, 245 Esophagus, aberrant right subclavian artery and, 243–245, 243f, 244f Excretory urography, in urinary bladder herniation, 395 Extramedullary plasmacytoma, pancreas and, 98–100, 98f F Familial adenomatous polyposis (FAP), 377 Familial Mediterranean fever, acute abdominal attack in, 315–317, 315f FAP (familial adenomatous polyposis), 377 Fascicular sign, 365 Fat necrosis, in lumbar hernia of Grynfellt, 382, 382f, 383 FDG PET. See 18F-fluorodeoxyglucose positron emission tomography (FDG PET) “Female prostate” sign, 411 Femoral hernia, 266 Fibrosis, retroperitoneal, 217–219, 217f, 219f FIGO staging system. See International Federation of Gynecology and Obstetrics (FIGO) staging system Fistula, colovesical, 406–408, 406f 18F-fluorodeoxyglucose positron emission tomography (FDG PET) in hepatic metastatic disease, 33 in pancreatic mucinous cystadenocarcinoma, 118 primary pancreatic lymphoma, 120, 120f Fluoroscopy, organoaxial gastric volvulus in hiatal hernia, 257–258, 257f Focal nodular hyperplasia (FNH), of liver, 5–8, 5f–7f Focal omental infarction, 372–374, 372f Fracture, penile, 488–489, 488f Fundal diverticulum, gastric, 322–324, 322f, 323f

INDEX

G Gadolinium benzyloxypropionictetraacetate (BOPTA), in focal nodular hyperplasia imaging, 7f Gadolinium-enhanced magnetic resonance imaging cervical carcinoma, 457 islet cell tumor of pancreas, 108 solid papillary epithelial neoplasm, 114 T1-weighted hepatic hemangioma, 3f intraductal papillary mucinous neoplasia, 81f T2-weighted Gartner duct cyst, 416, 416f, 417 leiomyoma, 419, 419f retroperitoneal schwannoma, 364f Gadopentate dimeglumine-enhanced imaging, splenic hemangioma, 137f Gallbladder acute acalculous cholecystitis and, 42–46, 42f, 44f–45f adenomyomatosis of, 53–55, 53f, 55f ascariasis of, 57 carcinoma of, 59–61, 59f choledochocele and, 62–64, 62f, 64f choledocholithiasis and, 68–70, 68f in Mirizzi syndrome, 65–67, 65f, 67f polyp of, 47–49, 47f, 49f porcelain, 50–52, 50f, 51f primary sclerosing cholangitis and, 71–73, 71f Gallstones, dropped, subhepatic abscess secondary to, 330–332, 330f Ganglioneuroma, adrenal, 240–242, 240f Gangrenous cholecystitis, 43, 44, 44f Gartner duct cyst, 416–418, 416f Gastric adenocarcinoma, 250–253, 250f, 251f Gastric carcinoid classification of, 320–321 pedunculated, 319–321, 319f Gastric fundal diverticulum, 322–324, 322f, 323f Gastric mucosa-associated lymphoid tissue (MALT) lymphoma, 246–248, 246f Gastrointestinal stromal tumor (GIST), 254–256, 254f, 255f Gastrointestinal tract lesions bowel pneumatosis with portal venous gas, 289–292, 289f, 291f in Crohn disease, 281–284, 281f, 282f desmoid tumor of anterior abdominal wall, 376–378, 376f diverticulosis, 296–298, 296f, 297f duodenal diverticulum, 261–263, 261f, 263f endometriosis implants in, 437 focal omental infarction, 372–374, 372f gastric adenocarcinoma, 250–253, 250f, 251f gastric fundal diverticulum, 322–324, 322f, 323f gastric MALT lymphoma, 246–248, 246f gossypiboma, 325–327, 325f

519

infectious colitis, 274–276, 274f intussusception, 285–287, 285f juxtacortical chondrosarcoma, 340–342, 340f pedunculated gastric carcinoid, 319–321, 319f perforated Meckel diverticulum, 368–371, 368f, 369f radiation enteritis, 360–362, 360f rectal adenocarcinoma, 309–311, 309f in sigmoid colon. See Sigmoid colon in small bowel. See Small bowel stromal, 254–256, 254f, 255f subhepatic abscess, 330–332, 330f ulcerative colitis, 305–308, 305f Germ cell tumors, 448 malignant testicular, 471–473, 472f Gerota fascia lumbar hernia of Grynfellt and, 266, 266f non-Hodgkin lymphoma and, 214, 214f Gestational trophoblastic disease (GTD), 432–435, 432f, 434f GIST (gastrointestinal stromal tumor), 254–256, 254f, 255f Glycogen storage disease, 10, 10f Gossypiboma, 325–327, 325f Gradient echo magnetic resonance imaging in-phase accessory spleen in pancreatic tail, 132, 132f, 134 hepatic adenoma, 9f, 12, 12f out-of-phase, accessory spleen, 132, 132f Gray-scale sonographic patterns, in tuberculous epididymo-orchitis, 484 Groove pancreatitis, 126–128, 126f classification of, 127 Grynfellt, lumbar hernia of, 266, 266f, 382–383, 382f GTD (gestational trophoblastic disease), 432–435, 432f, 434f H HCC. See Hepatocellular carcinoma (HCC) HCV. See Hepatitis C virus (HCV) infection Heart failure, high-output, hepatic lesions and, 22 Helicobacter pylori infection in gastric adenocarcinoma, 251 in gastric MALT lymphoma, 247, 248 Helminthic infestation, of biliary tract, 56–58, 56f Hemangioma hepatic, 1–3, 1f, 3f of spleen, 135–137, 135f, 137f Hemangiomatosis, 135 complications of, 136 Hemicolectomy, for cystadenocarcinoma, 358 Hemiscrotectomy, for dedifferentiated spermatic cord liposarcoma, 500 Hemoperitoneum hepatic adenoma and, 11 hepatic metastatic disease and, 32–34, 32f

520

INDEX

Hemorrhage. See also Spontaneous bleeding adrenal, 231–233, 231f, 232f Hepatic veins in hepatocellular carcinoma, 39, 40f obstruction of, 23 hepatic hemangioma and, 2 Hepatitis C virus (HCV) infection hepatic lymphoma and, 29, 30 intrahepatic cholangiocarcinoma and, 27 Hepatobiliary iminodiacetic acid (HIDA) scan, in acute acalculous cholecystitis, 44 Hepatocellular carcinoma (HCC), 38–41, 38f, 40f vascular malformations and, 23 Hereditary hemorrhagic telangiectasia (HHT). See Rendu-Osler-Weber syndrome Herlyn-Werner-Wunderlich syndrome, 417 Hernia(s) abdominal wall, 265–269, 265f–267f hiatal, organoaxial gastric volvulus in, 257–260, 257f lumbar, of Grynfellt, 266, 266f, 382–383, 382f obturator, small bowel obstruction and, 351–353, 351f spigelian, 328–329, 328f urinary bladder, 394–396, 394f HIDA (hepatobiliary iminodiacetic acid) scan, in acute acalculous cholecystitis, 44 Hilar cholangiocarcinoma, 26 Hormone therapy for adenomyosis, 414 for endometrial adenocarcinoma, 453 for endometrioma, 438 for leiomyoma, 422 multilocular mesothelial inclusion cyst, 355 for prostate carcinoma, 487 Howship-Romberg sign, 352 HTT (hereditary hemorrhagic telangiectasia). See Rendu-Osler-Weber syndrome Hydatid cysts, in liver, 14–15, 14f exophytic, 15 rupture of, 15 Hydatid disease, 14–17, 14f Hydatidiform mole, in gestational trophoblastic disease, 433–434 imaging findings, 434, 434f Hydronephrosis, in transitional cell carcinoma of urinary bladder, 401 Hyperplasia, focal nodular, of liver, 5–8, 5f–7f Hypersplenism, 136 Hypoplastic uterus, 442, 443 Hysterectomy for adenomyosis, 414 for endometrial adenocarcinoma, 453 for endometrioma, 438 for leiomyoma, 422 Hysteroscopic metroplasty, 443 I Imaging surveillance, microcystic adenoma of pancreas, 103

Immunotherapy in Crohn disease, 283 for primary pancreatic lymphoma, 121 for renal cell carcinoma, 209 for retroperitoneal fibrosis, 219 Incisional hernia, 267, 267f Inclusion cyst, multilocular mesothelial, 354–356, 354f Indium 111-labeled imaging, accessory spleen, 134 Infarcts focal omental, 372–374, 372f renal in abdominal aortic aneurysm, 178–180, 178f, 179f septic emboli causing, 160–162, 160f segmental testicular, 468–470, 469f in spleen, 160–162, 160f Infectious colitis, 274–276, 274f Inflammatory pseudotumor (IPT), splenic, 146–148, 146f Inner-tube sign, 57 Insulinoma, 107–109, 107f International Federation of Gynecology and Obstetrics (FIGO) staging system cervical carcinoma, 457 ovarian mucinous cystoadenocarcinoma, 449 Intraductal papillary mucinous neoplasia (IPMN), 79–82, 79f, 81f Intrahepatic cholangiocarcinoma, 25–28, 25f Intussusception, 285–287, 285f IPMN (intraductal papillary mucinous neoplasia), 79–82, 79f, 81f IPT (inflammatory pseudotumor), splenic, 146–148, 146f Ischemia, acute mesenteric, 270–273, 270f Islet cell tumor, pancreatic, 107–109, 107f nonfunctioning neuroendocrine type, 124 Isoechoicity, of cervical masses, 457 J Juxtacortical chondrosarcoma, 340–342, 340f K Kasabach-Merritt syndrome, hemangioma in hepatic, 2 splenic, 135 Kidney. See also Renal entries abscess of, 204–206, 204f angiomyolipoma of, 169–171, 169f lipid-poor, 172–174, 172f atrophic, secondary to reflux nephropathy, 175, 176f, 177 in autosomal dominant polycystic kidney disease, 166–168, 166f, 168f carcinoma of. See Renal cell carcinoma infarcts in abdominal aortic aneurysm and, 178–180, 178f, 179f septic emboli causing, 160–162, 160f

INDEX

lithium toxicity and, 190–191, 190f localized cystic disease of, 192–194, 192f metanephric adenoma of, 187–189, 187f metastases, from primary lung adenocarcinoma, 211–213, 211f multilocular cystic nephroma of, 195–197, 195f non-Hodgkin lymphoma involving, 214–216, 214f oncocytoma of, 184–186, 184f, 185f in pyelonephritis, 181–182, 181f retroperitoneal fibrosis and, 217–219, 217f, 219f in Von Hippel-Lindau disease, 198–200, 198f KIT receptor, 255 Klatskin tumor, 26 Klippel-Trénaunay-Weber syndrome, 135 Kommerell diverticulum, 244, 245 Kupffer cells, 10 L Laparoscopy for endometrioma, 438 for focal omental infraction, 374 for multilocular mesothelial inclusion cyst, 355 Laparotomy sponge, retained, 325–327, 325f, 327 removal of, 327 Leiomyoma, 419–422, 419f, 421f degenerative changes in, 422 submucosal, 420 Lipoma, urinary bladder, 397–398, 397f Liposarcoma dedifferentiated retroperitoneal, 333–335, 333f, 334f, 379–381, 379f, 380f spermatic cord, 498–500, 498f metastatic, 346–348, 346f myxoid, noncontrast appearance of, 347 Lithium toxicity, renal changes from, 190–191, 190f Liver. See also Hepatic entries adenoma of, 9–13, 9f–12f in autosomal dominant polycystic kidney disease, 166, 166f, 168f blood supply to, 21 carcinoma of hepatocellular, 38–41, 38f, 40f intrahepatic cholangiocarcinoma, 25–28, 25f focal nodular hyperplasia in, 5–8, 5f–7f hemangioma of, 1–3, 1f, 3f hydatid cysts in, 14–17, 14f lymphoma of, 29–31, 29f metastases adenocarcinoma in sigmoid colon with, 299–301, 299f calcified, in breast cancer patient, 35–37, 35f

521

in misdiagnosis of hepatic pyogenic abscess, 19 from pancreatic cancer, 32–34, 32f pyogenic abscess of, 18–20, 18f Thorotrast accumulation in, 152–154, 152f transplantation of. See Liver transplantation venous malformations in, 21–23, 22f Liver biopsy, in primary sclerosing cholangitis, 72 Liver transplantation for adenomatosis, 12 for hepatocellular carcinoma, 40 for primary sclerosing cholangitis, 73 “Long common channel” hypothesis, 63 Lumbar hernia of Grynfellt, 266, 266f, 382–383, 382f Lymph nodes, Thorotrast accumulation in, 152–154, 152f Lymphangioma pancreatic, 83–85, 83f retroperitoneal, 343–345, 343f Lymphoma cervical, 462–464, 462f gastric MALT, 246–248, 246f hepatic, 29–31, 29f primary pancreatic (non-Hodgkin), 120–122, 121f renal, 214–216, 214f sigmoid colon, 312–314, 312f spleen involvement in, 157–159, 157f testicular, 477–479, 477f Lynch II syndrome, 449 M Magnetic resonance angiography (MRA) aberrant right subclavian artery, 243, 243f, 244f, 245 acute mesenteric ischemia, 272 Magnetic resonance cholangiopancreatography (MRCP) adenomyomatosis of gallbladder, 54 in cholecystitis, acute acalculous, 45–46 in choledochal cyst diagnosis, 63–64, 64f in choledocholithiasis, 68, 68f, 69–70 in groove pancreatitis, 128 intraductal papillary mucinous neoplasia, 80, 81, 81f intrahepatic cholangiocarcinoma, 27 in Mirizzi syndrome, 66 pancreas divisum, 77, 77f, 78 Magnetic resonance imaging (MRI). See also Gadolinium-enhanced magnetic resonance imaging; T1-weighted magnetic resonance imaging; T2weighted magnetic resonance imaging gallbladder and bile duct lesions adenomyomatosis, 54 biliary ascariasis, 58 cholecystitis, acute acalculous, 44 polyp, 48

522

INDEX

Magnetic resonance imaging (MRI) (continued) gastrointestinal tract lesions gastric adenocarcinoma, 252 metastatic liposarcoma, 347 organoaxial gastric volvulus in hiatal hernia, 259 retained surgical sponge and, 327 hepatic lesions in hepatocellular carcinoma, 39, 40f metastasis from primary pancreatic cancer, 33 pancreatic lesions. See also Magnetic resonance cholangiopancreatography (MRCP) acinar cell carcinoma, 130 groove pancreatitis, 128 solid papillary epithelial neoplasm, 114 pelvic lesions arteriovenous malformation, 495, 495f, 496 cervical carcinoma, 457 dedifferentiated spermatic cord liposarcoma, 500 endometrial adenocarcinoma, 452, 453 extratesticular adenomatoid tumor, 475 ovarian dermoid, 445 penile metastases, 491 splenic lesions accessory spleen, 134 hemangioma, 137f in sarcoidosis, 140 urinary bladder lesions herniation, 395 lipoma, 398 MALT (mucosa-associated lymphoid tissue) lymphoma, gastric, 246–248, 246f Mayer-Rokitanski-Kuster-Hauser syndrome, 442 MDCT. See Multidetector computed tomography (MDCT) Mebendazole therapy, for biliary ascariasis, 58 Meckel diverticulum, perforated, 368–371, 368f, 369f Mesenteric fat, imaging of, 349–350, 349f Mesenteric ischemia, acute, 270–273, 270f Mesenteric metastases, small bowel carcinoid with, 336–339, 336f, 338f Mesentery, misty, 349–350, 349f Metanephric adenoma, 187–189, 187f Metastatic disease hepatic adenocarcinoma in sigmoid colon with, 299–301, 299f calcified, in breast cancer patient, 35–37, 35f from primary pancreatic cancer, 32–34, 32f mesenteric, small bowel carcinoid with, 336–339, 336f, 338f in pancreas, from renal cell carcinoma, 110–111, 110f penile, from prostate cancer, 490–491, 490f

renal, from primary lung adenocarcinoma, 211–213, 211f Metastatic liposarcoma, 346–348, 346f Metformin therapy, in polycystic ovary syndrome, 429 Methotrexate therapy, for testicular lymphoma, 477, 477f Metrifonate therapy, for schistosomiasis, 393 Metroplasty, hysteroscopic, 443 Microcystic adenoma, of pancreas, 101–103, 101f Microlithiasis, testicular, 480–482, 480f Microwave coagulation therapy, for hepatocellular carcinoma, 39 Mirizzi syndrome, 65–67, 65f, 67f Misty mesentery, 349–350, 349f MLCN (multilocular cystic nephroma), 195–197, 195f Monoclonal antibody therapy for gastric MALT lymphoma, 248 for splenic sarcoidosis, 140 Monoclonal gammopathy, extramedullary plasmacytoma and, 99 MRA. See Magnetic resonance angiography (MRA) MRCP. See Magnetic resonance cholangiopancreatography (MRCP) MRI. See Magnetic resonance imaging (MRI) Mucinous cystadenocarcinoma, pancreatic, 117–119, 117f Mucocele of appendix, 293–295, 293f, 295f porcelain appendix and, 357–359, 357f ruptured, management of, 295 Müllerian duct, anomaly classification, 441 Multidetector computed tomography (MDCT) abdominal wall hernias, 268 gastric MALT lymphoma, 247 hepatic adenoma, 11 Multilocular cystic nephroma (MLCN), 195–197, 195f Multimodality therapy, for hepatic lymphoma, 30 Murphy sign, 43, 44f Myelolipoma, adrenal, 224–226, 224f, 225f Myxoid liposarcoma, noncontrast appearance of, 347 N Nasogastric tube decompression, in gastric volvulus, 259 Necrosis, types of, 87 Nephrectomy, for renal cell carcinoma, 209 Nephroma, multilocular cystic, 195–197, 195f Nephrotoxicity, lithium-induced, 190–191, 190f Neurilemmoma, 363–365, 363f, 364f Neurinoma, 363–365, 363f, 364f Neuroendocrine tumor, nonfunctioning pancreatic, 123–125, 123f Node dissection, retroperitoneal, malignant testicular germ cell tumor, 473

INDEX

Noncontrast computed tomographic imaging adrenal hemorrhage, 231, 231f, 232, 232f gallbladder, porcelain, 51 hepatic lesions calcified metastases, 35, 35f, 36 in hepatocellular carcinoma, 39 pancreatic lesions intraductal papillary mucinous neoplasia, 79, 79f, 80–81 nonfunctioning neuroendocrine tumor, 123, 123f porcelain gallbladder, 51 renal lesions in cystic renal cell carcinoma, 201, 201f metanephric adenoma, 187f, 188 retroperitoneal lesions myxoid liposarcoma, 347 schwannoma, 363, 363f, 365 splenic lesions in autosplenectomy, 149, 149f, 150 hemangioma, 136 inflammatory pseudotumor, 147 Thorotrast accumulation, 152, 152f, 153 urinary bladder lesions hernia, 394, 394f, 395 stones, 385, 385f, 386 transitional cell carcinoma, 399, 399f Nonfunctioning neuroendocrine tumor, pancreatic, 123–125, 123f Non-Hodgkin lymphoma (NHL) involving kidney, 214–216, 214f involving pancreas, 120–122, 121f involving sigmoid colon, 312–314, 312f Nuclear imaging bile leak secondary to bile duct injury, 75 perforated Meckel diverticulum, 370 renal infarct, 178, 178f, 179, 179f O Obstruction appendiceal, 278 biliary tree. See Biliary tree obstruction common hepatic duct, 65–67, 65f, 67f hepatic. See Hepatic veins, obstruction of small bowel. See Small bowel, obstruction of Obturator hernia, 267, 267f small bowel obstruction and, 351–353, 351f Oncocytoma, 184–186, 184f, 185f Oophoropexy, for ovarian dermoid, 446 Oral contraceptives, hepatic adenoma and, 10 Orchiectomy high inguinal, for dedifferentiated spermatic cord liposarcoma, 500 for malignant testicular germ cell tumor, 473 for testicular lymphoma, 477, 477f Organ of Zuckerkandl, 228, 229f Organoaxial gastric volvulus, 257–260, 257f Ovary dermoid of, adnexal torsion secondary to, 444–446, 444f

523

mucinous cystoadenocarcinoma of, 447–450, 447f polycystic ovary syndrome, 428–430, 428f, 430f tumor classification, 448 P Palliative therapy for intrahepatic cholangiocarcinoma, 27 for small bowel carcinoid, 338 Pancreas abscess of, 89–91, 89f carcinoma of. See Pancreatic cancer extramedullary plasmacytoma of, 98–100, 98f intraductal papillary mucinous neoplasia of, 79–82, 79f, 81f islet cell tumor of, 107–109, 107f lymphangioma of, 83–85, 83f lymphoma (non-Hodgkin) of, 120–122, 120f metastases to, from renal cell carcinoma, 110–111, 110f microcystic adenoma of, 101–103, 101f nonfunctioning neuroendocrine tumor of, 123–125, 123f solid papillary epithelial neoplasm of, 113–115, 113f transection of, 95–97, 95f Pancreas divisum, 77–78, 77f pancreatitis risk in, 87 Pancreatic cancer acinar cell, 129–131, 129f hepatic metastatic disease from, 32–34, 32f mucinous cystadenocarcinoma, 117–119, 117f Pancreatic head, ductal adenocarcinoma of, 104–106, 104f Pancreatic tail, accessory spleen in, 132–134, 132f Pancreaticoduodenal groove, 127 Pancreaticoduodenectomy for groove pancreatitis, 128 in small bowel carcinoid, 338 Pancreatitis acute necrotizing, 86–88, 86f autoimmune, 92–94, 92f groove, 126–128, 126f classification, 127 wandering spleen and, 143 Papaverine therapy, for acute mesenteric ischemia, 272 Paraganglioma, adrenal medullary. See Pheochromocytoma, adrenal “Pearl necklace” sign, 54 Pelvic inflammatory disease (PID), 424–427, 424f, 426f Pelvic lesions adenomyosis, 412–414, 412f arteriovenous malformation, 495–497, 495f bicornuate uterus, 400f, 440–443, 440f, 442f cervical. See Cervix cystic teratoma, 459–461, 459f–461f

524

INDEX

Pelvic lesions (continued) endometrial adenocarcinoma, 451–453, 451f endometrioma, 436–439, 436f Gartner duct cyst, 416–418, 416f gestational trophoblastic disease, 432–435, 432f, 434f inflammatory disease with tubo-ovarian abscess, 424–427, 424f, 426f leiomyoma, 419–422, 419f, 421f ovarian. See Ovary prostate carcinoma, 486–487, 486f testicular. See Testis urethral diverticulum, 409–411, 409f Pelvic mass, visceral, juxtacortical chondrosarcoma mimicking, 340–342, 340f Penis fracture of, 488–489, 488f metastases, from prostate cancer, 490–491, 490f Percutaneous drainage of abscesses hepatic pyogenic, 19 pancreatic, 88 subhepatic, 331 of biloma, 76 Percutaneous image-guided biopsy, in gallbladder carcinoma diagnosis, 59, 59f Percutaneous therapy for hepatocellular carcinoma, 39 for hydatid disease, 16 microwave coagulation, for hepatocellular carcinoma, 39 Perforated Meckel diverticulum, 368–371, 368f, 369f Peritoneal cavity lesions abdominal wall hernia, 265–268, 265f–267f acute appendicitis, 277–279, 277f acute mesenteric ischemia, 270–273, 270f malignant mucocele of appendix, 293–295, 293f, 295f multilocular mesothelial inclusion cyst, 354–356, 354f porcelain appendix, 357–359, 357f PET. See 18F-fluorodeoxyglucose positron emission tomography (FDG PET); Positron emission tomography (PET) Pheochromocytoma, adrenal, 227–230, 227f, 228f, 229f cystic, 221 Phytobezoar, small bowel obstruction secondary to, 366–367, 366f PID (pelvic inflammatory disease), 424–427, 424f, 426f Plasmacytoma, extramedullary, pancreas and, 98–100, 98f “Plateau phase,” desmoid tumors, 378 Polycystic ovary syndrome (POS), 428–430, 428f, 430f

Polyp gallbladder, 47–49, 47f, 49f sigmoid colon, 302–304, 302f Polypoid mass, cholangiocarcinoma and, 73 Polypoidal lesion, radiologic criteria for, 300 Porcelain appendix, 357–359, 357f Porcelain gallbladder, 50–52, 50f, 51f Portal hypertension, in splenic AV fistula, 155–156, 155f Portal vein compression hepatic venous malformation and, 23 hydatid cysts and, 15 Portal venous system gas in, bowel pneumatosis with, 289–292, 289f, 291f in hepatocellular carcinoma, 39, 40f POS (polycystic ovary syndrome), 428–430, 428f, 430f Positron emission tomography (PET). See also 18F-fluorodeoxyglucose positron emission tomography (FDG PET) metastatic renal cell carcinoma to adrenal gland, 235 splenic involvement in lymphoma, 157, 157f, 158 Postcholecystectomy clips, 126f, 127 Postcontrast computed tomographic imaging adrenal pheochromocytoma, 229, 229f hepatic hemangioma, 3f pancreatic microcystic adenoma, 101, 101f, 102 renal lesions lithium-induced, 190, 190f, 191 localized cystic disease, 192, 192f, 193 multilocular cystic nephroma, 195, 195f, 196 in Von Hippel-Lindau disease, 198, 198f, 199 urinary bladder stones, 385, 385f, 386, 387f Postural maneuvers, in abdominal wall hernia imaging, 268 Praziquantel therapy, for schistosomiasis, 393 Pregnancy, gestational trophoblastic disease in, 432–435, 432f, 434f Primary sclerosing cholangitis (PSC), 71–73, 71f Prophylaxis cholecystectomy for porcelain gallbladder, 51 irradiation for testicular lymphoma, 477, 477f Prostate cancer, 486–487, 486f penile metastases from, 490–491, 490f PSC (primary sclerosing cholangitis), 71–73, 71f Pseudocystic sign, 346–348, 346f Pseudocysts, adrenal, 222 Pseudomembranous colitis, 275 Pseudomyxoma peritonei malignant mucocele of appendix with, 293–295, 293f, 295f ovarian mucinous cystoadenocarcinoma and, 448 porcelain appendix and, 358

INDEX

Pseudotumor, inflammatory splenic, 146–148, 146f Pyelonephritis, 181–182, 181f Pyrantel pamoate therapy, for biliary ascariasis, 58 R Radiation enteritis, 360–362, 360f Radiation therapy for adenocarcinoma in sigmoid colon, 300–301 for cervical carcinoma, 457 for cervical lymphoma, 464 for endometrial adenocarcinoma, 453 for extramedullary plasmacytoma, 99 for juxtacortical chondrosarcoma, 342 for metastatic liposarcoma, 347 for primary pancreatic lymphoma, 121 for prostate carcinoma, 487 for urachal adenocarcinoma, 405 Radiochemotherapy. See Chemoradiation therapy Radiofrequency ablation (RFA) of adrenal metastases, 236 for hepatic metastatic disease, 33 for hepatocellular carcinoma, 39 for renal metastases, 213 Radiography bladder stones, 386 bowel pneumatosis with portal venous gas, 290 cryptorchidism, 466 emphysematous cystitis, 389 in intussusception, 286 organoaxial gastric volvulus in hiatal hernia, 257–258, 257f, 259 porcelain gallbladder, 51 in schistosomiasis of urinary bladder and ureters, 392 small bowel obstruction, 352 tubo-ovarian abscess, 427 Radiologic follow-up for hepatic adenoma, 12 for pancreatic lymphangioma, 85 Radionuclear cystourethrography, atrophic kidney, 177 Radionuclide imaging, accessory spleen, 134 Radioscintigraphy in acute acalculous cholecystitis, 44 in adrenal pheochromocytoma, 229 Radiotracers, for radionuclide imaging of accessory spleen, 134 Rectal adenocarcinoma, 308f, 309–311 Red blood cells radiolabeled heat-damaged, for imaging of accessory spleen, 134 in sickle cell disease, 150 Reflux nephropathy, atrophic kidney secondary to, 175, 176f, 177

525

Renal cell carcinoma, 207–209, 207f cystic, 201–203, 201f classification of, 202t metastatic, to adrenal gland, 234–236, 234f pancreatic metastases from, 110–111, 110f subtype features in, 208–209 in Von Hippel-Lindau disease, 199, 208 Renal dialysis, in autosomal dominant polycystic kidney disease, 167 Renal failure, in autosomal dominant polycystic kidney disease, 166–167 Rendu-Osler-Weber syndrome hepatic venous malformation in, 23 splenic AV fistula in, 156 Retained surgical sponge, 325–327, 325f Rete testis, tubular ectasia of, 492–493, 492f Retractile testis, 467 Retrograde cystography, in urinary bladder herniation, 395 Retroperitoneal fibrosis (RPF), 217–219, 217f, 219f Retroperitoneal lesions dedifferentiated liposarcoma, 333–335, 333f, 334f, 379–381, 379f, 380f lumbar hernia of Grynfellt, 266, 266f, 382–383, 382f lymphangioma, 343–345, 343f metastatic liposarcoma, 346–348, 346f myxoid liposarcoma, 347 schwannoma, 363–365, 363f, 364f Retroperitoneal node dissection, malignant testicular germ cell tumor, 473 RFA. See Radiofrequency ablation (RFA) Rim sign in acute acalculous cholecystitis, 44 in renal infarct, 179 Rituximab therapy. See Immunotherapy Rokitansky-Aschoff sinuses, 54 Roundworm infestation, biliary tract, 56–58, 56f RPF (retroperitoneal fibrosis), 217–219, 217f, 219f S “Saddlebag” diverticula, 410–411 Salpingitis, imaging findings in, 425 Salpingo-oophorectomy, for ovarian dermoid, 446 Santorini duct, pancreas divisum and, 77, 77f Sarcoidosis, splenic, 139–141, 139f SAVF (splenic arteriovenous fistula), 155–156, 155f Schistosomiasis, in urinary bladders and ureters, 391–393, 391f Schmid’s triad, in acinar cell carcinoma of pancreas, 130 Schwannoma, retroperitoneal, 363–365, 363f, 364f Scintigraphy. See also Radioscintigraphy in gastric carcinoid, 321 in splenosis, 164

526

INDEX

Seminal vesicle invasion (SVI), prostate carcinoma and, 486–487 Septate uterus, 442, 442f Septic emboli, spleen and kidney infarcts caused by, 160–162, 160f Sex chord-stromal tumors, 448 Sickle cell disease, autosplenectomy from, 149–151, 149f Sigmoid colon adenocarcinoma in, 299–301, 299t colovesical fistula and, 406–408, 406f lymphoma of, 312–314, 312f polyp of, 302–304, 302f Single-photon emission computed tomography (SPECT), adrenal pheochromocytoma, 227, 227f Small bowel carcinoid of, with mesenteric metastases, 336–339, 336f, 338f obstruction of obturator hernia and, 351–353, 351f phytobezoar and, 366–367, 366f perforated Meckel diverticulum and, 368–371, 368f, 369f Solid papillary epithelial neoplasm (SPEN), 113–115 Somatostatin-receptor scintigraphy, gastric carcinoid, 321 Spaghetti sign, 57 SPECT (single-photon emission computed tomography), adrenal pheochromocytoma, 227, 227f SPEN (solid papillary epithelial neoplasm), 113–115 Spermatic cord liposarcoma, dedifferentiated, 498–500, 498f Sphincterotomy for bile leak, 76 endoscopic, in pancreas divisum, 78 Spigelian hernia, 328–329, 328f Spleen accessory, in pancreatic tail, 132–134, 132f arteriovenous fistula of, 155–156, 155f hemangioma of, 135–137, 135f, 137f infarcts in, 160–162, 160f inflammatory pseudotumor of, 146–148, 146f in lymphoma, secondary involvement, 157–159, 157f sarcoidosis of, 139–141, 139f in splenosis, 163–165, 163f Thorotrast accumulation in, 152–154, 152f wandering, 142–145, 142f, 144f Splenectomy for hemangioma of spleen, 136 for infarcts of spleen, 161 for inflammatory splenic pseudotumor, 147 Splenic arteriovenous fistula (SAVF), 155–156, 155f Splenopexy with splenic salvage, for wandering spleen, 144 Splenosis, 163–165, 163f

Spontaneous bleeding hepatic adenoma, 11, 11f hepatic hemangioma, 2 pelvic arteriovenous malformation and, 496 Spontaneous rupture hepatic hemangioma, 2 splenic, 136 Staging systems, for cancer in cervical carcinoma, 457 in endometrial adenocarcinoma, 452 in ovarian mucinous cystoadenocarcinoma, 449 Stein-Leventhal syndrome, 428–430, 428f, 430f Stent placement bile leak and, 76 primary pancreatic lymphoma and, 122 Steroid abuse, bleeding hepatic adenoma and, 11f Steroid therapy, for autoimmune pancreatitis, 93 Stripe sign, 57 Subhepatic abscess, 330–332, 330f Supportive treatment, for adrenal hemorrhage, 233 Surgical débridement acute necrotizing pancreatitis, 88 pancreatic abscess, 88 Surgical excision. See also Surgical resection accessory spleen, 134 choledochocele, 64 dedifferentiated spermatic cord liposarcoma, 500 desmoid tumor of anterior abdominal wall, 378 gastrointestinal stromal tumor, 255 islet cell tumor of pancreas, 109 juxtacortical chondrosarcoma, 342 metastatic liposarcoma, 347 multilocular mesothelial inclusion cyst, 355 pancreatic lymphangioma, 85 pelvic arteriovenous malformation, 497 perforated Meckel diverticulum, 370 porcelain appendix, 358 retroperitoneal lymphangioma, 344 Surgical management. See also Surgical débridement; Surgical excision; Surgical resection abdominal wall hernia, 268 in acute appendicitis, 279 in acute mesenteric ischemia, 272 adrenal cyst, 222 in biliary ascariasis, 58 bladder stones, 386 cervical carcinoma, 457 colovesical fistula, 407 in Crohn disease, 284 in diverticulosis, 298 duodenal diverticulum, 263 Gartner duct cyst, 418 gastric volvulus, 259 in gestational trophoblastic disease, 434

INDEX

hepatocellular carcinoma, 39 intussusception, 287 ovarian mucinous cystoadenocarcinoma, 449 penile fracture, 489 in polycystic ovary syndrome, 430 small bowel obstruction from obturator hernia, 353 from phytobezoar, 366, 366f, 367 spigelian hernia, 329 tubo-ovarian abscess, 427 uterine anomalies, 443 Surgical resection. See also Surgical excision in acinar cell carcinoma of pancreas, 130 adenocarcinoma in sigmoid colon, 300 adrenal ganglioneuroma, 240, 240f adrenal pheochromocytoma, 229 adrenocortical carcinoma, 238 bladder, in urachal adenocarcinoma, 405 calcified hepatic metastases, 36 dedifferentiated retroperitoneal liposarcoma, 379, 379f, 380 ductal adenocarcinoma of pancreatic head, 105 extratesticular adenomatoid tumor, 475 gastric adenocarcinoma, 252 hepatic adenoma, 12 hepatic hemangioma, 2 in hydatid disease, 16 intrahepatic cholangiocarcinoma, 27 mature cystic teratoma, 460 metanephric adenoma, 189 mucocele of appendix, 294, 295f multilocular cystic nephroma, 196 nonfunctioning neuroendocrine tumors of pancreas, 125 pancreatic mucinous cystadenocarcinoma, 119 pancreatic solid papillary epithelial neoplasm, 115 prostate carcinoma, 487 retroperitoneal liposarcoma, 335 retroperitoneal schwannoma, 365 small bowel carcinoid, 338 Surgical sponge, retained, 325–327, 325f SVI (seminal vesicle invasion), prostate carcinoma and, 486–487 T T1-weighted magnetic resonance imaging. See also Gradient echo magnetic resonance imaging adrenal gland lesions adrenocortical carcinoma, 238 cyst, 221 hemorrhage, 233 metastatic renal cell carcinoma and, 234, 234f, 235 myelolipoma, 225f, 226 pheochromocytoma, 227, 227f, 229 in cholecystitis, acute acalculous, 44 gadolinium-enhanced. See under Gadoliniumenhanced magnetic resonance imaging

527

gastrointestinal tract lesions desmoid tumor of anterior abdominal wall, 376, 376f, 378 juxtacortical chondrosarcoma, 340f, 341 small bowel carcinoid, 336, 336f hepatic lesions focal nodular hyperplasia, 6f, 7f intrahepatic cholangiocarcinoma, 27 pyogenic abscess, 19 pancreatic lesions acinar cell carcinoma, 130 lymphangioma, 84 lymphoma, 121 metastases, from renal cell carcinoma, 111 microcystic adenoma, 102 mucinous cystadenocarcinoma, 118 solid papillary epithelial neoplasm, 114 pelvic lesions adenomyosis, 414 arteriovenous malformation, 495, 495f, 496 bicornuate uterus, 440, 440f, 442 cervical lymphoma, 462, 462f, 463 cryptorchidism, 465, 465f, 466 endometrioma, 436, 436f, 438 Gartner duct cyst, 416, 416f, 417 in gestational trophoblastic disease diagnosis, 434 leiomyoma, 422 in mature cystic teratoma, 460, 461f ovarian mucinous cystoadenocarcinoma, 449 postgadolinium, penile metastases, 490–491, 490f segmental testicular infarct, 468, 469f, 470 renal lesions angiomyolipoma, 171 in autosomal dominant polycystic kidney disease, 167 lipid-poor angiomyolipoma, 173 metanephric adenoma, 189 non-Hodgkin lymphoma, 215 oncocytoma, 186 renal cell carcinoma, 208 retroperitoneal fibrosis, 218 in Von Hippel-Lindau disease, 199 retroperitoneal lesions lymphangioma, 344 schwannoma, 363, 363f, 364f, 365 splenic lesions hemangioma, 136, 137f inflammatory pseudotumor, 147 urinary bladder lesions urachal adenocarcinoma, 404 urethral diverticulum, 409, 409f, 410 T2-weighted magnetic resonance imaging adrenal gland lesions adrenocortical carcinoma, 238 cyst, 221 hemorrhage, 233 metastatic renal cell carcinoma and, 234, 234f, 235

528

INDEX

T2-weighted magnetic resonance imaging, adrenal gland lesions (continued) myelolipoma, 226 pheochromocytoma, 227, 227f, 229 in cholecystitis, acute acalculous, 44 gadolinium-enhanced. See under Gadoliniumenhanced magnetic resonance imaging gastrointestinal tract lesions desmoid tumor of anterior abdominal wall, 376, 376f, 378 duodenal diverticulum, 263 juxtacortical chondrosarcoma, 340f, 341, 342 rectal adenocarcinoma, 309, 309f, 310 small bowel carcinoid, 336, 336f hepatic lesions adenoma, 9f, 12, 12f focal nodular hyperplasia, 6f hemangioma, 3f intrahepatic cholangiocarcinoma, 27 pyogenic abscess, 19 pancreatic lesions acinar cell carcinoma, 130 lymphangioma, 84 lymphoma, 121 metastases, from renal cell carcinoma, 111 microcystic adenoma, 101, 101f, 102 mucinous cystadenocarcinoma, 118 solid papillary epithelial neoplasm, 114 pelvic lesions adenomyosis, 412, 412f, 414 bicornuate uterus, 440, 440f, 442, 442f cervical carcinoma, 455, 455f, 457 cervical lymphoma, 462, 462f, 463 cryptorchidism, 465, 465f, 466 endometrioma, 436, 436f, 438 Gartner duct cyst, 416, 416f, 417 in gestational trophoblastic disease diagnosis, 434 inflammatory disease with tubo-ovarian abscess, 425, 426f leiomyoma, 419, 419f, 422 malignant germ cell tumor of testis, 473 in mature cystic teratoma, 460, 461f ovarian mucinous cystoadenocarcinoma, 447, 447f, 449 penile fracture, 488, 488f, 489 polycystic ovary syndrome, 429, 430f prostate carcinoma, 486, 486f, 487 segmental testicular infarct, 468, 469f, 470 septate uterus, 442, 442f urethral diverticulum, 409, 409f, 410 renal lesions in autosomal dominant polycystic kidney disease, 167, 168f lithium-induced, 191 localized cystic disease, 194 metanephric adenoma, 189 multilocular cystic nephroma, 196 non-Hodgkin lymphoma, 215 oncocytoma, 186

renal cell carcinoma, 208 retroperitoneal fibrosis, 218 in Von Hippel-Lindau disease, 199 retroperitoneal lesions lymphangioma, 344 schwannoma, 363, 363f, 364f, 365 splenic lesions accessory spleen in pancreatic tail, 132, 132f, 134 hemangioma, 136, 137f inflammatory pseudotumor, 147 in sarcoidosis, 140 in urachal adenocarcinoma, 404 TACE (transcatheter arterial chemoembolization), for hepatocellular carcinoma, 40 Tapeworm infection, hydatid disease and, 14–17, 14f Technetium 99m scans accessory spleen, 134 in splenosis, 164 Teratoma, mature cystic, 459–461, 459f–461f Testis adenomatoid tumor of, extratesticular, 474–476, 474f dedifferentiated spermatic cord liposarcoma and, 498–500, 498f descent mechanisms, 466 lymphoma of, 477–479, 477f malignant germ cell tumor of, 471–473, 472f microlithiasis of, 480–482, 480f rete, tubular ectasia of, 492–493, 492f segmental infarct of, 468–470, 469f tuberculous epididymo-orchitis, 483–485, 483f undescended, 465–467, 465f types of, 467 Textiloma, 325–327, 325f Thin section computed tomographic imaging, intraductal papillary mucinous neoplasia, 80, 81 Thorotrast (thorium dioxide) accumulation, in liver, spleen and lymph nodes, 152–154, 152f Thrombosis, hydatid cysts and, 15 TNM (tumor-nodes-metastasis) system, 449 Todani classification, choledochal cysts, 62t, 63 Toxic megacolon, 307 Transcatheter arterial chemoembolization (TACE), for hepatocellular carcinoma, 40 Transection, pancreatic, 95–97, 95f Transitional cell carcinoma, of urinary bladder, 399–402, 399f–402f Transvaginal ultrasound adenomyosis, 412, 412f, 413 gestational trophoblastic disease, 432, 432f, 434, 434f leiomyoma, 421, 421f polycystic ovary syndrome, 428, 428f, 429 urethral diverticulum, 410 Triplication, of utero-ovarian ligament, 446

INDEX

Tuberculous epididymo-orchitis, 483–485, 483f Tuberous sclerosis, renal angiomyolipoma in, 170 Tubo-ovarian abscess, inflammatory pelvic disease with, 424–427, 424f, 426f Tubular ectasia, of rete testes, 492–493, 492f Tumor necrosis factor therapy, for splenic sarcoidosis, 140 Tumor-nodes-metastasis (TNM) staging system, 449 Tunica albuginea rete testis and, 493 trauma to, 488–489, 488f Turner syndrome, splenic hemangioma in, 135 U Ulcerative colitis, 305–308, 305f Ultrasound imaging. See also Transvaginal ultrasound adrenal gland lesions cyst, 220, 220f, 221 ganglioneuroma, 241 hemorrhage, 232 metastatic renal cell carcinoma and, 235 myelolipoma, 225 gallbladder and bile duct lesions in acute acalculous cholecystitis, 43 adenomyomatosis, 54, 55f bile leak secondary to bile duct injury, 74, 74f biliary ascariasis, 57–58 carcinoma, 60 polyp, 47, 47f, 48, 49f gastrointestinal tract lesions desmoid tumor of anterior abdominal wall, 378 duodenal diverticulum, 261, 261f, 262 in intussusception, 287 mucocele of appendix, 294 rectal adenocarcinoma, 309, 309f, 310 retained surgical sponge and, 327 retroperitoneal lymphangioma, 343, 343f, 344 hepatic lesions calcified metastases, 35, 35f, 36 focal nodular hyperplasia, 7 hemangioma, 2 in hepatocellular carcinoma, 38, 38f, 39 in hydatid disease, 15 metastasis from primary pancreatic cancer, 33 pyogenic abscess, 18, 18f, 19 pancreatic lesions lymphoma, 120, 120f microcystic adenoma, 102 mucinous cystadenocarcinoma, 118 pelvic lesions bicornuate uterus, 442 cervical carcinoma, 457 cervical lymphoma, 463 cryptorchidism, 466, 467

529

dedifferentiated spermatic cord liposarcoma, 500 endometrial adenocarcinoma, 453 endometrioma, 438 extratesticular adenomatoid tumor, 474f, 475 Gartner duct cyst, 417 inflammatory disease with tubo-ovarian abscess, 425, 426 malignant germ cell tumor of testis, 471, 472f, 473 mature cystic teratoma, 460, 460f ovarian dermoid, 445 ovarian mucinous cystoadenocarcinoma, 449 segmental testicular infarct, 468, 469f, 470 testicular lymphoma, 477, 477f, 478 testicular microlithiasis, 480, 480f, 481 tuberculous epididymo-orchitis, 483–485, 483f tubular ectasia of rete testis, 492, 492f renal lesions angiomyolipoma, 169, 169f, 170 autosomal dominant polycystic kidney disease, 167, 168f infarct, 178, 178f, 179, 179f lipid-poor angiomyolipoma, 173 localized cystic disease, 193 metanephric adenoma, 188 metastases, 212 oncocytoma, 184, 184f, 186 retroperitoneal fibrosis, 218 in Von Hippel-Lindau disease, 199 splenic lesions inflammatory pseudotumor, 147 splenosis, 164 urinary bladder lesions hernia, 396 stones, 386 Undescended testis, 465–467, 465f Unicornuate uterus, 442 Upper GI series duodenal diverticulum, 262, 263f gastric fundal diverticulum, 322, 322f, 323 organoaxial gastric volvulus, 259 pedunculated gastric carcinoid, 319, 319f Urachus, adenocarcinoma of, 403–405, 403f Ureters, schistosomiasis in, 391–393, 391f Urethral diverticulum, 409–411, 409f Urethroscopy, urethral diverticulum, 410 Urinary alkalization, for dissolution of bladder stones, 386 Urinary bladder colovesical fistula and, 406–408, 406f emphysematous cystitis of, 388–389, 388f herniation of, 394–396, 394f lipoma of, 397–398, 397f schistosomiasis in, 391–393, 391f stones in, 385–387, 385f, 387f

530

INDEX

Urinary bladder (continued) transitional cell carcinoma of, 399–402, 399f–402f and urachal adenocarcinoma, 403–405, 403f Urinary diversion, in transitional cell carcinoma of urinary bladder, 401 Urography in autosomal dominant polycystic kidney disease, 167, 168f urinary bladder lipoma, 398 Uterine artery embolization for adenomyosis, 414 in leiomyoma, 422 Uterine contractions, leiomyoma and, 422 Utero-ovarian ligament, triplication of, 446 Uterovaginal (Müllerian) anomalies, classification of, 441 imaging findings, 442–443 Uterus adenomyosis of, 412–414, 412f bicornuate, 440–443, 440f, 442f leiomyomas of, 419–422, 419f, 421f Müllerian duct anomaly classification, 441 imaging findings, 442–443 Uterus didelphys, 442

V Valsalva maneuver, in abdominal wall hernia imaging, 268 VCUG. See Voiding cystourethrography (VCUG) Venous malformations, hepatic, 21–23, 21f Ventral hernia, 266, 266f, 267f Vesicoureteral reflux (VUR), 175, 177 VIPoma, 108 Voiding cystourethrography (VCUG) atrophic kidney, 175, 176f, 177 urethral diverticulum, 410 Volvulus, organoaxial gastric, 257–260, 257f Von Hippel-Lindau disease, 198–200, 198f renal cell carcinoma in, 208 VUR (vesicoureteral reflux), 175, 177 W Wandering spleen, 142–145, 142f, 144f Whipple procedure for groove pancreatitis, 128 for islet cell tumor of pancreas, 109 Wirsung duct, pancreas divisum and, 77, 77f Z Zuckerkandl, organ of, 228, 229