Body CT The Essentials 9780071833646, 0071833641

Table of contents :
vii......Page 8
viii Co n t e n t s......Page 9
P a u l Sicuro, MD......Page 10
Z a chary R. Heeter, MD......Page 11
Preface......Page 12
1 The Physics of Computed Tomography......Page 14
C ommon Dos e T erminology......Page 20
C T - S p eci c Dos e T erminology......Page 21
S iz e - Specif c Dose Estimate......Page 22
F u n d a m ental Protocol Parameters......Page 23
A u tomatic Tu b e Curren t Modu l a tion a n d kVp Selection......Page 24
P rotocol Design and Clin ica l Setu p......Page 25
Co n Cl u s i o n......Page 26
Su g g e St e d R e a d i n g S......Page 27
e n h A n C e m e n T D u r A T i o n......Page 28
C a r d i a c Output......Page 29
Su g g e St e d R e a d I n g S......Page 30
Th y m u s......Page 32
G erm cell tumor......Page 34
Thymolipoma......Page 35
G erm Cell T u mors......Page 36
M edias t i n a l Fat Necros i s......Page 37
Ly m p h a d e n o p a t h y......Page 39
Neurof b r o m a......Page 40
H iatu s hernia......Page 41
Neurogenic Neoplas ms......Page 42
Media s tinitis......Page 43
Su g g e St e d R e A d i n g S......Page 44
Te c h n i q u e......Page 46
In ection......Page 47
E o s inophilic pn e u monia......Page 48
Ly m p h o m a......Page 49
Nodular Pattern......Page 50
Sarcoidosis......Page 51
Meta s ta s e s......Page 52
Pu l monary b rosis......Page 53
Pu l monary La n g e rha n cell histiocytosis......Page 54
L y mphoid interstitia l pneumon ia......Page 55
a Te L e c T a s is......Page 56
s o L i T a r y L u n g n o d u L e......Page 57
Lu n g c a n c e r......Page 58
Squ a mou s cell carcinoma......Page 59
Staging......Page 60
e m Ph y s e m a......Page 61
c o n g e n i T a L......Page 62
Systemic arteria l su p p l y to the lung......Page 63
L a rge vessel va s c u l itis......Page 64
P u l monary Arteriovenous Mal ormation......Page 65
RE E RENCES......Page 66
Te c h n i q u e......Page 68
Tr a c h e o b r o n c h o m a l a c i a......Page 69
M a l ign a nt tra c hea l neopla s ms......Page 70
D i u s e T r a cheal Dis eas e......Page 71
G ra n u l o matosis with polya n g iitis......Page 72
C a rdia c bron c hu s......Page 74
Bro n c h i e c t a s i s......Page 76
C y s tic b rosis......Page 77
L u ng neopla s ms......Page 78
Bro n c h i o li t i s......Page 79
H y p e rsen s itivity pn e u monitis......Page 80
R e s p iratory bronchiolitis......Page 81
Con s trictive bron c hiolitis......Page 82
Pl e u r a An a t o m y......Page 84
P l e u ra l e u s ion......Page 85
Chylothora x......Page 86
B ron c hopleura l a n d pleuropa renchyma l f s tu l a......Page 87
Meta s ta s e s......Page 88
P l e u ra l pla q u e s......Page 89
Di a P h r a g m An a t o m y......Page 90
Ch e s t W a l l An a t o m y......Page 92
Meta s ta s e s......Page 93
P l a s ma c y toma and mu l tiple myeloma......Page 94
C h es t W a l l In ection......Page 95
Nocardiosis......Page 96
T emporal Res olution......Page 98
Co r o n Ar y C T An g i o g r AP H y : in d iCATio n s......Page 99
L e t Circum ex Artery......Page 100
R i ght Coronary Artery......Page 101
C oronary Artery Anomalies......Page 102
m y o C A r d i u m M y ocardial Is chemic......Page 104
Pa p illary f b roela s toma......Page 105
Hemopericardium......Page 106
P ericardial Thickening......Page 107
TH o r A C i C Ao r T A An a t o m y......Page 108
A b e rrant right su b c l a v ian a rtery......Page 109
Pseudocoarctation......Page 110
A c u te a o rtic dissection......Page 111
T a k a y a s u arteritis......Page 112
G iant cell a rteritis......Page 113
SU G G E STED READIn G S......Page 114
A n a t omy and Phys i ology......Page 116
L i v er CT T echnique......Page 117
Cirrhosis......Page 118
F a tty liver disea s e......Page 119
V ira l hepatitis......Page 120
E c hin o c o c c a l in ection......Page 121
L iver cysts and polycystic disea s e......Page 122
H e p a tocellu l a r a d e noma......Page 123
H e p a tocellu l a r carcinoma......Page 125
Ly m p h o m a......Page 129
Meta s ta s e s......Page 130
T ransient hepa tic attenu a tion dif e ren c e s......Page 131
Peliosis hepatis......Page 132
Bi L i a r y S y S Te m An a t o m y......Page 133
C h oledochal Cys t s......Page 135
Ch o l e l i t h i a s i s......Page 136
A c u te cholecystitis......Page 137
Chronic cholecystitis......Page 138
P rimary sclerosin g chola n g itis......Page 139
I s c hemic cholangiopa thy......Page 140
Chola n g iocarcin o ma......Page 141
B iliary cysta d e noma a n d cysta d e nocarcinoma......Page 142
Su G G E STED READINGS......Page 143
An a t o m y......Page 144
P a n c r eatic Duct......Page 145
P a n c r eatic Ps eudomas s es......Page 146
Pancreatitis A c u t e Pancreatitis......Page 147
I n t ers t i t i a l Edematous Pancreatitis......Page 148
Peripa n c reatic collection s......Page 149
Necrotizing pancreatitis (pancreatic necros i s , peripancreatic necros i s ,......Page 150
Complication s o chronic pancrea titis......Page 151
M u c i n ous cys t i c neoplas m......Page 152
C y s t i c Neoplas m s......Page 153
So lid P a n c r e a t ic N e o p la s m s D u ctal Adenocarcinoma......Page 155
Neuroendocrine T u mors......Page 158
P a n c r eatic L y mphoma......Page 159
Su G G E STED READINGS......Page 160
An A t o m y......Page 162
Ct t e C h n i q U e......Page 163
V a riation in ren a l siz e s......Page 164
R enal Ectopy and Fus i on Anomalies......Page 166
A n omalies and V a r i a n t s o the Intrarenal C ollecting Sys t em and......Page 167
A n omalies and V a r i a n t s o the Bladder......Page 168
Ur o l i t h i A s i s......Page 169
r e n A l i n f e C t i o n s A n d in f l A m m A t o r......Page 171
C h r onic In ections......Page 173
r e n A l V A s C U l A r d i s e A s e......Page 174
B os n i a k Clas s i c a t i on Sys t em......Page 175
III In d e t e r m i n a t e c ys t......Page 176
B enign Primary Renal Mas s es......Page 178
M a l i gnant Primary Renal Mas s es......Page 179
M a l i gnan Secondary Renal Mas s es......Page 180
in t r A r e n A l C o l l e C t in g s y s t e m s ,......Page 181
C ongenital Ureteropelvic J u n c t i on Obs t r u c t i on......Page 182
Aden oca r ci n om a......Page 183
Nonneoplas t i c Bladder Mas s es......Page 184
SU g g E STED READi n g S......Page 185
A d ren a l a d e noma......Page 186
Cy s t / p s e u d o c y s t......Page 188
Pheochromocytoma......Page 189
Meta s ta s e s......Page 190
Me t a s ta s is......Page 191
B ilatera l a d ren a l hyperpla s ia......Page 192
R emote infection......Page 193
Ad r e n Al i n c i d e n t A l o m A s......Page 194
SU g g e St e d R e A d i Ng S......Page 195
Normal V a r i a n t s......Page 196
Sp l e Ni c l e Si o NS......Page 197
E c h i n ococcal cys t......Page 198
C y s tic/ n e c rotic splenic meta s ta s e s......Page 199
Sarcoidosis......Page 200
Sp l e Ni c i Nf a r c T S......Page 201
Su g g e STe d R e A d i n g S......Page 202
14 Gastrointestinal Tract......Page 204
At t e n u a t i o n......Page 205
En h a n c e m e n t......Page 206
H i a t a l Hernias......Page 207
G a s t r i c W a l l Thickening......Page 208
G a s tric Aden o c a rcin o ma......Page 209
CT Enterogra p hy......Page 211
An a t o m y......Page 212
Is c h e m i a......Page 213
“ Sma l l Bowel Feces” Sign......Page 214
Closed-Loop Obstru c tion......Page 215
Vo l v u l u s......Page 216
I n terna l H e rnia s......Page 217
Ly m p h o m a......Page 218
C a rcin o id Tumors......Page 219
Perforated Appendicitis......Page 220
M u c ocele o the Appendix......Page 221
Diverticulitis......Page 222
E p i p l oic Appendagitis......Page 223
I n f a m m a t ory Bowel Dis eas e......Page 224
I n ectious Colitis......Page 225
T oxic Megacolon......Page 226
Li p o m a......Page 227
C olorectal Cancer......Page 228
C T Colonography......Page 229
SU g g e STe D Re A Di Ng S......Page 230
P eritoneal Space: Broad Divis i ons......Page 232
S u p r a m es ocolic Compartment......Page 233
L e f t Su p ramesocolic Spa c e......Page 235
G r eater Omentum/ G a s t r ocolic Ligament......Page 236
S m a l l Bowel Mes entery......Page 237
h e m o P e r i t o n e u m......Page 238
P eritoneal Carcinomatos i s......Page 239
S erous Sur a c e Papillary Carcinoma o the Pe r ito n e u m......Page 240
S cleros i n g mesenteritis......Page 241
Su G G e STe D Re A DIn G S......Page 243
a b d o m i N a l a o R t a A b d ominal Aortic Aneurys ms......Page 244
M y c otic Aneurys m s......Page 245
A ortoenteric Fis t u l a s......Page 246
Pseudolipoma......Page 247
l y m p h N o d e s L y m p h Node Size......Page 248
Re t Ro p e Ri t o N e a l m a s s e s......Page 249
Neurogen ic tumors......Page 250
R etroperitoneal Fibros i s......Page 252
Su g g e St e d R e A d i n g S......Page 253
e x t r a P e r I t o n e a l S P a c e......Page 254
Pe r I n e u m......Page 255
In g u In a l r e g Io n ( H e r n Ia S )......Page 256
o v a r I a n l e S I o n S I d enti y i n g Ovarian Origin......Page 257
D i erential Diagnos i s......Page 259
S t a ging Ovarian Cancer......Page 260
C ervical Cancer......Page 261
E n d ometrial Cancer......Page 262
Su g g e St e D Re A DIn g S......Page 263
CT Te C h n i q u e Th o ra x......Page 264
S t ernal Fractures......Page 265
Pn e u m o th o r ax......Page 266
T r a cheobronchial Injury......Page 267
A c u t e T r a u m a t i c Aortic Injuries......Page 268
a b d o m i n a l a n d P e l v i C T r a u m a Hemope r i......Page 270
S olid Organ Injuries......Page 271
G r a d e V......Page 273
Pa n c reatic a n d du o d e n a l injuries......Page 274
B o w e l a n d mesenteric in j u ries......Page 275
G r a d e V......Page 277
B l a d d e r in j u ry......Page 278
P regn a n c y a n d a b d o min o p e l v ic tra u ma......Page 279
SU G G E STED READIn G S......Page 280
In d e x......Page 282

Citation preview

Body CT: The Essentials

Notice Medicine is an ever-changing science. As new research and clinical experience broaden our knowledge, changes in treatm ent and drug therapy are required. The authors and the publisher o this work have checked with sources believed to be reliable in their e orts to provide in orm ation that is com plete and generally in accord with the standards accepted at the tim e o publication. However, in view o the possibility o hum an error or changes in m edical sciences, neither the authors nor the publisher nor any other party who has been involved in the preparation or publication o this work warrants that the in orm ation contained herein is in every respect accurate or com plete, and they disclaim all responsibility or any errors or om issions or or the results obtained rom use o the in orm ation contained in this work. Readers are encouraged to con rm the in orm ation contained herein with other sources. For exam ple and in particular, readers are advised to check the product in orm ation sheet included in the package o each drug they plan to adm inister to be certain that the in orm ation contained in this work is accurate and that changes have not been m ade in the recom m ended dose or in the contraindications or adm inistration. This recom m endation is o particular im portance in connection with new or in requently used drugs.

Body CT: The Essentials David L. Coy, MD, PhD Attending Radiologist, Virginia Mason Medical Center Seattle, Washington Af liate Assistant Pro essor, Department o Radiology, University o Washington, Seattle, Washington

Eugene Lin, MD Attending Radiologist, Virginia Mason Medical Center Seattle, Washington Af liate Assistant Pro essor, Department o Radiology, University o Washington, Seattle, Washington

Jef rey P. Kanne, MD Associate Pro essor, Chie o Thoracic Imaging, Vice Chair o Quality and Sa ety, Department o Radiology, University o Wisconsin School o Medicine and Public Health, Madison, Wisconsin

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Chicago San Francisco Athens London Madrid New Delhi Singapore Sydney Toronto

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Copyright © 2015 by McGraw-Hill Education. All rights reserved. Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher. ISBN: 978-0-07-183364-6 MHID: 0-07-183364-1 The material in this eBook also appears in the print version of this title: ISBN: 978-0-07-176738-5, MHID: 0-07-176738-X. eBook conversion by codeMantra Version 1.0 All trademarks are trademarks of their respective owners. Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and to the bene t of the trademark owner, with no intention of infringement of the trademark. Where such designations appear in this book, they have been printed with initial caps. McGraw-Hill Education eBooks are available at special quantity discounts to use as premiums and sales promotions or for use in corporate training programs. To contact a representative, please visit the Contact Us page at www.mhprofessional.com. TERMS OF USE This is a copyrighted work and McGraw-Hill Education and its licensors reserve all rights in and to the work. Use of this work is subject to these terms. Except as permitted under the Copyright Act of 1976 and the right to store and retrieve one copy of the work, you may not decompile, disassemble, reverse engineer, reproduce, modify, create derivative works based upon, transmit, distribute, disseminate, sell, publish or sublicense the work or any part of it without McGraw-Hill Education’s prior consent. You may use the work for your own noncommercial and personal use; any other use of the work is strictly prohibited. Your right to use the work may be terminated if you fail to comply with these terms. THE WORK IS PROVIDED “AS IS.” McGRAW-HILL EDUCATION AND ITS LICENSORS MAKE NO GUARANTEES OR WARRANTIES AS TO THE ACCURACY, ADEQUACY OR COMPLETENESS OF OR RESULTS TO BE OBTAINED FROM USING THE WORK, INCLUDING ANY INFORMATION THAT CAN BE ACCESSED THROUGH THE WORK VIA HYPERLINK OR OTHERWISE, AND EXPRESSLY DISCLAIM ANY WARRANTY, EXPRESS OR IMPLIED, INCLUDING BUT NOT LIMITED TO IMPLIED WARRANTIES OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. McGraw-Hill Education and its licensors do not warrant or guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free. Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom. McGraw-Hill Education has no responsibility for the content of any information accessed through the work. Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages. This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise.

Dedication To Peggy and Will or their unlimited love and support, and to my residents and colleagues or their inspiration and encouragement. – DC I’m indebted to my colleagues who provided much o the material or this book and the time to write it, and to my current and ormer residents, who were the inspiration or writing the book. – EL To Elizabeth or all o her support and patience. – JK

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Contents Contributors.......................................................................................................................................................................................ix Pre ace ...............................................................................................................................................................................................xi

Chapter 1 The Physics o Computed Tomography ........................................................................................................... 1 Chapter 2 CT Radiation Dose and Management ............................................................................................................. 7 Chapter 3 Contrast Administration ................................................................................................................................ 15 Chapter 4 Mediastinum ....................................................................................................................................................19 Chapter 5 Lung ..................................................................................................................................................................33 Chapter 6 Airways .............................................................................................................................................................55 Chapter 7 Pleura, Diaphragm, and Chest Wall ............................................................................................................... 71 Chapter 8 Heart and Thoracic Aorta............................................................................................................................... 85 Chapter 9 Liver and Biliary .............................................................................................................................................103 Chapter 10 Pancreas .......................................................................................................................................................... 131 Chapter 11 Kidneys, Ureters, and Bladder ..................................................................................................................... 149 Chapter 12 Adrenal Glands .............................................................................................................................................. 173 Chapter 13 Spleen ............................................................................................................................................................. 183 Chapter 14 Gastrointestinal Tract .................................................................................................................................... 19 1 Chapter 15 Peritoneum and Peritoneal Spaces .............................................................................................................. 219

vii

viii Contents

Chapter 16 Retroperitoneum, Vessels, and Nodes ......................................................................................................... 231 Chapter 17 Pelvis ...............................................................................................................................................................241 Chapter 18 Trauma ........................................................................................................................................................... 251

Index .............................................................................................................................................................................................26 9

Contributors Claire K. Sandstrom, MD Assistant Pro essor Departm ent o Radiology University o Washington Seattle, Washington Claudia T. Sadro, MD Assistant Pro essor Departm ent o Radiology University o Washington Seattle, Washington David L. Coy, MD, PhD Attending Radiologist Departm ent o Radiology Virginia Mason Medical Center Seattle, Washington A liate Assistant Pro essor o Radiology University o Washington Seattle, Washington David Zamora, MS, DABR Medical Physicist Departm ent o Radiology University o Washington Seattle, Washington Ellen Hauptmann, MD Interventional Radiologist Departm ent o Radiology Virginia Mason Medical Center Seattle, Washington Eugene Lin, MD Attending Radiologist Departm ent o Radiology Virginia Mason Medical Center Seattle, Washington A liate Assistant Pro essor o Radiology University o Washington Seattle, Washington Evan Leitz, MD Abdom inal Im aging Fellow Departm ent o Radiology University o Washington Seattle, Washington

Evan Sirc, MD Attending Radiologist Radiology Medical Group o Santa Cruz County Santa Cruz, Cali ornia Geraldine Chen, MD Resident Physician Departm ent o Radiology University o Pennsylvania Philadelphia, Pennsylvania Jef rey P. Kanne, MD Associate Pro essor, Chie o Thoracic Im aging, Vice Chair o Quality and Sa ety, Departm ent o Radiology, University o Wisconsin School o Medicine and Public Health, Madison, Wisconsin Kalpana Kanal, PhD, DABR, FACR, FAAPM, FSCBTMR Associate Pro essor Director o Diagnostic Physics Departm ent o Radiology University o Washington Seattle, Washington Nathan Cross, MD, MS Resident Physician Departm ent o Radiology University o Washington Seattle, Washington Neal Conti, MD Attending Radiologist Departm ent o Radiology Virginia Mason Medical Center Seattle, Washington Orpheus Kolokythas, MD Director Magnetic Resonance Im aging Cantonal Hospital Winterthur Institute o Radiology Winterthur, Switzerland Paul Sicuro, MD Attending Radiologist Departm ent o Radiology Virginia Mason Medical Center Seattle, Washington ix

x Contributors Stephanie Cheng, MD Resident Physician Departm ent o Radiology Virginia Mason Medical Center Seattle, Washington Wendy Hsu, MD Attending Radiologist Residency Program Director Departm ent o Radiology Virginia Mason Medical Center Seattle, Washington

Zachary R. Heeter, MD Resident Physician Departm ent o Radiology Virginia Mason Medical Center Seattle, Washington

Preface Notwithstanding the increasing use o MR, CT holds the preem inent role as the m ost reliable and requently used im aging m odality or cross-sectional im aging o the chest, abdom en, and pelvis. In just seconds, m odern m ultidetector-row CT scanners can produce isotropic datasets with exceptional spatial resolution. In orm ation depicted by CT not only can provide a diagnosis but also im part im portant prognostic in orm ation, directly inf uencing patient care. Furtherm ore, the detailed anatom y depicted by CT is an im portant requisite in the planning o m inim ally invasive surgeries and im age-guided procedures. Our aim with Body CT: The Essentials is to present a tim ely, detailed, and practical review o CT im aging o the chest, abdom en, and pelvis that we hope will be use ul to trainees in diagnostic radiology and radiologists in

practice interested in body im aging. The chapters within the book are organized by organ system . In each chapter we have attem pted to keep in orm ation concise and tim ely, incorporating the latest advances in CT im aging and recom m endations or guidelines or im aging and ollow-up o ndings when available. The tables contained within each chapter include di erential diagnoses that are targeted to be sensible and practical rather than exhaustive. At the end o each chapter we present “suggested readings” or those interested in pursuing a m ore detailed review o relevant topics. We have also included technical chapters reviewing intravenous contrast adm inistration, scan param eters, and radiation physics so that quality studies can be per orm ed while m inim izing patient radiation exposure.

xi

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Ch a p t e r

1

Th Ph sics f C

p t

T

ph

Nathan Cross, MD, MS David Zamora, MS Kalpana Kanal, PhD, DABR, FAAPM, FSCBTMR, FACR

I. INTRODUCTION II. SCANNING HARDWARE a. X-Ray Generation b. Beam Filtration c. Detection

In Tr o d u CTIo n Com puted tom ography (CT) is at the heart o every m odern radiology departm ent because o its speed, reliability, and ability to separate overlapping structures. Although CT m ay seem distant rom plain lm radiography, tom osynthesis and ultim ately CT are the next logical progressions. Rather than im age rom a single stationary position, tom osynthesis uses a sm all am ount o source and detector rotation around a ocal point during the exposure to blur the tissue above and below the ocal plane. CT takes the concept urther, capturing data rom at least 180 degrees around the patient and calculating the anatom y o the entire volum e. At the dawn o CT, im age reconstruction was accom plished with com puters m arginally m ore com plex than a m odern calculator, thus the basic concepts are readily intelligible. The rst CT scanners, such as the original com m ercial scanner developed by Sir God rey Houns eld at EMI Central Research Laboratories in England, used a single source and a single detector. This is re erred to as a rstgeneration scanner today. CT im age acquisition com prises several discrete steps: 1. Acquisition o projections rom di erent angles rotating around the patient. 2. Assem bly o m ultiple projections into a slice (Reconstruction). 3. Stacking o m ultiple slices to create a 3-dim ensional volum e (3D Reconstruction). A rst-generation scanner only has a single detector elem ent and or each projection o every slice the source and detector are translated rom one side o the patient to the opposite, acquiring a series o linear rays that are

III. STUDY ACQUISITION IV. IMAGE PROCESSING V. IMAGE PROPERTIES AND STORAGE

assem bled into a single projection. The source-detector assem bly is then rotated several degrees around the patient and the projection acquisition process is repeated. Although there are som e advantages to this “parallel beam” arrangem ent (i.e., each ray within a projection is parallel, not a an-beam ), the tim e it takes to per orm all these steps is unacceptable. Later generations o scanners will use an-beam s to expose an array o detectors sim ultaneously, acquiring a single projection in a single exposure. The m odern scanner is m ore com plex than this original device but it can be broken into a logical sequence o discrete com ponents rom x-ray tube to detector to PACS station. Multiple technologies have led to a stepwise evolution o CT scanners depicted in Figure 1-1. A m odern CT work ow m ay start at the x-ray tube m ounted on the scanner but it extends to the radiologist, hospital network, and beyond. To review the com ponents o a scanner a logical approach starts with the orm ation o x-rays at the tube, subsequent ltration, conversion to light, detection, gantry rotation, repetition, and nally im age orm ation and dissem ination.

SCa n n In g H a r d w a r e X-Ray Generation The x-ray tube used in a CT scanner is not too dissim ilar rom the tubes used or radiography. The m ain di erence is the need or continuous, high radiation output over a longer period o tim e. The cathode is a wire lam ent, which em its electrons when a large current is supplied that overcom es the electron-binding energies. A side e ect o the applied current and the resistance o the lam ent is the 1

2 Body CT: The Essentials

H E T A

Figure 1-1 Generational CT Scanners CT scanners have ollowed a logical series o incremental improvement and complexity. F rs r o sc rs used a pencil beam o x-rays and a single detector element had to be translated across the eld o view to acquire the line o pixels in a single projection. The assembly was then rotated several degrees be ore repeating the process to acquire another projection. A s co r o CT im proved upon this idea by using a sm all an-beam which could radiate a small series o detector elements, which also had to be translated across the scanner’s eld o view or each projection. To urther accelerate the speed o acquisition, a hr r o sc r uses a wide an-beam and a wide array o detector elem ents. A projection at one point along the gantry’s rotation is acquired in one step without the need or detector or tube translation. This is the m odel or m any scanners currently on the m arket. A fo r hr o sc r uses a 36 0 -degree array o detector elements and a rotating source, which simpli es the slip ring and decreases the number o rotating components.

generation o heat, which necessitates a m etal or alloy with a high m elting point (e.g., tungsten). The “m A” or m illiam perage quanti es the electrical current running through the cathode, which correlates with the num ber o electrons em itted. O ten two lam ents o di erent sizes are constructed adjacent to each other allowing or di erent output characteristics depending on which is used. Electrons boiled o o the cathode lam ent are electrostatically accelerated toward the anode by the voltage applied between cathode and anode, described by the “kVp” or peak kilo-voltage o the system . When the electron strikes the anode, a variety o interactions can occur. The prim ary interaction with the anode is excitation resulting in in rared (heat) radiation. O the sm all raction o interactions that generate x-ray photons, Brem sstrahlung or “braking” radiation is the m ost requent interaction resulting in 80% to 9 0% o the produced x-ray photons. The spectrum o output x-rays encompasses a range o energies up to a m aximum

Filtra tion Collima tion Be a m S ha ping

Figure 1-2 CT Components A series o components are used to generate, and then lter x-rays which are transmitted through the patient. Those photons which are not attenuated reach the scintillator where they are converted to light photons which can be detected directly by a solid-state detector. This weak signal m ust be am pli ed and then converted to digital values which are read out and arranged into a orm at which is transmitted to the machine’s console and processed.

value, equivalent to the voltage between cathode and anode, kVp. Heat production by the cathode and anode accounts or a large raction o the energy input into an x-ray tube, and lim its its operation i not ef ciently dissipated. Several innovations in heat managem ent have improved CT x-ray tubes. Num erous materials, including tungsten, rhenium, m olybdenum , and graphite have been incorporated into the anode to increase electron interactions, slow wear, conduct heat, and absorb heat. A rotating anode allows or the heat to be spread in a circular track over the anode’s sur ace. A liquid gallium bearing reduces vibration rom ball bearings and increases the sur ace area conducting heat out o the anode into the housing assem bly. Som e tubes, rather than surrounding the anode and cathode with vacuum ll the space with oil, which is circulated to extract heat (Figure 1-2).

Beam Filtration The beam leaving the anode m ust be ltered, shaped, and collim ated to best penetrate the patient. The window on the x-ray tube allowing x-rays to leave the tube is m ade o a m aterial designed to attenuate low-energy x-rays, which will not penetrate to the detector and contribute to the im age’s contrast. As x-rays penetrate so t tissue, the lower-energy photons are pre erentially absorbed or scattered resulting in a relatively higher-energy beam , a process called “beam hardening.” Because patients are generally thicker in the

Chapter 1 The Physics of Computed Tomography 3 m iddle, there is m ore attenuation and hardening o the beam traversing the center o the patient. The result is a broad variation in the num ber o x-rays hitting di erent detector elem ents, with ewer hitting central detectors than peripheral detector elem ents. Detectors per orm optim ally when detecting over a narrow signal range. There ore, it is desirable to lim it this variation by attenuating the edges o the an-beam resulting in a m ore uni orm ux o photons reaching the detector. The lter is com m only a Te on block that is typically bow-tie shaped and placed in the beam path. Finally, pre-patient collim ators constrain the an-beam to the region o the bore occupied by the patient, elim inating peripheral radiation which m ight scatter.

e-

Z Axis

Detection X-rays pass through the patient interacting with tissue by absorption or scattering, which results in a m easured attenuation o the incident beam . The beam can be detected with a variety o di erent technologies. Early scanners used a scintillation crystal, which converted x-ray photons into light photons ollowed by a photom ultiplier tube that created an am pli ed electrical signal rom the light photons. Newer solid-state detectors use a scintillation m aterial such as cadm ium tungstate or a rare earth oxide ceram ic bonded to a photodiode. A photodiode is a silicon detector operating on sim ilar properties as a light-em itting diode (LED). A single detector would be o lim ited use in m odern high-speed scans, so a 2-dim ensional (2D) array o detectors is used to sim ultaneously m easure the wide beam traversing the patient at di erent spatial locations. A single-slice scanner uses a line o detectors that can num ber around 9 00 individual elem ents. Modern (m ultirow/ m ultislice/ m ultidetector) scanners em ploy m ultiple rows o detectors. A 320 -slice scanner is even available (which would em ploy 320 rows × ~9 0 0 elem ents per row = ~288,00 0 individual detector elem ents) (Figure 1-3). The usage o so m any detectors creates a trem endous am ount o data and consum es substantial power. To rapidly and continuously rotate the x-ray tube and detector around the patient without physical cable lim itations, slip-ring technology was necessary. A slip ring is a m echanism that provides an electrical connection across a rotating joint and allows or m ultiple data or power channels. The principle is to have two concentric cylinders, one rotating within the other, with a brush bridging the gap and contacting the inner ring as it spins. This can work, but needed re nem ent. Metal brushes or lam ents will wear, are noisy, and have lim ited current capacity; later versions use a m etal block pressed by a spring against a groove in the inner ring. Data is trans erred with optoelectronics, sim ilar to devices used in ber-optic transm ission.

STu d y a Cq u ISITIo n Scanning starts with positioning o the patient on the gantry. The goals o patient positioning are to ensure sa ety and

Rows

[[32/64/256/33 2 0]

De te ctor

Figure 1-3 Multidetector CT A m ultidetector CT arranges m ultiple elements in a series o rows. Scanners are o ten m arketed as 16 / 32/ 6 4/ 128/ 256 / 320 “slice” scanners, which re ers to the num ber o detector rows in the detector array. In a third-generation scanner this assem bly is rotated around the patient opposite to the x-ray source, as the patient m oves along the z-axis.

com ort, rem ove extraneous m aterial and extrem ities rom the area o interest, and center the patient. I contrast is being used, an IV will be placed, and connected to a syringe or an autom ated injector. Once the patient and team are ready, a scout im age is acquired, usually by positioning the x-ray source im m ediately below the patient table with detectors above and translating the table through the bore. Sim ilar to an of ce atbed scanner, a projection x-ray im age is acquired as the patient is m oved perpendicular to the an-beam . This generates an im age sim ilar to a plain lm , and is o ten re erred to as a scout or topogram . The topogram provides an overview o the patient’s anatom y so that the technologist can de ne which body region to scan. A technician uses so tware to set the scan param eters and prescribes the scan range overlaid on the topogram .

4

Body CT: The Essentials

The CT scan begins with the gantry rotating and speeding up to its operating angular velocity (i.e., number o seconds per gantry rotation). During acquisition, the table is translated through the bore either in a continuous motion or in discrete increments. In the case o a “helical” or “spiral” CT, where the patient table is moved continuously through the gantry, the distance the patient travels during one revolution o the gantry relative to the slice collimation (thickness o the slice) is described by the pitch. A pitch o 1 indicates that the detectors pass over the entire patient. I the pitch is increased to 2 the patient moves through the scanner aster and there is a gap, which the detector does not cover between each revolution. This is analogous to a Slinky, when the toy is compressed the metal o each revolution o the helix abuts the adjacent loop. I the toy is pulled apart slightly at both ends there is a small gap between revolutions. This can be advantageous as it allows the scan to proceed more quickly. In some cases there may be a second x-ray source and detector array at 90 degree to the primary set which may cover this “gap” as in some dual source CT systems. As the scanner irradiates each projection o every slice, each detector passes an analog signal to an analog to digital converter (ADC), which converts the signal into a binary number representing the intensity that exposed the detector element. An attenuation coef cient or the tissue that a beam encounters is calculated knowing the original intensity o the beam and the detected intensity using the equation I = I o × e(–u × x) where (I o = incident intensity, I = detected intensity, u = linear attenuation coef cient, x = thickness). To m ake these values m ore clinically relevant they are converted into Houns eld units (H U), which express the detected density relative to water. This conversion is calculated as H U = (µ t – µ w)/ µ w × K (µ t = attenuation coef cient o irradiated tissue, µ w = attenuation coef cient o water, K = scaling actor [1,000 ]). The im portance o the H U scale is the value corresponds to identi able densities. For exam ple, –1,00 0 is roughly the value o air, water is 0, blood is around 50 , so t tissue 20 to 70, and bone is 20 0 to 1,00 0.

Im a g e Pr o Ce SSIn g Once the data has been acquired, the CT gantry rotation decelerates and the computer renders the raw projection data as an image set. There are a variety o methods or turning the raw, sinogram, data into interpretable images. One o the earliest techniques used is called back projection (BP). It is a remarkably simple concept, easiest to understand with a “step and shoot” scan where the patient is incremented through the bore in discrete steps. At each o these steps, the scanner obtains a linear map o densities rom numerous angles/ projections as the detectors are rotated around the patient. To reconstruct the image the density map recorded across the line o detector elements is projected on top o each other. As each angle’s representation o the object

within the bore is averaged an image is slowly ormed. One o the weaknesses o this technique is a blurring e ect at the edge o objects. This can be improved by ltering the data slightly to increase the contrast at edges. These techniques, when used together, are called ltered back projection (FBP). More advanced reconstruction techniques such as modelbased iterative reconstruction attempt to use statistics and mathematical modeling o the components o the scanner to generate a more accurate representation o the data. The raw data or thin slice (~0.5–1.5-m m slice thickness) reconstructions are usually not used or clinical interpretation because o im age noise, and the large le size which causes arti acts and slow scrolling speeds. Instead, the m ean or average o several slices is used to create thicker slices. The voxels rom such a reconstruction have the sam e dim ensions within each slice but the third dim ension (the thickness o the voxel, or slice to slice distance) is larger. The original raw data likely had isotropic or near isotropic voxels m eaning all three dim ensions were equal or near equal. I m ultiplanar re orm ats are desired (i.e., oblique or o -axis reconstructions), isotropic or near-isotropic voxels are needed to avoid distorting anatom y. I non-isotropic voxels are used the reconstructions will have non-square pixels, and will im per ectly represent the original data. The im age can be ltered depending on the clinical intent o the reconstruction. Filters are usually applied with convolution, which takes a kernel and m oves it over the im age adjusting neighboring pixels to either sharpen or sm ooth the image. A sharpening kernel is com monly re erred to as a “bone kernel” used to accentuate ne pulm onary or osseous detail, but sim ultaneously increases noise. Alternatively a sm oothing or “so t-tissue” kernel can be applied to reduce noise at the expense o detail. Additional planes are o ten required to localize a structure. To create coronal, sagittal or oblique views, an algorithm takes the neighboring voxels across m ultiple slices and creates o -axis reconstructions. Two common specialized orms o reconstruction are the maximum intensity projection (MIP), and minimum intensity projection (MinIP). These reconstructions lump multiple slices together in a specialized way to make very speci c anatomy more conspicuous or clari y structures that course through many slices. MIPs and MinIPs take the entire stack o slices or a subset and or each pixel, the program looks at that pixel across all the slices in the im ages and nds the m axim um value. Once it has iterated through every pixel in the im age, the m axim um values are displayed as a single im age. The MinIP, used to look at the hypodense gas within the airway and bronchial tree, is very sim ilar except that when each pixel is reviewed across every slice the m inim um value is stored in the reconstruction. MIP series can be exceptionally valuable or nding sm all nodules in the lung where the radiologist is looking or a dense structure not connected to the vascular or bronchial tree. These projections sum m arize a large stack o im ages. The vessels appear as a continuous structure, rather than single cross-sectioned pro les, the result is that nodules are clearly delineated rom surrounding anatom y.

Chapter 1 The Physics of Computed Tomography 5 The raw data m ay also be sent to a “3D” workstation, which utilizes special so tware to reconstruct the data as a projection. Usually, the raw data is ltered in som e way: either by applying thresholds, autom atic segm entation, or m anual segm entation. These techniques isolate the anatom y o concern and then a sur ace rendering or volum etric rendering is per orm ed. Sur ace shading involves taking an area o high contrast on the raw data such as the edge o the m ediastinum , or the edges o bones and creating a hollow 3D shell o that structure. The structure is then “lit” by placing the object in a 3D environm ent with m odeled lights and applying a color or texture to its sur ace. A volum etric reconstruction treats the dataset as a large cloud o individual voxels assigning each voxel a color and a density/ opacity. The object, person, or organ is then reconstructed as viewed rom a certain angle with given lighting param eters. The end results o these techniques are 3D, o ten heavily edited, representations o the data, which are prone to a variety o arti acts and should be evaluated with care. Once the data has been reconstructed it is usually pushed to at least one production server, which distributes the data within the radiology departm ent. Depending on the size o the departm ent there m ay be m ultiple servers, which keep identical copies o the data and there m ay also be a hospital-wide server which provides a “light-weight” or com pressed version o the data to clinicians within an electronic m edical record or an im age viewer. The im age data is encapsulated in a orm at called DICOM, digital im aging and com m unications in m edicine, which is a standardized way o writing a le that m ixes the param eters the technologist and the scanner used to acquire the im age, with the patient’s identi ying in orm ation, and the im age data. DICOM has an associated vocabulary, which helps other com puters easily interpret the les regardless o m achine vendor or m odel. Grayscale and color values are also stored in such a way that they can be reproduced identically on a variety o di erent com puters and displays. CT im ages possess a large dynam ic range, which m eans that there is a wide spectrum o shades o H U in a CT im age. I you try and display the largest value in the im age as white and the sm allest num ber as black the result is a m iddle-gray washed out im age with white bones, black air, and m inim al so t-tissue contrast m aking it challenging to distinguish organs let alone pathology. The shades that contain clinical so t-tissue in orm ation are within a narrow range o values relative to the large spectrum H U in the whole dataset. To display the shades o gray use ul in so t-tissue evaluation a narrow range is displayed centered around the windowing “level.” Everything outside this narrow window is displayed as black or white depending on which side o the window the value alls.

Im a g e Pr o Pe r TIe S a n d STo r a g e Although a variety o so tware and hardware system s are used to package the in orm ation into a orm at a com puter

can interpret or you, the actual data o the im age is undam entally a string o 1’s and 0 ’s. A traditional pixel-based im age is stored as an array (a 2D grid) o pixels (px). A pixel is sim ply a rectangle with a speci c color value. The num ber o pixels along each axis o the im age is re erred to as the resolution o the im age and in CT is usually around 512 × 512 px. The eld o view (FOV) is the dim ensions o the space represented by the im age. For exam ple, a 512- × 512-px im age m ay represent a 32- × 32-cm FOV with pixel dim ensions o 0 .6 25 m m . A voxel is the 3D equivalent o a pixel, a rectangular or square box with a speci c color value. These are usually square and when assem bled in a large array orm a volum e. I the array has a high enough resolution it can be easy to orget that little squares are used at all. The color value stored or each pixel can be any num ber within a speci ed range. On early personal com puters this was a sm all range, 0 to 255 per red, green, and blue channel. This was described as an 8-bit channel, because 8 binary digits are needed to store each channel (28 = 256 ). For CT, on m odern scanners only a single channel, gray, is used and the analog to digital converter provides a 24-bit value, that is, a range o 0 to 16 ,777,215. This allows a m uch ner discrim ination o beam intensities as they hit the detector. The trade-o is storage size. I 24 bits are needed to describe the value o each pixel and a CT might have a 512- × 512-px slice resolution, with conservatively 200 slices, then 512 × 512 px × 200 slices = 52,428,800 voxels; 52, 428 k voxels × 24 bits = 1.3 billion bits = 150 Megabytes. The im age bit depth is relevant to interpretation as m ore subtle gradations in grayscale can contain use ul in orm ation distinguishing subtly di erent tissue densities. Most PACS workstations use 10-bit displays, which can display m ore shades o gray than typical 8-bit consum er grade m odels, but ar less than the bit depth o the im age (24 bits). Num erous orm ats are available to store im ages, including JPEG, GIF, PNG, TIFF, etc, and can be categorized as lossy and lossless orm ats. Lossy orm ats will sim pli y the im age to a varying degree to describe the im age with less data. To represent the im age with a smaller le size, equations that describe patterns or redundancies in the im age are used to store the im age at the expense o som e detail. A sim ple lossy exam ple is taking a block o black pixels that are alm ost the sam e shade and rather than listing each individually store the dim ensions o the block and its average shade. This represents the data m ore com pactly, thus requiring less storage space but inaccurately representing the original in orm ation. I this im age is a thum bnail or a preview no one will likely notice, but i that “sim pli cation” causes a hard edge to be orm ed where there really was not one, it m ight sim ulate pathology, such as a racture. A lossless orm at, attem pts to com pact the data into a sm aller space while still exactly representing the original copy. Lossless orm ats are appealing to radiologists since they decrease storage and transm ission dem ands while still m aintaining the original im age quality. The speed at which a CT scan can be per orm ed and the wide range o pathology it can reveal has lead to a

6

Body CT: The Essentials

phenom enal dem and or CT im aging. The ease with which these studies can be per orm ed provides the potential or overuse and inappropriate radiation exposure. The science o evaluating risks rom low dose radiation is extrem ely challenging and plagued by under-powered studies. These challenges and the appropriate use o radiation will be introduced in Chapter 2.

Su g g e St e d Re a d i n g S 1. Seeram E. Computed Tomography: Physical Principles, Clinical Applications, and Quality Control. 3rd ed. St. Louis, MO: Elsevier; 20 0 8. 2. Bushberg JT, Seibert JA, Leidholdt EM, Boone JM. The Essential Physics of Medical Imaging. 3rd ed. Philadelphia, PA: Lippincott William s and Wilkins; 20 12.

Ch a p t e r

2

CT R d t

D

dM

g m

t

David Zamora, MS, DABR Nathan Cross, MD, MS Kalpana Kanal, PhD, DABR, FACR, FAAPM, FSCBTMR

I. RADIATION RISKS IN CT II. RADIATION DOSE INDICATORS a. Common Dose Terminology b. CT-Speci c Dose Terminology i. CTDI and DLP ii. Size-Specif c Dose Estimate c. Ef ective Dose and Risk Estimation III. FACTORS AFFECTING CT DOSE a. Fundamental Protocol Parameters

Ra Dia Tio n Ris k s in CT All ionizing radiation carries with it the potential to harm an individual. CT can deposit m ore radiation dose per exam ination than other im aging m odalities and accounts or 50 % o the total collective m edical e ective dose delivered to US public.1 Further, the usage o CT as a diagnostic tool has increased dram atically over tim e with the increased availability o scanners, and a plethora o clinical applications. Public anxiety about radiation risks rom CT has been am pli ed by m edia coverage. This concern has driven manu acturers, researchers, and clinicians to minimize radiation dose rom CT through advances in technology, better radiation dose estim ation techniques, and to practically apply current dose reduction procedures. The e ects o radiation exposure in CT generally all within one o two categories: stochastic or determ inistic. Stochastic e ects encom pass cancer induction and the hereditary e ects o radiation dam age. Risk m odels o ten assum e that there is an increase in the probability o stochastic e ects with increased radiation dose, though accurate prediction is exceptionally dif cult. The second category, determ inistic e ects, describes radiation injury that will occur at a set dose threshold and above because o acute cellular dam age. Traditional determ inistic e ects include observable tissue reactions such as skin erythem a, epilation, the orm ation o cataracts and teratogenic e ects. To assess the likelihood o determ inistic e ects, dose to an

b. Advanced Dose Reduction i. Automatic tube current modulation and kVp selection ii. Current image reconstruction methods iii. Protocol design and clinical setup IV. MANAGING CT RADIATION DOSE a. Oversight o CT b. Minimizing CT Radiation Risk i. Radiation Dose Metric Monitoring ii. Protocol review V. CONCLUSION

organ is estim ated and com pared to accepted dose threshold values. The threshold or a particular e ect indicates that no reaction will take place below that level, but that the severity o the reaction increases with increased dose above the threshold. For CT, the prim ary concern lies with stochastic e ects or patients that receive m ultiple scans over his or her li etim e; however, determ inistic e ects such as epilation have been observed in high-dose procedures such as CT per usion.

Ra Dia Tio n Do s e in DiCa To Rs To understand the potential or dam age caused by ionizing radiation, a process o de ning how m uch ionizing energy is deposited m ust be established. The dose calculation process aim s to answer practical questions related to this potential: (1) How m uch radiation was used and how m uch energy was deposited?; (2) What type o radiation caused the dam age?; (3) What tissues did the radiation a ect and how sensitive are those tissues to radiation?; and, (4) What is the radiation detrim ent and increased risk to the patient? Each stage o the dose calculation process elucidates these deceptively com plicated questions.

Common Dose Terminology The topic o radiation dosimetry can be con using. The terminology is requently misused in literature and in practice, 7

8

Body CT: The Essentials

S ta nda rd Dos e Te rminology

CT Dos e Te rminology

Expo s ure – cha rge colle cte d pe r ma s s a ir (Coulombs /kg = C/kg) CTDI100 – ca lcula te d from expos ure me a s ure me nt in CTDI pha ntom (mGy) Abs o rbe d Do s e – e ne rgy de pos ite d pe r ma s s of ma te ria l (Gray = Gy) CTDIw – we ighte d ave ra ge of CTDI100 a t ce nte r/pe riphe ra l pos itions of CTDI pha ntom (mGy)

*WEIGHT BY RADIATION TYP E

Equivale nt Do s e (S ieve rt = S v)

CTDIvo l – CTDIw divide d by pitch (mGy)†

*WEIGHT BY TIS S UE TYP E

Effe c tive Do s e (S ieve rt = S v)

DLP – CTDIVol multiplie d by s ca n exte nt (mGy-cm)† *WEIGHT BY K-FACTOR

†

Co mmo nly dis playe d pro io r to irradiatio n and s ummarize d in do s e re po rt.

APPLICATIONS : S to c has tic Ris k, Radiatio n Pro te c tio n, Radiatio n S afe ty, Mo dality Co mparis o n

Radiatio n Ris k Es timatio n BEIR VII

Figure 2-1 Workf ow o com m on radiation dose term inology showing applied conversion actors, units, and com m on applications. SI units are presented in the gure, conventional units that m ay be encountered in the literature include: 2.58 × 10 −4 C/ kg = 1Roentgen [R]; 1Gy = 100 rad; 1Sv = 100 rem.

various updates to nomenclature and conversion actors have occurred over time, and the literature contains a mixture o SI and conventional units. Figure 2-1 o ers a linear workf ow o current terminology and the basic calculations that are applied (primarily SI units will be discussed). Most dose estim ates are rooted in a m easurem ent m ade by an air- lled ion-cham ber placed within a radiation eld. Incident radiation causes ionization o the air within the cham ber, leading to ree electrons and positive ions which are collected. Increasing signal indicates m ore ionization, and thus more radiation. This m easurem ent, termed exposure, is only de ned in air. The term absorbed dose describes the am ount o energy (Joule, J) rom radiation that was deposited per unit mass (kg) o any m aterial, given in units o Gray (1 Gy = 1 J/ kg). Absorbed dose can be estim ated by applying a correction actor to the exposure. For medical purposes, dose to tissue is o particular interest, and so organ dose would be an analog o absorbed dose. Di erent types o radiation deposit energy in di erent ways (e.g., quickly, in

a small volume; or slowly, spread out over a larger volume) and there ore have di erent biological e ects, so a collection o radiation weighting actors (ωr) have been developed. Multiplying the absorbed dose by the radiation weighting actor leads to the equivalent dose, in units o Sievert (1 Sv = 1 J/ kg). Finally, the term e ective dose (m Sv) was introduced as a metric to describe a non-uni orm patient dose as an equivalent whole-body dose. The e ective dose accounts or di erent tissue sensitivities by sum ming, over all tissues, the product o estim ated equivalent dose and published tissue weighting actors (ωT).2 In short, since e ective dose represents an equivalent whole-body dose, it can be used to com pare medical exam inations across di erent im aging modalities and over di erent body regions.

CT-Speci c Dose Terminology Because o the unique rotational delivery o radiation, a dose nom enclature or CT has evolved over tim e. Speci c

Chapter 2 CT Radiation Dose and Management

9

The CTDI 100 can be m easured at both the center and peripheral positions within the phantom . These m easurem ents are com bined into a weighted average o the m easurem ents, or CTDI w: 1 2 CTDI w = CTDI 10 0, center + CTDI 100 , periphery 3 3

Figure 2-2 Proper positioning o a CTDI body phantom (32-cm diam eter) or CTDI exposure m easurem ents is at the isocenter o a CT scanner. A CT pencil ion-cham ber is positioned in the upper peripheral through hole.

to CT are two dose indicators that are displayed by the system prior to irradiation o the patient and sum m arized in a dose report a ter exam ination com pletion: (1) com puted tom ography dose index (CTDI); (2) dose–length product (DLP). Figure 2-1 shows the relationship between the term inology used in CT dosim etry.

CT Dose Index and Dose Length Product Both CTDI and DLP are calculated rom exposure measurements within a cylindrical polymethyl methacrylate (PMMA) phantom. Two phantom sizes are commonly utilized to represent an adult abdomen (32-cm diameter) or an adult head (16-cm diameter). Each phantom has an array o through holes to hold a CT pencil ion-chamber (e.g., 100-mm length, volume o 3 cm 3) at the center or at one o the our peripheral locations within the phantom. Figure 2-2 shows proper positioning o a CTDI phantom within a CT scanner. The m etric “CTDI” has m ultiple variants that have becom e the standard in describing dose in CT. The CTDI is m eant to indicate average absorbed dose (in m Gy) in the acrylic phantom along the scan direction rom contiguous radiation exposures. In practice, an axial scan o the phantom at a single bed position centered over the CT pencil ion-cham ber is required. This exposure m easurem ent can be used to calculate the CTDI 100 using the equation: X LC (2-1) NT where X is the m easured exposure (Roentgen or C/ kg), is the conversion actor (m Gy/ R) o exposure to absorbed dose (mGy), L is the length o the CT ion-chamber (100 m m ), C is an ion-chamber correction actor, N is the number o active detector channels, and T is the channel width (in mm ). The product o N and T is comm only re erred to as the nom inal beam width, and represents the physical width o the radiation beam in the scan direction at isocenter. CTDI 10 0 =

(2-2)

Finally, a large portion o clinical scans are per orm ed in helical m ode, whereby the radiation beam either overlaps itsel (pitch < 1) or is extended over the scan direction (pitch >1); there ore, the CTDI vol is de ned as the CTDI w divided by the pitch. Consequently, high-pitch acquisitions will lead to a lower CTDI vol than would an equivalent lowpitch acquisition. Because the CTDI vol is appropriate to describe both axial and helical m ode acquisitions, it is displayed on all current CT scanner system consoles. A ull description o CTDI vol requires notation o the m easured or estim ated absorbed dose (in m Gy) and the size o the CTDI phantom . The im portance o noting the phantom size cannot be overstated, because or an identical technique, the CTDI vol in the 16 -cm head phantom is approxim ately twice that o the CTDI vol in the 32-cm body phantom . Finally, the second com m only displayed dose indicator is the DLP (units o m Gy-cm ), de ned as the product o the CTDI vol (m Gy) and the scan extent (cm ). Since the DLP takes into account the length o the CT scan, it serves as an indicator o total energy im parted to the standard phantom . For a given static CT technique, the CTDI vol would rem ain the sam e or all patients, but the DLP would increase or decrease with the longer or shorter scan extents (respectively) o individual patients.

Size-Specif c Dose Estimate The CTDI is de ned in an acrylic phantom and is not dose to any patient in particular. The two standard CTDI phantoms cannot accurately represent the vast array o possible patient sizes and densities. CTDI does provide a standardized m eans by which to compare CT scanner output within and between CT scanner system s because it is sensitive to changes in technique param eters (e.g., kVp, m As, lter, etc.). Recent e orts have worked to account or individual patient size by establishing conversion actors that can be applied to the standard CTDI vol. Am erican Association o Physicists in Medicine (AAPM) Report 204 suggests using the CT radiograph to measure the patient lateral (LAT), anterior–posterior (AP) dim ension, or LAT + AP dim ension to obtain an e ective diameter. Based on the e ective diameter, the tabulated conversion actor can be applied to the re erence 16 - or 32-cm CTDI phantom, as appropriate (size-speci c dose estimate [SSDE] = CTDI vol × conversion ).3 Generally, the conversion actor will be greater than one i the patient e ective diam eter is sm aller than the re erence phantom diam eter, and vice versa. Because o this, the SSDE or pediatric patients or smaller adult patients tends to be higher than the displayed CTDIvol. At this point in tim e, the SSDE

10

Body CT: The Essentials

should not be used to compute an updated DLP or an e ective dose using the m ethodology described below.

Ef ective Dose and Risk Estimation The estim ation o e ective dose rom a CT exam in ation m ay be done in a variety o ways. Characterizing radiation dose in term s o e ective dose is particularly help ul when attem pting to com pare the relative risks o exam inations in other m odalities or to other parts o the body. Although not speci c to any individual patient, the m ost direct m ethod o calculating e ective dose in CT is presented in AAPM Report 9 6 , whereby the e ective dose is de ned as the product o the DLP and a body-region speci c k- actor (units o m Sv/ [m Gy-cm ]). In addition, a set o k- actors is available or di erent age groups (0 -year old, 1-year old, 5-year old, 10 -year old, Adult) to account or a higher pediatric radiosensitivity.4 A m ore tim e-intensive m ethod o estim ating e ective dose involves applying Monte Carlo m ethods to calculate organ doses within a de ned m athem atical anthropom orphic m odel. In either m ethod, the e ective dose is not speci c to the individual patient, and does not ully describe speci c organ-speci c risk; however, it does provide a com parable dose m etric. Table 2-1 sum m arizes typical dose m etrics or com m on CT exam inations.4–6 Finally, substantial e ort has been directed toward estim ating additional cancer incidence and death attributable to radiation dose. The Biological E ects o Ionizing Radiation (BEIR) VII report has provided estim ated additional risk expressed as a percentage increase per Sievert o e ective dose.7 Again, these m ethods should be used only as a guideline, as the process is necessarily lled with assum ptions and generalizations. National guidelines such as the BEIR VII report can provide easy to use estim ations o risk, but are based on controversial and o ten lim ited data. Because o the exceptionally com plex prediction o risk and the need or large long-term cross-sectional studies, the biologic im plications o sm all-dose m edical radiation m ay never be well understood.

Fa CTo Rs a FFe CTin g CT Do s e The way in which a CT scan is executed can directly im pact the dose deposited into the patient. It is, there ore, very im portant understand the underlying technique param eters that drive changes in CTDI vol and/ or DLP. Sim ilarly, there exist patient-speci c actors such as size, sex, age, and radiation sensitivity that can also a ect the estim ation o radiation dose and risk.8 Methods to account or patient variation have been developed alongside dose reduction techniques.

Fundamental Protocol Parameters The peak tube voltage (kVp) is the voltage applied between the anode and cathode o the x-ray tube. Electrons are

T b 2-1. Typical Dose Metrics or Com m on CT Exam inations ef c iv DLp a Dos b (mGy-cm) (mSv)

Ber t c (y s)

S udy D sc i ion

Ct DIvola (mGy)

Ct h d w/ o IV con s

52

805

2

0.5

Ct N ck w/ IV con s

17

467

3

0.9

Ct C-s in w/ o IV con s

24

493

3

0.9

Ct L-s in w/ o IV con s

31

754

11

3.6

Ct ch s w/ IV con s

12

455

6

2.1

Ct bdom n w/ IV con s

15

566

8

2.7

Ct bdom n– lvis w/ IV con s

14

705

11

3.4

Ct ch s – bdom n– lvis w/ IV con s

15

799

12

3.9

D om a Cr Dos ind x r gis y (J n–Jun 2013 r o ) m di n v lu o Ct DIvol nd DLp sc n o ll DIr si s. a Ct DIvol nd DLp s n d s h m ximum v lu occu ing in ny s i s h oughou h n i x min ion. b ef c iv do s s im d using a a pM r o 96 k- c o s o n dul o ul ion. c B ckg ound quiv l n di ion im , c lcul d s s im d f c iv dos divid d by h s im d nnu l.

accelerated by this voltage, interact with the anode, and cause em ission o a spectrum o x-ray photons. The maximum photon energy (keV) o an x-ray that can be produced is lim ited to the selected peak tube voltage (kVp). As the kVp is increased, the maxim um and average x-ray photon energy increases. The type o interactions that occur between the patient’s body and the x-ray photons are a unction o the selected kVp. Generally, increasing the kVp is associated with increased photon penetration (im proved noise) and a worsening o low-contrast detectability, resulting rom less photo-electric (PE) absorption interactions. Regarding dose, i all other scan param eters are unchanged, the CTDI vol is roughly proportional to kVp2. In this scenario, i the kVp were doubled, CTDI vol would approxim ately exhibit a our- old increase. Because o this strong relationship, reducing kVp can be e ectively used to reduce dose in the particularly radiosensitive pediatric population or or sm aller adult patients. In som e im aging scenarios, such as

Chapter 2 CT Radiation Dose and Management CT angiography, dose reduction can be achieved with lower kVp at a com parable image quality when used in conjunction with intravenous iodine-based contrast; though decreasing the kVp leads to an increase in image noise, the contrast agent exhibits an increased PE attenuation (i.e., rom PE k-edge) which would lead to an increase in subject contrast. Two m ore param eters that are under the user’s control include the tube current (m A) and the tube rotation tim e (i.e., am ount o tim e per tube rotation, in seconds). These two param eters are o ten collectively re erred to as m As, de ned sim ply as the product o the selected m A and the tube rotation tim e (s). Modi ying m As is associated with increasing or decreasing the quantity o x-ray photons produced. Because o this, m As has a direct linear relationship with CTDI vol. Also, since im age noise is a unction o the num ber o photons detected, higher m As will lead to lower im age noise and vice versa.6 Discussed previously, a helical/ spiral m ode o acquisition allows or the assignm ent o a pitch actor, related to projection over-sampling (pitch 1) o the imaging volume. The equation or CTDIvol is de ned as the m easured CTDI w divided by the pitch. There ore, usage o a higher pitch will lead to a decrease in the CTDI vol. Alternatively, in situations or which the pitch is below one, the CTDI vol will increase because o the overlap o the rotating x-ray beam . The pre-patient lter (or “bow-tie lter”), m entioned in the previous chapter, is chosen with the goal o absorbing low-energy x-rays be ore passing through the patient. By doing this, patient radiation dose is decreased since m any o the low-energy x-rays would have been absorbed by the patient without contributing to the CT im age. As well, the shape o the lter leads to m ore uni orm x-ray intensity at the detector array. Selectable lter shapes are available or the im aging o di erent body regions or patient sizes (head, sm all body, large body, pediatric). It is im portant to m atch the lter to the im aging target so that a hom ogeneous dose distribution is achieved, without concentrating higher-dose regions at the patient’s skin entry or along the central axis. Pre-patient collimation o the x-ray beam occurs in the scan direction, and is comm only on the order o 1.25to 40 mm , and beyond. The collim ated radiation beam, or nom inal beam width is de ned by the detector con guration, and is the product o the number o detectors currently active (e.g., 1, 4, 16, 6 4 detectors) and the width o each detector (e.g., 0.6 25, 1.25 m m ). The selected protocol prescribes the detector con guration (i.e., num ber o active detector rows and the resulting acquisition thickness, such as 16 × 1.25 mm . Just as a shadow cast on the wall does not have a per ectly sharp edge when viewed up close, the an beam extends slightly beyond the detector rows resulting in dose without clinical utility. This penum bra or area o overbeaming is needed to ensure portion o the an beam covering the detector rows is homogeneous.8 The thickness o the penumbra is independent o the total beam width; as the total beam width is increased, the width o the penum bra relative to total beam width decreases unused dose. Stated

11

di erently, there is less wasted radiation when using larger beam widths, which there ore leads to a better dose ef ciency. It is also im portant to understand what param eters do not a ect the patient dose. Clinical application o such knowledge can im prove the quality o diagnostic in orm ation presented to the radiologist with no additional radiation detrim ent to the patient. Digital im age processing and reconstruction can increase the conspicuity o som e lesions or provide alternative views o the relevant anatom y. For exam ple, the technologist can reconstruct im ages at di erent thicknesses, using m axim um / m inim um intensity projections, in alternate or oblique planes, or at a di erent display eld o view. Di erent reconstruction kernels can im prove the conspicuity o low-contrast objects (sm oothing or low-pass lter, so t-tissue algorithm ) or very sm all objects (sharpening or high-pass lter, bone algorithm ). However, these lters do not add data, they only reprocess the existing im age to m ake ndings m ore apparent. There are inherent im age quality trade-o s with im age processing; properly optim ized, a trem endous opportunity exists to im prove diagnostic ability without additional radiation.

Advanced Dose Reduction Im provem ents in CT technology, im age reconstruction m ethods, and current scanning practices have allowed or urther reduction in patient dose, while m aintaining acceptable im age quality. The ollowing sections discuss the autom ated selection o protocol param eters, the application o cutting edge im age reconstruction m ethods, and practical considerations when designing scanning procedures.

Automatic Tube Current Modulation and kVp Selection The discussion o SSDE above notes that patient size can lead to inaccuracy in dose estim ation. Current scanners o er the ability to m odulate certain technical param eters based upon how large the system determ ines the patient to be. One com m on m ethod o determ ining the patient size is to utilize the CT radiograph (i.e., scout, topogram , surview, scano, etc.) as a m eans o estim ating the patient thickness. A com m on kVp value is 120 kV, but depending on the CT scanner, autom ated selection m ay choose an appropriately lower value based on the observed patient thickness. More com m only, the CT system generates a table o m A values that increases or decreases the current as the patient is scanned. With this mA modulation technique, the system will increase or decrease the m A depending upon the thickness and density o the body region determ ined in the CT radiograph. Modulation o the m A as the patient m oves in the scan direction is o ten term ed longitudinal or z-axis modulation. In addition to z -axis m odulation, som e CT system s also m odulate the m A as the x-ray tube rotates around an assum ed elliptical patient, called angular modulation. A lateral projection through a patient generally encounters m ore tissue thickness than a posterior–anterior view; consequently, there is a slight increase in m A as the system

12 Body CT: The Essentials approaches the lateral projection and a slight decrease in mA as the system approaches a PA or AP projection. O ten, both methods o mA modulation can be used independently, together, or not at all. The net result o using mA modulation is that lower x-ray tube output is used over thinner anatomy, and higher x-ray tube output is used over thicker anatomy, leading to a more consistent image noise (as determined by the user) throughout the tomographic images and more appropriate dose levels to match the body region.6 ,8

Current Image Reconstruction Methods Historically, ltered back-projection (FBP) has orm ed the backbone o reconstruction m ethodologies in CT. More recently, com putationally intensive iterative statistical de-noising, partial iterative, and m odel-based iterative reconstruction (MBIR) m ethods have becom e available com m ercially. The newer reconstruction m ethods utilize som e com bination o raw data (i.e., sinogram space) and im age data. To varying degrees, each m ethod o ers the opportunity to com putationally im prove the im age quality, m ost notably the im age noise.8,9 An im provem ent in the im age noise has led to im proved low-contrast detectability. Many clinics have used the im proved im age quality as an im petus or decreasing the radiation dose, o ten on the order o 20% to 6 0 %. Another recent technical advance called dual-energy CT has gained som e clinical utility because it o ers the ability to reconstruct additional im age sets at di erent calculated equivalent photon energies (keV) or at di erent weighted averages.8 Most im plem entations o dual-energy scanning rely upon either a secondary x-ray tube and detector array (i.e., dual-source system ) m ounted to the rotating gantry, or on rapid kVp-switching (between two values o kVp) within the prim ary x-ray tube. In either case, acquiring data at two di erent kVp values provides two unique attenuation data sets which can be com bined to o er im ages with im proved lesion conspicuity, or to generate additional im age sets such as virtual non-contrast (VNC). A dual-source system also o ers the bene t o im proved tem poral resolution because o the sim ultaneous acquisition o projection data. Im proved tem poral resolution is particularly help ul when im aging m oving objects.10 For exam ple, rapid im aging allows near-stationary capture o the heart, which is crucial in identi ying a variety o pathologies.

Protocol Design and Clinical Setup The design o the protocol and the m anner in which the patient is set up have im plications or patient dose. The rst stage o designing a protocol is to determ ine the clinical goal. De ning the clinical goal will determ ine the desired noise and resolution level, which in orm s the selection o protocol param eters. Not all protocols require the sam e level o im age quality, and the ALARA principle should guide the entire process.11 This includes high-level determ inations such as how m any phases are required or a study, down to what individual scan param eters are appropriate.

Som e exam ples include ull utilization o available technologies, such as VNC scans (a dual-energy technique), or appropriate training o the technologist sta to lim it the scan extent to the anatom y o interest as a m eans o reducing DLP and thus e ective dose. In addition, there are practical considerations when executing a given protocol. Discussed above, the usage o m A m odulation o ers the ability to m atch the x-ray tube output to the anatom y that is being im aged at any stage o a CT scan; however, the acquisition o the CT radiograph m ust be done correctly since it is driving the m A (and som etim es kVp) selection. The m ost im portant consideration when acquiring a CT radiograph is that the patient habitus is properly centered in the gantry. Since the CT radiograph is essentially a slot-scan planar radiograph, it is susceptible to patient m agni cation because o the diverging x-ray beam .8 Stated di erently, i the patient is positioned closer to the x-ray tube during CT radiograph acquisition, the planar projection o the patient will appear larger, and the m A will be m odulated up because the system expects that a larger patient is on the table. This can lead to an increase in dose. Additional shielding m ay be applied to protect speci c radiosensitive organs that m ay lie within or adjacent to the prim ary x-ray beam , such as breast tissue or the lens o the eye. Multiply Bism uth sheets have been used clinically in an attem pt to pre erentially lower dose at key regions o the body. Placem ent o Bism uth shielding has resulted in a reduction o dose deposition, but it is im portant to con rm that the im age quality has not been adversely a ected when used. Again, patient shielding needs to be used appropriately; when using in conjunction with m A m odulation techniques, the Bism uth shield should be placed on the patient a ter the CT radiograph, but be ore the actual CT scan to avoid autom ated selection o a higher m A value to overcom e the added attenuation. As an alternative, when using static m A techniques, the user m ay choose to reduce the overall m A value over the entire protocol in place o using patient shields.8

Ma n a g in g CT Ra Dia Tio n Do s e Given the clinical utility and burgeoning availability o CT, it is prudent to have system s in place to m onitor and ensure sa e usage o CT as a diagnostic tool. In every clinical decision, the physician m ust consider the relative bene ts and risks o a given CT procedure. Although it is accepted that CT delivers potentially dangerous radiation dose, the clinical utility o ten outweighs the risk. Multiple organizations have stated that the risks o m edical im aging below a certain threshold are sm all enough such that they are undetectable12 and discourage quantitative estim ation or such cases (Health Physics Society). On the other hand, because o the potential risk we ought not to apply m ore radiation to the patient that is necessary or the clinical task. The ollowing sections suggest ways in which a proper paradigm with respect to CT can be m aintained.

Chapter 2 CT Radiation Dose and Management

Oversight o CT The clinical environment in CT is highly com plex, and has a wide array o stakeholders that have varied experiences and opinions. Given this com plexity and the inherent risks presented by CT, there exists a collection o agencies and accrediting bodies. The goal o these di erent oversight bodies is to maintain patient and operator sa ety. All m anu acturers are subject to requirem ents put orth by the US Food and Drug Adm inistration (FDA). Additional regulations are en orced by the US Nuclear Regulatory Com mission (NRC) or the State in which the scanner is based. As well, voluntary accreditation can be achieved through di erent organizations, such as the Joint Comm ission, the Am erican College o Radiology (ACR), and the Intersocietal Accreditation Com m ission (IAC), among others. The aim s o voluntary accreditation range rom big picture process-oriented oversight to the de nition o speci c minim um per orm ance limits related to dose m etrics and im age quality.

Minimizing CT Radiation Risks The rst line o de ense against inappropriate use o CT radiation lies within the individual acility. Developing reasonable standard operating procedures and properly designed CT protocols goes a long way toward m inim izing radiation risk. It is im portant to m aintain a paradigm o not “m issing the orest or the trees.” This can be accom plished by developing a ram ework to determ ine the appropriateness o requesting a CT as com pared to other potential im aging m odalities that deposit m inim al or no radiation dose. Sim ilarly, an approach or the conditions under which a repeat exam ination is acceptable should be established. A clinic can have a ully optim ized clinical protocol; but, i that protocol is unnecessarily overutilized on a single patient or group o patients, urther optim ization should be per orm ed.

Radiation Dose Metric Monitoring It is di cult to determ ine where you are going with respect to CT dose i you do not know where you currently stand. Although im per ect, currently the best way to m onitor CT radiation dose is to gather and analyze the CTDI vol and/ or DLP and log them by procedure type. CTDI vol and DLP are not speci c to individual patients, but can serve as an indicator o relative CT output between and within institutions. The ability to m onitor CT dose m etrics m ay be lim ited by the scanner, hospital in rastructure, hospital nances, and even hospital sta ; there ore, the process o gathering CT dose data m ay require m ultiple logistical approaches. Recently, m ultiple com m ercially available dose databases have centralized the collection o CT dose m etrics. Using whatever m eans available, there is value to establishing a baseline collection o “norm al” values or CT dose in your institution by procedure. A variety o analysis and interpretation processes should be per orm ed on this data. In practice, the goal should be to generate a reasonable

13

process and approach or the purpose o im proving patient sa ety and clinical service. There are a variety o published diagnostic re erence levels (DRL) that o er “acceptable” re erence dose values or a lim ited collection o com m on CT exam inations.11,13 In those cases, a direct com parison can be m ade to the internal data. To com pare an individual site to others around the country, the ACR has developed the Dose Index Registry (DIR) to which acilities can send anonym ized patient study in orm ation.5 This in orm ation is com piled, categorized, and analyzed in a variety o ways to give the institution a better understanding o how its CT output com pares to other institutions around the country. Finally, internal CT dose data can be used in conjunction with the Medical Im aging and Technology Alliance (MITA) XR-25 CT DoseCheck standard, which is becom ing available on current or recent m odels o CT scanner.14 DoseCheck is so tware that is incorporated into the individual CT scanner system that allows the user to de ne noti cation values (NV) or a particular protocol or an alert value (AV) or dose accum ulation within a single exam ination. In both cases, the technologist is in orm ed via a system m essage that the dose exceeds expected levels prior to irradiation o the patient.

Protocol Review It is di cult or a single individual to sim ultaneously m aintain a high level o expertise in clinical application and workf ow, radiation dose, and current CT technology. Perhaps the best approach to the m anagem ent o protocol param eters is to orm a CT protocol com m ittee, consisting o representation rom physician, physicist, and technologist sta . In act, som e State and Accrediting bodies have m andated that a review o all CT protocols occur on som e periodic basis, such as annually. In this case, appropriate docum entation o changes and approval o the clinical CT protocols m ust be m aintained. With a f uid clinical atm osphere, it m ay be appropriate to have an ongoing process developed or protocol review. In this case, any individual m ay suggest a protocol m odication, which is orwarded to the CT protocol com m ittee or review. Upon review and approval by the protocol com m ittee m em bers, the requested change can be im plem ented by the hospital and the docum entation o changes can occur. In all cases, the clinic should con rm that they m eet the m inim um requirem ents that are set orth by the pertinent oversight authorities.

Co n Cl u s io n In this chapter, various im portant concepts were presented alongside recom m endations or how to suitably m anage radiation dose in CT. A CT scanner is a power ul diagnostic tool in the m odern Radiology departm ent, o ering rapid access to tom ographic im ages with good resolution and tissue contrast. Relative risks and clinical bene ts should always be considered when per orm ing a CT scan. There

14

Body CT: The Essentials

are m any actors that can a ect dose, including technical param eters, clinical setup, and patient-speci c inf uences. The responsibility or appropriate delivery o radiation lies with the end user. Su g g e St e d Re a d i n g S 1. National Council on Radiation Protection (NCRP), Ionizing radiation exposure o the population o the United States: recom m endations o the National Council on Radiation Protection and Measurem ents. (National Council on Radiation Protection and Measurem ents, Bethesda, MD, 200 9 ). 2. International Com m ission on Radiological Protection (ICRP), “ICRP Publication 10 3—The 20 07 Recom m endations o the International Com m ission on Radiological Protection,” Annals o the ICRP 37 (2–4), 2–4 (200 7). 3. Am erican Association o Physicists in Medicine (AAPM), Report No. 204, 20 11. 4. Am erican Association o Physicists in Medicine (AAPM), Report No. 9 6 , 20 08. 5. Am erican College o Radiology (ACR), “Dose Index Registry,” (20 13), vol. 2013. 6 . Bushberg JT. The Essential Physics o Medical Imaging. 3rd ed. Philadelphia, PA: Wolters Kluwer Health/ Lippincott William s & Wilkins; 20 12. 7. Com m ittee to Assess Health Risks rom Exposure to Low Level o Ionizing Radiation National Research Council, Health risks rom exposure to low levels o ionizing radiation : BEIR VII Phase 2. (National Academ ies Press, Washington, DC, 20 0 6 ).

8. Mahesh M. MDCT Physics: The Basics–Technology, Image Quality and Radiation Dose. Philadelphia, PA: Wolters Kluwer Health/ Lippincott William s & Wilkins: 20 0 9 . 9 . Xu Y, He W, Chen H , Hu ZH , Li J, Zhang TT. “Im pact o the adaptive statistical iterative reconstruction technique on im age quality in ultra-low-dose CT,” Clin Radiol. 20 13;6 8(9 ):9 0 2–9 0 8. 10 . Flohr TG, McCollough CH , Bruder H , et al. “First per orm ance evaluation o a dual-source CT (DSCT) system .” Eur Radiol. 16 (2):256 –26 8. 11. International Com m ission on Radiological Protection (ICRP). “ICRP Publication 10 2—Managing Patient Dose in MultiDetector Com puted Tom ography (MDCT).” J Radiol Prot. 20 08; 28(3):435–441. 12. Am erican Association o Physicists in Medicine (AAPM). “AAPM Position Statem ent on Radiation Risks rom Medical Im aging Procedures (PP 25-A),” (20 11). 13. International Com m ission on Radiological Protection (ICRP). “ICRP Publication 73:Radiological Protection and Sa ety in Medicine.” Ann ICRP. 19 9 6 ;26 (2):50 ; Tsapaki V, Aldrich JE, Sharm a R, Staniszewska MA, Krisanachinda A, Rehani M, Hu ton A, Triantopoulou C, Maniatis PN, Papailiou J, Prokop M. “Dose reduction in CT while m aintaining diagnostic con dence: Diagnostic re erence levels at routine head, chest, and abdom inal CT-IAEA-coordinated research project,” Radiology. (20 0 6 );240 (3):828–834; Berlin L, “Com m entary: ACR practice guidelines and technical standards,” JACR. (20 0 4);1(2):9 8–9 9 . 14. Medical Im aging and Technology Alliance (MITA), “Com puted Tom ography Dose Check,” (National Electrical Manu acturers Association (NEMA), 20 10), Vol. XR 25.

Ch a p t e r

3

C

t ast Ad

st at

Eugene Lin, MD

I. II. III. IV. V.

TIME TO PEAK ENHANCEMENT ENHANCEMENT DURATION SCAN DURATION SCAN DELAY PEAK ENHANCEMENT a. Arterial Enhancement

The contrast adm inistration protocol will determ ine when contrast enhancem ent peaks, how long enhancem ent lasts, the degree o peak enhancem ent, and how enhancem ent varies over tim e.

Tim e To Pe Ak e n h An Ce m e n T The tim e to peak enhancem ent is determ ined by co r s m ri l rriv l im and i j c io r io . Injection duration is the m ost im portant injectionrelated actor to consider in scan tim ing. Tim e to peak enhancem ent is earlier with shorter injection duration. Contrast m aterial arrival tim e can be determ ined by s bol s or bol s- r cki m ethods. Bolus tracking uses less exam ination tim e and less contrast m aterial, as it does not require two separate contrast injections. A test bolus is help ul in testing integrity o the injection site. The patient will be m ore prepared or the side e ects o the in jection, and heart rate variability can be evaluated prior to cardiac CT studies. The test bolus technique m ay be m ore appropriate or very short in jection durations as the bolus tracking m ay not have tim e to trigger.

e n h An Ce m e n T Du r ATio n I j c io r io is the prim ary actor determ ining enhancem ent duration. Longer injection duration results in longer enhancem ent duration.

b. Parenchymal Organ and Venous Enhancement c. Body Weight d. Cardiac Output e. Voltage VI. ENHANCEMENT OVER TIME VII. SALINE FLUSH

SCAn Du r ATio n The injection protocol should be optim ized or the scan duration. The scan duration should ideally be equal to the enhancem ent duration. As injection duration determ ines enhancem ent duration, injection duration should ideally be equal to scan duration.

SCAn De l Ay Scan delay should be determ ined by contrast arrival tim e, injection duration, and scan duration. One proposed schem e or calculating scan delay is: Sc

l y= P k

h cm

im − ½ (sc

r io )

Peak enhancem ent tim e = contrast m aterial arrival tim e + injection duration.

Pe Ak e n h An Ce m e n T Contrast adm inistration principles di er or arterial enhancem ent com pared to parenchym al organ and venous enhancem ent.

Arterial Enhancement For arterial enhancem ent, peak contrast enhancem ent is prim arily dependent upon io i f x (concentration o iodine × rate o injection). a. Arterial enhancement can be increased by increasing iodine concentration, increasing rate o injection or both. 15

Body CT: The Essentials

n a

Inje ction ra te

E

E

n

n

h

a

Conce ntra tion

h

n

c

c

e

e

m

m

e

e

n

n

t

t

16

Inje ction ra te

Conce ntra tion

Time

Time

Figure 3-1 Ef ect o Iodine Concentration on Arterial Enhancement I iodine concentration is increased and the volum e is unchanged, peak arterial enhancem ent will increase but the tim e o peak enhancem ent and enhancem ent duration will not change as injection duration is stable.

b. I io i co c r io is increased (Figure 3-1), and the volum e is unchanged, peak arterial enhancem ent will increase but the tim e o peak enhancem ent and enhancem ent duration will not change as injection duration is stable. One disadvantage o increasing iodine concentration is increased viscosity that m ay lim it contrast enhancem ent. Warm ing contrast m edia m ay decrease the viscosity. In addition, increased osm olality m ay increase adverse e ects. c. I r o i j c io is increased (Figure 3-2) and volum e is stable, peak arterial enhancem ent will increase but injection duration will decrease. This will shorten the tim e to peak enhancem ent and decrease enhancem ent duration. Keeping the injection duration stable would require a larger volum e o contrast. A ast injection rate with decreased injection duration is pre erred or m ultiphasic im aging o visceral organs. The ast injection rate will increase arterial enhancem ent, and the short injection duration results in a greater tem poral separation between phases. d. Som e studies suggest that peak enhancem ent is higher with lower concentrations o contrast injected at a higher rate; other studies show no di erence between the two approaches.

Parenchymal Organ and Venous Enhancement Parenchym al organ and venous enhancem ent is prim arily dependent upon o l io i os . High injection rates have m inim al e ect upon parenchym al and venous enhancem ent. For exam ple, although increases in injection rate will steeply increase the rate o arterial enhancem ent, peak hepatic enhancem ent will

Figure 3-2 Ef ect o Injection Rate on Arterial Enhancement I rate o injection is increased and volum e is stable, peak arterial enhancem ent will increase but injection duration will decrease. This will shorten the tim e to peak enhancem ent and decrease enhancem ent duration. Keeping the injection duration stable would require a larger volum e o contrast.

increase m uch m ore gradually, and only at injection rates < 3 m L/ s. Assum ing a xed iodine concentration, total iodine dose can be increased by keeping the sam e rate o injection and increasing volum e, or increasing the rate o injection with a xed injection duration. I the injection rate is kept constant, the injection duration will increase and the tim e to peak enhancem ent will increase. I the injection rate is increased with a xed injection duration, the scan tim ing should not be changed. This latter m ethod m ay be pre erable as it is m ore easily standardized.

Body Weight Body weight is the m ost im portant patient-related actor a ecting contrast enhancem ent. Larger patients have larger blood volum es, and contrast m edium dilution is greater resulting in lower blood iodine concentration and lower enhancem ent. Thus, larger patients require m ore iodine load than sm aller patients to reach the sam e m agnitude o enhancem ent. A 1:1 linear scale can be used to adjust iodine dose or body weight. However, this m ay overestim ate the am ount o contrast needed in obese patients who have a lower volum e o distribution than would be indicated by body weight ( at is less vascular than m uscle or visceral organs). Lean body weight and body sur ace area m ay be m ore use ul i iodine dose is adjusted or size.

Cardiac Output Decreased cardiac output will increase contrast enhancem ent, as there is less dilution o contrast. Decreased cardiac output will substantially increase peak aortic enhancem ent and renal enhancem ent, but has

Chapter 3 Contrast Administration a m inim al e ect on hepatic enhancem ent. In patients with hypovolem ic shock, bowel wall enhancem ent is also greatly increased.

Voltage Lower voltages such as 80 or 10 0 kVp will result in higher CT density o contrast, as these lower voltages are closer to the iodine k-edge o 33 keV. Im age noise will increase with lower voltages, but overall im age quality m ay not be a ected in som e cases i this is com pensated or by higher iodine density.

17

enhancem ent. These include biph sic, and exponentially decelerated m l iph sic injection m ethods.

SAl in e Fl u Sh A saline f ush will push unused contrast in the injection tubing and veins into the central blood volum e. This can decrease the am ount o contrast used and increase peak enhancem ent. In addition, it is help ul in reducing streak arti act rom dense venous contrast m aterial during thoracic CT exam inations. Su g g e St e d Re a d In g S

e n h An Ce m e n T o v e r Tim e Most protocols utilize iph sic injection (injection at a constant rate). Uniphasic injections will result in a peaked enhancem ent curve where enhancem ent progressively rises to a peak and then declines relatively rapidly. This o ten does not result in uni orm enhancem ent during im age acquisition. Other injection protocols m ay result in m ore o a plateau in peak contrast enhancem ent and thus m ore uni orm

1. Lin EC. Coronary com puted tom ography angiography: principles o contrast m aterial adm inistration. J Cardiovasc Comput Tomogr. 20 0 7;1(3):16 2–16 5. 2. Bae KT. Intravenous contrast m edium adm inistration and scan tim ing at CT: considerations and approaches. Radiology. 20 10 ;256 (1):32–6 1. 3. Flesichm ann D, Kam aya A. Optim al vascular and parenchym al contrast enhancem ent: the current state o the art. Radiol Clin North Am. 20 0 9 ;47(1):13–26 .

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Ch a p t e r

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Jef rey P. Kanne, MD

I. THE MEDIASTINUM II. ANTERIOR MEDIASTINUM a. Anatomy b. Thymus i. Thymoma ii. Lymphoma iii. Thymic cyst iv. Thymolipoma v. Thymic carcinoid vi. Thymic hyperplasia c. Germ Cell Tumors i. Teratoma ii. Malignant germ cell tumors d. Thyroid Masses e. Parathyroid Tumor . Mediastinal Lipomatosis g. Mediastinal Fat Necrosis III. MIDDLE MEDIASTINUM a. Anatomy

b. Lymphadenopathy c. Bronchogenic Cyst d. Esophageal Duplication Cyst e. Bronchogenic Carcinoma IV. POSTERIOR MEDIASTINUM a. Esophagus i. Dilated esophagus ii. Esophageal carcinoma iii. Esophageal varices iv. Hiatus hernia b. Neurogenic Neoplasms i. Peripheral nerves ii. Autonomic paraganglia iii. Sympathetic ganglia c. Miscellaneous i. Extramedullary hematopoiesis ii. Mediastinitis iii. Pancreatic pseudocyst

Th e Me d ia s Tin u M

a n Te r io r Me d ia s Tin u M

The m ediastinum (Figure 4-1) is the com partm ent located in the central thorax and is conf ned by the pleural sacs laterally, the sternum anteriorly, the spine posteriorly, the thoracic inlet superiorly, and the diaphragm in eriorly. The m ediastinum is traditionally divided into three com partm ents: anterior, m iddle, and posterior. A second schem e adds the superior m ediastinum , def ned by the thoracic inlet at the junction o the neck and chest, as a ourth com partm ent. CT o the m ediastinum is usually per orm ed ollowing intravenous adm inistration o iodinated contrast m aterial. Contrast-enhanced CT is especially help ul or evaluating known or suspected m ediastinal vascular lesions or or characterizing an indeterm inate m ediastinal m ass. H owever, unenhanced CT can be used or surveillance o known m ediastinal lesions including aortic aneurysm s.

Anatomy The anterior m ediastinum is located behind the sternum and in ront o the aorta, brachiocephalic vessels, and anterior pericardium . It extends superiorly to the anterior aspect o the thoracic inlet and extends in eriorly to the diaphragm . It contains at, lym ph nodes, internal m am m ary (thoracic) vessels, and thym us. The m ajority o m ediastinal m asses occur in the anterior com partm ent (Table 4-1).

Thymus The norm al thym us is a bilobed, triangular organ located in the anterior m ediastinum (Figure 4-2). The le t lobe is usually larger than the right. The thym us m ay also have a trapezoidal shape, especially in young wom en. With increasing age, the thym us undergoes atty degeneration and thus 19

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Body CT: The Essentials

B A

C

D

E

F

Figure 4-1 A–H. Contrast-enhanced Images o Normal Mediastinum Aortic arch (AA), ascending aorta (aAo), azygos vein (Az), descending aorta (dAo), Esophagus (E), hemiazygos vein (hAz), in erior vena cava (IVC), le t atrial appendage (LAA), le t atrium (LA), le t brachiocephalic vein (LBCV), le t common carotid artery (LCCA), le t in erior pulmonary vein (LIPV), le t internal jugular vein (LIJV), le t pulmonary artery (LPA), le t subclavian artery

(LSCA), le t superior pulmonary vein (LSPV), le t ventricle (LV), le t vertebral artery (LVA), main pulm onary artery (MPA), right atrial appendage (RAA), right atrium (RA), right brachiocephalic artery (RBCA), right brachiocephalic vein (RBCV), right common carotid artery (RCCA), right in erior pulmonary vein (RIPV), right internal jugular vein (RIJV), right pulmonary artery (RPA), right superior pulmonary vein (RSPV), right ventricle (RV), superior vena cava (SVC), thymus (T), thyroid (Th), trachea (Tr).

Chapter 4 Mediastinum

G

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H

Figure 4-1 (Continued )

becom es less apparent on CT. Tiny strands o at can be seen coursing through norm al thym ic tissue in adults.

Thymoma Thymoma (Figure 4-3) is the most common primary neoplasm o the anterior mediastinum, accounting or 20% o all mediastinal primary neoplasms in adults. Thymoma is o ten associated with other diseases, particularly myasthenia gravis, which occurs in 33% to 50% o patients with thymoma. These tumors most commonly arise anterior to the anterior pericardium and brachiocephalic vessels but also can occur along the cardiophrenic sulci, along the pericardium, and rarely in the neck. Thymomas are classi ed as either invasive or noninvasive, depending whether or not their capsule has been invaded. Thymomas tend to spread by direct extension, especially into the pleural and pericardial spaces. On CT, thym om as are typically round or lobulated. Foci o cystic degeneration or hem orrhage m ay be present

T b

in roughly one-third o thym omas, and approxim ately 20% contain calci cation. Findings suggesting invasive thym om a include lobular contour, m ediastinal at invasion, and great vessel invasion; the latter two are also seen with thym ic carcinom a. Pleural seeding m ay be detected on CT as subtle or extensive nodular pleural thickening.

Lymphoma The thym us m ay be the sole site o lym phom a or be a part o system ic disease. Hodgkin lym phom a (Figure 4-4) accounts or the m ajority o thym ic lym phom as, with m ost patients having the nodular sclerosing histopathologic subtype. Non-Hodgkin lym phom a, particularly di use large B-cell lym phom a, can also occur in the thym us. Although distinguishing thym ic lym phom a rom epithelial neoplasm s can be di cult, lym phom as tend to be “so t” tum ors, insinuating them selves between structures with little com pression.

4-1. Anterior Mediastinal Masses

Thymoma Lymphoma Germ cell tumor Caudal x nsion of hyroid goi r t hymic cys t hymic carcinoma t hymoli oma ec o ic ara hyroid ec o ic hyroid

Figure 4-2 Normal Thymus in a 20-year-old Man Contrast-enhanced CT im age shows a triangular, hom ogenous so t tissue structure (arrow) in the anterior m ediastinum .

22 Body CT: The Essentials

Figure 4-3 Thymoma Contrast-enhanced CT im age shows a heterogeneous, wellcircum scribed m ass (arrow) in the anterior m ediastinum . Calci cation and cystic degeneration can occur in thym om as.

Thymic cyst Thymic cysts (Figure 4-5) can occur anywhere in the neck or mediastinum along the normal developmental pathway o the thymus. They can be congenital, re ecting residua o the thymopharyngeal duct, or develop as a consequence o in ection or neoplasia. Most are incidentally detected on imaging and do not require urther management. However, i a sizeable so t tissue component is present, cystic degeneration in a neoplasm needs to be considered. Thymic cysts, especially those associated with treated neoplasm, can internally hemorrhage and ultimately develop mural calci cation.

Figure 4-5 63-year-old Woman with Thymic Cyst Unenhanced CT im age shows a hom ogeneous, water attenuation m ass (arrow) in the anterior m ediastinum .

Thymic carcinoid

Thym olipom a is rare, benign neoplasm , m ost com m only occurring in young adults. They grow very slowly and generally are detected when they are large, atty m asses in the anterior m ediastinum .

Carcinoid tum ors arising in the thym us (Figure 4-6 ) tend to be ar m ore aggressive than their pulm onary counterparts, prim arily as a result o high rates o local recurrence and m etastasis. Distinguishing between thym ic carcinoid and invasive thym ic epithelial tum ors by im aging is very di cult. Clinical m ani estations o endocrine dys unction

Figure 4-4 20-year-old Woman with Hodgkin Lymphoma Contrast-enhanced CT im age shows large in ltrating mediastinal m ass. Note the com pression o the superior vena cava (arrow).

Figure 4-6 Man with Thymic Carcinoid Contrast-enhanced CT im age shows a bilobed, heterogeneous m ass (arrow) in the anterior m ediastinum . Right hilar lym phadenopathy (arrowhead) is present.

Thymolipoma

Chapter 4 Mediastinum

A

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Figure 4-7 22-year-old Man with Thymic Hyperplasia Following Chemotherapy or Leukemia A. Contrast-enhanced CT image shortly ollowing chem otherapy shows lack o norm al thym ic tissue in the anterior m ediastinum . B. Contrast-enhanced CT im age 4 weeks later shows new triangular so t tissue (arrow) in the anterior m ediastinum , characteristic o norm al thym us.

B

such as Cushing syndrom e, which occurs in approxim ately one-third o patients, should suggest the diagnosis.

GCTs are typically classi ed as teratom as, pure sem inom as, and m alignant nonsem inom atous tum ors.

Thymic hyperplasia

Teratoma

Thym ic hyperplasia (Figure 4-7) is classi ed as either true thym ic hyperplasia (thym ic rebound) or lym phoid ( ollicular) hyperplasia o the thym us. True hyperplasia is de ned as abnorm al increase in size and weight o the thym us, typically as a rebound phenom enon occurring several m onths ollowing atrophy resulting rom treatm ents such as chem otherapy or corticosteroids. CT usually shows either a norm al-appearing thym us or dif use thym ic enlargem ent. Lym phoid thym ic hyperplasia is characterized by increased num ber o lym phoid ollicles in the thym us, but gland enlargem ent is uncom m on. Myasthenia gravis occurs in 6 0 % to 80 % o patients, and there is also a high association with other im m unologic disorders such as system ic lupus erythem atosus, rheum atoid arthritis, system ic sclerosis, and autoim m une thyroid disease.

Mature teratom a (Figure 4-8) is the m ost com m on m ediastinal GCT, accounting or approxim ately 75% o all

Germ Cell Tumors Prim ary m ediastinal germ cell tum ors (GCTs) are histopathologically indistinguishable rom their respective testicular and ovarian counterparts and nearly always occur in the anterior m ediastinum . They account or approxim ately 15% o prim ary m ediastinal neoplasm s in adults and are m ore com m on in children and younger adults. Benign m ediastinal GCTs are m ore com m on in wom en whereas m alignant m ediastinal GCTs are m ore com m on in m en.

Figure 4-8 37-year-old Man with Teratoma Containing Some Immature Elements Contrast-enhanced CT image shows a heterogeneous, wellcircumscribed mass in the anterior mediastinum. Note the presence o macroscopic at (arrowhead) within the mass. The overwhelming majority o mediastinal germ cell tumors in males are malignant.

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Body CT: The Essentials lower pole or isthm us into the anterior or m iddle m ediastinum . Retrotracheal extension can occur with thyroidal m asses arising rom the posterior m argin o the thyroid gland. Most o ten, m ediastinal extension o thyroid tissue is the result o multinodular goiter. Thyroid carcinom a and thyroiditis are very uncom m on causes o m ediastinal thyroidal m asses. Most intrathoracic goiters are detected incidentally on im aging, although signi cant airway com pression can occur in some patients.

Parathyroid Tumor

Figure 4-9 15-year-old Boy with Anterior Mediastinal Yolk Sac Carcinoma Contrast-enhanced CT im age shows a large heterogeneous m ass (arrow) in the anterior m ediastinum. Note the m ass ef ect on the large m ediastinal and right hilar vessels.

mediastinal GCT. These benign tum ors are typically encapsulated and contain oci o so t tissue, calci cation, and ossi cation. Macroscopic at is apparent in approxim ately hal o m ediastinal teratom as.

Ectopic parathyroid tissue (Figure 4-11) is a rare cause o anterior m ediastinal m ass. Most ectopic glands are unctional and are either hyperplastic or contain an adenom a. Parathyroid carcinom a is very rare. Anterior m ediastinal parathyroid tissue o ten m im ics a lym ph node on CT and is usually located in the superior aspect o the anterior m ediastinum . Patients usually present with signs and sym ptom s o hyperparathyroidism . Parathyroid scintigraphy and SPECT using 9 9 m Tc sestam ibi can localize ectopic parathyroid tissue to the anterior m ediastinum , which can be urther evaluated with CT.

Mediastinal Lipomatosis

Seminomas and nonseminomatous GCTs (Figure 4-9) are malignant and most commonly occur in men. They have propensity or local invasion as well as metastases, especially to lung and pleura. Malignant GCTs may be indistinguishable rom lymphoma or invasive thymic epithelial neoplasm.

Excessive accumulation o norm al at in the m ediastinum de nes mediastinal lipomatosis (Figure 4-12). It is m ost com monly associated with increased levels o serum cortisol such as corticosteroids or Cushing syndrome. Obesity may also result in an abundance o m ediastinal at. Mediastinal lipom atosis may be an incidental nding or be m istaken or a m ediastinal m ass on chest radiography. All com partm ents o the mediastinum m ay be involved, but the upper anterior m ediastinum is most com monly af ected.

Thyroid Masses

Mediastinal Fat Necrosis

The m ajority o mediastinal thyroid masses (Figure 4-10) extend in eriorly rom the neck, usually arising rom the

Sim ilar in m echanism to epiploic appendagitis, m ediastinal at necrosis (Figure 4-13) is a rare cause o acute chest

A

B

Figure 4-10 57-year-old Woman with Mediastinal Thyroid Axial (A) and coronal re orm atted (B) contrast-enhanced CT

im ages show enhancing thyroid tissue (arrows) extending into the upper m ediastinum .

Malignant germ cell tumors

Chapter 4 Mediastinum

A Figure 4-11 57-year-old Man with Hyperparathyroidism and Ectopic Parathyroid Tissue in the Anterior Mediastinum A. Coronal im age rom 9 9 m Tc sestam ibi scan shows ocal uptake (arrow) in the m ediastinum . B. Contrast-enhanced

Figure 4-12 68-year-old Morbidly Obese Man with Mediastinal Lipomatosis Contrast-enhanced CT im age shows abundant at (arrows) in the anterior m ediastinum . A sm all right pleural ef usion (arrowhead) is present, and their associated compressive atelectasis o the right upper lobe.

B CT im age shows a sm all ovoid so t tissue nodule (arrow) in the anterior m ediastinum , proven to be a parathyroid adenom a.

Figure 4-13 55-year-old Man with Acute Chest Pain and Mediastinal Fat Necrosis Unenhanced CT im age shows a well-circum scribed at attenuation m ass lesion (arrow) in the anterior m ediastinum .

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26 T b

Body CT: The Essentials 4-2. Middle Mediastinal Masses

Lymphadenopathy Bronchogenic cyst Esophageal neoplasm Hiatus hernia eso hag al varic s eso hag al du lica ion cys

pain or anterior m ediastinal m ass. The characteristic appearance on CT is that o an encapsulated at attenuation m ass within norm al m ediastinal at. Mediastinal at necrosis is indistinguishable rom atty neoplasm s. However, in the correct clinical setting, conservative m anagem ent with ollow-up im aging can be em ployed.

Mid d l e Me d ia s Tin u M Anatomy The middle mediastinum is located between the anterior and posterior compartments and contains the heart and pericardium, trachea and main bronchi, ascending aorta and aortic arch, central pulmonary arteries and veins, the superior and in erior venae cavae, and brachiocephalic vessels. The majority o diseases involving the mediastinum relate to the trachea or lymph nodes. Primary neoplasms and cysts can also develop in the middle mediastinum (Table 4-2).

Figure 4-14 53-year-old Woman with Sarcoidosis Coronal re orm atted contrast-enhanced CT im age shows bulky subcarinal (thin arrow), right paratracheal (arrowhead), and le t hilar (wide arrow) lym phadenopathy.

greater than 10 m m . Com m on causes o m ediastinal lym ph node enlargem ent include lym phom a, m etastases, granulom atous in ection, and sarcoidosis (Figure 4-14). In these conditions, the norm al m orphology o the lym ph node is o ten altered, with loss o the norm al atty hilum . In contrast,

Lymphadenopathy Lym ph node enlargem ent is a com m on cause o a m iddle m ediastinal m ass and is de ned by a short axis diam eter

A Figure 4-15 55-year-old Woman with Large Bronchogenic Cyst A. Un en h an ced CT im age sh ows a well-circu m scribed, hom ogen eou s m ediastin al m ass (arrow). B. Fat saturated

B T2-weighted MR im age shows dif use high T2 signal intensity in the m ass (arrow), re ectin g the high water content o the cyst.

Chapter 4 Mediastinum

27

lung edem a or pulm onary in am m ation can cause enlargem ent o m ediastinal lym ph nodes with preservation o norm al m orphology. A solitary hypervascular lym ph node should raise the suspicion or Castlem an disease, a benign lym phoproli erative disorder o unknown etiology.

Bronchogenic Cyst The m ajority o bronchogenic cysts (Figure 4-15) occur in the m iddle m ediastinum , usually near the tracheal carina. Patients m ay present with cough and chest pain related to m ass ef ect on adjacent structures, or they can be asym ptom atic. On CT, bronchogenic cysts are hom ogeneous and have well-de ned m argins. CT attenuation is low but can exceed 10 0 H U because o intracystic protein or calcium oxalate. Bronchogenic cysts do not enhance ollowing contrast adm inistration. MRI can be used to con rm the cystic nature o a suspected bronchogenic cyst with high attenuation.

Figure 4-17 71-year-old Woman with Small Cell Lung Carcinoma Contrast-enhanced CT im age shows a lobulated m ass (arrow) in the m iddle m ediastinum .

Esophageal Duplication Cyst Esophageal duplication cysts (Figure 4-16 ) m ay be di cult to distinguish rom bronchogenic cysts. However, they should be suspected when a m ediastinal cyst abuts or involves the wall o the esophagus.

Bronchogenic Carcinoma Prim ary lung cancer can arise in the m ediastinum , usually related to a large airway. Sm all cell lung carcinom a (Figure 4-17) should be suspected in sm okers or orm er sm okers presenting with a large, invasive m ediastinal m ass. Com pression o central airways or low-pressure vascular structures such as the superior vena cava is a com m on com plication o sm all cell lung carcinom a.

Po s Te r io r Me d ia s Tin u M The posterior m ediastinum extends rom the posterior m argin o the pericardium posteriorly to the paravertebral gutters. It contains the descending aorta, azygos and hem iazygos veins, thoracic duct, esophagus, autonom ic nerves, and at. The m ajority o posterior m ediastinal m asses are o esophageal or neural origin (Table 4-3).

Esophagus Dilated esophagus Disorders o m otility such as achalasia (Figure 4-18) or system ic sclerosis can lead to m arked esophageal dilation. Additional esophageal carcinom a can cause a stricture and resultant proxim al esophageal dilation. Chagas disease, caused by in ection by Trypanosoma cruz i, can result in esophageal dilation sim ilar to achalasia as a result o destruction o the autonom ic ganglia o the esophagus. Following esophagectom y, the stom ach is o ten pulled up into the chest and ashioned into a conduit. These gastric conduits can becom e distended.

T b

4-3. Posterior Mediastinal Masses

Schwannoma Neurof broma paraganglioma Ganglion uroma Figure 4-16 Woman with Esophageal Duplication Cyst Unenhanced CT im age shows hom ogeneous m ediastinal m ass lesion (arrow) abutting the esophagus.

Ganglion uroblas oma N uroblas oma

28

Body CT: The Essentials

A Figure 4-18 23-year-old Man with Achalasia Axial (A.) and sagittal re orm atted (B.) contrast-enhanced CT

B im ages show dif use esophageal dilation with a gas–watercontrast uid level (arrows).

Esophageal carcinoma Most esophageal carcinom as (Figure 4-19 ) arise near the esophagogastric junction. Adenocarcinom a and squam ous cell carcinom as are the m ost com m on. On CT, esophageal carcinom a can present as circum erential or eccentric wall thickening. Occasionally, a polypoid lum inal lling de ect m ay be present. Not uncom m only, CT shows little or no abnorm ality or early stage esophageal carcinom a. With advanced esophageal carcinom a, CT m ay show direct extension into adjacent structures or m etastatic lym phadenopathy.

Esophageal varices Esophageal varices (Figure 4-20 ) can m im ic other posterior m ediastinal m asses on chest radiography but are characteristic on CT. The m ajority orm near the esophagogastric junction as a com plication o portal hypertension. Varices resulting rom superior vena cava occlusion usually occur m ore cephalad.

Hiatus hernia

Figure 4-19 56-year-old Man with Esophageal Carcinoma Contrast-enhanced CT im age shows a large, heterogeneous m ass (arrow) expanding and obstructing the esophagus.

Hiatus hernia (Figure 4-21) is an extrem ely com m on cause o a posterior m ediastinal m ass. Large hernias are usually apparent on chest radiographs as a round or ovoid retrocardiac m ass containing a gas–liquid level. Sm aller hiatus hernias are not uncom m only detected on CT. Sliding type hiatus hernias are the m ost com m on and occur when the esophagogastric junction m igrates cephalad to its usual location. The less com m on paraesophageal hernias are

Chapter 4 Mediastinum

Figure 4-20 60-year-old Male Liver Transplant Recipient with Persistent Esophageal Varices Contrast-enhanced CT im age shows a large dilated varix (arrow) in the posterior m ediastinum .

characterized by herniation o the gastric cardia through the esophageal hiatus without displacem ent o the esophagogastric junction. Large hernias can result in an intrathoracic stom ach, o ten with an organoaxial volvulus. Surgical repair m ay be required to avoid an obstructing volvulus.

Neurogenic Neoplasms Neoplasm s o neural origin are com m on posterior m ediastinal m asses and arise rom peripheral nerves, autonom ic paraganglia, and sym pathetic ganglia. Most are evaluated with MRI, but they m ay be rst detected on CT.

Figure 4-21 66-year-old Man with Hiatus Hernia Unenhanced CT im age shows a portion o the gastric undus (arrow) in the lower m ediastinum .

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Figure 4-22 38-year-old Woman with Paraspinal Schwannoma Contrast-enhanced CT im age shows a large right paraspinal m ass. Note the extension through and widening o the neural oram en (arrow) by the m ass.

Peripheral nerves Neuro brom as, schwannom as (Figure 4-22), and m alignant nerve sheath tum ors (Figure 4-23) arise rom peripheral nerves and can be located im m ediately adjacent to the spine or course along the intercostal nerves. Schwannom as are the m ost com m on and can be detected incidentally or when they becom e large enough to cause m ass ef ect on adjacent structures. Those that involve the nerve root can expand and extend through the neural oram en. Schwannom as can contain oci o low attenuation

Figure 4-23 37-year-old Man with Neurof bromatosis Type 1 and Malignant Nerve Sheath Tumor Contrast-enhanced CT im age shows a very large and heterogeneous m ass (arrow) in the le t hem ithorax involving the chest wall. Two subcutaneous neuro brom as (arrowheads) are present.

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Body CT: The Essentials

on CT and o ten enhance ollowing the intravenous contrast adm inistration. Neuro brom as can be solitary or m ultiple and approxim ately 30% o patients have neuro brom atosis type 1. In contrast to schwannom as, m alignant degeneration can occur, particularly in patients with m ultiple neuro brom as. Malignant nerve sheath tum ors can occur in patients with and without neuro brom atosis type 1, but are m ore com m on in patients with the disease. In the absence o obvious destruction or invasion o adjacent structures, distinguishing these m alignant tum ors rom benign peripheral neural tum ors can be di cult or im possible.

Autonomic paraganglia Paragangliomas arise rom the autonomic paraganglia serving as chemoreceptors and are re erred to as pheochromocytomas when arising rom the adrenal gland. Functional paragangliomas can cause ushing or hypertension. On CT, thoracic paragangliomas are usually very hypervascular and are located in the posterior mediastinum or adjacent to the heart. Non unctioning paragangliomas, also called chemodectomas, can develop around the aortic arch, in the aortopulmonary window, or adjacent to the right pulmonary artery.

Sympathetic ganglia Neoplasms o the sympathetic ganglia include ganglioneuroma, ganglioneuroblastoma, and neuroblastoma. Neuroblastoma is a highly malignant neoplasm o young children that can occur in the chest or abdomen. Ganglioneuroblastomas are also malignant but are less aggressive than neuroblastoma. Ganglioneuromas are benign sympathetic nerve neoplasms that usually occur in adolescents and young adults.

Figure 4-24 12-year-old Girl with Beta Thalassemia and Extramedullary Hematopoiesis Contrast-enhanced CT shows hom ogeneous, high attenuation so t tissue m asses along the spine (arrows) and deep to the ribs (arrowheads).

encapsulated collection, usually with central low attenuation. Gas m ay be apparent in the abscess cavity. Mediastinitis without abscess typically m ani ests as sm all oci o m ediastinal uid, o ten accom panied by haziness in the adjacent at.

Pancreatic pseudocyst Pancreatic pseudocysts (Figure 4-26 ) can track into the m ediastinum and cause a m ediastinal m ass. A history o

Miscellaneous Extramedullary hematopoiesis Expansion o erythropoietic tissue into the paraspinal region and posterior m ediastinum can occur in patients with severe chronic anem ia, particularly those with thalassem ia (Figure 4-24). CT usually shows m ultiple lobulated paraspinal m asses that usually are o increased attenuation. Expansion o the m edullary spaces o bones or a history o anem ia m ay be clues to the diagnosis. A sul ur colloid nuclear m edicine scan can con rm extram edullary hem atopoiesis in cases o diagnostic uncertainty.

Mediastinitis Mediastinitis with or without abscess can af ect any m ediastinal com partm ent. Direct extension o diskitis or spinal osteom yelitis into the posterior m ediastinum can m im ic a m ediastinal m ass. Staphylococcal in ections and tuberculosis are the m ost com m on causes o diskitis/ osteom yelitis. Abscess or m ediastinitis can also arise in the anterior or m iddle com partm ents ollowing direct instrum entation or track in eriorly rom the neck (Figure 4-25). Mediastinal abscess on CT appears as an

Figure 4-25 24-year-old Woman with Mediastinitis Resulting rom Direct Extension o a Neck Abscess Contrast-enhanced CT im age shows uid pockets (arrows) in the anterior m ediastinum . Loculated pleural collections (arrowheads) have also developed.

Chapter 4 Mediastinum

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Su g g e St e d Re Ad i n g S 1. Marom EM. Advances in thym om a im aging. J Thorac Imaging. 20 13;28(2):6 9 –80 . 2. Jeung MY, Gasser B, Gangi A, et al. Im aging o cystic m asses o the m ediastinum . Radiographics. 20 0 2;22:S79 –S9 3. 3. Rossi SE, McAdam s H P, Rosado-de-Christenson ML, Franks TJ, Galvin JR. Fibrosing m ediastinitis. Radiographics. 20 0 1;21(3):737– 757. 4. Coulier B. Epipericardic at necrosis: CT diagnosis. JBR-BTR. 20 10 ;9 3(6 ):317–318. 5. Moeller KH , Rosado-de-Christenson ML, Tem pleton PA. Mediastinal m ature teratom a: im aging eatures. Am J Roentgenol. 19 9 7;16 9 :9 85–9 9 0 . 6 . Lee KS, Gilm J, Han CH , Han MC, Kim CW, Kim WS. Malignant prim ary germ cell tum ors o the m ediastinum : CT eatures. Am J Roentgenol. 19 89 ;153:9 47–9 51. 7. Drevelegas A, Palladas P, Scordalaki A. Mediastinal germ cell tum ors: a radiological-pathologic review. Eur Radiol. 20 0 1;11:19 25–19 32. 8. Tateishi U, Muller NL, Johkoh T, et al. Primary m ediastinal lymphom a: characteristic eatures o the various histological subtypes on CT. J Comput Assist Tomogr. 20 04;28:782–789 .

Figure 4-26 57-year-old Man with Mediastinal Extension o a Pancreatic Pseudocyst Coronal re orm atted contrast-enhanced CT im age shows a large encapsulated uid collection (arrow) in the lower m ediastinum . Dystrophic pancreatic calci cations (arrowhead) are the consequence o chronic pancreatitis.

pancreatitis or abdom inal ndings suggesting acute or chronic pancreatitis m ay be help ul in suggesting the diagnosis. Fluid sam pling reveals high levels o am ylase, conrm ing the diagnosis.

9 . Feung MY, Gasser B, Gangi A, et al. Im aging o cystic m asses o the m ediastinum . RadioGraphics. 20 0 2;22:S79 –S9 3. 10 . McAdams HP, Kirejczyk WM, Posado-de-Christenson ML, Matsumoto S. Bronchogenic cyst: imaging eatures with clinical and histopathologic correlation. Radiology. 2000;217:441–446. 11. Katabathina VS, Restrepo CS, Martinez-Jim enez S, Riascos RF. Nonvascular, nontraum atic m ediastinal em ergencies in adults: a com prehensive review o im aging ndings. Radiographics. 20 11;31(4):1141–116 0 . 12. Gupta R, Munoz JC, Garg P, Masri G, Nahm an NS Jr, Lam biase LR. Mediastinal pancreatic pseudocyst–a case report and review o the literature. MedGenMed. 20 0 7;9 (2):8.

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g

Jef rey P. Kanne, MD

I. TECHNIQUE II. PATTERNS OF LUNG ABNORMALITIES a. Consolidation i. In ection ii. Eosinophilic pneumonia iii. Organizing pneumonia iv. Lipoid pneumonia v. Lymphoma b. Ground-Glass Opacity i. Acute respiratory distress syndrome ii. Pneumocystis jiroveci pneumonia c. Nodular Pattern i. Sarcoidosis ii. Silicosis and coal worker’s pneumoconiosis iii. Miliary in ection iv. Metastases d. Septal Pattern i. Lung edema ii. Lymphangitic carcinomatosis e. Reticular Pattern i. Pulmonary brosis . Cysts i. Pulmonary Langerhans cell histiocytosis ii. Lymphangioleiomyomatosis iii. Lymphoid interstitial pneumonia g. Mosaic Attenuation h. Crazy-Paving i. Pulmonary alveolar proteinosis

Te c h n iq u e Com puterized tom ography (CT) o the chest is com m only per orm ed to evaluate patients with known or suspected pulm onary disease. Traditionally, routine chest CT is perorm ed with helical acquisition and 3- to 5-m m slice-thickness reconstructions. However, because m any pulm onary structures and abnorm al ndings are sm aller than 3 m m , im aging o the chest is pre erably per orm ed using highresolution CT (H RCT) technique. Because o natural con-

III. ATELECTASIS IV. SOLITARY LUNG NODULE V. LUNG CANCER a. Histopathology i. Adenocarcinoma ii. Squamous cell carcinoma iii. Small cell lung carcinoma b. Staging VI. EMPHYSEMA VII. CONGENITAL a. Pulmonary Sequestration b. Congenital Pulmonary Airway Mal ormation c. Miscellaneous Congenital Lesions i. Congenital lobar overinf ation ii. Systemic arterial supply to the lung iii. Intrapulmonary bronchogenic cyst VIII. PULMONARY VASCULAR DISEASE a. Acute Pulmonary Thromboembolism b. Chronic Pulmonary Thromboembolism c. Pulmonary Artery Sarcoma d. Vasculitis i. Large vessel vasculitis ii. Small vessel vasculitis e. Pulmonary Arteriovenous Mal ormation

trast between air and tissue, H RCT o the lungs can be per orm ed with low tube current. Most m odern scanners have autom atic exposure control, which can result in signi cant dose savings, especially in the chest. For average adults, 120 kVp is suf cient. In larger adults, 140 kVp m ay be required, and 100 kVp can be used in sm aller adults. Volumetric H RCT should be strongly considered as the standard routine chest CT protocol. Images should be reconstructed with both so t tissue and high spatial requency convolution kernels at 1- to 1.5-mm slice thickness. Coronal and 33

34

Body CT: The Essentials

sa ittal re ormations can be immensely help ul in evaluatin the lun s and can be enerated rom ori inal scan data or, on some PACS, on-the- y. Thick slab (10 mm) slidin maximum intensity projections (MIPs) are very use ul or improvin detection o small lun nodules. I small airways disease is suspected, limited end expiratory ima es can be obtained every 10 to 20 mm. Prone ima es do not need to be per ormed routinely and can be reserved or patients in whom the dia nosis o interstitial brosis is equivocal in the dependent lun on inspiratory ima es. Furthermore, the scan ran e or prone ima es can be restricted to the re ion o carina throu h the diaphra m as most patients with interstitial brosis have basal predominant disease. For most thoracic indications, the use o intravenous contrast is not necessary. For lun patholo y, contrast is rarely indicated as it adds little-to-no additional in ormation and can result in streak arti act in the superior vena cava. Contrast administration can be use ul in sta in o lun carcinoma, especially when radio raphy shows extensive abnormalities or su ests mediastinal, hilar, or chest wall involvement.

Pa TTe r n s o f Lu n g a b n o r m a LiTie s Pulm onary disease is com m only rouped into three cate ories: airspace, interstitial, and airways. However, this classi cation is rau ht with problem s as m any lun diseases af ect m ultiple com partm ents o the lun s. Furtherm ore, the im a in ndin s o interstitial, airspace, and airways diseases can overlap. A better approach to thinkin about lun disease is to inte rate the pattern(s) o disease on CT with clinical in orm ation. For exam ple, m ulti ocal lun consolidation in an acutely ill patient with ever, leukocytosis, and productive cou h is m ost likely the result o in ection whereas m ulti ocal consolidation in a patient with interm ittent ever and dry cou h over several weeks is m ore likely to re ect a chronic in am m atory process such as or anizin pneum onia (OP).

Consolidation Lun consolidation (Table 5-1) is de ned as increased attenuation o the lun that obscures the underlyin architecture. Consolidation m ost com m only is the result o alveolar llin , prim arily by blood, pus, water, cells, protein, or a com bination thereo . Determ inin the cause o lun consolidation rom im a in alone is o ten di cult; and interation o clinical in orm ation is essential or providin the m ost appropriate dif erential dia nosis.

In ection Pulm onary in ection rem ains a com m on cause o m orbidity and m ortality in im m unocom petent and im m unocom prom ised patients, alike. The dia nosis o pneumonia is typically m ade by a com bination o history and physical exam ination, supportin laboratory data, and chest radio raphy. Chest CT is usually per orm ed on patients with

T l 5-1. Com m on Causes o Lun Consolidation Di gnosis

Clu s o Di gnosis

In c ion

F v , l ukocy osis, c n ilobul nodul s

h mo

g

a cu y oxi , v sculi is, conn c iv issu dis s

ed m

S l ick ning, l u l c diom g ly

a r DS/ a Ip

a cu

O g nizing n umoni

Sub cu s non oduc iv ib onc i l, dis ibu ion;

C onic osino ilic n umoni

p i l nons gm n l dis ibu ion, u lob domin nc , blood osino ili

Li oid n umoni

Lownu ion oci, d nd n o ions o lung, min l oil ing s ion, o n d bili d i ns

Lung d noc cinom (o n mucinous sub y )

Di us , symm ic, nodul s o n s n , slowly og ss s ov im

s i

usions,

o y ilu , y ox mi n ion wi coug ; i l, nd ilobul v s d lo sign

suspected com plications such as em pyem a or on im m unosuppressed patients with norm al or near norm al chest radio raphs but with a hi h clinical suspicion o pulm onary in ection. However, as with chest radio raphy, the speci c pattern o im a in ndin s on CT is nonspeci c or determ inin a causative or anism or even broad cate ory o patho en. Further com plicatin the issue is the act that m ore than one pattern can exist in the sam e patient. Lobar pneumonia rst develops in the periphery o the lun and spreads to the adjacent alveoli, resultin in lun consolidation (Fi ure 5-1). Pleural boundaries and host immune response usually con ne in ection to a sin le lobe, althou h total lobar consolidation is uncommon because most patients receive treatment early in the course o disease. Air broncho rams are requently present, as the lar e airways are not typically involved. The most common causes o lobar pneumonia include Streptococcus pneumoniae, Haemophilus inf uenzae, Klebsiella pneumoniae, Mycobacterium tuberculosis, and Legionella pneumophila. However, other or anisms such as Blastomyces dermatitidis, Nocardia asteroides complex, and respiratory tract viruses can also cause lobar pneumonia. Bronchopneumonia is typically a multi ocal, multilobar process characterized by oci o peribronchial consolidation with or without associated centrilobular nodules. In contrast to lobar pneumonia, air broncho rams are less common with bronchopneumonia because o in ammation o the lar er airways. Some de ree o volume loss may be apparent. The most requent causes o bronchopneumonia include

Chapter 5 Lung 35

Figure 5-1 Streptococcus Pneumoniae In ection Unenhanced CT ima e shows dense consolidation in the ri ht upper and lower lobes with air broncho rams (arrow). Several lar e nodular oci o consolidation (arrowhead) are in the le t upper lobe.

Staphylococcus aureus, H . inf uenzae, un i, and aspiration pneumonia. Round pneum onia is a variant o lobar pneum onia and m ore com m only af ects children, m ost o ten as an early presentation o S. pneumoniae in ection. In adults, other in ections such as endem ic un i and Q ever (Coxiella burnetii) should also be considered.

Eosinophilic pneumonia Eosinophilic pneumonia describes a ran e o acute and chronic lun diseases that can be idiopathic or related to dru reaction or in ection. Simple pulmonary eosinophilia, also called Loe er syndrome, consists o blood eosinophilia and eetin oci o lun consolidation. CT shows patchy, nonse m ental consolidation and round- lass opacity with a peripheral and upper lobe predominance in approxim ately 40% o patients. Chronic eosinophilic pneumonia (CEP)

Figure 5-2 Chronic Eosinophilic Pneumonia Contrast-enhanced CT im a e shows bilateral patchy oci o peripheral consolidation and round- lass opacity.

is characterized by alveolar llin o in amm atory cells o which most are eosinophils. The m ajority o patients also have blood eosinophilia, and 50% o patients with CEP have asthma. CT typically shows peripheral and patchy lun consolidation (Fi ure 5-2), round- lass opacity with or without crazy-pavin , linear and band-like opacities, and a mid and upper zone predom inance. Most patients respond quickly to corticosteroid therapy. Acute eosinophilic pneumonia (AEP) is a severe, acute ebrile illness that can pro ress to respiratory ailure. Most cases o AEP are idiopathic, but dru reactions or inhalation o smoke (particularly tobacco sm oke) can cause AEP. Bronchoalveolar lava e uid shows a hi h num ber o eosinophils. CT ndin s are similar to those o lun edem a with septal thickenin , round- lass opacity, consolidation, and pleural ef usions. Pro nosis is ood with rapid response to corticosteroid therapy. Hypereosinophilic syndrome is de ned by persistent blood eosinophilia or at least 6 m onths and m ultior an tissue in ltration by eosinophils. CT ndin s include bilateral lun nodules, o ten peripherally located and surrounded by a halo o roundlass opacity. Pro nosis is poor.

Organizing pneumonia OP is a com m only encountered histolo ic pattern o lun injury characterized by the presence o ranulation tissue plu s in the alveoli and alveolar ducts with chronic in am m ation in the surroundin tissues. Com m on causes o OP include in ection, dru reaction, colla en-vascular disease, in am m atory bowel disease, hypersensitivity pneum onitis, aspiration, and radiation-induced lun injury. In som e patients, no cause is determ ined and the term cryptogenic organizing pneumonia (COP) is used. The typical CT ndin s o OP are patchy consolidation and round- lass opacity, o ten with a peribronchial, peripheral, and perilobular distribution (Fi ure 5-3). Air broncho ram s are requently

Figure 5-3 Cryptogenic Organizing Pneumonia Unenhanced CT im a e shows bilateral peribronchial consolidation and round- lass opacity. Note a developin reversed halo si n with consolidation (arrows) surroundin a ocus o round- lass opacity.

36

Body CT: The Essentials

Figure 5-4 Lipoid Pneumonia Unenhanced CT im a e shows a ocus o consolidation containin at attenuation (arrowhead).

Figure 5-5 Primary Pulmonary Lymphoma CT im a e shows peribronchial nodular consolidation (arrow) with surroundin round- lass opacity.

apparent in areas o consolidation, and the bronchi m ay have thickened walls and m ildly dilated lum ens. Scattered sm all and lar e nodules m ay also be present, re ectin oci o OP. The reversed halo or atoll si n describes a crescent or rin -shaped opacity o consolidation surroundin a ocus o round- lass opacity and occurs in approxim ately 20 % o patients with COP. Althou h the reversed halo si n can occur in other diseases such as in ection and vasculitis, it usually re ects the presence o an OP reaction.

(MALT) lymphomas (MALTomas) can present as solitary or multiple lar e lun nodules. Eccentric air broncho rams may be apparent, re ectin the airway-centric ori in o this neoplasm.

Lipoid pneumonia Lipoid pneumonia results rom recurrent aspiration o lipid-containin substances. O ten patients with lipoid pneum onia are debilitated and aspirate m ineral oil that is used to treat chronic constipation. Patients are usually asym ptom atic, and abnorm alities are detected on radio raphy per orm ed or nonspeci c si ns and sym ptom s. CT ndin s include low-attenuation consolidation (Fi ure 5-4), septal thickenin , and crazy-pavin .

Lymphoma Lymphoma can arise primarily in the lun or af ect the lun as part o a systemic lymphoproli erative disorder. Lun consolidation occurs in two-thirds o patients with pulmonary lymphoma (Fi ure 5-5), and lar e nodules develop in approximately 40%. Low- rade mucosa-associated lymphoid tissue

Ground-Glass Opacity Ground-glass opacity is de ned as increased attenuation o the lun without obscuration o the underlyin architecture; thus, vessels and airways are still visible. As with consolidation, round- lass opacity is the result o alveolar llin , primarily by blood, pus, water, cells, protein, or a combination thereo (Table 5-2). However, expansion o the pulmonary interstitium can also lead to round- lass opacity, as the amount o aerated lun per unit volume is diminished. Similar to lun consolidation, narrowin the dif erential dia nosis or round- lass opacity requires inte ration o clinical in ormation. Importantly, the acuity o the patient’s illness is key to narrowin the dif erential dia nosis. For example, dif use round- lass opacity in a patient presentin with acute respiratory illness, in ection (especially i immunocompromised), acute lun injury, edema, and pulmonary hemorrha e should be considered. For patients with a more subacute presentation, consider entities such as dru reaction, interstitial pneumonia, smokin -related interstitial pneumonia (respiratory bronchiolitis and desquamative interstitial pneumonia), and hypersensitivity pneumonitis.

Chapter 5 Lung 37 T l 5-2. Com m on Causes o Extensive g round- lass Opacity Di gnosis

Clu s o Di gnosis

pn umoni (PJP, vi l, Mycoplasma)

F v , l ukocy osis, consolid ion, nodul s

a r DS/ a Ip

a cu s i o y ilu , consolid ion o n s n

ed m

S

h mo

g

l

ick ning o

n

s n

a cu y oxi , v sculi is, conn c iv issu dis s

Nons cif c in s i i l n umoni

Sub l u l s ing, icul ion m yb s n , conn c iv issu dis s

h y s nsi ivi y n umoni is

Sub cu s n ion, mos ic nu ion, lobul i ing, oo ly d f n d c n ilobul nodul s

Acute respiratory distress syndrome Acute respiratory distress syndrome (ARDS) is an acute hypoxic respiratory illness that is characterized histopatholo ically by di use alveolar damage. Patients require m echanical ventilation, and m ortality rates are hi h. Patients present with pro ressive dyspnea and hypoxia that evolves over hours to days. Causes are num erous and include in ection, inhalational injury, aspiration, sepsis, and traum a. Idiopathic ARDS is term ed acute interstitial pneum onia (AIP). Early in the course o ARDS, CT shows extensive round- lass opacity o ten accom panied by consolidation (Fi ure 5-6 ). Dependent portions o lun m ay be m ore extensively involved. ARDS resultin rom extrapulm onary causes is m ore likely to have a round- lass

Figure 5-7 Pneumocystis jiroveci Pneumonia CT im a e shows extensive round- lass opacity in both lun s. Subtle superim posed lines are in the ri ht upper lobe, creatin a crazy-pavin pattern.

predom inance and a uni orm distribution, whereas ARDS resultin rom pulm onary disease is m ore likely to have equal extent o round- lass opacity and consolidation with asym m etric lun involvem ent. As ARDS evolves, or anization and brosis ensue. CT shows clearin o consolidation with developm ent o reticulation, traction bronchiectasis, and cystic spaces (sim ilar to em physem a).

Pneumocystis jiroveci pneumonia Pneumocystis jiroveci pneumonia (PJP) occurs in im m unocom prom ised patients with de ciency o T-cell unction. The incidence o PJP has dim inished because o widespread prophylaxis in the United States and im proved treatm ent or H IV in ection. However, it rem ains the m ost com m on opportunistic in ection in patients with AIDS. The m ost com m on CT ndin o PJP is extensive round- lass opacity (Fi ure 5-7), requently in a central or perihilar distribution. Superim posed thin-walled cysts or pneum atoceles m ay be present, particularly in patients with AIDS.

Nodular Pattern

Figure 5-6 Acute Respiratory Distress Syndrome Unenhanced CT ima e shows extensive round- lass opacity and crazy-pavin in the mid and anterior lun s with dense consolidation in the posterior lun s. Pneumomediastinum (arrow) and subcutaneous as have developed as a result o barotrauma.

Three m ain patterns o dif use nodularity on CT include centrilobular, perilym phatic, and random . Distin uishin am on these patterns o dif use nodularity is im portant as each has its own airly lim ited dif erential dia nosis. With a centrilobular pattern o nodules, nodules are located in or around the centrilobular core, which consists o the terminal bronchus and lobular artery. They are airly evenly spaced and do not touch pleural sur aces or inter ace with lar e airways and vessels. Most commonly, a centrilobular pattern is the result o small airways disease (see Chapter 6), typically in ectious bronchiolitis. When nodules in a centrilobular pattern are poorly de ned (“ uzzy” or round- lass attenuation), the dif erential dia nosis is usually limited to

38

Body CT: The Essentials

either hypersensitivity pneumonitis or respiratory bronchiolitis. Tree-in-bud (branchin Y- or V-shaped) opacities are a variant o centrilobular nodules and are almost always the result o in ectious bronchiolitis. Aspiration bronchiolitis can also result in tree-in-bud opacities and should be considered in the settin o risk actors or aspiration, ravitationally dependent distribution, and other ndin s o aspiration such as endobronchial debris and retained uid or debris in the esopha us. Nodules in a perilymphatic distribution localize to the subpleural lun , lar e bronchovascular bundles, and around the centrilobular core. The pulmonary ssures are ideal locations to assess or perilymphatic nodules because subpleural interstitium abuts both sides o the ssures. The dif erential dia nosis o perilymphatic nodules is most commonly related to sarcoidosis. Lymphan itic carcinomatosis can also lead to perilymphatic nodularity, but septal thickenin is typically evident as well. Other causes o a perilymphatic pattern o nodules include silicosis, coal worker’s pneumoconiosis (CWP), and chronic beryllium disease. The perilymphatic nodules in sarcoidosis and berylliosis tend to have more irre ular shapes, whereas the nodules associated with silicosis and CWP typically are more rounded. Exposure history in conjunction with ima in ndin s is nearly always su cient or establishin a dia nosis o pneumoconiosis. Dif use nodules that are neither in a centrilobular nor a perilym phatic distribution are considered to be in a random distribution. A m iliary pattern o nodules consists o a random distribution o dif use tiny (4–6

Ct ollow-u in 12 mon s

Ct ollow-u in 6–12 mon s, n 18–24 mon s i s bl

>6–8

Ct ollow-u in Ct ollow-u in 3–6 6–12 mon s, n mon s, n 9–12, 18–24 mon s i nd 24 mon s i s bl s bl

>8

Follow-u Ct 3, 9, nd 24 mon s, dyn mic con s n nc d Ct , pet , nd/ o bio sy

Guid lin s m lign ncy.

ly only o

i n s 35 y

so

S m s o low- isk i n

g o old

wi ou known

the result o ranulom atous in am m ation or in ection such as sarcoidosis or histoplasm osis (Fi ure 5-22). Coarse, dystrophic or “popcorn” calci cation can develop in som e

Figure 5-22 Remote Histoplasmosis Unenhanced CT im a e shows a well-de ned le t lower lobe nodule (arrow) with lam ellar pattern o calci cation.

Chapter 5 Lung 45 T l 5-6 . Fleischner Society g uidelines or Follow-up o Incidentally Detected Subsolid Nodules Nodul t y

M n g m n r comm nd ions

Soli

y u

g ound-gl ss, ≤5 mm

No ollow-u

Soli

y u

g ound-gl ss >5 mm

Ct ollow-u ollow-u o

Soli

y

Mul i l

-solid nodul s

u

g ound-gl ss, ≤5 mm

3 mon s, nnu l Ct l s 3y s i sis n

FDG pet no

comm nd d

Ct ollow-u 3 mon s. I sis n , Ct ollow-u o l s 3 y s i solid com on n 10 mm

Follow-u Ct

Consid

2 nd 4 y

s

Mul i l u g ound-gl ss >5 mm wi ou domin n l sion

Ct ollow-u 3 mon s, Ct ollow-u o l s 3y s i sis n

Domin n nodul (s) wi o solid com on n

Ct ollow-u 3 mon s, i sis n , bio sy o s c ion, s ci lly i solid com on n >5 mm

-solid

Comm n s

l

FDG pet no

n

-

c us s comm nd d

Subsolid nodules are those that are pure round- lass attenuation or part-solid/ part round- lass attenuation. Pure round- lass nodules can re ect ocal brosis, ocal in am m ation, atypical adenom atous hyperplasia, or lowrade adenocarcinom a. A part-solid/ part round- lass nodule is m ore likely to represent a low- rade adenocarcinom a, but still has a sim ilar dif erential dia nosis as a purely round- lass nodule. Mana ement o these nodules is dif erent than or solid nodules (Table 5-6 ). Because low- rade adenocarcinom as row slowly, it is im portant to com pare these lesions across m ultiple studies. In addition to linear rowth, increasin attenuation or developm ent o solid com ponents should prom pt biopsy or resection, as these ndin s m ay be indicators o invasion. Cavitation within a lun nodule usually si ni es tissue necrosis and com m unication with an airway or air spaces. Both beni n and m ali nant nodules can cavitate, thus, this ndin is nonspeci c. Com m on causes o cavitary lun nodules include in ection, prim ary lun carcinom a, and m etastases.

Lu n g c a n c e r Figure 5-23 Pulmonary Hamartoma/ Mesenchymoma Unenhanced CT im a e shows a lobulated ri ht m iddle lobe nodule (arrow) with coarse, “popcorn” calci cation.

pulmonary hamartomas/ mesenchymomas (Fi ure 5-23). When calci cations are eccentric or stippled, the nodule is indeterminate because dystrophic calci cation can develop in lun carcinomas and carcinoid tumors. In the settin o matrix ormin sarcomas such as osteosarcoma or chondrosarcoma, metastases may be calci ed, so comparison to previous studies is prudent and short-term ollow-up may be warranted.

Lung cancer remains the leadin cause o cancer-related death amon men and women. Approximately 85% o lun cancers occur in current and ormer smokers, and ci arette smokin remains the reatest risk actor or developin lun cancer. CT plays a central role in the dia nosis and sta in o lun cancer and is routinely used in surveillance ollowin therapy. The recently published National Lun Screenin Trial (NLST), a multicenter trial o approximately 55,000 current and ormer smokers, showed that annual screenin with low-dose CT can result in decreased lun -cancer– related mortality in hi h-risk patients. Althou h lun -cancer screenin with CT is currently not in widespread use at the time o this writin , recent recommendations by the US Preventive Services Task orce endorsin annual lun -cancer

46

Body CT: The Essentials

CT screenin in hi h-risk patients reatly increase the likelihood o proli eration o screenin pro rams.

Histopathology Lun carcinom a is traditionally divided into small cell lung carcinoma (SCLC) and non–small cell lung carcinoma (NSCLC) based on histopatholo y, and this division alon with sta e direct therapy. However, advances in system ic treatm ent o NSCLC with im m unolo ic a ents tar eted to certain anti ens on tum or cell sur aces have increased the im portance o m ore speci c histopatholo ic dia noses o NSCLC as well as testin or variation enetic m utations such as Eg FR, EML4-ALK translocation, and KRAS. In addition, the World Health Or anization recently revised the classi cation system or lun adenocarcinom as, better re ectin understandin o the biolo y o these neoplasm s.

Adenocarcinoma Adenocarcinoma is the m ost com mon type o lun cancer, accountin or rou hly one-third o all lun cancers and or the vast majority o lun cancers in never smokers. They most com m only present as peripheral nodules, more o ten in the upper lobes, with spiculated or lobulated mar ins. Air broncho ram s or cystic “bubbly” lucencies m ay also be present. Some adenocarcinom as are subsolid or part-solid, re ectin com ponents o lepidic rowth (Fi ure 5-24). In addition, adenocarcinoma can m ani est as consolidation, mim ickin pneumonia (Fi ure 5-25). This type o adeno-

Figure 5-24 Adenocarcinoma with Lepidic Growth Component Unenhanced CT ima e shows a part-solid nodule with peripheral round- lass opacity (arrow), presumably re ectin lepidic rowth.

Figure 5-25 Mucinous Adenocarcinoma Unenhanced CT im a e shows m ass-like consolidation (arrow) in the le t lower lobe with scattered solid and subsolid nodules (arrowheads) in both lun s, re ectin endobronchial spread o tumor.

carcinom a should be suspected when “pneum onia” ails to resolve or an area o consolidation slowly enlar es over tim e. Scattered solid and subsolid nodules m ay also be present, and cystic “bubbly” lucencies may be apparent.

Squamous cell carcinoma Squamous cell carcinomas m ost com m only arise in the se m ental or subse m ental airways. They are usually solid on CT, and up to one-third may cavitate (Fi ure 5-26 ).

Figure 5-26 Squamous Cell Carcinoma Unenhanced CT im a e shows a cavitary m ass (arrow) in the le t lower lobe with nodular m ar ins.

Chapter 5 Lung 47 Obstructive pneum onia or atelectasis in the af ected bronchopulm onary se m ent m ay be apparent on CT.

Small cell lung carcinoma SCLC is the m ost m ali nan t o the neuroendocrine lun neoplasm s and is hi hly a ressive. Most patients present with advanced disease (extensive sta e), o ten with a hilar or m ediastinal m ass (Fi ure 5-27). Rarely, SCLC is dia nosed on biopsy o a solitary lun nodule. SCLC has a stron relationship to sm okin and can produce neoplastic syn drom es such as Lam bert–Eaton m yasthen ic syn drom e. Survival is poor, even with lim ited sta e disease.

Staging Non–sm all cell lun carcinom a is sta ed with TNM system , sim ilar to other cancers (Tables 5-7 and 5-8). Sta in both predicts pro nosis as well as uides therapy. Survival rates depend directly on the sta e, with survival rates allin precipitously with locore ional and system ic spread o cancer. Localized lun carcinom a (T1) is usually treated

Figure 5-27 Small Cell Lung Carcinoma Contrast-enhanced CT im a e shows a bulky, in ltratin le t hilar m ass, which narrows the le t m ain and lobar bronchi (arrowhead).

with sur ery alone. Lar er tum ors and those with ipsilateral hilar lym ph node m etastases are usually treated with a com bination o sur ery, radiation therapy, and system ic chem otherapy. Treatm ent o m ore advanced lun cancers

T l 5-7. Seventh Edition o the TNM Sta in System or Lun Cancer t

N

M

t 1 : ≤2 cm t 1b: >2 cm bu ≤3 cm

No inv sion oxim l o lob b onc us Su ound d by lung o visc l l u

N1: I sil l il , in lob , lob , s gm n l, o subs gm n l lym nod

M1 : pl u l o ic di l m lign n usion o umo nodul (s), s umo nodul (s) in con l l lung

t 2 : >3 cm bu ≤5 cm

Inv sion o m in b onc us (≥2 cm dis l o c in ) Visc l l u inv sion

N2: I sil l m di s in l nod (subc in l is lw ys consid d i sil l)

M1b: ex

t 2b: >5 cm bu ≤7 cm

Obs uc iv l c sis o n umoni x nding o ilum wi ou o l lung involv m n

N3: Con l l m di s inum, ilum lung, o i sil l o con l l sc l n o su cl vicul nod

t 3: >7 cm

Inv sion o m in b onc us ( 2) and m ost com m only a ects m en with chronic obstructive lung disease (Figure 6 -1).

Tracheobronchomegaly, also termed Mo nier-K hn syndrome, usually results rom atrophy o the longitudinal elastic bers and the muscularis m ucosa. Patients usually present during the third and ourth decades o li e with recurrent in ections o the respiratory tract. On CT, tracheobronchom egaly is de ned as a coronal diameter greater than 25 mm and a sagittal diameter o 27 m m in m en or a coronal diam eter greater than 21 m m and a sagittal diameter greater than 23 mm in women. Furtherm ore, the dilated trachea o ten has a corrugated appearance, and num erous diverticula are o ten present (Figure 6 -3). Most patients with tracheobronchomegaly also have bronchiectasis and TBM.

Postintubation stenosis

Tracheobronchomalacia

The incidence o postintubation stenosis has decreased with the advent o low-pressure, high-volum e endotracheal tube balloon cu s and with lower thresholds or tracheostomy. Postintubation stenosis results in a characteristic hourglass appearance o the trachea at the thoracic inlet. Axial CT can underestimate the extent o luminal narrowing,

Tracheobronchomalacia (TBM) is characterized by excessive airway collapse on expiration and is caused by weakness in cartilage and other tissues o the airway walls. TBM can result rom congenital airway weakness or compression rom a vascular ring or sling, or it can be acquired, most commonly rom chronic obstructive lung disease. TBM is best detected

Saber-sheath trachea

Chapter 6 Airways

A Figure 6-2 Postintubation Stenosis A. Axial CT im age shows irregular narrowing and thickening o the trachea (arrow) at the thoracic inlet. B. Coronal oblique

57

B m inim um intensity projection shows the extent and severity o stenosis (arrows) to advantage.

on expiratory CT as the a ected airways m ay have a norm al appearance on inspiratory CT (Figure 6 -4). Furtherm ore, volum etric dynam ic expiratory CT (scanning during orced exhalation) is superior to end-expiratory im aging or determ ining the severity o large airway collapse. A threshold o greater than 70 % tracheal and bronchial cross-sectional narrowing on expiratory CT provides the best balance between sensitivity and speci city or TBM. O note, the bronchus interm edius can com pletely collapse even in norm al individuals at expiration. Lunate trachea re ers to tracheal m orphology where the coronal diam eter exceeds the sagittal diam eter and is highly associated with TBM.

Excessive Dynamic Expiratory Collapse Excessive dynamic expiratory collapse (EDAC) is distinguished rom TBM by preservation o the norm al supporting cartilage but redundancy or weakness o the posterior airway membrane. With EDAC, inspiratory CT usually shows norm al large airways, but expiratory CT shows excessive anterior bowing o the posterior membrane (Figure 6 -5). Figure 6-3 Mounier-Kuhn Syndrome Coronal re orm atted CT im age shows tracheobronchom egaly with corrugated appearance o the large airways and num erous diverticula (arrowheads). Used with perm ission o Arlene Sirajuddin, M.D., Chicago, IL.

Tracheal Neoplasms Malignant tracheal neoplasms Primary tracheal malignancies are uncom m on, yet they account or 9 0 % o all tracheal neoplasm s. Sq amo s cell

58 Body CT: The Essentials

A

B

Figure 6-4 Tracheobronchomalacia A. Inspiratory CT im age shows severe f attening o the anterior

and posterior tracheal walls with lum inal narrowing. B. Expiratory CT im age shows severe airway collapse.

carcinoma (SCC) is the m ost com m on prim ary tracheal neoplasm . It occurs m ost o ten in older m en and is associated with cigarette sm oking. In contrast, adenoid cystic carcinoma (ACC), a type o salivary gland neoplasm , occurs in younger adults with no sex predilection. On CT, SCC typically m ani ests as a polypoid, solitary lling de ects protruding into the tracheal lum en (Figure 6 -6 ). Direct extension into other m ediastinal structures such as the esophagus as well as m etastases to regional lym ph nodes m ay be apparent. Rarely, tracheal SCC can cause a di use in ltrative process characterized by di use irregular and nodular wall thickening on CT. ACC usually appears as a sm ooth ocal m ass on CT (Figure 6 -7). Up to hal o the tracheal circum erence can be involved, and the longitudinal extent o the tum or typically exceeds the cross-sectional extent. Metastases are uncom m on, but local recurrence can result because o incom plete resection.

Respiratory papillomatosis

A

B

Figure 6-5 Excessive Dynamic Airway Collapse A. Inspiratory CT image shows normal appearance o the trachea.

B. Expiratory CT im age shows severe collapse o the trachea with anterior bowing o the posterior tracheal m em brane (arrow).

Respiratory papillomatosis results rom the in ection with hum an papillom a virus (H PV), which typically occurs during birth. In m ost patients, in ection is lim ited to the larynx. Tracheal and bronchial involvem ent is rare and is characterized by orm ation o tiny endolum inal nodules (Figure 6 -8). Spread to the lung can occur and m ani ests as thin-walled cysts and nodules. Trans orm ation to SCC is an extrem ely rare com plication.

Di use Tracheal Disease Most di use tracheal diseases are inf am m atory processes and are o ten part o a system ic illness. Patients m ay present with signs and sym ptom s related to airway involvem ent, such as cough or dyspnea, or with other system ic m ani estations.

Chapter 6 Airways

Figure 6-6 Squamous Cell Carcinoma Contrast-enhanced CT im age shows a polypoid m ass (arrow) with irregular m argins and heterogeneous attenuation extending into and narrowing the tracheal lum en.

59

Figure 6-8 Respiratory Papillomatosis CT im age shows sm all m ural nodules (arrowheads) protruding into the tracheal lumen.

Relapsing polychondritis Relapsing polychondritis (RPC) is a systemic inf amm atory disorder o cartilage that prim arily a ects cartilages in the ears, nose, joints, and tracheobronchial tree. Respiratory tract involvement is the most comm on cause o morbidity and m ortality. In the early stages o RPC, the tracheal and m ain bronchial walls thicken with ongoing inf am mation. In the later course o the disease, the central airways becom e di usely narrowed, and the cartilaginous segm ents o ten calci y. CT shows di use large airway wall thickening and lum inal narrowing. Sparing o the posterior tracheal wall, which lacks cartilage, is characteristic and helps distinguish RPC rom other di use tracheal diseases (Figure 6 -9 ).

Granulomatosis with polyangiitis

Figure 6-7 Adenoid Cystic Carcinoma Contrast-enhanced CT image shows a smoothly marginated mass (arrow) in the right lateral wall o the trachea. The tumor extends circum erentially into the remainder o the tracheal wall (arrowheads).

Gran lomatosis with polyangiitis (GPA), orm erly known as Wegener granulom atosis, is a system ic vasculitis associated with C-ANCA and PR-3 autoantibodies. The kidneys, paranasal sinuses, and respiratory tract are com m only involved. Tracheal involvem ent m ost com m only occurs in the subglottic region and is characterized on CT by irregular, circum erential, and patchy wall thickening with variable degrees o stenosis (Figure 6 -10 ). Respiratory tract involvem ent in GPA can be lim ited to the airways or can include lung nodules and m asses with or without cavitation, consolidation, and ground-glass opacity.

60

Body CT: The Essentials

Figure 6-9 Relapsing Polychondritis Unenhanced CT image shows thickening o the tracheal wall with characteristic sparing o the posterior membrane (arrowhead).

A Figure 6-11 Tracheobronchial Amyloidosis A. Contrast-enhanced CT image shows circum erential thickening o the tracheal wall with several oci o calci cation (arrowheads).

Figure 6-10 Granulomatosis with Polyangiitis Unenhanced CT im age shows eccentric thickening (arrow) o the trachea with m oderate lum inal narrowing.

B B. Sagittal oblique re ormation shows di use tracheal involvement (arrows).

Chapter 6 Airways

61

Tracheobronchial amyloidosis

In ammatory bowel disease

Tracheobronchial amyloidosis is the m ost com m on orm o localized am yloidosis to a ect the respiratory tract. Characteristic CT ndings are di use, circum erential tracheobronchial wall thickening (Figure 6 -11). Calci cations are present in approxim ately 50 % o patients. Disease is usually lim ited to the large airways.

In ammatory bowel disease is an uncommon cause o pulmonary disease, but can a ect the tracheobronchial tree in a small number o patients. Di use sclerosing tracheobronchitis can develop with ulcerative colitis, independently o bowel activity and even years a ter colectomy. Patients with Crohn disease can develop a granulomatous tracheobronchitis.

Tracheobronchopathia osteochondroplastica

In ection

Tracheobronchopathia osteochondroplastica (TO) is a rare cause o signi cant tracheal narrowing and is characterized by small hamartomatous nodules arising in the tracheal rings. Most patients are older men with chronic obstructive lung disease. Like RPC, the posterior membrane is characteristically spared. Most patients are asymptomatic, but occasionally the size and extent o nodules can lead to obstructive signs and symptoms.

Respiratory tract viruses are the most com mon cause o large airway in ection in North Am erica. The subglottic trachea and larynx are most o ten involved, and narrowing or tissue edem a is typically occult on imaging. Endobronchial t berc losis usually involves the distal trachea and m ain bronchi. Initially, the airway walls become thickened and lum ens narrowed secondary to inf am mation and edem a. Contrast-enhanced CT m ay show wall enhancem ent. Findings o lung in ection need not be present. With healing, scar can develop and lead to stricture orm ation, typically a ecting a long segm ent. Other less com mon causes o large airway in ection include endem ic ungal in ection, aspergillosis (Figure 6 -12), zygomycosis, and Klebsiella rhinoscleromatis.

Sarcoidosis Although noncaseating granulomata are requently ound in the airways o patients with sarcoidosis, symptomatic large airway disease is uncom mon. Central airways can be compressed by adjacent enlarged lymph nodes. Mediastinal and hilar lymphadenopathy, bilateral perilym phatic lymphadenopathy, or both can help establish the diagnosis.

Br o n c h i Normal Anatomy The airways branch dichotom ously rom the trachea to the alveoli with approxim ately 23 generations. Bronchi contain both cartilage and brom uscular tissue. Central bronchi are nam ed by the respective lung, lobe, or segm ent they supply, sim ilar to the adjacent pulm onary artery (Figure 6 -13). As with the trachea, the central bronchi contain a posterior m em brane that norm ally bows orward on expiration.

Congenital Anomalies Tracheal bronchus Tracheal bronch s is anomalous origin o a bronchus rom the trachea, carina, or main bronchi (Figure 6 -14). The anom alous origin most o ten arises 2 cm rom the carina. The most comm on orm o a tracheal bronchus is a replaced right upper lobe apical segmental bronchus. Less o ten, the entire right upper lobe is supplied by a tracheal bronchus. Replaced tracheal bronchi are m ore than twice as comm on as supernum erary tracheal bronchi.

Cardiac bronchus

Figure 6-12 Endobronchial Aspergillosis Contrast-enhanced CT im age shows a branching tubular opacity (arrow), representing m ucus and debris. Aspergillus was detected on bronchoalveolar lavage f uid and culture.

A cardiac bronch s is a supernum erary bronchus that arises rom the in erom edial aspect o the bronchus interm edius that is directed toward the heart (Figure 6 -15). Reported incidence ranges rom 0 .0 7 to 0 .5%. Most o ten, it is a blind-ending diverticulum , but occasionally a cardiac bronchus supplies a ew secondary pulm onary lobules.

62 Body CT: The Essentials

A B

C

E Figure 6-13 Normal Bronchial Anatomy (A–H). Bronchus interm edius (BI), le t lower lobe basal trunk bronchus (LLLb), le t lower lobe superior segm ental bronchus (LLLs), le t m ain bronchus (LM), le t upper lobe in erior lingular bronchus (LULi), le t upper lobe lingular bronchus (LULl), le t upper lobe superior lingular bronchus (LULs), le t lower lobe anterom edial basal segm ental bronchus (LLLa), le t lower lobe lateral basal segm ental bronchus (LLLl), le t lower lobe posterior basal segm ental bronchus (LLLb), right lower lobe anterior basal segm ental bronchus (RLLa), right lower lobe basal trunk bronchus (RLLb), right lower lobe bronchus

D

F (RLL), right lower lobe lateral basal segm ental bronchus (RLLl), right lower lobe m edial basal segm ental bronchus (RLLm), right lower lobe posterior basal segm ental bronchus (RLLp), right lower lobe superior segm ental bronchus (RLLs), right m ain bronchus (RM), right m iddle lobe bronchus (RML), right m iddle lobe lateral segm ental bronchus (RMLl), right m iddle lobe m edial segm ental bronchus (RMLm), right upper lobe anterior segm ental bronchus (RULan), right upper lobe apical segm ental bronchus (RULa), right upper lobe bronchus (RUL), right upper lobe posterior segm ental bronchus (RULp), trachea (Tr).

Chapter 6 Airways

G

63

H

Figure 6-13 Normal Bronchial Anatomy (Continued )

Bronchial atresia

Bronchiectasis

Bronchial atresia describes ocal interruption o a segm ental airway with norm al developm ent o the distal airways. Airways distal to the atretic segm ent becom e dilated and lled with m ucus, orm ing a bronchocele (Figure 6 -16 ). Lung distal to the atresia lls via collateral f ow and becom es hyperinf ated secondary to air trapping. The le t upper lobe is m ost com m only a ected. Most o ten, bronchial atresia is an incidental nding.

Bronchiectasis is de ned as irreversible dilation o a bronchus and can be ocal or di use (Table 6 -2). In ection is the m ost com m on cause o bronchiectasis. Bronchiectasis is traditionally classi ed into cylindrical, varicose, and cystic types based on m orphology, although this distinction is less im portant than determ ining the cause, severity, and distribution. CT is the diagnostic study o choice or establishing a diagnosis o bronchiectasis. Bronchial dilation is de ned as internal bronchial diam eter greater than that o the diam eter o the adjacent pulm onary artery. However, bronchial dilation can occur in norm al individuals, particularly those

Figure 6-14 Tracheal Bronchus CT im age shows the right upper lobe bronchus (arrow) originating rom the trachea at the level o the aortopulm onary window.

Figure 6-15 Cardiac Bronchus CT im age shows a bronchus (arrow) arising rom the in erom edial aspect o the bronchus interm edius.

64

Body CT: The Essentials

Figure 6-16 Bronchial Atresia Contrast-enhanced CT im age shows several dilate, m ucous- lled bronchi (arrowheads) in the right lower lobe, which has di use air trapping. The right lower lobe bronchus was blind-ending.

living at higher altitudes, and as a norm al variant o ageing in older patients. Usually, abnorm ally dilated bronchi are associated with wall thickening, contour abnorm alities, and endobronchial debris. Other direct CT ndings include lack o tapering m ore than 2 cm distal to a bi urcation or bronchi touching the m ediastinal pleura or visible less than 1 cm rom the costal pleura. CT ndings o ten associated with bronchiectasis include tree-in-bud opacities distal to the abnorm al bronchus, m osaic attenuation, and atelectasis distal to abnorm al airways.

Cystic brosis Cystic f brosis (CF) is a common cause o chronic lung disease in children and young adults and the most common cause o respiratory ailure in this population. CF is caused by an autosomal recessive mutation in the CF transmembrane regulator (CFTR) protein that results in abnormally viscous mucus, decreased mucociliary clearance, and recurrent and chronic Tab

Figure 6-17 Cystic Fibrosis CT im age shows di use central bronchiectasis (arrows) with bronchial wall thickening and endobronchial debris. Background m osaic attenuation ref ects air trapping as a m ani estation o sm all airways involvem ent.

bacterial in ections. Most patients are diagnosed in childhood, but some CFTR mutations result in milder disease, which may not present until adulthood. Bronchiectasis is the hallmark o CF on CT (Figure 6-17). Bronchiectasis tends to be central with a mid and upper lung predominance, although all lobes are usually involved. Bronchial wall thickening, mucoid impaction, and mosaic attenuation may be present.

Allergic bronchopulmonary aspergillosis Allergic bronchop lmonary aspergillosis (ABPA) is characterized by hypersensitivity to endobronchial growth o Aspergillus fumigatus and eosinophilia. The majority o patients have asthma, but ABPA occurs in up to 10% o patients with CF. CT ndings o ABPA include central bronchiectasis (o ten varicose) and mucus plugging (Figure 6-18). High-attenuation

6-2. Causes o Bronchiectasis

Congenit l de ect

Mounie -Ku n synd ome Willi ms–C m bell synd ome

In ection

B cte i , mycob cte i

Dys unction mucocili y Cystic b osis cle nce Dyskinetic cili y synd ome Immunode ciency

h y og mm globulinemi , t ns l nt

h y e immunity

a lle gic b onc o ulmon y s e gillosis r eum toid t itis

In

l tion l inju y

a s i tion G st oeso ge l ef ux Smoke nd ume in l tion

Figure 6-18 Allergic Bronchopulmonary Aspergillosis Coronal re orm atted im age rom contrast-enhanced CT shows dilated bronchi with high-attenuation m ucus (arrowheads) and peripheral consolidation (arrow) in the le t upper lobe, the latter ref ecting associated eosinophilic pneum onia.

Chapter 6 Airways

65

Figure 6-20 Endobronchial Carcinoid Contrast-enhanced CT im age shows an ovoid, sm oothly m arginated enhancing nodule (arrowhead) in the le t upper lobe bronchus, resulting in le t upper lobe collapse (arrow).

Figure 6-19 Dyskinetic Cilia Syndrome Coronal re orm atted CT im age shows extensive basal predom inant bronchiectasis. Small centrilobular nodules are present in the le t upper lobe, and there is a background o m osaic attenuation rom patchy air trapping.

mucus, which is present in up to one-third o patients with ABPA, is highly suggestive o the diagnosis and is believed to be related to a high concentration o metal ions (e.g., calcium, iron) trapped in thick mucus. Tree-in-bud opacities, mosaic attenuation, and peripheral consolidation and ground-glass opacity may also accompany bronchiectasis.

Dyskinetic cilia syndrome Dyskinetic cilia syndrome (DKS), also known as prim ary ciliary dyskinesia, is characterized by decreased m ucociliary clearance and chronic sinopulm onary in ection as a result o abnorm al structure and unction o epithelial cilia. Bronchiectasis develops in a majority o patients, and approxim ately 50% o patients also have situs inversus totalis. Kartagener syndrome is a subtype o DKS that includes bronchiectasis, chronic sinusitis, and situs inversus totalis. CT shows bilateral bronchiectasis with a m id and lower lung zone predom inance (Figure 6 -19 ). Tree-in-bud opacities may also be present, ref ecting accompanying bronchiolitis.

Endobronchial Lesions Lung neoplasms L ng neoplasms account or the majority o endobronchial lesions in adults. SCC and adenocarcinoma occur m ost com m only in current or orm er sm okers. Patients m ay

present with hemoptysis, recurrent pneum onia, or new or worsening cough. On CT, a so t tissue attenuation endobronchial lesion m ay be apparent. More com mon, patients present with larger m asses, o ten with associated lymphadenopathy and obstructive atelectasis. Endobronchial carcinoid is the most com mon airway neoplasm in children and young adults. Most arise in the central bronchi, and patients can present with hem optysis or signs and sym ptom s related to obstruction. On CT, endobronchial carcinoids usually have smooth margins and are oriented along the long axis o the airway. They are o ten hypervascular on contrastenhanced CT (Figure 6 -20). Less comm on primary endobronchial neoplasm s include m ucoepiderm oid carcinoma, ACC, hamartoma, and lipom a. Endobronchial metastases can occur, especially with melanom a and adenocarcinom as.

Broncholith Broncholiths occur when an adjacent calci ed lymph node erodes into the airway lumen. Remote histoplasmosis is the most common cause, but tuberculosis, sarcoidosis, silicosis, and coal workers’ pneumoconiosis can also lead to broncholith ormation. Most patients develop signs and symptoms including chronic cough, recurrent in ection, hemoptysis, or lithoptysis (expectorating calci c ragments). On CT, broncholiths appear as a calci c attenuation body in the airway lumen (Figure 6-21). An extraluminal component may be apparent, and other calci ed lymph nodes are usually present.

Foreign bodies Aspirated oreign bodies are m ore com mon in children than adults, with ood being the m ost comm on in adults. Most aspirated oreign bodies are occult on radiography, so CT is usually per orm ed. CT may show a lling de ect within the airway or atelectasis or obstructive pneumonia distal to the lesion (Figure 6 -22). Expiratory CT m ay be help ul in localizing an endobronchial oreign body because it can show air trapping in the segment distal to the obstruction.

66

Body CT: The Essentials

Figure 6-21 Broncholith rom Remote Histoplasmosis Coronal oblique re ormatted im age rom unenhanced CT shows a portion o a calci ed subcarinal lym ph node (arrow) protruding into the bronchus interm edius.

Mucous pseudotumor Retained m ucus in the central airways is a com m on nding and is usually located dependently and has a characteristic low attenuation, bubbly appearance on CT (Figure 6 -23). However, mucus can occasionally m im ic an endobronchial

Figure 6-23 Mucous Pseudotumor Unenhanced CT im age shows low-attenuation m ucus (arrow) in the right m ain bronchus.

m ass lesion when it is thick and sticky. Rescanning the area in question ollowing vigorous coughing is usually su cient to distinguish a xed so t tissue lesion rom the m obile or expectorated m ucus.

Br o n c h io l e s Normal Anatomy Term inal (m em branous) and respiratory bronchioles are sm all airways that lack cartilage and subm ucosal glands. Term inal bronchioles are purely conducting airways that give rise to respiratory bronchioles, which are partially alveolated and participate in gas exchange. Although norm al bronchioles are below the resolution o CT, CT plays a central role in the evaluation o sm all airways diseases.

Bronchiolitis

Figure 6-22 Aspirated Straight Pin Causing Postobstructive Pneumonia Coronal re orm atted im age rom unenhanced CT shows a linear m etallic oreign body (arrow) in the le t m ain bronchus. Extensive le t lung consolidation (asterisk) is present.

Bronchiolitis describes a broad spectrum o inf ammatory and brotic diseases that a ect the bronchioles (Table 6-3). Several classi cation systems have been described on the basis o clinical eatures, histopathology, or CT ndings. Although the CT ndings o bronchiolitis will be emphasized in this chapter, integrating clinical and histopathologic in ormation can result in a more accurate diagnosis. Cell lar bronchiolitis is the most common orm o bronchiolitis

Chapter 6 Airways Tab

67

6-3. Types o bronchiolitis and com m on causes

In ection

r es i to y t ct vi us Mycob cte i Mycoplasma Aspergillus (es eci lly in immunocom omised)

r es i to y b onc iolitis

Cig ette smoking

Follicul b onc iolitis

r eum toid t itis Sjög en synd ome Immunode ciency C onic in ection

a s i tion b onc iolitis

Sw llowing diso de s Dementi Subst nce buse

h y e sensitivity neumonitis

B cte i , mycob cte i , ungi, vi n ntigens, low molecul weig t com ounds

Const ictive b onc iolitis

postin ectious In l tion o umes (NO 2, SO 2) G t-ve sus- ost dise se C onic llog t ejection in lung t ns l nt r eum toid t itis Inf mm to y bowel dise se D ug e ction

and is de ned by a preponderance o inf ammatory cells in and around the small airways. In ection is the most common cause o cellular bronchiolitis. CT mani estations o cellular bronchiolitis include poorly de ned or solid centrilobular nodules, tree-in-bud opacities, or both. Constrictive bronchiolitis (CB) describes brosis o the bronchioles that can cause

Figure 6-25 Mycobacterium avium Complex In ection CT im age shows scattered tree-in-bud opacities (arrowhead) and m iddle lobe and lingular bronchiectasis (arrows).

airway wall thickening with luminal narrowing ranging rom subtle to obliteration. Mosaic attenuation (air trapping on expiratory CT) is an indirect sign o CB on CT.

In ectious bronchiolitis A wide variety o organisms cause in ectious bronchiolitis including respiratory tract viruses, bacteria, mycobacteria, and ungi. Although CT generally per orms poorly in determ ining the causative organism , additional CT ndings m ay suggest a speci c diagnosis. For example, coexistent cavitary lesions, especially in the upper lobes or superior segm ents o the lower lobes suggest t berc losis (Figure 6 -24), whereas bronchiectasis in the m iddle lobe and lingula avors nont berc lo s mycobacterial in ection (Figure 6 -25). Mycoplasma should be suspected when centrilobular nodules and lobular ground-glass opacity are present.

Aspiration bronchiolitis Di se aspiration bronchiolitis (DAB) describes chronic bronchiolitis as a result o recurrent aspiration o oreign m aterial. The m ajority o patients have swallowing disorders. DAB should be suspected in patients with recurrent bronchopneum onia, especially in dependent portions o the lungs. CT ndings o DAB include centrilobular nodules, tree-in-bud opacities, and varying degrees o peribronchial consolidation (Figure 6 -26 ). Bronchiectasis m ay orm in the a ected areas with a long-standing disease.

H ypersensitivity pneumonitis

Figure 6-24 Tuberculosis CT im age shows extensive tree-in-bud opacities in the right upper lobe. Foci o bronchiectasis are also present, and there is a large cavity in the le t upper lobe.

Bronchiolitis is a central eature o hypersensitivity pne monitis (HP), a di use lung disease characterized by delayed-type hypersensitivity im m unologic response to an extrinsic inhaled antigen. The bronchiolitis com ponent is characterized by lym phocytic bronchiolitis with occasional loosely orm ed granulom ata. Com m on causes o H P include m icroorganism s associated with agriculture ( arm er’s lung), avian antigens (bird ancier’s lung), and

68

Body CT: The Essentials

Figure 6-26 Aspiration Bronchiolitis CT image shows extensive tree-in-bud opacities with relative sparing o the anterior middle lobe and lingula. Note the thickening o the esophagus (arrow) rom esophagitis and dysmotility.

Figure 6-28 Respiratory Bronchiolitis CT im age shows scattered poorly de ned centrilobular nodules (arrows) in the upper lobes.

nontuberculous m ycobacteria (hot tub lung and m etalworking f uid lung). The presence o di use poorly de ned centrilobular nodules on CT is highly suggestive o H P in the correct clinical setting (Figure 6 -27). Lobular areas o air-trapping or patchy ground-glass opacity urther support the diagnosis. The other m ani estations o H P are discussed in Chapter 5.

RB-ILD include upper lobe predom inant poorly de ned centrilobular nodules and patchy ground-glass opacity (Figure 6 -28). Patients with RB-ILD typically have m ore extensive disease, and CT ndings o RB are o ten incidentally detected in current or orm er sm okers.

Follicular bronchiolitis

Respiratory bronchiolitis (RB) is a condition o cigarette sm okers characterized by accum ulation o pigm ented m acrophages in and around the respiratory bronchioles. Mild chronic inf am m ation m ay be present. The vast m ajority o patients are asym ptom atic. RB-associated interstitial l ng disease (RB-ILD) develops in a very sm all num ber o sm okers, presents as dyspnea with m ild-to-m oderate restrictive physiology and decreased di usion capacity, and is characterized histopathologically by RB. CT ndings o RB/

Follic lar bronchiolitis (FB), also re erred to as pulm onary lym phoid hyperplasia, is characterized by orm ation o lym phoid ollicles around the airways. FB is associated with im m unode ciency, collagen vascular disease (especially rheum atoid arthritis and Sjögren syndrom e) and other autoim m une disorders, system ic hypersensitivity reactions, in ection, lym phoproli erative disorders, and other causes o chronic airway inf am m ation. CT ndings o FB include di use centrilobular nodules, patchy groundglass opacity, and peribronchial and subpleural nodules (Figure 6 -29 ).

Figure 6-27 Subacute Hypersensitivity Pneumonitis rom Exposure to Birds CT im age shows di use poorly de ned centrilobular nodules.

Figure 6-29 Follicular Bronchiolitis in Rheumatoid Arthritis CT im age shows centrilobular (arrows) and subpleural (arrowheads) nodules as well as bronchial wall thickening.

Respiratory bronchiolitis

Chapter 6 Airways

69

A

B

Figure 6-30 Constrictive Bronchiolitis rom Inf ammatory Bowel Disease A. Inspiratory CT im age shows m osaic attenuation and m ild

cylindrical bronchiectasis. B. Expiratory CT im age con rm s the presence o air trapping.

Dif use panbronchiolitis

CB) should be suspected i there is disproportionate involvem ent o one lobe. Di se idiopathic p lmonary ne roendocrine cell hyperplasia (DIPNECH) should be considered when scattered lung nodules are present.

Di se panbronchiolitis (DPB) a ects almost exclusively adults o Japanese heritage and is characterized by progressive bronchiolitis and chronic sinusitis. CT ndings are similar to other chronic airway disorders and include centrilobular nodules, tree-in-bud opacities, bronchiectasis and bronchial wall thickening, mosaic attenuation, and air trapping.

Constrictive bronchiolitis Constrictive bronchiolitis (CB) results in dyspnea, cough, and airf ow obstruction. Causes include in ection, drug reaction, chronic gra t-versus-host disease ollowing hematopoietic stem cell transplant, chronic allogra t rejection ollowing lung transplant, connective tissue disease, and inhalation injury. The diagnosis is o ten established by a com bination o CT and clinical ndings, as the disease may be missed on biopsy because o the patchy nature o the lesions and the di culty in recognizing obliterated bronchioles. The CT ndings o CB are mosaic attenuation on inspiratory CT and lobular air trapping on expiratory CT (Figure 6 -30). Bronchial dilation and wall thickening and bronchiectasis may also be present. Occasionally, centrilobular nodules are present. Swyer–James–MacLeod syndrom e (postin ectious

Su GGESTED READINGS 1. Abbott GF, Rosado-de-Christenson ML, Rossi SE, Suster S. Im aging o sm all airways disease. J Thorac Imaging. 20 0 9 ;24:285–29 8. 2. Boiselle PM. Im aging o the large airways. Clin Chest Med. 20 0 9 ;29 :181–19 3. 3. Ngo AV, Walker CM, Chung JH , et al. Tum ors and tum orlike conditions o the large airways. AJR Am J Roentgenol. 20 13;20 1(2):30 1–313. 4. Boiselle PM, O’Donnell CR, Bankier AA, et al. Tracheal collapsibility in healthy volunteers during orced expiration: assessm ent with m ultidetector. Radiology. 20 0 9 ;252(1):255–26 2. 5. Bonavita J, Naidich DP. Im aging o bronchiectasis. Clin Chest Med. 20 12;33(2):233–248. 6 . Bains SN, Judson MA. Allergic bronchopulm onary aspergillosis. Clin Chest Med. 20 12;33(2):26 5–281. 7. Javidan-Nejad C, Bhalla S. Bronchiectasis. Radiol Clin North Am. 20 0 9 ;47(2):289 –30 6 .

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Ch a p t e r

7

P

,D p

, nd C

W

Je rey P. Kanne, MD

I. PLEURA a. Anatomy b. Pleural E usion and Other Collections i. Pleural e usion ii. Hemothorax iii. Chylothorax iv. Empyema v. Pneumothorax vi. Bronchopleural and pleuroparenchymal f stula c. Pleural Neoplasm i. Solitary f brous tumor ii. Mesothelioma iii. Metastases iv. Lymphoma d. Miscellaneous i. Pleural plaques ii. Pleural thickening and f brothorax iii. Splenosis

Pl e u r a Anatomy Two pleural layers de ne the ple ral space. The par etal ple ra lines the m ediastinum , diaphragm , and inner surace o the thoracic wall and consists o a single layer o m esothelial cells and underlying supporting connective tissue and, along the chest wall, varying am ounts o extrapleural at. The v sceral ple ra is tightly adherent to the lung and contains underlying connective tissue and blood supply. The parietal pleura receives sensory neural input and derives its blood supply rom the system ic circulation. The visceral pleura lacks sensory neural input and derives its blood supply prim arily rom the bronchial arteries. The pleural space contains approxim ately 10 m L o uid, produced prim arily by the parietal layer, allowing the two layers o pleura to m ove sm oothly against each other during respiration.

II. DIAPHRAGM a. Anatomy i. Eventration ii. Hernia III. CHEST WALL a. Anatomy b. Chest Wall Masses i. Lipoma ii. Neurogenic tumors iii. Metastases iv. Primary malignancies v. Plasmacytoma and multiple myeloma vi. Miscellaneous c. Chest Wall In ection i. Actinomycosis ii. Nocardiosis iii. Tuberculosis iv. Postoperative in ection

The ple ral ss res are located between the lobes o the lung and are contiguous with the pleural space (Figure 7-1). Each ssure represents two layers o visceral pleura and the potential space between them. The m ajor or oblique ssures separate the lower lobes rom the remainder o the lung. The m inor or horizontal ssure separates the right upper and m iddle lobes. A range o accessory ss res has been described, with the right er or accessory ss re being the most comm on, occurring in approximately 10% to 15% o patients (Figure 7-2). Fissures are incom plete in the majority o patients, providing pathways or collateral air ow between the lobes and the direct spread o in ection or neoplasm . In contrast to other accessory ssures, the azy os ss re (Figure 7-3), which occurs in approxim ately 1% o patients, consists o our layers o pleura, two parietal and two visceral, and re ects a congenital m igration anom aly o the azygos vein. Although com m only re erred to as an

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72 Body CT: The Essentials

A

B

Figure 7-1 Normal Pulmonary Fissures Axial (A) and coronal re orm atted (B) CT im ages show the right

m ajor (thin arrow) and m inor (arrowhead) and le t m ajor (wide arrow) ssures.

“azygos lobe,” the partially isolated lung is just a norm al portion o the right upper lobe and has the expected vascular and bronchial supply. The er or p lmo ary l ame t (Figure 7-4) is orm ed by the junction o the visceral and parietal pleurae at the

hilum and separates the m edial aspect o the pleural space into the anterior and posterior com partm ents, although uid can accum ulate on both sides o the ligam ent. In eriorly, the in erior pulm onary ligam ent can widen and som etim es extend all the way to the diaphragm , where it joins the diaphragm atic pleura.

Pleural E usion and Other Collections Pleural e usion Ple ral ef s o s (Figure 7-5) result rom increased uid production, decreased resorption, or both. Congestive heart ailure, pneum onia, and m alignancy are the m ost com m on causes o pleural e usion. In addition, pleural e usions

Figure 7-2 Right In erior Accessory Fissure CT im age shows the norm al location o the in erior accessory ssure (arrow) joining the right m ajor ssure and partially separating the right lower lobe m edial basal segm ent rom the anterior basal segm ent.

Figure 7-3 Azygos Fissure Contrast-enhanced CT im age shows the azygos vein (arrow) passing through the right lung. The vein is extrapleural and is separated rom the lung by two layers o parietal pleura and two layers o visceral pleura.

Chapter 7 Pleura, Diaphragm, and Chest Wall 73

Figure 7-4 In erior Pulmonary Ligament CT im age shows the norm al appearances o the in erior pulm onary ligam ents (arrowheads) and the associated intersublobar septum (arrows).

can develop in the setting o large volum e abdom inal ascites when uid crosses the diaphragm through congenital de ects or via the lym phatics. CT is som etim es help ul in determ ining the likely cause o pleural e usion such as one associated with pneum onia. However, CT typically cannot determ ine whether or not a pleural e usion is transudative

Figure 7-6 Hemothorax Unenhanced CT im age shows a high-attenuation–loculated pleural collection (arrow). Note the presence o extrapleural at (arrowhead) super cial to the pleural blood collection in contrast to an extrapleural hem atom a, which can display extrapleural at internally.

versus exudative or sterile versus in ected. Thoracentesis, typically per orm ed under ultrasound guidance, is usually required to characterize a pleural collection.

Hemothorax Hemothorax is the accum ulation o blood in the pleural space and m ost com m only results rom thoracic traum a. Nontraum atic hem othorax is rare and can occur in the setting o m alignancy or pulm onary em bolism . Acute hem othorax is characterized by a high-attenuation pleural collection (usually between 30 and 70 Houns eld units) or a uid level in the pleural space (Figure 7-6 ). As blood products break down, a subacute hem othorax m ay be indistinguishable rom a sim ple pleural e usion. Pleural thickening with or without calci cation can develop as a consequence o hem othorax.

Chylothorax

Figure 7-5 Simple Transudative Pleural E usion Contrast-enhanced CT im age shows a sm all pleural e usion (asterisk) layering dependently.

Chylothorax re ers to accum ulation o uid with high triglyceride content in the pleural space. Approxim ately 50 % o chylothoraces result rom tum or, particularly lym phom a. Injury to the thoracic duct, m ost o ten during surgery, can also lead to chylothorax. When the lower thoracic duct is transected, an isolated le t chylothorax can develop. Isolated right chylothorax can orm when the upper thoracic duct is transected. Less com m on causes o chylothorax include slow leakage rom pleural lym phatics and m igration o chylous ascites rom the abdom en into the pleural space. Lym phangioleiom yom atosis, a rare lung disease characterized by di use cysts, can also produce chylothorax. Chylothorax m ay be indistinguishable rom a sim ple pleural e usion on CT. Rapid accum ulation and lower CT attenuation (less than water) m ay be suggestive.

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Figure 7-8 Spontaneous Pneumothorax Unenhanced CT image shows gas (asterisk) located nondependently in the le t pleural space. The thin visceral pleura (arrowhead) can be seen along the sur ace o the lung.

ropare chymal or ple rop lmo ary st la) as the result o traum a surgery, in ection, tum or, or radiation. In som e patients, the direct com m unication between airway and pleura is apparent on CT, especially on thin section reconstructions (Figure 7-9 ). Indirect clues include enlarging pneum othorax or ailure o pneum othorax to resolve Figure 7-7 Pneumonia and Empyema rom Streptococcus pneumoniae In ection Contrast-enhanced CT image shows heterogeneous consolidation with small pockets o gas (arrow) in the right lung with an adjacent pleural collection (asterisk). Note how the atelectatic right lower lobe (arrowhead) enhances homogeneously.

Empyema An empyema is an in ected pleural collection. Although CT can suggest the presence o em pyem a, direct uid sam pling is required to con rm the diagnosis. Findings on CT suggesting em pyem a include thickening and enhancem ent o the parietal and visceral pleura separated by uid (split pleura sign) and increased attenuation or haziness in the adjacent extrapleural at (Figure 7-7).

Pneumothorax P e mothorax is de ned as air within the pleural space (Figure 7-8). Causes include traum a, iatrogenic injury such as surgery or central venous catheter placem ent, ruptured subpleural bulla or bleb, in ection, and m alignancy. Radiography is usually suf cient or the detection and ollow-up o pneum othorax, but CT can be help ul to assess pleural drain position, to distinguish pneum othorax rom a large bulla, or when the pleura is obscured by extensive subcutaneous gas or other arti act.

Bronchopleural and pleuroparenchymal f stula The pleura can directly com m unicate with a peripheral airway (bro chople ral st la) or lung parenchym a (ple -

Figure 7-9 Bronchopleural Fistula Unenhanced CT image shows persistent right pneumothorax (asterisk) despite pleural drainage. Note the direct com m unication (arrow) between the right lower lobe and the pleural space.

Chapter 7 Pleura, Diaphragm, and Chest Wall 75 despite appropriate drainage, unexplained intrapleural gas, or developing em pyem a. Following pneum onectom y, the rem aining pleural space gradually lls with liquid. New or increasing gas in the pneum onectom y space indicates bronchopleural stula, usually the result o in ection at the bronchial stum p. In patients who ail percutaneous or surgical drainage, an open window thoracotom y (Clagett window or Eloesser ap) m ay be per orm ed by resecting a portion o the chest wall and m arsupializing the skin into the wound, allowing open drainage o the in ected pleural space. The space is m aintained with packing and can ultim ately be closed with a m uscle ap and skin gra t once the pleural in ection has cleared.

Pleural Neoplasm Solitary f brous tumor Sol tary bro s t mors (SFT) occur alm ost anywhere in the body, but the m ajority o them arise in the pleura (Figure 7-10 ). They develop rom m esenchym al cells below the m esothelium , o ten growing rom a stalk into the pleural space. SFTs m ay be large at presentation because o little or no sym ptom s. A sm all num ber o patients m ay present with paraneoplastic syndrom es such as digital clubbing or

Figure 7-11 Pleural Mesothelioma Contrast-enhanced CT im age shows a di use so t tissue rind (arrows) with an associated e usion in the le t pleural space.

sym ptom atic hypoglycem ia. Most have a benign course, but som e exhibit aggressive behavior such as local recurrence or invasion o the chest wall or m ediastinum . On CT, SFTs are usually hom ogeneous pleural so t tissue m asses, usually growing along the in erior and posterior aspects o the pleura or within a ssure. Larger SFTs m ay be m ore heterogeneous, re ecting areas o hem orrhage or necrosis. However, these ndings do not necessarily im ply m alignant behavior.

Mesothelioma Mesothel oma is the m ost com m on prim ary malignant neoplasm o the pleura and most o ten is a consequence o asbestos exposure with a latency o up to several decades. Accompanying pleural e usion is com mon, a ecting up to 9 5% o patients, and m ay be the only nding on im aging. Other CT ndings o mesotheliom a include di use nodular pleural thickening, including along the ssures (Figure 7-11). Other ndings on CT suggesting mesotheliom a include direct chest wall, m ediastinum, or diaphragmatic invasion; and bone or lym ph node metastases. Pleural plaques, which are a biom arker o asbestos exposure, are present in the contralateral hemithorax only in approxim ately hal o the patients. The sarcom atoid variant o m esothelioma m ay contain large masses or areas o calci cation, ossi cation, or at rom various types o dedi erentiation. Figure 7-10 Solitary Fibrous Tumor o the Pleura Contrast-enhanced CT im age shows a biconvex so t tissue m ass in the posterior right hem ithorax. Note how the m ass orm s obtuse angles (arrows) with the adjacent chest wall, indicating an extrapulm onary location.

Metastases Metastases com prise the m ajority o m alignant pleural neoplasm s (Figure 7-12), with lung cancer being the m ost com m on cause o pleural m etastases. Other neoplasm s that com m only m etastasize to the pleura are adenocarcinom as

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Figure 7-12 Breast Carcinoma Metastatic to the Pleura Unenhanced CT im age shows a sm all right pleural e usion (asterisk). Nodular thickening o the m ediastinal pleura (arrow) is highly suggestive o m alignant pleural disease.

Figure 7-13 Pleural Lymphoma Unenhanced CT im age shows a large right pleural e usion and several nodular oci o pleural so t tissue (arrows).

o the breast, gastrointestinal tract, and ovary, usually by hem atogenous seeding o the pleura, o ten directly rom the adjacent lung. CT shows sm all, lenticular nodules orm ing obtuse m argin with the chest wall. Pleural e usions are requently present. Adding a slight delay to scanning, ollowing intravenous contrast m aterial injection m ay m ake enhancem ent o pleural m etastases m ore conspicuous.

Pleural thickening and f brothorax Focal and di use ple ral th cke can be the result o empyema, hemothorax, organizing e usion, or instrumentation.

Lymphoma Although the pleura can be the sole site o lymphoma, direct extension rom the m ediastinum or chest wall is m ore com m on. Both Hodgkin and non-Hodgkin lym phom a can involve the pleura. On CT pleural lym phom a can m ani est as a solitary pleural m ass or extensive pleural thickening (Figure 7-13).

Miscellaneous Pleural plaques H yalinizing ple ral plaq es are a biom arker o asbestos exposure, usually developing 20 years a ter exposure (Figure 7-14). They orm on the parietal pleura along the diaphragm as well as anterolateral, posterior lateral, and paraspinal aspects o the m id thorax. Plaques are usually bilateral and have varying degrees o calci cation.

Figure 7-14 Asbestos-related Pleural Plaques Unenhanced CT im age shows bilateral high-attenuation plaques (arrows) along the costal m argin. Note the m esa- or table-like con guration.

Chapter 7 Pleura, Diaphragm, and Chest Wall 77

Figure 7-15 Fibrothorax Contrast-enhanced CT im age shows di use pleural thickening and calci cation (arrows). Note decreased volum e in the le t hem ithorax. H ypertrophy o the extrapleural at (arrowhead) typically indicates a long-standing in am m atory process.

When circum erential, di use pleural thickening is re erred to as a brothorax and results in a restrictive e ect on the underlying lung (Figure 7-15). Extensive calci cation can develop and commonly is associated with remote empyema or hemothorax.

Splenosis Thoracic sple os s occurs as a result o im plantation o the splenic tissue in the chest ollowing injury to the diaphragm and spleen (Figure 7-16 ). Nodules o splenic tissue develop blood supply rom the pleural vessels and m ani est on CT as homogeneous pleural nodules with similar attenuation and enhancement as spleen. Clues to the diagnosis include a history o traum a to the ipsilateral side, surgically absent spleen, abdom inal splenosis, and diaphragm atic de ect. A nuclear m edicine sul ur colloid study is diagnostic when the diagnosis is in doubt.

Dia Ph r a g m Anatomy The diaphragm is the prim ary m uscle o respiration and also serves as a barrier between the chest and the abdom en. Muscle bers attach to the chest wall. CT is very use ul or

Figure 7-16 Pleural Splenosis rom Remote Trauma with Splenic Rupture Coronal re orm atted unenhanced CT im age shows colon and at herniating through a diaphragm atic de ect (arrowheads). The pleural nodule (arrow) represents splenic tissue that seeded the pleural space at the time o injury. In cases where the diagnosis is unclear, a sul ur colloid scan is diagnostic.

evaluating the diaphragm , particularly with the use o sagittal and coronal re orm ations.

Eventration Diaphragm atic eve trat o is a ocal bulge resulting rom a congenital thinning o the m uscle (Figure 7-17). Typically, only a portion o the hem idiaphragm is involved, m ost o ten the anterom edial aspect o the right hem idiaphragm . On CT, a sharp transition m ay be apparent at the edge o the eventration. Diaphragm atic eventration can be m istaken or diaphragm atic hernia.

Hernia D aphra mat c her as can be congenital or acquired. Bochdalek her as (Figure 7-18), which account or 9 0 % o congenital diaphragm atic hernias, likely result rom a de ect in the pleuroperitoneal olds. They occur m ost com m only and, depending on the de ect size, can contain retroperitoneal at, stom ach, bowel, liver, spleen, and kidney. In adults, the vast m ajority o posterior diaphragm atic de ects are m ore likely acquired than congenital with increasing incidence with age, weight, and chronic obstructing pulm onary disease. Mor a her as are located anterom edially, m ost o ten on the right, and occur with ailure o the

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Body CT: The Essentials

B

A

Figure 7-17 Diaphragmatic Eventration Axial (A) and sagittal re orm atted (B) unenhanced CT im ages show an elevated but intact right hem idiaphragm (arrows).

A Figure 7-18 Bochdalek Hernia Axial (A) and sagittal re orm atted (B) unenhanced CT im ages

B show a ocal posterior de ect (arrow) in the posterior le t hem idiaphragm with upward herniation o perinephric at.

Chapter 7 Pleura, Diaphragm, and Chest Wall 79

A

B

Figure 7-19 Morgagni Hernia Axial (A) and coronal re orm atted (B) contrast-enhanced

CT im ages show herniation o colon (arrow) through an anterom edial de ect (arrowhead) in the right hem idiaphragm .

transverse septum to use to the lateral body (Figure 7-19 ). They account or ewer than 10% o congenital diaphragm atic hernias and m ay also be acquired, as there is an association with obesity. Most occur on the right and contain at covered by peritoneum and parietal pleura. Transverse colon and, less com m only, other upper abdom inal organs can be contained in the hernia sac. H atal her as are com m only encountered in routine CT scanning o the chest. Two m ain types o hiatal hernias occur. The sliding-type hiatal hernia accounts or 9 5% o all hiatal hernias and is characterized by intrathoracic displacem ent o the esophagogastric junction. In paraesophageal hernias, the esophagogastric junction and gastric cardia

rem ain subdiaphragm atic whereas the undus and som etim es the rem ainder o the stom ach herniate into the chest through a de ect in the phrenicoesophageal m em brane.

A

B

Figure 7-20 Normal Chest Wall Anatomy (A–D). Contrast-enhanced CT im ages show normal chest wall anatom y. Anterior scalene (As), in raspinatus (IS), intercostal m uscles (IC), latissim us dorsi (LD), m iddle scalene (Ms),

pectoralis m ajor (PM), pectoralis m inor (Pm), serratus anterior (SA), subscapularis (SSc), supraspinatus (SS), teres m inor (Tm), trapezius (TR). (continued )

Ch e s t Wa l l Anatomy The chest wall (Figure 7-20) consists o the ribs, sternum, thoracic spine, thoracic as well as the surrounding musculature, at, skin, ascia, and supplying nerves, arteries, and veins. The ax lla is bound by the pectoralis major and minor muscles anteriorly and by the subscapularis, teres major, and

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Body CT: The Essentials

C Figure 7-20

(Continued)

latissimus dorsi muscles posteriorly. The axilla contains lymph nodes, the brachial plexus, and the axillary artery and veins. The external, internal, and innerm ost tercostal m scles are located between the ribs. The intercostal nerve, artery, and vein course between the internal and innerm ost intercostal m uscles along the undersur ace o the ribs. Although breast tissue is readily apparent on CT, it is best evaluated with m am m ography and, when appropriate, MRI and ultrasound.

D

Primary malignancies Prim ary chest wall m alignancies are ar less com m on than m etastases, and prim ary m alignant so t tissue neoplasm s (Figure 7-25) occur m ore requently than prim ary m alignant bone neoplasm s. Cho drosarcoma (Figure 7-26 ) is the m ost com m on prim ary chest wall m alignant neoplasm and usually arises rom the anterior chest wall. Malignant neoplasm s o the Ew am ly o sarcomas are rare and

Chest Wall Masses Patients with palpable chest wall m asses are o ten rst evaluated with CT. A m etallic BB or other m arker should be placed on the palpable abnorm ality at the tim e o im aging.

Lipoma L poma (Figure 7-21) is the m ost com m on benign neoplasm o the chest wall. Lipom as can be subcutaneous and palpable or intram uscular and incidentally detected on CT. They have characteristic hom ogeneous at attenuation and a thin capsule. The presence o so t tissue elem ents or localized pain should raise the suspicion o a liposarcom a.

Neurogenic tumors Sim ilar to the posterior m ediastinum , neurogenic tum ors such as schwa oma (Figure 7-22) and e ro broma can occur in the chest wall, m ost com m only arising rom the intercostal nerves.

Metastases Metastases (Figures 7-23 and 7-24) are the m ost com m on m alignant neoplasm s o the chest wall. They usually develop in the advanced stages o m alignancy. Bone m etastases are the m ost com m on and can be either lytic or blastic. Early m etastases to bone m arrow m ay be occult on CT but readily apparent on FDG PET or MRI.

Figure 7-21 Intramuscular lipoma Contrast-enhanced CT im age shows a hom ogeneous atty m ass (arrow) in the right lateral chest wall.

Chapter 7 Pleura, Diaphragm, and Chest Wall 81

Figure 7-22 Intercostal Schwannoma Contrast-enhanced CT im age shows a hom ogeneous so t tissue m ass (arrow) arising rom the undersur ace o a rib.

highly aggressive, and can develop in the chest wall o young adults.

Figure 7-24 Chest Wall Metastases rom Renal Cell Carcinoma nenhanced CT im age shows so t tissue m asses (arrows) in the right lateral chest wall involving the ribs, extrapleural and intercostal spaces, and extending into m ore super cial m usculature (arrowhead).

Plasmacytoma and multiple myeloma Plasmacytoma (Figure 7-27) and m yelom atous lesions can occur anywhere in the chest wall, particularly in the bones. They typically m ani est as expansile, destructive lesions, but occasionally can have a perm eative appearance.

Figure 7-23 Intramuscular Renal Cell Carcinoma Metastasis Contrast-enhanced CT shows an intram uscular hypervascular so t tissue nodule (arrow) in the le t lateral chest wall.

Figure 7-25 So t tissue Sarcoma Unenhanced CT im age shows an encapsulated so t tissue m ass (arrow) in the le t axilla. Note the intram uscular lipom a (arrowhead) in the pectoralis m ajor.

82 Body CT: The Essentials

Figure 7-26 Chondrosarcoma Contrast-enhanced CT image shows an expansile, destructive mass (arrow) containing cartilaginous matrix arising rom the sternum.

Miscellaneous Sebaceo s cyst On CT, sebaceo s cysts are ound just deep to the skin and have low attenuation and a thin capsule.

Elasto broma dors Elasto broma dors (Figure 7-28) are benign pseudotum ors o broelastic tissue that m ost com m only occur in the subscapular region and are benign in approxim ately 50 % o patients. On CT, elastobrom as have sim ilar attenuation to skeletal m uscle and contain streaks o at. They occur m uch m ore requently in wom en.

Figure 7-28 Elastof broma Dorsi Contrast-enhanced CT im age shows bilateral so t tissue m asses (arrows) deep in the latissim us dorsi m uscles just below the scapulae. Note the attenuation sim ilar to m uscle and the presence o at.

that occurs in the deep so t tissues. Nearly a quarter o desmoids occur in the chest wall, particularly around the shoulder, and there is emale preponderance. These in ltrative lesions are prone to local recurrence ollowing resection.

Chest Wall In ection Chest wall in ections can occur rom direct extension rom adjacent lung in ection (Figure 7-29 ), hematogenous spread o pathogens, or as a com plication o traum a or surgery.

F bromatos s (desmo d) Deep (m sc loapo e rot c) bromatos s, or desmo d, is a benign, rare broelastic proli eration

Figure 7-27 Plasmacytoma Contrast-enhanced CT im age shows an expansile, destructive m ass (arrow) in the sternal body.

Figure 7-29 Empyema Necessitatis Contrast-enhanced CT im age shows a com plex le t pleural collection containing liquid and gas. The collection extends through a chest wall de ect (arrow) into the chest wall (asterisk).

Chapter 7 Pleura, Diaphragm, and Chest Wall 83

Tuberculosis Mycobacterium tuberculosis in ection can extend rom in ected lung or pleura (em pyem a necessitatis) or be a localized in ection. Cutaneous stulae are not uncom m on. Hem atogenous dissem inated can result in tuberculous spondylitis (Pott disease) with paraspinal abscess.

Postoperative in ection Chest wall in ection can com plicate sternotom y and thoracotom y. Com m on organism s include Staphylococcus aureus, Staphylococcus epidermidis, and Pseudomonas aeruginosa. Risk actors include obesity, tobacco abuse, diabetes m ellitus, and chronic obstructive lung disease. Su g g ESTED READi n g S 1. Nam SJ, Kim S, Lim BJ, et al. Im aging o prim ary chest wall tum ors with radiologic-pathologic correlation. Radiographics. 20 11;31(3):749 –770 . 2. Ayres J, Gleeson F. Im aging o the pleura. Semin Respir Crit Care Med. 20 10 ;31(6 ):6 74–6 88.

Figure 7-30 Actinomycosis Contrast-enhanced CT im age shows a low attenuation so t tissue m ass (arrow) extending rom the right m iddle lobe, through the adjacent rib, and into the anterior chest wall so t tissues.

Actinomycosis Chest wall in ection with Actinomyces species is typically the result o direct extension rom a lung abscess (Figure 7-30 ). Risk actors include poor dentition, aspiration, and recent dental procedures with m icroaspiration.

Nocardiosis Sim ilar to actinom ycosis, chest wall in ection with Nocardia asteroides complex typically results rom direct extension rom lung in ection. In contrast, however, patients typically have cell-m ediated im m une de ciency such as solid organ transplant or long-term high-dose corticosteroid use.

3. Kanne JP, Yandow DR, Moham m ed TL, Meyer CA. CT ndings o pulm onary nocardiosis. AJR Am J Roentgenol. 20 11;19 7(2):W26 6 –W272. 4. Chelli Bouaziz M, Jelassi H , Chaabane S, Ladeb MF, Ben Miled-Mrad K. Im aging o chest wall in ections. Skeletal Radiol. 20 0 9 ;38(12):1127–1135. 5. Morris BS, Maheshwari M, Chalwa A. Chest wall tuberculosis: a review o CT appearances. Br J Radiol. 20 0 4;77(9 17):449 –457. 6 . Gallardo X, Castañer E, Mata JM. Benign pleural diseases. Eur J Radiol. 20 0 0 ;34(2):87–9 7. 7. Helm EJ, Matin TN, Gleeson FV. Im aging o the pleura. J Magn Reson Imaging. 20 10 ;32(6 ):1275–1286 . 8. Cardillo G, Lococo F, Carleo F, Martelli M. Solitary brous tum ors o the pleura. Curr Opin Pulm Med. 20 12;18(4):339 –346 . 9 . Gill RR. Im aging o m esotheliom a. Recent Results Cancer Res. 20 11;189 :27–43. 10 . Roberts H C. Im aging the diaphragm . Thorac Surg Clin. 20 0 9 ;19 (4):431–450 . 11. Mullins ME, Saini S. Im aging o incidental Bochdalek hernia. Semin Ultrasound CT MR. 20 0 5;26 (1):28–36 .

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Ch a p t e r

8

H a ta

Th

ac c A ta

Eugene Lin, MD Je rey P. Kanne, MD

I. CARDIAC CT: TECHNICAL FACTORS a. Temporal Resolution b. Radiation Dose, Temporal Resolution, and Heart Rate c. Prospective Triggering versus Retrospective Gating II. PATIENT PREPARATION III. CORONARY CT ANGIOGRAPHY: INDICATIONS IV. CORONARY ARTERIAL ANATOMY a. Le t Main Coronary Artery b. Le t Anterior Descending Artery c. Le t Circumf ex Artery d. Right Coronary Artery e. Coronary Artery Anomalies V. MYOCARDIUM a. Myocardial Ischemic b. Neoplasms i. Myxoma ii. Papillary f broelastoma iii. Angiosarcoma c. Miscellaneous i. Lipomatous hypertrophy o the interatrial septum

CAr d iAC CT: Te CH n iCAl FACTo r s The CT technology and dose-reduction techniques relevant to cardiac CT are discussed in Chapters 1 and 2. There are two additional technical actors that are specif cally relevant to cardiac CT: tem poral resolution and gating.

Temporal Resolution Tem poral resolution is the ability to resolve ast-m oving objects; it is com parable to shutter speed or a cam era. For m ost applications o CT, tem poral resolution is o little

VI. PERICARDIUM a. Anatomy b. Pericardial E usion c. Hemopericardium d. Pericardial Thickening e. Pericardial Cyst . Pericardial Neoplasm VII. THORACIC AORTA a. Anatomy b. Congenital i. Aberrant right subclavian artery ii. Right aortic arch iii. Double aortic arch iv. Cervical aortic arch v. Other aortic arch anomalies vi. Coarctation and hypoplasia vii. Pseudocoarctation c. Aortic Aneurysm d. Acute Aortic Syndrome i. Acute aortic dissection ii. Intramural hematoma iii. Penetrating atherosclerotic ulcer e. Aortitis i. Takayasu arteritis ii. Giant cell arteritis

im portance as the structures im aged have m inim al or no m otion. However, tem poral resolution is vital during cardiac CT. The coronary arteries are optimally evaluated when there is the least cardiac m otion. This occurs during the “rest” periods, which are typically in m id-diastole (diastasis). The tim e o diastasis shortens substantially as heart rate increases. Thus, low heart rates are optim al or cardiac CT. As current generation CT scanners have minim um gantry rotation times o around 270 m s and the m ean duration o the cardiac rest period is around 120 m s, urther techniques are necessary to adequately im age the coronary arteries. 85

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Body CT: The Essentials

High tem poral resolution in cardiac CT is prim arily achieved through partial sca reco structio , where im ages are reconstructed rom a 180 -degree gantry rotation. In noncardiac CT, high tem poral resolution is not needed, and im ages are reconstructed rom a ull 36 0-degree gantry rotation. Using partial scan reconstruction will alm ost double the tem poral resolution. Dual-source CT scanners have double the tem poral resolution o single-source scanners.

Radiation Dose, Temporal Resolution, and Heart Rate During a helical retrospectively gated study that im ages the heart throughout the cardiac cycle, all phases o the heart should be seen by the detector at any z-axis rotation. For this to occur in conjunction with partial scan reconstruction, the table cannot m ove quickly or there will be gaps in the acquired data. Thus, cardiac CT is typically per orm ed with a low pitch. As pitch is inversely related to radiation dose, helical retrospectively gated CT m ay be associated with high radiation doses. The tem poral resolution, radiation dose, and heart rate are interrelated. Although it is generally desirable in term s o im age quality to scan at lower heart rates, high heart rates m ay allow or dose reduction with dual-source CT. At higher heart rates, the R-R interval is shorter, and it takes less tim e to acquire data rom all phases o the cardiac cycle. Thus, cardiac CT can potentially be per orm ed at a higher pitch at higher heart rates, which would lower radiation dose. However, single-source CT scanners typically do not have the tem poral resolution to scan at high heart rates. A dual-source scanner with higher tem poral resolution would allow the heart to be im aged at higher heart rates, which allows pitch to be increased and lowers radiation dose. Nevertheless heart rate reduction has som e advantages in term s o dose reduction: it will allow or certain dosereduction techniques, such as prospective triggering, tube current modulation, and single volum e data acquisition to be m ore optim ally used. For exam ple, i tube current m odulation is em ployed, the relative length o time that the current is reduced is longer with lower heart rates.

Prospective Triggering Versus Retrospective Gating In a helical retrospectively gated study, the heart is im aged throughout the cardiac cycle. The coronary arteries are typically viewed during diastole where there is the least m otion, and the rem aining portion o the data can be used to evaluate unction or is not used at all. With prospective electrocardiographic triggering (step and shoot m ode) the x-ray tube is only turned on during a prede ned phase (typically in diastole) o the R-R interval, and data are only available rom this speci c phase. This technique is associated with signi cantly lower radiation doses than retrospective gating, but unctional data are not available. Prospective trig-

gering is optim ally used with a low and regular heart rate. Prospective triggering is optim ally suited or 256 - and 320slice scanners that can cover the craniocaudal dim ension o the heart in one rotation; this allows or im aging o the heart within the span o a single heartbeat.

PATie n T Pr e PAr ATio n A low heart rate, as previously noted, will increase the duration o the cardiac rest period and, thus, decrease m otion arti acts and also allow or som e dose-reduction techniques to be optim ally em ployed. Ideally, the heart rate should be less than 6 0 beats/ m inute or both optim al im age quality and reduction o radiation dose. However, studies with su cient im age quality can be obtained at substantially higher heart rates with the higher tem poral resolution o dual-source CT scanners. In addition, radiation dose can be m inim ized during retrospectively gated dual-source CT by utilizing a higher pitch at these high heart rates. Beta-blocker adm inistration is o ten used to reduce heart rate during coronary CT angiography (CCTA). Oral m etoprolol can be adm inistered 1 hour be ore the study. I the target heart rate is not achieved, intravenous m etoprolol or esm olol can be adm inistered. A sam ple protocol would be to adm inister 5 m g o intravenous m etoprolol, ollowed by 2.5 to 5 gm each 5 m inutes as needed, with a m axim um o 30 m g. Side e ects o beta blockers include bronchospasm , bradycardia, atrioventricular block, hypotension, allergic reaction, and Raynaud phenom enon. Contraindications to beta-blocker adm inistration are: Severe chronic obstructive pulm onary disease or asthm a Atrioventricular block type II Mobitz or type III Severe bradycardia (heart rate < 50 beats/ m inute) Severe hypotension (systolic blood pressure < 100 m m H g) Acute congestive heart ailure Allergy to beta blockers In addition, beta blockers m ay trigger or aggravate sym ptom s o aortic stenosis, carotid stenosis, and pulm onary em bolism . It should be noted that beta-blocker adm inistration can potentially dim inish the value o ventricular unction analysis as it can lower ejection raction, stroke volum e, and cardiac output.

Co r o n Ar y CT An g io g r APH y : in d iCATio n s The ollowing indications were considered appropriate or CCTA in 20 10 appropriateness criteria: • Detection o CAD in sym ptom atic patients without known heart disease, either nonacute or acute presentations. • Detection o CAD in patients with new onset or newly diagnosed clinical heart ailure and no prior CAD. • Preoperative coronary assessm ent prior to noncoronary cardiac surgery.

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• Patients with prior ECG exercise testing—norm al test with continued sym ptom s or interm ediate risk Duke treadm ill score. • Patients with prior stress im aging procedures—discordant ECG exercise and im aging results or equivocal stress im aging results. • Evaluation o new or worsening sym ptom s in the setting o a past norm al stress im aging study. • Risk assessm ent post revascularization—sym ptom atic i post coronary artery bypass gra ting or asym ptom atic with prior le t m ain coronary stent greater than or equal to 3 m m . In general, CCTA should be per orm ed in sym ptom atic patients with low or interm ediate probability o disease. It is not currently indicated or asym ptom atic people. Measurem ent o coronary calcium m ay be appropriate or risk strati cation in asym ptom atic patients at interm ediate risk.

Co r o n Ar y Ar Te r iAl An ATo m y The le t anterior descending artery (LAD) and posterior descending artery (PDA) run in the anterior and posterior interventricular grooves, respectively. The circumf ex and right coronary artery (RCA) run in the atrioventricular groove. Coro ary domi a ce typically re ers to the artery rom which the PDA originates.

Figure 8-2 Le t-dominant System Volum e-rendered CT im age dem onstrates a le t-dom inant system with the posterior descending artery (arrowhead) and a posterolateral branch (white arrow) arising rom the circum f ex artery (black arrow).

Right domi a t (89%) (Figure 8-1): Both the PDA and the posterolateral le t ventricular branches arise rom the RCA. Le t domi a t (8%) (Figure 8-2): Both the PDA and the posterolateral branches arise rom the circum f ex. Codomi a t (3%) (Figure 8-3): The PDA arises rom the RCA. The posterolateral branches arise rom the circum f ex.

Le t Main Coronary Artery The le t m ain coronary artery is short and usually bi urcates into the LAD and the circum f ex (Figure 8-4). In approxim ately 30 % o cases the le t m ain artery will tri urcate, with a ramus i termedius artery between the LAD and the circum f ex. The ram us interm edius artery will supply a lateral wall territory between the rst diagonal and the rst obtuse m arginal territories.

Le t Anterior Descending Artery The LAD is variable in length and can term inate be ore the apex, supply the apex, or supply the distal in erior wall. The LAD gives rise to diago al branches supplying the anterolateral wall and to septal per orators supplying the interventricular septum . Figure 8-1 Right-dominant System Volum e-rendered CT im age o the right coronary artery dem onstrates a right-dom inant system with right ventricular (acute) m arginal (long arrows), posterior descending artery (short arrow), and posterior ventricular (arrowhead) branches.

Le t Circum ex Artery The le t circum f ex artery gives o obtuse margi al branches that supply the posterolateral wall. In m any cases, particularly in a right-dom inant system , the rst obtuse

88 Body CT: The Essentials m arginal branch will be larger than the circum f ex. The circum f ex artery is the vessel that rem ains in the atrioventricular groove.

Right Coronary Artery

Figure 8-3 Codominant System Volum e-rendered CT im age dem onstrates a codom inant system with the posterior descending artery (arrow) arising rom the right coronary artery and a posterior ventricular branch (arrowhead) arising rom the circum f ex.

A Figure 8-4 Le t Coronary Arteries Volum e-rendered (A) and m ultiplanar reconstruction (B) CT im ages in two patients dem onstrate the le t anterior

There are two arteries that can arise rom the proxim al RCA (Figure 8-5). The rst branch o the RCA is o ten the co us artery. In 50 % o cases, the conus artery arises rom the RCA, in the other cases, it arises rom the aorta. The conus artery heads anteriorly toward the co us (right ventricular outf ow tract). The second branch o the RCA is o ten the si oatrial (SA) odal artery. In 55% o cases, the SA nodal artery arises rom the RCA, in the other cases, it arises rom the circum f ex. The SA nodal artery heads posteriorly toward the SA ode. The SA node is located in the superior aspect o the crista termi alis o the right atrium (Figure 8-6 ) (near the junction o the superior vena cava and the right atrium ). The crista term inalis is a vestigial rem nant located between the right atrial appendage and the sinus venosus. The crista term inalis can result in a right atrial “pseudom ass” on CT. The branches rom the RCA are called acute margi al or right ve tricular margi al arteries. However, the acute m arginal branch is also used to re er to the largest m arginal artery that arises at the in erior aspect o the right border o the heart, coursing toward the apex.

B descending artery (1), rst septal per orator (2), rst diagonal (3), ram us interm edius (4), circum f ex artery (5), and rst obtuse m arginal (6).

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At the in erior aspect o right atrioventricular groove, the right coronary artery, i dom inant, bi urcates into the PDA and posterolateral le t ve tricular bra ch. The PDA runs along the undersur ace o the heart in the posterior interventricular groove and gives rise to septal per orators supplying the posterior third o the interventricular septum . The posterolateral branch supplies the posterior and lateral le t ventricular walls. The atriove tricular (AV) odal artery arises rom the RCA in m ost cases, but can also arise rom the circum f ex or rom both the RCA and circum f ex. I it arises rom the RCA, it typically originates rom the proxim al posterolateral branch. It heads superiorly through the septum to the AV ode, which is in the in erior aspect o the interatrial septum .

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Figure 8-5 Conus and Sinoatrial Node Arteries A. Axial m axim um intensity projection im age dem onstrates the conus artery (arrow) arising rom the right coronary artery. B. Axial m axim um intensity projection im age dem onstrates the sinoatrial node artery (arrow) arising rom the right coronary artery. C. Volum e-rendered CT im age o the right coronary artery dem onstrates the conus artery (arrow) heading anteriorly and the sinoatrial node artery (arrowhead) heading posteriorly.

Coronary Artery Anomalies Coronary artery anom alies can be broadly classi ed as anom alies o origin, anom alies o course, and anom alies o term ination. In anom alous cases, the coronary arteries should be identi ed by their location rather than by their origin or speci c branches. The right coronary artery lies in the right atrioventricular groove and supplies the right ventricular ree wall. The LAD lies in the anterior interventricular groove and supplies the anterior interventricular septum (the LAD need not give rise to the diagonal bran ches). The le t circum lex artery lies in the le t atrioventricular groove and supplies the le t ventricular ree wall.

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Body CT: The Essentials

Figure 8-6 Crista Terminalis Axial CT im age dem onstrates the crista term inalis (arrow) in the superior right atrium .

Most anom alies are incidental ndings but m ay be im portant during surgical planning to avoid accidental vascular injury. Only a ew anom alies are potentially m alignant, with the potential to result in ischem ia, in arction, or sudden cardiac death. These include origin o artery rom the opposite coronary sinus with interarterial

A Figure 8-7 Anomalous Le t Coronary Artery A. Axial CT demonstrates the le t main coronary artery (arrow) arising rom the right coronary sinus with a common origin with the

course, pulm onary artery origin, and coronary artery stulae. Patients with anom alous coronary artery origin rom the pulm onary arteries show sym ptom s in in ancy or early childhood. Origin o the le t coronary artery rom the right coronary sinus, with an i terarterial course between the aorta and pulm onary artery (Figure 8-7) has the highest association with ischem ia, in arction, and sudden cardiac death, particularly related to exercise. Origin o the RCA rom the le t coronary sinus with an interarterial course (Figure 8-8) is also potentially m alignant, but is less o ten associated with m ortality. The anom alous coronary arteries can also take a retroaortic, prepulmo ic, or septal course. In the septal (also known as intram yocardial or tunneled) course, the LCA arises rom the right coronary sinus, courses through the interventricular septum , and then bi urcates in the LAD and circum f ex a ter reaching the interventricular groove. This anom aly is usually asym ptom atic but som e reports have linked it to sudden cardiac death. Coro ary artery stulas are usually congenital and can be sym ptom atic i large. They are well visualized by CCTA. Coronary artery stulas originate rom the RCA in twothirds o cases and the le t coronary system in a quarter o cases. More than 9 0 % drain into the right atrium , coronary sinus, or right ventricle. On CCTA, contrast opaci cation o the receiving cham ber/ vessel (shu t sig ) (Figure 8-9 ) is use ul or determ ining the exact site o entry o the stula. However, this nding will be obscured i there is a

B right coronary artery. B. This anomalous artery courses between the aorta and the pulmonary artery. This nding can predispose to the patient to ischemia, in arction, and sudden cardiac death.

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signi cant am ount o preexisting contrast in the receiving cham ber/ vessel.

m y o CAr d iu m Myocardial Ischemic

Figure 8-8 Anomalous Right Coronary Artery (RCA) Axial CT im age o an anom alous RCA arising rom the le t coronary sinus, with an interarterial course between the aorta and the pulm onary artery.

A Figure 8-9 Coronary Artery Fistula Volum e-rendered CT im age (A) dem onstrates a stula rom the le t anterior descending artery (arrow) to the right ventricular

Ischem ic heart disease rem ains the m ost com m on cause o death in the United States. Acute m yocardial in arction is rarely detected on CT as these patients usually are evaluated with catheter coronary angiography. However, patients presenting with atypical signs and sym ptom s o acute m yocardial ischem ia m ay undergo chest CT or pulm onary em bolism or acute aortic pathology. Regional hypoper usion characterized by decreased attenuation (Figure 8-10) m ay be present on contrast-enhanced chest CT and m ay be m ore conspicuous with cardiac gating. More o ten, the sequelae o m yocardial ischem ia or m yocardial in arction are detected on CT. Rem ote m yocardial in arction appears as a region o thinned m yocardium , aneurysm , or m yocardial calci cation in a de ned coronary artery territory (Figure 8-11). Fatty atrophy o the subendocardium o ten indicates a rem ote partial-thickness in arct. Le t ventricular aneurysm s and pseudoaneurym s can also be detected at CT. Thrombus m ay be present adjacent to an akinetic or hypokinetic segm ent o m yocardium .

B outf ow tract (RVOT) (arrowhead). Coronal CT image (B) dem onstrates a sm all jet o contrast in the region o the shunt entrance (arrow) into the RVOT.

92 Body CT: The Essentials

Figure 8-10 Acute Myocardial Ischemia Contrast-enhanced CT im age shows ull thickness decreased attenuation (arrowheads) in the apical m yocardium o the le t ventricle. Coronary angiography showed occlusion o the le t anterior descending coronary artery.

Figure 8-12 Myxoma Contrast-enhanced CT im age shows a low attenuation m ass (asterisk) in the le t atrium attached to the ossa ovalis (arrow) by a sm all pedicle.

Neoplasms

round or ovoid le t atrial m ass arising rom the ossa ovalis, usually attached by a narrow pedicle (Figure 8-12). Calcication is com m on. Occasionally, distinguishing between m yxom a and throm bus can be di cult on CT. Findings that avor m yxom a over throm bus include origin at the ossa ovalis, a villous shape, m obility, and prolapse through the m itral valve. However, because o potential overlap o ndings between m yxom a and throm bus, urther characterization with cardiac MRI or echocardiography is usually warranted.

Prim ary cardiac neoplasm s are rare, and approxim ately 75% are benign. They m ay be incidentally detected on CT per orm ed or other reasons or m ay be discovered in patients undergoing cardiac CT or chest pain or other cardiac signs and sym ptom s. Magnetic resonance im aging (MRI) is o ten per orm ed to urther characterize cardiac m asses and to help distinguish neoplasm rom throm bus.

Myxoma Myxomas constitute 25% to 50% o all prim ary cardiac neoplasm s. Nearly 75% arise in the le t atrium with approxim ately 25% occurring in the right atrium and rarely in the ventricles. On CT, m yxom a m ost com m only appears as

Figure 8-11 Remote In arct Contrast-enhanced CT shows thinning and calci cation (arrowhead) o the le t ventricular apex. Throm bus (arrow) has orm ed adjacent to this akinetic segm ent.

Papillary f broelastoma Papillary broelastoma is the second m ost com m on benign prim ary cardiac neoplasm , and over 9 0 % arise rom the endocardial sur ace o the cardiac valves (Figure 8-13). The

Figure 8-13 Papillary Fibroelastoma Axial oblique MIP rom contrast-enhanced CT shows a sm all so t tissue nodule (arrow) arising rom the posterior leaf et o the m itral valve.

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Figure 8-14 Primary Cardiac Angiosarcoma Contrast-enhanced CT im age shows a large, heterogeneous m ass (asterisk) in the right aspect o the heart.

Figure 8-15 Lipomatous Hypertrophy o the Interatrial Septum Contrast-enhanced CT shows expansion o the interatrial septum with at (arrow). Note the ocal narrowing (asterisk) at the ossa ovalis.

aortic valve is m ost requently involved, accounting or approxim ately 30 % o cases. Patients usually present with signs and sym ptom s o em bolization. Most are occult on CT because o their sm all size, and they are usually detected at echocardiography.

inner layer. The pericardium norm ally contains 15 to 50 m L o serous f uid. On CT, the pericardium is a thin layer o tissue surrounding the heart. Mediastinal at super cial to and epicardial at deep to the pericardium m ake it m ore conspicuous on CT. The norm al pericardium is usually 2 m m in thickness and is considered abnorm al when it exceeds 4 m m in thickness. The pericardium is typically thicker over the right ventricle and thinner over the lateral and posterior aspects o the le t ventricle. Norm al pericardial f uid tends to pool around the base o the heart and anteriorly. The pericardium is divided into the transverse and oblique sinuses, and each sinus contains several recesses (Figure 8-16 ). Knowledge o these norm al pericardial recesses is im portant as not to con use them with lym ph nodes or other f uid collections.

Angiosarcoma A giosarcoma is the m ost com m on prim ary m alignant neoplasm o the heart. CT shows a heterogeneous m ass (Figure 8-14) that usually arises rom the right atrial ree wall. In ltration o the adjacent m yocardium and pericardium is com m on, and m ass e ect on the right heart cham bers is usually evident. Areas o contrast enhancem ent and necrosis are com m on. Prognosis is poor.

Miscellaneous Lipomatous hypertrophy o the interatrial septum Lipomatous hypertrophy o the i teratrial septum (LHIS) is a benign proli eration o at in the interatrial septum . Most o ten an incidental nding, it has been associated with cardiac dysrhythm ias in a sm all num ber o patients. LH IS characteristically appears on CT as a dum bbell-shaped hom ogeneous at attenuation m ass in the interatrial septum (Figure 8-15). The ossa ovalis is located at the narrowed waist o the atty m ass.

Pe r iCAr d iu m Anatomy The pericardium consists o parietal and visceral layers. The parietal layer has a brous outer layer and a serous

Pericardial E usion Pericardial ef usio is an abnorm al accum ulation o f uid in the pericardial sac (Figure 8-17). CT is superior to echocardiography or detecting sm all e usions and those that are loculated. Pericardial e usions can be the result o pericarditis or m ay occur in the setting o cardiac or renal ailure. Transudative e usions usually have attenuation less than 20 H U whereas exudative e usions typically have attenuation between 20 and 6 0 H U. Pericardial e usion with irregular thickening or nodularity is highly suggestive o m alignancy.

Hemopericardium Hemopericardium is the accum ulation o blood in the pericardial space. It can develop a ter cardiac surgery or pericardiocentesis or can result rom chest traum a or

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cardiac or aortic rupture. Rapid accum ulation o blood in the pericardial space usually leads to cardiac tam ponade and death. Slower accum ulation o hem opericardium causes m ore gradual onset o signs and sym ptom s. CT shows high-attenuation f uid in the pericardial sac, usually around 30 to 50 H U, depending on hem atocrit and age o blood products (Figure 8-18).

Figure 8-16 Pericardial Sinuses and Recesses A. Anterior superior aortic recess (A). B. Posterior superior aortic recess (PA) and le t pulmonary artery recess (L). C. Oblique sinus (O). D. Posterior recess (P). E. Right pulm onic vein recess (arrowheads).

Pericardial Thickening Pericardial thicke i g can develop in the setting o acute or chronic pericarditis. With acute pericarditis, the pericardium is usually thickened and enhances ollowing intravenous contrast adm inistration. A pericardial e usion m ay be present. With chronic pericarditis,

Chapter 8 Heart and Thoracic Aorta

Figure 8-17 Pericardial E usion Contrast-enhanced CT im age shows a m oderate volum e circum erential pericardial f uid collection (asterisk).

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Figure 8-20 Pericardial Cyst Contrast-enhanced CT im age shows an ovoid, hom ogeneous, water-attenuation m ass (arrow) adjacent to the lateral wall o the le t ventricle.

calci ication can develop (Figure 8-19 ). Con strictive physiology m ay or m ay not be present and does not correlate with the degree o thickening or the presence o calci cation.

Pericardial Cyst

Figure 8-18 Hemopericardium Contrast-enhanced CT im age shows a uni orm ly highattenuation, circum erential pericardial collection (arrow).

Pericardial cysts occur when an outpouching o redundant pericardium becom es pinched o during developm ent. When a sm all com m unication exists between the pericardial sac and the apparent pericardial cyst, pericardial diverticulum is pre erred. Approxim ately 80 % o pericardial cysts occur at the right cardiophrenic angle. On CT, pericardial cysts are typically located adjacent to the heart. They are round or ovoid and have sm ooth, thin walls. Attenuation is hom ogeneous and that o water (0 to 10 H U), and pericardial cysts do not enhance (Figure 8-20 ).

Pericardial Neoplasm Metastases are the m ost com m on neoplasm s to a ect the pericardium , occurring in up to 10 % o patients with cancer (Figure 8-21). Most have coexistent lung m etastases, and lung carcinom a is the m ost com m on prim ary site, accounting or approxim ately one-third o patients. Prim ary pericardial neoplasm s are rare, and pericardial mesothelioma accounts or hal .

TH o r ACiC Ao r TA Anatomy Figure 8-19 Pericardial Calcif cation and Thickening Unenhanced CT im age shows thickening and calci cation (arrows) o the pericardium along the atrioventricular grooves.

The thoracic aorta is divided into the root, ascending segm ent, arch, and descending segm ent. The aortic root consists o the three (right, le t, noncoronary) si uses o Valsalva (Figure 8-22). The sinotubular junction is located just

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Body CT: The Essentials that occurs in 0.5% to 1.0% o the population. The ARSCA arises as the last arch vessel, distal to the le t subclavian artery, and crosses the mediastinum behind the esophagus and courses superolaterally toward the right upper extrem ity (Figure 8-23).

Right aortic arch

Figure 8-21 Metastatic Sarcoma Contrast-enhanced CT image shows a large so t tissue mass (arrow) in the pericardium, invading into the adjacent myocardium.

beyond the sinuses o Valsalva. The ascending aorta extends rom the sinotubular junction to the rst arch branch vessel. The aortic arch normally has three branches: right brachiocephalic, le t common carotid, and le t subclavian arteries. The descending aorta begins just beyond the last arch vessel. The aortic isthmus is a ocal segment o the descending aorta that attaches to the ligamentum arteriosum, the remnant o the ductus arteriosus. The descending aorta gives rise to the bronchial, intercostal, and spinal arteries.

A right aortic arch occurs in approxim ately 0 .1% o the population. The two m ost com m on variations o right aortic arch are mirror image bra chi g (MIB) and aberra t le t subclavia artery (ALSCA) (Figure 8-24). Right aortic arch with MIB is alm ost always associated with cyanotic congenital heart disease, m ost com m only tetralogy o Fallot (TOF). Right aortic arch with ALSCA is m ost com m only an incidentally detected anatom ic variant. Congenital heart disease, m ost com m only TOF, occurs in approxim ately 10 % o patients with right aortic arch and ALSCA. The ALSCA o ten arises rom an outpouching o the distal arch term ed the diverticulum o Kom m erell. Although this con guration results in a vascular ring, the vast m ajority o patients have no signs or sym ptom s related to the ring.

Double aortic arch

The m ost com m on congenital anom aly o the thoracic aorta is an aberra t right subclavia artery (ARSCA)

Double aortic arch is a rare congenital variant but is the m ost com m on cause o a sym ptom atic vascular ring. Usually the right aortic arch is larger an d located m ore cephalad than the le t. Most patients present in in ancy with di culty eeding or stridor rom m ass e ect o the vascular ring. Treatm en t is ligation o the ring, usually at the posterior aspect o the le t arch. There is no increased inciden ce o congenital heart disease with double aortic arch

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Figure 8-22 Normal Aortic Root A. Axial contrast-enhanced CT im age shows the norm al le t sinus o Valsalva (L), which can be mistaken or an aneurysm

because o the oblique orientation o the aortic root. B. Double oblique re ormation in the plane o the aortic valve shows the normal le t (L), right (R), and noncoronary (N) sinuses o Valsalva.

Congenital Aberrant right subclavian artery

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Figure 8-23 Aberrant Right Subclavian Artery A. Contrast-enhanced CT image shows the right subclavian artery (arrow) arising rom the aortic arch distal to the right brachiocephalic (B), le t com m on carotid (C), and le t subclavian

(S) arteries. B. Coronal MIP shows the right subclavian artery (arrow) crossing the posterior m ediastinum and the le t subclavian artery (arrowhead).

Cervical aortic arch

Other aortic arch anomalies

Cervical aortic arch is a rare anom aly in which the arch o the aorta is located in the lower neck. Anom alous branching o the arch vessels is com m on.

Other anatom ic variations o the aortic arch occur with varying requencies. Di erent patterns o arch vessel branching are encountered including a com m on origin o the right brachiocephalic and le t com m on carotid arteries and the le t vertebral artery arising rom the arch.

Coarctation and hypoplasia Aortic coarctatio is de ned as a ocal congenital narrowing o the aorta. Most coarctations occur just beyond the ligam entum arteriosum . Approxim ately 50 % o patients with aortic coarctation have a bicuspid aortic valve. Aortic hypoplasia is de ned as an abnorm ally sm all caliber o the aorta. The aorta can be di usely hypoplastic or it can be lim ited to a segm ent, o ten the arch. H ypoplasia m ay coexist with coarctation.

Pseudocoarctation Figure 8-24 Right Aortic Arch Contrast-enhanced CT im age shows a right aortic arch with aberrant le t subclavian artery arising rom a diverticulum o Kom m erell (arrow).

Aortic pseudocoarctatio is a ocal kink in the aorta, usually at the isthm us, that does not result in signi cant (< 10 m m H g) pressure change across the narrowing

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Figure 8-27 Sinus o Valsalva Aneurysm Contrast-enhanced CT im age shows ocal outpouching (arrow) rom the right sinus o Valsalva.

Aortic Aneurysm

Figure 8-25 Aortic Pseudocoarctation Sagittal oblique re orm ation rom contrast-enhanced CT shows a ocal kink and m ild narrowing (arrow) at the aortic isthm us. Atherosclerotic calci cations in this area m ay be the result o increased turbulence.

(Figure 8-25). The exact etiology is unclear but m ay be related to abnorm al m igration o the em bryonic arches that give rise to the aorta. As with coarctation, approxim ately 50 % o patients with pseudocoarctation have a bicuspid aortic valve.

The norm al adult thoracic aorta has a diam eter o up to 40 m m . The ascending aorta is usually larger than the arch and descending aorta. Thoracic aortic ectasia is abnorm al enlargem ent o the aorta and thoracic aortic a eurysm is de ned as an aortic diam eter greater than 50 m m . Atherosclerosis is the m ost com m on cause o aortic dilation. Aortic aneurysm s can be classi ed as usi orm (Figure 8-26 ) or saccular. A uloaortic ectasia is de ned as abnorm al enlargem ent o the aortic root and the ascending aorta, o ten with e acem ent o the sinotubular junction. Causes include Mar an syndrom e, Ehlers–Danlos syndrom e, syphilis, and idiopathic cystic m edial necrosis. Si us o Valsalva a eurysms (Figure 8-27) can be congenital or acquired. Underlying weakness o the elastic lam ina at the junction o the aortic annulus and the aortic m edia is believed to be the underlying m echanism . Congenital causes include Ehlers–Da los, and acquired causes include in ection, traum a, and atherosclerosis. Because o the oblique orientation o the aortic root with respect to the transaxial acquisition plane o CT, sinus o Valsalva aneurysm s can be m issed or erroneously diagnosed on axial im ages alone.

Acute Aortic Syndrome Acute aortic sy drome is de ned as an acute presentation o patients with one o several li e-threatening aortic pathology. These conditions include aortic dissection, penetrating atherosclerotic ulcer (PAU), intram ural hem atom a (IMH ), and aneurysm al leak.

Acute aortic dissection Figure 8-26 Fusi orm Ascending Aortic Aneurysm Contrast-enhanced CT im age shows usi orm dilation o the ascending aorta.

Acute aortic dissectio occurs when an intim al tear occurs and f owing blood dissects into the aortic m edia. Driven by high pressure, blood tracking the aortic wall creates a alse

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Figure 8-28 Stan ord Type A Aortic Dissection Contrast-enhanced CT im age shows an intim al f ap (arrows) in both the ascending and descending aorta. The ascending aorta is aneurysm al.

Figure 8-29 Stan ord Type B Aortic Dissection Contrast-enhanced CT image shows true (T) and alse (F) lumens in the proximal descending aorta. Note the thin low-attenuation ocus (arrow) in the alse lumen, ref ecting the cobweb sign.

lum en, which m ay develop several. The Stan ord classi cation is used to characterize aortic dissection as it dictates m anagem ent. Type A aortic dissectio s involve the ascending aorta (Figure 8-28). Most arise just beyond the aortic valve in the right lateral wall o the ascending aorta. Type B aortic dissectio s do not involve the ascending aorta, and m ost arise near the ligam entum arteriosum . Type A dissections are treated with surgical repair, whereas type B dissections are usually m anaged m edically. Surgical intervention or type B dissections, either with open or endovascular repair, m ay be required or progressive disease or with end-organ ischem ia. Contrast-enhanced CT clearly shows the intim al f ap separating the true and alse lum en. The intim al f ap is usually convex toward the alse lum en, which is usually larger and has slower f ow. Throm bi m ay orm in the alse lum en. With type A dissection, the alse lum en is typically located along the right anterolateral wall o the ascending aorta, spiraling distally along the posterolateral wall o the descending aorta. The cobweb sig describes thin, low-attenuation linear oci ref ecting incom pletely dissected m edia and is speci c or the alse lum en (Figure 8-29 ). On non-gated or im properly gated studies, pulsatile m otion o the ascending aorta can m im ic dissection. Arti act rom dense contrast in large m ediastinal veins, intravascular devices, or m ediastinal clips can cause streak arti act, possibly m im icking an intim al f ap.

(Figure 8-30 ). Subsequent contrast-enhanced CT shows persistent wall thickening and preserved lum en. Although the diagnosis o IMH is usually straight orward with appropriate CT technique, atherosclerotic thickening, throm bus, and throm bosed dissection can occasionally m im ic IMH . MRI m ay be use ul in distinguishing am ong these.

Intramural hematoma I tramural hematoma (IMH) develops when blood collects in the aortic wall without an intim al tear. This can occur with bleeding rom the vaso vasorum or rom hem orrhage rom an atherosclerotic plaque. IMH is also classi ed with the Stan ord system . IMH is best detected on unenhanced CT im ages as thickening and increased attenuation o the aortic wall relative to blood pool that extends longitudinally

Penetrating atherosclerotic ulcer Pe etrati g atherosclerotic ulcer (PAU) occurs when ocal intim al erosion occurs at the site o an atherosclerotic plaque. IMH or, rarely, dissection can ensue. Most PAUs occur in the descending aorta, particularly in the m id segm ent (9 0 %), likely because o the higher requency o atherosclerosis. PAU appears sim ilar to IMH on unenhanced CT. Contrast-enhanced im ages show ocal outpouching o the aorta, usually in the m id descending segm ent, at the site o IMH (Figure 8-31). Associated atherosclerotic plaque is o ten evident. Com plications include em bolization o plaque or clot rom the PAU as well as aneurysm , IMH , and rupture. Short-term ollow-up is advised or patients who are being m anaged m edically.

Aortitis Aortitis is an inf amm atory process o the aortic wall that can result rom in ection or, m ore com monly, nonin ectious causes such as vasculitis. Aortitis is a comm on com ponent o Takayasu arteritis and giant cell arteritis, both large vessel vasculitides. Long-standing ankylosing spondylitis and relapsing polychondritis can also lead to aortitis.

Takayasu arteritis Takayasu arteritis is a large vessel vasculitis that has a propensity to involve the aorta and its branch vessels.

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A Figure 8-30 Intramural Hematoma with Aortic Rupture A. Unenhanced CT im age shows thickening and increased attenuation (arrow) o the descending aortic wall. Extensive

B m ediastinal hem atom a (asterisk) is present. B. Contrastenhanced CT im age at the sam e level shows preservation o the aortic lum en.

The m ajority o patients are young em ales. Earlier in the course o disease, patients m ay present with constitutional sym ptom s such as ever and night sweats. Later on, sym ptom s related to vascular stenosis or occlusion predom inate. CT ndings include concentric wall thickening, stenosis, occlusion, and throm bosis. The outer layers o the aortic wall m ay show enhancem ent relative to the intim a. Calci cation m ay develop with long-standing inf am m ation. The abdom inal aorta is m ost com m only involved, ollowed by the descending thoracic aorta and aortic arch.

Giant cell arteritis

Figure 8-31 Penetrating Atherosclerotic Ulcer Contrast-enhanced CT im age shows a ocal lum inal outpouching (arrow) in the m id descending aorta with adjacent m ural thickening.

Gia t cell arteritis (GCA) is a chronic vasculitis o large and m edium size vessels. Super cial cranial arterial involvem ent is com m on, hence the synonym tem poral arteritis. Most patients are older than 50 years, and there is a strong association with polym yalgia rheum atica. Aortic involvem ent usually leads to annuloaortic ectasia or ascending aortic aneurysm . Aortic insu ciency and aortic dissection are other m ani estations o GCA. CT can show circum erential aortic wall thickening or aortic dilation or both. Arch branch vessels are also com m only involved (Figure 8-32).

Chapter 8 Heart and Thoracic Aorta

A

101

B

Figure 8-32 Giant Cell Arteritis A. Contrast-enhanced CT image shows circum erential mural thickening (arrow) and luminal narrowing o the proximal le t

subclavian artery. B. Sagittal oblique re ormatted image shows ocal wall thickening and luminal narrowing in the proximal le t subclavian artery (arrow) and in the descending aorta (arrowhead).

SUGGESTED READIn GS

6 . Kini S, Bis KG, Weaver L. Norm al and variant coronary arterial and venous anatom y on high-resolution CT angiography. AJR Am J Roentgenol. 20 0 7;188(6 ):16 6 5–16 74.

1. Taylor AJ, Cerqueira M, Hodgson JM, et al. ACCF/ SCCT/ ACR/ AH A/ ASE/ ASNC/ NASCI/ SCAI/ SCMR 20 10 Appropriate Use Criteria or Cardiac Com puted Tom ography. A Report o the Am erican College o Cardiology Foundation Appropriate Use Criteria Task Force, the Society o Cardiovascular Com puted Tom ography, the Am erican College o Radiology, the Am erican Heart Association, the Am erican Society o Echocardiography, the Am erican Society o Nuclear Cardiology, the North Am erican Society or Cardiovascular Im aging, the Society or Cardiovascular Angiography and Interventions, and the Society or Cardiovascular Magnetic Resonance. Circulation. 20 10 ;122(21):e525–e555. 2. Mahesh M, Cody DD. Physics o cardiac im aging with m ultiplerow detector CT. Radiographics. 20 07;27(5):149 5–1509 . 3. Prim ak AN, McCollough CH , Bruesewitz MR, Zhang J, Fletcher JG. Relationship between noise, dose, and pitch in cardiac m ultidetector row CT. Radiographics. 20 06 ;26 (6 ):1785–179 4. 4. Pannu H K, Alvarez W Jr, Fishm an EK. Beta-blockers or cardiac CT: a prim er or the radiologist. AJR Am J Roentgenol. 20 0 6 ;186 (6 Suppl 2):S341–S345. 5. Dodd JD, Ferencik M, Liberthson RR, Niem an K, Brady TJ, Ho m ann U. Evaluation o e cacy o 6 4-slice m ultidetector com puted tom ography in patients with congenital coronary stulas. J Comput Assist Tomogr. 20 08;32(2):26 5–270 .

7. Sundaram B, Patel S, Agarwal P, Kazerooni EA. Anatom y and term inology or the interpretation and reporting o cardiac MDCT: part 2, CT angiography, cardiac unction assessm ent, and noncoronary and extracardiac ndings. AJR Am J Roentgenol. 20 0 9 ;19 2(3):584–59 8. 8. Ahm ad F, Chesire N, Ham ady M. Acute aortic syndrom e: pathology and therapeutic strategies. Postgrad Med J. 20 0 6 ;8(9 6 7):30 5–312. 9 . Restrepo CS, Ocazionez D, Suri R, Vargas D. Aortitis: im aging the spectrum o the in ectious and inf am m atory conditions o the aorta. Radiographics. 20 11;31(2):435–451. 10 . Sche el H , Baum ueller S, Stolzm ann, et al. Atrial m yxom as and throm bi: com parison o im aging eatures on CT. AJR Am J Roentgenol. 20 0 9 ;19 2(3):6 39 –6 45. 11. Rajiah P, Kanne JP, Kalahasi V, Schoenhagen P. Com puted tom ography o cardiac and pericardiac m asses. J Cardiovasc Comput Tomogr. 20 11;5(1):16 –29 . 12. Kanne JP, Godwin JD. Right aortic arch and its variants. J Cardiovasc Comput Tomogr. 20 10 ;4(5):29 3–30 0 . 13. Rajiah P, Kanne JP. Computed tomography o the pericardium and pericardial disease. J Cardiovasc Comput Tomogr. 2010;4(1):3–18.

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Ch a p t e r

9

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nd B l

David L. Coy, MD, PhD Orpheus Kolokythas, MD

I. LIVER a. Anatomy and Physiology b. Liver CT Technique c. Cirrhosis and Di use Liver Disease i. Cirrhosis ii. Fatty liver disease iii. High density liver d. Hepatic In ections i. Viral hepatitis ii. Hepatic abscesses iii. Echinococcal in ection iv. Schistosomiasis e. Benign Liver Lesions i. Liver cysts and polycystic disease ii. Hemangioma iii. Focal nodular hyperplasia iv. Hepatocellular adenoma v. Inf ammatory pseudotumor . Liver Neoplasms i. Hepatocellular carcinoma ii. Fibrolamellar hepatocellular carcinoma iii. Hepatoblastoma iv. Hepatic angiosarcoma v. Epithelioid hemangioendothelioma vi. In antile hemangioendothelioma vii. Lymphoma viii. Metastases g. Liver Hemorrhage h. Vascular Phenomena

Liv e r Anatomy and Physiology The liver is the largest abdom inal organ. It is located in the right upper quadrant and invested by peritoneum except or upper posterior m argin or bare area that contacts the diaphragm and com m unicates with the retroperitoneal space. Liver unctions include m etabolism o intestinally absorbed nutrients and toxins; synthesis o bile salts,

i. Transient hepatic attenuation di erences ii. Hepatic congestion iii. Hepatic shunts iv. Hepatic in arction v. Peliosis hepatis II. BILIARY SYSTEM a. Anatomy b. Choledochal Cysts i. Caroli disease c. Biliary Hamartomas d. Cholelithiasis e. In ammatory and In ectious Processes o the Gallbladder i. Acute cholecystitis ii. Acalculous cholecystitis iii. Chronic cholecystitis iv. Adenomyomatosis . In ammatory and In ectious Processes o the Bile Ducts i. Primary sclerosing cholangitis ii. In ectious cholangitis iii. Ischemic cholangiopathy iv. Drug- and toxin-induced cholangiopathies v. IgG4 cholangiopathy g. Gallbladder Neoplasms h. Neoplasm o the Biliary Tract i. Cholangiocarcinoma ii. Biliary cystadenoma and cystadenocarcinoma i. Periampullary Carcinoma

enzym es, album in, and coagulation actors; storage o glycogen; and horm onal regulation. The liver has a dual blood supply. The portal vein delivers low-pressure venous blood rom the splanchnic circulation and comprises 75% to 80% o the hepatic in ow which accounts or the propensity o the liver to be a target or metastases and in ection originating rom the gastrointestinal tract. The remaining 20% to 25% o the hepatic in ow arrives rom the hepatic arteries that are at systemic pressure. 103

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Body CT: The Essentials

Caudate lo be

1 7

4a

2

8

3 4b 6

5

Le ft he patic lo be

Rig ht he patic lo be Figure 9-1 Couinaud Classif cation The le t and right hepatic lobes are divided by the m iddle hepatic vein. The le t hepatic lobe is divided into segm ents II, III, IVa, and IVb by the le t hepatic vein and plane o the le t portal vein.

The right hepatic lobe is divided into segm ents V, VI, VII, and VIII by the right hepatic vein and the plane o the right portal vein. The caudate lobe is a longitudinal posterior lobe that drains directly in to the IVC and is designated as segment I.

The liver passively receives portal in ow, having no ability to control or regulate the portal vein. In contrast, the liver can regulate hepatic arterial in ow up or down to compensate or the changes in portal in ow so as to maintain a near constant total hepatic in ow. This has been termed the hepatic arterial b er response and can be seen as an alteration o liver enhancement on dynamic CT examinations (e.g., TH ADs). There are m ultiple classi cations or describing segm ental anatom y o the liver. One o the m ost com m only used system s that is pre erred by hepatic surgeons is the Co ina d classi cation (Figure 9 -1) which is a unctional system that divides the liver into eight segm ents each with its own vascular in ow and out ow, and biliary drainage. The m iddle hepatic vein divides the liver into le t and right hepatic lobes. The right lobe is divided into segm ents V, VI, VII, and VIII by the right hepatic vein and the plane o the right portal vein. The le t hepatic lobe is divided into segm ents II, III, IVa, and IVb by the le t hepatic vein and plane o the le t portal vein. The caudate lobe is a posterior, vertically oriented m idline lobe that is designated as segm ent I. It receives in ow rom the le t and right portal veins and arterial in ow rom le t and right hepatic artery branches, and drains directly into the IVC. Lymphatic drainage o the liver occurs through multiple pathways. As a rule o thumb, superior segments (i.e.,

segments II, IVa, VII, and VIII) drain predominantly to the posterior mediastinal and anterior cardiophrenic lymph nodes. In erior segments (i.e., segments III, IVb, V, and VI) drain mainly to the porta hepatis and portocaval lymph nodes.

Liver CT Technique Routine evaluation o the liver with contrast-enhanced CT is per ormed during portal venous phase enhancement in which the liver parenchyma has its maximum enhancement and there is contrast enhancement o the portal and hepatic veins. This phase provides maximum sinusoidal enhancement allowing or the best contrast between the parenchyma and ocal lesions with a hypovascular component. Characterization o liver masses and screening or hypervascular lesions are per ormed with a multiphase contrast-enhanced CT consisting o a late arterial, a portal venous and an equilibrium phase. An unenhanced phase be ore contrast injection is optional. The late arterial enhancement phase scan is per ormed when the contrast is still predominantly in the arterial system with only a small amount having reached the portal vein. During arterial phase imaging the liver parenchyma demonstrates little enhancement because the contrast-enhanced hepatic arteries account or only a minority o the blood supply to normal liver parenchyma. However,

Chapter 9 Liver and Biliary 105 hypervascular liver tumors, supplied solely rom hepatic artery branches, have their greatest enhancement and conspicuity against the adjacent liver parenchyma during arterial phase imaging. Timing o the scan or late arterial phase ensures that the contrast has reached the arterioles o the tumor by the time o the scan, The interval rom contrast injection to late arterial and portal venous phases o enhancement are about 35 and 70 seconds, respectively. However, or an individual patient the optimal timing scan can be variable, in uenced by technical actors such as contrast injection rate and volume and patient actors such as cardiac output. There ore the use o triggers, such as contrast bolus triggering or test contrast injection is pre erred over a xed time interval between contrast injection and scan initiation. A nal interstitial or equilibrium (also called delayed) phase obtained 5 to 10 minutes a ter contrast injection is help ul or characterization o slowly enhancing lesion such as cavernous hem angiom as, washout o hyperenhancing lesions such as hepatocellular carcinoma (H CC), or progressive delayed enhancem ent o masses with brous characteristics such as cholangiocarcinom a. A ter approxim ately 3-5 minutes an equal amount o contrast is present in the blood pool (sinusoids) and in the interstitial space (third space), which is why it is also called equilibrium phase.

Cirrhosis and Di use Liver Disease Cirrhosis Hepatic cirrhosis is a generic term or irreversible, endstage hepatic injury caused by any di use liver disease. It is characterized by brosis, regenerative nodules, and distor-

A Figure 9-2 Macronodular and Micronodular Cirrhosis A. Portal venous phase CT in a patient with macronodular cirrhosis because o sarcoidosis with macronodular distortion o the hepatic parenchyma and capsule (arrowheads) with signs o signi cant portal hypertension including enlarged caliber o main portal vein and large le t upper quadrant and varices (white arrows). Note laminated enhancement in the main portal vein (black arrow)

tion o liver vasculature with orm ation o abnorm al arteriovenous connections. Alcoholism and hepatitis C are the m ost com m on etiologies in the United States whereas hepatitis B and C are the m ost com m on etiologies worldwide. Other causes o cirrhosis include prim ary biliary cirrhosis (PBC), prim ary sclerosing cholangitis (PSC), hem ochrom atosis, Wilson disease, Budd–Chiari syndrom e, nonalcoholic steatohepatitis (NASH ), cryptogenic cirrhosis, and granulom atous diseases. Mild orm s o liver brosis are not usually detected by CT. The im aging eatures o severe brosis representing hepatic cirrhosis can vary and are in uenced by the underlying etiology. In m ost instances o cirrhosis there is an overall decrease in liver volum e with atrophy o right liver and m edial segm ents (segm ent IV) m ost usually a ected. H ypertrophy o the caudate lobe is a com m on nding. The caudate – right lobe ratio can be m easured on transverse im ages o the liver. A ratio o greater than 0 .6 5 has a sensitivity o 84% and speci city o 100 % or the diagnosis o cirrhosis. Liver atrophy results in the widening o portal ssures and o the physiologic indentations o the liver such as expansion o the gallbladder ossa. Regenerating nodules are always present in cirrhosis but may not be visible on im aging. Micronodules (< 3 m m) are most comm only associated with alcohol and chronic in ectious hepatitis. Macronodules ranging rom 3 mm up to several centimeters in size are m ost comm only associated with viral hepatitis, PSC, and other causes o cirrhosis (Figure 9 -2). The greatly increased incidence o H CC in patients with cirrhosis results rom malignant trans orm ation o regenerating nodules. Over tim e regenerating

B caused by incomplete mixing o venous blood with and without intravenous contrast. B. Portal venous phase CT in a man with micronodular alcoholic cirrhosis demonstrating shrinkage o the liver and nodular contour (arrowhead). The enlarged hepatic artery (arrow) results rom arteriovenous shunting within the liver. Gallbladder wall edema (dashed arrow) may result rom hypoalbumenia or portal hypotension.

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Body CT: The Essentials

nodules may become dysplastic by developing areas o cellular atypia. Dysplastic nod les may progress and develop into H CC with subsequent neovascularization rom the hepatic arterial supply. Siderotic nod les are regenerating nodules that contain increased iron levels which result in them having increased attenuation and making them visible as dense nodules on unenhanced CT. They have a higher propensity or malignant trans ormation than non-siderotic nodules. Fibrosis in cirrhotic livers appears as linear bands between regenerating nodules that m ay have a di use lacey or reticular pattern. On unenhanced and arterial and portal venous enhancem ent phases hepatic brosis is usually hypoattenuating, but on equilibrium phase brosis m ay be denser than the adjacent liver parenchym a owing to its slow, progressive enhancem ent. Occasionally hepatic brosis can have a m ore ocal or con uent appearance, which is a requent nding in cirrhosis caused by PSC. The slow, progressive enhancem ent characteristics o brosis on CT and MR can help di erentiate con uent brosis rom a tum or. Focal con uent brosis is not a speci c nding or cirrhosis as it can result rom other causes such as traum a, ocal hepatic in am m ation, and radiation therapy. Recognition o cirrhosis on imaging is essential, not only because o the inherent clinical implications o end-stage liver disease, but also because the spectrum o hepatic masses and lesions encountered in a cirrhotic liver varies considerably rom those in a noncirrhotic liver. Benign lesions such as simple cyst, hemangioma, adenoma, and ocal nodular hyperplasia (FNH) are common liver lesions in patients without cirrhosis, but these lesions are uncommon or rare in patients with cirrhosis. Liver metastases and hepatic lymphoma are also uncommon in cirrhosis. On the other hand, the risk o HCC which is the most common malignant primary neoplasm o the liver is much higher in patients with cirrhosis. A minority o H CCs arise in noncirrhotic livers. The brosis and architectural distortion o cirrhosis usually lead to portal hypertension. The im aging ndings o portal hypertension include ascites, splenom egaly, recanalized um bilical vein, and gastroesophageal, m esenteric, and splenorenal varices. Although portal hypertension is a requent nding in cirrhosis, the presence o portal hypertension does not necessarily indicate that liver cirrhosis is present as there are m any other causes o portal hypertension such as portal vein obstruction, in ltrative liver disease, hepatic vein obstruction, and right heart ailure. It is im portant to recognize that nodularity o the liver can be caused by entities other than end-stage liver cirrhosis. Treated hepatic m etastases—m ost com m only breast cancer m etastases, di use sm all hepatic m etastases, hepatic sarcoidosis, and regenerating nodules rom chronic Budd–Chiari syndrom e or portal venous throm bosis can result in nodularity o the liver parenchym a (pse docirrhosis), and in som e instances also cause portal hypertension.

Fatty liver disease Liver steatosis results rom the intracellular accum ulation o triglycerides in hepatocytes. The m ost com m on causes

Figure 9-3 Hepatic Steatosis (Fatty Liver) Portal venous phase CT demonstrating hypoattenuation o the liver. The attenuation o the liver is 20 H U less than that o the paraspinal m uscles. Note the geographic area o ocal atty sparing (arrowhead) along the porta hepatitis which is a com m on location or ocal sparing or ocal at deposition.

are alcohol-induced liver disease and nonalcoholic atty liver disease (NAFLD) which is requently associated with m etabolic syndrom e and insulin resistance. Other com m on etiologies include acute viral hepatitis, drugs (e.g., corticosteroids, chem otherapeutics), and alterations o diet (e.g., starvation and total parenteral nutrition). NASH re ers to NAFLD accom panied by signs o hepatic in am m ation and brosis on histologic analysis. In the absence o cirrhosis, NAFLD and NASH cannot be di erentiated rom one another by CT or other im aging m odalities. NAFLD has becom e the m ost com m on liver disease in the econom ically developed world with a prevalence o 33% to 35%. In the United States NASH is the third m ost com m on cause o cirrhosis ollowing hepatitis C and alcoholism . Liver steatosis can be detected on unenhanced CT by the presence o lipid, which decreases the attenuation o the liver (Figure 9 -3) (Table 9 -1). The norm al attenuation o T bl 9-1. Low Density Liver Di use: F y liv h ic cong s ion ( cu cu ic inju y)

i is,

ilu ,

Focal: Cys a bsc ss h ic m ss (b nign o m lign n ) Foc l (c c is ic loc ions o is, g llbl dd oss , dj c n o lci o m lig m n ) Foc l b osis

Chapter 9 Liver and Biliary 107 the liver parenchym a is 50 to 6 5 H U, which is about 8 to 10 H U denser than the unenhanced spleen. Steatosis is considered to be present when the liver attenuation on unenhanced CT is less than 48 H U or when the liver attenuation is less than that o the spleen. Contrast-enhanced CT in the portal venous and later phases has a lower sensitivity or the detection o steatosis than unenhanced CT. Severe liver steatosis can be diagnosed on contrast-enhanced CT i the hepatic attenuation is 20 to 25 H U less than that o the spleen or i hepatic attenuation is less than that o paraspinal m uscles. Most requently atty liver presents as di use hypoattenuation o the liver. Less com m on patterns o liver steatosis include ocal at deposition in an otherwise norm al appearing liver and areas o ocal sparing in a di usely atty liver. Focal at deposition or sparing requent occur adjacent to the alci orm ligam ent, in the porta hepatis, and in the gallbladder ossa but it can occur anywhere in the liver and can be m istaken or a m ass. Features on CT that suggest ocal at or ocal at sparing would include (1) occurrence in a characteristic location, (2) lack o m ass e ect on adjacent vessels and structures, (3) geographic con guration rather than having rounded borders, (4) degree o contrast enhancem ent sim ilar or less than that o norm al liver parenchym a. In instances where it is uncertain whether a hypoattenuating lesion on CT represents a m ass or a pseudolesion due to ocal at deposition or sparing chem ical shi t MR im aging should be considered.

High density liver There are several conditions that result in the liver having increased attenuation on unenhanced CT (Figure 9 -4) (Table 9 -2). Am iodarone is a cardiac antiarrhythm ic agent that contains iodine and causes increased hepatic iodine levels. Secondary hemochromatosis (hemosiderosis) is the m ost com m on cause o hyperdense liver parenchym a and is caused by iron deposition within the reticuloendothelial system caused by m ultiple blood trans usions, excessive exogenous iron supplem entation, or anem ia with ine ective erythropoiesis (e.g., thalassem ia). Primary hemochromatosis is an autosom al recessive m etabolic disorder that results in increased intestinal iron uptake and iron deposition in the liver, pancreas, heart, pituitary gland, and thyroid. Iron within hepatocytes results in cellular dam age and can lead to cirrhosis and increased risk o H CC. MR is m ore sensitive and accurate or detection and quanti cation o intrahepatic iron than CT.

Hepatic In ections Viral hepatitis Viral hepatitis is the most common in ection o the liver. Hepatitis A is an acute in ection that is usually sel -limited but can result in ulminant liver ailure in 2% o cases. Unlike the other orms o viral hepatitis A is transmitted via ecal–oral route and does not result in chronic liver disease. Hepatitis B, C, and D and other viral pathogens causing viral

Figure 9-4 Hemosiderosis (Secondary Hemochromatosis) in a Cirrhotic Patient Unenhanced CT dem onstrates di usely increased attenuation o the liver parenchym a in a patient with cirrhosis who developed hem osiderosis rom repeat trans usions because o the variceal bleeding. There are dense lym ph nodes in the gastrohepatic ligam ent that show the sam e high attenuation as the liver. Iron deposition in the reticuloendothelial system is a pattern associated with hem osiderosis.

hepatitis are blood-borne in ections that can result in chronic liver disease and cirrhosis. Worldwide hepatitis B is the most common orm o viral hepatitis with vertical transmission rom mother to child being the most common route o in ection. Hepatitis B is a carcinogenic in ection o the hepatocyte and carries the risk or the development o H CC independent rom chronicity o in ection, extent o liver injury, or presence o cirrhosis. In the economically developed countries hepatitis C is the most common viral hepatic in ection. Approximately 50% o individuals with acute hepatitis C will progress to chronic hepatitis with 10% to 20% progressing to cirrhosis. Hepatitis D is a de ective virus that requires the presence o hepatitis B to exist. Hepatitis D in ection may

T bl 9-2. High Density Liver Di use: a miod on h mosid osis ( iculo ndo li l sys m) p im y moc om osis Wilson dis s (co d osi ion) Gold d osi ion ( m n o um oid) Focal: Foc l y s ing (c c is ic loc ions o is, g llbl dd oss , nd dj c n o lci o m lig m n ) h mo g ( xclud und lying m ss)

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develop at the same time as or ollowing hepatitis B in ection. The propensity to progress to cirrhosis is greater in individuals with combined hepatitis B and D than in those with only hepatitis B. The diagnosis o acute hepatitis is m ade by sym ptom s and serologies. On im aging liver requently appears norm al. In cases o severe ulm inant viral hepatitis CT m ay dem onstrate hepatom egaly, periportal edem a, severe gallbladder wall thickening, portal hypertension, and di use or ocal hepatic steatosis but these ndings are not speci c or viral hepatitis. In chronic hepatitis there are usually no im aging ndings unless there has been progression to cirrhosis. The im portance o im aging in viral hepatitis lies m ore in the detection o com plications, nam ely H CC and detection o cirrhosis and portal hypertension.

Hepatic abscesses Pyogenic liver abscesses are usually a sequela o ascending cholangitis or an enteric in ection transm itted via the portal vein. Although they are not uncom m on in poorer countries, their incidence in the Western world is decreasing and m ostly related to acute appendicitis, diverticulitis, and in am m atory bowel disease. On CT pyogenic abscesses are usually solitary, large, and o ten located in the posterior right hepatic lobe. Acute liver abscess initially appears as a cluster o sm all (< 2 cm ) cysts (cl ster sign) (Figure 9 -5) that over tim e coalesce into a uid-containing abscess cavity surrounded by a thick wall and requently a hypodense rim caused by edem a (do ble target sign). Gas within the abscess cavity is com m on. The presence o signs and sym ptom s o in ection are im portant clinical actors that can help di erentiate a pyogenic abscess rom necrotic or m ucinous m etastasis and biliary cystadenom a. Amebic abscesses are m ost com m on in poorer countries and caused by the parasite Entameba histolytica. Like pyogenic abscesses, am ebic abscesses are requently large

Figure 9-6 Amebic Abscess Contrast-enhanced CT in a Som ali wom an dem onstrating a unilocular amebic abscess in the right hepatic lobe with enhancing inner rim (black arrow), representing granulation tissue and in am mation o the hepatic parenchym a, surrounded by a hypodense outer edem atous rim (black arrowhead). There is gas within the abscess (white arrowhead) and delayed contrast enhancem ent o the parenchym a peripheral to the abscess because o the vascular com pression (white arrow).

and solitary lesions m ost com m only located in the right hepatic lobe. The im aging eatures are very sim ilar to that o a pyogenic abscess with a uid abscess surrounded by a thick wall and a hypodense rim because o the hepatic edem a (Figure 9 -6 ). Extension to the chest wall and across the diaphragm into the right pleural space is com m on. F ngal abscesses m ost com monly occur in im munocom prom ised individuals and Candida species is the m ost com mon pathogen. In contrast to pyogenic and amebic abscesses, ungal abscesses are com monly numerous, distributed in both hepatic lobes, and are microabscesses m easuring less than 2 cm . On CT m icroabscesses are sm all hypodensities requently with a surrounding ring o enhancement on the portal venous phase because o the hyperemia rom the in amm atory response o the liver. The presence o a surrounding ring on equilibrium phase can result rom a surrounding brous capsule. Fungal m icroabscesses are also requently present in the spleen, which can help to di erentiate them rom sm all metastases.

Echinococcal in ection

Figure 9-5 Pyogenic Hepatic Abscess Contrast-enhanced CT demonstrates an early abscess in le t liver with clusters o sm all abscesses that will coalesce over tim e.

Echinococcus granulosus is a canine tapeworm that causes hydatid liver disease (cystic echinococcosis). It is most common in the Mediterranean basin and in Latin America whereas Echinococcus multilocularis is a ox tapeworm endemic in the northern hemisphere, especially in Central Europe and Siberia. Humans are an intermediate host in ected by ingestion o contaminated ood or water. The parasites enter the gastrointestinal tract and gain access to the portal circulation and are ltered by the liver. E. granulosus

Chapter 9 Liver and Biliary 109

Figure 9-7 Hepatic Hydatid Cyst Contrast-enhanced CT in a patient with a hydatid cyst (Echinococcus granulosus). The endocyst (arrow) has detached rom the cyst capsule (arrowhead) resulting in the linguine sign.

results in hydatid cysts in the liver. On CT hydatid cysts are usually well-de ned cyst that may be simple in appearance, contain multiple internal septations, or contain multiple peripheral daughter cysts. The detachment o the parasitic endocyst rom the cyst capsule results in a oating membrane (ling ine sign) (Figure 9-7). Peripheral calci cations are present in up to 50% o cases. E. multilocularis results in alveolar echinococcosis which is more aggressive than hydatid cysts. On CT it has an in ltrating growth pattern and di use calci cations that make it dif cult to distinguish rom metastases.

Schistosomiasis Schistosom iasis is caused by one o three di erent parasites that live in warm countries with prom inent water pathways such as Northeastern A rica and Japan. Both Schistosoma japonicum and Schistosoma mansoni invade the portal system and liver causing parenchym al brotic septae and calci cations (S. japonicum) and chronic periportal in am m ation (S. mansoni), resulting in intrahepatic periportal brosis and portal hypertension. On CT calci cations are requently present. Periportal brotic tissue m ani ests as a thick hypovascular rim surrounding the intrahepatic portal veins with late brotic enhancem ent. Schitosom iasis can result in hepatic cirrhosis and increased risk or H CC.

Benign Liver Lesions Liver cysts and polycystic disease Sim ple hepatic cysts are biliary cysts that do not com municate with the bile ducts. The incidence ranges rom 1% to 14% and they are m ore com mon in wom en. Hepatic

Figure 9-8 Polycystic Liver Disease Contrast-enhanced CT o a patient with adult polycystic kidney disease. Im age through the liver at the right portal venous bi urcation (arrow) dem onstrating innum erable sim ple and partially calci ed cysts distorting the liver parenchym a. Note the innum erable cysts in both kidneys (stars).

cysts can be solitary or multiple and range in size orm a ew millimeters to 25 cm. Simple hepatic cysts are usually incidental ndings, but can be symptomatic i large or i they become in ected or hemorrhage. On CT simple hepatic cysts are de ned water density lesions with a thin wall and sharp margin that do not enhance a ter contrast administration. Polycystic liver (Figure 9-8) occurs in individuals with adult polycystic kidney disease (ADPKD) or the much less common adult polycystic liver disease (ADPLD). Approximately 30% to 70% o individuals with ADPKD have hepatic involvement. In both ADPKD and ADPLD there are innumerable hepatic cysts but patients with ADPLD do not have renal involvement. Hepatic brosis may occur in patients with ADPKD polycystic liver disease. Patients with polycystic liver regardless o the etiology may have pain rom hepatomegaly, portal hypertension resulting rom portal vein compression, or early satiety resulting rom extrinsic gastric compression. Other hepatic cysts include Caroli disease, biliary ham artom as, and biliary cystadenom as, which are urther detailed in the biliary section. The di erential diagnosis o hepatic cysts includes hydatid cysts, abscess, biliary cystadenom a, and m ucinous and cystic m etastases (Table 9 -3).

Hemangioma Hem angiom as are the m ost com mon benign noncystic lesion in the liver. They are ound in individuals o all ages with a reported prevalence o 1% to 20% and slightly m ore com mon in em ales. Hem angiom as are rare in cirrhotic livers there ore hem angiom a-like lesions in cirrhosis should always prom pt comparison with previous im aging and careul ollow-up or biopsy (Table 9 -4).

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Body CT: The Essentials

T bl 9-3. Hepatic Cysts D v lo m n l cys a bsc ss Cys ic o n c o ic n o l sm Bilom s Bili y

m

om s

Bili y cys d nom C oli dis

s

The presence o m ultiple liver hem angiom as is com m on. Hemangiomatosis is de ned as the presence o 10 or m ore hem angiom as within one liver. Hem angiom atosis m ay be indistinguishable rom angiosarcom a m etastases, because both m ay dem onstrate nodular centripetal enhancem ent. The coexistence o hem angiom as, FNH , and adenom as is com m on especially in young wom en. Even though all the three entities are benign, care ul analysis o each lesion is m andatory to di erentiate lesions that require urther im aging or ollow-up rom benign hem angiom as, which are “leave alone” lesions.

Focal nodular hyperplasia Microscopically hem angiom as represent dilated venous spaces supplied by hepatic arteries. Hem angiom as are benign, incidental lesions that are usually o no clinical signi cance other than not con using them or a m alignancy. Giant hemangiomas de ned as hem angiom as m easuring greater than 4 to 12 cm in size have been reported to spontaneously rupture during pregnancy or estrogen treatm ent and have been reported to cause throm bocytopenia (Kasabach–Merritt syndrom e). On CT caverno s hemangiomas are hypodense lesions that dem onstrate centripetal enhancem ent with peripheral nodular discontinuous enhancem ent on arterial and portal venous phase that progresses and coalesces on equilibrium and m ore delayed phases (Figure 9 -9 ). A continuous ring o peripheral enhancem ent on early contrast phases is not a typical nding or hem angiom as. Sim ilarly contrast washout or attenuation greater than blood pool are not typical ndings and should prom pt consideration o other entities such as abscess, m etastases, and prim ary m alignancy. Although arterial–portal venous shunting is m ore com m on with m alignant lesions; it does occur with hem angiom as and results in a geographic area o hyperenhancem ent (TH AD) adjacent to the hem angiom a. Capillary hemangiomas (f ash- lling hemangiomas) are usually smaller than 2 cm and dem onstrate imm ediate, hom ogeneous enhancem ent on the rst contrast-enhanced CT, whether it is arterial or portal venous phase (Figure 9 -10). Like cavernous hem angiom as they ollow blood pool attenuation and should remain isoattenuating to blood pool on equilibrium phase, which helps to di erentiate them rom other hypervascular lesions such as metastases. Atypical hemangiomas are hem angiom as that do not dem onstrate the classic enhancem ent characteristics described earlier. Frequently these are large hem angiom as with brotic or hyalinized com ponents and occasionally central dystrophic calci cations. The enhancem ent eatures o atypical hem angiom as are variable and can include slow, m odest enhancem ent that is less than that o the blood pool or heterogeneous contrast enhancem ent on equilibrium and delayed phases. Because the im aging eatures o atypical hem angiom as are not speci c and can overlap with hepatic tum ors, tissue sam pling m ay be necessary i there are no com parison studies to docum ent long-term stability.

Focal nodular hyperplasia (FNH ) is a benign m al orm ation o hepatic parenchym a that is considered to be a ham artom atous lesion. It is the second m ost com m on benign hepatic “tum or” with a prevalence o 0 .9 % and em ale-tom ale predom inance o 8:1. In approxim ately 20 % o cases there are m ultiple FNH s present. It is not uncom m on or FNH s, adenom as, and hem angiom as to coexist in the sam e liver. On noncontrast CT FNH s are lobulated lesions that are usually isoattenuating or hypoattenuating to adjacent liver parenchym a. On arterial phase FNH s are hypervascular with the exception o the radial brous septations and a central scar that are hypovascular. On portal venous and equilibrium phase contrast-enhanced CT FNH s are usually isoattenuating to the surrounding parenchym a and m ay be dif cult to distinguish rom adjacent norm al liver parenchym a except or subtle displacem ent o adjacent liver vessels or by the delayed enhancem ent o a central scar (Figure 9 -11). The m ost im portant di erential diagnosis is brolam ellar hepatocellular carcinom a (FLC), which usually occurs in young adults and can dem onstrate hyperenhancem ent with a central scar, sim ilar to FNH (Table 9 -5). However, FLC is usually large at the tim e o detection and dem onstrates heterogeneous areas o arterial enhancem ent, eatures atypical or FNH . The central scar in FLC m ay be calci ed and i present can help di erentiate FLC rom FNH ; however, the absence o a calci cation does not exclude FLC. Both FNH and FLC m ay show washout and a pseudocapsule on equilibrium phase, but these ndings tend to be m ore pronounced in brolam ellar carcinom a. Atypical im aging eatures or FNH include presence o at, heterogeneous enhancem ent, calci cations, and growth and i present should prom pt tissue sam pling or liver MRI with hepatospeci c contrast agents.

Hepatocellular adenoma Hepatocellular cell adenom a is the m ost com m on benign neoplasm o the liver. Eighty- ve percent occur in wom en and there is a strong association with the use o oral contraceptives. Other risk actors include anabolic steroid use, pregnancy, and glycogen storage diseases. Although these are benign lesions there is a risk o intratum oral hem orrhage, hem operitoneum , and m alignant trans orm ation in adenom as greater than 5 cm in size.

Chapter 9 Liver and Biliary 111

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Figure 9-9 Cavernous Hemangioma Two cavernous hem angiom as o di erent sizes in a young m an. On unenhanced CT (A) both hem angiom as are hypodense (white arrows). With arterial phase enhancem ent (B) the giant exophytic hem angiom a in le t lobe shows classic peripheral nodular discontinuous centripetal enhancem ent that progresses on portal venous (white arrows) (C) and delayed phase CT (D). The sm aller hem angiom a in segm ent VIII

has sim ilar enhancem ent eatures with peripheral nodular centripetal enhancem ent (black arrows in C). On the delayed phase CT (D) contrast enhancem ent has progressed to the center o the sm aller hem angiom a (white arrow) whereas in the giant hem angiom a the contrast has progressed but has not reached the center o the giant hem angiom a (star). The enhancem ent characteristics are typical or hem angiom as o these sizes.

Hepatic adenom as can be categorized into three subtypes that have di ering clinical behavior and im aging eatures: (1) in am m atory adenom as; (2) hepatocyte nuclear actor (H NF)-1 α –m utated adenom as; and (3) β -catenin– m utated adenom as. Inf ammatory (teleangiectatic) adenomas are m ost com m on subtype accounting or 40 % to 50% o hepatic adenom as and m ost com m only occur in young wom en using oral contraceptives. The risk or intratum oral hem orrhage is the greatest in this subtype with hem orrhage associated with 30 % o in am m atory adenom as. The risk o hem orrhage is greater i an in am m atory adenom a m easures greater than 5 cm . About 10% o in am m atory ade-

nom as m ay develop m alignant degeneration. On CT and MR in am m atory adenom as dem onstrate intense hyperenhancem ent on arterial phase that persists into the portal venous and equilibrium phases. Intratum oral hem orrhage is requently present. HNF-1 α –m tated (steatotic) adenomas account or 30 % to 40% o hepatocellular adenom as. They occur exclusively in wom en and are strongly associated with the use o oral contraceptives. Am ong the subtypes o adenom as, they are the least aggressive subtype with very sm all risk or bleeding when less than 5 cm in size and m inim al or no risk or m alignant degeneration. In about 50 % o cases m ultiple adenom as are present. H NF-1 α –m utated adenom as

112 Body CT: The Essentials

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Figure 9-10 Capillary ( ash-f lling) Hemangioma Contrast-enhanced CT demonstrating a sm all ash- lling hem angiom a. On arterial phase (A) there is enhancem ent o nearly the entire lesion (arrows) and a perilesional hypervascular

transient hepatic attenuation di erence (TH AD, arrowhead). The attenuation o the hem angiom a on portal venous (B) and equilibrium phase (C) ollows blood pool attenuation (com pare to IVC and aorta).

are characterized by the accum ulation o intracellular lipids that m ay be detected by chem ical shi t MRI which has a sensitivity o 86 % to 100 % or diagnosis o this subtype o adenom a. In about 7% o hepatocellular adenom as there is m acroscopic accum ulation o at that can be identi ed on unenhanced CT by the presence o areas o negativeattenuation (H U) values. On CT this subtype requently dem onstrates avid enhancem ent on the arterial phase that does not persist into the portal venous and delayed phases. This subtype o ten occurs in the setting o hepatic steatosis. β-catenin–m tated adenomas constitute about 10% to 15% o all hepatocellular adenom as and is the m ost com m on subtype in m en. This subtype is associated with anabolic steroid use, glycogen storage disease, and am ilial adenom atous polyposis. O all hepatocellular adenom as, β -catenin–m utated subtypes have the highest risk o m alignancy and are considered borderline neoplasm s. Risk actors or m alignant degeneration include m ale gender, adenom as m easuring greater than 5 cm , and anabolic steroid usage. The β -catenin–m utated subtype o adenom a has variable im aging characteristics. Approxim ately 10% o all hepatocellular adenom as are unclassi ed. Hepatocell lar adenomatosis (Figure 9 -12) is arbitrarily de ned as the presence o 10 and m ore liver adenom as and m ost com m only occurs in young obese wom en, o ten in association with the use o oral contraceptives. Any o the subtypes o liver cell adenom a m ay be involved. Di erentiating a small adenoma rom FNH can be dif cult because their im aging eatures overlap with one

another. Internal hemorrhage in adenomas and central scar in FNH are characteristic eatures that i present can help to di erentiate the two; however, these eatures are present in ewer than 50% o cases. Liver MRI with a hepatospeci c contrast agent m ay be use ul in di erentiating FNH rom adenom as. In young emales discontinuation o oral contraceptives should result in regression o estrogen-associated adenom as.

In ammatory Pseudotumor Hepatic in ammatory pseudotumors are ocal in ammatory lesions o uncertain etiology. Patients present with abdominal pain and ever. The imaging eatures o hepatic in ammatory pseudotumors are nonspeci c. The lesion may be a solitary or multi ocal mass. On contrast-enhanced CT the enhancement characteristics are variable, but requently heterogeneous. Because the imaging eatures are not speci c and overlap with malignant tumors histological sampling is requently needed. I malignancy has been excluded then in ammatory pseudotumors can be treated with nonsteroidal anti-in ammatory drugs and observation.

Liver Neoplasms Hepatocellular carcinoma Hepatocellular carcinom a (H CC) is the m ost com m on prim ary hepatic m alignancy and the second m ost com m on m alignancy in the liver ollowing m etastases. About 9 0 % o patients with H CC have cirrhosis and over 75% o H CCs result rom viral hepatitis. Risk actors or the developm ent

Chapter 9 Liver and Biliary 113

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Figure 9-11 Focal Nodular Hyperplasia Liver CT in a 31-year-old em ale with ocal nodular hyperplasia (FNH ). On unenhanced CT FNH is isoattenuating to the surrounding liver except or the sm all central hypoattenuating scar (arrow in A). On arterial phase contrast-enhanced CT (B) the FNH dem onstrates avid hom ogeneous enhancem ent with the exception o the central hypovascular scar. On portal venous

phase (C) the central scar rem ains hypovascular whereas the enhancing com ponents o the FNH are nearly isoattenuating with the surrounding liver parenchym a. A thin peripheral rim o com pressed hepatic vessels m im icks a capsule. Equilibrium phase (D) shows delayed enhancem ent o the brotic central scar (arrow in D) whereas the rest o the FNH is isoattenuating.

o H CC are hepatitis B and C, hepatitis rom excessive alcohol consum ption, NASH , a atoxin B exposure, and m etabolic diseases such as hem ochrom atosis. In patients with cirrhosis H CC develops at a rate o 1% to 4% o patients per year. H CC is m ost prevalent in older individuals with the exception o the brolam ellar H CC that occurs in young adults. H CC has three m ajor growth patterns: (1) a solitary or m assive H CC; (2) m ulti ocal H CC; and (3) di use, in ltrative H CC. On unenhanced CT H CC is hypodense in a nonsteatotic liver with variable but predom inantly strong hyperenhancem ent on late arterial phase (Figure 9 -13)

because it draws its blood supply rom the arterial in ow. I cirrhosis is present the di erential diagnosis o a hypervascular lesion is lim ited—arterioportal venous shunt, dysplastic nodules, and H CCs. Flash- lling hemangiomas are rare in cirrhosis and adenomas and FNH s should not be diagnosed in a cirrhotic liver. On equilibrium phase H CCs usually dem onstrate hypoattenuation (washo t) relative to the remainder o the liver. The appearance o H CCs on portal venous phase is variable. Large H CCs com m only have a heterogeneous or mosaic appearance because o intralesional nodules and brous septations, necrosis, and som etim es the presence o at. A pseudocapsule on equilibrium phase

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Body CT: The Essentials

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Figure 9-12 Hepatic Adenomatosis Fem ale with history o oral contraceptive use and num erous hepatic adenom as that are m inim ally visible on unenhanced (A) and equilibrium phase CT (D). The dom inant hypervascular adenom a (arrowheads) and other sm aller adenom as have

heterogeneous enhancem ent on arterial (B) and portal venous phase CT (C). A sm all adenom a in right liver (black arrow in D) dem onstrates a ocus o at, best seen on equilibrium phase (arrow in D).

CT has a positive predictive value or the diagnosis o H CC o 9 5%. Vascular invasion o the portal and hepatic veins is also a com m on nding in large H CCs. Another typical eature o larger H CC is the presence o smaller satellite nodules in the im mediate proxim ity o the dom inant m ass. About 15% o H CCs have the di use in ltrative pattern o growth with heterogeneous enhancem ent and subtle or no contrast washout on CT (Figure 9 -14). H CC m etastases occur with large solitary tumors or in the setting o multiple sm aller tumors with the most comm on sites o involvement being the lung, abdominal lymph nodes, and bone. Imaging eatures that best correlate with H CC in patients with cirrhosis are hypervascular enhancement, washout on portal venous or delayed contrast phases, the presence o a pseudocapsule, and lesion growth. Lesion size is also a

very important actor in that hypervascular lesions measuring less than 10 mm are much more likely to represent a regenerating nodule or a hypervascular shunt, both o which are expected ndings in patients with cirrhosis. H yperenhancing lesions measuring 20 mm or greater in a cirrhotic liver are likely to represent H CC and in most instances an imaging diagnosis is considered suf cient or treatment without urther need o histologic diagnosis. H yperenhancing lesions measuring 10 to 19 mm in a cirrhotic liver have intermediate probability o representing H CC, but the probability increases when multiple characteristics are present in the same lesion so a hypervascular lesion with washout and growth or a pseudocapsule has greater probability o representing H CC. The American College o Radiology (ACR) has published the Liver Im aging Reporting an d Data System

Chapter 9 Liver and Biliary 115

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Figure 9-13 Hepatocellular Carcinoma Contrast-enhanced CT in a emale with hepatitis B dem onstrates a 2.5 cm H CC in segm ent VIII that is hypervascular with m osaic enhancem ent (i.e., intratum oral nodules o variable

enhancem ent) on arterial phase (A) and hypoattenuating (“washout”) with surrounding hyperdense pseudocapsule on equilibrium phase (arrow in B).

(LI-RADS) reporting system or the reporting and risk strati cation o ocal liver lesions in patients at risk or the development o H CC. The diagnostic per ormance o CT in diagnosis o H CC in patients with cirrhosis has sensitivities

o 55% to 80% and speci cities o 89% to 96% which is superior to ultrasound, but slightly in erior to MRI. Because liver CTs are multiphasic studies, they are one o the highest radiation dose CT scans per ormed in abdominal imaging which

A

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Figure 9-14 Inf ltrative Hepatocellular Carcinoma Coronal image rom contrast-enhanced CT in a male with cirrhosis rom hepatitis C. In segment VIII there is a hypervascular H CC (arrowheads in A), that is dif cult to distinguish because o the surrounding hypervascular per usion abnorm ality (TH AD)

caused by the expansile tum or throm bus in the portal vein (arrow in A). Ten-m inute delayed contrast-enhanced CT does not dem onstrate discernible washout or surrounding pseudocapsule which is typical or di use H CC.

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Body CT: The Essentials

raises concern or potential cumulative radiation exposure in patients who are likely to be subject to numerous scans over the course o their lives as part o screening or or ollowup o liver lesions. Because o this concern and the superior diagnosis per ormance o MRI or detection o H CC, liver MRI is being employed with increasing requency or patients at risk or H CC.

Fibrolamellar hepatocellular carcinoma Fibrolamellar hepatocellular carcinoma (FLC) is a histologic variant o H CC which di ers rom conventional H CC in several ways. It occurs in young individuals with the average age o 26 years and is not associated with cirrhosis, di use liver disease, or other risk actors or H CC. At presentation 80% to 90% o FLCs are large solitary lobulated masses. They are heterogeneous masses with hyperenhancement on arterial phase CT. Fibrous septations that coalesce to orm a central scar are present in 70% o cases and are hypoenhancing on arterial and portal venous phase CT but may demonstrate delayed enhancement on equilibrium phase. Central calci cations are present in over 50% o cases, but absence o a central calci cation does not exclude H CC. The primary di erential diagnosis is FNH that shares the same epidemiology and imaging eatures o a scar and hypervascular enhancement on arterial phase. FNH is usually homogeneously hypervascular whereas FLC has heterogeneous enhancement. Washout and pseudocapsules are more common in FLC than FNH . In cases where an FNH cannot be distinguished rom FLC on CT, MR with a hepatobiliary contrast agent should be considered because FLCs show no or mild patchy uptake in delayed hepatospeci c phases o enhancement, whereas FNH s commonly have strong enhancement.

o involvem ent. Hepatic angiosarcoma m ost comm only a ects older individuals but can occur in younger adults. On CT hepatic angiosarcom as are large hypervascular masses that are requently m ulti ocal. Central or irregular peripheral enhancement on arterial phase with progressive contrast enhancement or washout on equilibrium phase may be present. Small angiosarcom as m ay m im ic hemangiomas since both types o lesions m ay dem onstrate centripetal nodular enhancem ent. Central nodular enhancem ent with persistent blood pool enhancem ent on equilibrium phase however is more comm on in angiosarcom a.

Epithelioid hemangioendothelioma Epithelioid hemangioendothelioma (EHE) is a rare vascular neoplasm o variable malignant potential that occurs in young and middle-aged adults with slight emale predominance. EH E is usually m ulti ocal with a peripheral subcapsular distribution. Over tim e sm aller lesions coalesce into larger con uent mass. Retraction o the adjacent liver capsule is a com mon nding. On unenhanced CT EH E is hypoattenuating. On contrast-enhanced CT EH E have an avascular hypoenhancing outer rim with a aintly enhancing inner rim on arterial phase (Figure 9 -15). The central portion o EH E m ay not enhance or enhance only on delayed im aging. Because o its m ulti ocality and potential or malignancy liver transplantation is considered the treatm ent o choice.

In antile hemangioendothelioma

Hepatoblastoma is the most com mon primary pediatric malignant hepatic tum or. Ninety percent o cases present in the rst 5 years o li e with a slight male predom inance o 1.5:1. A ter the th year o li e H CC is the most comm on primary hepatic m alignancy. In 80% o cases hepatoblastom a presents as a large solitary mass. Serum alpha- etoprotein levels are elevated in 9 0% o cases. On unenhanced CT hepatoblastom as are usually hypoattenuating and 50% have calci cations. On contrastenhanced CT they are usually hypervascular on arterial phase with washout on portal venous phase. Fibrous septations sim ilar to H CC are also com m only present.

In antile hem angioendotheliom a (juvenile hem angiom a) is a benign vascular m alignancy and the m ost com m on liver m ass in in ants with 9 0% occurring in the rst 6 m onths o li e with a slight m ale predom inance. In about hal the cases it presents as a solitary liver m ass and in the other hal o cases it is a m ulti ocal liver m ass. In 10% to 6 8% o patients with m ulti ocal liver lesions, there can have involvem ent o other organs such as skin or chest. Although benign in antile hem angiom as can lead to com plications o high-output cardiac ailure due to arteriovenous shunts or Kasabach–Merritt syndrom e due to intratum oral platelet sequestration. On CT speckled calci cations are present in 50 % o cases. On contrast-enhanced CT enhancem ent o in antile hem angioendotheliom as are sim ilar to those o hem angiom as in adults with progressive centripetal nodular enhancem ent that ollows blood pool attenuation. Because o the high ow through the tum or the hepatic arteries and veins m ay be enlarged.

Hepatic angiosarcoma

Lymphoma

Hepatic angiosarcom a is an aggressive primary or m etastatic m alignancy o the liver. It is rare but the most com mon prim ary hepatic sarcoma. Risk actors include exposure to polyvinyl chloride, arsenic, steroids, or thorotrast, but most patients have no history o exposure. At the tim e o presentation the m ajority o patients have metastases with liver, spleen, lung, and bone being the most requent sites

Primary hepatic lymphoma is rare, but up to hal o patients with lymphoma have hepatic involvement. In Hodgkin disease there is usually di use in ltration o the liver. In nonHodgkin disease there may be discrete nodules or di use in ltration. On CT primary hepatic lymphoma may present as a large solitary mass with central necrosis or multiple masses. In secondary hepatic involvement there are multiple

Hepatoblastoma

Chapter 9 Liver and Biliary 117

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Figure 9-15 Epithelioid Hemangioendothelioma Contrast-enhanced CT in m iddle-aged patient with peripherally located epithelioid hem angioendotheliom a that is hypovascular

on arterial (A) and portal venous (B) phases with central enhancem ent and peripheral contrast washout on the 10-m inute delayed phase (C).

hypoattenuating, hypoenhancing masses that may show encasement o intrahepatic vessels without narrowing o the vessel lumen (vessel penetration sign). Frequently the liver ndings are accompanied by signi cant lymphadenopathy or splenomegaly which can be help ul to distinguish lymphoma rom other etiologies o liver masses. In the di use in ltrative orm o hepatic lymphoma the liver is enlarged but there are no discrete hepatic masses.

on equilibrium and later phases o contrast-enhancem ent hypervascular m etastases m ay show washout or prolonged hyperenhancem ent relative to the adjacent liver parenchym a. With success ul system ic or liver directed treatm ent a local brotic response associated with treated m etastases

Metastases Metastases are the most common malignant liver neoplasms in patients over 40 years o age. Gastrointestinal primary tumors commonly metastasize to the liver via the portal circulation but breast and lung primary neoplasms and melanoma may metastasize to the liver via the hepatic arteries. Metastases to the liver tend to have im aging characteristics sim ilar to the prim ary tum or. Most hepatic m etastases are hypodense on unenhanced CT. Colon and breast m etastases som etim es contain calci cations (Figure 9 -16 ). Metastases rom lung, gastrointestinal, and breast prim ary carcinom as are usually hypoenhancing on contrastenhanced CT despite the act that they derive their blood supply predom inantly rom the hepatic arteries. When m etastases have increased vascularity com pared to the adjacent liver parenchym a they are hypervascular and avidly enhance on arterial phase contrast enhancem ent such as with intrahepatic m etastases o H CC or m etastases rom m elanom a or renal cell, thyroid, neuroendocrine carcinom as. On portal venous and m ore com m only

Figure 9-16 Hepatic Metastases Contrast-enhanced CT in patient with two colorectal hepatic m etastases (arrows) with central necrosis, lobulated m argins, and punctate calci cations at the transition between necrotic and viable tum or tissue (arrowheads).

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Body CT: The Essentials

m ay cause retraction o the hepatic capsule and result in pseudocirrhosis.

Liver Hemorrhage Spontaneous liver hemorrhage in the absence o trauma or anticoagulation is rare but can be associated with underlying liver disease and be li e threatening. A thorough search or an underlying hepatic mass should be made in any person with spontaneous hepatic hemorrhage. In some instances the hepatic hemorrhage may obscure an underlying mass there ore patients with unexplained liver hemorrhage and unrevealing evaluation should be reevaluated a ter the acute hemorrhage has cleared. Liver masses most commonly associated with spontaneous hemorrhage are H CC, adenoma, and metastases. Hemorrhage associated with FNH and hemangiomas is rare. Di use liver diseases including hepatic amyloidosis and H ELLP syndrome can also result in spontaneous liver hemorrhage (Figure 9-17). In the rst 24 to 72 hours liver hemorrhage is hyperattenuating making it visible on unenhanced CT. Over time it becomes more hypoattenuating. Large hemorrhages result in hepatic enlargement and hemoperitoneum i there is disruption o the hepatic capsule.

Vascular Phenomena Transient hepatic attenuation dif erences Transient hepatic attenuation di erence (TH AD) is a transient alteration o liver enhancement usually seen on arterial or portal venous phases o contrast-enhanced CT o the liver (Figure 19-18). They result rom the local mismatches in ow rom hepatic arteries and portal veins. TH ADs do not persist into equilibrium and later post contrast enhancement phases.

A Figure 9-18 Transient Hepatic Attenuation Di erence (THAD) Coronal im age rom contrast-enhanced CT demonstrating a TH AD because o the portal vein throm bosis. The segm ental hepatic artery branch is well dem onstrated (arrow in A) within

Figure 9-17 Hepatic Hemorrhage Contrast-enhanced CT demonstrating m ultiple hem orrhages in a patient with am yloidosis. The liver is enlarged and m ildly com pressing the right kidney.

H ypervascular TH ADs can result rom the hepatic arterial bu er response to decreased portal venous ow in which there is com pensatory increase in arterial ow to maintain total ow. The increased ow through the hepatic artery results in additional delivery o concentrated contrast rom the aorta on arterial phase which leads to areas o increased enhancement during early contrast-enhanced phases. This m ost requently occurs when portal vein branches becom e obstructed m ost com monly by throm bus, compression, or direct tumor invasion. TH ADs caused by portal vein obstruction are usually wedge shaped and extend to the periphery

B the geographic area o hyperattenuation (“straight border sign,” arrowheads in A) caused by throm bus o a segm ental portal vein branch (arrow in B). The TH AD does not persist into the portal venous phase (B).

Chapter 9 Liver and Biliary 119 T bl 9-4. H yperenhancing Liver Lesions Noncirrhotic liver h m ngiom ( s ing- lling) Foc l nodul y l si a d nom h y v scul m s s s h oc llul c cinom Cirrhotic liver h oc llul c cinom Dys l s ic nodul r g n ing nodul

o the liver. Their size will vary depending on the size and territory o the obstructed portal vein. I a lobar portal vein is obstructed the TH AD will involve the entire a ected lobe. Another m echanism or developm ent o TH ADs is regional hypervascularity in which the portal vein ow is not com prom ised but increased hepatic arterial ow is stim ulated by the presence o a tum or, in ection, or abscess— akin to a siphon e ect (Figure 9 -27). In cases where TH AD is caused by a neoplasm it is im portant to delineate the TH AD rom the underlying m ass to accurately assess and ollow-up lesions because the presence and size o TH ADs will vary between scans (Table 9 -6 ).

Hepatic congestion Hepatic congestion is the stasis o blood in the hepatic venous system and sinusoids because o im paired hepatic venous out ow. The m ost com m on cause is elevated central venous pressures caused by right heart disease or constrictive pericarditis but other etiologies include acute hepatitis, throm botic, and neoplastic obstruction. On CT hepatic congestion due to right heart ailure is accom panied by dilation o the IVC and intrahepatic veins, which m ay contain contrast on the early phases ollowing contrast adm inistration because o the retrograde ow o contrast rom the right atrium . During the portal venous phase parenchym al enhancem ent has a m arble per usion pattern (Figure 9 -19 ). By the equilibrium phase, enhancem ent o the liver parenchym a is usually uni orm . Signs o portal hypertension are requently present. Long-standing hepatic congestion caused by heart ailure can result in cirrhosis.

T bl 9-5. Liver Lesions with Central Scar Foc l nodul

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po a cu

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Hepatic shunts Hepatic shunts are aberrant congenital or acquired vascular connections that can occur within or extrinsic to the liver. Congenital shunts are rare and usually portosystemic shunts. Since many congenital hepatic shunts are symptomatic in childhood, diagnosis is usually made by Doppler ultrasound. CT, however, can also demonstrate vascular pathologies and has the potential to characterize regenerative nodules that are o ten associated with these congenital anomalies. Rarely small intrahepatic portosystemic shunts may be encountered in adults. On CT the most common appearance is o a centimeter- or smaller-sized nodule that has blood pool attenuation with a visible eeding portal vein and draining hepatic vein extending into the nodule (Figure 19-20). Acquired hepatic shunts are usually hypervascular arterioportal com m unications that are acquired by biopsy or traum a. They are usually asym ptom atic, but their recognition is im portant so that they are not m istaken or a hypervascular tum or. Post-biopsy shunts are typically located in a lateral portion o the right liver o ten with a transverse orientation to the liver capsule, corresponding the tract o the biopsy needle. Intentional shunts such as transjugular intrahepatic portosystem ic shunt (TIPSS) and extrahepatic portocaval shunts (Denver shunt and Warren shunt) are per orm ed to decreased portal hypertension and reduce the rate o ascites orm ation and decrease the risk or variceal bleeding.

Hepatic in arction Because o the dual blood supply o the liver a hepatic in arct requires occlusion or comprom ise o the hepatic artery and portal vein serving the sam e vascular territory. The most com m on clinical scenarios or hepatic in arction are acute vascular comprom ise o orthotopic liver transplantation or alterations in coagulability such as m ay occur in shock, sepsis, sickle cell anemia, and in patients using oral contraceptives. On CT in arctions are sharp hypovascular lesions that extend to the capsule. In contrast to con uent brosis that m ay have a triangular shape and extend to the capsule, hepatic in arctions do not enhance on equilibrium or delayed phase contrast-enhanced CT.

Peliosis hepatis

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T bl 9-6 . Conditions associated with TH ADs

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Peliosis hepatis is a rare disorder that results rom m icroscopic dilatation o hepatic sinusoids that can range in size rom 1 m m to several centim eters. Its etiology is not understood, but it can be associated with system ic wasting diseases and in ections such as AIDS and tuberculosis,

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Body CT: The Essentials

A Figure 9-19 Hepatic Congestion A. Mosaic enhancem ent pattern in a 6 5-year-old patient with a m etastasis obstructing hepatic venous out ow (obstructing m ass not shown). The central portal veins o a hepatic lobule enhance

B with contrast (arrows in A), whereas the periphery o the hepatic lobule is hypoattenuating resulting in the polygonal or chickenwire appearance. B Marble enhancem ent pattern o the liver (arrows) in a patient with right heart ailure.

m alignancies, and with drugs such as corticosteroids and oral contraceptives. In 20% to 50% o cases no associated condition is identi ed. Peliosis hepatis does not usually result in sym ptom s, although it has been reported to lead to hepatic ailure and portal hypertension in som e cases and rarely hepatic rupture with hem orrhage. On contrast-enhanced CT peliosis hepatitis can dem onstrate centripetal or centri ugal enhancem ent with a ring o enhancem ent on equilibrium phase (Figure 9 -21). The diagnosis o peliosis hepatis on im aging should always be con rm ed with biopsy or close ollow-up, since it is a rare condition with variable im aging eatures and the potential con used with a m alignancy.

BiLia r y Sy STe m Anatomy

Figure 9-20 Intrahepatic Portosystemic Shunt Contrast-enhanced CT demonstrating a small incidental portosystemic shunt (arrow) with a eeding portal vein branch and draining hepatic vein branch (arrowheads) Source: Used with permission rom the University o Washington, as developed as part o the Liver Imaging Atlas (http:/ / liveratlas.org/ ) © 2010-2013.

The intrahepatic bile ducts parallel the portal venous system. The right hepatic lobe (segments V to VIII) is drained by the right hepatic duct, which is ormed by the joining o a posterior branch that drains the posterior segments (VI and VII) and an anterior branch draining the anterior segments (V and VIII). The le t hepatic lobe is drained by the le t hepatic duct that is ormed by ducts converging rom the le t hepatic segments (II to IV). Le t hepatic and right hepatic ducts join

Chapter 9 Liver and Biliary 121 T bl 9 -8. Extrahepatic Biliary Distention without Intrahepatic Distention e ly obs uc ion o

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Figure 9-21 Hepatic Peliosis Contrast-enhanced CT in a 36 -year-old m ale with AIDS dem onstrating num erous hypervascular lesions with irregular shapes and som e with low-attenuation centers (arrows) m im icking ocal nodular hyperplasia.

together to orm the common hepatic duct. Conventional biliary anatomy is present in 58% o individuals. Common anatomic variants o the upper biliary tree include right posterior branch draining directly into the hepatic duct which is present in up to 19% o individuals. Another variant present in 11% o individuals is a tri urcation at the biliary hilum in which the right anterior and right posterior branch ducts and the le t hepatic duct all converge together at the same point, so that there is no right hepatic duct. Drainage o an aberrant right branch duct into the common hepatic duct or the cystic duct is present in up to 5% o individuals. The cystic duct joins with the common hepatic duct to orm the common bile duct typically in the upper third o the extrahepatic bile duct. Variants in cystic duct anatomy include cystic duct insertion into the right hepatic duct and low insertion in which the cystic duct inserts into the lower extrahepatic bile duct, which is present in up to 9% o individuals. Anatomic variation o biliary system is common and clinically important in those patients undergoing surgery or other interventional procedures as ailure to recognize anatomic variants can lead to iatrogenic bile duct injuries. In m ost individuals there is some variation in the caliber o the extrahepatic bile duct. The upper lim its o nor-

I

m al caliber in a person 50 years o age or younger is 5 to 6 m m. In older individuals the caliber o the bile duct tends to be larger with the accepted upper lim its o norm al o 7 to 8 m m . In patients who have undergone cholecystectomy a caliber o 10 m m is the generally accepted upper limit o normal size (Table 9 -7 and Table 9 -8). The lower bile duct passes through the pancreatic head in m ost individuals but in 30 % o people it passes within a groove along the posterior m argin o the pancreatic head. The bile duct passes through the m edial wall o second duodenal segm ent where it is encom passed by the sphincter o Oddi com plex. In the duodenal wall the bile duct and pancreatic duct (duct o Wirsung) run alongside one another and usually join together to orm a short com m on channel that drains to the m ajor duodenal papilla (Figure 9 -22).

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Figure 9-22 Normal Pancreaticobiliary Junction Coronal im age rom a contrast-enhanced CT through the pancreaticobiliary junction (arrowheads). The com m on bile duct and pancreatic duct use in the sphincter o Oddi com plex. In contrast, an aberrant long comm on channel occurs when the bile duct and pancreatic duct join together in the pancreatic head allowing re ux o bile into the pancreatic duct and pancreatic juice into the bile duct.

122 Body CT: The Essentials

Norma l

Type 1

Type 4a

Type 2

Type 4b

Type 3

Type 5

Figure 9-23 Todani classif cation o choledochocysts

A long common channel is an anom aly in which the bile and pancreatic ducts use in the pancreatic head, above the sphincter o Oddi com plex. This aberrant connection allows re ux o pancreatic juice into the bile duct, which is associated with type I choledochocysts, and re ux o bile into the pancreatic duct, which can cause pancreatitis.

Choledochal Cysts

Figu 9-24 t y I C ol doc ocys Coronal image rom contrast-enhanced CT demonstrates usi orm dilation o the extrahepatic bile duct (arrowheads). There was a long common channel (arrow) between the bile duct and the pancreatic ducts. Gallbladder (labeled G) was decompressed.

Choledochal cysts are congenital anom alies o the biliary system that are distinguished by cystic or usi orm dilation o the biliary tree. Most choledochal cysts are diagnosed in childhood but up to 20 % to 40% o patients m ay present in adulthood. In children the classic triad o ndings are jaundice, abdom inal pain, and right upper quadrant m ass. However, in adults the m ost com m on sym ptom is nonspeci c abdom inal pain. Fem ales are our tim es m ore likely to be a ected than m ales. The Todani classi cation system divides choledochal cysts into ve categories based on their m orphology: (Figure 9 -23) Type I— usi orm dilation o the extrahepatic bile duct (Figure 9 -24); Type II—diverticulum originating rom the extrahepatic bile duct; Type III—choledochocele (cystic dilation o the intram ural portion o

Chapter 9 Liver and Biliary 123 the lower bile duct); Type IVa— usi orm dilation o extrahepatic duct with cystic dilation o the intrahepatic ducts; Type IVb—cystic dilation o the extrahepatic duct with no involvem ent o the intrahepatic duct; and Type V—cystic dilation o the intrahepatic ducts (Caroli disease). Choledochal cysts are associated with stones in the cyst, gallbladder, and dilated intrahepatic ducts. Rupture can result in bile peritonitis in children, but is uncom m on in adults. Patients are at increased risk o biliary m alignancy. The presence o wall thickening or enhancing nodules within choledochal cysts are ndings associated with neoplasm . Extrahepatic choledochal cysts that are sym ptom atic or have ndings worrisom e or the presence o neoplasm are usually resected; however, even a ter resection o choledochal cysts patients rem ain at increased risk o m alignancy elsewhere in the biliary system .

Caroli disease Caroli disease is characterized by saccular ectasia o intrahepatic bile ducts that can have a di use or segm ental distribution in the liver. Although it is categorized under the Todani classi cation system or choledochal cysts. Caroli disease is not associated with aberrant long com m on hepatobiliary channel, but rather is a rare developm ental abnorm ality o intrahepatic bile duct. On im aging Caroli disease presents as dilated cystic structures that com m unicate with the biliary tree. The presence o an enhancing central portal vein radical surrounded by dilated bile ducts (central dot sign) (Figure 9 -25) is a nding suggestive o Caroli disease. Intrahepatic stones are a com m on nding.

Figure 9-26 Biliary Hamartomas Contrast-enhanced CT demonstrates m ultiple sm all wellde ned biliary hamartom as scattered through the liver. These do not com m unicate with the bile ducts and are o no clinical signi cance but should not be con used or pathology.

Caroli disease accom panied by hepatic Caroli syndrome.

brosis is called

Biliary Hamartomas Biliary ham artom as (von Meyenb rg complexes) are developm ental lesions that represent em bryonic bile duct rem nants that persist because o the incom plete involution during the developm ent. They present as m ultiple sm all intrahepatic cysts m easuring rom 1 to 15 m m in size (Figure 9 -26 ). Unlike Caroli disease, biliary ham artom as do not com m unicate the bile duct. They are o no clinical signi cance but are im portant to recognize so as to not conuse them with m etastases or other pathology.

Cholelithiasis

Figure 9-25 Caroli Disease Coronal image rom contrast-enhanced CT demonstrates saccular ectasia o the intrahepatic bile ducts. There is an enhancing portal vein branch (arrow) that results in the “central dot” sign.

Gallstones orm rom supersaturation o bile com ponents. Cholesterol is the m ajor com ponent o gallstones except or pigm ent stones in which calcium salts o bile are the predom inate constituents. Approxim ately 20 % o gallstones contain calci cation and som e gallstones m ay develop nitrogen gas within central ssures (Mercedes Benz sign). Ultrasound is the im aging m odality o choice or detection o gallstones, but CT has reported sensitivity o up to 78% or detection o gallstones. Most patients with gallstones are asym ptom atic. In sym ptom atic patients biliary colic is usually caused when gallstones transiently obstruct the gallbladder neck or cystic duct with sym ptom s resolving when the gallstone alls back into the gallbladder or passes into the com m on bile duct. Once gallstones enter the com m on bile duct

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Body CT: The Essentials

Figure 9-27 Choledocholithiasis Coronal im age rom a contrast-enhanced CT dem onstrates a aintly visible gallstone (arrowhead) in a dilated com m on bile duct alongside a biliary stent.

(choledocholithiasis) they may cause obstruction and jaundice (Figure 9 -27). Other com plications associated with gallstones include acute cholecystitis, obstruction o the bile and cystic ducts (Mirizzi syndrome), pancreatitis, biliary stula, and cholangitis (Table 9 -9 ). Spillage o gallstones during laparoscopic cholecystectomy is reported in up to 6 % to 8% o surgeries and is associated with the development o indolent peritoneal abscess, usually located near the liver that can present rom 1month to 10 years a ter surgery.

In ammatory and In ectious Processes o the Gallbladder Acute cholecystitis In 9 0 % to 9 5% o cases acute cholecystitis is caused by obstruction o the cystic duct by gallstones. Because o its greater sensitivity or detection o gallstones and ability to assess or a Murphy sign ultrasound is superior to CT and the best im aging m odality or patients with suspected acute

inc

cholecystitis. However, i there is uncertainty as to the etiology o a patient’s pain or the presentation is atypical or acute cholecystitis, CT m ay be per orm ed be ore a right upper quadrant ultrasound. The CT ndings o acute cholecystitis include gallbladder distention, gallbladder di use wall thickening (>4 m m wall thickness), m ucosal hyperenhancem ent, and pericholecystic edema or uid. H yperenhancem ent o hepatic parenchyma along the gallbladder ossa because o the secondary hyperemia (CT rim sign) m ay be present (Figure 9 -28). The presence o di use gallbladder wall thickening has low speci city or acute cholecystitis as it can also be caused by hypoalbuminem ia, ascites, acute or chronic hepatitis, and chronic cholecystitis (Table 9 -10). Com plications o acute cholecystitis are more likely to occur in elderly and debilitated patients and are associated with greater patient m orbidity and higher m ortality rates. T bl 9-10 . Gallbladder Wall Thickening Incom l a cu

dis n ion (dif us )

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Figure 9-28 Gangrenous Cholecystitis with Per oration Coronal im age rom contrast-enhanced CT demonstrate thickened gallbladder wall with ocal de ect (black arrow) and contained pericholecystic abscess (white arrows). Note the hyperenhancem ent (TH AD) o the liver around the gallbladder ossa (arrowheads) which represents the CT rim sign.

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Chapter 9 Liver and Biliary 125 Gangreno s cholecystitis occurs in 2% to 38% o patients and is associated with increased risk o gallbladder per oration. On CT gangrenous cholecystitis m ay m ani est as areas o decreased m ucosal enhancem ent, mucosal de ects, or sloughed m ucosa. Gallbladder per oration occurs in 8% to 12% o cases o acute cholecystitis (Figure 9 -28). The m ost requent site o per oration is the gallbladder undus, but a transm ural de ect in the gallbladder is visualized in only 70% o cases. In patients with gallbladder per oration diagnosis o acute cholecystitis m ay be con ounded by the decompressed state o the gallbladder that results rom peroration. The per oration can result in ree spillage into the peritoneal space or result in a ocal pericholecystic abscess. Prom pt diagnosis is essential as the m ortality rate in patients with gallbladder per oration can be as high as 24%. Emphysemato s cholecystitis results rom secondary in ection o the gallbladder wall by gas- orming organism s in patients with acute cholecystitis and o ten leads to other complications such as per oration and has a mortality rate o 15%. Hemorrhagic cholecystitis is an uncomm on com plication o acute cholecystitis in which necrosis o the gallbladder wall results in hem orrhage into the gallbladder lum en and is associated with an increased mortality rate.

Acalculous cholecystitis Between 5% and 10 % o cases o acute cholecystitis are not associated with gallstones. Acalculous cholecystitis m ost com m only occurs in critically ill patients who are on total parenteral nutrition. The im aging eatures o acalculous cholecystitis include gallbladder distention, m ild gallbladder wall thickening, and the presence o viscous biliary sludge in the absence o gallstones. In general ultrasound is m ost com m only used in patients with suspected acalculous cholecystitis. CT has the advantage o being able to show in am m atory changes around the gallbladder which can be dif cult to detect by ultrasound; however, in practice the diagnosis o acalculous is requently dif cult to m ake because patients tend to have m ultiple m edical com orbidities and cannot be reliably assessed or the presence o a Murphy sign because o sedation or obtundation. Patients with acalculous cholecystitis are at high risk or gallbladder necrosis and per oration. The treatm ent o choice is gallbladder drainage and antim icrobial therapy.

Chronic cholecystitis Chronic cholecystitis is de ned by chronic in ammatory changes in the gallbladder wall that occurs in the setting o chronic cholelithiasis. On CT di use gallbladder wall thickening and gallstones – i visible by CT – are the most common ndings (Figure 9-29 ). Unlike acute cholecystitis the gallbladder may be contracted and acute in ammatory changes around the gallbladder are absent. An uncommon complication o chronic cholecystitis is per oration with ormation o a stula tract with an adjacent viscous with the most common sites o stula ormation being the duodenum, colon, and stomach. Gallstones pass through the s-

Figure 9-29 Chronic Cholecystitis Contrast-enhanced CT demonstrates di use chronic wall thickening o the gallbladder (arrowheads) in a patient with chronic right upper quadrant pain. The gallbladder was rem oved and at histologic analysis chronic cholecystitis with a sm all, contained ocus o neoplasia was identi ed.

tula and i suf ciently large can obstruct the lumen o the a ected viscous. Gallstone ile s is a mechanical obstruction o small bowel by intraluminal gallstones via cholecystoenteric stula (Figure 9-30). The most common location o gallstone impaction in the small bowel is the ileum ollowed by the jejunum and the duodenum.

Adenomyomatosis Adenomyomatosis is a benign hyperplastic condition characterized by the presence o intramural diverticula. The dilated diverticula are re erred to as Rokitansky–Ascho sin ses. It can occur at any age, but is most common in individuals 50 years or older with emales being more commonly a ected than males and concomitant cholelithiasis present in 90% o individuals. On imaging adenomyomatosis presents as gallbladder wall thickening that can be di use, segmental, or ocal. The ocal orm presents as a ocal area o intramural wall thickening most commonly at the gallbladder undus that can resemble a gallbladder polyp or mass (Figure 9-31). In the segmental or annular orm there is a ring o circumerential gallbladder wall thickening and luminal narrowing usually in the mid portion o the gallbladder. In the di use orm the gallbladder wall is di usely thickened and the gallbladder appears contracted. Di erentiating benign adenomyomatosis rom gallbladder neoplasm by imaging is challenging because the imaging eatures between the two are very similar. The presence o small intramural cysts in areas o gallbladder wall thickening (string o pearls sign) is a nding associated with adenomyomatosis but is not always present, and better detected by MRI than CT.

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Body CT: The Essentials

A

B

Figure 9-30 Gallstone Ileus Contrast-enhanced CT in a patient with chronic cholecystitis dem onstrates a cholecystoenteric stula with oral contrast and

air lling the gallbladder (arrowheads in A) and dilated sm all bowel resulting rom im pacted gallstone in the ileum (arrow in B).

In ammatory and In ectious Processes o the Bile Ducts Primary sclerosing cholangitis

Figure 9-31 Focal Adenomyomatosis Contrast-enhanced CT demonstrating ocal wall thickening o the gallbladder at the undus (arrowheads) with a tiny intram ural cyst. Gallbladder wall thickening rom adenom yomatosis can be ocal, circum erential, or di use and be dif cult to discern rom a neoplasm by CT. G, gallbladder.

Prim ary sclerosing cholangitis (PSC) is an idiopathic in am m atory disease characterized by brosis o the biliary tree. The m edian age o diagnosis is 40 years old and 70% o cases occur in m en. There is a strong association with ulcerative colitis with 70% o patients with PSC having ulcerative colitis; however, only 3% to 7% o patients with ulcerative colitis develop PSC. There is a weaker association with Crohn disease. In m ost patients PSC is a progressive disease leading to biliary cirrhosis and liver ailure but the rate o progression is variable and unpredictable. The m edian survival rom the tim e o diagnosis is 11.8 years. Liver transplantation is the only proven therapy. The hallm ark im aging ndings o PSC are developm ent o m ulti ocal biliary strictures that m ay vary rom 1to 2 m m to 1 cm in length. The presence o biliary strictures with intervening norm al or near-norm al calibered segm ents results in the bile ducts taking on a beaded appearance. Sm all biliary diverticula are present in approxim ately 25% o patients with PSC. Over tim e there is obliteration o the sm all peripheral intrahepatic bile ducts resulting in the intrahepatic ducts taking on a pr ned tree appearance. In about 70 % to 80 % o PSC strictures are distributed in both the intrahepatic and extrahepatic bile ducts. Approxim ately 10 % o individuals with PSC have strictures only within the intrahepatic bile ducts and another 10% o individuals

Chapter 9 Liver and Biliary 127 have strictures only in the extrahepatic ducts. Gallbladder involvem ent o PSC is present in 15% o patients. Intrahepatic bile duct calculi develop in 8% o patients with PSC. Mural wall thickening o bile ducts is a com m on nding in PSC. The presence o bile duct wall thickening, particularly when nodular or irregular can m ake it dif cult to di erentiate PSC rom coexistent cholangiocarcinom a, which occurs in up to 15% o patients with PSC. Features that suggest a cholangiocarcinom a superim posed on PSC include signi cant progression o biliary stricturing with m arked dilation o bile ducts, intraductal lling de ects greater than 1 cm in size, and the presence o a m ass on cross-sectional im aging. As PSC progresses cirrhosis develops and perihepatic lym phadenopathy is a requent nding. Large regenerative nodules are com m on in PSC and can be easily con used with hepatic tum ors. The presence o biliary strictures is a com m on nding in m ost cholangiopathies. There ore other secondary causes o sclerosing cholangitis, detailed next, should be excluded be ore the diagnosis o PSC is m ade.

In ectious cholangitis Bacterial ac te cholangitis is a li e-threatening in ection o the biliary tree that m ost requently develops in the setting o biliary stasis. The classic presentation o ever, pain, and jaundice (Charcot triad) is present in m any but not all patients. Up to 80% o patients with bacterial acute cholangitis have obstructing gallstones in the com m on bile duct. Biliary m alignancies and recent instrum entation o the biliary tree are also associated with developm ent o bacterial cholangitis. On im aging there is alm ost always dilation o the intrahepatic bile ducts that can be di use or have a central or segm ental distribution. Because o the high association with obstructive choledocholithiasis, dilation o the com m on bile duct is requently present. On CT bile duct walls m ay be thickened. The liver parenchym a m ay dem onstrate patchy or a wedge-shaped area o hyperenhancem ent surrounding the in ected bile ducts. Pneum obilia can result rom gas- orm ing organism s or recent instrum entation. Com plications o bacterial acute cholangitis include developm ent o an intrahepatic abscess (Figure 9 -32), which occurs in 24% o cases, and portal vein throm bosis, which occurs in 16 % o cases. Treatm ent consists o decom pression o the biliary tree and antim icrobial therapy. Rec rrent pyogenic cholangitis (oriental cholangiohepatitis) is characterized by recurrent episodes o ascending cholangitis and is m ost com m on in patients rom Southeast Asia. Pigm ented intrahepatic and extrahepatic bile duct stones are present and m ay be visible on unenhanced CT. Other im aging ndings include di use dilation o the extrahepatic and central intrahepatic bile ducts with strictures o peripheral intrahepatic bile ducts. Atrophy o the le t hepatic lobe or posterior right hepatic segm ents is a requent nding in individuals with long-standing disease. AIDS-cholangiopathy a ects HIV-in ected individuals who are severely immunocompromised with CD4 counts less than 100 per mm 2. Multiple viruses including cytomegalovi-

Figure 9-32 Cholangitis with Hepatic Abscess Coronal im age rom contrast-enhanced CT demonstrates dilated intrahepatic bile duct (arrowhead) with developing peripheral hepatic abscess (arrows).

rus and H IV itsel , and other opportunistic pathogens such as Cryptosporidium parvum have been implicated as etiologic agents although no pathogen is identi ed in hal o patients. The imaging ndings overlap with those o PSC including multi ocal strictures, caliber irregularities, and pruning o the bile ducts. Papillary stenoses and long extrahepatic bile duct strictures are present and there is requently wall thickening o the extrahepatic bile duct and gallbladder. In addition to patients with AIDS-cholangiopathy viral pathogens can cause cholangitis in patients ollowing orthotopic liver transplant. Outside o the economically developed countries biliary parasites are the common causes o in ectious cholangitis, either by direct in ection o the bile ducts or by causing increased susceptibility o an individual to bacterial cholangitis. The most common pathogens include species o Echinococcus, Clonorchiasis, Opisthorchiasis, and Ascariasis. Dilated bile ducts and intraductal lling de ects are common ndings in biliary parasitic in ection, but speci c ndings vary depending on the pathogen.

Ischemic cholangiopathy Because the intrahepatic bile ducts derive their per usion largely through the hepatic arterial supply im pairm ent o hepatic arterial ow rom vascular disease or iatrogenic injury m ay cause bile duct ischem ia leading to developm ent o m ultiple biliary stenoses. Abrupt cessation o hepatic arterial ow such as with hepatic artery throm bosis in the setting o liver transplant m ay lead to bile duct necrosis with developm ent o bilom as and biliary leakage.

128

Body CT: The Essentials

Drug- and toxin-induced cholangiopathies Radiation therapy and hepatic arterial in usion o chem otherapeutic agents are known to cause biliary strictures. The pathogenesis is not ully understood.

IgG4 cholangiopathy IgG4 autoimmune sclerosing cholangitis commonly occurs in patients with autoimmune pancreatitis, but biliary disease may be present in patients without pancreatic involvement. CT ndings include thick, enhancing bile duct walls with stricturing and upstream duct dilation. The extrahepatic ducts with or without involvement o the intrahepatic bile ducts are the most requent patterns o disease distribution. The presence o a stricture in the biliary hilum with associated so t tissue thickening o the bile duct can mimic a cholangiocarcinoma. Biliary strictures resolve with corticosteroid therapy.

Gallbladder Neoplasms Gallbladder neoplasm s occur in patients greater than 50 years o age with peak incidence in the eighth decade. Gallstones are a risk actor and present in up to 9 0% o cases. Other risk actors include m ural gallbladder calci cations (porcelain gallbladder) and anom alous pancreaticobiliary duct junction. Patients requently present with right upper quadrant abdom inal pain and weight loss. Up to 9 0% o gallbladder neoplasm s are adenocarcinom as. The imaging appearance o gallbladder neoplasm can be o (i) ocal m ural wall thickening; (ii) a polypoid gallbladder mass; or (iii) di use gallbladder wall thickening. About 6 0% o gallbladder neoplasms occur in the gallbladder undus. The imaging eatures o gallbladder neoplasms can overlap with benign gallbladder diseases—gallbladder carcinoma requently occurs in the setting o chronic cholecystitis. Ultrasound is most commonly used or detailed imaging o the gallbladder wall and can be help ul in di erentiating mobile gallstones or biliary sludge rom an intraluminal gallbladder mass. On CT the presence o mural contrast enhancement and nodularity, particularly with severe gallbladder wall thickening o 1cm or greater are ndings associated with gallbladder neoplasms. The vast majority o gallbladder polyps are benign cholesterol polyps; however, polyps measuring greater than 10 mm or that have greater enhancement than the gallbladder wall are suspect or a neoplasm and patients should be re erred or consideration o cholecystectomy. The m ost com m on sites or gallbladder carcinom a m etastases are the liver – through direct invasion rom the gallbladder ossa and hem atogenous spread, regional lym ph nodes via lym phatic spread, and the peritoneum by direct invasion. The prognosis with cancer con ned to the gallbladder is good; however, the m ajority o patients present with locally advanced, unresectable disease (Figure 9 -33). Metastases to the gallbladder wall are not com m on but can be seen in patients with m elanom a, breast cancer, and H CC prim ary neoplasm s. On CT m etastases tend to present as ocal gallbladder wall thickening or an intralum inal

Figure 9-33 Invasive Gallbladder Neoplasm Coronal im age rom contrast-enhanced CT demonstrates a hypoenhancing gallbladder neoplasm with direct invasion into the liver (black arrowheads) and direct extension to the peritoneum and colon (white arrowheads; C, colon).

m ass that is indistinguishable rom a prim ary gallbladder neoplasm with the exception that there m ay not be gallstones present.

Neoplasm o the Biliary Tract Cholangiocarcinoma Cholangiocarcinoma is a malignant neoplasm, usually an adenocarcinoma, arising rom the epithelium o the bile ducts. Risk actors include PSC, choledochocysts, Caroli disease, choledocholithiasis, hepatolithiasis, and in ection with liver ukes. The typical age at presentation is 50 to 70 years and the incidence is slightly higher in men. In 65% o cases cholangiocarcinoma arises in the extrahepatic bile ducts. In 35% o cases it arises around the biliary hilum and in 10% o cases it arises in the peripheral intrahepatic bile ducts. Patients with hilar or extrahepatic cholangiocarcinomas typically present with painless jaundice and weight loss. Patients with intrahepatic cholangiocarcinoma are rarely jaundiced and tumors tend to be large at the time o diagnosis. Superimposed in ectious cholangitis can occasionally be the presenting symptom in a patient with undiagnosed cholangiocarcinoma or in those patients whose biliary ducts have been instrumented. Cholangiocarcinoma is divided into three morphologic growth patterns. The mass- orming type is most commonly associated with intrahepatic cholangiocarcinomas. On CT this type presents as a hypodense mass with dilated bile ducts radiating rom the mass. On contrast-enhanced CT there is requently peripheral enhancement o the mass on arterial and portal venous phases with progressive centripetal enhancement on delayed sequences (delayed enhancement) owing to the brous nature o the tumor that results in slow di usion o iodinated contrast into and out o the interstitial

Chapter 9 Liver and Biliary 129

Figure 9-34 Intrahepatic Cholangiocarcinoma Delayed phase contrast-enhanced CT dem onstrates dilation o le t intrahepatic bile ducts with an abrupt obstruction (arrows) and a aintly visible hyperdense cholangiocarcinom a (arrowhead).

spaces o the tumor (Figure 9-34). Areas o necrosis within the tumor and satellite nodules may be present. Liver parenchymal atrophy as evidence by crowding o obstructed bile ducts and capsular retraction are also requent ndings associated with the mass- orming type o cholangiocarcinoma. The intrad ctal growth type o cholangiocarcinom a is a papillary adenocarcinoma that can super cially spread throughout the biliary m ucosa and can arise in intrahepatic, hilar, and extrahepatic bile ducts. The intraductal intrahepatic cholangiocarcinom a has a better prognosis than other types o cholangiocarcinoma. On CT the intraductal cholangiocarcinom a presents with dilation o upstream bile ducts that can be mild to severe, but a stricture m ay or m ay not be visible. I the tum or is larger than 1 cm it may be visible as a hypodense m ass. Cholangiocarcinomas at the biliary hilum (Klatskin tumor) are most commonly the perid ctal in ltrating type (Figure 9-35). On CT in ltrating tumors present as ocal segment o bile duct wall thickening with obliteration o the lumen. Di erentiating an in ltrating cholangiocarcinoma rom a benign stricture can be challenging. Imaging eatures that avor malignancy include a long segment stricture with irregular margins, asymmetric luminal narrowing, or ductal enhancement or a stricture with periductal so t tissue. In ltrating type cholangiocarcinoma is also the most common type arising in the common hepatic and common bile ducts.

Figure 9-35 Cholangiocarcinoma at the Biliary Hilum Coronal image rom contrast-enhanced CT demonstrates periductal in ltrating mass at the biliary hilum (arrows) with obliteration o the bile duct lumen and dilation o intrahepatic bile ducts.

On CT biliary cystadenom as appear as solitary cystic m asses with a well-de ned capsule that enhances on portal venous and equilibrium phase. Internal septations are com m on (Figure 9 -36 ). Di erentiation o benign cystadenom a rom a m alignant cystadenocarcinom a by im aging is usually not possible. Cyst size does not correlate with m alignancy. The presence o solid nodules, upstream biliary dilation and TH ADs are ndings that are m ore com m on with cystadenocarcinom as; however, their absence does not exclude cystadenocarcinom a. Because o the di culty in di erentiating the two and because biopsy does not exclude the possibility o uture m alignant degeneration surgical resection is the treatm ent o choice.

Biliary cystadenoma and cystadenocarcinoma Biliary cystadenom a is a rare benign cystic neoplasm that arises rom the biliary epithelium . Eighty- ve percent o biliary cystadenom as occur intrahepatically with slight predom inance in the right hepatic lobe (55%). The rem aining 15% arise in the extrahepatic bile ducts. Cystadenom as can vary rom 1.5 to 35 cm in size.

Figure 9-36 Biliary Cystadenoma Coronal im age rom contrast-enhanced CT dem onstrates a septated biliary cystadenom a in the right liver (arrowheads). There were no enhancing nodules or m asses which are ndings associated with cystadenocarcinom as.

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Body CT: The Essentials m orphology and di use abnorm alities. AJR Am J Roentgenol. 19 9 9 ;173:10 31–10 36 . 7. Dodd GD 3rd, Baron RL, Oliver JH 3rd, Federle MP. Spectrum o im aging ndings o the liver in end-stage cirrhosis: part II, ocal abnorm alities. AJR Am J Roentgenol. 19 9 9 ;173:1185–119 2. 8. Gallego C, Miralles M, Marin C, Muyor P, Gonzalez G, Garcia-Hidalgo E. Congential hepatic shunts. RadioGraphics. 20 0 4;24:755–772. 9 . Gore RM, Mathieu DG, White EM, Ghahrem ani GG, Panella JS, Rochester D. Passive hepatic congestion: cross-sectional im aging eatures. AJR Am J Roentgenol. 19 9 4;16 2:71–75. 10 . Gouya H , Vignaux O, Legm ann P, de Pigneux G, Bonnin A. Peliosis hepatis: triphasic helical CT and dynam ic MRI ndings. Abdom Imaging. 20 0 1;26 :50 7–50 9 . 11. Ham er OW, Aguirre DA, Casola G, et al. Fatty liver: im aging patterns and pit alls. RadioGraphics. 20 0 6 ;26 :16 73–16 53. 12. Iannaccone R, Federle MP, Brancatelli G, et al. Peliosis hepatis: spectrum o im aging ndings. AJR Am J Roentgenol. 20 0 6 ;187:W43–W52.

Figure 9-37 Periampullary Carcinoma Coronal image rom contrast-enhanced CT demonstrates a mass (arrow) resulting in obstruction o the common bile duct (labeled B) and the pancreatic duct (labeled P). Most periampullary neoplasms are not directly visible on CT, but their presence can be in erred by dilation o the bile duct and pancreatic duct. G, gallbladder.

13. Mortele KJ, Ros PR. Anatom ic variants o the biliary tree: MR cholangiographic ndings and clinical applications. AJR. 20 0 1;177:389 –39 4. 14. Mortele KJ, Ros PR. Cystic ocal liver lesions in the adult: di erential CT and MR im aging eatures. RadioGraphics. 20 0 1;21:89 5–9 10 . 15. Mortele KJ, Segatto E, Ros PB. The in ected liver: radiologicpathologic correlation. RadioGraphics. 20 0 4;24:9 37–9 55.

Periampullary Carcinoma Tum ors within 2 cm o the papilla can arise rom the am pulla, pancreatic duct, bile duct, or duodenum . Even with detailed histopathology analysis the exact origin o the tum or rom am ong the our possible candidates o ten cannot be de nitively determ ined. In 75% o cases dilation o the bile duct down to the level o the m ajor papilla is present. Dilation o the pancreatic duct is present in 6 7% o cases (Figure 9 -37). A m ass is not usually visible on CT. Su GGESTED READINGS 1. Catalano OA, Sahani DV, Forcione DG, et al. Biliary in ections: spectrum o im aging ndings and m anagem ent. RadioGraphics. 20 0 9 ;29 :2059 –20 80 . 2. Chen WP, Chen JH , H wang JI, et al. Spectrum o transient hepatic attenuation di erences in biphasic helical CT. AJR Am J Roentgenol. 19 9 9 ;172:419 –424. 3. Chung EM, Cube R, Lewis RB, Conran RM. From the archives o the AFIP: pediatric liver m asses: radiologic-pathologic correlation part 1. Benign tumors. RadioGraphics. 20 11;30 :80 1–826 . 4. Chung EM, Lattin GE Jr, Cube R, et al. From the archives o the AFIP: pediatric liver m asses: radiologic-pathologic correlation part 2. Malignant tum ors. RadioGraphics. 2011;31:483–507. 5. Chung YE, Kim M, Park YN, et al. Varying appearances o cholangiocarcinom a: radiologic-pathologic correlation. RadioGraphics. 20 09 ;29 :6 83–700 . 6 . Dodd GD 3rd, Baron RL, Oliver JH 3rd, Federle MP. Spectrum o im aging ndings o the liver in end-stage cirrhosis: part I, gross

16 . Hussain SM, Terkivatan T, Zondervan PE, et al. Focal nodular hyperplasia: ndings at state-o -the-art MR im aging, US, CT, and pathologic analysis. RadioGraphics. 20 0 4;24:3–17. 17. Katabathina VS, Menias CO, Shanbhogue AK, Jagirdar J, Paspulati RM, Prasad SR. Genetics and imaging o hepatocellular adenomas: 2011update. RadioGraphics. 2011;31:1529 –1543. 18. Koyam a T, Fletcher JG, Johnson CD, Kuo MS, Notohara K, Burgart LJ. Prim ary hepatic angiosarcom a: ndings at CT and MR im aging. Radiology. 20 0 2;222:6 6 7–6 73. 19 . Miller WJ, Dodd GD 3rd, Federle MP, Baron RL. Epithelioid hem angioendotheliom a o the liver: im aging ndings with pathologic correlation. AJR Am J Roentgenol. 19 9 2;159 :53–57. 20 . Palacios E, Shannon M, Solom on C, Guzm an M. Biliary cystadenom a: ultrasound, CT, and MRI. Gastrointest Radiol. 19 9 0 ;15:313–316 . 21. Sm ith EA, Dillm an JR, Elsayes KM, Menias CO, Bude RO. Cross-sectional im aging o acute and chronic gallbladder in am m atory disease. AJR. 20 0 9 ;19 2:188–19 6 . 22. Sm ith MT, Blatt ER, Jedlicka P, Strain JD, Fenton LZ. Fibrolam ellar hepatocellular carcinom a. RadioGraphics. 20 0 8;28:6 0 9 –6 13. 23. Torabi M, Hosseinzadeh K, Federle MP. CT o nonneoplastic hepatic vascular and per usion disorders. RadioGraphics. 20 0 8;28:19 6 7–19 82. 24. Tsou YK, Lin CJ, Liu NJ, Lin CC, Lin CH , Lin SM. In am m atory pseudotum or o the liver: report o eight cases, including three unusual cases, and a literature review. J Gastroenterol Hepatol. 20 0 7;22:2143–2147. 25. Yu J, Turner MA, Fulcher AS, Halvorsen RA. Congenital anomalies and normal variants o the pancreaticobiliary tract and the pancreas in adults: part I, biliary tree. AJR. 2006;187:1536–1543.

Ch a p t e r

10

Pancreas David L. Coy, MD, PhD Zachary R. Heeter, MD

I. ANATOMY a. Pancreatic Duct b. Anatomic Variants c. Pancreatic Pseudomasses II. PANCREAS CT TECHNIQUE III. PANCREATITIS a. Acute Pancreatitis b. Interstitial Edematous Pancreatitis c. Acute Necrotizing Pancreatitis d. Complications o Acute Pancreatitis i. Peripancreatic collections ii. Pancreatic f stulas

Anatomy The pancreas has both exocrine and endocrine unctions. The vast m ajority o the pancreatic parenchym a is devoted to its exocrine unction o producing bicarbonate and digestive enzym es that are delivered via the pancreatic duct to the duodenum to neutralize gastric acid and aid digestion o com plex m olecules in chym e. Endocrine unction is per orm ed by the Islets o Langerhans that are com posed o a cluster o insulin-secreting β -cells and less num erous glucagon-secreting α -cells and som atostatin-secreting δ-cells. The Islets o Langerhans are distributed through the pancreas and account or 1% to 2% o the pancreatic parenchym a. The pancreas resides in the anterior pararenal space o the retroperitoneum in an oblique transverse plane spanning rom the inner curve o the duodenal sweep to the splenic hilum . The parenchym a is divided into ve segm ents (Figure 10 -1). The head is adherent to the second and third duodenal segm ents. The hook-like process o the lower head that extends dorsal to the superior m esenteric vein and artery is the ncinate process. The pancreatic neck (genu) lies ventral to the m esenteric vein and artery. The parenchym a le t o the neck consists o the body and tail. The precise boundary between the pancreatic

iii. Chronic pancreatitis iv. Complications o chronic pancreatitis IV. PANCREATIC CYSTIC LESIONS a. Benign Cysts b. Cystic Neoplasms c. Management o Pancreatic Cysts V. SOLID PANCREATIC NEOPLASMS a. Ductal Adenocarcinoma b. Neuroendocrine Tumors c. Pancreatic Lymphoma d. Pancreatic Parenchymal Metastases VI. POSTOPERATIVE PANCREAS

body and tail is arbitrary but the tail is usually de ned as the le t end o pancreas that lies ventral to the le t kidney. The body and tail lie ventral to the splenic vein. Em bryologically the pancreas is derived rom ventral and dorsal buds that arise in the oregut. During developm ent the ventral bud rotates clockwise where it uses with the larger dorsal bud. The ventral pancreatic bud orm s the uncinate process and part o the pancreatic head and the dorsal bud orm s the neck, body, tail, and the rem ainder o the pancreatic head. The pancreas is not enclosed in a capsule and although it is a retroperitoneal organ it has continuity with peritoneal organs through re ections and ligam ents o the peritoneum . These connections are clinically im portant because they are pathways or pancreatic diseases to travel into other spaces and organs. The transverse m esocolon extends across the head and lower body and tail o the pancreas. It allows pancreatic disease to spread to the transverse colon and subsequen tly to the greater om entum and gastrocolic ligam ent because o their com m on in sertion on the transverse colon . Laterally the transverse m esocolon is contiguous with the splenorenal an d phrenocolic ligam ents. At the uncin ate process the transverse m esocolon is con tiguous with the root o the sm all bowel m esentery. The head o the pancreas can 131

132 Body CT: The Essentials Common he pa tic duct

Anatomic Variants

Live r Aorta

Cys tic duct Common he pa tic a rte ry

Ga llbla dde r

S upe rior me s e nte ric a rte ry S ple nic a rte ry Common bile duct Ta il

Acce s s ory pa ncre a tic duct of S a ntorini

Ne ck Hee a d

Body B

S ple nic ve in Pa ncre a s

Minor duode na l pa pilla Ma jor duode na l pa pilla

Ma in pa ncre a tic duct

Uncina te

He pa topa ncre a tic a mpulla Duct of Wirs ung Duode num S upe rior me s e nte ric ve in

Infe rior me s e nte ric a rte ry

Figure 10-1 Pancreas Anatomy The pancreas lies in an oblique plane and is divided into ve segm ents: the head is adherent to the second and third segment o the duodenum ; the uncinate process is the lower portion o the head that extends to the le t o the SMV; the neck is the segm ent ventral to the SMV; the parenchyma to the le t o the neck are the body (closest to the neck) and tail ( urthest rom the neck). Pancreatic juice drains via the m ain pancreatic duct usually through the duct o Wirsung into the duodenum through the m ajor duodenal papilla. The duct o Santorini is usually dim inutive.

com m unicate with the liver and lesser curvature o the stom ach via the hepatoduoden aland gastrohepatic ligam ents. The tail o the pancreas can com m unicate with the spleen and greater curvature o the stom ach via the splen orenal and gastrosplenic ligam ents.

Ann lar pancreas is a rare variant in which the pancreas com pletely or partially encircles the second duodenal segm ent because o the ailure o the ventral pancreatic bud to rotate with the duodenum during developm ent. In about 10 % o cases there is duodenal obstruction that presents early in the postnatal period with gastrointestinal or biliary obstruction. In the extram ural type the ventral pancreas encircles the duodenum and the annular ventral duct joins the dorsal duct to drain through the m ajor duodenal papilla (Figure 10 -2). In the intram ural type the ventral pancreas is incorporated into the duodenal wall and an annular ventral duct is not present because sm all ducts rom incorporated pancreas drain directly into the duodenal lum en. Ectopic Pancreas occurs in 1% to 14% o individuals. The m ost com m on sites or ectopic pancreatic tissue are the stom ach, duodenum , and jejunum but it can occur anywhere in the gastrointestinal tract. The am ount o ectopic tissue is usually sm all, less than 2 cm in size, m aking it di cult to diagnosis prospectively. Com plications rom ectopic pancreas include ectopic acute pancreatitis, adenocarcinom a, bowel intussusception, and hem orrhage. Pancreas divis m results rom ailure o the dorsal and ventral ducts to use such that the m ain pancreatic duct drains exclusively through the accessory duct o Santorini and m inor duodenal papilla. The duct o Wirsung drains the ventral pancreatic head but does not com m unicate with the m ain pancreatic duct. This is present in 4% to 10% o the population but is m ore com m on in patients with pancreatitis in which the reported incidence is as high as 38%. There are m any other ductal variants including

Pancreatic Duct When the pancreatic buds use during developm ent their ducts usually join together and in m ost individuals pancreatic juice drains through the main pancreatic d ct (duct o the pancreatic tail and body derived rom the dorsal bud) and d ct o Wirs ng (duct o the pancreatic head derived rom the ventral bud) to the m ajor duodenal papilla (Figure 10 -1). The accessory d ct (d ct o Santorini) derived rom the dorsal bud drains to the m inor duodenal papilla. The accessory duct is usually dim inutive and m ay not com m unicate with the m ain pancreatic duct. The norm al pancreatic duct caliber varies by segm ent with the upper lim its o norm al 3.5 m m in the head, 2.5 m m in the body and 1.5 m m in the tail. Because there is no generally accepted de nition o “distal” and “proxim al” with respect to the pancreatic duct this term inology should be avoided and instead segm ents o pancreatic duct should be described by their location in the pancreas—pancreatic head, body, or tail.

Figure 10-2 Ann lar Pancreas Contrast-enhanced CT demonstrating a near-complete extramural annular pancreas (arrowheads) encircling the second segment o the duodenum (d) that was an incidental nding in a middle-aged woman.

Chapter 10 Pancreas

133

a bi d or duplicated m ain pancreatic duct that are m ore com m only im aged by MR or endoscopic pancreatography. The pancreatic duct and com m on bile duct join together at the sphincter o Oddi. An anomalo s pancreaticobiliary j nction occurs when the pancreatic and bile ducts use together be ore the sphincter o Oddi resulting in long common channel (15 m m ) that allows pancreatic juice to re ux into the bile ducts and is associated with the developm ent o choledochocysts.

Pancreatic Pseudomasses Variations in the shape, contour, and texture o the pancreas are com m on. These norm al anatom ic variants as well as pancreatic and peripancreatic disease can m im ic a pancreatic neoplasm . Recognition o com m on anatom ic variants helps to avoid this diagnostic pit all; however, in som e instances it m ay be necessary to per orm a pancreatic CT or MRI or in rare circum stances obtain tissue or histologic analysis to dif erentiate a true m ass rom a benign “pseudom ass” caused by anatom ic variation. Fat replacement (lipomatosis) o the pancreatic parenchyma is a common nding in elderly, diabetics, and obese patients and can be mistaken or pancreatic disease. The deposition o adipose is requently heterogeneous or segmental with sparing o other segments. The at deposition results in hypoattenuation o the pancreatic parenchyma that can mimic a hypoattenuating neoplasm or pancreatitis. The most common patterns o at deposition are in the anterior pancreatic head with sparing o the uncinate process, body, and tail and at deposition o the anterior head, body and tail with sparing o the uncinate process (Figure 10-3). Fat depo-

Figure 10-3 Focal Lipomatosis o Pancreas Mimicking a Neoplasm Contrast-enhanced CT in a patient with ocal at deposition in the pancreatic head (arrows) with sparing o the uncinate process (arrowhead). Focal at deposition was con rm ed by MRI. Focal pancreatic lipom atosis can m im ic pancreatitis or a pancreatic neoplasm . d, second segm ent o the duodenum .

sition may be dif use involving the entire pancreatic parenchyma (Figure 10-4). Lipomatosis may be so pronounced that minimal or no pancreatic parenchyma is visible on CT with the pancreatic duct surrounded by at that is indistinguishable rom peripancreatic at. Accessory splenic tissue (splenules) is a com m on nding and when located adjacent to or within the pancreatic

A

B

Figure 10-4 Di se Lipomatosis o Pancreas A. Contrast-enhanced CT images rom an elderly patient with dif use at replacement o the pancreatic parenchyma (arrowheads). B. Image rom the same patient demonstrates

hypoenhancing spiculated ductal adenocarcinoma (arrow) abutting the superior mesenteric vein and easily visualized because o the pancreatic lipomatosis.

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Body CT: The Essentials

tail can resemble a pancreatic mass (Figure 13-2 in Chapter 13). The nodule can be recognized as an accessory spleen based on its enhancem ent m irroring that o the adjacent spleen.

Pancreas CT Technique The CT technique used to evaluate the pancreas and pancreatic disease depends on the clinical objectives. In patients with acute pancreatitis the aim o imaging is to delineate the severity and extent o disease by assessing or the presence o pancreatic necrosis, uid collections, and other complications such as hemorrhage or pancreatic stula. Routine CT abdomen with portal venous phase contrast enhancement is the rst-line imaging choice. Because CT has low sensitivity or detection o noncalci ed gallstones, abdominal ultrasound is use ul to assess or gallstones which are a requent cause o pancreatitis. Beyond the initial diagnosis, repeat imaging is indicated in those patients with worsening abdominal pain, signs or symptoms o in ection, or deteriorating clinical course to evaluate or progression and developing complications. Because patients with severe pancreatitis are subject to multiple CTs that increases their cumulative radiation exposure, MR is becoming more requently used or ollow-up imaging o patients with pancreatitis. In addition to assessment o uid collections and pancreatic necrosis, MR also of ers the advantage o being more sensitive than CT or detection o gallstones. In patients with a suspected or known pancreatic mass multiphase contrast-enhanced pancreas CT with multiplanar re ormats is used or detection and staging o pancreatic neoplasms. Many protocols include an initial scan without intravenous contrast to identi y calci ed gallstones and pancreatic calci cations; however, to minimize radiation exposure the noncontrast sequence i needed should be per ormed with very low-dose technique. The contrastenhanced portion o a pancreas CT relies on rapid contrast injection rates, up to 6 mL/ s, to maximize peak arterial enhancement. With ast multichannel scanners and high injection rates, adequate arterial phase timing can be challenging. The time interval rom initiation o contrast injection to peak pancreatic parenchymal enhancement is in uenced by multiple actors including the contrast injection rate and volume, and patient’s cardiac output. Because o variability between patients a bolus tracking technique is pre erable or determining the optimal timing o the scan as opposed to using a xed time delay between contrast injection and initiation o the scan. With a bolus tracking technique a region o interest, usually the abdominal aorta at the level o the celiac artery, is monitored a ter contrast injection. The rst contrast-enhanced phase is the pancreatic phase which is initiated 10 to 15 seconds a ter the aorta has reached a predetermined threshold enhancement value—typically 150 H U. Pancreatic phase enhancement is a late arterial phase in which the pancreatic parenchyma has the greatest amount o enhancement. Because pancreatic adenocarcinomas are hypoenhancing their conspicuity is greatest when

the remainder o the pancreatic parenchyma is at maximal enhancement. The pancreatic phase is also well suited or imaging o hypervascular masses such as neuroendocrine tumors, especially or small lesions that may be isoattenuating to the pancreas on portal venous phase imaging making them di cult to detect on a scan with only a portal venous enhancement phase. The pancreatic phase is also use ul or detailed evaluation o arterial anatomy that is necessary or staging o pancreatic adenocarcinoma and essential or surgical planning. A second scan ollowing the pancreatic phase is per ormed during portal venous enhancement to evaluate the portal, superior mesenteric, and splenic veins as well as the liver and other solid organs. This phase occurs around 60 to 70 seconds a ter contrast injection. Thin section re ormations are necessary or evaluating local extension o pancreatic adenocarcinoma, particularly vascular involvement as discussed below.

Pancreatitis Acute Pancreatitis Acute pancreatitis is an acute in am m atory process o the pancreas caused by activation o pancreatic enzym es within the pancreatic ducts that leads to autodigestion o the pancreas and peripancreatic tissues. The extravasated uid can track away rom the pancreas to involve other spaces and organs in the abdom en, pelvis, and thorax. Gallstones and alcohol are the etiologic agents or greater than 80 % o adult acute pancreatitis in developed countries whereas m alnutrition is the m ost com m on cause worldwide. Pancreatic neoplasm s can also cause pancreatitis and should be considered in any patient with an unexplained cause o pancreatitis. The clinical diagnosis o acute pancreatitis requires two o the ollowing three eatures: (1) abdom inal pain characteristic o pancreatitis; (2) elevated serum am ylase or lipase levels; and (3) characteristic im aging ndings on CT. The serum am ylase and lipase values do not correlate with the severity o pancreatitis. Im aging can be used to con rm the diagnosis o acute pancreatitis although in early or very m ild cases the pancreas m ay appear norm al. The objectives o im aging in patients with acute pancreatitis are to determ ine the extent o disease—the presence o pancreatic and peripancreatic necrosis and uid collections—and to detect other im portant ndings and com plications such as presence o gallstones, venous throm bosis, pseudoaneurysm , or unsuspected obstructing neoplasm . Routine im aging is not necessary in patients with m ild pancreatitis who are responding to supportive therapy. Patients with their rst episode o pancreatitis, are over 40 years o age, or have no identi able cause o pancreatitis, are an exception and CT should be considered to exclude an underlying pancreatic m ass. Diagnostic im aging is warranted in patients who are not im proving with conservative therapy, have a decline in their clinical status, or have signs or sym ptom s suggesting in ection or other com plication.

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and 10-6 ). Enhancem ent o the pancreatic parenchym a ollowing intravenous contrast is usually norm al, but in cases o severe pancreatitis enhancem ent can be heterogeneous because o the presence o interstitial edem a and indistinguishable rom the early stages o developing pancreatic necrosis. In m ild cases o acute pancreatitis the pancreas m ay appear norm al except or m ild edem a in the peripancreatic so t tissues. In m ore severe orm s o acute IEP, peripancreatic uid collections m ay be present.

Acute Necrotizing Pancreatitis

Figure 10-5 Mild Ac te Interstitial Edemato s Pancreatitis Contrast-enhanced CT demonstrates m ild acute interstitial edem atous pancreatitis in the pancreatic head and uncinate process. Linear hypodensities in the pancreatic parenchym a represent interstitial edema. There is edem a uid ( at stranding) in the peripancreatic at (arrows) and extending into m esentery (arrowhead) between the superior m esenteric artery and vein.

Interstitial Edematous Pancreatitis Acute interstitial edematous pancreatitis (IEP) mani ests with ocal or dif use enlargement o the pancreas (Figures 10-5

Figure 10-6 Ac te Interstitial Edemato s Pancreatitis Ca sed by Occ lt Neoplasm Contrast-enhanced CT dem onstrates m ild acute interstitial edematous pancreatitis in the pancreatic body and tail with mild edema in the peripancreatic so t tissues (black arrowheads) caused by an occult ductal adenocarcinoma. Although the neoplasm was not visible on pancreas CT, its presence was in erred by mild dilation o the main pancreatic duct (white arrowhead) that terminated abruptly (white arrow) in a 59 -year-old patient with unexplained pancreatitis. The hypodensity partially imaged in the right liver was a benign cyst.

Acute necrotizing pancreatitis occurs less requently than IEP, accounting or 20% to 30 % o acute pancreatitis, but is associated with a signi cantly higher risk o com plication and m ortality that generally correlates with the extent o pancreatic necrosis. On CT necrosis is de ned as nonenhancem ent o pancreatic parenchym a ollowing adm inistration o intravenous contrast and can be ocal or involve the entire gland. Pancreatic necrosis develops in the rst 24 to 48 hours a ter onset o sym ptom s. CT per orm ed during the rst 48 hours a ter onset o sym ptom s can be equivocal or dif erentiating pancreatic necrosis rom acute IEP because heterogeneous enhancem ent o pancreatic parenchym a can be present in both necrotizing and edem atous pancreatitis, and sm all intraparenchym al uid collections in edem atous pancreatitis m ay be indistinguishable rom sm all areas o necrosis (Figure 10 -7). By 72 hours a ter onset o sym ptom s areas o necrosis coalesce and becom e better de ned which im proves the diagnostic accuracy o CT or diagnosis o pancreatic necrosis. The speci city o CT or necrotizing pancreatitis is 100 % and the sensitivity is 10 0% or large or extended areas o necrosis and 50 % or sm all areas o pancreatic necrosis. Extravasation o pancreatic enzym es into the peripancreatic so t tissues results in peripancreatic at necrosis. In 75% to 80 % o cases o necrotizing pancreatitis, pancreatic parenchym al n ecrosis and peripan creatic necrosis occur together, but in about 20 % o cases peripancreatic necrosis m ay be present without visible pancreatic necrosis. Peripancreatic necrosis m ani ests as heterogeneous areas o n onenhancem ent that are m ost requently located in the lesser sac and retroperitoneum adjacent to the pancreas. Patien ts with peripancreatic necrosis without pan creatic parenchym al necrosis have a ewer com plications than those patients with pancreatic necrosis, but the com plication rate is higher than in those patients with IEP. CT Severity Index (CTSI) is a m orphologic assessm ent o acute pancreatitis (Table 10 -1) based on the presence o peripancreatic collections and pancreatic necrosis. The m axim um CTSI score is 10. On the CTSI scale 0 to 3 points is m ild pancreatitis, 4 to 6 points is m oderate pancreatitis, and 7 to 10 points is severe pancreatitis. Generally, the clinical severity o acute pancreatitis correlates with the m orphologic assessm ent. Patients with a CTSI o 0 to 1 point have very low m orbidity and no m ortality resulting

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Body CT: The Essentials

A

B

C

Figure 10-7 Evol tion o Necrotizing Pancreatitis A. Contrast-enhanced CT per orm ed within 24 hours a ter onset o symptom s reveals peripancreatic edema (arrow) and heterogeneous enhancement o the pancreatic body and tail (arrowheads). At this point the im aging ndings demonstrate acute pancreatitis, but are equivocal or dif erentiating necrotizing pancreatitis rom interstitial edematous pancreatitis. B. Contrast-enhanced CT per ormed several days a ter onset o symptoms demonstrates necrosis o the pancreas and peripancreatic at resulting in acute necrotic collections (arrowheads). C. Contrast-enhanced CT per orm ed 2 m onths later reveals active extravasation o intravenous contrast (arrows) rom a pseudoaneurysm o the gastroduodenal artery (not shown). The necrotic collections (now term ed walled of necrosis) becam e in ected and were drained with large percutaneous drains (arrowhead).

rom pancreatitis. In contrast, patients with CTSI o 7 to 10 points can have m ortality rate o 17% and greater than 9 0 % com plication rate.

Complications o Acute Pancreatitis Peripancreatic collections Peripancreatic collections m ost requently develop in the pancreatic bed and peripancreatic tissues, but the collections can extend into peritoneal spaces and organs via peritoneal re ections or dissect through the retroperitoneum into the pelvis or occasionally the m ediastinum . The revised Atlanta classi cation standardizes the term inology used or describing the uid and necrotic collections resulting rom acute pancreatitis (Table 10-2). Collections are classi ed on the basis o the presence o absence o necrosis and tim e rom onset o pancreatitis.

Ac te peripancreatic f id collections resulting rom IEP usually resolve without need or drainage. Pse docysts are encapsulated uid collections present 4 weeks or longer a ter onset o IEP. Pseudocysts should contain no enhancing internal septations or nodules, but m ay contain som e nonenhancing debris early on. The natural course o pseudocysts is to resolve slowly over tim e although about 50% o pseudocysts com m unicate with the pancreatic duct which can result in growth or recurrence. Drainage m ay be necessary i a pseudocyst is sym ptom atic, or in the rare circum stance that it becom es in ected. In contrast to acute peripancreatic uid collections and pseudocysts, 40 % to 70 % o collections associated with necrotizing pancreatitis becom e in ected. Because im aging cannot reliably distinguish whether a com plex necrotic collection is in ected, percutaneous or endoscopic aspiration o uid is usually required to diagnose a

Chapter 10 Pancreas Table 10 -1. CT Severity Index (CTSI) or Acute Pancreatitis C

c

is ic

Ct SI Sco

Pancreatic inf ammation Non (no m l) Foc l o di us nc ic nl g m n p i nc ic in mm ion Singl cu uid coll c ion t wo o mo cu uid coll c ions

0 1 2 3 4

Pancreatic parenchymal necrosis Non nc s < 30% o 30%–50% o nc s > 50% o nc s

0 2 4 6

M ximum Ct SI sco is 10. Sco o 0–3 is mild mod nc i is, nd 7–10 is s v nc

nc i is.

i is, 4–6 is

137

pancreatic abscess. The presence o gas within a uid collection is not a help ul nding or diagnosis o an in ected collection because it is rarely present in pancreatic abscesses and is m ore com m on to result rom a pancreaticoenteric stula. Drainage o in ected collections is critical as patient m ortality approaches 10 0 % i le t untreated. The approaches to drain in ected collections include percutaneous drainage, open or laparoscopic necrosectom y, and in select instances internal drainage by endoscopically placed drains. Other com plications arising rom acute pancreatitis include hem orrhage that can occur rom venous bleed or through developm ent o pse doane rysms o the splenic, gastroduodenal, and pancreaticoduodenal arteries. Veno s thromboembolism occurs in approxim ately 10 % o patients with acute pancreatitis and m ost com m only involves the splenic, superior m esenteric, and portal veins. Occlusion o the portal system veins either by throm bus or extrinsic com pression rom a peripancreatic collection results in the developm ent o intra-abdom inal varices.

Table 10 -2. Revised Atlanta Criteria o Fluid Collections Resulting rom Acute Pancreatitis ty

t im om ons o nc i is

o Coll c ion

F

u s

Comm n s

Interstitial edematous pancreatitis a cu i nc (a pFC)

ic uid coll c ion

ps udocys

≤ 4 w ks

h omog n ous, uid nu ion, no d b is. No d f n bl w ll. ex nc ic.

In c ion x m ly . r solv s wi ou d in g

> 4 w ks

enc sul d nd w ll ci cumsc ib d. e ly in cou s m y con in som d b is, bu b com s mo omog n ous ov im . Usu lly x nc ic.

In c ion is . D in g indic d o in c ion o i sym om ic

≤ 4 w ks

h og n ous a, d b is, locul d bu no d f n bl w ll. In nc ic nd/ o x nc ic.

D in i in c d I no in c d d cision o d in b s d on clinic l cou s

> 4 w ks

h og n ous a, d b is, nc sul d. In nc ic nd/ o x nc ic.

D in i in c d I no in c d d cision o d in b s d on clinic l cou s

Necrotizing pancreatitis (pancreatic necrosis, peripancreatic necrosis, or pancreatic and peripancreatic necrosis) a cu

n c o ic coll c ion (a NC)

W ll d-o n c osis (WON)

a

e ly in cou s o a NC nd WON uid c n omog n ous. Sources: a d d om t oni r F. t vis d a l n cl ssif c ion o cu nc i is: i s im o nc Radiology. 2012; 262: 751–764. nd B nks pa , Boll n t L, D v nis C l., Cl ssif c ion o cu nc nd d f ni ions by in n ion l cons nsus. Gut. 2013; 62: 102-111.

o diologis nd i s c on m n. i is - 2012: r vision o a l n cl ssif c ions

138

Body CT: The Essentials

Pancreatic f stulas In a subset o patient with necrotizing pancreatitis a disconnected d ct or pancreatic st la m ay occur. Necrosis o the pancreatic duct epithelium results in disruption o the main pancreatic duct by which an active segment o pancreatic parenchyma may become isolated rom the remainder o the gastrointestinal tract. The enzymes and uid produced by the isolated (or “orphaned”) parenchymal segment have no channel into the duodenum which leads to development o an uncontrolled leak o pancreatic juice into the peripancreatic tissues, peritoneal space (pancreatic ascites), or pleural space (pancreatic ple ral e sion). The enzymes within the collection can also result in development o a stula to an adjacent viscous such as the stomach, duodenum, small bowel, colon, or bile duct. Treatment options include endoscopic therapy with placement o pancreatic duct stents bridging the disconnected ductal segment, placement o percutaneous or internal drains, and surgical intervention such as partial resection o the isolated pancreatic segment or surgical revision o pancreatic ductal drainage.

Chronic pancreatitis Chronic pancreatitis is de ned as irreversible in am m atory dam age to the pancreas that results in m orphologic and unctional abnorm alities. In the United States 75% o cases o chronic pancreatitis are caused by alcoholism . Worldwide alcoholism and m alnutrition are the m ost com m on etiologies. On im aging chronic pancreatitis m ani ests with gland atrophy and caliber enlargem ent and irregularity o the m ain pancreatic branch ducts. Intraductal stones are

m ost com m on in alcoholic, tropical, and idiopathic orm s o chronic pancreatitis (Figure 10-8). A toimm ne pancreatitis accounts or 1% to 10 % o chronic pancreatitis and is characterized by IgG4-positive plasm a cell in ltration o the pancreas resulting in brosis. Unlikely other types o chronic pancreatitis, it responds to corticosteroid therapy. Patients with autoim m une pancreatitis are requently over 50 years o age although it has been described in all age groups, and m en are twice as likely as wom en to be af ected. The m ost requent presenting signs and sym ptom s include jaundice, weight loss, abdom inal pain, and diabetes m ellitus. Interestingly patients do not present with severe abdom inal pain or classic attacks o acute pancreatitis. There are several m orphologic patterns o autoim m une pancreatitis: (1) the di se orm with an enlarged, eatureless (“sausage-shaped”) pancreatic parenchym a requently surrounded by a hypoattenuating halo and dif use narrowing o the pancreatic duct and pancreatic segm ent o the lower bile duct (Figure 10-9 ); (2) the ocal orm m ost requently af ects the pancreatic head with ocal enlargem ent o the pancreatic parenchym a and segm ental stenosis o pancreatic duct and lower bile duct within the pancreatic head—m im icking a pancreatic adenocarcinom a; and (3) m lti ocal orm with two or m ore segm ents o ocal pancreatic enlargem ent and segm ental ductal stenosis. Groove (parad odenal) pancreatitis is an uncom m on orm o chronic pancreatitis af ecting the pancreaticoduodenal groove that is the space between the head o the pancreas and the duodenum . Groove pancreatitis leads to scarring within the groove and a varying degree o chronic pancreatitis within the pancreatic head. Clinically, patients m ay present with duodenal or biliary strictures. The scar can resem ble a pancreatic neoplasm , but unlike m ost neoplasms it demonstrates slow progressive enhancement. Cystic change within the medial wall o the duodenum m ay be present. Chronic pancreatitis ca sed by cystic brosis causes exocrine pancreatic insu ciency in young adults. On CT the pancreas may be atrophic or demonstrate varying degrees o atty replacement o the pancreatic parenchyma, the degree o which correlates with exocrine insu ciency. A less common pattern is or the pancreatic parenchyma to be replaced by numerous cysts o varying sizes (pancreatic cystosis). Tropical pancreatitis presents in young patients and is associated with m alnutrition. Calculi develop within a dilated pancreatic duct and there is a tendency or the calculi to be large.

Complications o chronic pancreatitis Figure 10-8 Chronic Pancreatitis Contrast-enhanced CT dem onstrating an atrophic, calci ed (black arrowheads) pancreas in patient with idiopathic chronic pancreatitis. The pancreatic duct (white arrowheads) is obstructed by a large stone (white arrow).

Pse docysts are present in up to 25% o patients with chronic pancreatitis and can be located within, adjacent, or ar rom the pancreas. A pancreatic st la is caused by a leak o pancreatic juice through a duct disruption and can result in recurrent pancreatic ascites or pleural ef usions that are distinguished by their elevated amylase levels. Veno s occl sion

Chapter 10 Pancreas

139

A

B

Figure 10-9 Di se A toimm ne Pancreatitis A. Contrast-enhanced CT in a patient with dif use autoim m une pancreatitis dem onstrating ef aced, eatureless pancreatic parenchym a surrounded by a hypoattenuating halo (arrows) with obstruction o the lower bile duct resulting in placem ent o a biliary stent (arrowhead). B. Six weeks ollowing steroid

treatm ent the pancreas has becom e atrophic (arrows) and the surrounding hypoattenuating halo is resolving. Com pression o the bile duct has resolved (com pare caliber o bile duct in A and B) and pancreatic duct is visible. A pseudocyst is present in the pancreatic body.

results in abdominal varices. The splenic vein is more commonly af ected than the superior mesenteric or portal veins. Obstruction o the main pancreatic or side branch ducts may result rom in ammatory strictures, intraluminal calculi, or proteinaceous debris. Stricturing o the lower bile duct can result rom chronic pancreatitis in the pancreatic head. Patients with chronic pancreatitis are at increased risk or developm ent o ductal adenocarcinom a. In patients with chronic pancreatitis in which there is obstruction o the pancreatic or bile duct, it m ay be di cult or im possible to dif erentiate a sequelae o chronic pancreatic rom a developing pancreatic neoplasm and tissue sam pling m ay be necessary.

they develop a brous capsule. The capsule enhances, but pseudocysts should not have any internal enhancing nodules or septations—a characteristic that distinguishes them rom m ucinous carcinom as and other cystic neoplasm . A solitary tr e pancreatic cyst is rare and m ost com m only ound in in ants. Most true pancreatic cysts are associated genetic diseases in which cysts develop in m ultiple organs. About 5% to 10 % o patients with adult polycystic kidney disease (APCKD) can have sm all pancreatic cysts. Involvem ent o the pancreas is usually m uch less than that o the kidneys and liver. Von Hippel–Linda disease is an autosom al dom inant disorder associated with visceral cysts. Pancreatic cysts are present in 50% to 70 % o these patients and cysts m ay also be ound in the spleen, adrenal

Pancreatic Cystic Lesions Pancreatic cystic lesion can be divided into benign and neoplastic etiologies (Table 10-3). The imaging eatures o the cyst and the patient’s gender and age can be help ul in determining the etiology o a pancreatic cyst (Table 10-4). Analysis o the cyst uid either rom percutaneous or endoscopic aspiration may also provide additional use ul in ormation.

Table 10 -3. Cystic Lesion o the Pancreas Pseudocyst Intraductal papillary mucinous neoplasm (IPMN) Serous microcystic adenoma Mucinous cystic neoplasm

Benign Cysts Pse docysts occur in the setting o acute or chronic pancreatitis and are the m ost com m on cause o pancreatic cysts accounting or 30 % o pancreatic cysts. On CT pseudocysts early in their course can have a com plex appearance because o the presence o internal debris, but over tim e they becom e m ore hom ogeneous and well m arginated as

Cys ic n u o ndoc in Lym

o

t u

nc

i

li l cys ic cys

Cys ic d noc cinom Cys ic n o l sm

umo

140

Body CT: The Essentials

Table 10 -4. Im aging Features o Cystic Pancreatic Lesions L sion

Incid nc

t y ic l p i n

ps udocys

Common

V i bl

V i bl

Unilocul

r

t in, b own uid Unlik ly i h ig a myl s no is o y o nc i is a bou l communic wi nc ic duc

IpMN

Common

eld ly

Uncin bu v i bl

Unilocul , m c ocys ic, o cys wi solid com on n s

r

Viscous uid Mucin h ig Cea V i bl a myl s

S ous cys d nom

r l iv ly common

eld ly F> M

V i bl

Mic ocys ic, m c ocys ic, o unilocul

Cn l t in uid c lcif d sc Low Cea (mic ocys ic)

a sym om ic B nign

Mucinous cys ic n o l sm

r l iv ly common

Middl g d m l s

85% in body o il

M c ocys ic

S l o mu l c lcif c ions in 10%

Viscous uid Mucin h ig Cea V i bl a myl s

C lcif c ions co l wi lik li ood o m lign ncy

Solid s udo umo

r

Young m l s

t il

V i bl

30%

Bloody uid Low Cea

M y b solid o cys wi solid com on n s

Cys ic n u o ndoc in umo

r

V i bl

V i bl

Cys wi solid V i bl com on n s

t in uid Low Cea

Usu lly non unc ion l

Cys ic d noc cinom

r

eld ly

V i bl

Cys wi solid Uncommon com on n s

V i bl

M y communic wi nc ic duc

t u cys s

r

V i bl

V i bl

Unilocul

No usu lly s m l d

Usu lly mul i l Von h i l–Lind u

ill y

t y ic l Loc ion

Mo

glands, or kidneys. Patients with von Hippel–Lindau are at increased risk or developing pancreatic neoplasm s— serous cystadenom a, islet cell tum or, and adenocarcinom a. They are also at risk or developm ent o renal cell carcinom as and pheochrom ocytom as. As noted previously, patients with cystic brosis m ay develop pancreatic cysts that likely result rom occlusion o pancreatic ducts caused by inspissated m ucin. Lymphoepithelial cysts contain keratinaceous debris and are rare.

Cystic Neoplasms Intrad ctal papillary m cino s neoplasms (IPMN) account or 20 % o all cystic pancreatic lesions and tend to occur in older patients with a m ean age o 6 5 years at the tim e o presentation. IPMNs have m alignant potential that varies

ology

Fluid C lcif c ions C c

No

is ics

Comm n s

Communic s wi nc ic duc M y b mul i l Dil d duc s

by their site o involvem ent—branch duct, m ain duct, or com bined (branch and m ain duct). On CT branch d ct (side branch) IMPNs can present as a single cyst (unilocular cyst) or a cyst with a ew septations (m acrocystic) or a m ultiseptated cyst (m icrocystic type). A connection to the pancreatic duct is present, but m ay not be visible on CT. The uncinate process is the m ost requent location or branch duct IPMNs, but they occur anywhere in the pancreas. Carcinom a is ound in approxim ately 25% o branch duct IPMNs and invasive carcinom a in 15% o cases. Findings associated with m alignant degeneration o side branch IPMNs include (1) internal com plexity—the presence o m ural nodules or solid enhancing com ponents; (2) size greater than 3 cm ; (3) large caliber com m unication with the m ain pancreatic duct; and (4) presence o abdom inal pain. Approxim ately 30 % o patients with branch duct IMPNs have m ulti ocal disease and up to 29 % o patients

Chapter 10 Pancreas

Figure 10-10 Combined (Branch and Main Duct) Type IPMN Contrast-enhanced CT demonstrating 5-cm IPMN in the pancreatic head (arrow). The pancreatic duct was dilated (not shown) and at endoscopy there was mucin extruding through the duct o Wirsung (not shown) and duct o Santorini (arrowhead). Main duct and combined type IPMNs have an increased risk o containing an invasive carcinoma component that was present in this IPMN.

m ay have a synchronous or m etachronous neoplasm o other organs. Main d ct and combined (branch and main d ct) IPMNs present with dif use or segmental dilation o the main pancreatic duct with or without a communicating cyst, depending on whether it is main duct or a combined type (Figure 10-10). Pancreatic parenchymal atrophy is a requent nding making these lesions di cult to distinguish rom the changes o chronic pancreatitis. On CT the pancreatic duct is dilated and the wall may enhance. At endoscopy up to hal o patients will have a “ sh-mouth” papilla because o the extrusion o excess mucin into the duodenum. Because the rates o pancreatic adenocarcinoma and invasive carcinoma are high in patients with IPMNs involving the main duct – 70% and 43%, respectively – resection is recommended in patients who are surgical candidates with a reasonable li e expectancy. Imaging eatures associated with malignant degeneration o main duct IPMNs include (1) presence o mural nodules or enhancing components; (2) large unilocular cystic components; (3) enhancement o the main pancreatic duct wall; and (4) main duct caliber greater than 18 mm. M cino s cystic neoplasms account or up to 10% o pancreatic cysts. Unlike IPMNs they do not com m unicate with the pancreatic duct. On CT m ucinous cystic neoplasm s are solitary unilocular cysts with enhancing walls and thick or nodular internal septations and alm ost always located in the pancreatic body or tail (Figure 10-11). Calcication o the capsule or septations occurs in up to 10% o m ucinous cystic neoplasm s. The m ean age at presentation is 47 years and 9 5% o patients are em ales. Im aging

141

Figure 10-11 Mucinous Neoplasm Large m ucinous neoplasm in the pancreatic tail containing m ural nodules (arrowheads) and wall calci cation (arrow). Invasive carcinoma was present on histopathology.

eatures associated with m alignancy or invasion include (1) cyst size greater than 4 cm ; (2) presence o m ural nodules, thickened septations, or calci cation; and (3) obstruction o the m ain pancreatic duct. Because o their m alignant potential it is recom m ended that all m ucinous cystic neoplasm be resected. Microcystic sero s cystadenomas are generally benign neoplasm s that account or 20% o all pancreatic cystic lesions. The m ean age at presentation is 6 2 years and 75% o cases occur in em ales. The most com m on CT appearance is o a cystic lesion containing sm all or honeycom b cysts and radiating brous septations converging into a central scar that is calci ed in 30% o lesions (Figure 10 -12). Serous cystadenom as m ost comm only occur in the pancreatic body and tail. The macrocystic (oligocystic) serous cystadenom a variant presents a unilocular cyst or a cluster o centim eter-sized cysts that can resem ble an IMPN or m ucinous neoplasm but is distinguished by its lack o com m unication with the pancreatic duct and by the contents o its uid. There is also a solid sero s cystadenoma variant that presents as a hypervascular solid m ass with im aging eatures sim ilar to a neuroendocrine neoplasm or hypervascular m etastasis. Patients with von Hippel–Lindau disease can develop m ulti ocal m acrocystic cystadenom as. Malignant trans orm ation o serous cystadenom as is rare and patients with classic m icrocystic serous cystadenom as are usually not resected unless they becom e sym ptom atic. Solid pse dopapillary t mors are rare usually benign tum ors that occur in younger patients with a m ean age o 22 years, and 9 1% occur in em ales. The im aging eatures o these tum ors are variable and can range rom a solid m ass to com plex cyst with hem orrhage or necrosis.

142 Body CT: The Essentials

A

B

Figure 10-12 Serous Cystadenomas in Two Patients Contrast-enhanced CT in two patients reveal (A) large microcystic serous cystadenoma with small cysts and radiating brous septations

that converge to a calci ed central scar (arrow) and (B) Macrocystic (unilocular) variant o a serous cystadenoma (arrowhead) that is indistinguishable by imaging rom an IMPN or mucinous tumor.

Peripheral calci cations are present in 30% o cases. Rupture can result in hem operitoneum . Acinar cell carcinoma is an uncom m on neoplasm in adults that is associated with excessive pancreatic enzym e production and can result in lipase hypersecretion syndrom e with elevated serum lipase levels and at necrosis. On CT acinar cell carcinom as present as large m asses with central cystic or necrotic areas and calci cations. Men are twice as likely to be af ected as em ales and the prognosis is poor. Cystic variants o solid neoplasm s occur in about 5% o neuroendocrine tum ors and rarely in ductal adenocarcinom as.

evaluation o the pancreatic ducts and whether there m ay be com m unication between the cyst and the pancreatic duct which is an im portant distinguishing eature. MR also has the added bene t o not requiring additional patient exposure to ionizing radiation. Pancreatic cysts with internal com plexity, dilation o m ain pancreatic or side branch ducts, or size approaching 3 cm should be characterized with pancreas MRI and/ or endoscopic ultrasound including aspiration o cyst uid. Analysis o the cyst uid or am ylase, m ucin, and CEA levels, and or cytology can be help ul in establishing the etiology o the cyst (Table 10 -4). In patients with a pancreatic cyst who have sym ptom s directly re erable to the cyst such as steatorrhea, hyperam ylasem ia, epigastric pain, weight loss, recent-onset diabetes, or jaundice, the risk o m alignancy is increased. Patients with sym ptom atic pancreatic cysts greater than 3 cm are generally re erred or surgical resection. Sym ptom atic patients with cysts less than 3 cm typically go on to endoscopic ultrasound and aspiration o cyst uid with subsequent ollow-up or surgical consultation based on the results o the cyst uid analysis.

Management o Pancreatic Cysts Published guidelines or the evaluation and workup o patients with pancreatic cysts dif er between specialty groups and organizations and have not been prospectively validated. Pancreatic cysts are com m only detected on crosssectional im aging with a requency o 2.6 % on CT and 19 .9 % on MRI which has greater sensitivity or detection o sm all cysts (< 10 m m ). The m ajority o pancreatic cysts are benign with 75% to 9 0 % being stable over long-term ollow-up. Cyst size is an im portant actor as the likelihood o neoplasm in a sim ple pancreatic cyst m easuring less than 3 cm is less than 3% in asym ptom atic patients. The length and tim ing o ollow-up or an asym ptom atic sim ple pancreatic cyst m easuring less than 3 cm varies am ong the published guidelines with a range o 1 to 4 years’ stability recom mended to establish benign etiology. Pancreas MR with MRCP is generally pre erred over CT or ollowup o pancreatic cysts because it provides m ore detailed

Solid Pancreatic Neoplasms Ductal Adenocarcinoma Pancreatic ductal adenocarcinom a accounts or 9 0% o all pancreatic neoplasm s. In the United States it is the second m ost comm on gastrointestinal malignancy and the ourth most com m on cause o cancer deaths. Risk actors include chronic pancreatitis, cigarette sm oking, and longstanding diabetes m ellitus. Up to 10% m ay be associated with am ilial disorders that include hereditary pancreatitis,

Chapter 10 Pancreas

Figure 10-13 Pancreatic Head Ductal Adenocarcinoma with Double Duct Sign Coronal im age rom contrast-enhanced CT demonstrates a hypoenhancing ductal adenocarcinom a (m arked A) in the pancreatic head resulting in obstruction o the bile duct (white arrow) and pancreatic duct (black arrow).

Peutz–Jeghers syndrom e, hereditary nonpolyposis colorectal carcinom a, am ilial adenom atous polyposis, and von Hippel–Lindau disease. Patients requently present with symptoms o abdominal or back pain, weight loss, or jaundice which are usually indicators o advanced stage disease. On CT pancreatic ductal adenocarcinoma is m ost com m only a hypodense slowly enhancing pancreatic m ass with poorly de ned m argins. It is m ost conspicuous on contrastenhanced CT during peak pancreatic enhancem ent in the late arterial phase in which the hypodense mass is best delineated rom the enhanced pancreatic parenchym a. Even with optim al CT technique up to 15% o ductal adenocarcinom as are isoattenuating on CT and cannot be visualized, but their presence m ay be in erred by secondary signs such as an abrupt pancreatic duct obstruction. The do ble d ct sign re ers to obstruction o the pancreatic and bile ducts caused by a ductal adenocarcinom a in the pancreatic head (Figure 10-13). Other secondary im aging ndings or pancreatic ductal adenocarcinoma include ocal contour de orm ity or enlargem ent o the pancreas especially in the setting o pancreatic atrophy and pancreatic duct obstruction with abrupt cut-of (Figure 10-6 ). Because these ndings m ay also be caused by anatom ic variation or chronic pancreatitis endoscopic ultrasound and biopsy m ay be necessary to determ ine the etiology (Table 10-5). Up to 70% o ductal adenocarcinomas arise in the pancreatic head with the remaining 30% evenly distributed in the pancreatic body and tail (Figure 10-14). The m ajority o patients are greater than 6 0 years o age at presentation (Table 10-6 ). These tum ors are highly invasive and the m ajority o patients present with locally advanced or m etastatic disease.

143

Figure 10-14 Ductal Adenocarcinoma Contrast-enhanced CT demonstrates m ild ullness and hypoattenuation o the pancreatic tail (arrowheads) caused by ductal adenocarcinom a.

The most commonly used staging system or patients with ductal adenocarcinoma is the American Joint Committee on Cancer (AJCC) based on TNM (tumor/ lymph node/ metastases) staging. Patients are also requently classi ed into a clinical management category based on their radiographic and endoscopic sonographic staging. The clinical management categories are resectable, borderline resectable (i.e., tumors that are involved with nearby structures but neither clearly resectable nor clearly unresectable), locally advanced nresectable (i.e., tumors that are too involved with adjacent structures or curative resection despite there being no evidence o distant metastatic disease), and disseminated (metastatic). The aim o imaging in patients with ductal adenocarcinoma is to delineate the local extent o disease, evaluate or the presence o metastatic disease including hepatic Table 10 -5. Mim ics o Pancreatic Neoplasm s a n omic v i n Foc l

d

osi ion

S l nul C onic

nc

Duod n l div

i is iculum

Duod n l n o l sm ps udocys a n u ysm p i nc

ic lym

d no

y

M ss in dj c n o g ns (s om c , l

kidn y, l

d n l)

144

Body CT: The Essentials

Table 10 -6 . Features o Solid Pancreatic Neoplasm s L sion

Incid nc

t y ic l p i n

a d noc cinom

Common

eld ly

70% in d

h y o n ncing, inf l iv

N u o ndoc in umo

Uncommon

V i bl

V i bl

hy n ncing, 20% l ss lik ly cys ic

Func ion l l sions usu lly sm ll Insulinom >G s inom >Gluc gonom Non unc ion l l sions mo lik ly o b l g nd cys ic MeN-1

Lym

om

Uncommon

V i bl

V i bl

Singl m ss, di us inf l ion, o mul i l m ss s

No

S cond y lym om muc mo lik ly n im y nc ic lym om p nc ic duc no usu lly obs uc d Lym d no y b low n l v ins

s s s

Uncommon

eld ly

V i bl

Singl m ss, di us inf l ion, mul i l m ss s

Uncommon

Usu lly occu s in s ing o dv nc d s g dis s wi known im y n o l sm

Solid s ous cys d nom

r

eld ly m l

V i bl

hy n m ss

Non

r v i n o s ous cys d nom

Solid s udo umo

r

Young m l s

t il

V i bl

30%

C n by cys ic o solid

M

ill y

t y ic l Loc ion

Mo

metastasis, peritoneal carcinomatosis, and pulmonary metastasis to allow or accurate staging and provide anatomic detail necessary or surgical planning in those patients with potentially resectable disease. Determining the local extent o disease includes evaluation o tumor involvement o adjacent major vessels – celiac artery, common hepatic artery, superior mesenteric artery, portal vein, and superior mesenteric vein – which greatly impacts resectability. The rst-order branches o these vessels near the tumor should also be evaluated. Lack o tumor invasion into a vessel is de ned as the presence o clear at plane without tumor contact o the vessel wall. In those vessels that normally contact the pancreatic parenchyma such as the upper superior mesenteric vein and lower portal vein only normal pancreatic parenchyma should contact the vessel wall and there should be no abnormal de ormation o the vessel lumen. The teardrop sign re ers to de ormation o the superior mesenteric vein lumen into a teardrop shape caused by tumor invasion. Lack o tumor contact with a vessel wall has a

ology

ncing

C lcif c ions

Comm n s

r

M lign n

strong negative predictive value or tumor invasion o the vessel. Tumor ab tment is de ned as tumor contact with a vessel wall that may be up to 180 degrees o the vessel circum erence. Tumor encasement is any contact with a vessel wall that involves greater than 180 degrees o the vessel circum erence. The resectable category consists o those patients with no evidence o metastatic disease – that is no liver m etastases, peritoneal carcinomatosis, or pathologic lym phadenopathy – and no tumor involvement o the celiac, superior m esenteric, and comm on hepatic arteries and no involvem ent o superior mesenteric and portal veins. The resectable category corresponds to AJCC stage I or II and accounts or less than 20% o patients with ductal adenocarcinoma. The nresectable category corresponds to AJCC stage III or IV and consists o patients who have distant m etastatic disease including pathologic lym phadenopathy outside o the norm al surgical eld or pancreatoduodenectom y (Whipple procedure) or locally advanced disease with

Chapter 10 Pancreas

145

A

B

Figure 10-15 Unresectable Ductal Adenocarcinoma in the Pancreatic Body Contrast-enhanced CT in patient with locally advanced ductal adenocarcinoma in the pancreatic body. A. Axial im age during axial phase dem onstrates in ltrating neoplasm (arrowheads) with encasem ent o the celiac axis (arrow) abutm ent o the

aorta and invasion o the le t adrenal gland. B. Coronal im age during portal venous phase dem onstrates m ultiple collateral vessels (arrow) in the porta hepatis resulting rom occlusion o the superior mesenteric vein and lower portal vein by the ductal adenocarcinoma (arrowheads).

vascular invasion as de ned by encasem ent o superior m esenteric artery, abutm ent o the celiac artery, or m ore than short segm ent involvem ent o the com m on hepatic artery; occlusion o the superior m esenteric vein or portal vein that is longer than can be surgically reconstructed; or abutm ent or encasem ent o the aorta or IVC (Figure 10 -15). In these patients there is no role or surgical resection and system ic therapy is the standard o care. The National Com prehensive Cancer Network (NCCN) criteria or borderline resectable category or ductal adenocarcinom a in the pancreatic head include involvem ent o the superior m esenteric vein or portal vein ranging rom narrowing, lum en distortion, or even occlusion provided the tum or and af ected vein segm ent can be resected and the vein reconstructed; gastroduodenal artery encasem ent extending up to the hepatic artery with short segm ent abutm ent or encasem ent o the hepatic artery provided that the celiac artery is uninvolved; and tum or abutm ent o the SMA. In practice, the speci c criteria used to de ne the borderline resectable category varies between institutions. The positive predictive value o CT or determ ining a locally invasive nonresectable tum or is 89 % to 100%. Older studies using single detector CTs reported negative predictive values o 74% to 79 % with the understaging o CT m ost requently caused by sm all undetected hepatic and peritoneal metastases, and incorrect estimation o vascular invasion. The accuracy o vascular staging with the use o m ultidetector CTs has im proved and has been reported to be up to 9 9 %. In patients with initial locally advanced, borderline resectable disease who received chem otherapy or downstaging, the accuracy o CT or determ ining resect-

ability ollowing therapy is lower than in initially resectable patients and is m ost requently because o the overestim ation o vascular involvement due to in am matory changes and brosis resulting rom treatm ent that can resemble residual in ltrative tum or.

Neuroendocrine Tumors Pancreatic neuroendocrine tumors arise rom the Islet Cells and account or 1% to 2% o pancreatic neoplasms. They can be associated with von Hippel–Lindau disease, multiple endocrine neoplasia type I (MEN 1), and neuro bromatosis type I. On contrast enhanced CT they are usually solid, and hyperenhance during arterial phase, and at portal venous phase can be hyperdense, isoattenuating, or hypodense to normal pancreatic parenchyma (Figure 10-16). Approximately 5% o neuroendocrine tumors are cystic, requently with a hyperenhancing rim. Functional pancreatic endocrine tumors typically present as small m asses that are discovered because the patient is symptomatic rom excess horm one production. Ins linomas are the most com mon unctional pancreatic endocrine tumor. They occur in all segm ents o the pancreas with equal requency, usually measure less than 2 cm, and 9 0% are benign. Patients with insulinom as present with symptoms o hypoglycem ia. Gastrinomas are the second m ost comm on neuroendocrine tum or and patients present with Zollinger–Ellison syndrome consisting o abdominal pain, gastric ulcers, and diarrhea. Gastrinom as occur more comm only in the duodenum than the pancreas and 6 0% to 70% are malignant. Gl conomas are large at presentation measuring 7 to 8 cm and are most

146

Body CT: The Essentials

Pancreatic Parenchymal Metastases In autopsy series m etastases to the pancreas are present in 3% to 12% o patients with advanced m alignancy. The m ost requent prim ary sources o m etastases to the pancreas are lung cancers, breast cancers, gastrointestinal cancers, renal cancers, and m elanom as. Pancreatic m etastases usually occur in the setting o advanced stage disease and discovery o a pancreatic m etastasis be ore the prim ary source is known is extrem ely rare. On CT m etastases to the pancreas can present as a single pancreatic m ass, a dif usely in ltrating m ass, or less requently at m ultiple ocal pancreatic m asses. The m etastases can be locally invasive and result in obstructive pancreatitis sim ilar to ductal adenocarcinom a. Som e pancreatic m etastases, particularly those originating rom renal cell carcinom as m ay have enhancem ent characteristics that closely ollow those o the prim ary neoplasm . Figure 10-16 Neuroendocrine Tumor Contrast-enhanced CT reveals a hyperenhancing non unctional neuroendocrine tum or in the pancreatic tail (arrowheads). Non unctioning neuroendocrine tum ors tend to be large at presentation and m ay have central necrosis.

commonly located in the pancreatic body and tail. Most are malignant and patients present with the 4D’s—dermatitis, diarrhea, diabetes m ellitus, and deep venous throm bosis. VIPomas secrete vasointestinal polypeptide that causes watery diarrhea, hypokalemia, and achlorhydria. Tumors are 5 to 6 cm on average and heterogeneous because o the central necrosis or cystic change. They most requently occur in the pancreatic tail and are usually malignant. Non unctional pancreatic endocrine tum ors are m ore com m on than unctional tum ors. They tend to be larger, 5 to 6 cm on average, and are requently heterogeneous because o internal hem orrhage or cystic change. Non unctional tum ors are the m ost com m on pancreatic endocrine tum or type in patients with von Hippel–Lindau and MEN1. These tum ors occur with equal requency through the pancreas and at the tim e o presentation 6 0% to 80 % o patients have m etastases.

Pancreatic Lymphoma The pancreas is secondarily involved in 30% o patients with non-Hodgkin lymphoma but primary lymphoma o the pancreas is rare with ewer than 2% o extranodal non-Hodgkin lymphomas arising in the pancreas. The incidence increases to 5% in patients with AIDS-related non-Hodgkin lymphoma. Pancreatic lymphoma can present as a homogeneous bulky mass or with dif use involvement o the pancreas that may mimic pancreatitis. Lymphoma may be in ltrative, but unlike ductal adenocarcinoma the pancreatic duct is not usually obstructed when invaded and there is no luminal narrowing o encased vessels. The presence o lymphadenopathy below the renal veins can occur with pancreatic lymphoma but virtually excludes pancreatic adenocarcinoma.

Postoperative Pancreas Pancreatic resection is one o the m ost requent treatm ents or pancreatic cystic neoplasm s, neuroendocrine tum ors, and the only curative therapy or the m inority o patients who have resectable ductal adenocarcinom a. Partial pancreatectom y or revision o pancreatic drainage is indicated in patients with chronic pancreatitis who are sym ptom atic and re ractory to other therapies. Understanding the norm al postoperative anatom y and anastom oses is essential to accurate interpretation o CT in these patients. Pancreaticod odenectomy (Whipple proced re) consists o en block resection o the pancreatic head, duodenum , distal stom ach, gallbladder, lower bile duct, and included lym ph nodes with pancreaticojejunostom y, hepaticojejunostomy, and gastrojejunostom y anastomoses. In the pylor s-sparing Whipple proced re there is preservation o the distal stom ach and proxim al duodenum so that a duodenojejunostom y anastomosis is per ormed instead o a gastrojejunostomy. Postoperative pneum obilia is usually present and air m ay also be present in the pancreatic duct. In patients who have undergone Whipple procedure reactive lymphadenopathy and perivascular edem a are com m on in the rst 2 m onths ollowing surgery. In the case o patients who have undergone Whipple procedure or ductal adenocarcinom a these norm al postoperative ndings can be m istaken or recurrent tumor. However unlike recurrent neoplasm , which progresses over tim e, postoperative lym phadenopathy and perivascular cu ng decrease and either resolve or stabilize over time. The m ost requent complications ollowing Whipple surgery are delayed gastric em ptying, anastom otic leak, and uid collections. Obstruction o the biliary or pancreatic ducts by anastomotic strictures is uncom mon. Distal Pancreatectomy is per orm ed to resect the pancreatic body and tail with the resection occurring at or just to the le t o the superior m esenteric vein. The spleen is also o ten rem oved. There are no anastom oses. The m ost

Chapter 10 Pancreas com m on com plications o distal pancreatectom y are pancreatic stula, uid collections, and splenic vein throm bus. The P estow proced re is per ormed or drainage o the pancreatic duct in patients with chronic pancreatitis. The pancreatic duct rom uncinate process to pancreatic tail is longitudinally opened and debrided. The pancreas is then anastomosed in a side-to-side ashion with a longitudinally opened jejunal loop (pancreaticojejunostomy) so the pancreatic duct is open to the bowel lumen through its entire length. Su GGESTED READINGS 1. Balthazar EJ. Acute pancreatitis: assessm ent o severity with clinical and CT evaluation. Radiology. 200 2;223:6 03–6 13.

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10 . National Com prehensive Cancer Network (NCCN) Clinical Practice Guidelines in Oncology: Pancreatic Adenocarcinom a Version I. 20 13. www.nccn.org. Accessed July 25, 20 13. 11. Ram an SP, Salaria SN, H ruban RH , Fishm an EK. Groove pancreatitis: Spectrum o im aging ndings and radiologypathology correlation. AJR 20 13;20 1:W29 –W30 . 12. Sahani DV, Rajgopal K, Saokar A, Fernandez-del Castillo C, Brugge WR, Hahn PF. Cystic pancreatic lesions: a sim ple im age-based classi cation system or guiding m anagem ent. RadioGraphics. 20 0 5;25:1471–1484. 13. Sandrasegaran K, Patel A, Fogel EL, Zyrom iski NJ, Pitt H A. Annular pancreas in adults. AJR. 20 0 9 ;19 3:45–46 0 .

2. Berland LL, Silverm an SG, Gore RM, et al. Managing incidental ndings on abdom inal CT: white paper o the ACR incidental ndings com m ittee. JACR. 20 10 ;7:754–773.

14. Sandrasegaran K, Tann M, Jennings SG, et al. Disconnection o the pancreatic duct: an im portant but overlooked com plication o severe acute pancreatitis. Radiographics. 20 0 7; 27:1389 –140 0 .

3. Borghei P, Sokhandon F, Shirkhoda A, Morgan D. Anom alies, anatom ic variants, and sources o diagnostic pit alls in pancreatic im aging. Radiology. 20 13;26 6 :28–36 .

15. Scatarige JC, Horton KM, Sheth S, Fishm an EK. Pancreatic parenchym al m etastases: observations on helical CT. AJR. 20 0 1;176 :6 9 5–6 9 9 .

4. Dewhurst CE, Mortele KJ. Cystic tum ors o the pancreas: im aging and m anagem ent. Radiol Clin N Am. 2012;50:46 7–486 .

16 . Tam m EP, Balachandran A, Bhosale PR, et al. Im aging o pancreatic adenocarcinom a: update on staging/ resectability. Radiol Clin N Am. 20 12;50 :40 7–428.

5. Kucera JN, Kucera S, Perrin SD, Caracciolo JT, Schm ulewitz N, Kedar RP. Cystic lesions o the pancreas: radiologicendosonographic correlation. RadioGraphics. 2012;32:E283–E30 1. 6 . Lesniak RJ, Hohenwalter MK, Taylor AJ. Spectrum o causes o pancreatic calci cations. AJR. 200 2;178:79 –86 .

17. To’o KJ, Ram an SS, Yu NC, et al. Pancreatic and peripancreatic diseases m im icking prim ary pancreatic neoplasia. RadioGraphics. 20 0 5;25:9 49 –9 6 5.

7. Merkle EM, Bender GN, Brambs H J. Imaging ndings in pancreatic lymphoma: dif erential aspects. AJR. 2000;174:671–675.

18. Theoni RF. The revised Atlanta classi cation o acute pancreatitis: its im portance or the radiologist and its ef ect on treatm ent. Radiology. 20 12;26 2:751–76 4.

8. Morgan DE, Waggoner CN, Canon CL, et al. Resectability o pancreatic adenocarcinom a in patients with locally advanced disease downstaged by preoperative therapy: a challenge or MDCT. AJR. 2010;19 4:6 15–6 22.

19 . Vikram R, Balachandran A, Bhosale PR, Tam m EP, Marcal LP, Charnsangavej C. Pancreas: peritoneal re ections, ligam entous connections, and pathways o disease spread. RadioGraphics. 20 0 9 ;29 :e34.

9 . Mortele KJ, Rocha TC, Streeter JL, Taylor AJ. Multim odality im aging o pancreatic and biliary congenital anom alies. RadioGraphics. 20 06 ;26 :715–731.

20 . Yam auchi FI, Ortega CD, Blasbalg R, Rocha MS, Jukem ura J, Cerri GG. Multidetector CT evaluation o the postoperative pancreas. RadioGraphics. 20 12;32:743–76 4.

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Ch a p t e r

11

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David L. Coy, MD, PhD

I. ANATOMY II. CT TECHNIQUE III. CONGENITAL ANOMALIES AND ANATOMIC VARIANTS a. Renal Anomalies and Variants i. Variation in renal contour ii. Variation in renal sizes b. Renal Agenesis c. Renal Ectopy and Fusion Anomalies d. Anomalies and Variants o the Intrarenal Collecting System and Ureters e. Anomalies and Variants o the Bladder IV. NEPHROCALCINOSIS V. UROLITHIASIS VI. RENAL INFECTIONS AND INFLAMMATORY DISEASE a. Acute In ections b. Chronic In ections VII. RENAL VASCULAR DISEASE a. Renal In arcts

An At o m y The kidneys are retroperitoneal organs located in the per re al space which is orm ed by Gerota ascia that contains the kidneys, proxim al ureters, adrenal glands, and perinephric at. The a ter or parare al space lies anterior to the perirenal space and contains the pancreas, duodenum , ascending and descending segm ents o colon, and variable am ount o at. The poster or parare al space is a sm all space de ned by the ascia o psoas and quadratus lum borum m uscles and the posterior m argin o the perirenal space. On norm al studies the boundaries o the retroperitoneal com partm ents are not visible, but the perinephric and anterior pararenal spaces m ay be delineated based on the organs that they contain. The kidneys are bean-shaped paired organs m easuring 9 to 13 cm in length that lie adjacent to and parallel with

VIII. RENAL CYSTIC DISEASE a. Bosniak Classi cation System b. Renal Cystic Diseases IX. RENAL TUMORS a. Benign Primary Renal Masses b. Malignant Primary Renal Masses c. Malignant Secondary Renal Masses X. INTRARENAL COLLECTING SYSTEMS URETERS AND BLADDER a. Papillary Necrosis b. Congenital Ureteropelvic Junction Obstruction c. Benign Masses o the Collecting Systems d. Urothelial Tumors i. Transitional cell carcinoma ii. Squamous cell carcinoma iii. Adenocarcinoma e. Nonneoplastic Bladder Masses . Cystitis

the psoas m uscles on both sides o the lum bar spine such that the lower pole o the kidney is slightly anterior and lateral to the upper pole. The le t kidney is usually located slightly higher than the right kidney. The re al h lum is a recessed ssure in the m edial aspect o the m idpoint o the kidney through which the renal vessels, nerves, and the collecting system pass to enter into the re al s us, a central cavity in the kidney lled with variable am ounts o at. The renal parenchym a consists o the outer renal cortex and the inner m edullary space that contains a variable num ber o renal pyram ids. The base o each renal pyram id is covered by renal cortex and the apex o the pyram id is the renal pap lla that is directed into the central renal sinus that contains the collecting system , renal artery and vein branches, and a variable am ount o at. Colum s o Bert are orm ed by extension o renal cortex between the renal pyram ids (Figure 11-1). 149

150

Body CT: The Essentials Re na l p a re nc hyma

Corte x Me d ulla P a p illa Ca p s ule Ca lyx

Column Hilum P yra mid

P e lvis Ure te r

Figure 11-1 Renal Anatomy (line drawing) Renal parenchym a consists o the outer cortex and the inner m edullary space that contains the renal pyram ids. The papilla

o the renal pyram id is directed into the central renal sinus and is drained by a calyx. The in undibula connect the calyces to the renal pelvis.

The trare al collect system is the portion o the urinary collecting system contained in the renal sinus which consists o calyces, in undibula, and the renal pelvis. The cone-shaped calyx cups the papilla to drain the urine em erging rom the tip o papilla. The ree edge o the calyx that orm s the rim o the cup surrounding the papilla is the or x. In the upper and lower poles o the kidneys several renal papillae m ay drain into a compou d calyx. Urine ows rom the calyx through the u d bulum a slender channel that connects the calyces to the renal pelvis. In som e individuals the renal pelvis m ay extend through the hilum into the perinephric space (extrare al pelv s). The portion o the renal pelvis that extends beyond the renal sinus is requently patulous; however, an extrarenal pelvis should not be con used or pathologic dilation or obstruction as the rem ainder o the collecting system contained within the renal sinus will have norm al caliber. The ureters are conduits or transport o urine between the renal pelvis and the bladder. Urine is m oved toward the bladder by peristaltic contractions. The ureters course entirely through the retroperitoneal space. In the lower abdom en they course over the psoas m uscles and iliac vessels be ore entering the pelvis. In the pelvis the ureters curve laterally and then course m edially to insert into the posterior in erior bladder. The ureters course obliquely through the bladder wall or approxim ately 2 cm be ore

term inating at the ureteral ori ces. The oblique intram ural course o the ureters orm s the ureterovesicle junction (UVJ) which is the narrowest segm ent o the ureter and unctions to prevent vesicoureteral re ux o urine. The urinary bladder is a hollow viscus that lies in the deep pelvis. It is extraperitoneal but the bladder dom e and upper portion o the lateral walls are covered by peritoneum . Its shape and wall thickness vary depending on the am ount o urine it contains. The bladder trigone is a sm ooth triangular-shaped segm ent in the posterior in erior bladder with the upper two vertices ormed by the ureteral ori ces and the lower midline vertex ormed by the bladder neck.

Ct t e Ch n iq Ue CT-KUB is a low-radiation dose CT per orm ed without the use o intravenous or oral contrast that is speci cally designed to detect calculi within the kidneys, ureters, and bladder. Because o the noise and lack o contrast its diagnostic per orm ance or detection o conditions other than urolithiasis is lim ited. On the current generation o CT scanners thin (1.25–2.5 m m ) slice axial scans with coronal and sagittal re orm ats are per orm ed. CT urography (CTU) is a m ultiphasic CT and is designed to evaluate renal parenchym a and collecting system s and is m ost com m only used or patients with hem aturia. A low-dose CT-KUB is rst per orm ed to

Chapter 11 Kidneys, Ureters, and Bladder 151 evaluate or calculi within the collecting system . This is ollowed by contrast-enhanced CT with 10 0 to 150 m L o iodinated contrast adm inistered intravenously at an injection rate o 3 to 4 m L per second. The patient is scanned during nephrographic phase in which there is com plete, uni orm enhancem ent o the renal parenchym a which occurs approxim ately 9 0 to 120 seconds ollowing contrast adm inistration. An excretory phase scan per orm ed 3 to 8 m inutes ollowing contrast adm inistration. Concentrated contrast excreted into the collecting system allows or detailed exam ination o the intrarenal collecting system and ureters. Because o concern or patient radiation exposure rom m ultiphasic CT exam inations, a “split-bolus” technique in which the contrast is ractionated into two tim ed injections to allow or a single post-contrast scan is being used with greater requency. With this technique about a third o the intravenous contrast is adm inistered ollowed by a several m inute delay a ter which the rem aining two-thirds o contrast is adm inistered. A single scan is per orm ed 10 0 seconds a ter the second contrast adm inistration in which there is sim ultaneous excretory and nephrographic phase enhancem ent rom the rst and second contrast injections, respectively. In this way the num ber o post–contrast-enhanced CTs is reduced to one scan. Potential lim itations o the split-bolus technique include di cultly in characterization o sm all renal lesions located adjacent to the collecting system lled with concentrated contrast. Variation in the typical im aging appearance o benign incidental ndings such as benign liver hem angiom as by the dual contrast injection technique m ay result in additional im aging studies (Figure 11-2). Renal CT is per orm ed or evaluation o the kidneys or renal m asses. An unenhanced CT o the kidneys is perorm ed ollowed by contrast-enhanced CT in corticom edullary and nephrographic phases o enhancem ent which occur at approxim ately 20 to 80 seconds and 9 0 to 120 seconds, respectively, ollowing adm inistration o intravenous contrast. During the corticom edullary phase there is contrast enhancem ent o the renal cortex but little enhancem ent o the renal m edulla. This phase is help ul or evaluation o hypervascular tum ors and the arterial anatom y is usually well delineated. A nephrographic phase with hom ogeneous contrast enhancem ent o the renal cortex and m edulla is essential as the likelihood o detecting a sm all renal m ass is greater than on corticom edullary phase enhancem ent. As a corollary, because routine contrast-enhanced CT o the abdom en is com m only per orm ed 6 0 to 80 seconds a ter intravenous contrast adm inistration when the kidneys are in corticom edullary phase o enhancem ent sm all m edullary renal lesions m ay be inadvertently m issed on routine portal venous phase contrast-enhanced CT. In som e instances a renal CT m ay include a delayed excretory phase scan to evaluate the intrarenal collecting system ; however, because the lower ureters and bladder are not im aged a renal CT is not su cient or hem aturia evaluation. The overall sensitivity o CT or detection o renal m asses is about 9 6 %. When a suspected renal cell

carcinom a (RCC) is identi ed a close inspection o the vasculature should be per orm ed due to the propensity o RCCs to invade and extend into the renal vein and IVC. Regional retroperitoneal lym ph nodes, liver, lung bases, and the bones should also be closely evaluated, as these are the m ost requent locations or regional and distant RCC m etastases. CT cystogram is used or evaluation o bladder leak, rupture, or stula orm ation. CT through the pelvis is per orm ed a ter the bladder has been lled with diluted contrast via a Foley catheter. The volum e o contrast can range rom 20 0 to 50 0 m L but should be su cient to m ildly distend the bladder so as to not m iss a sm all leak. The presence o excreted contrast in the bladder rom an intravenous contrast adm inistration m ay not su ciently distend to bladder to detect a sm all leak and there ore does not substitute or a CT cystogram in cases where a bladder leak is suspected.

Co n g e n it Al An o m Al ie s An d An At o m iC VAr iAn t s Renal Anomalies and Variants Variation in renal contour There is considerable variation in renal shape. A dromedary hump re ers to a bulge in the contour o the le t upper kidney caused by m olding or im pression o the spleen (Figure 11-3). Despite the bulging contour the thickness o the renal parenchyma is normal and it should not be mistaken or a m ass. Pers ste t etal lobat o s are sm all indentations in the lateral renal contour that result rom incom plete usion o round renal lobules during development. The indentations in the renal contour are sm all, smooth, and distributed in between the renal pyramids as opposed to indentations in the renal contour caused by scarring which can be large, irregular, and directly overlying a renal pyramid. A prominent m edial bulge o the renal parenchyma extending into the renal sinus at the midpoint o the kidney is a prom e t colum o Bert . It divides the renal pelvis between the upper and lower poles and is associated with partial or complete duplication o the collecting system. The presence o ocal scarring or renal atrophy within a kidney may result in com pensatory hypertrophy o the remaining normal parenchym a within the same kidney and urther distort the renal contour. On CT the presence o a renal contour abnorm ality rom a prominent column o Bertin or ocal hypertrophy can be dif erentiated rom a neoplasm, because they are com posed o renal parenchym a they will enhance equally and sym metrically with normal renal parenchym a in the ipsilateral and contralateral kidneys.

Variation in renal sizes The renal length m easured rom upper to lower poles ranges rom 9 to 13 cm with longer length correlating with m ale gender and body habitus. There is norm ally m ild

152 Body CT: The Essentials

A

B

C

Figure 11-2 Unenhanced and Contrast-Enhanced CT o Le t Kidney Coronal im ages through the le t kidney in the sam e patient rom unenhanced CT (A) and contrast-enhanced CT (B–D). B Corticom edullary phase enhancem ent occurs about 20 to 80 seconds ollowing contrast adm inistration and is use ul or determ ining the enhancem ent characteristics o renal lesions, but sm all renal lesions in the m edullary space m ay be m issed.

D

C. Nephrographic enhancem ent phase occurs about 9 0 to 120 secon ds ollowin g con trast adm in istration an d the hom ogeneous enhancem ent o the renal parenchym a is use ul or detecting sm all renal lesions. D. Split-bolus technique ( rom dif erent exam ination than B and C) perm its sim ultaneous excretory phase and nephrographic phases to be obtained with a single scan.

Chapter 11 Kidneys, Ureters, and Bladder 153 t ab

11-2. Bilateral Sm all Kidneys

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Figure 11-3 Dromedary Hump Contrast-enhanced CT dem onstrates contour a bulge in the lateral contour o the le t kidney (arrow) due to impression o the spleen on the upper pole.

asym m etry in the renal lengths with the m ean renal length being 10 .8 cm or the right kidney and 11.1cm or the le t kidney with standard deviations o about 1.3 cm . The presence o a unilateral sm all kidney can result rom partial nephrectom y, hypoplasia, or atrophy caused by chronic ischem ia or prior injury rom in ection, vesicoureteral re ux, or in arction (Table 11-1). Sm all bilateral kidneys usually result rom a chronic disease (Table 11-2). Unilateral renal enlargem ent m ost com m only results rom com pensatory hypertrophy due to injury or chronic disease in the contralateral kidney (Table 11-3). Bilateral renal enlargem ent is m ost com m only seen in patients with diabetes m ellitus, and acute in am m atory conditions (e.g., glom erulonephritis, interstitial nephritis) (Table 11-4).

Renal Agenesis Unilateral renal agenesis occurs in approxim ately 1:50 0 live births and usually discovered on prenatal sonography or as an incidental nding in adults. The pathogenesis is unknown. With the absence o one kidney there is com pensatory hypertrophy o the rem aining kidney. Generally, patients with a solitary kidney are asym ptom atic and otherwise have a norm al li e expectancy; however, when discovered on prenatal ultrasound a detailed etal anatom ic survey should be per orm ed because o 11-1. Unilateral Sm all Kidney

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During etal development the kidneys ascend rom the pelvis to the abdom en. Interruption o this ascent results in the kidney being located in an abnorm al position. The m ost com mon orm o renal ectopy is a pelv c k d ey in which a kidney is located in anterior to the sacrum and occurs

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an association between renal agenesis and chrom osom al abnorm alities. B lateral re al a e es s (class c Potter seque ce) occurs in 1:40 0 0 to 1:80 0 0 etuses and results in severe oligohydram nios and pulm onary hypoplasia with a m ortality rate o nearly 10 0 % in the antenatal period. On CT im aging patients with unilateral renal agenesis will have an absent kidney and absent ipsilateral renal artery. The ipsilateral adrenal gland can have a attened, elongated con guration (ly dow adre al la d) or can be absent in 8% to 10% o cases. The contralateral kidney will dem onstrate com pensatory hypertrophy. I the renal ossa is em pty on CT a search should be m ade in the pelvis and contralateral abdom en to exclude renal ectopia. Agenesis can be dif erentiated rom ipsilateral nephrectom y by the presence o surgical clips and a renal artery stum p. Renal agenesis is associated with the presence o other genitourinary anom alies. In m ales associated anom alies include ipsilateral sem inal vesicle cysts, ipsilateral hypoplasia o the testis, and hypospadias. In em ales unicornuate and bicornuate uterine anom alies are associated with renal agenesis.

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Body CT: The Essentials

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risk o injury in blunt abdominal traum a. On CT horseshoe kidneys are positioned in the lower abdomen and the renal axis is inverted with the lower poles being directed m edially due to them being joined together. There is also renal m alrotation with the renal pelvises being oriented anteriorly which is associated with stone ormation and ureteropelvic junction (UPJ) obstruction.

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with an incidence o 1:500 to 1:1000. Crossed renal ectopy occurs in about 1:1000 individuals and results when two kidneys are located on the sam e side o m idline. In 9 0% o cases the two kidneys are at least partially used to one another (crossed used ectopy). In m ost cases the ureter o the ectopic kidney courses to the contralateral side and inserts norm ally into the bladder. Horseshoe k d ey is the most com m on orm o renal usion anom aly occurring in 1:400 adults and is twice as com mon in males (Figure 11-4). The horseshoe shape is due to usion o the two kidneys across the m idline at their lower poles by an isthm us o renal parenchym a or brous tissue. Horseshoe kidneys are positioned in the lower abdomen due to arrest o normal renal ascent caused by the midline isthmic tissue being unable to pass over the trunk o the in erior mesenteric artery. Horseshoe kidneys have variant vascular anatomy with m ultiple renal arteries that can originate rom the aorta or iliac arteries. Horseshoe and pelvic kidneys have a higher

Figure 11-4 Horseshoe kidney Contrast-enhanced CT dem onstrates usion o the kidneys across m idline through their lower poles (arrowhead). The kidneys are located in the lower abdom en because isthm us cannot pass over the in erior m esenteric artery (arrow) trunk. Note that kidneys are m alrotated with the renal pelvises directed anteriorly.

Anomalies and Variants o the Intrarenal Collecting System and Ureters Duplication o the collecting system is present in 0 .7% o adults and results rom developm ent o two ureteric buds such that the upper and lower poles o the kidneys are separated rom one another. The degree o separation is variable. Partially duplication can range rom a bi d renal pelvis with upper and lower pole pelvises draining into a single com m on ureter to the upper and lower pole pelvises each having its own ureter that at som e point join together into a single ureter (Figure 11-5). In a com plete duplicated system there are separate lower and upper pole m oieties each with its own ureter that inserts into the urinary bladder. The Meyer–We ert rules o com plete

Figure 11-5 Duplicated Collecting System Coronal oblique MIP reconstruction o contrast-enhanced CT during excretory phase dem onstrates a duplicated le t collecting system with two ureters. The lower ureters inserts at the normal location whereas the upper ureter inserts m edial and in erior to the lateral ureter.

Chapter 11 Kidneys, Ureters, and Bladder 155 duplicated system s state that the ureter o the upper pole m oiety has an ectopic insertion into the bladder that is usually in erior and m edial to the norm al ureteral insertion and is prone to obstruction. The ureter o the lower pole m oiety has a norm al (orthotopic) insertion into the urinary bladder, but there is an increased incidence o vesicoureteral re ux. The ectopic insertion o the upper pole m oiety can occur in the bladder neck, urethra, or vagina and can be a cause o leakage or enuresis in young em ales. The ureter o the upper pole m oiety also has an increased propensity to develop an ureterocele—a ocal dilation o the distal ureter located within the bladder wall proxim al to the ureteral ori ce. On contrast-enhanced CT the presence o collecting system duplication should be suspected when a kidney contains a prom inent column o Bertin and has increased renal length. When two ureters are present it can be di cult to discern whether the ureters join together at som e point (partial duplication) or have separate insertions into the bladder (complete duplication). In such cases excretory phase contrast-enhanced CT can be used to provide greater detail o the ureteral anatom y. The dropp l ly s on excretory urography in a duplicated collecting system re ers downward and lateral displacem ent o a contrast- lled lower pole m oiety due to direct m ass ef ect by a dilated upper pole moiety that is poorly enhancing due to obstruction. Me acalycos s (co e tal me acalyces) is de ned by dif use, sym m etric enlargem ent o calyces in absence o obstruction or dilation o other segm ent o the collecting system . This m ay be congenital or acquired. The enlarged calyces have a squared or polygonal con guration and m ay be m ore num erous (polycaliosis) than usual. Megacalycosis is requently unilateral and can be associated with in ection and stone orm ation due to urine stasis. Retrocaval (c rcumcaval) ureter is a rare congenital anomaly in which the right ureter courses posterior and medial to the IVC (Figure 11-6). On imaging there is an abrupt medial deviation o the upper right ureter which may take a hook-like or J con guration. On rontal radiograph a retrocaval ureter will course medial to the right lumbar pedicles.

Figure 11-6 Retrocaval Ureter Excretory phase contrast-enhanced CT demonstrates contrastlled right ureter (arrow) extending posterior to the IVC (labeled i).

Figure 11-7 Right Orthotopic Ureterocele Contrast-enhanced CT demonstrates right ureterocele (arrowhead) protruding into the urinary bladder.

Co e tal (pr mary) me aureter is a dilated ureter that is caused by an aperistaltic segment in the distal ureter resulting in a unctional obstruction. Treatment consists o excision o the adynamic distal segment and ureteral reimplantation. In addition to ectopic ureteroceles that occur in duplicated collecting systems, ureteroceles may develop in a nonduplicated system with the ureter inserting into the bladder at the normal location (orthotop c ureterocele). On CT orthotopic ureteroceles present as cystic dilations o the intramural portion o the distal ureter that protrude into the bladder lumen (cobra head s ) on excretory contrast-enhanced CT (Figure 11-7).

Anomalies and Variants o the Bladder Bladder exstrophy is a rare developm ental anom aly in which there is eversion o the bladder that protrudes through a de ect in the anterior abdom inal wall. It is m ore com m on in m ales and is associated with epispadias. The presence o an abnorm ally wide sym physis pubis and pelvic surgical clips rom surgical correction are ndings that m ay be seen in children and adults. Patients are at increased risk or squam ous cell carcinom a o the bladder. The urachus is a m idline tubular structure connecting the anterior bladder dom e to the um bilicus. Norm ally the urachus involutes be ore birth becom ing the m edian um bilical ligament; however, the entire urachus or segm ents o the urachus can persist resulting in an urachal rem a t a omaly (Figure 11-8). A ully patent persistent urachus is usually identi ed in in ants due to urine leakage rom the um bilicus and is associated with the presence o posterior urethral valves and ventral wall de ects. In contrast patients with segmental or incom plete patency o the urachus are usually asym ptom atic. Urachal s us is patency o the umbilical end o the urachus. Urachal cyst results rom patency o m id portion o the urachus with obliteration o the bladder and umbilical ends. Urachal d vert culum represents

156

Body CT: The Essentials

Figure 11-8 Urachal Diverticulum Sagittal im age rom contrast-enhanced CT dem onstrates a short urachal diverticulum (arrows) arising rom the anterior bladder (labeled b) in the m idline. The rem ainder o the urachus is involuted into the m edian um bilical ligam ent (arrowheads) that extends to the um bilicus (labeled u).

patency o the bladder end o the urachus. As opposed to other congenital or acquired bladder diverticula, an urachal diverticulum arises rom the anterior bladder dom e in the midline. In requently urachal cysts can become in ected and patients with urachal rem nants are at risk or development o adenocarcinoma within the remnant. Co e tal bladder d vert cula typically occur close to the ureteral ori ce and can result in vesicoureteral re ux due to compression on the intramural segment o the distal ureter.

n e p h r o CAl Cin o s is Nephrocalcinosis re ers to calcium deposition in the renal parenchym a and is classi ed based on the predom inant location o involvem ent. Medullary ephrocalc os s is calcium deposition in the central kidney that spares the renal cortex. The m ost com m on causes are renal tubular acidosis type I, m edullary sponge kidney disease (MSK), hyperparathyroidism , and other hypercalcem ic states. Medullary spo e k d ey d sease is a sporadic condition in which the collecting tubules in the renal pyram ids are abnorm ally dilated resulting in developm ent o tiny stones within the pyram ids. MSK can af ect one or both

Figure 11-9 Medullary Sponge Kidney Disease Coronal oblique m axim um intensity projection reconstruction rom contrast-enhanced CT in excretory phase dem onstrating striations o contrast (paint-brush sign) in the renal papillae o le t kidney resulting rom ectasia o the renal tubules in a person with m edullary sponge kidney disease.

kidneys and can have a segm ent or uni orm distribution within a kidney. Segm ental distribution o m edullary nephrocalcinosis is a help ul sign to dif erentiate MSK rom other causes o m edullary nephrocalcinosis. Occasionally the sm all stones can pass into the collecting system resulting in nephrolithiasis. On CT MSK presents with tiny calci cations in the renal pyram ids and som etim es clusters o tiny calculi in the calyces. On excretory phase contrastenhanced CT contrast lling o the dilated distal collecting tubules results in pa t brush appearance o the renal pyram ids (Figure 11-9 ). Cort cal ephrocalc os s is less com m on than m edullary nephrocalcinosis and m ani ests as calcium deposition in the renal cortex. Etiologies or cortical nephrocalcinosis are chronic glom erulonephritis, oxalosis, and acute cortical necrosis. Other causes o renal calci cation are listed in Table 11-5.

Ur o l it h iAs is Urolithiasis af ects up to 14% o men and 6% o women during their li etimes. Although the pathogenesis o stone ormation in the urinary tract is not ully understood patients

Chapter 11 Kidneys, Ureters, and Bladder 157 t ab a

11-5. Renal Calci cations oscl osis o sm ll

N

n l

i l b nc

s

oli i sis

M dull y n oc lcinosis r n l ubul cidosis M dull y s ong kidn y dis h y c lc mic s s p ill y n c osis

s

Co ic l n oc lcinosis C onic glom ulon i is Ox losis a cu co ic l n c osis C onic ns l n j c ion r mo

in c ion o in

c ion

t umo s—r CC, Wilms’ umo

with metabolic disorders such as hypercalciuria and gout, or with recurrent in ections are at risk or development o calculi. There are ve subtypes o calculi. Calcium with varying amounts o oxalate and phosphate accounts or 70% to 80% o all urinary tract calculi. These are the most radiodense urinary tract calculi and easily visible on abdominal radiographs. Struvite-apatite stones account or 15% to 20% o all urinary calculi and are caused by urinary in ections by urease-producing gram-negative bacteria such as Proteus, Klebsiella, and Pseudomonas. Struvite-apatite stones are more common in women and account or 70% o all sta hor calcul – branched calculi that ll two or more calices so as to resemble the antlers o a stag (Figure 11-10). Struvite-apatite calculi are less radiodense than calcium stones but visible on plain radiographs. Uric acid stones account or 5% to 10% o all urinary tract calculi and occur in patients with low urine

Figure 11-10 Staghorn Calculus Coronal im age rom unenhanced CT dem onstrates a large branched staghorn calculus (arrow) lling several calyces in the upper pole o the right kidney.

pH. These stones are too radiolucent to be seen on plain radiographs, but are visible on CT. Cystine stones account or about 3% o all urinary tract calculi and occur in patients with cystinuria an autosomal-recessive inherited disorder o renal absorption. These are not as radiodense as calcium stones but are usually visible on plain abdominal radiograph. Medication-induced calculi result rom precipitation o a medication or its metabolites in the urine and account or about 1% o all urinary tract calculi. Protease inhibitors such as indinavir used in the treatment o H IV in ection can produce stones that may be too radiolucent to be visible even on CT. Although about 9 0 % o urinary tract calculi are radiodense the sensitivity o plain radiographs or detection o urolithiasis is only about 6 0%. In patients with ank pain or hem aturia and suspected urolithiasis CTKUB is the imaging m odality o choice having a sensitivity and speci city approaching 100 % or detecting urinary tract calculi. CT also has the added bene ts o providing additional clinically use ul in orm ation such as whether a stone is causing hydronephrosis 1 or elucidating alternative diagnoses in sym ptom atic patients in which urolithiasis is not present. The degree o obstruction caused by a stone does not correlate with its size as sm all stones m ay result in m uch m ore severe obstruction than larger stones. Stone size and location correlate with the probability o passage through the collecting system . Stones m easuring 4 m m or less have a spontaneous passage rate o greater than 70%. The rate o spontaneous passage decreases with increasing size and is approxim ately 30% or stones m easuring 9 to 10 m m . Generally, stones that are located in the distal ureter have a greater chance o spontaneous passage with a passage rate o approxim ately 75% or stones in the distal ureter and UVJ com pared to 50% or stones located at the UPJ. The m ost com m on locations or ureteral calculi to becom e lodged are at the UPJ, where the ureters pass over the iliac vessels, and the ureterovesicle junction. The aim o imaging in nephrolithiasis is to determ ine the size and location o stones and associated com plications such as hydronephrosis. Diagnosis o stones in the intrarenal collecting system on CT-KUB is usually straight orward; however, positive identi cation o ureteral stones can be challenging i the ureter is obscured by bowel or other adjacent structures because it may be di cult to discern whether a visualized retroperitoneal calci cation represents a stone in a nonvisualized ureter, a phlebolith, or other calci cation. Secondary imaging signs help ul in the diagnosis o a ureteral stone include the presence o hydronephrosis or hydroureter to the level o the stone and the presence o a rim o so t tissue (r m s ) surrounding the calculus due to wall thickening o the ureter (Figure 11-11); however, the absence o these signs does not exclude a ureteral stone. The presence o perinephric edema uid surrounding a kidney 1

Pelv cal ectas s re ers to distention o the intrarenal collecting system rom any cause whereas the term hydro ephros s is used in this text to describe dilation o the intrarenal collecting system caused by obstruction. However m any authors use these term s interchangeably.

158

Body CT: The Essentials t ab

11-6 . H ydronephrosis

UpJ obs uc ion S on , blood clo , ungus b ll t umo Cong ni l C ossing v ss l U

l obs uc ion S on , blood clo , ungus b ll t umo ex insic com ssion by m ss r o i on l b osis

pain and microscopic hematuria. Bladder stones are easily visible on CT. Stones that have a spiked appearance are called jacksto es because they resemble the shape o a jack toy.

Figure 11-11 Le t Ureteral Calculus with Rim Sign Unenhanced CT with 5-m m calculus in the m id le t ureter surrounded by a rim o so t tissue due to ureteral in am m ation (arrow).

is a nding that can be associated with the presence o an ipsilateral calculus or recently passed calculus but is not speci c as it can also be seen in cases o pyelonephritis, various orm s o renal dys unction, and as a norm al nding in som e individuals. The comet-ta l s in which a calci ed phlebolith – representing the com et – is associated with a linear sclerosed vein – representing the comet tail – is describe in many re erences but has poor reliability in dif erentiating a pelvic phlebolith rom a distal ureteral stone. In cases where a nonobstructing stone cannot be dif erentiated rom a phlebolith, or i there is suspicion or a radiolucent druginduced stone based on patient history, an excretory phase contrast-enhanced CT can be per orm ed to better delineate the ureters. On CT the presence o obstructive hydronephrosis rom stones, and other causes o obstruction, can result in delayed contrast enhancement o the obstructed kidney or rupture o the calyceal ornices with leakage o urine and contrast into the renal sinus (pyelos us extravasat o ) (Tables 11-6 to 11-8). Primary bladder stones are calculi that develop within the bladder as opposed to stones that originate in the upper collecting system but have spontaneously passed into the bladder. Approximately 70% o primary bladder stones are associated with conditions causing urinary stasis such as bladder outlet obstruction, neurogenic bladder, and bladder diverticula. Less common etiologies include oreign bodies such as chronic indwelling Foley catheters and bladder in ection with urea-splitting bacteria. Bladder stones are more common in men and patients may present with suprapubic

r e n Al in f e Ct io n s An d in f l Am m At o r y d is e As e Acute In ections Acute pyelo ephr t s is caused by bacterial in ection o the kidney that usually has ascended rom the lower urinary tract or less com monly is seeded by hem atogenous spread o in ection. In patients under the age o 50 years acute pyelonephritis is more comm on in em ales but the incidence is equal in men and wom en over 50 years o age. Routine im aging o the kidneys and urinary tracts is not indicated in adults with uncom plicated pyelonephritis. In patients who are not responding to appropriate therapy within the rst 72 hours, are at risk or severe com plications (i.e., diabetic, im munocomprom ised, or elderly patients), or have history o prior urologic surgery or stones, im aging o the kidneys and collecting system is warranted to evaluate or complications such as developm ent o a renal abscess and CT is the im aging modality o choice. In patients with acute pyelonephritis contrast-enhanced CT is pre erred because the kidneys may appear normal and small intrarenal abscesses may not be visible on unenhanced CT. On contrast-enhanced CT acute pyelonephritis mani ests as wedge-shaped areas o decreased or striated t ab 11-7. Nonobstructive Causes o Pelvicaliectasis or H ydroureter V sicou

l

ux

p im y m g u M g c liosis r li v d c onic obs uc ion

Chapter 11 Kidneys, Ureters, and Bladder 159 t ab

11-8. Delayed or Striated Nephrogram s

Bil l dif us h y o nsion a cu ubul n c osis Bil l obs uc ion Bil l n l y s nosis Bil l n l v in obs uc ion Unil l dif us Obs uc ion r n l y s nosis r n l v in obs uc ion py lon i is Con usion S gm n l (“s o d n V sculi is ( .g., oly g nulom ous) emboli py lon i is

og m”) i is nodos , SLe, W g n

parenchymal enhancement that extend rom the renal pyramids to the cortex that may be solitary or multi ocal with involvement o one or both kidneys. The imaging eatures o acute pyelonephritis can overlap with those o renal in arctions; however, renal in arctions may be associated with a thin rim o cortical enhancement (cort cal r m s ) which i present can help to dif erentiate an in arction rom pyelonephritis. The patient’s clinical presentation and presence o pyuria can be use ul to distinguish between the two. I the areas o decreased enhancement within the kidney appear round then hematogenous seeding should be considered. Secondary signs o acute pyelonephritis include ocal or dif use renal enlargement, stranding o the perinephric at, and thickening o Gerota ascia (Figure 11-12). However, stranding o the perinephric at is nonspeci c ndings that can be seen in many dif erent conditions such as pyelonephritis, renal vein thrombosis, trauma, and in some asymptomatic individuals. Re al abscess is an uncom m on complication o bacterial pyelonephritis that m ost comm only occurs in diabetic and im munocom prom ised patients. Interestingly up to 20% o patients with renal abscesses have negative urine cultures. On contrast-enhanced CT renal abscesses present as unilocular or m ultilocular low-attenuation lesions (0–20 H U) that do no enhance centrally due to the presence o necrosis and pus but have an enhancing rim (Figure 11-13). The abscess may be contained within the renal parenchyma or extend into the perinephric space. A renal abscess can resem ble a cystic or necrotic renal neoplasm on im aging but i the patient has signs or sym ptom s o in ection then the diagnosis o renal abscess should be made. In circumstances where the urine cultures are negative or other clinical param eters are equivocal or in ection presumptive

Figure 11-12 Acute Pyelonephritis Coronal im age rom unenhanced CT dem onstrates enlargement o the le t kidney and stranding o the perinephric at and thickening o Gerota ascia (arrowheads) due to acute severe pyelonephritis. Perinephric stranding is a nonspeci c nding that occurs with hydronephrosis, renal vein occlusion, and other conditions. The absence o perinephric stranding does not exclude pyelonephritis.

antim icrobial treatment with short-interval im age ollow-up is a reasonable approach. Emphysematous Pyelo ephr t s is a rare li e-threatening necrotizing in ection o the kidney with gas orming organisms. Ninety percent o cases occur in patients with poorly controlled diabetes. Gas within the renal parenchyma or perinephric space is present on CT and requently visible on radiographs (Figure 11-14). Emphysematous pyel t s is a less

Figure 11-13 Acute Pyelonephritis with Small Renal Abscess Contrast-enhanced CT in a patient with acute pyelonephritis in le t kidney. The le t kidney has decreased enhancem ent com pared to the right kidney (labeled k) and there is ocal enlargem ent with a sm all central abscess (arrow) surrounded by a thick enhancing wall. There is m ild stranding o the le t perinephric at with loss o the at plane between the kidney and spleen (arrowhead).

160

Body CT: The Essentials

Figure 11-14 Emphysematous Pyelonephritis Unenhanced CT dem onstrates an enlarged le t kidney containing gas within the parenchym a indicating em physem atous pyelonephritis. A ureteral stent is present in the le t renal pelvis.

severe orm o necrotizing in ection in the urinary tract that is characterized by gas within the collecting system. Alternative etiologies or gas within the collecting system such as a stula, trauma, and instrumentation should be excluded be ore making the diagnosis o emphysematous pyelitis. Pyo ephros s re ers to an in ected and obstructed collecting system . It should be suspected in patients with an obstructed urinary collecting system and ever or other signs o in ection. I untreated, it can result in loss o renal unction or sepsis. Ultrasound is the m ost com m only used im aging m odality. The im aging eatures o pyonephrosis on CT include a dilated, obstructing urinary collecting system and wall thickening and hyperenhancem ent o the renal pelvis and ureter. The presence o pus is rarely detected on CT but m ore com m only identi ed by ultrasound.

Figure 11-15 Ref ux Nephropathy Coronal im age rom contrast-enhanced CT dem onstrates chronic parenchym al scarring and prom inence o the intrarenal collecting system in the right kidney caused by chronic vesicoureteral re ux. Incidentally the le t kidney contains a prominent colum n o Bertin (labeled b).

Chronic In ections Chro c atroph c pyelo ephr t s re ers to renal scarring with thinning o the renal cortex and m edullar and blunting o the calyces that can result rom severe ocal pyelonephritis or stones. Renal scarring caused by vesicoureteral re ux is re ux ephropathy (Figure 11-15). Xa tho ra ulomatous pyelo ephr t s (XGN) is a chronic in ection o the renal parenchyma that is usually associated with obstruction o part or all o the intrarenal collecting system, requently by a staghorn calculus. The in ection may extend into the perinephric space and adjacent organs, and develop sinus tracts to the skin or colon. On CT the af ected kidney is usually enlarged and non unctioning. Staghorn calculi are requently present and the renal pelvis is small and contracted. Areas o branching hypoattenuation extending rom the renal pelvis can resemble hydronephrosis but actually represent renal parenchyma replaced with lipid-laden macrophages. The con guration o these areas o hypoattenuation around a small renal pelvis can resemble a bear’s paw (bear paw s ). Focal XGN involving a portion o a kidney is less common than dif use involvement and its imaging eatures may resemble those o a hypovascular or necrotic renal neoplasm (Figure 11-16). The presence o

Figure 11-16 Focal Xanthogranulomatous Pyelonephritis Coronal im age rom contrast-enhanced CT dem onstrates a com plex cystic m ass in the upper pole o the right kidney (black arrowheads) with invasion into the liver (white arrowhead) and obliteration o the upper pole collecting system (black arrow). Although staghorn calculi are requently associated with this condition no renal stones were present in this patient.

Chapter 11 Kidneys, Ureters, and Bladder 161 a staghorn calculus and contracted renal pelvis or invasion into psoas should raise suspicion or ocal XGN. Treatm ent o choice or patients with XGN is nephrectom y. Re al Tuberculos s results rom hem atogenous seeding o Mycobacterium tuberculosis. Although both kidneys are seeded the im aging ndings are usually visible in only one kidney. The in ection is indolent and m ay progress slowly to involve the ureters and bladder. The classic clinical presentation is sterile pyuria. One o the earliest im aging eatures associated with renal tuberculosis is papillary necrosis resulting in clubbing o the calyces. Over the course o the in ection renal parenchym a m ay develop hypoattenuating, hypoenhancing areas sim ilar to acute pyelonephritis that can coalesce and calci y over tim e. Stricturing o the in undibula with dilation o calyces is a hallm ark nding associated with renal tuberculosis. I severe, the in undibular strictures can isolate the calyx rom the rest o the collecting system resulting in an “am putated” calyx. The stricturing can also involve renal pelvis and ureter resulting in them having a distorted appearance. At the end stage the kidney becom es shrunken and calci ed (putty k d ey) and is non unctional (auto ephrectomy) (Figure 11-17). Fu al ect o o urinary tract is uncommon but can occur in the clinical settings o diabetes, renal transplantation, chronic indwelling catheters, and immunosuppression. The imaging ndings are variable and can include papillary necrosis, abscess ormation, renal calci cation, and development o ungal balls that mani est as round contrast lling de ects in the renal pelvis, ureters, or bladder.

in 2% to 5% o all patients with hypertension and nearly all patients with atherosclerotic renal vascular disease have hypertension. F bromuscular dysplas a (FMD) is an angiopathy that accounts or 10 % o renal artery stenoses. The renal arteries are af ected in 6 0 % to 70 % o patients with FMD with the extracranial internal carotid, vertebral, iliac, and m esenteric arteries less requently af ected. Fem ales are three tim es m ore likely than m en to have FMD. Med al f broplas a is the m ost com m on subtype o FMD accounting or 80 % o cases and results in segm ents o dilation and brosis in the af ected artery. On arterial phase contrast-enhanced CT FMD o the renal arteries m ani ests as areas o alternating dilation and stenosis (str o pearls s ) that usually spares the proxim al third o renal artery in contradistinction to renal atherosclerosis (Figure 11-18). The right renal artery is m ore com m only af ected than the le t renal artery and bilateral involvem ent is present in 40 % o cases. Com plications o renal artery FMD include hypertension, renal artery dissection, renal throm boem bolism , and aneurysm rupture. Angioplasty is the pre erred treatm ent. Takayasu arter t s (TA) is an in am m atory vasculitis that af ects the aorta and its m ajor branches and is a rare cause o renal artery stenosis in the United States. Over 9 0% o all cases occur in young wom en and it is m ost requent in Asians. During the initial phase o TA

r e n Al VAs CUl Ar d is e As e Atherosclerosis accounts or greater than 9 0 % o all renal artery stenosis with the vast m ajority o signi cant atherosclerotic lesions being ostial—occurring within 1 cm o renal artery origin. Renal artery atherosclerosis is ound

Figure 11-17 End-Stage Renal Tuberculosis (Putty Kidney) Coronal im age rom unenhanced CT dem onstrates a sm all non unctioning right kidney with dystrophic calci cations resulting rom renal tuberculosis.

Figure 11-18 Fibromuscular Dysplasia o the Renal Arteries Coronal oblique im age rom contrast-enhanced CT in a young em ale dem onstrating caliber irregularity with beaded appearance o the right (black arrow) and le t (white arrow) renal arteries due to brom uscular dysplasia.

162 Body CT: The Essentials contrast-enhanced CT dem onstrates hyperenhancem ent and thickening o af ected arterial walls indicating acute vasculitis. In the late “pulseless” stage vascular stenoses and pseudoaneurysm s develop. Other orm s o vasculitis that can af ect the kidneys include polyarter t s odosa and drug-induced vasculitis associated with m etham phetam ine and other illicit drugs which result in developm ent o m icroaneurysm s in sm all renal artery branches that can rupture resulting in intraparenchym al or subcapsular renal hem atom as. The m icroaneurysm s are diagnosed on conventional angiography but too sm all to be seen on CT. Renal in arctions and segm ental or “spotted” delayed nephrogram m ay be present on CT.

Renal In arcts Renal in arctions most com m only result rom throm boem bolic disease with the heart being the m ost com mon source. Less com mon causes include renal artery dissection resulting rom FMD, aortic dissection, traum a, vasculitis, and iatrogenic injury. On contrast-enhanced CT renal in arcts most comm only present as wedge-shaped area o severe hypoenhancem ent involving both the medulla and cortex (Figure 11-19 ). The cort cal r m s re ers to a thin rim o cortical enhancement that results rom capsular collateral per usion that i present is a use ul nding to distinguish sm all in arction rom the decreased enhancement associated with acute pyelonephritis. In the chronic phase renal in arcts develop into parenchym al scarring and thinning.

r e n Al Cy s t iC d is e As e Renal cysts are a common nding present in hal o patients 50 years or older. In the vast majority o patients simple cysts are asymptomatic incidental ndings. Rarely, a cyst may hem-

Figure 11-20 Peripelvic Cysts Axial im age rom contrast-enhanced CT (split-bolus technique) in a patient with m ultiple bilateral peripelvic cysts that are delineated rom the contrast- lled intrarenal collecting system . The in undibulum in the le t kidney is distorted by the cysts.

orrhage, become in ected, or grow su ciently large to result in discom ort. On CT simple cysts should be homogeneous containing no internal septations and have water density (0–20 H U). The cyst wall should be imperceptible and the inter ace with the renal parenchyma sharp. There should be no enhancement o the cyst on contrast-enhanced CT. Exophyt c cysts are cysts that extend rom the renal parenchyma into the perinephric at. Parapelv c cysts are cysts originating rom the renal parenchyma that protrude into the renal sinus. Uncommonly parapelvic cysts can become su ciently large to compress and obstruct portions o the adjacent intrarenal collecting system. Per pelv c cysts (Figure 11-20) are multiple small con uent cysts that arise in the renal sinus and are usually bilateral and thought to be lymphatic in origin. Imaging eatures help ul in distinguishing between hydronephrosis and renal sinus cysts is that in hydronephrosis the dilated calyces and renal pelvis are contiguous with one another and the ureter in contrast to sinus cysts that are not interconnected to one another. In hydronephrosis dilation o the collecting system ef aces or obscures the sinus at surrounding calyces which is not the case or sinus cysts except in the uncommon circumstance when a parapelvic cyst obstructs part o the collecting system. In cases where there is uncertainty or suspicion or compression o the intrarenal collecting system by a parapelvic cyst an excretory phase contrast-enhanced CT can be used to delineate the contrast- lled collecting system rom nonenhancing cysts (Figure 11-20).

Bosniak Classi cation System

Figure 11-19 Renal In arct Coronal image rom contrast-enhanced CT in a patient with in arct o the entire le t kidney due to traumatic dissection o the renal artery (not shown). The thin rim o enhancement along the renal capsule results rom collateral per usion (cortical rim sign).

The Bos ak class f cat o system (Table 11-9) is used to categorize and strati y complex cysts by their risk o malignancy based on their CT imaging eatures (Figure 11-21). Determination o whether there is enhancement present is an important eature to the classi cation (Table 11-10). CT enhancement is determined by measuring the attenuation o a cyst or portion o a cyst on unenhanced CT and comparing to the same

Chapter 11 Kidneys, Ureters, and Bladder 163 t ab

11-9 . Bosniak Classi cation o Renal Cystsa,b

Bosni k C go y I Simple Cyst

Im ging F

u s

h omog n ous 0–20 h U No in n l s ions o c lci c ions t in o im c ibl w ll nd s in No c lci c ions No n nc m n

r isk o M lign ncy (%)

r comm nd ion c

0

Igno

c

II Minimally complex cyst

F w, i lin in in n l s ions c n v ess n i lly 0 c iv d bu no m su bl n nc m n Fin c lci c ion o s o - ick n d c lci c ion in w ll o s ions Uni o mly ig nu ing, non n ncing l sions xo y ic o i con in d wi in n l nc ym m su ≤ 3cm

Igno

IIF Moderately complex cyst requiring ollow-up

Mul i l i lin in in n l s ions c n v c iv d bu no m su bl n nc m n Minim l ick ning o w ll o s ions t ick o nodul w ll o s l c lci c ion Uni o mly ig nu ing, non n ncing l sions m su >3cm nd n i ly in n l

5–25

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50–60

Su gic l l sion. U ology consul ion.d

100

Su gic l l sion. U ology consul ion.d

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IV C go y III l sion con ins n ncing so issu Cystic malignancy com on n s ind nd n o s o w lls. a

Is l GM, Bosni k Ma . h ow I do i : v lu ing n l m ss s. Radiology 2005; 236: 441–450 b Dunnick Nr , S ndl CM, N w ous Jh t x book o U o diology, 5 d. Li inco Willi ms & Wilkins 2013: 109-110. c B l nd LL, Silv m n SG, Go r M, l. M n ging incid n l ndings on bdomin l Ct : w i o a Cr incid n l ndings commi . J Am Coll Radiol 2010; 7:754–773. d Fo i n s wi limi d li x c ncy o s v como bidi i s IIF l sion m su ing 1.5 cm o l ss m y no qui ollow-u nd im ging ollow-u o c go y III nd IV l sions m y b o i . e t o im l du ion o ollow-u o c go y IIF l sions is no s l d.

location on nephrographic phase contrast-enhanced CT. For complex or heterogeneous cysts multiple small areas should be measured and compared with care taken to exclude renal sinus at and normal renal parenchyma rom the measurement so as to minimize measurement error. Generally i a region in a cystic lesion increases its attenuation on a contrast-enhanced scan by less than 10 H U compared to the unenhanced CT it is considered to be nonenhancing and i the attenuation increases by 20 H U or greater it is considered to be enhancing. An attenuation increase o 10 to 19 H U it is considered indeterminate and an alternative imaging modality such as MRI or ultrasound may be considered. Pseudoe ha ceme t re ers to an apparent increase in attenuation o small (≤ 15 mm) intrarenal cysts that occurs on contrast-enhanced CT as a result rom beam-hardening

ef ects. In cases where it is uncertain whether a small intrarenal lesion has true enhancement or pseudoenhancement on CT, contrast-enhanced MRI may be help ul. Bosniak category I and II cysts are benign and should be ignored. H yperdense cysts have an attenuation greater than 20 H U but that do not enhance which generally requires both an unenhanced and contrast-enhanced CT to con rm. However, in a sm all series it has been shown that hom ogeneous hyperdense lesions with attenuation o 70 H U or greater on unenhanced CT had a greater than 9 9 % probability o being benign. H yperdense cysts that are entirely intrarenal and measure greater than 3 cm are classi ed as Bosniak category IIF. Bosniak category IIF cysts are m oderately complex cysts that require imaging ollow-up. Follow-up should be

164

Body CT: The Essentials

A

B

C

D

E Figure 11-21 Bosniak Classi cation o Renal Cysts CTs o renal cysts in m ultiple patien ts. A. Category I cyst is hom ogeneous with water attenuation and an imperceptible wall. B. Category II cyst—hyperdense cyst on unenhanced CT with no change in attenuation on contrast-enhanced CT (not shown ). C. Category IIF cyst—cyst with m in im ally thicken ed septation

but n o m easurable en han cem en t. D. Category III cyst—cyst with several thickened septations in which enhancem ent could be m easured. E. Category IV cyst—patient with autosom al dom inant polycystic kidney disease and com plex cyst in le t lower kidney that contains an enhancing nodule.

Chapter 11 Kidneys, Ureters, and Bladder 165 t ab 11-10 . H yperattenuating (40–70 H U) Renal Masses on Unenhanced CT Non n ncing B nign y d ns cys r n l m om en ncing F oo ngiomyoli om M lign n cys (Bosni k c go y III o IV) V scul m l o m ion o n u ysm r n l c ll c cinom

per orm ed with renal CT or MRI at 6 and 12 m onths and therea ter, although the duration o ollow-up required to establish the benign etiology o an IIF lesion is not settled. On ollow-up im aging interval growth o a category IIF cyst should be noted, but in and o itsel does not indicate m alignancy. Progression o worrisom e morphologic eatures such as increasing num ber o internal septations, increasing septal or wall thickening, or developm ent o com ponents with m easurable enhancem ent are ndings worrisome or m alignancy. Category III and IV cysts are considered to be surgical lesions. Approximately hal o category III lesions are benign but cannot be reliably distinguished rom m alignancies by imaging and biopsy o category III lesions is generally avoided because o the concern or alse negative results due to undersampling. There ore category III lesions are generally rem oved. However, in select circum stances such as when there is suspicion that a complex cystic lesion may represent pyelonephritis or a renal abscess, biopsy to establish the correct diagnosis is indicated. The management o category III and IV lesions in the general population is surgery, but in patients with limited li e expectancy or signi cant comorbidities imaging ollow-up may be appropriate.

Renal Cystic Diseases Renal cystic diseases are a group o disorders that are characterized by the presence o m ultiple renal cysts and are a com m on cause o end-stage renal disease in adults. Hereditary diseases that result in renal cystic disease include autosomal dom a t polycyst c k d ey d sease (ADPKD) which has an incidence o 1:40 0 to 10 0 0 births. Most patients will develop renal cysts by the age o 30 and 45% will develop end-stage renal disease. On CT the kidneys in patients with ADPKD are grossly enlarged due to the presence o innum erable large (> 3 cm ) cysts with very little, i any norm al renal parenchym a visible. Cyst-associated com plications include cyst hem orrhage, in ection, and rupture. Patients with ADPKD m ay also have hepatic, pancreatic, or splenic cysts. Patients are not at increased risk or RCC, but there is an association with intracranial and aortic aneurysm s.

Medullary cyst c k d ey d sease (MCKD) is a rare inherited disorder that results in end-stage renal disease. On CT the kidneys are norm al sized or sm all and contain m ultiple sm all (< 3 cm ) cysts. Renal cystic disease is also associated with tuberous scleros s and vo H ppel–L dau d sease (VH L). Patients with VH L requently have pancreatic cysts and the presence o renal and pancreatic cysts in a patient is m ore likely to be due to VH L than ADPKD. Patients with VH L are at increased risk or developm ent o RCCs. Autosomal recess ve polycyst c k d ey d sease (ARPKD) is a rare inherited renal cystic disease that can result in renal ailure at birth, in the early postnatal period, or in older children. Hepatic involvem ent correlates with age at which ARPKD presents. In ants typically have little hepatic involvement whereas hepatic brosis is com m on at presentation in older children. Ultrasound is the m ost comm only used im aging m odality or these patients. Nonhereditary orm s o renal cystic disease include acqu red cyst c k d ey d sease that results as a consequence o end-stage renal disease. Approxim ately 50% o patients undergoing dialysis have acquired cystic kidney disease and the incidence correlates with the length o tim e on dialysis, approaching 100 % or patients undergoing dialysis or greater than 10 years. On CT the kidneys are sm all and contain m ultiple cysts o varying sizes. Mult cyst c dysplast c k d ey d sease is a rare developm ent disorder with an incidence o 1:430 0 births that results in a non unctional kidney. In children the af ected kidney is enlarged with a nonreni orm shape and contains num erous cysts and no recognizable renal parenchym a. In adults the af ected kidney is non unctional with central so t tissue surrounded by peripheral cysts. A m ulticystic dysplastic kidney can resem ble a cystic neoplasm but can be distinguished by nonvisualization o the renal collecting system and renal vessels. There is an association with vesicoureteral re ux in the contralateral kidney and posterior urethral valves. Medullary spo e k d ey d sease is also associated with renal cysts and can be identi ed by the presence o m edullary nephrocalcinosis. Local zed re al cyst c d sease is a rare nonprogressive condition characterized by m ultiple renal cysts located in one kidney or a segm ent o one kidney. Patients are usually asym ptom atic. On CT the af ected kidney will contain a large group o m ultiple cysts o various sizes with intervening atrophic renal tissue.

r e n Al t Um o r s Benign Primary Renal Masses AMLs are com m on benign m esenchym al neoplasm s that are com posed o variable am ounts o adipose tissue, sm ooth m uscle cells, and dysm orphic vessels (Figure 11-22). In 80% o patients AMLs occur sporadically and present as a solitary predom inantly at-containing m ass. Sporadic

166

Body CT: The Essentials t ab

11-11. Fat-Containing Renal Masses

a ngiomyoli om X n og nulom ous py lon m co g s)

Figure 11-22 Angiomyolipoma Contrast-enhanced CT through le t kidney dem onstrates an exophytic m ass (white arrowheads) that contains at (white arrow). Note the ocal indentation o the m ass in the renal cortex (black arrowhead) which can be help ul in distinguishing an exophytic AML rom a perirenal m ass.

AMLs are our tim es m ore com m on in wom en. Generally, AMLs m easuring less than 4 cm are usually ound as an incidental nding. Patients with larger AMLs can present with ank pain, hem aturia, and palpable m ass. In 20% o patients AMLs are associated with tuberous sclerosis. Approxim ately 80 % o patients with tuberous sclerosis have AMLs that are m ultiple in 75% o cases and bilateral in 50% o cases. Sm all intratum oral aneurysm s in AML can result in spontaneous hem orrhage. AMLs m easuring greater than 4 cm or having aneurysm s m easuring greater than 5 m m are at increased risk or hem orrhage and m ay be prophylactically treated with em bolization. On CT the classic appearance o a renal AML is a at-containing m ass with variable am ount o enhancing so t tissue and intralesional aneurysm s. About 5% o AMLs contain m inim al at ( at-poor variant) and can be di cult to dif erentiate rom other renal tum ors on CT. Features that have been reported to dif erentiate at-poor AMLs rom RCC include an angular inter ace o an exophytic lesion with the renal parenchym a, hom ogeneity, attenuation greater than 38 H U on unenhanced CT, and hom ogeneous enhancem ent. AMLs very rarely contain calci cations, there ore a at-containing renal m ass that contains calci cations is unlikely to represent AML and alternative diagnoses such as at-containing RCC or liposarcom a should be considered (Table 11-11). Exophytic AMLs m ay resem ble a perirenal liposarcom a, but the exophytic AML can have an angular inter ace or ocal indentation o the renal cortex which can be a help ul nding to distinguish an exophytic m ass rom a perirenal m ass. O cocytomas are gen erally con sidered to be ben ign n eoplasm s an d accoun t or about 5% o all ren al tum ors.

r n l c ll c cinom (

)

Li om / li os com (

)

i is (li id-con ining

They ten d to occur in older patien ts with peak in ciden ce in the seven th decade. On CT on cocytom as are usually well-dem arcated large exophytic en han cin g solid tum ors that are hom ogen eous i less than 3 cm but larger tum ors ten d to be heterogen eous. Calci ication s m ay be presen t. A cen tral stellate n on en han cin g ibrous scar an d “spoke wheel” appearan ce o the eedin g arteries on an giography are in din gs suggestive o but n ot speci ic or an on cocytom a. Because on cocytom as can n ot be reliably di eren tiated rom RCCs by im agin g they are resected. Mult locular cyst c ephromas (MLCNs) are uncom m on benign renal neoplasm s with a bim odal age distribution occurring in young boys and m iddle-aged wom en. On CT MLCNs are requently large m easuring 10 cm or greater with m ultiple cysts and enhancing septations. The dif erential diagnosis includes m ulticystic RCC, m ulticystic dysplastic kidney, and abscess. Surgical resection is usually advised.

Malignant Primary Renal Masses Re al cell carc omas account or 85% o all renal m alignancies and are twice as com m on in m en as wom en. RCCs can occur at any age, but the peak incidence is in the sixth decade. Risk actors or developm ent o RCC include tobacco usage, VH L, and hem odialysis. Patients can present with hem aturia, ank pain, and nonspeci c constitutional sym ptom s although about hal o RCCs are ound incidentally. Approxim ately 30 % o patients with RCC have m etastases at the tim e o presentation. In patients with RCC the role o im aging is to detect and de ne the tum or and anatom y relevant or surgery or interventional therapy, provide staging in orm ation, and evaluate the contralateral kidney. The renal vein and IVC should be closely exam ined as RCCs have a propensity to extend into the renal vein and IVC. Retroperitoneal lym ph nodes, liver, lung bases, and bones should be care ully evaluated as these are the m ost com m on places or regional and distant m etastatic disease. Clear cell RCC accounts or 70 % o all RCCs. About hal o patients are stage 1 or 2 at presentation and the overall 5-year survival is 55% to 6 5%. They are cortically based hypervascular neoplasm s. On CT clear cell RCCs are hypervascular renal tum ors that have m axim al enhancem ent during the corticom edullary phase and

Chapter 11 Kidneys, Ureters, and Bladder 167

Figure 11-23 Renal Cell Carcinoma Coronal im age rom contrast-enhanced CT demonstrating papillary renal cell carcinom a that is hypovascular and has invaded into the renal vein (arrow).

generally have greater enhancem ent than the other subtypes o RCC. Cystic change is present in 15% and calci cation present in 10 % to 15% o clear cell RCCs. Capsular or renal vein invasion is present in 45% o patients at presentation. Pap llary RCC accounts or 10% to 15% o all RCCs and is the m ost com m on subtype in patients with end-stage kidney disease and is the m ost com m on subtype to have m ultiocal or bilateral tum ors. It is slow growing and the overall 5-year survival rate is 80 % to 9 0 %. On CT papillary RCCs are m ost com m only hom ogeneous, hypovascular m asses (Figure 11-23). Large papillary RCCs are usually m ore heterogeneous on CT due to the presence o necrosis, internal hem orrhage, and calci cation. Although rare, m acroscopic at resulting rom cholesterol-laden m acrophages can be present in these tum ors. Chromophobe RCCs account or about 5% o all RCCs and occur in older patients with men and women equally af ected. Eighty-six percent o patients are stage 1or 2 at presentation and this subtype has a 5-year survival rate o 90%. Chromophobe RCCs have relatively homogeneous enhancement on contrast-enhanced CT and can demonstrate a “spoke wheel” pattern o enhancement similar to oncocytomas. Renal vein invasion is present in 5% o patients. Despite their avorable prognosis patients with large tumors are at risk or development o hepatic metastases. Collect duct carc oma accounts or less than 1% o all RCCs but is the m ost aggressive subtype. It can occur at any age but the m ean age at presentation is 55 years and m en are m ore com m only af ected. One-third o patients have m etastases at the tim e o presentation and less than one-third survive m ore than 2 years rom presentation. On

CT collecting duct carcinom as are hypovascular in ltrative tum ors with a heterogeneous appearance due to necrosis, internal hemorrhage, and calci cation. Mult locular cyst c RCC is a rare subtype accounting or less than 1% o all RCCs. They have an excellent prognosis with no reported cases o metastatic disease. The mean age o presentation is 51 years and men are three times more likely to be af ected than emales. On CT multilocular cystic RCC presents as a multiloculated cystic tumor with thickened septations and septal or wall calci cations in 20% o cases. Re al medullary carc oma is an extrem ely rare RCC that occurs alm ost exclusively in patients with sick cell trait. The prognosis is poor with a m ean survival o 15 weeks. On CT renal m edullary carcinom as are hypovascular, in ltrative neoplasm s requently with internal hem orrhage and necrosis. The liver and lung are the m ost com m on sites o m etastatic disease. W lms’ tumor ( ephroblastoma) is the m ost com m on m alignan t tum or in children and adolescents and is rare in adults. In children Wilm s’ tum ors are m ost requen tly diagn osed by ultrasound. On CT they are large (> 10 cm ) hypoenhancin g m asses that can invade the renal vein. Bilateral in volvem ent is present in 5% to 10 % o cases. The lungs are the m ost com m on site or m etastatic disease. In adults Wilm s’ tum ors are indistinguishable rom RCC. Renal sarcom as account or 1% to 3% o all m alignant renal neoplasms and are highly aggressive tumors that carry a grave prognosis. These are primary mesenchymal tumors and do not represent sarcomatoid degeneration o an RCC which is also associated with poor prognosis. Le omyosarcomas account or 50% to 6 0% o primary renal sarcom as and occur in patients 40 to 70 years o age. The 5-year survival is 29 % to 36 %. On CT these tumors are usually expansile, large well-de ned masses that can have delayed enhancement due to the presence o brous stroma. They are requently heterogeneous due to central necrosis. The location o the tumor will depend on whether the leiom yosarcom a arose rom the smooth m uscle cells o the renal capsule, parenchyma, sinus, or vessels.

Malignan Secondary Renal Masses Re al lymphoma m ost com m only occurs in the setting o widespread B-cell non-H odgkin lym phom a with the kidneys representing a site o extranodal spread in about 11% o patients. Renal involvem ent in H odgkin disease is less com m on occurring in only 1% o patients. Prim ary renal lym phom a, isolated to the kidney with no nodal involvem ent is very rare. The im aging pattern o renal lym phom a can vary on CT. In 50 % o cases renal lym phom a presents as m ultiple hom ogeneous, hypoenhancing renal lesions with bilateral involvem ent in 50 % to 70 % o cases. In 25% o cases it can m ani est as an in ltrating hilar m ass and in 10 % o cases as a perirenal m ass (Table 11-12) (Figure 11-24). In 5% o patien ts lym phom a can be a solitary m ass. In

168

Body CT: The Essentials

t ab

11-12. Perinephric Masses

t ab 11-13. Contrast Filling De ects in the Collecting System

h m om p in

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Lym

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approxim ately 10 % o patients renal lym phom a has an in ltrative pattern o growth with no distinct m ass but rather dif use renal enlargem ent. I bulky retroperitoneal lym phadenopathy is present the ureters m ay be laterally deviated. Because renal lym phom a arises in the setting o widespread disease the diagnosis is not usually in doubt. Although m etastases to the kidneys rom solid organ tum ors are reported to be present in 2% to 20 % patients in autopsy series, clinically re al metastases are uncom m on. Metastases can result rom hem atogenous or lym phatic spread, or direct invasion. The prim ary neoplasm s m ost com m only associated with renal m etastases are lung, breast, and gastrointestinal m alignancies, and m elanom a. The im aging eatures are variable and can range rom a solitary lesion to m ultiple lesions to an in ltrative lesion. Except or m elanom a m ost m etastases are hypoenhancing and not distinguishable rom prim ary renal neoplasm s by their im aging characteristics; however, because renal m etastases tend to occur in the setting o widespread m etastatic disease the diagnosis is not usually a dilem m a.

Papillary necrosis is a condition in which the renal pyramids become ischemic leading to necrosis and cavitation o the papillary tips. The causes o papillary necrosis include analgesic overuse (including nonsteroidal anti-in ammatory drugs), sickle-cell disease, in ections especially renal tuberculosis, and diabetes mellitus. The imaging ndings o papillary necrosis are best seen on excretory phase contrast-enhanced CT. Sloughed renal papillae may migrate into the collecting system and present as contrast lling de ects (Table 11-13). In the medullary orm o papillary necrosis a central cavity in the papillary tip orms resulting in a ocal outpouching o contrast rom the calyx into the papillary tip on excretory phase CT (Figure 11-25). In the papillary orm erosions rom the calyceal ornices extend into the papillary tip which can result in a lobster claw appearance o contrast on excretory phase CT.

Figure 11-24 Renal Lymphoma Coronal im age rom contrast-enhanced CT demonstrating a bulky m ass extending rom the upper retroperitoneum into the renal hilum with encasem ent o the renal artery (arrow).

Figure 11-25 Papillary Necrosis Contrast-enhanced excretory phase CT dem onstrating a sm all ocus o contrast lling in the papillary tip (arrow) resulting rom papillary necrosis.

in t r Ar e n Al Co l l e Ct in g s y s t e m s , Ur e t e r s , An d Bl Ad d e r Papillary Necrosis

Chapter 11 Kidneys, Ureters, and Bladder 169

Benign Masses o the Collecting Systems F broep thel al polyps are benign brous polyps o the collecting system that can result in ank pain and hem aturia. They are usually solitary, sm ooth long tubular ll de ects ound in the ureters, m ost com m only the proxim al ureters. They can resem ble a blood clot, but are usually solitary, have so t tissue attenuation (35–45 H U) which is less than that o m ost blood clots. Bladder le omyomas are benign m asses that usually occur in m iddle-aged wom en and m ost com m only arise in the bladder trigone. On im aging, these are sm ooth m ural bladder wall m asses that project into the bladder lum en in 6 0 % o cases, outside o bladder in 30% o cases, and both inside and outside o the bladder in the rem aining cases.

Urothelial Tumors Transitional cell carcinoma

Figure 11-26 Le t Ureteropelvic Junction Obstruction Coronal im age rom contrast-enhanced CT demonstrating hydronephrosis o the le t intrarenal collecting system with norm al sized ureter. Thinning o the renal parenchym a indicates chronicity.

When the papillary tip sloughs of it may migrate into the collecting system resulting in the calyx taking on a blunted or round shape. I the papillary tip remains in the calyx it can calci y and mani est as lling de ect within an otherwise round, blunted calyx on excretory phase CT.

Congenital Ureteropelvic Junction Obstruction Congenital UPJ obstruction is a unctional or anatom ic obstruction preventing ow o urine rom the renal pelvis into the proxim al ureter that is caused by an abnorm ality o the sm ooth m uscle that prevents transm ission o the peristaltic wave across the UPJ. Extrinsic com pression rom renal vessels crossing over the UPJ m ay exacerbate a congenital UPJ obstruction. On CT UPJ obstruction m aniests as a dilated intrarenal collecting system with a norm al caliber proxim al ureter (Figure 11-26 ). A ter the possibility o an obstructing stone or underlying m ass have been excluded as causes or obstruction, a close inspection o the renal vessels should be m ade to determ ine i a vessel crossing the UPJ is present. In som e cases a preoperative contrast-enhanced CT angiogram m ay be help ul. Identi cation o crossing vessels is essential or preoperative planning because their presence is associated with lower success rates or endoscopic-based therapy.

Transitional cell carcinom a (TCC) is the m ost com m on m alignancy o the urinary tracts accounting or 9 5% o all urothelial tum ors. Tobacco use, arsenic ingestion, cyclophospham ide treatm ent, and Balkan nephropathy are risk actors associated with the developm ent o TCC. About 9 7% o TCCs arise in the bladder, 2% to 3% arise in the intrarenal collecting system , and about 1% arise in the ureter. Patients with TCC require care ul staging and surveillance o the urinary system because o the high risk or m ultiple sites o disease and recurrence. About 2% to 4% o patients with bladder TCC will develop upper tract TCC and 40% o patient with upper tract TCC will develop bladder TCC. The incidence o TCC is higher in m en and peaks in the seventh decade. CTU is the diagnostic imaging m odality o choice or evaluation o the collecting systems in patients with hem aturia. It has a sensitivity and speci city o greater than 9 5% or detection or urothelial tum ors. The aim o CT in patients with TCC is to detail the tum or detect synchronous tumors and provide staging in ormation. Neither CT nor MRI can accurately determine the depth o TCC invasion into the bladder or collecting system ; however, CT is use ul in evaluation o regional and distant lymph nodes or nodal m etastases and or evaluation o the lungs, liver, and bones which are requent sites o metastatic disease. In the intrarenal collecting system TCCs present as lling de ects that may be smooth (sessile orm) or nodular (papillary orm) and can be multi ocal (Table 11-13). In undibular involvement results in in undibular stenoses (Figure 11-27). Involvement o the renal pelvis leads to its distortion or obliteration. TCCs in the renal sinus can in ltrate into the renal parenchyma resulting in enlargement or expansion o the kidney with a hypoenhancing mass (Table 11-14). With in ltrative TCCs the kidney retains its reni orm shape and there is obliteration o the collecting system which are ndings help ul in distinguishing an in ltrative TCC rom other renal tumors. The dif erential diagnosis or lling de ects in the intrarenal collecting system includes calculi, blood clot,

170

Body CT: The Essentials t ab 11-15. Focal Bladder Wall Thickening or Filling De ect Blood clo enl g d

os

Fol y c Uo

gl nd x nding in o bl dd o o

b s

o ign body

li l umo (mos commonly t CC)

Fungus b ll U

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endom

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a myloidosis Figure 11-27 Transitional Cell Carcinoma o the Intrarenal Collecting System Contrast-enhanced excretory phase CT dem onstrates a nodular transitional cell carcinom a in the lower pole o the le t kidney resulting in in undibular stenosis (arrows). This patient was treated or a transitional cell carcinom a o the bladder several years be ore this examination.

papillary necrosis, and ungus ball. The majority o TCCs in the intrarenal collecting system have a good prognosis. Standard treatment is nephroureterectomy. TCC o the ureters is about 100 times less comm on than TCC o the bladder. TCCs present as papillary or sessile m asses on CT. The papillary orm is m ore comm on and has a better prognosis than the sessile orm that tends to be higher grade at presentation. About 75% o ureteral TCCs arise in the distal ureter and 2% to 5% o patients have bilateral tumors on presentation. Ureteral TCCs present as ureteral stenoses that m ay or may not result in hydronephrosis. In the urinary bladder TCCs all into two general categories. Super cial tum ors account or 80 % o bladder TCCs and are usually low grade or carcinom a-in-situ at presentation. They have a very low risk o m etastases but 70 % recur within 3 years and 10 % to 20 % o recurrences will progress to invasive disease. The invasive TCCs extend through the bladder wall m aking them higher stage and are associated with a less avorable prognosis. On CT bladder TCCs m ost com m only m ani est as ocal bladder wall thickening (Table 11-15) (Figure 11-28). Dif use bladder wall thickening is m ore likely to be caused by cystitis than a bladder tum or.

t ab

Squamous cell carcinoma Pure squam ous cell carcinom as account or 3% to 4% o all urothelial tum ors. It is m uch m ore prevalent in Egypt and locations where schistosom iasis in ections are m ore com m on. Other risk actors include bladder stones and chronic indwelling catheters. Squam ous cell carcinom as tend to be m ulti ocal and invasive. On im aging squam ous cell carcinom a cannot be dif erentiated rom TCC. The prognosis o patients with squam ous cell carcinom a is poor.

Adenocarcinoma Adenocarcinom a o the bladder represents 1% to 2% o all bladder neoplasm s. About two-thirds are prim ary adenocarcinoma and one-third arise in urachal rem ants. Cystitis glandularis, a m etaplasia o the bladder urothelium associated with chronic in ection is a risk actor or adenocarcinom a as

11-14. In ltrative Renal Masses

Inv siv

nsi ion l c ll c cinom

Lym o oli iv dis l sm cy om )

s ( .g., lym

X n og nulom ous y lon r n l c ll c cinom

i is

om , l uk mi ,

Figure 11-28 Transitional Cell Carcinoma o the Bladder Contrast-enhanced CT demonstrates a nodular transitional cell carcinom a along the anterior wall o the bladder (arrow). A reservoir or a penile prosthesis is located to the le t o the bladder.

Chapter 11 Kidneys, Ureters, and Bladder 171

Figure 11-30 Emphysematous Cystitis Unenhanced CT dem onstrates intram ural gas within the bladder wall due to em physem atous cystitis. Bladder is decompressed by a Foley catheter. Figure 11-29 Endometrioma o the Bladder Sagittal im age rom contrast-enhanced CT in young wom en with a history o endometriosis dem onstrating a sm ooth intramural m ass in the superior bladder wall (arrow).

is presence o an urachal remnant. Adenocarcinom a cannot usually be dif erentiated rom TCC on im aging; however, the presence o a nodular enhancem ent or a m ass in an urachal rem nant is highly suspect or adenocarcinom a.

Nonneoplastic Bladder Masses The vast m ajority o bladder tum ors are urothelial neoplasms. Uncomm on nonneoplastic bladder tum ors include e dometr omas (Figure 11-29 ) and ammatory pseudotumors. Malacoplak a is a chronic granulom atous condition associated with Escherichia coli urinary tract in ections that m ost requently occurs in m iddle-aged wom en and is m ore com mon in diabetic or imm unocom promised patients. The bladder is the most comm on site organ in the genitourinary tract. Patients present with hematuria. On CT m alacoplakia can present as a single or m ultiple bladder m asses, or di use bladder thickening. Cyst t s cyst ca and cyst t s la dular s result rom chronic in am m ation due to in ection, calculi, or bladder outlet obstruction that causes m etaplasia o urothelium . The dif erence between the two lies in the m etaplastic t ab

11-16 . Dif use Bladder Wall Thickening

D com

Cystitis Acute in ection o the bladder is m ost requently caused by bacterial pathogens. The m ost com m on nding is di use bladder wall thickening which is a nonspeci c nding (Table 11-16 ) that can be associated with in ectious or in am m atory causes o cystitis. Emphysematous cyst t s is a necrotizing in ection o the bladder that m ost requently occurs in diabetic patients and on CT m ani ests with gas within the bladder wall (Figure 11-30 ). Gas within the bladder lum en without intram ural involvem ent is m ore likely to be due to a cause other than in ection such as Foley placem ent or instrum entation (Table 11-17). Patients undergoing pelvic radiation or therapy with cyclophospham ide chem otherapy are at risk or hem orrhage cystitis. At im aging there m ay be ocal or dif use bladder wall thickening present. Chronically, the ef ects o radiation lead to interstitial cystitis resulting in the bladder having a contracted appearance. Patients are also at risk or developm ent o com plex stulas with bowel or the vagina.

ss d bl dd

In c ious cys i is In in

dif erentiation; however, in practice both usually occur together. They can occur at any age, but are m ore com m on in m en. On im aging patients m ay have sm all nodular or polypoid lling de ects. There is a risk or developm ent o adenocarcinom a and patients should be m onitored.

mm o y cys i is ( .g., s i i l cys i is)

t ab

11-17. Gas in Bladder Lum en

di ion, Cy ox n, Fol y c

Ou l obs uc ion

Fis ul wi

N u og nic bl dd

em

o ins um n

ion

colon, sm ll bow l, o v gin

ys m ous cys i is

172 Body CT: The Essentials SUg g ESTED READi n g S 1. Coll DM, Varanelli MJ, Sm ith RC. Relationship o spontaneous passage o ureteral calculi to stone size and location as revealed by enhanced helical CT. AJR. 20 02;178:101–103. 2. Craig WD, Wagner BJ, Travis MD. From the archives o the AFIP pyelonephritis: radiologic-pathologic review. Radiographics. 20 0 8;28:255–276 . 3. Jung DC, Kim SH , Jung SI, H wang SI, Kim SH . Renal papillary necrosis: review and comparison o ndings at multidetector row CT and intravenous urography. Radiographics. 2006 ;26 :1827–1836 . 4. Dunnick NR, Sandler, CM, Newhouse JH . Textbook of Uroradiology. 5th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013. 5. Dyer RB, Chen MY, Zagoria RJ. Classic signs in uroradiology. Radiographics. 200 4;24:S247–S280. 6 . Glodny B, Unterholzner V, Ta erner B, et al. Norm al kidney size and its in uencing actors – a 6 4-slice MDCT study o 1040 asym ptom atic patients. BMC Urology. 20 09 ;9 :19 . 7. Gotway MB, Araoz PA, Macedo TA, et al. Im aging ndings in Takayasu’s arteritis. AJR. 20 05;184:19 45–19 50 . 8. Israel GM, Bosniak MA. How I do it: evaluating renal m asses. Radiology. 200 5;236 :441–450. 9 . Jonisch AI, Rubinowitz AN, Mutalik PG, Israel GM. Can high-attenuation renal cysts be dif erentiated rom renal cell carcinom a at unenhanced CT? Radiology. 200 7;243:445–450 .

12. Katabatina VS, Vikram R, Nagar AM, Tam boli P, Menias CO, Srinivasa RP. Mesenchym al neoplasm s o the kidneys in adults: im aging spectrum with radiologic-pathologic correlation. Radiographics. 20 10 ;30 :1525–1540 . 13. Prassad SR, Hum phrey PA, Catena JR, et al. Com m on and uncom m on histologic subtypes o renal cell carcinom a: im aging spectrum with pathologic correlation. Radiographics. 20 0 6 ;26 :179 5–180 6 . 14. Sheth S, Ali S, Fishm an E. Im aging o renal lym phom a: patterns o disease with pathologic correlation. Radiographics. 20 0 6 ;26 :1151–116 8. 15. Silverm an SG, Mortele KJ, Tuncali K, Jinzaki M, Cibas ES. H yperattenuating renal m asses: etiology, pathogenesis, and im aging evaluation. Radiographics. 20 0 7;27:1131–1143. 16 . Vikram R, Sandler CM, Ng CS. Im aging and staging o transitional cell carcinom as: part I, lower urinary tract. AJR. 20 0 9 ;19 2:1488–149 3. 17. Vikram R, Sandler CM, Ng CS. Imaging and staging o transitional cell carcinom as: part 2, upper urinary tract. AJR. 20 0 9 ;19 2: 1481–1487. 18. Wolin EA, Hartm an DS, Olson JR. Nephrographic and pyelographic analysis o CT urography: dif erential diagnosis. AJR. 20 13;20 0 :119 7–120 3. 19 . Wong-You-Cheong JJ, Woodward PJ, Manning MA, Sesterhenn IA. Neoplasm s o the urinary bladder: radiologic-pathologic correlation. Radiographics. 20 0 6 ;26 :553–580 .

10 . Kam badakone AR, Eisner BH , Catalano OA, Sahani DV. New and evolving concepts in the im aging and m anagem ent o urolithiasis: urologists’ perspective. Radiographics. 20 10 ;30 : 6 0 3–6 23.

20 . Yang CW, Shen SH , Chang YH , et al. Are there use ul CT eatures to dif erentiate renal cell carcinom a rom lipid-poor renal angiom yolipom a? AJR. 20 13;20 1:10 17–10 28.

11. Katabathina VS, Kota G, Dasyam AK, Shanbhogue AKP, Prasad SR. Adult renal cystic disease: a genetic, biological, and developm ental prim er. Radiographics. 20 10;30:150 9 –1523.

21. Yu JS, Kim KW, Lee H J, Lee YJ, Yoon CS, Kim MJ. Urachal rem nant diseases: spectrum o CT and US ndings. Radiographics. 20 0 1;21:451–46 1.

Ch a p t e r

12

A

a Ga

Geraldine Chen, MD David L Coy, MD, PhD

I. ANATOMY AND VARIANTS II. ADRENAL MASSES a. Neoplasms i. Adrenal adenoma ii. Endocrine abnormalities due to adenomas and other adrenal masses iii. Pheochromocytoma iv. Myelolipoma v. Adrenocortical carcinomas vi. Metastases

An At o m y An d VAr iAn t s The adrenal glands play a major role in endocrine homeostasis. Each gland is composed o the nn r m ulla that originates rom em bryonic neural crest cells and secretes epinephrine and norepinephrine, and the outer cortex that is derived rom em bryonic mesoderm . The ou r cor x has three distinct layers: the outerm ost zona lom rulosa, which secretes aldosterone; the middle zona fasc cula a, which secretes glucocorticoids; and the inner zona r cular s, which secretes androgens. Both adrenal glands lie anterosuperiorly to the kidneys within Gerota ascia and are surrounded by perinephric at. The right adrenal gland lies posterior to the IVC and between the right hepatic lobe laterally and the diaphragm atic crus m edially. The le t adrenal gland lies posterom edial to the distal pancreatic body and tail and lateral to the aorta and le t diaphragm atic crus. The adrenals are best viewed on thin slice (1.25–2.5 m m ) CT. They are thin triangular-shaped structures with the body located superiorly and an inverted Y- or V-shape orm ed by the m edial and lateral lim bs (Figure 12-1). The body m easures about 9 m m and each lim b is 2 to 4 m m in thickness. Intravenous contrast m ay be used to better distinguish the glands rom the surrounding vessels and also assess the vascularity o any lesions that are detected. A r nal aplas a, or congenital absence o the bilateral adrenal glands, is exceedingly rare and atal within the rst 2 to 3 days o li e i not recognized. Un la ral a r nal a n s s

vii. Collision tumors viii. Lymphoma ix. Neuroblastic tumors b. Nonneoplastic Adrenal Masses i. Bilateral adrenal hyperplasia ii. Adrenal hemorrhage iii. Adrenal cysts iv. Infectious diseases III. ADRENAL INCIDENTALOMAS

is rare and occurs in conjunction with ipsilateral renal agenesis. However, in 90% o in ants with unilateral renal agenesis the ipsilateral adrenal gland is present. In these cases, the adrenal gland ipsilateral to the renal agenesis can have a attened discoid shape (lying down adrenal) (Figure 12-2). Most commonly, absence o one or both o the adrenal glands is iatrogenic, having resulted rom surgical adrenalectomy or i the ipsilateral kidney is absent, rom radical nephrectomy.

Ad r e n Al m As s e s Neoplasms Adrenal adenoma Adrenal adenom as are benign neoplasm s o the adrenal cortex present in 1% to 9 % o the general population and are com m only encountered as an incidental nding on CT. They are typically a well-de ned, hom ogeneous nodule m easuring less than 3 cm in size. Sixty to 9 0 % o adenom as are lipid-rich with their attenuations ranging rom –2 to 16 Houns eld Unit (H U) on a nonenhanced CT. Using an attenuation threshold o ≤ 10 H U on nonenhanced CT o a hom ogeneous and less than 3 cm adrenal nodule has a diagnostic sensitivity o 71% and a speci city o 9 8% or lipid-rich adenom as (Figure 12-3). L p -poor a nomas have attenuations o greater than 10 H U on unenhanced CT which m akes them di cult to dif erentiate rom other adrenal m asses. However the 173

174

Body CT: The Essentials

A

B

Figure 12-1 Normal Adrenal Glands Axial (A) and coronal (B) im ages rom contrast-enhanced CT

dem onstrating normal adrenal glands (arrows) with thin lim bs and characteristic inverted V or Y shape.

per usion characteristics o adenom as, nam ely their rapid washout, can be exploited to diagnose lipid-poor adenom as on contrast-enhanced CT. Contrast washout m ay be calculated by absolu p rc n a washou (APW) or r lav p rc n a washou (RPW). The enhanced attenuation value (EA) is m easured during the portal venous phase and the delayed attenuation value (DA) is m easured 15 m inutes a ter contrast adm inistration. The APW calculation also requires a pre-contrast attenuation value (PA).

Figure 12-2 Discoid Adrenal Gland Contrast-enhanced CT in patient with right pelvic kidney (note the colon in the right renal ossa) dem onstrating right adrenal gland with a attened or discoid con guration (arrows). Discoid con guration is also associated with ipsilateral renal agenesis. Le t adrenal gland is not shown.

APW =

EA- DA × 10 0 %, EA- PA

RPW =

EA- DA × 10 0 % EA

Both benign and m alignant lesions can avidly enhance; however, benign adenom as dem onstrate greater washout than adrenal corticocarcinom as and m etastases. Using a threshold o APW ≥ 6 0 % and/ or RPW ≥ 40% has sensitivity o 82% to 100 % and a speci city o 9 2% to 100 % or diagnosis o lipid-poor adenom as (Figure 12-4). However, up to 16 % o pheochrom ocytom as can m im ic the contrast washout characteristics o adrenal adenom as and thereore should be considered in adrenal m asses with eatures atypical or adenom as, such as heterogeneous attenuation and enhancem ent or size greater than 3 cm .

Figure 12-3 Lipid-Rich Adrenal Adenoma Unenhanced CT in a patient with a le t adrenal nodule (arrow) having attenuation o 8 H U, consistent with an adrenal adenom a, and normal right adrenal gland (arrowhead).

Chapter 12 Adrenal Glands

175

A

B

C

Figure 12-4 Lipid-Poor Adrenal Adenoma Unenhanced CT o 15-m m le t adrenal nodule (arrow) with attenuation o 35 H U (A). Contrast washout protocol dem onstrated an attenuation o 115 H U on (B) initial postcontrast scan and 56 H U on (C) delayed post-contrast scan. This corresponds to APW o 74% and DPW o 51% (see text or details), consistent with a lipid-poor adenom a.

Chem ical shi t MRI using T1-weighted in-phase and out-o -phase sequences is a technique that is also requently used or diagnosis o adrenal adenomas. Protons o intracellular lipids resonate at a lower requency than water protons. In out-o -phase imaging the signal rom the water protons and at protons within the sam e voxel subtract rom one another which results in decreased signal intensity com pared to the in-phase im age. The diagnostic per orm ance o chem ical shi t MRI or detection o lipid-rich adenom as is equivalent to that o unenhanced CT. However, in adenom as that contain a lesser lipid content such that their attenuation on enhanced CT is greater than 10 H U but less than 30 H U chemical shi t MRI is su ciently speci c to detect the lipid and diagnose an adenom a (Table 12-1).

t ab

12-1. Low Density (0–10 H U) Adrenal Lesions

Adenoma Cyst/ pseudocyst h yd id dis Cys ic Cys ic m

s (

)

oc omocy om ( s sis (

)

)

176

Body CT: The Essentials

Endocrine abnormalities due to adenomas and other adrenal masses Adrenal neoplasms can be classi ed as hyper unctioning or nonhyper unctioning based on excess hormone production. Ninety- ve percent o adenom as are nonhyper unctioning. The clinical presentation o patients with hyper unctioning adenom as or other hyper unctional adrenal masses will depend on the hormone produced in excess. An aldosterone-secreting adenoma causes Conn synrom , which is characterized by hypertension and hypokalemia. Prim ary hyperaldosteronism is caused by an adrenal adenom a in 80% o cases and adrenal hyperplasia in the rem aining instances. Adenom as that secrete aldosterone tend to have the lowest-attenuation values. Cush n synrom results rom inappropriately high levels o glucocorticoids. Patients present with hypertension and insulin resistance, with the characteristic appearance o central obesity, moon acies, and hirsutism. Most instances o Cushing syndrome are due to exogenous steroid administration. Up to 30% o cases are due to endogenous hyper secretion by an adrenal adenoma (20%) or adrenal corticocarcinom a (10%). In contrast, Cush n s as is caused by pituitary hypersecretion o adrenocorticotropic hormone (ACTH ), which results in bilateral adrenal hyperplasia and over secretion o glucocorticoids. The presence o an adrenal nodule in patients with Cushing symptom s can be con ounding because it can represent a nonhyper unctioning adenoma, a dom inant nodule in ACTH -dependent hyperplasia, or a hyper unctioning adenoma. The presence o contralateral adrenal atrophy can be a clue that an adenoma is hyper unctioning; however, in patients with Conn syndrome or Cushing disease adrenal venous sam pling may be necessary.

An ro n al syn rom resulting in precocious puberty in boys and masculinization o em ales can rarely result rom an adenoma or adrenocortical carcinom a. A son s as is caused by adrenal insu ciency and m ani ests with atigue, weakness, anorexia, and hypotension. The most common acute etiologies o adrenal insu ciency are bilateral adrenal hem orrhage and granulom atous in ection.

Pheochromocytoma Pheochromocytomas are neoplasms o the adrenal m edulla that are usually benign. They are said to ollow the “rul of 10”; that is, approxim ately 10% are bilateral, 10% are extraadrenal, 10% occur in children, 10% are m alignant, and 10% are asymptom atic. Extra-adrenal pheochrom ocytom as are known as para an l omas and occur along the sym pathetic chain ganglia, but are m ost requent at the aortic bi urcation in the organ o Zuckerkandl. Pheochrom ocytom as are associated with various am ilial syndrom es: m ultiple endocrine neoplasia (MEN) types IIa and IIb, von Hippel–Lindau syndrome, Neuro bromatosis type I, Sturge–Weber syndrome, and Carney triad. About hal o the patients with pheochromocytomas present with new-onset hypertension that may be paroxysmal or re ractory to treatment; however, less than 1% o hypertensive patients have a pheochromocytoma. Other symptoms such as palpitations, diaphoresis, headache, and ushing result rom excess catecholamine secretion. Clinical symptoms and elevated urine levels o catecholamine breakdown products o metanephrine and vanillylmandelic acid establish the diagnosis. Pheochromocytomas are requently greater than 3 cm in size, which is larger than most adenomas, but smaller than most adrenocortical carcinomas. Asymptomatic lesions tend

A

B

Figure 12-5 Pheochromocytoma Two patients with pheochrom ocytom as: A. Axial im age rom unenhanced CT dem onstrating normal le t adrenal gland (arrowhead) and a sm all, hom ogeneous right pheochrom ocytom a (arrows) with appearance sim ilar to the lipid-poor adenom a.

B. Coronal im age rom contrast-enhanced CT dem onstrating large heterogeneous le t pheochrom ocytom a (large white arrows) with cystic areas (small black arrow) and a norm al right adrenal gland (arrowhead).

Chapter 12 Adrenal Glands to be larger at presentation than those that are symptomatic. Smaller pheochromocytomas tend to be homogeneous, whereas larger pheochromocytomas are more heterogeneous due to internal hemorrhage, necrosis, or cystic degeneration (Figure 12-5). Up to 10% o pheochromocytomas are calci ed. Though most pheochromocytomas have attenuation values greater than 10 H U, which readily distinguishes them rom lipid-rich adenomas, macroscopic at or cystic degeneration may be present and could mimic an adenoma on unenhanced CT. Solid pheochromocytomas avidly enhance with intravenous contrast and retain contrast on delayed images, though up to 16% can have more rapid contrast washout similar to that o an adrenal adenoma. Biopsy o pheochrom ocytom as should be approached with caution as it can result in li e-threatening com plications o severe hypertension, arrhythm ias, or hem orrhage due to catecholam ine release. Many authors recom m end per orm ing urine catecholam ine screening be ore per orm ing biopsy or surgery o an indeterm inate adrenal m ass; although, biopsy o unsuspected pheochrom ocytom as in patients with negative urine catecholam ine screens and no com plication rom the biopsy has been reported.

Myelolipoma Myelolipomas are benign tumors composed o mature adipose tissue intermixed with hematopoietic elements resembling bone marrow. Adrenal myelolipomas are non unctional and in the vast majority o patients are asymptomatic and discovered incidentally. Rarely, they may be symptomatic due to mass ef ect, necrosis, or internal hemorrhage. Myelolipomas are usually unilateral and occur in the right adrenal

Figure 12-6 Myelolipoma Contrast-enhanced CT dem onstrating a predom inantly atcontaining right adrenal myelolipom a (arrowheads) and norm al le t adrenal gland (arrow). Usually 70 % to 80 % o m yelolipom as occur in the right adrenal gland. In a m inority o cases the m yeloid com ponent predom inates and there is only a m odest am ount o at. Calci cations are present in 25% o m yelolipom as, but not in this patient.

t ab

177

12-2. Fat Containing Adrenal Lesions

Myelolipoma p

oc omocy om

a d noco ic l c cinom Collision umo Li os com (

)

gland in 70% to 80% o cases. Extra-adrenal myelolipomas occur in the retroperitoneal space and are uncommon. Most m yelolipom as are predom inantly com posed o at giving them a distinctly low attenuation on CT im aging, interspersed with denser m yeloid tissue content (around 20–30 H U) (Figure 12-6 ). Less requently m yelolipom as will contain a greater am ount o m yeloid tissue than at. Though m acroscopic at is characteristic o m yelolipom as, at can also be present in atypical pheochrom ocytom as and a m inority o adrenocortical carcinom as. Sm all calci cations are present in up to 25% o m yelolipom as. Pseudocapsules can result rom hem orrhage or represent a surrounding rim o norm al adrenal tissue. In rare cases, m yelolipom as m ay coexist with another tum or in the sam e adrenal gland resulting in a coll s on umor. The m ost com m on counterpart in a m yelolipom a collision tum or is an adrenal adenom a (Table 12-2).

Adrenocortical carcinomas Adrenocortical carcinom as (ACC) are rare with an incidence o 1 to 2 per m illion. They have a bim odal distribution af ecting patients in the rst and ourth decades, and can be associated with Li–Fraum eni, Carney com plex, and Beckwith–Wiedem an syndrom es. Sixty percent o ACCs are hyper unctioning and present sim ilarly to their benign adenom a counterparts with variably m ixed Cushing syndrom e, hyperaldosteronism , or em inization or virilization. Those that are non unctional tend to be larger and are m ore likely to have m etastases when diagnosed. The m ost com m on sites or distant m etastases are the liver, lung, and bone. Aggressive local disease is com m on at presentation. On CT im aging, ACCs are typically large m asses with a m ean size o 10 cm and the m ajority m easuring greater than 6 cm . They have a heterogeneous appearance due to necrosis and internal hem orrhage. They enhance heterogeneously and m ay have a peripheral rim o nodular enhancem ent. Unlike benign adenom as, ACCs retain contrast resulting in slow contrast washout rate (APW < 6 0%, RPW < 40%). The m ost reliable im aging nding or ACC is an adrenal m ass with size greater than 4 cm and heterogeneous enhancem ent (Figure 12-7) (Table 12-3).

Metastases The adrenal glands are a requent site o m etastases exceeded only by lung, liver, and bone. In patients without

178

Body CT: The Essentials

Figure 12-7 Adrenocortical Carcinoma Contrast-enhanced CT dem onstrates a large, heterogeneous le t adrenocortical carcinom a (arrows). This patient had liver m etastases (arrowheads) at presentation. Metastases are com m on at presentation.

a known prim ary cancer, m etastases to the adrenal as a presentation or an unsuspected prim ary neoplasm is exceedingly rare; however, in cancer patients, up to 50 % o discovered adrenal m asses are m etastases. The m ost com m on prim ary neoplasm s causing adrenal m etastases are lung cancer, gastrointestinal cancers (e.g., gastric, colorectal, pancreatic), renal cancers, and lym phom a. Metastases are bilateral in up to hal o the cases, and there is a slight le tsided predom inance (1.5:1) with unilateral involvem ent. A m inority o patients with bilateral adrenal m etastases m ay develop adrenal insu ciency. On CT imaging, metastases appear sim ilar to other m alignant lesions. They m ay be a round heterogeneous m ass or result in dif use enlargement o the gland (Figure 12-8). Like other m alignant lesions, they enhance with contrast administration, but dem onstrate a slow washout rate (APW < 6 0%, RPW < 40%) compared to benign adenomas. In rare circum stances, intracellular lipid content in m etastases rom clear cell renal cell carcinom a and hepatocellular carcinom a may result in low attenuation and resem ble an adenom a. Occasionally metastases m ay occur in an existing adenom a, thus orming a collision tumor.

Collision tumors Adrenal collision tum ors occur when histologically distinct tum ors coexist adjacent to one another without signi cant t ab

12-3. Large (> 4–6 cm ) Adrenal Masses

Adrenocortical carcinoma Pheochromocytoma Metastasis ad n l

mo

g

Figure 12-8 Bilateral Adrenal Metastases Contrast-enhanced CT demonstrates bilateral adrenal m etastases (arrows) in a patient with lung cancer. A lytic vertebral m etastasis (black arrowhead) is also present.

m ixture. Adrenal collision tum ors are usually com posed o an adenom a and a m etastasis or m yelolipom a. The im aging eatures o collision tum ors are variable based on the com ponent neoplasm s.

Lymphoma Prim ary lym phom a arising in the adrenals is extrem ely rare. Secondary adrenal lym phom a occurs in about 4% o patients with non-Hodgkin lym phom a. Bilateral adrenal involvem ent is present in 43% o these patients and m ay result in adrenal insu ciency. CT im aging characteristics are varied ranging rom a discrete m ass to ill-de ned in ltrative expansion o the adrenal gland. Early disease m ay be di cult to detect because it m ay m ani est only as nonspeci c dif use enlargem ent. The m ass m ay be hom ogeneous or heterogeneous with necrotic or cystic com ponents. Adrenal calci cations can develop ollowing treatm ent.

Neuroblastic tumors Neuroblastic tumors are derived rom neural crest cells and include benign an l on uromas composed o mature gangliocytes and stroma, an l on uroblas omas o intermediate malignancy, containing both mature and immature gangliocytes, and malignant n uroblas omas composed o immature and undif erentiated gangliocytes. About one-third o neuroblastic tumors arise rom the adrenal medulla with the remainder occurring along the paravertebral sympathetic chain in the retroperitoneum or posterior mediastinum. The majority o patients with benign an l on uromas are asymptomatic, even with large tumors. Some o these tumors may secrete catecholamines, vasoactive intestinal peptide, or androgens, leading to variable degrees o diarrhea, perspiration, hypertension, and virilization. Ganglioneuromas are well-de ned homogeneous or mildly heterogeneous

Chapter 12 Adrenal Glands t ab

179

12-4. Bilateral Adrenal Enlargem ent/ Masses

Adrenal Hyperplasia Adenomas Metastases h mo

g

Inf c ion Lym p

Figure 12-9 Ganglioneuroma Coronal im age rom unenhanced CT dem onstrates a le t adrenal ganglioneurom a (arrow) containing ne, speckled calci cations which are present in about 50 % o these lesions. The patient was asym ptom atic which is typical or these lesions.

masses with modest enhancement ollowing intravenous contrast. About hal o ganglioneuromas contain calci cations, which can be ne and speckled or coarse (Figure 12-9). Interestingly, these tumors have a tendency to encase vessels without causing obstruction, similar to lymphoma. N uroblas oma is the third m ost com m on m alignant tum or in children, com prising 10 % o pediatric cancers, but accounting or 15% o pediatric cancer deaths. Neuroblastom as are large and heterogeneous m asses with 80 % to 9 0 % containing calci cations. There m ay also be areas o low attenuation secondary to central necrosis and hem orrhage. It m ay invade by direct extension into adjacent structures such as the psoas and paraspinal m uscles, as well as into the epidural space through neural oram ina. Sim ilar to ganglioneurom as, vascular encasem ent and com pression is com m on.

om

oc omocy om

in an ACTH -independent ashion. Idiopathic unilateral hyperplasia has also been reported (Table 12-4).

Adrenal hemorrhage Blunt abdom inal traum a accounts or 80 % o adrenal hem orrhages. Nontraum atic causes o adrenal hem orrhage include coagulopathy, physiologic stress (i.e., surgery, sepsis, shock), and spontaneous hem orrhage in underlying adrenal tum ors (e.g., ACC, pheochrom ocytom a, m etastases). Clinically, patients m ay present with pain in the upper abdom en, ank, or back. Adrenal insu ciency due to hem orrhage is rare but can occur with large bilateral adrenal hem atom as. On CT im aging, adrenal hem orrhage m ost requently appears as a high-attenuation round or oval adrenal m ass, or less requently as sm ooth enlargem ent o the gland (Figure 12-10 A). The attenuation o acute to subacute hem orrhage ranges rom 50 to 9 0 H U. Associated ndings include at stranding in the surrounding perirenal at and extension into the perinephric space. Over tim e m ost hem orrhages resolve. Chronic hem atom as can calci y or develop into a pseudocyst (Figure 12-10B).

Adrenal cysts

Nonneoplastic Adrenal Masses Bilateral adrenal hyperplasia Bilateral adrenal hyperplasia typically occurs in instances o excess ACTH . In Cush n s as , excess ACTH is produced by a pituitary adenom a. Ectopic ACTH -producing neoplasm s m ay also be the source o excess ACTH . Overstim ulation o the adrenal glands by excess ACTH leads to thickening o adrenal gland lim bs. A m ean adrenal lim b width o ≥ 5 m m based on m easurem ents rom the lim bs o both glands has been used as a diagnostic criterion or bilateral adrenal hyperplasia. Without treatm ent, long-term stim ulation by ACTH m ay cause the adrenal glands to becom e nodular in appearance, leading to b la ral mul no ular hyp rplas a. Excess ACTH m ay also be the result o con n al a r nal hyp rplas a, where an enzym e de ect results in im paired cortisol and/ or aldosterone synthesis, leading secondarily to increased pituitary ACTH stim ulation. In rare instances, bilateral adrenal hyperplasia occurs

Adrenal cysts are uncom m on and have a prevalence o about 1in 50 0 to 150 0 , but com prise up to about 5% o incidental adrenal lesions. They are usually solitary and occur with equal requency in the le t and right adrenal glands, but can be bilateral in about 8% to 10 % o cases. Adrenal cysts can be broadly classi ed into three categories: benign cysts, pseudocysts, and parasitic cysts. Benign a r nal cys s (54%) have thin walls and water attenuation (< 20 H U). They m ay be unilocular or m ultilocular with septations, som etim es containing m ural calci cations. Benign adrenal cysts are asym ptom atic, but rarely m ay cause pain or other sym ptom s i they are large (Figure 12-11). They m ay be di cult to distinguish rom an adrenal adenom a on unenhanced CT, however on contrastenhanced CT cysts do not enhance, unlike adenom as. A r nal ps u ocys s (39 %) are encapsulated by a brous wall and are there ore not true cysts. Pseudocysts can result rom previous hemorrhage or in arction o norm al adrenal tissue or an adrenal tum or. They are most

180

Body CT: The Essentials

A

B

Figure 12-10 Bilateral Adrenal Hemorrhage A. Contrast-enhanced CT dem onstrates spontaneous bilateral adrenal hem orrhages (arrows) in a patient ollowing abdom inal surgery. There is stranding o the at surrounding the adrenal glands (arrowheads) which is a com m on nding in acute adrenal

hem orrhage. B. Contrast-enhanced CT on the sam e patient several years later dem onstrates evolution o the hem orrhages into sm all bilateral adrenal pseudocysts (arrows). Calci cations have developed in the le t adrenal gland.

comm only unilocular but have a complex and heterogeneous appearance due to the presence o debris and hemorrhage in various stages. Because o their complex appearance it can be di cult to distinguish a benign pseudocyst rom a cystic neoplasm . Although rare, cystic degeneration o adrenal adenom as, pheochromocytomas, and ACC has been reported and should be considered in cystic adrenal m asses measuring 5 to 6 cm or larger with com plex eatures, such as thick walls or septations and high-attenuation uid. Paras c a r nal cys s (7%) are usually secondary to Echinococcus in ection and occur in less than 1% o patients with hydatid disease. Echinococcal cysts are usually m ultiseptated and m ay contain daughter cysts attached to septa, or ree oating inside the cyst.

Infectious diseases Granulom atous disease o the adrenal glands is m ost com m only due to adrenal ub rculos s, though disseminated histoplasm osis or blastom ycosis can af ect the adrenal glands in im munocomprom ised patients. Hal o the patients with dissem inated histoplasm osis develop Addison disease due to in ltration o the adrenal glands. Imaging characteristics on CT are similar regardless o etiology o in ection and depend on the time course o the disease. Initially there is bilateral hom ogeneous adrenal enlargement with central hypoattenuation due to necrosis and a peripheral enhancing rim. In chronic disease there is adrenal atrophy with variable calci cation and cystic degeneration. Pneumocystis jiroveci m ay dissem inate rom the lungs i not adequately treated. In the adrenals, as well as other abdom inal organs and lym ph nodes, this m ay lead to developm ent o punctate or coarse calci cations. Adrenal abscesses are rare, usually occurring in neonates with pre-existing adrenal hemorrhage. On CT imaging, the adrenals appear as a cystic mass with thickened walls. H ydatid cysts rom Echinococcus in ection m ay also occur in the adrenals as previously described (Table 12-5). t ab

12-5. Adrenal Calci cations

Adrenal cyst Remote hemorrhage Remote infection Figure 12-11 Adrenal Cyst Contrast-enhanced CT dem onstrates a large right adrenal cyst (arrowheads). The cyst is hom ogeneous and has a thin wall which avors benign etiology, but was resected because o its size and patient being sym ptom atic.

My loli om N u obl s om t

d lym

om

Chapter 12 Adrenal Glands

Ad r e n Al in c id e n t Al o m As Incidentalomas are incidental adrenal masses measuring 1 cm or greater that are detected by cross-sectional imaging perormed or an unrelated reason. Adrenal incidentalomas are present in 3% to 7% o the imaged population. Benign nonhyper unctioning adrenal adenomas are the most common etiology, comprising 50% to 80% o incidentalomas. Because the prevalence o adenomas is high in the general population, an incidentally discovered small adrenal mass in an oncologic patient has a reasonable probability o being benign, even though the adrenal gland is a common site or metastases. When an adrenal incidentalom a is discovered, the goal o im aging is to dif erentiate a benign “leave alone” lesion rom one that warrants urther workup (Figure 12-12). Features characteristic o a m yelolipom a or an adenom a establish benign etiology and require no urther im aging.

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Adrenal m asses that have been stable or a year or longer are also likely to be benign. An adrenal m ass o indeterm inate etiology m easuring less than 4 cm with suspicious im aging eatures such as irregular m argins or heterogeneous attenuation, or in a patient with a history o cancer should be evaluated by unenhanced adrenal CT. I the attenuation m easures less than or equal to 10 H U then the m ass is a benign adenom a. I attenuation is greater than 10 H U then an adrenal contrast washout protocol should be per orm ed to detect lipid-poor adenom a, or a benign nonenhancing cyst or hem atom a. I the etiology o the m ass rem ains uncertain a ter adrenal protocol CT then biochem ical screening or pheochrom ocytom a and biopsy are appropriate. I the adrenal m ass has benign im aging eatures – sm ooth m argins and hom ogeneous, low attenuation – and the patient has no history o neoplasm then it is likely that the lesion is

Figure 12-12 Proposed Imaging Workup of an Incidental Adrenal Mass Based on American College of Radiology Recommendations Adapted rom Berland LL, Silverman SG, Gore RM, et al. Managing incidental ndings on abdominal CT: white paper o the ACR incidental ndings committee. JACR. 2010;7:754–773. Notes: 1Imaging eatures diagnostic or adenoma are attenuation ≤ 10 H U on unenhanced CT or signal loss on chemical shi t MR (CS-MR). 2I patient has signs o symptoms o adrenal hyper unction consider biochemical evaluation. 3 Consider biochemical testing to exclude pheochromocytoma. 4Benign imaging eatures include smooth margins, homogeneous attenuation, and low density. 5Suspicious imaging eatures include irregular margins, heterogeneous attenuation, and necrosis.

182 Body CT: The Essentials benign and ollow-up CT or MR m ight be considered in 12 m onths to docum ent stability and con rm benign etiology. Biochem ical screening m ight also be considered to exclude a sm all pheochrom ocytom a. In patients with an adrenal m ass that is not a m yelolipom a or adenom a and m easures greater than 4 cm surgical consultation should be considered as m asses o this size have a greater probability o being m alignant. Biochemical screening or pheochrom ocytom a should be considered be ore biopsy or surgery. SUg g e St e d Re Ad i Ng S 1. Berland LL, Silverm an SG, Gore RM, et al. Managing incidental ndings on abdom inal CT: white paper o the ACR incidental ndings com m ittee. JACR. 20 10 ;7:754–773. 2. Blake MA, Cronin CG, Boland GW. Adrenal im aging. AJR. 20 10 ;19 4:1450 –146 0. 3. Blake MA, Kalra MK, Sweeney AT, et al. Distinguishing benign rom m alignant adrenal m asses: m ulti-detector row CT protocol with 10-m inute delay. Radiology. 20 06 ;238:578–585.

4. Blake MA, Mannudeep KK, Maher MM, et al. Pheochromocytoma: an im aging cham eleon. Radiographics. 20 0 4;24:S9 8–S9 9 . 5. Johnson PT, Horton KM, Fishm an EK. Adrenal m ass im aging with Multidetector CT: pathologic conditions, pearls, and pit alls. Radiographics. 20 0 9 ;29 :1333–1351. 6 . Lonergan GJ, Schwab CM, Suarez ES, Carlson SL. Neuroblastom a, ganglioneuroblastom a, and ganglioneurom a: radiologic-pathologic correlation. Radiographics. 20 0 2;22: 9 11–9 34. 7. Rao P, Kenney PJ, Wagner BJ, Davidson AJ. Im aging and pathologic eatures o m yelolipom a. Radiographics. 19 9 7;17: 1373–1385. 8. Rozenbilt A, Morehouse H T, Am is ES Jr. Cystic adrenal lesions: CT eatures. Radiology. 19 9 6 ;20 1:541–548. 9 . Taf el M, Haji-Mom enian S, Nikolaidis P, Miller FH . Adrenal im aging: a com prehensive review. Radiol Clin North Am. 20 12; 50 :219 –243. 10 . Lingam RK, Sohaib SA, Vlahos I, et al. CT o prim ary hyperaldosteronism (Conn’s Syndrom e): the value o m easuring the adrenal gland. AJR. 20 0 3;181:843–849 .

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I. THE NORMAL SPLEEN a. Size b. Density c. Peritoneal Space d. Normal Variants II. POLYSPLENIA/ ASPLENIA III. SPLENOSIS IV. SPLENIC LESIONS a. Cystic Splenic Lesions i. Differential diagnosis ii. Nonneoplastic cysts

iii. Benign cystic neoplasms iv. Cystic/ necrotic splenic metastases b. Solid Nonvascular Lesions i. Lymphoma ii. Sarcoidosis iii. Metastases iv. Infection c. Vascular Lesions i. Hemangioma ii. Hamartoma iii. Angiosarcomas V. SPLENIC INFARCTS

Th e No r m a l Sp l e e N

Density

Size

On noncontrast im ages, the spleen is hom ogeneous in density. The spleen is equal or slightly less in density than the norm al liver. The noncontrast CT attenuation values are typically in the range o 40 to 6 5 H U.

Spleen m easurem ents (upper lim it o norm al): L th (craniocaudal dim ension): 10 to 12 cm W th (longest splenic diam eter on any transverse im age): 8 to 11cm Th ck ss (distance between the inner and outer borders o the spleen at the level o the hilum ): 3 to 4 cm The thickness is usually the least valuable m easurem ent. More tim e-consum ing m ethods or estim ating splenic volum e include calculation o a spl c x by m ultiplying the length, width, and thickness (upper lim it o norm al 480 cm 3), or calculating the volum e rom the areas o each cross-sectional im age. In practice, the splenic size is o ten assessed subjectively. A speci c but insensitive sign o splenic enlargem ent is visualization o the splenic edge at or below the in erior third o the le t kidney. Spl om aly can be due to an extensive range o in ectious, hem atological, congestive, in am m atory, in ltrative, and neoplastic causes. The m ost com m on causes in developed countries include in ectious m ononucleosis, in ltration rom hem atological m alignancy, and portal hypertension.

Peritoneal Space The spleen is surrounded by the le t posterior subphrenic (perisplenic) space. Like the liver, there is a bar ar a o th spl (F r 15-8) which is not peritonealized. This bare area is adjacent to the superior le t kidney.

Normal Variants A lobule o splenic tissue extending m edially rom the posterior aspect o the spleen is a very com m on variant (Figure 13-1). Less com monly, a lobule can be seen involving the anterior spleen. There can be norm al splenic cle ts which should not be con used with lacerations. Accessory spleens (spl l s) are com m on variants which can be usually be easily characterized. These are usually seen in the hilum . A splenule in the pancreatic tail (Figure 13-2) is a variant which is im portant to di erentiate rom a pancreatic m ass. A splenule will typically enhance 183

184

Body CT: The Essentials

p o l y Sp l e Nia / a Sp l e Nia Polysplenia and asplenia are related to situs am biguous, de ned as an abnorm al arrangem ent o the organs and vessels in contrast to the orderly arrangem ent in situs solitus or situs inversus. In polysplenia (bilateral le t sidedness or le t isom erism ), the spleen is divided into m ultiple m asses which together equal the m ass o the norm al spleen, typically rom two to six in num ber and ranging rom 1to 6 cm in diam eter. In asplenia (bilateral right sidedness or right isom erism ) the spleen is absent. There is a wide range o associated abnorm alities in both conditions. Figure 13-1 Normal Variant Medial Lobule A prom inent lobule o splenic tissue extends m edially, anterior to the upper pole o the le t kidney. This is the typical location or this nding, but occasionally the medial lobule can extend posterior to the upper pole le t kidney, displacing it anteriorly.

in an identical ashion to the spleen. I there is a question as to whether a lesion is a splenule the attenuation o the lesion can be com pared to the spleen be ore and a ter contrast adm inistration. The “wa r ” spl is a congenital variant in which there is laxity o the suspensory splenic ligam ents, allowing the spleen to m ove out o the le t upper quadrant. The wandering spleen is prone to torsion. A ter contrast adm inistration, the spleen will usually dem on strate heterogen eous (o ten arci orm or wavelike) en han cem en t (Figure 13-2) i im aged early (typically be ore 1m in u te). This m ay be secon dary to variable blood ow in di erent splenic com partm ents. On portal phase im ages, the spleen will typically dem onstrate hom ogen eous enhancem ent.

Sp l e No SiS Splenosis (Figure 13-3) is autotransplantation o splenic tissue, usually the result o traumatic rupture or splenectom y. Splenosis is m ost comm only noted in the peritoneum but can involve the retroperitoneum , pleura, lung, pericardium, and subcutaneous tissue. Most patients with splenosis are asym ptom atic but splenosis may m im ic neoplasm on CT. The nodules enhance sim ilarly to normal spleen on CT, ranging rom 75 to 9 7 H U approximately 1m inute a ter the start o contrast injection. In some cases, scintigraphy may be necessary to con rm the suspected diagnosis.

Sp l e Nic l e Sio NS The di erential diagnosis o splenic lesions is broad. In sym ptom atic patients with m ultiple splenic nodules, but no known m alignancy, the m ost com m on etiologies are lym phom a, in ection, and sarcoid. In asymptomatic patients with multiple nodules, sarcoid, nonlym phom atous m etastatic disease, and benign tum ors such as hem angiom atosis are m ost com m on.

A

B

Figure 13-2 Splenule in Pancreatic Tail, and Arterial Phase Splenic Enhancement A splenule in the pancreatic tail (arrow) could potentially be con used with a hypervascular pancreatic m ass such as a neuroendocrine tum or. The enhancem ent o the splenule

ollows the spleen on arterial (A) and portal (B) phase im ages which is help ul in di erentiation rom a pancreatic tumor. The heterogeneous enhancem ent o the spleen in A is a norm al variant on arterial phase im ages; the splenic enhancem ent becom es uni orm on the later portal phase im ages (B).

Chapter 13 Spleen

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185

B

Figure 13-3 Splenosis A. Splenic tissue is present in the right cardiophrenic angle (arrow) in a patient with prior splenectom y. This is dif cult to

de nitely diagnose as splenic tissue on CT, but is con rm ed to be splenic tissue by white blood cell scintigraphy (B).

Splenic lesions can be classi ed as cystic, solid and nonvascular, or vascular.

Nonneoplastic cysts

Cystic Splenic Lesions Dif erential diagnosis Cystic splenic lesions can be nonneoplastic, benign neoplasm s, or cystic/ necrotic m etastases (Table 13-1). With the exception o echinococcal cysts, benign cystic splenic lesions typically cannot be di erentiated. Echinococcal cysts should be considered in an at-risk patient population i daughter cysts or m em brane detachm ent is seen, and particularly i sim ilar cystic liver lesions are present. Lym phangiom as should be considered in children. The possibility o cystic/ necrotic m etastases should always be considered in patients with cancer. Pancreatic pseudocyst and abscess are also possible etiologies with the proper clinical history. T b

The nonneoplastic cysts can be congenital, post-traum atic, or hydatid. Co tal cysts have a true epithelial lining. Posttra mat c cysts, which may be more common in the United States, represent the nal stage o evolution o splenic hematomas. Both types o cysts typically appear as spherical, circumscribed, water-density lesions with no enhancement. Compared to congenital cysts, post-traumatic cysts are more likely to have calci ed portions and septations (Figure 13-4). Both types o cysts are o ten asymptomatic, although patients with larger cysts can present with ullness or pain. Patients can also present acutely with cyst rupture or in ection.

13-1. Cystic Splenic Lesions

Post-traumatic cyst Congenital cyst Pancreatic psuedocyst Echinococcal cyst a bsc ss Lym

ngiom

Cys ic m

s sis

Figure 13-4 Splenic Cyst Two com m on etiologies o splenic cysts are post-traum atic and congenital. This cyst is m ost likely post-traum atic given the septation and calci cation.

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A

B

Figure 13-5 Cystic Serosal Metastasis A. A peripheral lesion in the spleen in a patient with ovarian cancer has the appearance o a nonspeci c cyst. However, a CT

per orm ed 3 m onths earlier (B) dem onstrates that this cystic lesion was previously sm aller (arrow); it represents a serosal im plant rom ovarian cancer.

H ydatid disease is a zoonotic in ection typically caused by Echinococcus granulosus, and rarely caused by Echinococcus multilocularis. The spleen is the third m ost com m on site o involvem ent, a ter the liver and lung. Splenic ch ococcal cysts are rare in the United States, but a com m on cause o splenic cysts worldwide. Patients are usually asym ptom atic, although large or secondarily in ected cysts m ay be sym ptom atic. Im aging ndings which suggest echinococcal cysts include daughter cysts (either peripheral or di use) and m em brane detachm ent (the “f oat l ly” s ). Cyst wall calci cation is m ore com m on than in other benign cystic lesions. There is typically no enhancem ent. In greater than 70% o cases o splenic echinococcal disease, other organs, m ost com m only the liver, are involved.

Cystic m etastases m ay show peripheral and septal enhancem ent.

Benign cystic neoplasms The prim ary benign cystic neoplasm to be considered is lympha oma. Lym phangiom as are m ost com m on in children and are typically asym ptom atic. The cystic type is the m ost com m on in the spleen. They appear as single or m ultiple cystic lesions, som etim es m ultiloculated, which are o ten subcapsular in location. Minim al or no enhancem ent o the cyst wall and septations is seen a ter contrast adm inistration. Cyst wall calci cation can occasionally be seen. Lymphangiomas usually cannot be di erentiated rom nonneoplastic cysts.

Cystic/ necrotic splenic metastases Splenic metastases are uncommon and usually multiple. Isolated splenic metastases are rare. The most common tumors to metastasize to the spleen are breast, lung, ovary, and melanoma. A cystic appearance can be seen in mucinous metastases or secondary to necrosis. Melanoma can also cause cystic metastases. Metastatic ovarian cancer can produce cystic serosal implants along the splenic sur ace (Figure 13-5).

Solid, Nonvascular Lesions These lesions have greater attenuation than the cystic lesions. They may demonstrate some enhancement but less than the vascular lesions which have greater enhancement than the splenic parenchyma. The primary considerations are metastases, lymphoma, sarcoidosis, and in ection (Table 13-2).

Lymphoma Splenic involvem ent in Hodgkin disease (H D) and nonHodgkin lym phom a (NH L) is com m on, but isolated or prim ary splenic involvem ent, alm ost always secondary to NH L, is rare. Overall, CT has low sensitivity (ranging rom 22% to 6 5%) or the diagnosis o splenic involvem ent in lym phom a. The spleen may appear norm al with microscopic involvem ent. Imaging m ani estations include splenomegaly without ocal lesions, and solitary and multi ocal nodules. In patients with lym phom a, m assive splenom egaly is highly suggestive o splenic involvem ent. However, m ild to m oderate splenom egaly is less speci c and can be nonneoplastic, particularly in patients with NH L. T b

13-2. Solid, Nonvascular, Splenic Lesions

Lymphoma Metastases Sarcoidosis Infection (mycobacterial, fungal) Inf mm o y s udo umo

Chapter 13 Spleen

Figure 13-6 Splenic Lymphoma A hypodense central splenic m ass is present with additional peripheral areas o hypodensity. This nding is not speci c and could be seen in other disorders including metastases and sarcoid, but adenopathy in the splenic hilum (arrow) is m uch m ore likely to be present in lym phom a com pared to other disorders.

Focal splenic involvem ent appears as single or m ultiple hypodense oci with little or no enhancem ent. Rarely, rim enhancem ent can be seen. Calci cation is rare but can be seen in aggressive or treated lesions. The nodules m ay be greater than 1 cm or m iliary (< 1 cm ). The nodules secondary to NH L are o ten larger than nodules secondary to H D. H D o ten results in nodules which are less than 1 cm in size. These sm all nodules m ay be dif cult to di erentiate rom in ection. Extrasplenic ndings can be help ul in diagnosing splenic lymphoma. Adenopathy in the splenic hilum (Figure 13-6 ) is som etim es noted in patients with splenic lym phom a, particularly in NH L. This is not com m only seen in other conditions. In patients with H D, splenic involvem ent is very com m on i there is known hepatic involvem ent.

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Figure 13-7 Splenic Sarcoidosis Multiple solid-appearing splenic nodules are present in a patient with sarcoidosis. Other possible etiologies are metastatic disease, lym phom a, and in ection. The liver is also involved in approxim ately 50% o cases o splenic sarcoidosis. The appearance o the liver in this case m ay be secondary to brosis.

Metastases Splenic m etastases can appear solid (Figure 13-8) or cystic. The m ost com m on tum ors to m etastasize to the spleen are breast, lung, ovary, and m elanom a. These can range in size rom a ew m illim eters to several centim eters. Splenic m etastases do not have distinguishing im aging characteristics; however, isolated splenic m etastases are rare.

Sarcoidosis Splenic involvem ent occurs in 24% to 59 % o patients with sarcoidosis. Patients are usually asym ptom atic. Splenic sarcoidosis m ay appear as splenom egaly and/ or m ultiple nodules. Splenic nodules are hypodense with little or no enhancem ent. They range rom 1m m to 2 cm in size. Calci cation is rare. Extrasplenic ndings (Figure 13-7) m ay be help ul in suggesting the diagnosis. There is requent concom itant abdom inal adenopathy. Hepatic nodules will be noted in 50 % o patients with splenic nodules. However, splenic sarcoidosis is dif cult to distinguish rom lym phom a by im aging alone. A negative chest radiograph does not exclude splenic sarcoidosis. A norm al chest radiograph is seen in 25% o patients with sarcoidosis and splenic nodules.

Figure 13-8 Splenic Metastasis A splenic m etastasis is noted in a patient with m elanom a. The m ost com m on tum ors to m etastasis to the spleen are breast, lung, ovary, and m elanom a. Splenic m etastasis are nonspeci c in appearance but typically appear solid as in this case; they can occasionally appear cystic (Figure 13-5).

188 Body CT: The Essentials T b

13-3. Vascular Splenic Lesions

Hemangioma h m

om

a ngios com h m ngio ndo h m ngio

liom

icy om

In ection Bacterial abscesses are rare and m ight m im ic a cystic splenic lesion rather than a solid lesion. However, m ycobacterial and ungal (Candida, Aspergillus, Cryptococcus) in ections usually appear as hypodense lesions which are m ore dense than cysts. These o ten have a m iliary pattern with extensive lesions less than 1cm in size. The sm all and relatively uni orm size o these lesions can be help ul in distinguishing in ection rom other lesions. Typically the liver and possibly the kidneys will also be involved. CT m ay have lim ited sensitivity or early ungal in ection.

Figure 13-9 Splenic Hemangioma (Presumed) Coronal CT dem onstrates a splenic lesion with heterogeneous enhancem ent. This dem onstrated long-term stability and is presum ed to be a hem angiom a. Sm all splenic (capillary) hem angiom as m ay enhance hom ogeneously. Larger splenic (cavernous) hem angiom as dem onstrate di erent patterns o delayed enhancem ent, including progressive centripetal enhancem ent and discrete m ottled areas o heterogeneous density (as seen in this case).

Vascular Lesions Vascular splenic lesions have areas which enhance m ore than the surrounding splenic parenchym a. The m ost com m on vascular lesion is a hem angiom a. Other lesions to consider include ham artom a and angiosarcom a (Table 13-3).

Hemangioma Splenic hemangiomas are the m ost comm on benign primary neoplasm o the spleen, and the second most com mon ocal lesion a ter cysts. Most incidentally detected vascular splenic lesions will be hemangiomas. They are m ost o ten seen in patients between the ages o 30 and 50 with a slight male sex predilection. Splenic hem angiom as have been associated with Klippel–Trenaunay–Weber syndrome. Most splenic hem angiom as are less than 2 cm and there is occasional calci cation. Sm all splenic (capillary) hem angiom as, like sm all liver hem angiom as, m ay enhance hom ogeneously. Larger splenic (cavernous) hem angiom as, unlike liver hem angiom as, do not typically have peripherally enhancing nodules; the initial enhancem ent is m ore ring like. Di erent patterns o delayed enhancem ent have been described, including progressive centripetal enhancem ent and discrete m ottled areas o heterogeneous density (Figure 13-9 ).

Hamartoma Splenic ham artom as (also called nodular hyperplasia or splenom as) are rare lesions com posed o m al orm ed pulp elem ents. They can be seen at any age and have no sex predilection. Splenic ham artom as have been associated with tuberous sclerosis and Wiskott–Aldrich like syndrom e. They should also be considered in younger patient with throm bocytopenia.

Ham artom as have an enhancem ent pattern which is som ewhat sim ilar to hem angiom as. They o ten dem onstrate di use heterogeneous early contrast enhancem ent and hom ogeneous persistent delayed enhancem ent. However, the early contrast enhancem ent is typically m ore heterogeneous than seen in hem angiom as.

Angiosarcomas Angiosarcom as usually occur in the age range o 50 to 79 years and have a slight male sex predilection. Unlike hepatic angiosarcoma there is no association with exposure to vinyl chloride or arsenic, although there m ay be som e association with Thorotrast. Most patients with angiosarcoma have splenomegaly. The tumors can appear as low-attenuation areas with possible cystic and necrotic areas and hemorrhage. There is typically heterogeneous enhancement and occasionally extensive calci cation. Distant m etastases at presentation are com m on, but angiosarcom a usually does not m etastasize to abdom inal lym ph nodes, which can be help ul in distinguishing an avascular angiosarcoma rom lymphoma. Hem angioendotheliom a and hem angiopericytom a are other vascular lesions which som etim es cannot be distinguished rom angiosarcom a by im aging.

Sp l e Nic iNf a r c TS Splenic in arcts are usually due to throm boem bolic or hem atological etiologies. In older patients em bolic events are m ost com m on etiology. In patients under 40 , associated hem atological disorders are the m ost com m on etiology. Splenic in arcts can be asym ptom atic or present with

Chapter 13 Spleen

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2. Bezerra AS, D’Ippolito G, Faintuch S, Szejn eld J, Ahm ed M. Determ ination o splenom egaly by CT: is there a place or a single m easurem ent? AJR Am J Roentgen. 20 0 5;184:1510 –1513. 3. Nelson RC, Chezm ar JL, Peterson JE, Bernardino ME. Contrastenhanced CT o the liver and spleen: com parison o ionic and nonionic contrast agents. AJR Am J Roentgenol. 19 89 ;153: 9 73–9 78. 4. Ben Ely A, Zissin R, Copen L, et al. The wandering spleen: CT ndings and possible pit alls in diagnosis. Clin Radiol. 20 0 6 ;6 1(11):9 54–9 58. 5. Fulcher AS, Turner MA. Abdom inal m ani estations o situs abnorm alities in adults. Radiographics. 20 0 2;22(6 ):1439 –1456 . 6 . Warshauer DM, Molina PL, Worawattanakul S. The spotted spleen: CT and clinical correlation in a tertiary care center. J Comput Assist Tomogr. 19 9 8;22:6 9 4–70 2.

Figure 13-10 Splenic Infarct A typical appearance o splenic in arction is noted with a wedgeshaped area o hypodensity extending to the capsule. A “cortical rim” sign o peripheral enhancem ent is noted rom residual capsular ow.

abrupt le t upper quadrant pain. On contrast-enhanced CT, splenic in arcts are classically sharply m arginated, peripheral wedge-shaped hypodense de ects. However, this classic appearance is seen in less than hal o acute in arcts, and in arcts can be poorly m arginated, round, or heterogeneous. In patients with larger in arcts, a “cortical rim” sign (Figure 13-10 ) o peripheral contrast enhancem ent rom residual capsular ow can som etim es be seen. I splenic in arcts are identi ed, the study should be care ully evaluated or renal and intestinal in arcts which o ten coexist. Su g g e STe d Re Ad i n g S 1. Am enta PS, Am enta PS II. The anatom y o the spleen. In: Bowdler AJ, ed. The Spleen: Structure, Function, and Clinical Signif cance. London: Chapm an and Hall Medical; 19 9 0 .

7. Warshauer DM, Hall H L. Solitary splenic lesions. Semin Ultrasound CT MR. 20 0 6 ;27:370 –388. 8. Kam aya A, Weinstein S, Desser TS. Multiple lesions o the spleen: di erential diagnosis o cystic and solid lesions. Semin Ultrasound CT MR 2, http:/ / www.ncbi.nlm .nih.gov/ pubm ed/ 170 48454. 9 . Urrutia M, Mergo PJ, Ros LH , Torres GM, Ros PR. Cystic m asses o the spleen: radiologic-pathologic correlation. Radiographics. 19 9 6 ;16 :10 7–129 . 10 . Bhatia K, Sahdev A, Reznek RH . Lym phom a o the spleen. Semin Ultrasound CT MR. 20 0 7;28(1):12–20 . 0 0 6 6 ;27:389 –40 3. 11. Abbott RM, Levy AD, Aguilera NS, Gorospe L, Thom pson WM. From the archives o the AFIP: prim ary vascular neoplasm s o the spleen: radiologic-pathologic correlation. Radiographics. 20 0 4;24:1137–116 3. 12. Yu RS, Zhang SZ, Hua JM. Im aging ndings o splenic ham artom a. World J Gastroenterol. 20 0 4;10 :26 13–26 15. 13. Thom pson WM, Levy AD, Aguilera NS, Gorospe L, Abbott RM. Angiosarcom a o the spleen: im aging characteristics in 12 patients. Radiology. 20 0 5;235:10 6 –115. 14. Rom ano S, Scaglioni M, Gatta G, et al. Association o splenic and renal in arctions in acute abdom inal em ergencies. Eur J Radiol. 20 0 4;50 (1):48–58. 15. Gayer G, Zissin R, Apter S, Atar E, Portnoy O, Itzchak Y. CT ndings in congenital abnorm alities o the spleen. Br J Radiol. 20 0 1;74:76 7–772.

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Eugene Lin, MD Evan Leitz, MD Wendy Hsu, MD

I. BOWEL WALL a. Thickening b. Attenuation c. Enhancement d. Pneumatosis II. STOMACH a. Technique b. Anatomy c. Hiatal Hernias d. Gastric Volvulus e. Gastric Wall Thickening i. Gastritis ii. Peptic Ulcer Disease . Gastric Neoplasms i. Gastric Adenocarcinoma ii. Gastrointestinal Stromal Tumor iii. Gastric Lymphoma III. SMALL BOWEL a. Technique i. CT Enterography b. Anatomy c. Measurements d. Ischemia e. Small Bowel Obstruction i. “Small Bowel Feces” Sign ii. The “Whirl” Sign . Complicated Small Bowel Obstructions i. Closed-Loop Obstruction ii. Volvulus iii. Internal Hernias

g. Intussusception h. Small Bowel Tumors i. Adenocarcinoma ii. Lymphoma iii. Carcinoid Tumors iv. Metastases IV. COLON a. Anatomy b. Normal Measurements c. Appendicitis i. Appendix Size and Appearance ii. Secondary Signs iii. Perforated Appendicitis iv. Pitfalls d. Mucocele o the Appendix e. Diverticulitis i. Diverticulitis Versus Carcinoma . Epiploic Appendagitis i. Omental Infarction g. Ischemic Colitis h. Inf ammatory Bowel Disease i. Distribution ii. Bowel Wall iii. Other Findings i. In ectious Colitis j. Toxic Megacolon k. Sigmoid Volvulus l. Cecal Volvulus m. Lipoma n. Lymphoma o. Colorectal Cancer p. CT Colonography

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Bo w e l w a l l The bowel wall can be assessed by the degree and distribution o thickening, attenuation, and enhancem ent.

Thickening The m ost nonspeci c type o bowel wall thickening is thickening with hom ogeneous so t tissue attenuation. This is m ost o ten neoplastic when greater than 3 cm , whereas thickening secondary to benign etiologies is usually less than 2 cm .

Attenuation The “wat r halo” s n can have two or three layers. The “tar t” s n (Figure 14-1) dem onstrates a three-layer appearance to the bowel wall with a contrast-enhanced inner (m ucosal) and outer (serosal) layer around a m iddle layer o decreased attenuation which is secondary to subm ucosal edem a or in am m ation. Occasionally, the outer enhanced layer is not seen and the bowel wall has a twolayer appearance, or “doubl halo” s n (Figure 14-2). The water halo sign is nonspeci c and can be seen in m any in ectious and in am m atory processes but is rarely associated with m alignancy. The “ at halo” s n (Figure 14-3) appears as at attenuation (< 10 H U) in the subm ucosa between the inner and outer layers o so t tissue attenuation. It appears as a three-layer bowel wall, resem bling the “target” sign but with lower density centrally. It is associated with chronic in am m atory bowel disease, and is m ore prevalent in ulcerative colitis (UC) than Crohn disease (CD). However, this sign can also be norm al variant in the term inal ileum and colon when the appearance o the bowel is otherwise norm al.

Figure 14-1 Bowel Wall Enhancement with “Target” Sign Thickening and enhancement o m ultiple loops o ileum (arrows) is present. This dem onstrates a three-layer “target” sign, with enhancem ent o the serosal and mucosal layers and a low (water) density subm ucosa. This is a variant o the “water halo” sign (another variant is the “double halo” sign). This nding is nonspeci c but is typically not associated with m alignancy.

Figure 14-2 Bowel Wall Enhancement with “Double Halo” Sign Thickening and enhancement o m ultiple sm all bowel loops in the le t abdom en is noted. A two-layer “double halo” appearance is seen which is a variant o the “water halo” sign without the enhancing outer (serosal) layer seen in the three-layer “target” sign (Figure 14-1). This nding is nonspeci c but is typically not associated with m alignancy.

H yperdensity in the bowel wall on noncontrast im ages is consistent with ntramural h morrha (typically in the subm ucosa), but this nding is only seen in a m inority o patients with intram ural hem orrhage. The m ost com m on cause o sm all bowel intram ural hem orrhage is anticoagulation; other causes include bleeding disorders, vasculitis, m alignancy, and ischem ia. A ter contrast adm inistration, subm ucosal hem orrhage can appear as either hom ogeneous wall thickening, or a “target” sign. Intram ural hem orrhage usually has a greater degree o wall thickening and shorter segm ent o involvem ent com pared to bowel ischem ia.

Figure 14-3 Fat Halo Sign Subm ucosal at density is noted in the term inal ileum (arrows) in a patient with Crohn disease. This sign is usually associated with chronic in am m atory bowel disease. It can be distinguished rom the m ore nonspeci c “target” sign secondary to subm ucosal edem a by lower attenuation (< 10 H U) in the subm ucosa. Intram ural at can be a norm al variant in the colon and distal ileum , but in these cases the at layer is usually thin and the bowel loops are undistended or collapsed. In addition, there are other signs o in am m atory bowel disease in this case such as bowel wall thickening and bro atty proli eration.

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Increased bowel wall enhancem ent (greater than venous opaci cation) can be seen with vasodilatation and/ or intram ural vessel injury with interstitial leakage. Causes o increased enhancem ent include active in am m atory bowel disease, and “shock bowel” in hypotensive traum a patients. Although decreased bowel wall enhancem ent is a speci c sign o bowel ischem ia, increased enhancem ent can also be seen in bowel ischem ia (Figure 14-5) secondary to reper usion and increased vascular perm eability.

Figure 14-4 Decreased Bowel Wall Enhancement Secondary to Small Bowel In arction Decreased enhancem ent o the sm all bowel wall is the m ost speci c sign o ischem ia (arrowhead). A discrete transition is noted rom enhancing (arrow) to nonenhancing bowel in the sam e loop. Note that the wall o the sm all bowel is very thin. Although bowel wall thickening is a nonspeci c sign o ischem ia, a paper thin bowel wall can be seen in arterio-occlusive sm all bowel in arction.

Pneumatosis

Decreased bowel wall enhancem ent (Figure 14-4) is a speci c sign o ischem ia in the proper clinical setting.

Pneum atosis intestinalis (PI) (Figure 14-6 ) is de ned as the presence o gas in the bowel wall. It is o ten best visualized on lung windows. PI is secondary to a wide range o underlying conditions which range rom benign to li e-threatening. Proposed m echanism s are dissection o gas into the bowel wall rom the bowel lum en or lungs (through the m ediastinum and retroperitoneum ), and entry o gasorm ing bacilli into the bowel wall through m ucosal rents or overdistension. The etiologies o PI have been classi ed into our broad categories: bowel necrosis, m ucosal disruption, increased m ucosal perm eability, and pulm onary disease (Table 14-1).

Figure 14-5 Decreased, Increased, and Normal Bowel Wall Enhancement Coronal CT in a patient with sm all bowel ischem ia dem onstrates areas o decreased (long arrow), increased (arrowhead), and norm al (short arrow) bowel wall enhancem ent. The increased bowel wall enhancem ent in the setting o ischem ia m ay be secondary to reper usion and increased vascular perm eability.

Figure 14-6 Small Bowel Pneumatosis Secondary to Obstruction Pneum atosis o the small bowel is present secondary to a severe small bowel obstruction. Although the presence o pneumatosis raises the suspicion or ischemia, ischemic bowel was not present in this case. The lack o additional ndings such as bowel wall thickening and mesenteric edema (which would typically be present in a venous ischemia related to obstruction) suggests that the pneumatosis could be related to the obstruction alone.

Enhancement

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T b

14-1. Etiologies o Pneum atosis Intestinalis

In s in l isc

mi / in

c ion

In s in l obs uc ion pulmon y ( .g., s m , m c

nic l v n il ion)

Mucos l dis u ion ( .g., ic ulc dis s , in mm o y bow l dis s , c us ic ing s ion) I

og nic ( .g., ndosco ic

oc du s, b ium n m )

Immunologic l dis u b nc s ( .g., s ns l n ion, c mo y)

oids, o g n

In c ions ( .g., clos idium di cil , a IDS n

ocoli is)

Mo ili y diso d s ( .g., scl od m , j junoil l by ss) p im y n um osis ( .g., n um osis cys oid s in s in lis)

The bowel wall gas can have a circular, bubbly, or linear appearance. Although a linear pattern m ay be m ore associated with bowel ischem ia, both the bubbly and linear appearance can be seen in benign and li e-threatening conditions. However, the circular pattern has been associated

with pneum atosis cystoides intestinalis and is som etim es benign when identi ed in the colon. The presence o additional ndings such as bowel wall thickening, ascites, m esenteric stranding, dilatation, decreased bowel wall enhancem ent, arterial and venous occlusion, and portom esenteric gas (Figure 14-7) is help ul in suggesting a li e-threatening cause o PI. PI con ned to the sm all bowel is m ore worrisom e, whereas PI con ned to the colon is m ore requently benign. The com bination o pneum atosis and portom esenteric gas is associated with bowel ischem ia in approxim ately 70% o cases, but portom esenteric gas can also be seen in nonischem ic conditions with a m ore avorable outcom e. In patients with ischem ia, PI can be seen in both transm ural in arction, and partial m ural ischem ia with viable bowel. In one study, pneum operitoneum was equally associated with benign and li e-threatening PI. Gas trapped with eces at the m ucosal sur ace can result in a “pseudopneum atosis” appearance. A help ul sign or distinguishing pseudopneum atosis is that i a ree gas– uid level is present, the apparent pneum atosis will stop at the gas– uid level.

STo m a c h Technique Standard abdom inal CT protocols are typically not optim ized or stom ach evaluation. I m ore detailed evaluation o the stom ach is desired, distention may be achieved using water as a negative oral contrast agent. In addition, some institutions administer e ervescent (gas-producing) crystals to im prove distention o the antidependent portions o the stom ach.

Anatomy

Figure 14-7 Pneumatosis with Portal Venous Air Extensive pneum atosis is noted with portal venous air (arrows). The com bination o pneum atosis and portal venous air is associated with bowel ischem ia in approxim ately 70 % o cases; however, portom esenteric gas can som etim es be noted in nonischem ic conditions with a m ore avorable outcom e.

The stomach is generally divided into our anatomic segments. The cardia surrounds the gastroesophageal (GE) junction. The undus is the most cephalad portion o the stomach extending superiorly rom the cardia and abuts the le t hemidiaphragm in a patient with conventional anatomy. The gastric body constitutes the bulk o the stomach and extends in eriorly rom the undus. The antrum is the most distal portion o the stomach and connects to the duodenum through the pyloric sphincter. No clear demarcating eatures distinguishing the gastric segments are evident on CT. On arterial phase im aging, a layered enhancem ent pattern m ay be visualized with the relatively hypoenhancing subm ucosa separating the enhancing m ucosal and m uscular layers. This enhancem ent pattern is not com m only seen on portal venous phase im ages.

Hiatal Hernias Hiatal hernias can be separated into two general categories— sliding and paraesophageal types. The surgical classi cation

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B

Figure 14-8 Mesentero-axial volvulus Coronal CT im ages dem onstrate rotation o the stom ach around the short axis. The stom ach appears upside down with the

antrum and pylorus (A) superior to the undus and GE junction (B). Severe gastric wall thickening is noted. (Im ages courtesy o Christine Menias MD, Scottsdale, AZ).

is o ten utilized and separates these hernias into our categories. Type I (sliding) hernias are the most common with the GE junction displaced superiorly into the thorax. Type II hernias are strictly paraesophageal, with the GE junction in the normal in radiaphragmatic position. Type III are “mixed” demonstrating eatures o both sliding and paraesophageal type components. A type IV hernia is the most severe orm, representing a complete intrathoracic stomach.

5 m m , and can norm ally m easure up to 12 m m . Caution should be taken when determ ining gastric wall thickness to not include rugal olds. Gastric wall thickening is nonspeci c nding on CT with potential etiologies including in am m atory, in ltrative, and m alignant causes. Although the distribution o wall thickening and clinical history m ay suggest a m ore speci c etiology, diagnosis m ust o ten be de erred to endoscopy with direct visualization and biopsy o the abnorm ality detected on CT. Gastric wall thickening o 1cm or greater on CT has a sensitivity o 10 0 % but speci city o less than 50 % or m alignant or potentially m alignant stom ach lesions. Gastric wall thickening greater than 1 cm that is also ocal, eccentric, and enhancing is m ore speci c (9 2%) but m uch less sensitive or m alignancy. Benign causes o gastric wall thickening include gastritis and peptic ulcer disease.

Gastric Volvulus CT is particularly use ul to assess or com plications o type III and IV hiatal hernias such as volvulus. A gastric volvulus is described on the basis o the rotational m orphology. An or anoax al volvulus occurs around the longitudinal axis o the stom ach and is the m ost com m on type. A m snt roax al volvulus (Figure 14-8) is the result o the stom ach rotating around the m esenteric (short) axis. Either type o gastric volvulus can result in li e-threatening com plications. CT can play an im portant role in identi ying associated obstruction with dilation o the rotated gastric lum en. Uncom m only, ischem ia m ay be evident by gastric pneum atosis. A search or extralum inal gas adjacent to a gastric volvulus can be use ul as a sign o gastric wall necrosis and per oration.

Gastric Wall Thickening Most o the norm al gastric wall should not exceed 5 m m in thickness when the stom ach is well distended. However, the thickness o the gastric antrum com m only exceeds

Gastritis The m ost com m on appearance o gastritis on CT is di use gastric wall thickening. In som e cases, a m ore ocal gastritis can result in a region o thickened and nodular gastric wall which can m im ic a neoplasm . Gastritis m ay be suggested when the thickened gastric wall has decreased attenuation as a result o edem a. The CT ndings are generally nonspeci c although certain eatures m ay suggest a particular etiology. For exam ple, patients with Zollinger–Ellison (ZE) syndrom e develop gastritis due to gastric acid hypersecretion resulting rom a gastrinom a tum or. CT m ay dem onstrate additional ndings suggesting ZE syndrom e such as

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Figure 14-10 Gastric Carcinoma Di use gastric wall thickening is noted in the body and antrum , with loss o the norm al rugal old pattern com pared to the undus (arrow). Figure 14-9 Per orated Ulcer A dilated stom ach, retroperitoneal uid, and extralum inal air is present secondary to a per orated pyloric ulcer. The ulcer itsel (arrow) is visualized as a sm all outpouching.

in am m atory changes in the duodenum rom associated ulcers, a hypervascular pancreatic tum or representing the gastrinom a, or liver m etastases.

Peptic Ulcer Disease Uncom plicated peptic ulcer disease is typically not identi ed on standard CT exam inations. Per orated gastric and duodenal ulcers (Figure 14-9 ) can som etim es present with an acute abdom en. CT ndings o bowel per oration include extralum inal air bubbles adjacent to the bowel wall, ree air, segm ental wall thickening, perivisceral at stranding, abscess or in am m atory m ass, and extralum inal uid or contrast. Occasionally, the ulcer itsel will be visualized as a sm all outpouching in the wall. CT can accurately identi y the site o per oration in the m ajority o cases, with the location o extralum inal air bubbles and segm ental wall thickening being the m ost help ul signs or localization.

Gastric Neoplasms Most gastric neoplasm s are benign and are o ten not detected by CT. These include an approxim ately equal percentage o m ucosal and subm ucosal lesions. H yperplastic polyps are the m ost com m on, with other lesions including adenom atous polyps, leiom yom as, lipom as, and neural tum ors.

Gastric Adenocarcinoma Gastric adenocarcinom a is the m ost com m on m alignant gastric tum or. CT is an im portant adjunct to endoscopic ultrasound (EUS) in evaluating and staging gastric cancer.

The CT appearance o gastric adenocarcinom a (Figure 14-10 ) is variable, including ocal thickening o ten with associated m ucosal irregularity or a di usely in ltrating lesion with loss o the norm al rugal old pattern (linitis plastica). A less com m on appearance is that o a large exophytic m ass. Conventional CT has a high prim ary tum or detection rate (85%–9 5%) in patients with advanced gastric cancer, but has a m ore lim ited role in early gastric cancer. EUS is the typical diagnostic m odality o choice or local (T) staging o gastric cancer. However, dedicated gastric CT with three dim ensional (3D) virtual gastroscopy techniques is valuable in evaluating early gastric cancer and has achieved sim ilar diagnostic accuracy to EUS in assessing T stage and serosal involvem ent. Blurring o the serosal contour and increased attenuation o the serosal contour suggests T4 disease. The tum or can then spread directly via peritoneal re ections into the liver, pancreas, and transverse colon. Regional lym ph nodes can be considered involved when the short-axis diam eter is greater than 6 m m or perigastric nodes, and greater than 8 m m or extraperigastric nodes. In a m eta-analysis, CT had a sensitivity o 6 3% to 9 2% and a speci city o 50 % to 88% or lym ph node m etastasis rom gastric cancer. Hem atogenous m etastases m ost com m only involve the liver; less com m on sites include the lungs, adrenal glands, kidneys, bones, and brain. Intraperitoneal m etastases can also occur; i these seed the ovaries they are known as Krukenberg tum ors (Figure 17-12).

Gastrointestinal Stromal Tumor Gastrointestinal strom al tum or (GIST) is a rare so t tissue sarcom a, but the m ost com m on m esenchym al tum or o the gastrointestinal tract. Historically, they were classi ed as leiom yom as or leiom yosarcom as but are now recognized as a distinct tum or type, arising rom the interstitial cells o Cajal. Nearly 9 0% o GISTs display strong im m unohistochem ical staining or KIT (a tyrosine kinase growth

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A

B

C

D

Figure 14-11 Gastrointestinal Stromal Tumor—Spectrum o Appearances A. Intralum inal GIST (arrow) with hom ogeneous appearance and m inimal enhancem ent. B. Dum bbell appearance with intralum inal (arrow) and extralum inal (arrowhead) com ponents.

The intralum inal com ponent dem onstrates central cavitation with stulation to the gastric lum en. C. Sm all extralum inal GIST (arrow) with hom ogeneous enhancem ent. D. Large extraluminal GIST with central necrosis.

actor receptor). GISTs have a peak age incidence o 50 to 6 0 years. They can arise anywhere in the gastrointestinal tract but the m ajority are in the stom ach (6 0%–70 %) or sm all intestine (20 %–30%), m ost com m only in the duodenum . All GISTs have m alignant potential, with up to 30 % being rankly m alignant. However, GISTs less than 2 cm typically have a very low risk o recurrence. Size is the best predictor o m alignancy on im aging. GISTs can have three general appearances: intralum inal, extralum inal, and dum bbell type (Figure 14-11). Sm all GISTs m ay be intralum inal, appearing as hom ogeneous sharply m arginated m asses with m oderate contrast enhancem ent. Larger GISTs are typically extralum inal with

heterogeneous enhancem ent, central necrosis, m ucosal ulceration, and possible stulation to the bowel lum en. Calci cation is rare. Large tum ors can also have a “dum bbell” appearance with both intralum inal and extralum inal com ponents. As the bowel is typically not concentrically involved, bowel obstruction is rare. Aneurysm al dilation (which is also seen in lym phom a) can som etim es occur. GISTs typically metastasize to the liver (m ost com m on) and the peritoneum . Lym ph node m etastases are rare and lym phadenopathy o ten suggests another diagnosis. Advanced GISTs can be treated with the tyrosine kinase inhibitor im atinib (Gleevec; Novartis Pharm a, Basel, Switzerland). The response evaluation criteria or GISTs a ter

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A

B

Figure 14-12 Gastrointestinal Stromal Tumor—Treatment Response A. A liver m etastasis rom a GIST (arrow) dem onstrates peripheral enhancem ent. B. A ter treatm ent with the tyrosine

kinase inhibitor im atinib (Gleevec; Novartis Pharm a, Basel, Switzerland), the lesion is actually slightly larger, but the density is decreased and the enhancem ent is no longer identi ed. This is consistent with treatm ent response.

treatm ent with a targeted, cytostatic agent like im atinib di er rom the typical response evaluation a ter cytotoxic agents. Treatm ent with im atinib results in a decrease in the size o GISTs, but this response will o ten take 3 to 4 m onths, or longer, be ore satis ying traditional tum or response criteria based upon size. Responding GISTs will dem onstrate a change in the pattern o enhancem ent, in 1 to 2 m onths, rom heterogeneous hyperattenuation to hom ogeneous hypoattenuation (Figure 14-12), regardless o change in tum or size. Responding GISTs m ay even increase in size. There ore, response criteria or GISTs a ter im atinib therapy include a decrease in tum or density. In addition, the developm ent o intratum oral enhancing nodules, without a change in tumor size, is o ten the earliest sign o disease progression.

the level o the renal hila. Transpyloric spread is m ore likely in lym phom a but can also be seen in carcinom a.

Gastric Lymphoma Although gastric lym phom a (usually non-Hodgkin lym phom a) is substantially less com m on than adenocarcinom a or GIST, the stom ach is the m ost com m on site (50 % o cases) o gastrointestinal lym phom a. Prim ary gastric lym phom as o ten originate as a low-grade m ucosa-associated lym phoid tissue (MALT) lym phom a associated with Helicobacter pylori in ection. In these cases, gastric wall thickening m ay be m inim al or undetectable by CT. Lowgrade MALT lym phom as can progress to high-grade B-cell lym phom a which m ay be detected by CT. Gastric lym phom a o ten cannot be reliably di erentiated rom gastric adenocarcinom a on CT. Features suggestive o lym phom a include greater and m ore di use m ural thickening, a lesser degree o enhancem ent, and preservation o the perigastric at planes. Lym phom a is less likely to result in narrowing or obstruction o the gastric lum en. Perigastric adenopathy can be seen in both conditions but the adenopathy in gastric lym phom a o ten extends below

Sm a l l Bo w e l Technique Standard CT protocols not speci cally designed to evaluate the sm all bowel typically em ploy positive oral contrast. However, positive contrast agents can lim it visualization o the m ural eatures o the gastrointestinal tract. Positive contrast can decrease visualization o enhancing bowel tum ors, and inter ere with assessm ent o the degree o m ural enhancem ent. Bowel wall and intraluminal hem orrhage can also be obscured. Although water is a use ul contrast agent or evaluation o the stom ach, it will usually result in unsatisactory distention o the jejunum and ileum secondary to slow transit and rapid absorption. There ore, neutral oral contrast agents with attenuation sim ilar to water are typically used or speci c evaluation o the sm all bowel. Oral contrast is som etim es not adm inistered in cases o suspected sm all bowel obstruction (SBO) as the contrast will be stagnant and becom e diluted in the uid- lled dilated loops o bowel. In addition, the retained intralum inal uid contents m ay serve as a “natural” negative oral contrast agent.

CT Enterography CT enterography is a technique which utilizes oral intake o large volum es o neutral contrast agents and rapid adm inistration o intravenous contrast to improve evaluation o the sm all bowel wall. Im aging can be per orm ed in the “enteric” phase, starting approxim ately 45 seconds a ter initiation o intravenous contrast, where mural enhancement is m axim al. Potential applications o CT enterography (Figure 14-13)

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A

Figure 14-13 CT Enterography: Meckel Diverticulum A. A right lower quadrant bleeding site (arrow) is demonstrated on a technetium-99m tagged red cell bleeding scan. B. CT enterography examination demonstrates a small Meckel diverticulum (arrow) in the ileum as the etiology o the bleed (active extravasation was not identi ed during the enterography examination). The tissue protruding into the bowel lumen is likely secondary to ectopic gastric mucosa. B

include the evaluation o active CD, small bowel neoplasms, and gastrointestinal bleeding. Evaluation o gastrointestinal bleeding is usually done using a m ultiphase protocol with precontrast, arterial phase, and delayed im aging. There are som e potential pit alls in evaluating m ural enhancem ent. During the enteric phase, the jejunum will typically enhance m ore than the ileum , and nondistended

sm all bowel loops may appear to enhance m ore than distended loops.

Anatomy The small bowel can be divided into three anatomic sections: (1) duodenum , (2) jejunum , and (3) ileum .

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The duodenum is the shortest segm ent o sm all bowel extending rom the gastric pylorus to the ligam ent o Treitz. With conventional em bryologic sm all bowel rotation, the duodenum will have a typical “C-loop” orientation wrapping around the head o the pancreas. Only the rst portion o the duodenum (the bulb) is intraperitoneal whereas the rest o the duodenum is retroperitoneal. The second (descending) portion o the duodenum is the entry site or the m ajor pancreaticobiliary papilla, which m ay be visualized on CT i the duodenal lum en is distended with uid or oral contrast. The third (transverse) portion o the duodenum passes posterior to the superior m esenteric vessels. This segm ent m ay o ten appear com pressed between the superior m esenteric vessels anteriorly and the IVC and aorta posteriorly. The ourth (ascending) portion o the duodenum transitions to the jejunum at the ligam ent o Treitz where the sm all bowel again becom es intraperitoneal. The jejunum and ileum combined are approximately 5 to 7 m in length. The jejunum constitutes approximately 40% o this length, and primarily lies in the le t upper quadrant. The ileum makes up the distal 60% o small bowel and lies in the right lower quadrant ending at the ileocecal valve. On contrast-enhanced CT, the normal jejunum may be distinguished by the closely spaced valvulae conniventes ( eathery appearance) relative to the more widely spaced bowel olds in the ileum. However, there is otherwise no anatomic point o transition between the jejunum and the ileum.

Measurements The sm all bowel is considered dilated i the diam eter is greater than 2.5 to 3 cm . The sm all bowel wall is considered abnorm ally thickened i it m easures greater than 3 m m despite adequate lum inal distension. The m ost m arked wall thickening (> 2 cm ) is usually due to neoplasm s and occasionally intram ural hem orrhage. CD, ischem ia secondary to venous throm bosis, and vasculitis can also result in substantial intram ural thickening.

Figure 14-14 Renal In arct and Bowel Ischemia Multiple le t renal in arcts are present in conjunction with a superior mesenteric artery embolus (arrow). Identi cation o renal and splenic in arcts should prompt a search or evidence o bowel ischem ia.

Figure 14-15 Small Bowel Obstruction Secondary to an Adhesive Band The “ at notch” sign (arrow), as well as a “beak” sign, is a typical appearance in obstruction rom adhesive bands. The at notch sign in particular is not seen in obstruction rom matted adhesions.

Ischemia Acute sm all bowel ischem ia is secondary to arterial occlusion (m ost com m only rom cardiac em boli) in 6 0 % to 70 % o cases, m esenteric venous throm bosis in 5% to 10 % o cases, and nonocclusive ischem ia in 20% to 30 % o cases. Venous causes include neoplastic and in amm atory conditions involving the m esentery, hypercoagulability states, and bowel obstruction, where the ischemia arises rom venous compromise rom com plicated obstruction and m icrovascular occlusion secondary to overdistension. Venous ischem ia m ay di er in appearance rom arterial ischem ia, o ten resulting in greater bowel wall thickening, and more stranding and ascites. In patients with suspected arterial ischem ia, m esenteric CT angiography should be considered to best evaluate the m esenteric vessels or em boli or throm botic occlusion. In addition, arterial sm all bowel ischem ia is o ten seen in conjunction with other em bolic ndings (Figure 14-14), such as renal and splenic in arcts. Nonspeci c signs o sm all bowel ischem ia include bowel wall thickening, bowel dilatation, m esenteric stranding and ascites, and abnorm al attenuation. Bowel wall thickening is the m ost com m only seen nding in sm all bowel ischem ia but is very nonspeci c. The bowel wall

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Figure 14-16 Small Bowel Obstruction Secondary to a Carcinoid Tumor Coronal CT demonstrates a carcinoid mesenteric metastasis (arrow) causing a small bowel obstruction. A central calci cation is present which is com m only seen in carcinoid m esenteric m etastases.

tends to be thicker in venous occlusion. However, a paper thin wall (Figure 14-4) can be seen a ter transm ural arterioocclusive in arction. Bowel dilation tends to be seen in the later stages o ischem ia. Mesenteric stranding and ascites are m ore com m on in venous occlusion. On precontrast im ages, the bowel wall can be abnorm ally hyperdense rom hem orrhage, or abnorm ally hypodense rom edem a. Pneum atosis, portom esenteric gas (Figure 14-7), and abnorm al enhancem ent (Figures 14-4 and 14-5) are more speci c signs o ischem ia but relatively insensitive. Although pneum atosis can be seen in a wide range o nonischem ic conditions it can be a relatively speci c sign o ischem ia in the proper clinical setting. The presence o pneum atosis in bowel ischem ia does not always indicate transm ural in arction; this is more likely i portomesenteric gas is also seen. Decreased or absent bowel wall enhancem ent a ter contrast is the most speci c sign o ischemia but may be di cult to detect, particularly i positive contrast was employed. However, increased bowel wall enhancem ent secondary to reperusion and increased vascular perm eability can also be seen in bowel ischem ia and m ay indicate viability.

Small Bowel Obstruction Computed tomography has become the primary imaging modality or the diagnosis o SBO with both high sensitivity and speci city, particularly in cases o high-grade obstruction. Criteria or a mechanical SBO on CT include proximally dilated small bowel loops (de ned as > 2.5–3 cm—outer wall

Figure 14-17 Small Bowel Obstruction Secondary to an External Hernia Coronal CT dem onstrates a sm all bowel obstruction secondary to a hernia (arrow). In addition to evaluating the bowel outside the hernia sac, the bowel contents inside the sac should be evaluated or signs o strangulation (not present in this case).

to outer wall), a transition point, and distal normal caliber or decompressed bowel loops. An adynamic ileus typically demonstrates di use bowel dilation with no clear transition point. CT is valuable in identi ying the source o a m echanical SBO. Postoperative adhesions have becom e the m ost com m on cause in Western countries. The diagnosis o SBO secondary to adhesions is usually one o exclusion in a patient with a postoperative abdom en; however, occasionally a “ at notch” s n (Figure 14-15) at the site o obstruction can be seen which is suggestive o an adhesive band. The next m ost likely causes o SBO are m alignancy (Figure 14-16 ) and hernias (Figure 14-17). In patients with SBO, the “small bow l c s” s n (Figure 14-18) is help ul in determ ining the site o obstruction. The “wh rl” s n (Figure 14-19 ) is help ul in suggesting a com plicated SBO (particularly volvulus) that m ay require m ore urgent surgical intervention.

“Small Bowel Feces” Sign The “sm all bowel eces” sign re ers to a eculent appearance in a dilated sm all bowel loop secondary to particulate

202 Body CT: The Essentials Som e reports suggest that it is associated with interm ittent low-grade obstructions which usually do not require surgical intervention, but one report suggests it m ay be associated with higher-grade obstructions and bowel ischem ia.

The “Whirl” Sign The “whirl” sign re ers to central vessels producing a whirllike pattern, partly or com pletely encircled by bowel loops. Both the vessels and the bowel should be a ected and there should be at least 9 0 degrees o intestinal rotation. The whirl sign has been typically associated with sm all bowel volvulus but is relatively nonspeci c, and has been described in patients with other disorders such as large bowel volvulus, internal hernia, as well as asym ptom atic patients and patients with previous hem icolectom y and several other surgeries. This sign is signi cant prim arily when seen in conjunction with a SBO.

Complicated Small Bowel Obstructions Figure 14-18 “Small Bowel Feces” Sign Fecalization o small bowel contents is noted immediately proximal to the transition point (arrow) o a small bowel obstruction. This sign is help ul in determining the point o obstruction.

m aterial interm ingled with gas bubbles. It is a speci c but insensitive sign o SBO i it is seen in conjunction with sm all bowel dilation (cystic brosis, in ectious and m etabolic enteropathies, and re ux through the ileocecal valve can result in this nding in nondilated bowel). It is m ost help ul or identi ying the site o obstruction, which will usually be just distal to the area o eculent-appearing m aterial. Otherwise, the signi cance o this sign is controversial.

It should be determined whether an SBO may require urgent surgical intervention. In addition to the grade o obstruction, the presence o the whirl sign, m esenteric edema, and ascites are associated with the need or surgery, whereas the sm all bowel eces sign m ay be inversely associated. In particular, com plicated SBOs requiring urgent surgical intervention are o ten closed-loop obstructions (usually secondary to adhesive bands) with signs o ischem ia. Accurate identi cation o com plicated SBOs at high risk or ischem ia is im portant. Clos d-loop obstruct on, volvulus, and nt rnal h rn as can result in vascular com prom ise and ischem ia. These classi cations can overlap, or exam ple, volvulus is a orm o closed-loop obstruction, but closed-loop obstruction can occur without volvulus. All ndings noted in the bowel ischem ia section can be help ul in evaluating or potential ischem ia secondary to SBO. However, the m ost speci c sign is lack o bowel wall enhancem ent. Other im aging ndings which m ay be m ore com m only associated with bowel necrosis secondary to SBO are increased m esenteric attenuation, ascites, and radial distribution.

Closed-Loop Obstruction

Figure 14-19 “Whirl” Sign A “whirl” sign is noted in the right abdomen secondary to volvulus. In a de nitive “whirl” sign, both the vessels and bowel loops should be involved and there is at least 90 degrees o rotation.

Closed-loop obstruction (Figure 14-20) re ers to obstruction o the small bowel at two separate points. These two points o obstruction will typically be in close proximity as they result rom a single process. The segment o bowel between the two points o obstruction will typically be more dilated than the bowel upstream o the proximal obstruction. I the closed loop rotates along its axis, a volvulus can also result. The most common cause is postoperative adhesive bands. Other causes include internal hernias, congenital bands, and malrotation. Signs o closed-loop obstruction include a U- or C-shaped con guration o the abnormal small bowel loops, a beakshaped con guration o the dilated loops toward the obstruction (“beak” sign), a radial distribution o mesenteric vessels

Chapter 14 Gastrointestinal Tract

A

203

B

Figure 14-20 Closed-Loop Obstruction with Bowel Ischemia Coronal (A) and axial (B) im ages in patient with sm all bowel obstruction. A radial con guration o the obstructed sm all bowel loops is present. A “beak” sign is noted as the loops converge on

the site o obstruction (arrow). Severe edem a in the m esentery associated with the closed-loop obstruction is suspicious or venous ischem ia. This m ay be relatively early as only a ew o the obstructed bowel loops are thickened.

converging toward the point o obstruction (appearing like spokes o a wheel, or “balloons on a string”), and the “whirl” sign.

rior m esenteric artery (SMA) axis resulting in a closedloop obstruction. This occurs m ore com m only in the pediatric population, with intestinal m alrotation putting patients at increased risk. The “superior m esenteric vein (SMV) rotat on” s n is associated with m d ut malrotat on (Figure 14-21) and re ers to an abnorm al position o the SMV on the le t ventral side o the SMA. The whirl sign has

Volvulus A sm all bowel (or m idgut) volvulus occurs when there is abnorm al twisting o the sm all bowel around the supe-

A Figure 14-21 Intestinal Malrotation There are two signs o intestinal malrotation: the superior mesenteric vein (arrow) is to the le t o the superior mesenteric artery (SMV rotation sign) in A.; in B., the third portion o

B the duodenum (arrow) extends into the right abdomen rather than across the midline and the jejunum (arrowhead) is in the right abdomen. Although no volvulus is present in this case, malrotation can predispose to volvulus.

204

Body CT: The Essentials

a variable sensitivity (15%–6 7%) or volvulus. Another sign o sm all bowel volvulus is m ultiple transition points with a posterior location (due to the attachm ent o the sm all bowel m esentery to the retroperitoneum , the bowel is drawn posteriorly during a volvulus).

Internal Hernias Internal hernias are less com m on and de ned by protrusion o a segm ent o sm all bowel through a m esenteric or peritoneal de ect (which m ay be present in a postoperative abdom en) into a di erent com partm ent within the abdom inal cavity. Internal hernias are o ten di cult to diagnose but should be suspected i there are abnorm ally located, encapsulated, and crowded bowel loops, o ten displacing adjacent structures, with a higher index o suspicion in patients with prior surgeries with Roux-en-Y loop orm ation. Abnorm al m esenteric vasculature (displacem ent, crowding, whirl, engorgem ent) is o ten seen in association with internal hernias. In one study, m esenteric whirl was the m ost predictive sign o internal hernia; however, m inor

A

C

degrees o whirl should be interpreted with caution as this can be seen in patients without internal hernia or volvulus. Historically, the m ost com m on types o internal hernias were paraduod nal (53%), with a m uch lesser incidence o oram en o Winslow, pericecal, and intersigm oid hernias. Most paraduodenal hernias are le t sided (75%), occurring through Landzert ossa behind the ourth portion o the duodenum . However, with m ore new surgical procedures per orm ed using a Roux loop, the num ber o internal hernias is increasing and these postsurgical cases m ay be the m ost com m on types o internal hernias in som e clinical practices. The incidence o internal hernias a ter laparoscopic Roux-en-Y gastric bypass (Figure 14-22) is higher com pared to open surgery. A ter Roux-en-Y gastric bypass, internal hernias can occur through the de ect in the transverse mesocolon (m socol c w ndow), through the enteroenterostomy m esenteric de ect (transm s nt r c) and through the space between the Roux lim b mesentery and transverse m esocolon (P t rs n h rn a). Mesocolic window hernias occur with retrocolic placem ent o the Roux loop, a portion o which

B Figure 14-22 Internal Hernia A ter Roux-en-Y Gastric Bypass A. A Roux-en-Y gastric bypass with antecolic placem ent o the Roux loop (arrow) is noted. This predisposes to transm esenteric hernias. Transm esocolic internal hernias are seen with retrocolic placem ent. B. A “whirl” sign is seen near the site o obstruction near the distal anastom osis (arrow). Dilated sm all bowel loops adjacent to the abdom inal wall (arrowhead) are a typical nding in transm esenteric hernias. C. A transm esenteric internal hernia a ter gastric bypass typically occurs at the enteroenterostom y m esenteric de ect and is thus m ore distal than a transm esocolic or Petersen hernia. In this case, both the Roux loop (arrowhead) and proxim al sm all bowel (arrow) are dilated, indicated the distal nature o the obstruction.

Chapter 14 Gastrointestinal Tract

Figure 14-23 Intussusception Coronal CT dem onstrates a colocolic intussusception involving the transverse colon. A sausage-shaped appearance is noted with the m obile bowel segm ent (intussusceptum ) (labeled I), surrounded by m esenteric at and vessels and the outer receiving segm ent (intussuscipiens) (arrows).

then herniates through the m esocolic window; in these cases there are m ultiple, o ten dilated, loops o bowel above the transverse colon and the distal jejunal anastomosis is in a high position (norm ally it is near the m id-le t kidney level). In Petersen hernias, clustered bowel loops are typically seen posterior to the transverse colon, anterior to the pancreas, and above the sm all bowel mesentery. Transm esenteric hernias occur a ter antecolic Roux loop placem ent and are in erior to m esocolic window and Petersen hernias. The colon is typically displaced superiorly, and the herniated sm all bowel loops are o ten adjacent to the abdom inal wall.

Intussusception Intussusception (Figure 14-23) re ers to invagination o a more proximal segment o bowel into the lumen o a more distal segment o bowel. Ileoileal intussusception is the most common location, with ileocolic and colocolic variants also occurring. CT will demonstrate a bowel-within-bowel con guration o ten with either a target appearance when imaged transversely or a “sausage-shaped” mass containing mesenteric at and vessels when imaged longitudinally. The outer ring o so t tissue is the receiving segment (intussuscipiens). The enclosed mesenteric at and an inner ring o so t tissue is the mobile telescoped bowel segment (intussusceptum). In contrast to intussusceptions in adults involving the colon, which are associated with lead points, sm all bowel

205

Figure 14-24 Duodenal Adenocarcinoma A mass is noted narrowing the duodenum with adjacent adenopathy (arrow). The di erential diagnosis includes metastases, carcinoid, gastrointestinal stromal tumor, and lymphoma. Carcinoid tumors may demonstrate hyperenhancement. Lymph nodes metastases are rare in gastrointestinal stromal tumor. Lymphoma is more common in the distal small bowel.

intussusceptions are usually transient and nonobstructive, with no clinical signi cance. In particular, shorter nonobstructive intussusceptions (< 3.5 cm ) with a sm aller diam eter (< 3 cm ) tend to be idiopathic. A m inority o sm all bowel intussusceptions m ay be secondary to lead-point tum ors and require surgery. More than one-hal o colonic intussusceptions are associated with m alignant lesions such as adenocarcinom a and lym phom a. Benign lesions causing intussusception include lipom a and adenom atous polyp.

Small Bowel Tumors Small bowel neoplasms are relatively uncommon, with malignant small bowel tumors making up less than 2% o all gastrointestinal tumors. In addition, primary small bowel neoplasms are much less common than metastatic diseases.

Adenocarcinoma Greater than hal o small bowel adenocarcinomas occur in the duodenum (Figure 14-24) with a majority o remaining tumors ound in the jejunum. CT ndings include a short segment mass resulting in an annular stricture. This mass o ten results in an associated obstruction or serves as a lead point or intussusception. Adjacent lymphadenopathy is common.

Lymphoma Lymphoma o the small bowel is more common in the distal small bowel, in contrast to adenocarcinoma. Small bowel

206

Body CT: The Essentials

Figure 14-25 Bowel Lymphoma with Aneurysmal Dilatation Bowel wall thickening and aneurysm al dilatation o the term inal ileum is noted secondary to lym phoma. This may be secondary to replacem ent o the m uscularis propria and destruction o the autonom ic nerve plexus. Aneurysm al dilatation can also be seen in adenocarcinom a, gastrointestinal strom al tum or, and necrotic m etastases.

lymphoma can appear as an in ltrating lesion, a polypoid lesion, multiple nodular de ects, and an endoteric–exoteric mass with ulceration and stula ormation. The lumen can be widened rather than narrowed. This has been called “an urysmal d latat on” (Figure 14-25) and may be secondary to destruction o the muscle wall and myenteric plexus by in ltrating tumor. Lymphoma typically does not invoke a desmoplastic reaction and obstruction is relatively rare compared to other tumors o comparable size. Cavitation o a lymphomatous small bowel mass is more common than in adenocarcinoma and may result in an enteroenteric or enterocolonic stula. Bulky mesenteric and retroperitoneal lymphadenopathy on CT should raise the suspicion or the diagnosis o lymphoma.

Figure 14-26 Carcinoid CT enterography study dem onstrates m ural enhancem ent in thickened segm ent o ileum (arrow) along with a spiculated m esenteric m ass (arrowhead) adjacent to the abnorm ally thickened loop, consistent with ileal carcinoid with a m esenteric m etastasis. Without the sm all bowel abnorm ality, sclerosing m esenteritis could be considered in the di erential diagnosis.

Carcinoid tum ors can spread to the m esentery via direct extension or local lym phatics. These m etastases (Figure 14-26 ) present as spiculated or ill-de ned m esenteric m asses which m ay result in tethering o adjacent sm all bowel loops rom a resultant desm oplastic reaction. Central punctate calci cations (Figure 14-16 ) are com m on. A carcinoid m esenteric m etastasis m ost resem bles sclerosing m esenteritis, but desm oid tum or, GIST, sarcom a, lym phom a, or m etastases rom other prim aries are also in the di erential diagnosis. I m esenteric m etastases are visualized, the liver should be closely evaluated or additional m etastatic disease. Sm all bowel carcinoids are m ulticentric (Figure 14-27) in 20% to 30% o patients. Such patients are younger, have a signi cantly greater risk o developing carcinoid syndrom e, and generally have a poorer prognosis than patients with solitary lesions.

Carcinoid Tumors Carcinoid tumors are the most common primary small bowel tumor distal to the ligament o Treitz (second overall behind adenocarcinoma). The majority o gastrointestinal carcinoids are ound within 60 to 90 cm o the ileocecal valve; 50% are in the appendix and 33% in the small intestine. Carcinoids account or 50 % o all appendiceal tum ors. Appendiceal carcinoids rarely m etastasize and typically have a very indolent clinical course compared to carcinoids in other locations. They may be ound incidentally or present with appendicitis. Sm all bowel carcinoids m ay be di cult to detect when con ned to the bowel wall. Metastatic oci o carcinoid tum ors are generally m ore readily detected than the prim ary m ass on CT. The prim ary tum or m ay appear as a well-de ned enhancing m ural m ass that is better visualized with negative or neutral intralum inal contrast. It is not uncom m on or the prim ary tum or to be occult on CT.

Figure 14-27 Multi ocal Carcinoid CT enterography exam ination demonstrates m ultiple hypervascular m ucosal/ subm ucosal lesions (arrows) secondary to m ulti ocal carcinoid.

Chapter 14 Gastrointestinal Tract

Metastases Metastases to the sm all bowel have a range o appearances and result rom hem atogenous spread, direct invasion, or peritoneal seeding. Direct invasion o the sm all bowel rom pancreatic or colon cancer is not uncom m on. Malignancies spreading hem atogenously to the sm all bowel include bronchogenic and breast carcinom a and m elanom a. Mesenteric m etastases rom peritoneal carcinom atous m ay be seen with ovarian, gastric, or colon carcinom as and can result in tethering o the adjacent sm all bowel.

co l o n Anatomy The large intestine consists o the cecum , ascending colon, transverse colon, descending colon, sigm oid colon, and rectum . The junction between the colon and rectum has been arbitrarily de ned as 12 cm rom the anal verge by rigid protoscopy (as the surgical landm arks are not visualized by endoscopy). The rectosigm oid junction is roughly at the sacral prom ontory (anterior edge o the rst sacral segm ent). The ascending colon, descending colon, and lower one-third o the rectum are extraperitoneal. The cecum , ascending colon, and m ost o the transverse colon are supplied by the superior m esenteric artery. The descending colon, sigm oid colon, and upper rectum are supplied by the in erior m esenteric artery, whereas the lower rectum is supplied by the internal iliac arteries.

Normal Measurements The diam eter o the cecum m easures up to 9 cm . The transverse colon is usually less than 6 cm. The rem aining colon is usually sm aller in caliber than the transverse colon, although the caliber o the rectum varies greatly. The normal thickness o the colonic wall depends upon the degree o distension. In well-distended segments (> 4 cm), the thickness should be less than 3 mm. However, less than 5 mm is normal in segments between 2 and 4 cm in caliber, and 6 to 8 mm thickness may be normal in contracted segments.

Appendicitis Appendix Size and Appearance In healthy adults the appendix ranges rom 3 to 10 m m in size. Although a threshold diam eter o 6 to 7 m m has been used or the diagnosis o appendicitis, appendiceal diam eters between 6 and 10 m m as an isolated nding are indeterm inate as norm al appendices can be in this size range. Secondary signs such as at stranding are needed or the de nitive diagnosis o appendicitis when the appendix is in this size range. The presence o increased intralum inal uid is also help ul in distinguishing appendicitis rom a distended (6 –10 m m ) norm al appendix. I appendiceal intralum inal uid has a m axim um depth o greater than 2.6 m m , this suggests appendicitis (Table 14-2).

T b

207

14-2. CT Findings in Appendicitis

Siz > 10 mm Siz b w n 6 nd 10 mm, wi inc s d in lumin l uid (d a hy

ndic l w ll n

s cond y signs, o > 2.6 mm)

ick ning (> 3 mm)

nc m n , mu l s

if c ion

S cond y signs p i ndic l s nding ex lumin l uid ex lumin l, o in mu l i p l gmon, bsc ss C c l ick ning, c c l b , nd c c l

ow

d sign

Appendiceal wall thickening (> 3 m m ), hyperenhancem ent, and m ural strati cation are additional signs o appendicitis. On noncontrast im ages, 30 % o in am ed appendixes are hyperdense relative to the cecal wall. The presence o appendicoliths has a low positive predictive value or appendicitis; however, visualized appendicoliths in the setting o appendicitis are associated with a higher risk o per oration. The presence o contrast or gas in the appendix should not be used to exclude appendicitis. A sm all am ount o contrast or gas can enter an in am ed appendix i the obstruction is not at the base, and gas can be present because o gas- orm ing m icroorganism s. However, intram ural or extralum inal air are signs o appendicitis. Appendicitis is very unlikely i the appendix cannot be visualized and there are no in am m atory ndings.

Secondary Signs In a prescreened population, periappendiceal at stranding had a sensitivity o 87% and a speci city o 74% or appendicitis. Thickening o the lateral conal ascia, extralum inal uid, phlegm on, and abscess are other signs. These signs m ay not be speci c as other right lower quadrant in am m atory disorders can result in these ndings. Focal in am m atory thickening o the cecum has a sensitivity o 6 9 % and is m ost com m only seen in the apex. Circum erential cecal thickening is less likely to be caused by appendicitis, instead it suggests colitis. I positive contrast is adm inistered, other cecal signs (Figure 14-28) are the “c cal arrowh ad” s n ( unneling o the cecal contrast or air toward the appendiceal origin) and “c cal bar” s n (in am ed cecal wall between the cecal lum en and the appendix). Both these signs are insensitive.

Perforated Appendicitis Signs o per orated appendicitis (Figure 14-29) include phlegmon, abscess, extraluminal gas, extraluminal appendicolith,

208 Body CT: The Essentials

Figure 14-30 Tip Appendicitis Appendicitis is noted involving only the tip o the appendix. The m ore proxim al appendix (arrow) appears norm al.

Figure 14-28 Appendicitis Appendicitis with an obstructing appendicolith dem onstrates m ultiple signs o appendicitis: dilated appendix, increased intralum inal uid, periappendiceal at stranding, cecal bar sign (in am ed cecal wall between the cecal lum en and the appendix) (arrow) and cecal (arrowhead) sign ( unneling o contrast or air toward the appendiceal origin) (arrowhead).

and ocal de ect in the enhancement o the appendiceal wall. The presence o an appendicolith is associated with a greater risk o per oration. Larger appendiceal diameters are also associated with per oration, with a mean diameter o 15 mm noted in per orated appendicitis. Abscess and extraluminal air are the most speci c signs o per oration, but have low sensitivity.

Figure 14-29 Per orated Appendicitis An extralum inal appendicolith and right lower quadrant abscess are noted secondary to per orated appendicitis. Abscess and extralum inal air are the m ost speci c signs o per orated appendicitis, but have low sensitivity.

Pitfalls The entire appendix m ust be visualized to exclude tip appendicitis (Figure 14-30 ). Other right lower quadrant in ectious and in ammatory conditions can potentially mimic appendicitis on imaging, but typically can be di erentiated on the basis o imaging ndings speci c to each disorder. These potential mimics include CD, right-sided, or speci cally appendiceal diverticulitis, in ectious enterocolitis, and tubo–ovarian abscess.

Mucocele o the Appendix A m ucocele re ers to a dilated appendix with abnorm al intralum inal accum ulation o m ucus, secondary to obstruction

Figure 14-31 Appendiceal Mucocele A tubular cystic structure (arrow) contiguous with the cecum is consistent with an appendiceal m ucocele. Etiologies include m ucosal hyperplasia, m ucinous cystadenom a, and m ucinous cystadenocarcinom a. The presence o curvilinear m ural calci cation is help ul in m aking the diagnosis o m ucocele, but is present in less than 50% o cases.

Chapter 14 Gastrointestinal Tract

Figure 14-32 Right Colonic Diverticulitis In am m ation o a right colonic diverticulum (arrow) is noted, secondary to diverticulitis. Right colonic diverticulitis has a m uch higher prevalence in Asian countries (accounting or up to 75% o cases) and patients o ten present at a younger age com pared to those with le t-sided disease.

o the lum en. A sim ple m ucocele results when the obstruction is nonneoplastic with norm al m ucosa. Mucoceles can also be caused by m ucosal hyperplasia, m ucinous cystadenom a, and cystadenocarcinom a. On CT, m ucoceles (Figure 14-31) typically appear as well-circum scribed tubular or spherical m asses o low attenuation, contiguous with the cecal base. The presence o curvilinear m ural calci cation suggests the diagnosis but is seen in less than 50 % o cases. Intralum inal gas suggests superin ection. Appendicitis with associated m ucocele can be di cult to di erentiate rom appendicitis without m ucocele. Cystic dilatation o the appendix, m ural calci cation, and lum inal diam eter greater than 1.3 cm suggests an associated m ucocele in a patient with appendicitis.

Diverticulitis Mostly 9 0% o cases o diverticulitis in Western countries occur in the le t colon, prim arily in the sigmoid. Right colonic diverticulitis (Figure 14-32) has a m uch higher prevalence in Asian countries (accounting or up to 75% o cases) and patients o ten present at a younger age com pared to those with le t-sided disease. Pericolonic in am m ation is seen in virtually all cases o diverticulitis. Focal colonic wall thickening is very com m on, and can be eccentric or circum erential. H owever, circum erential wall thickening can also be seen with m uscular wall hypertrophy in diverticulosis. Diverticula are noted in 84% to 9 7% o cases o diverticulitis, and

209

Figure 14-33 Diverticulitis with Fistulas Sigm oid diverticulitis is noted with stulas to the uterus (black arrow) and vagina (white arrow).

an in am ed diverticulum is seen in 30 % o cases. Fascial thickening near the pelvic side wall m ay be an early sign o diverticulitis. Engorged vessels supplying the in am ed segm ent can also be seen. I positive contrast is adm inistered, an associated nding in diverticulitis is the “arrowh ad” s n, also seen in appendicitis (Figure 14-28). Contrast is unneled toward the apex o the in am ed diverticulum , creating an arrowhead-shaped collection o contrast. Com plications o diverticulitis, such as abscess, per oration, and stula (Figure 14-33) are well dem onstrated by CT. Mim ics o diverticulitis include carcinom a, epiploic appendagitis, and ischem ic colitis.

Diverticulitis Versus Carcinoma Diverticulitis and colon cancer can som etim es be di cult to di erentiate by CT. The m ost help ul di erentiating ndings are the presence o nonin am ed and in am ed diverticula, m ild degree o enhancem ent, target enhancem ent pattern, pericolonic in am m ation, abscess orm ation, ree air and length greater than 10 cm in diverticulitis, and pericolonic lym ph nodes (Figure 14-34) and lum inal m ass in colon cancer. Pericolonic in am m ation out o portion to the degree o bowel thickening is the m ost speci c nding or diverticulitis. In right-sided diverticulitis the m ost help ul ndings in di erentiating the disease rom colon cancer are preserved wall enhancem ent and in am ed diverticula (Table 14-3).

210

Body CT: The Essentials

Figure 14-34 Colon Cancer Thickening o the sigm oid colon is noted secondary to colon cancer. Enlarged nodes adjacent to the thickened colon (arrow) suggest the diagnosis o colon cancer, as nodal enlargem ent is not typically seen in diverticulitis. In addition, discrete diverticula are not noted.

T b

14-3. Diverticulitis versus Colon Cancer Div

iculi is

Colon C nc

p icolonic in mm ion (ou o o o ion o bow l w ll ick ning)

+

-

p icolonic d m

+

-

Fluid oo o m s n y

+

-

L ng

+

-

+

-

M s n ic v scul ngo g m n

+

-

S w oo us ick ning

l

+

-

a ow d-s ick ning

d w ll

+

-

+

-

+

-

-

+

-

+

-

+

+ /-

+




+

-

ex

In

> 10 cm lumin l i o

m d div

uid

icul

p s v d w ll n nc m n

n

Lumin l m ss p icolonic lym S ould

nod s

o m ion

L ng

< 5 cm

D g

o

n

t g

n

nc m n

n

nc m n

Figure 14-35 Epiploic Appendagitis An in am ed or in arcted epiploic appendage is noted with a “hyperattenuating ring” sign (arrow) secondary to in am ed visceral peritoneum . The anterior border o the sigm oid colon is the m ost com m on location or epiploic appendagitis. The at stranding is greater than the colonic wall thickening in this case, which is help ul in di erentiating epiploic appendagitis rom other colonic in am m atory processes.

Epiploic Appendagitis Epiploic appendices are peritoneal pouches arising rom the serosal sur ace o the colon, containing adipose tissue and blood vessels. These appendices can undergo torsion with resulting ischemia and in arction. Epiploic appendagitis most commonly mani ests in men in the ourth to th decades o li e. It is most common in the sigmoid colon (53%), ollowed by the descending colon and right hemicolon. An in amed or in arcted epiploic appendage appears as a 1- to 4-cm ovoid at-density lesion abutting the anterior colonic wall. A relatively speci c sign is the “hyp ratt nuat n r n ” (Figure 14-35) s n, which is a 2- to 3-mm hyperdense rim surrounding the ovoid mass. This represents in amed visceral peritoneum covering the appendage. Another relatively speci c sign is the “c ntral dot” s n which is a central hyperattenuating round or linear area corresponding to engorged or thrombosed central vessels. However, the absence o these signs does not exclude epiploic appendagitis. One help ul sign in di erentiating epiploic appendagitis rom other in am m atory processes is that at stranding is m ore pronounced than wall thickening (wall thickening is typically asym m etric i present). Epiploic appendagitis should be di erentiated rom diverticulitis, appendicitis, m esenteric panniculitis, and om ental in arction.

Chapter 14 Gastrointestinal Tract

211

is most com m only seen adjacent to the sigm oid colon. Omental in arctions typically lack a hyperattenuating rim. In some cases, it m ay not be possible to di erentiate the two entities, but both conditions are sel -lim ited.

Ischemic Colitis

Figure 14-36 Omental In arction Stranding is present anterior to the right transverse colon (arrow). Compared to epiploic appendagitis, omental in arction is typically larger, right sided, and does not have a hyperattenuating ring.

Omental Infarction Om ental in arctions (Figure 14-36 ) are rare and usually idiopathic, but can m im ic the appearance o epiploic appendagitis. They typically involve the right-sided epiploic vessels. Unlike epiploic appendagitis, omental in arctions are occasionally seen in pediatric patients. The lesion in omental in arction is typically larger than the lesion in epiploic appendagitis. Om ental in arctions typically occur next to the cecum and ascending colon, whereas epiploic appendagitis

Ischem ic colitis (Figure 14-37) typically occurs in elderly patients due to a sudden loss o blood ow. Nonocclusive ischem ia secondary to low- ow states is m ore com m on than ischem ia secondary to arterial or venous occlusive disease. In m any cases, the colitis develops a ter the lowow episode has resolved and the colonic changes are secondary to reper usion. The m ost vulnerable areas are the splenic exure at the junction between the superior m esenteric artery and in erior m esenteric artery distributions, and the sigm oid colon at the junction between the in erior m esenteric artery and hypogastric artery distributions. The distribution and length o bowel wall thickening are the prim ary diagnostic criteria or ischem ic colitis. The length o the segm ent involved is typically 10 cm or m ore, with a m ean a ected length o 19 cm . The distribution is segm ental without discontinuity. The descending and sigm oid colon are the m ost com m only involved areas, with splenic exure involvem ent o ten seen in conjunction. Right-sided ischem ic changes are m ore typical in younger patients a ter hem orrhagic shock rom traum a. The appearance o the ischem ic colon depends on the stage and severity o the process. A colon segm ent with a super cial m ucosal injury m ay be spastic and could be m isinterpreted as contraction. Bowel wall thickening, thum bprinting, pericolonic stranding, and ascites are nonspeci c signs o ischem ic colitis. Mural strati cation, hom ogeneous wall attenuation, or bowel wall hem orrhage can be seen. I there is in arction, the colon m ay be dilated with a thin unenhanced wall. Pneum atosis and venous gas are also signs o bowel in arction. Ischem ic changes o the rectum are rare due to collateral blood supply. Thus sparing o the rectum avors ischem ic colitis over other orm s o colitis. However, elderly patients with atherosclerosis and predisposing actors such as hem odynam ic disturbance can develop ischem ic protosigm oiditis. In addition, cocaine users can develop ischem ia in the right colon or the rectosigm oid colon. Rarely, isolated cecal ischem ia can occur i the cecal arteries arise directly rom the ileal or colic artery.

Inf ammatory Bowel Disease

Figure 14-37 Ischemic Colitis Coronal CT dem onstrates colonic wall thickening and pericolonic stranding involving a long segm ent o the descending colon (arrowhead) extending to the splenic exure.

In am m atory bowel disease o ten presents in patients in their early 20 s but late onset can be seen in the 6 0 s or 70 s. The usual absence o ascites in in am m atory bowel disease is help ul in di erentiating it rom in ectious colitis in which ascites is com m on. CD (Figure 14-38) and UC (Figure 14-39 ) have som e distinguishing im aging eatures.

212 Body CT: The Essentials

Distribution UC is typically le t sided or di use, whereas CD is typically right sided or di use. The rectum is alm ost always involved in UC, but can be spared in CD. Proli eration o perirectal at with increased attenuation is o ten seen in UC. The term inal ileum in UC can be thin walled and dilated due to backwash ileitis, whereas the term inal ileum in CD can be thickened and narrowed.

Bowel Wall

Figure 14-38 Crohn Disease Enhancement o the term inal ileum (arrow) and sigm oid colon (arrowhead) is noted in patient with active Crohn disease. A “double halo” pattern o enhancem ent is noted, along with prom inent vasa recta supplying the abnorm al bowel loops (“com b” sign).

The degree o bowel wall thickening in CD is usually greater than in UC. CD, along with pseudom em branous colitis, produces the m ost severe degree o wall thickening am ong all types o colitis. The wall thickening in UC is usually sym m etric and continuous. The wall thickening in CD is usually asym m etric (along the m esenteric border), with skip areas. Pseudodiverticula can be seen along the antim esenteric border. The “water halo” sign (Figures 14-1, and 14-2), is seen in both CD and UC and represents active disease. Hom ogeneous bowel wall enhancem ent in CD suggests quiescence. The presence o intram ural at (“ at halo” sign) (Figure 14-3) indicates past or chronic in am m ation. However, intram ural at in the colon and term inal ileum can be a norm al variant i the bowel otherwise appears norm al. CT enterography is best suited to evaluate the bowel wall in CD. CTE ndings o bowel wall thickening, mural strati cation, mural hyperenhancement, increased perienteric at attenuation, and engorged vasa recta correlate with active CD. Mural hyperenhancement is the most sensitive sign o active CD.

Other Findings The “comb” s n describes engorged m esenteric vessels supplying the bowel wall. Although associated with CD, this sign can be seen with any cause o bowel wall in am m ation, but it is not usually seen in carcinom a. In am m atory adenopathy is m ore com m only seen in CD than in UC. However, as patients with CD have an increased risk o lym phom a and carcinom a, the possibility o neoplasm should also be considered. Fibro atty proli eration o the m esentery (creeping at) (Figure 14-3) is associated with CD.

In ectious Colitis

Figure 14-39 Ulcerative Colitis Thickening o the descending and sigm oid colon is noted (arrows) with a norm al-appearing right colon. This appearance is m ore typical o ulcerative colitis which is usually di use or le t sided. Crohn disease is usually di use or right sided.

In ectious colitis typically has CT eatures o wall thickening, pericolonic stranding, and ascites. Pancolitis is common, however, predominant right-sided (with or without ileum involvement) and le t-sided involvement are also seen. The various etiologies usually cannot be di erentiated on CT. A ew orm s o in ectious colitis have m ore speci c ndings. Tub rculos s can m im ic CD. The nodes are typically larger in tuberculosis, and separation o the bowel loops is due to these enlarged nodes rather than the broatty in ltration seen in CD. Mural strati cation is typically

Chapter 14 Gastrointestinal Tract

Figure 14-40 Pseudomembranous Colitis Di use severe colonic wall thickening (arrows) is noted along with ascites. Pseudom embranous colitis (PMC) and Crohn disease (CD) result in the m ost severe bowel wall thickening o all the types o colitis. The severity o the wall thickening is help ul in distinguishing PMC rom other types o colitis. The ascites and extent o involvem ent are im aging ndings which distinguish PMC rom CD.

not seen in tuberculosis. Am ebiasis can produce a coneshaped cecum without ileal involvem ent. Ps udom mbranous col t s (PMC) (Figure 14-40) is due to the overgrowth o Clostridium dif cile a ter the use o antibiotics. Untreated, it can result in toxic megacolon or per oration. PMC o ten mani ests as a pancolitis, but can also be right sided, or start in the rectum and then involve the le t colon. PMC produces one o the most severe degrees o wall thickening o all the types o colitis, with the exception o CD. CT ndings include a markedly thickened colonic wall with low attenuation, thumbprinting, pericolonic stranding, and ascites. I positive contrast is administered, the “accord on” s n can be noted due to contrast trapped between thickened haustral olds. Although this nding suggests PMC, it is not speci c and can be seen with any cause o severe bowel wall thickening. The severity o the bowel wall thickening helps di erentiate PMC rom other orms o colitis, and the presence o ascites is help ul in di erentiating PMC rom CD. N utrop n c col t s (typhlitis) is seen in im m unosuppressive conditions. The typical CT ndings o colitis, wall thickening, pericolonic stranding, and uid are noted, but the ndings are con ned to the right colon, o ten involving the ileum as well.

Toxic Megacolon Toxic m egacolon (Figure 14-41) is a li e-threatening com plication o severe acute colitis. Although typically associ-

213

Figure 14-41 Toxic Megacolon Dilatation o the transverse colon, wall thinning, dim inished haustral pattern, and multiple nodular pseudopolyps (arrows) are present in a patient with in am m atory bowel disease and toxic m egacolon.

ated with in am m atory bowel disease, toxic m egacolon can com plicate in ectious colitis o diverse causes, PMC, ischem ic colitis, and obstructive colon cancer. Toxic m egacolon is typically diagnosed on radiography. CT ndings o toxic m egacolon include dilatation, m ost com m only o the transverse colon (> 6 cm ), loss o the norm al haustral pattern, segm ental wall thinning, and nodular pseudopolyps.

Sigmoid Volvulus Sigm oid volvulus accounts or 6 0 % to 75% o all cases o colonic volvulus. The typical signs o sigm oid volvulus can o ten be seen on the scanogram . These include a “co eebean” shape o the dilated sigm oid (the central line o the bean is the apposed loops o the ascending and descending sigm oid), and cephalic extension o the sigm oid colon in relation to the transverse colon (the “north rn xposur ” s n) (Figure 14-42). Proxim al colonic dilatation is noted in approxim ately hal o the cases. On CT, the whirl sign can be noted due to volvulus in any location. A whirl sign to the le t o m idline is highly accurate in di erentiating a sigm oid rom a cecal volvulus, in which the whirl sign is to the right o m idline. In suspected sigm oid volvulus, the identi cation o two transition points on CT would be m ore speci c, but this is only identi ed in slightly m ore than hal o the cases. There are other CT signs o volvulus. I two lim bs o a bowel loop orm a com plete twist, the site o the twist m ay be visualized on CT as two crossing transition points oriented in opposite directions, called the “x marks th spot” s n (Figure 14-43). I there is twisting o a single lim b, a “spl twall” s n (Figure 14-42) m ay be seen where the single loop

214

Body CT: The Essentials

A Figure 14-42 Sigmoid Volvulus Scanogram (A) dem onstrates the “northern exposure” sign with cephalic extension o the “co ee bean” shaped dilated sigm oid colon superior to the transverse colon, secondary to sigm oid

B volvulus. Arrow in (B) dem onstrates the “split wall” sign with m esenteric at between decom pressed bowel at the site o the twist in a single loop. The “split wall” and “x m arks the spot” sign can be seen in sigm oid and cecal volvulus.

at the site o the twist appears as two decom pressed bowel loops separated by m esenteric at.

Cecal Volvulus Cecal volvulus accounts or 25% to 40% o all cases o colonic volvulus. Typical signs o cecal volvulus can o ten be seen on the scanogram. The cecum is distended more than 10 cm, and is o ten directed toward the le t upper quadrant. The “cof b an” s n (Figure 14-44) described in sigmoid volvulus has also been described in cecal volvulus; in this case, the line o the co ee bean is secondary to haustration at the ileocecal valve. The distal colon is usually decompressed. The CT whirl sign is to the right o the m idline in cecal volvulus. Two transition points are m ore speci c, but a single transition point is o ten seen. The “x m arks the spot” and “split wall” signs are insensitive but speci c signs in cecal volvulus. The ileum is involved in the torsion in approxim ately hal o the cases o cecal volvulus.

Lipoma Figure 14-43 Sigmoid Volvulus Two crossing transition points oriented in orthogonal directions are noted (arrow) in a patient with sigm oid volvulus. This “x m arks the spot” sign can be seen in sigm oid and cecal volvulus and is secondary to two lim bs o a bowel loop orm ing a com plete twist.

The colon is the m ost com m on site o bowel lipom as, ollowed by the sm all bowel and stom ach. The cecum is the m ost com m on location, ollowed by the right colon. Colonic lipom as (Figure 14-45) are usually solitary. On CT, lipom as appear as a hom ogeneous m ass with Houns eld

Chapter 14 Gastrointestinal Tract

A

215

B

Figure 14-44 Cecal Volvulus A. A dilated cecum with a “co ee bean” shape is noted in a patient with cecal volvulus. The “co ee bean” sign can be seen

in both sigm oid and cecal volvulus. B. A right-sided “whirl” sign (arrow) is noted along with a dilated cecum (arrowhead); in sigm oid volvulus the “whirl sign” is to the le t o m idline.

units between –80 and –120 . Lipom as are usually ound incidentally, but can cause intussusception, and lipom as greater than 2 cm can ulcerate and result in anem ia. Intussuscepted lipom as m ay show som e loss o at density which can obscure the diagnosis. In the ileocecal valve, lipom atosis which has an appearance o sym m etric enlargem ent is m uch m ore com m on than a true lipom a o the valve.

o ten non-Hodgkin lym phom a o B-cell origin) m ost o ten a ects the cecum and rectum . Features that are help ul in distinguishing lym phom a rom adenocarcinom a are term inal ileum extension, well-de ned m argins with preserved at planes, and lack o invasion into adjacent structures. Lym phom a is less likely to cause obstruction as it does not elicit a desm oplastic response.

Lymphoma

Colorectal Cancer

Colorectal lym phom a is rare, constituting 6 % to 12% o gastrointestinal lym phom as. Prim ary lym phom a (m ost

The sensitivity o standard CT or the detection o prim ary colorectal cancer (CRC) is variable and dependent upon tum or size. CRC can appear as a discrete so t tissue m ass narrowing the colonic lum en, a necrotic m ass resem bling an abscess, or ocal wall thickening. Diverticulitis is som etim es in the di erential diagnosis; the im aging eatures in Table 14-3 m ay be help ul to di erentiate cancer rom diverticulitis. Com plications o prim ary colonic m alignancies include obstruction, abscess, and stula, all o which can be readily diagnosed by CT. Pericolonic tum or extension (T3) disease can be suggested by blurring o the surrounding at planes; however, this nding is very nonspeci c. In one system atic review, CT had a sensitivity o 77% and a speci city o 3% or T-staging o colon cancer. However, CT m ay have better accuracy or diagnosis o T4 disease, such as invasion o other organs. For nodal (N) staging, CT had a sensitivity o 76 % and a speci city o 55%. The prim ary value o CT is in detection o distant m etastasis. The liver is the prim ary organ to be involved

Figure 14-45 Colon Lipoma A lipom a (arrow) in the transverse colon is noted.

216

Body CT: The Essentials

with m etastases rom CRC. In a m eta-analysis o prospective studies, CT had a sensitivity o 74% on a per-lesion basis, and 84% on a per-patient basis or liver m etastasis. However, CT m ay be less sensitive or sm all (< 1 cm ) liver m etastasis than MRI. Distal rectal cancer can produce isolated pulm onary m etastases without liver m etastases, as the m iddle and in erior hem orrhoidal veins drain into the in erior vena cava (the superior hem orrhoidal vein drains into the portal vein). The accuracy o CT detection o peritoneal carcinom atosis depends on tum or size and location, and is poor or sm all peritoneal im plants.

CT Colonography CT Colonography (CTC) is a minimally invasive technique or the detection o CRC. CTC may be per ormed or screening in the average risk asymptomatic population greater than 50 years o age or or evaluation o patients presenting with symptoms such as bleeding and altered bowel habits. It is an option or patients with incomplete optical colonoscopy (OC) and those at increased risk or sedation complications. Contraindications to CTC include acute colitis or diverticulitis, recent deep endoscopic biopsy, and recent colorectal surgery. Protocols or CTC balance optim izing detecting true lesions with m aintaining low-radiation dose. Patient preparation includes cathartics or colon cleansing. Solid and liquid stool tagging is increasingly used to di erentiate polyp rom stool (Figure 14-46 ). Carbon dioxide or room air is insuf ated to distend the colon. The patient is scanned in the supine, prone, and i necessary, one o the decubitus positions to m axim ize visualization o the m ucosal sur ace. Antispasm olytics such as glucagon m ay be used. Multide-

Figure 14-46 Cecal Polyp 2D im age rom CT colonography per orm ed with solid and liquid stool tagging reveals a sessile polyp (arrow) in the cecum subm erged in the contrast pool. 2D and 3D search m ethods are com plem entary or interpretation.

Figure 14-47 Sessile Polyp 3D virtual endoscopic view CT colonography dem onstrates a sessile polyp (arrow) at the splenic exure.

tector (≥ 4 slice) CT im ages are acquired with ≤ 3 m m slice thickness and ≤ 2 m m reconstruction interval. The primary targets o CTC are large (≥ 10 mm) polyps, or which OC with polypectomy is recommended. Sensitivity o CTC or large polyps is ≥ 9 0 %. The 3% rate or detection

Figure 14-48 Pedunculated Polyp 3D virtual endoscopic view dem onstrates a pedunculated polyp in the sigm oid colon. The diam eter o the head (white arrow) should be m easured, excluding the stalk (black arrow).

Chapter 14 Gastrointestinal Tract o advanced neoplasia by screening CTC is sim ilar to the rate by OC. Up to 70% o patients have extracolonic ndings at screening CTC. The m ajority o incidental ndings at screening CTC are clinically insigni cant, but workup o incidental lesions m ay increase the potential or patient harm and incur additional cost. Two dimensional (2D) and 3D search methods are com plem entary or interpretation. Adequate colonic distention is important or detection o polyps as well as circum erentially in ltrating masses. 2D im ages are viewed with a colon setting (window o 2000 H U and level o 0 H U) or lesion detection, but so t tissue windows con rm the diagnosis o lipom as. 3D virtual endoscopy views allow intralum inal assessm ent visually similar to OC. Size, m orphology, and location o each lesion are reported. Polyps can be sessile (Figure 14-47), pedunculated (Figure 14-48), or at. A CT Colonography Reporting and Data System (C-RADS) has been developed to prom ote standard reporting, but im plem entation o C-RADS and m anagem ent or polyps less than 1 cm is variable among institutions. For sm all (6 –9 m m) polyps, the patient m ay be re erred to OC or surveillance CT. The Am erican College o Radiology does not currently advocate the reporting o diminutive (≤ 5 m m ) polyps is necessary due to the extrem ely low likelihood o CRC.

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s

Eugene Lin, MD

I. ANATOMY a. Contents b. Peritoneal Space: Broad Divisions c. Supramesocolic Compartment i. Right supramesocolic space ii. Lesser sac iii. Left supramesocolic space d. Greater Omentum/ Gastrocolic Ligament e. Transverse Mesocolon . Small Bowel Mesentery g. Sigmoid Mesocolon II. DISTRIBUTION OF FLUID III. PERITONEAL ENHANCEMENT IV. HEMOPERITONEUM V. PERITONEAL CALCIFICATION VI. DIFFUSE SOLID PERITONEAL DISEASE

An At o m y Contents The peritoneum is a m esothelial m em brane which lines the inner sur ace o the abdom inal cavity (parietal peritoneum ) and extends to cover som e o the solid organs and m ost o the bowel (visceral peritoneum ). The peritoneal cavity is a potential space between these layers which contains a sm all am ount (50–100 cc) o serous uid. In practice, the term “intraperitoneal” is used to re er to both the peritoneal cavity, and to organs and bowel which are covered by visceral peritoneum . However, “intraperitoneal” organs and bowel are covered by visceral peritoneum but not actually in the peritoneal cavity which is a potential space between the parietal and visceral peritoneum . I trap rito Liver Spleen Ovaries

al str ct r s:

a. b. c. d. e. . g.

Peritoneal Carcinomatosis Peritoneal Tuberculosis Malignant Peritoneal Mesothelioma Peritoneal Lymphomatosis Peritoneal Sarcomatosis Desmoplastic Small Round Cell Tumor Serous Sur ace Papillary Carcinoma o the Peritoneum VII. CYSTIC PERITONEAL MASSES a. Di erential Diagnosis b. Pseudomyxoma Peritonei VIII. SOLID MESENTERIC MASSES a. Di erential Diagnosis b. Sclerosing Mesenteritis c. Mesenteric Fibromatosis/ Desmoid Tumor

Stom ach, rst portion o the duodenum , jejunum , ileum , cecum , appendix, transverse colon, sigm oid colon, and upper two-thirds o rectum . The double layer in oldings o visceral peritoneum which suspend organs and bowel are known as ligam ts, om ta, a d m s t ri s. These provide structural support, and are conduits or vascular and nerve supply. This has been re erred to as the s bp rito al space, and provides a network o connections between the peritoneum and extraperitoneum .

Peritoneal Space: Broad Divisions The transverse m esocolon divides the peritoneal cavity into supram esocolic and in ram esocolic com partm ents (Figure 15-1). The supram esocolic com partm ent consists o the right and le t supram esocolic com partm ents, and the lesser sac. The in ram esocolic com partm ent is divided into the abdom inal and pelvic regions by the sigm oid m esocolon.

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Body CT: The Essentials BA

L GP C

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L LO

LS GS L LO

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IVC

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M T

Figure 15-2 Axial View o Abdomen Ao, aorta; GPC, greater peritoneal cavity; GSL, gastrosplenic ligam ent; IVC, in erior vena cava; L, liver; LO, lesser om entum ; LS, lesser sac; LK, le t kidney; RK, right kidney; S, stom ach; SP, spleen; SRL, splenorenal ligam ent.

GC TC SB G R

Right Supramesocolic Space

UT

B

PD

Pu

The right com partm ent can be divided into s bphr ic and s bh patic spaces, but these spaces com m unicate reely. The portion o this space situated between the posterior liver and anterior right kidney is called the h pator al fossa or Moriso po ch.

Figure 15-1 Sagittal View o Abdomen and Pelvis Ao, aorta; B, bladder; BA, bare area; D, duodenum , G, greater om entum ; GC, gastrocolic ligament; L, liver; LO, lesser om entum ; LS, lesser sac; P, pancreas; PD, pouch o Douglas; Pu, pubis; R, rectum ; S, stomach; SB, sm all bowel; TM, transverse m esocolon.

The abdom inal in ram esocolic com ponent is divided in the right and le t regions by the sm all bowel m esentery. The right a d l ft paracolic g tt rs are part o the in ram esocolic com partm ent. The m ost in erior portion o the peritoneal cavity is the r cto t ri po ch (po ch of Do glas) in em ales, and the r ctov sical po ch in m ales.

Supramesocolic Compartment There are three m ajor regions in the supram esocolic com partm ent, right and le t, and the lesser sac (the lesser sac is som etim es included in the right com partm ent) (Figure 15-2). These are divided by two sets o roughly vertically oriented ligam ents, the alci orm ligam ent and lesser om entum (gastrohepatic and hepatoduodenal ligam ents) on the right, and the phrenicocolic, splenorenal, and splenocolic ligam ents on the le t (Figure 15-3). The le t-sided gastrosplenic ligam ent is part o the greater om entum .

Figure 15-3 Le t-Sided Ligaments The gastrosplenic (arrowhead) and splenorenal ligam ents (arrow) are noted in a patient with gastric cancer and ascites. The phrenicocolic ligam ent is absent or underdeveloped; i present, it o ten lim its cephalic extension o uid rom the pelvis in the le t peritoneal space.

Chapter 15 Peritoneum and Peritoneal Spaces

Figure 15-4 Bare Area o Liver Ascites extends around the liver except or the bare area (arrow). Fluid in this region would be secondary to a pleural ef usion.

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Figure 15-5 Falci orm Ligament The alci orm ligam ent (arrow) is noted in a patient with severe ascites.

A portion o the right lobe o the liver is directly attached to the diaphragm and posterior abdominal wall, without intervening peritoneum. This area o direct attachment is called the bar ar a (Figure 15-4). The peritoneal re ections at the margins o the bare area are the coro ary ligam ts. As ascites cannot extend posterior to the liver in the region o the bare area, uid in this region is usually pleural. The bare area can also communicate with the right perirenal space. The falciform ligam t (Figure 15-5) separates the right and le t subphrenic spaces; however, it is only an incom plete barrier to the spread o uid between these two spaces. The alci orm ligam ent connects the anterior abdom inal wall to the le t liver and extends in eriorly to the

level o the um bilicus. The base o the alci orm ligam ent contains between its layers the ro d ligam t (ligam t m t r s) and the paraum bilical veins. The alci orm ligam ent is contiguous with the coronary ligam ents over the diaphragm atic sur ace. In addition, the alci orm ligam ent is contiguous with the hepatoduodenal ligam ent. This is a route or pancreatic in am m ation to spread through the gastrohepatic ligam ent to the alci orm ligam ent, resulting in Cullen sign around the um bilicus. The l ss r om t m suspends the lesser curvature o the stomach and the proxim al duodenum rom the liver. It com prises the gastrohepatic and hepatoduodenal ligam ents. The gastroh patic ligam t (Figure 15-6 ) contains the le t

A

B

Figure 15-6 Gastrohepatic Ligament In ltration o the gastrohepatic ligam ent is noted in a patient with gastric cancer. A. In ltration o the gastrohepatic ligam ent (arrowhead) extends into the contiguous ssure or

the ligam entum venosum (arrow). B. The le t gastric artery (arrow) lies in the gastrohepatic ligam ent and is irregular due to surrounding tum or in ltration.

222 Body CT: The Essentials

A

B

Figure 15-7 Lesser Sac Anatomy Positive oral contrast is noted in the lesser sac in a patient with gastric per oration. A. Coronal CT im age dem onstrates the superior (black arrow), in erior (arrowhead) and splenic (white arrow) recesses o the lesser sac. B. Contrast is present in the in erior recess o the lesser sac (arrow) between the pancreas and the stom ach. C. The superior recess (white arrow) is noted extending around the caudate lobe, distinct rom the gastrohepatic ligam ent (black arrow). The splenic recess (arrowhead) is also noted. C

gastric artery and vein, and lymph nodes. It attaches to the ssure or the ligam entum venosum . The gastrohepatic ligam ent can be identi ed on CT by identi ying the le t gastric artery and contiguity with the ssure or the ligam entum venosum . The h patod od al ligam t carries the portal triad; it is the caudal ree edge o the gastrohepatic ligam ent, and extends rom the second portion o the duodenum to the porta hepatis. Pancreatic disease can spread to the porta hepatis and liver via the hepatoduodenal ligament.

Lesser Sac The lesser sac (Figure 15-7) is between the posterior gastric wall and pancreas and is typically collapsed on CT. The lesser sac is covered anteriorly by the lesser om entum , which orm s the boundary between the right subhepatic space and the lesser sac. The s p rior r c ss of th l ss r sac extends around the caudate lobe; uid in the superior recess should be distinguished rom gastrohepatic

ligam ent disease. The i f rior r c ss of l ss r sac typically extends slightly below the transverse colon. The spl ic r c ss of th l ss r sac lies at the hilum o the spleen. The lesser sac com m unicates with the rest o the peritoneal space (gr at r sac) via the foram of Wi slow which is about 3 cm in size, anterior to the in erior vena cava, posterior to the hepatoduodenal ligam ent, caudal to the caudate lobe, and cephalad to the duodenal bulb. Fluid in the lesser sac is usually secondary to extension o greater sac ascites. Isolated lesser sac uid could be a postoperative nding a ter gastric or hepatobiliary surgery, or can be related to pancreatitis, cholecystitis, or gastric peroration.

Left Supramesocolic Space The le t supram esocolic space is less com plex. It can be divided into the le t perihepatic, le t subphrenic, and perisplenic spaces, but these spaces all comm unicate. Below

Chapter 15 Peritoneum and Peritoneal Spaces

Figure 15-8 Bare Area o Spleen Fluid com pletely surrounds the spleen except or the “bare area” (arrow). Fluid posterior to the bare area (arrowhead) is in the pleural space.

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abdom inal cavity. The greater om entum can be identi ed on CT by ollowing the gastroepiploic arteries and veins and their in erior epiploic branches. The greater om entum attaches to the superior transverse colon. This portion o the om entum between the caudal stom ach and transverse colon is known as the gastrocolic ligam t or s pracolic ligam t (Figure 15-9 ). The gastrocolic ligam ent is anterior to the in erior portion o the lesser sac (above the gastrocolic ligam ent the anterior portion o the lesser sac is orm ed by the stom ach and lesser om entum ). The greater om entum is contiguous with the gastrosplenic ligam ent on the le t and the transverse m esocolon at the transverse colon. The greater om entum is a com m on site or peritoneal carcinom atosis. Gastric cancer can spread directly through the gastrocolic ligam ent, and pancreatic disease can spread through the m esocolon into the om entum .

Transverse Mesocolon

The greater om entum hangs in eriorly rom the greater curvature o the stom ach, extending over the anterior

The transverse m esocolon suspends the transverse colon in the abdom inal cavity and separates the supram esocolic and in ram esocolic spaces. On CT, the transverse m esocolon is between the pancreas and transverse colon, and contains the m iddle colic artery and vein. The root o the transverse m esocolon extends rom the in ra-am pullary portion o the second portion o duodenum through the in erior anterior edge o the pancreas. At the level o the uncinate process, the m esocolon is contiguous with the sm all bowel m esentery. Laterally, the m esocolon is contiguous with the splenorenal and phrenicocolic ligam ents. The m esocolon and gastrocolic ligam ent have a com m on insertion into the transverse colon (Figure 15-10 ).

Figure 15-9 Gastrocolic Ligament and Greater Omentum Coronal CT in patient with gastric cancer demonstrates peritoneal implants in the gastrocolic ligament (black arrow) as well as in the more in erior greater omentum (white arrows). The gastrocolic or supracolic ligament is the superior portion o the greater omentum between the caudal stomach and the transverse colon. It is anterior to the in erior aspect o the lesser sac.

Figure 15-10 Transverse Mesocolon and Greater Omentum Axial CT in a patient with gastric cancer dem onstrate the transverse m esocolon (arrowhead) and the greater om entum (arrow). The transverse m esocolon, greater om entum, and gastrocolic ligam ent all connect to the transverse colon.

the spleen, the phr icocolic ligam t separates the perisplenic space rom the rest o the peritoneal cavity and limits cephalic extension o uid rom the pelvis. As in the liver, a “bar ar a” o the spleen (Figure 15-8) is present. Gastric or pancreatic disease can spread to the splenic hilum via the gastrosplenic, splenorenal, and phrenicolic ligam ents.

Greater Omentum/ Gastrocolic Ligament

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Body CT: The Essentials static peritoneal seeding m edial to the cecum . As the sm all bowel m esentery separates the right and le t in ram esocolic spaces, processes in the right in ram esocolic space above the m esentery will typically not extend into the pelvis due to the cecal attachm ent o the m esentery. However, processes in the le t in ram esocolic space below the m esentery can extend reely into the pelvis.

Sigmoid Mesocolon The sigm oid m esocolon divides the in ram esocolic space into the abdom inal and pelvic regions. The sigm oid m esocolon (Figure 15-12) is a V-shaped old which attaches the sigm oid colon to the posterior abdom inal wall. The apex o the V is anterior to the le t com m on iliac artery and le t ureter, and right and le t lim bs extend in eriorly into the pelvis. The sigm oid m esocolon contains the sigm oid and superior rectal vessels.

Figure 15-11 Small Bowel Mesentery A portion o the sm all bowel m esentery is noted (arrows) in a patient with gastric cancer and ascites. The sm all bowel m esentery runs rom the duodenojejunal exure (ligam ent o Treitz) to the ileocecal valve and can be identi ed on CT by tracing the course o the superior m esenteric artery and vein. Because o its course, peritoneal im plants are o ten noted at the m edial border o the cecum .

The tran sverse m esocolon is a pathway or spread o pan creatic disease to the tran sverse colon . This pre erentially in volves the in erior border o the colon , in con trast to spread o disease rom the stom ach alon g the gastrocolic ligam en t which in volves the superior border.

Small Bowel Mesentery The sm all bowel m esentery (Figure 15-11) is a an-shaped old connecting the sm all bowel with the root o the m esentery, which runs rom the duodenojejunal exure (ligam ent o Treitz) to the ileocecal valve. The m esentery can be identi ed on CT by tracing the course o the superior m esenteric artery and vein. The sm all bowel m esentery is contiguous with the transverse m esocolon at the uncinate process. The oblique course o the m esentery rom superior le t to in erior right accounts or the prevalence o m eta-

Figure 15-12 Sigmoid Mesocolon Both the sigm oid m esocolon (arrow) and the in erior portion o the sm all bowel m esentery (arrowhead) are noted in patient with gastric cancer and ascites. The sigm oid m esocolon has a typical “V” shaped con guration; it divides the in ram esocolic space into abdom inal and pelvic regions.

Chapter 15 Peritoneum and Peritoneal Spaces

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DiSt r ib u t io n o f f l u iD Peritoneal uid will seek the gravity-dependent spaces in the pelvis, and then ascend cephalad in the paracolic gutters to reach the subdiaphragm atic spaces (Figure 15-13). Most o the uid will ascend via the right paracolic gutter, as the le t paracolic gutter is shallow and cephalad extension m ay be lim ited by the phrenicocolic ligam ent. The alci orm ligam ent m ay lim it extension rom the right to le t subdiaphragm atic spaces. Fluid can then extend caudally back into the pelvis through the in ram esocolic com partm ent. As the sm all bowel m esentery separates the right and le t in ram esocolic spaces and extends obliquely rom superior le t to in erior right, processes in the right in ram esocolic space above the m esentery will typically not extend into the pelvis due to the cecal attachm ent o the m esentery. Thus peritoneal uid and disease is m ost likely to collect in: The dependent peritoneal recesses o the pelvis (retrouterine pouch in wom en, retrovesical space in m en) Right paracolic gutter Right subdiaphragm atic space

Figure 15-14 Peritoneal Enhancement CT in a patient with bowel per oration demonstrates increased peritoneal enhancem ent (arrows) secondary to peritonitis. Ascites and ree air are also present.

Right lower quadrant (near the term ination o the sm all bowel m esentery at the ileocecal junction) Superior aspect o sigm oid m esocolon

R

S

Pe r it o n e Al e n h An c e m e n t

S

The norm al peritoneum enhances to a sim ilar degree as the liver. Abnorm al peritoneal enhancem ent (Figure 15-14) can be suspected when it is greater than that o the liver.

h e m o Pe r it o n e u m

TM

RIMC

S

B M

L P

G

LIMC

Blood in the peritoneal cavity (Figure 15-15) can usually be distinguished rom other uids by attenuation. Unclotted extravascular blood typically m easures 30 to 45 Houns eld

G P R

RP S

LP S

Figure 15-13 Flow o Fluid in the Peritoneal Cavity LIMC, le t in erior m esocolic space; LPG, le t paracolic gutter; LPS, le t pararectal space; RIMC, right in erior m esocolic space; RPG, right paracolic gutter; RPS, right pararectal space; RSS, right subphrenic space; SBM, sm all bowel m esentery; TM, transverse m esocolon.

Figure 15-15 Hemoperitoneum H yperdense uid consistent with hem operitoneum is noted in the le t peritoneal space (arrow). This is denser than the uid in the right peritoneal space (arrowhead).

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Body CT: The Essentials ta

15-2. Dif use Solid Peritoneal Disease

Peritoneal carcinomatosis p i on l ub culosis M lign n

i on l m so

p i on l lym

liom

om osis

p i on l s coidosis p i on l s com osis p i on l myloidosis D smo l s ic sm ll ound c ll umo S ous su Figure 15-16 Peritoneal Calcif cation Peritoneal calci cation (arrow) is noted rom m etastatic ovarian cancer. Other com m on etiologies o peritoneal calci cation include peritoneal dialysis and prior peritonitis.

units (H U), whereas clotted blood (usually closer to the site o bleeding) typically m easures 45 to 70 H U. However, blood m ay m easure less than 30 H U in patients with low hem atocrit or in hem orrhage greater than 48 hours old.

Pe r it o n e Al c Al c if ic At io n Benign calci cation o ten has a sheet-like appearance. Malignant calci cation (Figure 15-16 ) is o ten associated with nodal calci cation (Table 15-1).

Dif f u Se So l iD Pe r it o n e Al DiSe ASe

c

ill y c cinom o

i on um

ascites, which m ay be loculated, along with m ultiple so t tissue nodules. Calci cations are o ten seen with m etastases rom m ucin-producing prim ary tum ors such as colon adenocarcinom a.

Peritoneal Tuberculosis Tuberculous peritonitis (Figure 15-17) is in the spectrum o granulomatous peritonitis, which includes other in ectious agents such as histoplasmosis and pneum ocystis, oreign m aterial, sarcoidosis, and Whipple disease. There are several ndings which can be help ul in dif erentiating tuberculous peritonitis rom carcinom atosis. High-density ascites (25– 45 H U) can be seen secondary to tuberculosis; however, the ascites can also be near water density. Mesenteric changes are m ore likely to present in tuberculosis, and m esenteric

Dif use solid peritoneal disease will be secondary to peritoneal carcinom atosis in the m ajority o cases. The other prim ary consideration in endem ic areas is peritoneal tuberculosis (Table 15-2).

Peritoneal Carcinomatosis The m ost com m on etiologies are cancers o the ovary, colon, stom ach, and pancreas. Typically there is substantial ta

15-1. Peritoneal Calci cation

Peritoneal dialysis Prior peritonitis Malignancy M conium

i oni is

p i on l ub culosis hy pos su gic l

y oidism o o ic ossi c ion

In c ion ( n umocys is ji ov ci) a myloidosis

Figure 15-17 Peritoneal Tuberculosis Ascites and omental nodularity are present in a patient with peritoneal tuberculosis. In this case, the ndings closely resemble peritoneal carcinomatosis and the diagnosis would require a high index o suspicion. The presence o high-density ascites and a greater degree o mesenteric involvement (such as large lowdensity or calci ed nodules) can suggest peritoneal tuberculosis instead o carcinomatosis in the proper clinical setting.

Chapter 15 Peritoneum and Peritoneal Spaces nodules in tuberculosis are o ten larger, and m ay have lowdensity centers and/ or calci cation. Peritoneal tuberculosis m ay have m inimal sm ooth peritoneal thickening with pronounced enhancem ent. Irregular peritoneal thickening and peritoneal nodules are m ore com m on in carcinom atosis. In addition, other signs o tuberculosis are o ten present, such as hepatic and splenic m icroabscesses, splenom egaly and splenic calci cation, low-attenuation adenopathy, and in am m atory cecal and term inal ileal thickening.

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does not involve the ovaries. It should be considered in a postm enopausal wom an when there is the appearance o peritoneal carcinom atosis without an ovarian or gastrointestinal tract abnorm ality.

c y St ic Pe r it o n e Al m ASSe S Di erential Diagnosis

Malignant mesothelioma is the most common primary malignant peritoneal neoplasm. Approximately 35% o all mesotheliomas arise solely rom the peritoneum and 50% to 70% o these are associated with asbestos exposure. Peritoneal mesothelioma can occur in a ocal orm, with a large, usually upper abdominal, mass with scattered peritoneal nodules, or a dif use orm without a de nable mass. Ascites is variable but usually is not massive. The diagnosis can be suggested by concomitant asbestos-related lung and pleural disease.

The dif erential diagnosis o cystic peritoneal m asses is very broad (Table 15-3). Mucinous carcinom atosis (Figure 15-18) is a prim ary consideration i there is a known prim ary neoplasm . Pseudom yxom a peritonei is less com m on but can have a sim ilar appearance. Nonpancreatic pseudocysts and prim ary lesions o lym phatic, m esothelial, and enteric origin should also be considered. In the em ale pelvis, ovarian lesions are the prim ary consideration. Ovarian lesions as well as peritoneal inclusion cysts are discussed in Chapter 17. Rarely, typically ovarian lesions such as cystic teratom a can present outside the ovaries. The presence o at in a cystic m ass suggests a cystic teratom a.

Peritoneal Lymphomatosis

Pseudomyxoma Peritonei

Peritoneal lym phomatosis can be prim ary or secondary. Primary peritoneal lym phom atosis is rare and typically seen in im m unocomprom ised patients who are in ected with the hum an imm unode ciency virus. The presence o extensive adenopathy in typical areas involved by lymphom a can be help ul in dif erentiating secondary lymphomatosis rom carcinom atosis. However, prim ary lymphom atosis can mani est as malignant ascites not associated with adenopathy, organomegaly, or m asses. The ascites in lym phomatosis is o ten not loculated.

Pseudomyxom a peritonei is a rare condition describing intraperitoneal accumulation o gelatinous or m ucinous m aterial. It is more comm on in wom en. The m ajority o cases o classic pseudom yxoma peritonei develop rom

Malignant Peritoneal Mesothelioma

Peritoneal Sarcomatosis Peritoneal sarcom atosis is associated with gastrointestinal strom al tum ors (GISTs), liposarcom a, and leiom yosarcom a. Distinguishing eatures o sarcom atosis include variable ascites, heterogeneous bulky m asses, and hypervascularity with or without hem operitoneum .

Desmoplastic Small Round Cell Tumor Desm oplastic sm all round cell tum or is an aggressive m alignancy seen in young adults and adolescents. There m ay be a m ale sex predilection. This entity should be considered in young patients with peritoneal disease in the absence o an organ-based prim ary site. The m asses m ay have hem orrhage, necrosis, and punctate calci cations.

Serous Sur ace Papillary Carcinoma o the Peritoneum Serous sur ace papillary carcinom a o the peritoneum occurs in postm enopausal wom en. It is histologically indistinguishable rom ovarian serous papillary carcinom a, but

Figure 15-18 Mucinous Carcinomatosis A cystic peritoneal lesion is present secondary to peritoneal m etastases rom m ucinous colon carcinom a. This case is atypical in that only a single lesion is identi ed, but the peripheral calci cation (arrow) is a clue to the diagnosis.

228 Body CT: The Essentials ta

15-3. Cystic Peritoneal Masses

Mucinous carcinomatosis Abscess Nonpancreatic pseudocyst Lymphatic origin: Simple lymphatic cyst, lymphangioma Mesothelial origin: Simple mesothelial cyst, benign cystic mesothelioma (peritoneal inclusion cyst), malignant cystic mesothelioma Enteric origin: Enteric duplication cyst, enteric cyst Serous and mucinous cystadenoma and cystadenocarcinoma: Ovarian and nonovarian Cystic teratoma: Ovarian and nonovarian ps udomyxom

i on i

U og ni l cys h yd id cys

low-grade appendiceal mucinous neoplasm s which rupture or penetrate into the peritoneal cavity. Wom en o ten have synchronous appendiceal and ovarian tumors; som e authors believe that the ovarian tumors are metastases rom an appendiceal primary but this is controversial. The early deposits accum ulate in the typical areas o stasis resulting rom the circulation o uid. The peritoneal sur aces o the bowel tend to be spared. Mucin is usually low in CT attenuation, but areas o so t tissue attenuation unrelated to m ucin can be seen. Curvilinear or am orphous calci cations m ay be present. The prim ary nding that is help ul in dif erentiating pseudomyxom a rom simple ascites is scalloping o the visceral sur aces o the intraperitoneal organs (Figure 15-19 ),

usually the liver and spleen. In these cases, the appendiceal region and ovaries should be care ully evaluated. Pseudom yxom a peritonei should be dif erentiated orm peritoneal m ucinous carcinom atosis secondary to an invasive higher-grade m ucinous carcinom a as the prognosis in the later is substantially poorer. Mucinous carcinom atosis tends to involve the chest m ore requently, and can invade the visceral organs and spread via hem atogenous or lym phatic routes.

So l iD m e Se n t e r ic m ASSe S Di erential Diagnosis Predom inately m esenteric lesions have a dif erent dif erential diagnosis than m ore dif use peritoneal abnorm alities (Table 15-4). I a m esenteric m ass is spiculated, the prim ary entities that should be considered are carcinoid and sclerosis m esenteritis. Otherwise, lym phom a, m etastases, sarcom a, desm oids, and GIST should be the prim ary considerations. Several im aging eatures can be help ul in the dif erential diagnosis o m esenteric lesions (Table 15-5). GIST and carci oid t mors are discussed in Chapter 14.

Sclerosing Mesenteritis Sclerosing m esenteritis is an idiopathic disorder with varied degrees o brosis, at necrosis, and in am m ation. It has been associated with other idiopathic in amm atory disorders such as retroperitoneal brosis and orbital pseudotum or. There is a m ale gender predilection. It typically involves the small bowel m esentery, but can also involve the m esocolon. It is also known by num erous other term s, including retractile mesenteritis and mesenteric panniculitis. The term m esenteric panniculitis is typically used when in am mation predominates. M s t ric pa ic litis typically m ani ests as increased attenuation without a so t tissue m ass. This appearance has been term ed “misty m s t ry.” However, this appearance ta

15-4. Solid Mesenteric Masses

Lymphoma Metastases Carcinoid Gastrointestinal stromal tumor Sarcoma Sclerosing mesenteritis M s n Figure 15-19 Pseudomyxoma Peritonei Pseudom yxom a peritonei is present secondary to rupture o an appendiceal mucinous neoplasm . Scalloping o the visceral sur ace o the liver and spleen (arrows) distinguishes pseudom yxom a rom sim ple ascites.

ic b om osis/ d smoid umo

pl xi o m n u o b om Inf mm o y s udo umo ex

l u l soli

y b ous umo

Chapter 15 Peritoneum and Peritoneal Spaces ta

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15-5. Features o Solid Mesenteric Masses C cinoid

Scl osing M s n i is

D smoid

GISt

S com

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d m gin

p s v ion o v ss ls

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is not speci c or m esenteric panniculitis and is also associated with edema, in amm ation, and hem orrhage. Neoplastic etiologies are also possible, speci cally early stage lym phoma, or rarely lipom atous tum ors. Misty m esentery m ay also be associated with coexisting abdom inal and extraabdom inal tumors. The solid orm o sclerosing m esenteritis has also been associated in some studies with coexisting m alignancy. There ore, identi cation o misty mesentery should prompt a care ul search or etiologies o edema and in am m ation, and signs o malignancy. In the absence

Figure 15-20 Mesenteric Panniculitis An area o increased m esenteric attenuation dem onstrates a tum oral pseudocapsule (peripheral band o increased attenuation) (arrows) and a at ring or halo sign (preserved at attenuation around the vessels in the involved area). These signs are associated with m esenteric panniculitis. H owever, the at halo sign has also been described in lym phom a, and tum oral pseudocapsules can be seen in benign and m alignant lipom atous tum ors. The identi cation o this nding should prom pt a search o possible etiologies o edem a and in am m ation, and or coexisting abdom inal and extraabdom inal tum ors. Follow-up studies could dem onstrate stability or resolution and rule out early stage lym phom a.

o an identi able etiology, ollow-up CT exam inations are o ten indicated to assess stability. Two imaging signs have been associated with mesenteric panniculitis (Figure 15-20): the fat ri g or halo sig (preservation o at attenuation around the vessels in the involved area) and a t moral ps docaps l (peripheral band o so t tissue attenuation). However, the at halo sign has also been described in lymphoma, and tumoral pseudocapsules can be seen in benign and malignant lipomatous tumors. The solid orm o sclerosing m esenteritis (Figure 15-21) has been re erred to as r tractil m s t ritis and o ten presents as a spiculated m ass which m ay kink or xate the adjacent sm all bowel, potentially resulting in obstruction. Calci cation and occasionally cystic change can be seen. The at ring sign is som etim es seen in retractile m esenteritis. The typical appearance can m im ic a carcinoid m esenteric m etastasis. The presence o m ural thickening or a m ass in the sm all bowel suggests the diagnosis o carcinoid.

Figure 15-21 Sclerosing Mesenteritis Coronal CT im age dem onstrates a spiculated m esenteric lesion with calci cation. The prim ary dif erential diagnosis is m esenteric m etastasis rom carcinoid which can have a very sim ilar appearance. The presence o m ural thickening or mass in the sm all bowel would suggest the diagnosis o carcinoid.

230

Body CT: The Essentials connections and pathways o disease spread. Radiographics. 20 0 9 ;29 :e34. 3. Raptopoulos V, Gourtsoyiannis N. Peritoneal carcinom atosis. Eur Radiol. 20 0 1;11:219 5–220 6 . 4. Tirkes, T, Sandrasegaran K, Patel AA, et al. Peritoneal and retroperitoneal anatom y and its relevance or cross-sectional im aging. Radiographics. 20 11;32:437–451. 5. Seo BK, Ha H K, Kim AH , et al. Segm ental m isty m esentery: analysis o CT eatures and prim ary causes. Radiology. 20 0 3;226 : 86 –9 4. 6 . Lubner M, Menias C, Rucker C, et al. Blood in the belly: CT ndings o hem operitoneum . Radiographics. 20 0 7;27(1):10 9 –125. 7. Agarwal A, Yeh BM, Breim an RS, Qayyum A, Coakley FV. Peritoneal calci cation: causes and distinguishing eatures on CT. AJR Am J Roentgenol. 20 0 4;182:441–445.

Figure 15-22 Desmoid Tumor A slightly heterogeneous m ass (arrow) is present adjacent to the pancreas in a patient with a prior proctocolectom y due to Gardner syndrom e. In patients with Gardner syndrom e desm oid tum ors occur m uch m ore requently (4%–29 %) than in the general population, and are o ten seen a ter proctocolectom y. Abdom inal desm oids are nonspeci c in appearance, but m ore o ten have well-de ned borders com pared to the irregular borders typically seen in carcinoid and sclerosing m esenteritis. The history suggests the diagnosis in this case. The dif erential diagnosis includes lym phom a, m etastases, gastrointestinal strom al tum or, and carcinoid.

Mesenteric Fibromatosis/ Desmoid Tumor Mesenteric brom atosis is part o the spectrum o deep brom atoses, which include intra-abdom inal, extra-abdom inal and abdom inal wall brom atoses. The m esentery is the m ost com m on site o an intra-abdom inal brom atosis. Mesenteric brom atosis (Figure 15-22) has no gender predilection and can be seen in a wide age range. A m inority o cases are associated with the Gardner syndrom e variant o am ilial adenom atous polyposis. In these patients desm oid tum ors occur m uch m ore requently (4–29 %) than in the general population, and are o ten seen a ter proctocolectom y. On CT, desm oid tum ors are variable in density and enhancem ent. The predom inantly m yxoid lesions m ay be hypoattenuating and do not enhance, whereas other lesions are iso- or hyperdense com pared to m uscle and have m ild enhancem ent. More than two-thirds o lesions have wellde ned borders, the rem aining lesions have an in ltrative outer m argin. Su GGe STe D Re ADIn GS 1. Coakley FV, H ricak H . Im aging o peritoneal and m esenteric disease: key concepts or the clinical radiologist. Clinical Radiology. 19 9 9 ;54:56 3–574. 2. Vikram R, Balachandran A, Bhosale PR, Tam m EP, Marcal LP, Charnsangavej C. Pancreas: peritoneal re ections, ligam entous

8. Rodriguez E, Pom bo F. Peritoneal tuberculosis versus peritoneal carcinom atosis: distinction based on CT ndings. J Comput Assist Tomogr. 19 9 6 ;20 (2):26 9 –272. 9 . Ha H K, Jung JI, Lee MS, et al. CT dif erentiation o tuberculous peritonitis and peritoneal carcinom atosis. AJR Am J Roentgenol. 19 9 6 ;16 7(3):743–748. 10 . Kim Y, Cho O, Song S, Lee H , Rhim H , Koh B. Peritoneal lym phom atosis: CT ndings. Abdom Imaging. 19 9 8;23:87–9 0 . 11. Rha SE, Ha H K, Kim AY, et al. Peritoneal leiom yosarcom atosis originating rom gastrointestinal leiom yosarcom as: CT eatures. Radiology. 20 0 3;227:385–39 0 . 12. Pickhardt PJ, Bhalla S. Unusual nonneoplastic peritoneal and subperitoneal conditions: CT ndings. Radiographics. 2005;25:719–730. 13. Bellah R, Suzuki-Bordalo L, Brecher E, Ginsberg JP, Maris J, Pawel BR. Desm oplastic sm all round cell tum or in the abdom en and pelvis: report o CT ndings in 11 af ected children and young adults. AJR Am J Roentgenol. 20 0 5;184: 19 10 –19 14. 14. Morita H , Aoki J, Taketom i A, Sato N, Endo K. Serous sur ace papillary carcinom a o the peritoneum : clinical, radiologic, and pathologic ndings in 11 patients. AJR Am J Roentgenol. 20 0 4;183:9 23–9 28. 15. Sulkin TV, O’Neill H , Am in AI, Moran B. CT in psuedom yxom a peritonei: a review o 17 cases. Clin Radiol. 20 0 2;57(7):6 0 8–6 13. 16 . Levy AD, Cantisani V, Miettinen M. Abdom inal lym phangiom as: im aging eatures with pathologic correlation. AJR Am J Roentgenol. 20 0 4;182:1485–149 1. 17. Stoupis C, Ros PR, Abbitt PL, Burton SS, Gauger J. Bubbles in the belly: im aging o cystic m esenteric or om ental m asses. Radiographics. 19 9 4;14:729 –737. 18. Levy AD, Rim ola J, Mehrotra AK, Sobin LH . From the archives o the AFIP: benign brous tum ors and tum orlike lesions o the m esentery: radiologic-pathologic correlation. Radiographics. 20 0 6 ;26 :245–26 4. 19 . Horton KM, Lawler LP, Fishm an EK. CT ndings in sclerosing m esenteritis (panniculitis): spectrum o disease. Radiographics. 20 0 3;23:156 1–156 7. 20 . McLaughlin PD, Filippone A, Maher MM. The “m isty m esentery”: m esenteric panniculitis and its m im ics. AJR Am J Roentgenol. 20 13;20 0 :W116 –W123.

Ch a p t e r

16

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, n N

Eugene Lin, MD

I. RETROPERITONEAL ANATOMY II. ABDOMINAL AORTA a. Abdominal Aortic Aneurysms b. Aneurysm Rupture c. Mycotic Aneurysms d. In ammatory Aneurysms e. Aortoenteric Fistulas III. INFERIOR VENA CAVA a. Congenital Abnormalities and Normal Variants i. Circumaortic and retroaortic le t renal vein ii. Le t-sided IVC iii. Double IVC iv. Interruption o the IVC with azygous or hemiazygous continuation

Re t Ro p e Rit o Ne a l a Na t o m y The retroperitoneum extends rom the diaphragm to the level o the pelvic viscera. It is bounded anteriorly by the parietal peritoneum and elsewhere by the ascia surrounding the m usculature (Figures 16 -1 and 16 -2). At the level o the kidneys, the retroperitoneal space is divided into the perirenal space, anterior pararenal space, and posterior pararenal space. The a r or parar al spac is bounded anteriorly by the parietal peritoneum , posteriorly by the anterior renal ascia, and laterally by the lateral conal ascia. The la ral co al asc a is orm ed by the usion o the anterior and posterior renal ascia. The anterior pararenal space contains the pancreas, duodenum , and ascending and descending colon. The pos r or parar al spac contains m ostly at. The l mbar r a l is a cle t between the m edial border o the posterior pararenal space and the lateral border o the quadratus lum borum at pad. Both the anterior and posterior pararenal spaces com m unicate in eriorly with the pelvic extraperitoneal spaces and superiorly with the diaphragm atic sur ace and bare area o the liver. The p r r al spac surrounds the kidneys and adrenals. It is bounded anteriorly by the anterior renal ascia and posteriorly by the posterior renal ascia. Bridging brous

v. Pseudolipoma vi. Retrograde IVC contrast opacif cation b. IVC Thrombosis IV. LYMPH NODES a. Lymph Node Size b. Lymph Node Density c. Lymph Node Anatomy V. RETROPERITONEAL MASSES a. Primary Retroperitoneal Lesions i. Sarcomas ii. Neurogenic tumors iii. Fat-containing retroperitoneal lesions iv. Cystic retroperitoneal lesions b. Retroperitoneal Fibrosis

septa in the perinephric at interconnect the renal capsule with the anterior and posterior renal ascia. The perirenal spaces m ay com m unicate across the m idline, and with the pelvic extraperitoneal spaces and the diaphragm atic surace and bare area o the liver. There are potential retroperitoneal spaces within the ascial planes separating the perirenal and pararenal spaces which can contain uid collections. This has been labeled the r asc al spac . There is a potential r rom s rc (or a r or r asc al) spac in the anterior renal ascia, and a potential r ror al (or pos r or r asc al) space in the posterior renal ascia. These potential spaces com municate across the m idline and with the pelvic extraperitoneal spaces. The bridging septa in the perinephric space can act as conduits between the perinephric and inter ascial spaces.

a b d o m iNa l a o Rt a Abdominal Aortic Aneurysms The abdominal aorta is considered dilated i it exceeds 3 cm in maximum diameter. As wall tension in aortic aneurysms is proportional to mean vessel radius, the maximum diameter o the aneurysm is predictive o rupture. Once an aneurysm surpasses 5.5 cm in anterior to posterior diameter, 231

232 Body CT: The Essentials

L

D P

D P RM

ARF

AO

AP S

IVC

LCF DC

AC

LK

RK RRS

PPS

P RK

Figure 16-1 R rop r o al Spac s Ao, aorta; AC, ascending colon; APS, anterior pararenal space; ARF, anterior renal ascia; D, duodenum ; IVC, in erior vena cava; L, liver; LCF, lateroconal ascia; P, pancreas; LK, le t kidney; PPS, posterior pararenal space; PRF, posterior renal ascia; RK, right kidney; RMP, retrom esenteric inter ascial plane; RRS, retrorenal inter ascial space.

intervention is typically considered. A patient presenting with symptoms o acute aortic syndrome with an aneurysm greater than 7 cm has a high likelihood o aneurysm rupture. I intervention is planned, help ul ndings to report include the m axim um anterior to posterior diam eter o the aneurysm sac, the distance between the lowerm ost renal artery and the start o the aneurysm , the shape and angulation o the neck, the diam eter and condition o the iliac arteries, the am ount and change in m ural throm bus and calci cation in the aneurysm , the num ber o location o the

Figure 16-2 R rop r o al Spac s Patient with severe pancreatitis. APS, anterior pararenal space; LC, lateroconal inter ascial plane; PPS, posterior pararenal space; QL, quadratus lumborum; RMP, retromesenteric inter ascial plane; RRS, retrorenal inter ascial space. There is a small amount o uid extending into the lumbar triangle (arrow) between the quadratus lum borum and medial posterior pararenal space.

Figure 16-3 Aortic Aneurysm Rupture Blood is noted predom inately in the right anterior pararenal space secondary to aneurysm rupture. Focal discontinuity o aortic calci cations is present at the site o the rupture.

renal arteries, and the presence o a retroaortic le t renal vein. Approxim ately 5% o abdom inal aortic aneurysm s are juxtarenal or suprarenal, which increases surgical risk.

Aneurysm Rupture Rupture m ost com m only involves the posterolateral aorta with hem orrhage into the retroperitoneum . Blood can extend into the pararenal space, perirenal space, inter ascial (usually retrorenal) space or psoas m uscle. However, rupture can also involve the anterior or anterolateral aorta with hem orrhage into the peritoneum . Ruptures into the bowel, typically the duodenum , or very rarely into the in erior vena cava can also occur. Focal discontinuity in otherwise circum erential calcication can be seen in ruptured aneurysm s (Figure 16 -3). However, this is only a help ul sign i it is a new nding as m ural calci cation is o ten discontinuous. H yperattenuating crescents in the peripheral aortic lum en, term ed the “cr sc ” s (Figure 16 -4), have been attributed to hem orrhage into the aneurysm wall or m ural throm bus. A crescent can be considered hyperattenuating i it is well de ned, and o higher attenuation than the psoas m uscle on enhanced scans or the patent lum en on nonenhanced scans. The “crescent” sign indicates rank or im pending rupture. Signs o chronic-contained rupture include draping o the posterior aorta over the adjacent vertebral body, and associated vertebral body erosion.

Mycotic Aneurysms In ected (mycotic aneurysm s) are rare, accounting or only 0.7% to 2.6 % o aortic aneurysm s, and are m ost o ten pseudoaneurysm s. They can result rom seeding by septic em boli or contiguous spread rom an adjacent source such

Chapter 16 Retroperitoneum, Vessels, and Nodes

233

In ammatory Aneurysms In am m atory aneurysm s should be suspected i signi cant perianeurysm al brosis or in am m ation is present. Im aging can dem onstrate a rind o enhancing so t tissue anterior and lateral to the aorta, typically sparing the posterior wall. Like atherosclerotic aneurysm s the in rarenal aorta is typically involved but the patients are o ten younger and are usually sym ptom atic. There is a strong m ale sex predilection and association with sm oking. The etiology is poorly understood but m ay be related to retroperitoneal brosis and various autoim m une diseases.

Aortoenteric Fistulas Figure 16-4 Aortic Aneurysm Rupture Noncontrast CT dem onstrates a hyperattenuating crescent (arrows) in an abdom inal aortic aneurysm . This indicates rank or im pending rupture, in this case periaortic hem orrhage is present consistent with rank rupture.

Prim ary aortoenteric stulas are very rare an d alm ost always associated with preexisting aortic aneurysm s. Secondary aortoenteric stulas are m uch m ore com m on, but still relatively rare, and occur as com plications o aortic reconstructive surgery with or without stent-gra t placem ent. Eighty percent o secondary aortoenteric stulas (Figure 16 -5) a ect the duodenum , typically the third and ourth portions. As these stulas occur as a com plication o perigra t in ection, it is dif cult to di erentiate an aortoenteric stula rom perigra t in ection. The m ost speci c but rare signs o aortoenteric stula are extravasation o aortic contrast m aterial into the bowel lum en, and leakage o enteric contrast m aterial into the periaortic space. Ectopic gas, ocal bowel wall thickening, and breach o the aortic wall are also help ul signs but can also be occasionally seen with perigra t in ection alone.

as vertebral osteom yelitis. Unlike atherosclerotic aortic aneurysm s which usually occur in the in rarenal abdom inal aorta, the m ajority o in ected aneurysm s occur in the thoracic or suprarenal abdominal aorta. Im aging ndings o in ected aneurysm s include saccular shape and lobular contours, and ndings o in ection such as periaortic in ammation, gas, abscess, and adjacent vertebral body abnormalities related to spread o in ection. The expansion rate o m ycotic aneurysm s is typically aster than that o atherosclerotic aneurysm s. Rapidly expanding saccular aneurysm s should raise suspicion or in ected aneurysm .

A Figure 16-5 Aortoenteric Fistula A. Extralum inal air is present between the aortic lum en and the third portion o the duodenum . Eighty percent o secondary aortoenteric stulas involve the duodenum . B. Coronal CT

B dem onstrates stranding and extralum inal air in the region o the third portion o the duodenum . Used with perm ission o Christine Menias MD, Washington University, St. Louis, MO

234

Body CT: The Essentials

Pseudoaneurysm orm ation, loss o at place between the bowel and aorta, and perigra t uid and so t tissue thickening can be seen in both aortoenteric stula and perigra t in ection alone. Note that ectopic gas and perigra t uid and so t tissue thickening m ay be norm al ndings a ter surgery. Ectopic gas should be considered abnorm al a ter 4 weeks, and perigra t uid and so t tissue thickening should be considered abnorm al a ter 3 m onths. As it is dif cult to di erentiate aortoenteric stula rom perigra t in ection alone by im aging, a high index o suspicion is necessary in patients with clinical m ani estations. Eighty percent o patients with a secondary aortoenteric stula will present with gastrointestinal bleed.

iNf e Rio R Ve Na Ca Va

Figure 16-6 Azygous Continuation o the In erior Vena Cava The hepatic IVC is absent and the in rarenal IVC drains into an enlarged azygous vein.

Congenital Abnormalities and Normal Variants Congenital abnorm alities are typically not clinically signi cant, but should be recognized to avoid con usion with pathology such as adenopathy.

Circumaortic and retroaortic le t renal vein The le t renal vein can have a retroaortic course, or there can be two le t renal veins, one o which courses anterior and the other posterior to the aorta. This is usually clinically insigni cant but m ay be relevant in the preoperative planning o nephrectom y. Com pression o the retroaortic renal vein between the aorta and vertebral body can result in a “posterior nutcracker syndrom e” with periureteric varices, hem aturia, proteinuria, and ank pain.

Le t-sided IVC The in rarenal IVC is to the le t o the aorta. At the level o the le t renal vein, it crosses anterior to the aorta to join the right renal vein and orm a norm al right superior IVC.

Retrograde IVC contrast opacif cation Retrograde contrast opaci cation o the IVC and hepatic veins (Figure 16 -8) has been associated with right-sided heart disease. However, this is o ten a norm al variant at aster injection rates (> 3 m L/ s).

IVC Thrombosis Arti actual lling de ects in the IVC are com m on and should be di erentiated rom throm bus. The m ost com m on cause is lam inar ow caused by m ixing o opaci ed blood rom the renal veins with nonopaci ed blood rom the lower extrem ities. Bland IVC thrombus most commonly spreads rom the lower-extremity veins, but can be isolated. External compression, venous stasis, and oreign bodies such as catheters and

Double IVC There is both a right and le t in rarenal IVC. The le t IVC typically drains into the le t renal vein, which joins a single right-sided suprarenal IVC.

Interruption o the IVC with azygous or hemiazygous continuation The hepatic IVC is absent. The in rarenal IVC drains into the azygous system (Figure 16 -6 ) (or the hem iazygous system in the case o a le t IVC).

Pseudolipoma Prom inent pericaval at may appear to project into the lum en o the IVC above the caudate lobe and appear as an apparent intralum inal lesion (Figure 16 -7). This is m ost comm on in patients with chronic liver disease in whom prom inent pericaval at collections can develop.

Figure 16-7 Pseudolipoma o the In erior Vena Cava Prominent pericaval at (arrow) projects into the in erior vena cava which can mimic an intraluminal lipoma or liposarcoma. This is most o ten seen as the IVC passes through the diaphragm.

Chapter 16 Retroperitoneum, Vessels, and Nodes t

16-1. Upper Lim its in Size or Lym ph Nodes r

oc u l s

p

c di c: 8 mm

G s o U po

lters predispose to IVC thrombus ormation. Malignancies such as renal cell, hepatocellular, and adrenocortical carcinoma can extend directly into the IVC (Figure 16-9). However, as malignancy predisposes to thrombus through hypercoagulability, it may be dif cult to di erentiate tumor rom bland thrombus in the setting o malignancy. Enhancement o tumor thrombus can be seen which is help ul in di erentiating it rom bland thrombus.

l y m p h No d e s Lymph Node Size Metrics used to m easure a lym ph node include the greatest axial diam eter, the m inim al (short) axial diam eter, and a ratio o these two values. Lym ph node m easurem ent in the

Figure 16-9 Malignant Thrombosis o the In erior Vena Cava A right renal cell carcinom a is present (arrow) with m alignant throm bus extending into the in erior vena cava. The presence o peripheral enhancem ent and vascularity in the throm bus is consistent with a m alignant etiology.

c : 6 mm

ic lig m n : 8 mm - o ic

c v ls

gion: 9 mm

c : 10 mm

po

is: 7 mm

Low

- o ic: 11 mm

M s n

Figure 16-8 Retrograde Contrast Opacif cation o the In erior Vena Cava Retrograde IVC opaci cation can be associated with right heart disease, but in this case it is secondary to rapid contrast injection (rates > 3 cc/ s).

235

ic: 5 mm

short axis m ay be the m ost reproducible and the optim al predictor o m alignancy. The accuracy o size evaluation o lym ph nodes by CT depends upon the prim ary tum or type. The norm al range o lym ph node size m ay vary throughout the body. In particular, retrocrural and m esenteric nodes tend to be sm aller, whereas axillary and inguinal nodes m ay be larger and still be nonm alignant (Table 16 -1). However, in practice, a single size cuto o 1 cm in short-axis dim ension is o ten used throughout the body. A cluster o nodes which are upper norm al in size is o ten pathologic. Benign lym ph nodes tend to have a m ore oval shape, whereas m alignant lym ph nodes tend to be m ore rounded (short axis-to-long axis ratio > 0 .7).

Lymph Node Density A visualized atty hilum generally indicates a benign node. Calci ed (Figure 16 -10 ) and low-density (Figure 16 -11) nodes have speci c etiologies (Tables 16 -2 and 16 -3).

Figure 16-10 Nodal Calcif cation Calci cation in a le t pelvic node is secondary to m etastasis rom m ucinous adenocarcinom a. The di erential diagnosis o nodal calci cation in the abdom en and pelvic includes in am m atory etiologies (e.g., tuberculosis, histoplasm osis), treated lym phom a, and m etastases rom sarcom a and m ucinous adenocarcinom a.

236

Body CT: The Essentials t

16-3. Low-Density Abdom inal Lym ph Nodes Mycob c

ium ub culosis

Mycob c

ium vium-in

W i

l dis

c llul

s

C li c dis s (c vi synd om )

ing m s n

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nod

Primary Retroperitoneal Lesions Prim ary retroperitoneal m alignancies are rare. Retroperitoneal sarcom as should be the prim ary consideration, ollowed by neurogenic tum ors. Figure 16-11 Low-Density Nodes Low-density retroperitoneal nodes are present in a patient with m ycobacterium avium -intracellulare in ection. Other etiologies o low-density abdominal nodes include m ycobacterium tuberculosis, Whipple disease, and celiac disease.

Lymph Node Anatomy As pelvic lym ph nodes m ay be m ore dif cult to identi y than abdom inal lym ph nodes, an overview o pelvic lym ph node anatom y in provided (Figures 16 -12 to 16 -14).

Re t Ro p e Rit o Ne a l m a s s e s The retroperitoneal origin o a m ass can be suggested by anterior displacem ent o retroperitoneal organs such as the kidneys, ureters, pancreas, ascending and descending colon, parts o the duodenum , and the retroperitoneal vessels. I a lesion arises rom a retroperitoneal organ, the organ will either appear em bedded in the lesion, or a sharp “beak”-like de ect will be seen in the organ at the inter ace with the lesion. The m ost com m on m alignant lesions in the retroperitoneum not arising rom an organ are lym phom a and m etastatic nodal disease. Lym phom a (Figure 16 -15) will o ten not signi cantly com press the adjacent structures, and calci cation and necrosis are rare be ore treatm ent. Lym phom a can result in an appearance o com plete aortic encasem ent which is typically not seen with prim ary retroperitoneal neoplasm s such as sarcom as or neurogenic tum ors. t

Sarcomas The m ost com m on prim ary retroperitoneal sarcom as are liposarcom a, leiom yosarcom a, and m alignant brous histiocytom a. With the exception o well-di erentiated liposarcom a, the sarcom as tend to exhibit greater contrast enhancem ent than lym phom a. L posarcomas (Figure 16-16 ) are the most common type o retroperitoneal sarcoma. There are ve subtypes o liposarcoma: well di erentiated, myxoid, pleomorphic, round cell, and dedi erentiated. Well-di erentiated liposarcomas typically have substantial visible at content on CT. They may resemble lipomas, but are typically large (> 10 cm), have so t tissue components and less than 75% at content, and o ten have thicker and more irregular septa that enhance a ter contrast administration. However, in adults, deeper and more central primary at-containing lesions are more likely to be malignant. Thus, unlike the musculoskeletal system, retroperitoneal lipomas are rare in adults and any at-containing lesion should be considered a potential liposarcoma. Myxoid liposarcomas typically have lower attenuation than muscle

16-2. Calci ed Abdom inal Lym ph Nodes Inf mm o y condi ions ( .g., ub culosis, is o l smosis) t

d lym

om

M

s

ic s com

M

s

ic mucinous umo s

Figure 16-12 Common Iliac Lymph Nodes A, com m on iliac artery; V, com m on iliac vein. There are three com m on iliac nodal chains: lateral (long white arrow), m iddle (black arrow), and m edial (short white arrow).

Chapter 16 Retroperitoneum, Vessels, and Nodes

Figure 16-13 External Iliac Lymph Nodes A, external iliac artery; V, external iliac vein. There are three external iliac nodal chains: lateral (long white arrow), middle (short white arrow), and medial (black arrow). Medial chain nodes near the obturator internus muscle are also called obturator nodes.

237

Figure 16-15 Lymphoma Extensive retroperitoneal adenopathy is noted in a patient with non-Hodgkin lym phom a. The aorta is com pletely encased by the con uent adenopathy and displaced anteriorly rom the spine. This nding is help ul in di erentiating lym phom a rom prim ary retroperitoneal tum ors and retroperitoneal brosis.

and may even appear cystic. Slowly progressive contrast enhancement can di erentiate a myxoid liposarcoma rom a cystic lesion. A pleomorphic or round cell liposarcoma may not contain visible mature at and cannot be di erentiated rom the other sarcomas. Calci cation in a liposarcoma is o ten a sign o dedi erentiation. L omyosarcomas are the second m ost com m on type o retroperitoneal sarcom a and have a em ale predom inance. Leiomyosarcom as can be separate rom , or arise rom the in erior vena cava. In erior vena cava involvem ent suggests leiom yosarcom a but is not speci c as other sarcom as can secondarily invade this structure. Leiom yosarcom as tend to have m ore central necrosis than other sarcom as. Retroperitoneal mal a f bro s h s ocy oma is the third m ost com m on type o retroperitoneal sarcom a and has a m ale predom inance. It typically cannot be di erentiated rom the other sarcom as, but is m ore likely to contain calci cation than a leiom yosarcom a.

Neurogenic tumors

Figure 16-14 Internal Iliac Lymph Nodes (1) Presacral node; (2) lateral sacral node (adjacent to the lateral sacral artery); (3) anterior node (anterior to the anterior division o the internal iliac artery). The term hypogastric node has been used to re er to both the m ost cephalic o the internal iliac nodes, and the entire internal iliac nodal group.

10% to 20% o prim ary retroperitoneal tum ors are neurogenic tum ors (Figure 16 -17). They typically occur in a younger age group than the sarcomas. Neurogenic tumors include rv sh a h mors (schwannom a, neuro brom a), mors ar s rom a l o c c lls (ganglioneurom a, neuroblastom a), and para a l o c mors (paragangliom a, pheochrom ocytom a). Schwannom a is the m ost likely neurogenic tum or in an adult. Schwannom as are typically sharply circum scribed m asses, with larger m asses o ten undergoing degenerative changes with cyst orm ation, calci cation, or hem orrhage. The m ost com m on site or paragangliom as (extraadrenal pheochrom ocytom a) in the retroperitoneum is at

238 Body CT: The Essentials

A Figure 16-16 Liposarcoma Liposarcom as are the m ost com m on retroperitoneal sarcom a. A. A liposarcom a is present posterior to the right colon. The presence o a thickened wall and internal so t tissue com ponents

B di erentiate this lesion rom a lipom a. Lipom as are rare in the retroperitoneum . The retroperitoneal m ass in (B) is also a liposarcom a, but it does not contain mature at and cannot be di erentiated rom other sarcom as.

A B

C Figure 16-17 Retroperitoneal Neurogenic Tumors The di erential diagnosis or a solid retroperitoneal m ass includes m etastases, lym phom a, and prim ary retroperitoneal lesions such as sarcom as and neurogenic tum ors. Neurogenic tum ors include nerve sheath tum ors (schwannom a, neuro brom a), tum ors arising rom ganglionic cells (ganglioneuroma, neuroblastom a), and paraganglionic tum ors (paragangliom a, pheochrom ocytom a). Schwannom a (A) is the m ost com m on neurogenic tum or in an adult. The lesion in B in a ganglioneurom a. Ganglioneurom as are rare

benign neurogenic tum ors that can arise anywhere along the paravertebral sym pathetic plexus or in the adrenal m edulla. They are typically hom ogeneous lesions with attenuation less than m uscle, as seen in this case. The lesion in C is a paragangliom a. These neurogenic lesions are dif cult to di erentiate rom each other and nonneurogenic tumors. The hypervascular nature o the paragangliom a is a help ul di erentiating eature. Up to 6 0% o paragangliomas are unctional in which case the diagnosis can be m ade by correlation with sym ptom s and laboratory catecholam ine values.

Chapter 16 Retroperitoneum, Vessels, and Nodes t

16-4. Fat-Containing Retroperitoneal Lesions

t

16-5. Cystic Retroperitoneal Lesions

Myelolipoma

S

Angiomyolipoma

Lymphocele

Liposarcoma

U inom

Li om / li om osis

h m om

Li obl s om

B onc og nic cys

t

Cys ic d g n ion o solid n o l sm (n u og nic umo , s com )

om

h ib nom

t bl 15-3 (Cys ic p i on l M ss s) nd dd:

e id moid o d moid cys s ( the renal hila and the organs o Zuckerkandl. The organs o Zuckerkandl are located anterior to the aorta at the level o the in erior m esenteric artery origin. Paragangliom as are m ore likely to be m alignant (up to 40%) than adrenal pheochrom ocytom as (up to 10 %) and are unctional in up to 6 0 % o patients. On CT paragangliom as o ten appear as well-circum scribed, hypervascular m asses (usually 3 cm or larger) with possible necrosis, uid– uid levels, calci cation, or hem orrhage.

Fat-containing retroperitoneal lesions Fat-containing lesions (Table 16-4) arising rom the kidney and adrenal gland are usually angiomyolipomas and myelolipomas, respectively. Angiomyolipomas o ten contain enlarged vessels with possible aneurysm ormation which can be helpul in di erentiating a renal angiomyolipoma rom a perirenal liposarcoma which is typically relatively avascular. Rarely, both angiomyolipomas and myelolipomas can be seen in the retroperitoneum separate rom the kidney or adrenal. Rare at-containing lesions include primary retroperitoneal teratoma and hibernoma. Teratomas (Figure 16-18), like

Figure 16-18 Retroperitoneal Teratoma Fat and calci cation is noted in a retroperitoneal teratom a. The di erential diagnosis includes liposarcom a. Retroperitoneal teratomas are rare lesions; the presence o a at– uid level (not present in this case) would suggest teratom a rather than liposarcom a.

239

t ilgu o n u n

ic cys s (

o c l) o c l)

other germ cell tumors, can rarely originate in an extragonadal location, o ten near the midline. Teratomas occur predominately in emale patients with a bimodal age distribution in the rst 6 months o li e and early adulthood. Fat– uid levels and calci cation are help ul ndings in di erentiating a teratoma rom other at-containing lesions. Hibernomas are composed o brown at. The presence o enlarged sur ace vessels can be help ul in suggesting this diagnosis.

Cystic retroperitoneal lesions Cystic retroperitoneal lesions can be neoplastic or nonneoplastic. The nonneoplastic lesions include pancreatic and nonpancreatic pseudocyst, lym phocele, urinom a, and hem atom a (Table 16 -5). Cystic lym phangiom as usually occur in the head and neck but rarely can occur in the retroperitoneum . They are m ore com m on in m en and can be seen at any age. Cystic lym phangiom as appear as thin-walled m ulti-septated cystic m asses which insinuate between rather than de orm ing retroperitoneal structures. The wall and septations usually enhance. Occasionally areas o at density can be seen. Retroperitoneal bronchogenic cysts are rare and typically ound in the upper retroperitoneum adjacent to the diaphragm atic crura. Typically ovarian tum ors such as m ucinous cystadenom a and cystic teratom a can also present prim arily in the retroperitoneum . Occasionally paragangliom as and other neurogenic tum ors can appear cystic, and leiom yosarcom as can have large areas o cystic degeneration. Myxoid liposarcom as can appear cystic, but will dem onstrate slowly progressive contrast enhancem ent. In the retrorectal space, cystic lesions are o ten developm ental cysts such as epiderm oid and derm oid cysts, and enteric (tailgut) and neurenteric cysts.

Retroperitoneal Fibrosis Retroperitoneal brosis can occur rom the chest to the pelvis but m ost comm only involves the region between the

240

Body CT: The Essentials 3. Lee SL, Ku YM, Rha SE. Com prehensive review o the inter ascial plane o the retroperitoneum : norm al anatom y and pathological entities. Emerg Radiol. 20 10 ;17(1):1155–116 1. 4. Budovec JJ, Pollem a M, Grogan M. Update on m ultidetector com puted tom ography angiography o the abdom inal aorta. Radiol Clin North Am. 20 10 ;48(2):283–30 9 . 5. Schwartz SA, Taljanovic MS, Smyth S, et al. CT ndings o rupture, impending rupture, and contained rupture o abdominal aortic aneurysms. AJR Am J Roentgenol. 20 07;188:W57–W6 2. 6 . Rakita D, Newatia A, Hines JJ, Siegel DN, Friedm an B. Spectrum o CT ndings in rupture and im pending rupture o abdom inal aortic aneurysm s. Radiographics. 20 0 7;27:49 7–50 7.

Figure 16-19 R rop r o al F bros s Con uent so t tissue is present around the aorta and ureters in a patient with retroperitoneal brosis. Unlike lym phom a, retroperitoneal brosis typically does not li t the aorta o the spine, and the ureters are displaced m edially rather than laterally.

renal hila and the pelvic brim . It is more comm on in m en and typically presents rom 40 to 6 0 years o age. Two-thirds o cases are idiopathic, the other third are linked to causes such as m edication (ergot derivatives), radiation, hem orrhage, urine extravasation, in ection, or tum or. Patients with retroperitoneal brosis are som etim es a ected by brosing processes in other com partm ents such as m ediastinal brosis, sclerosing m esenteritis, and Riedel thyroiditis. Retroperitoneal brosis (Figure 16 -19 ) usually appears as a well-de ned sheath o so t tissue enveloping the aorta, in erior vena cava, iliac vessels, and ureters. It can cause vascular com pression and ureteral com pression leading to hydronephrosis. Unlike lym phadenopathy rom lym phom a, the so t tissue m ass rom retroperitoneal brosis typically does not li t the aorta o the spine and usually will not displace the ureters laterally (instead the ureters are o ten displaced m edially). The so t tissue will enhance to a variable degree; the early-stage in am m atory brosis m ay be hypervascular whereas the m ature brosis m ay be hypovascular. Retroperitoneal m etastatic im plants can result in m alignant retroperitoneal brosis. This typically cannot be di erentiated rom benign brosis without biopsy, but m alignant retroperitoneal brosis is m ore likely to have illde ned m argins and to displace the aorta anteriorly and the ureters laterally. Su g g e St e d Re Ad i n g S 1. Goenka AH , Shah SN, Rem er EM. Im aging o the retroperitoneum . Radiol Clin N Am. 20 12;50 :333–355. 2. Thornton FJ, Kandiah SS, Monkhouse WS, Lee MJ. Helical CT evaluation o the perirenal space and its boundaries: a cadaveric study. Radiology. 20 01;218:6 59 –6 6 3.

7. Vu QDM, Menias CO, Bhalla S, Peterson C, Wang LL, Bal e DM. Aortoenteric stulas: CT eatures and potential m im ics. Radiographics. 20 0 9 ;29 :19 7–20 9 . 8. Kandpal H , Sharm a R, Gam angatti S, Srivastava DN, Vashisht S. Im aging the in erior vena cava: a road less traveled. Radiographics. 20 0 8;28:6 6 9 –6 89 . 9 . Yeh BM, Kurzm an P, Foster E, Qayyum A, Joe B, Coakley F. Clinical relevance o retrograde in erior vena cava or hepatic vein opaci cation during contrast-enhanced CT. AJR Am J Roentgenol. 20 0 4;183(5):1227–1232. 10 . Dor m an RE, Alpern MB, Gross BH , Sandler MA. Upper abdom inal lym ph nodes: criteria or norm al size determ ined with CT. Radiology. 19 9 1;180 (2):319 –322. 11. Lucey BC, Stuhl aut JW, Soto JA. Mesenteric lym ph nodes: detection and signi cance on MDCT. AJR Am J Roentgenol. 20 0 5:184(1):41–44. 12. Schwartz LH , Bogaerts J, Ford R, et al. Evaluation o lym ph nodes with RECIST 1.1. Eur J Cancer. 20 0 9 ;45:26 1–26 7. 13. McMahon CJ, Ro sky NM, Pedrosa I. Lym phatic m etastases rom pelvic tum ors: anatom ic classi cation, characterization, and staging. Radiology. 20 10 ;254:31–46 . 14. Nishino M, Hayakawa K, Minam i M, Yam am oto A, Ueda H , Takasu K. Prim ary retroperitoneal neoplasm s: CT and MR im aging ndings with anatom ic and pathologic diagnostic clues. Radiographics. 20 0 3;23:45–57. 15. Rajiah P, Sinha R, Cuevas C, Dubinsky TJ, Bush WH Jr, Kolokythas O. Im aging o uncom m on retroperitoneal m asses. Radiographics. 20 11;31:9 49 –9 76 . 16 . Rha SE, Byun JY, Jung SE, Chun H J, Lee H G, Lee JM. Neurogenic tum ors in the abdom en: tum or types and im aging characteristics. Radiographics. 20 0 3;23:29 –43. 17. Craig WD, Fanburg-Sm ith JC, Henry LR, Guerrero R, Barton JH . Fat-containing lesions o the retroperitoneum : radiologicalpathological correlation. Radiographics. 20 0 9 ;29 :26 1–29 0 . 18. Israel GM, Bosniak MA, Slywotzky CM, Rosen RJ. CT di erentiation o large exophytic renal angiom yolipom as and perirenal liposarcom as. AJR Am J Roentgenol. 20 0 2;179 :76 9 –773. 19 . Yang DM, Jung DH , Kim H , et al. Retroperitoneal cystic m asses: CT, clinical, and pathologic ndings and literature review. Radiographics. 20 0 4;24(5):1353–136 5. 20 . Degesys GE, Dunnick NR, Silverm an PM, Cohan RH , Illescas FF, Castagno A. Retroperitoneal brosis: use o CT in distinguishing am ong possible causes. AJR Am J Roentgenol. 19 9 6 ;146 :57–6 0 .

Ch a p t e r

17

P

is

Eugene Lin, MD

I. INTRAPERITONEAL SPACE II. EXTRAPERITONEAL SPACE III. PERINEUM IV. FEMALE PELVIS V. INGUINAL REGION (HERNIAS) VI. ACUTE FEMALE PELVIC DISEASE a. Adnexal Torsion b. Pelvic In ammatory Disease/ Tubo–Ovarian Abscess

VII. OVARIAN LESIONS a. Identi ying Ovarian Origin b. Di erential Diagnosis c. Nonovarian Cystic Lesions d. Staging Ovarian Cancer VIII. UTERINE LESIONS a. Leiomyomas b. Cervical Cancer c. Endometrial Cancer

In t r a Pe r It o n e a l SPa c e The pelvic intraperitoneal space contains the ovaries, sm all intestine, sigm oid colon, and upper two-thirds o the rectum . The r ro ri po ch (po ch o Do las) is the m ost dependent portion o the peritoneal space in em ales; in m ales, the r rov sical po ch is the m ost dependent. Intraperitoneal m asses im press the bladder dom e, and displace the sigm oid posteriorly and superiorly, and the ureters posteriorly and laterally.

e x t r a Pe r It o n e a l SPa c e The extraperitoneal space is in erior and posterior to the peritoneal space and contains the uterus, bladder, pelvic ureters, ascending and descending colon, lower one-third o the rectum , iliac vessels, and lym phatics. Extraperitoneal m asses displace the bladder posteriorly or m edially, the ureters m edially or anteriorly, and the iliac vessels m edially. The pelvic extraperitoneal space consists o the anterior pr v sical and p riv sical spaces and the posterior r c al x rap ri o al and pr sacral spaces. The pelvis extraperitoneal spaces com m unicate with the anterior and posterior pararenal and (occasionally) perirenal spaces o the retroperitoneum . The prevesical space (Figure 17-1) is the largest extraperitoneal space. This extends superiorly to the um bilicus; posterior to the pubis it is known as the spac o R zi s.

Figure 17-1 Prevesical Space H em orrhage is presen t in the prevesical space secon dary to m ore in erior pelvic ractures. A substantial am ount o uid in the prevesical space will assum e a “m olar tooth” con guration where the “roots” o the m olar are on both sides o the bladder (short arrows). The bladder (labeled B) is displaced posteriorly an d m edially by a prevesical space collection; peritoneal uid would displace the bladder in eriorly. The prevesical space com m unicates with the presacral space (long arrow).

241

242 Body CT: The Essentials

A

B

Figure 17-2 Pelvic Intraperitoneal Space Peritoneal uid in the pelvis can assum e a “m olar tooth” con guration similar to prevesical space uid (see Figure 17-1), but the “roots” o the m olar (arrows) in A are above the bladder.

B. Coronal CT dem onstrates in erior displacement o the bladder. Prevesical space uid would displace the bladder posteriorly and m edially.

The prevesical space is continuous with the presacral space, rectus sheath, and em oral sheath. Most uid collections in the prevesical space are the result o spontaneous or post-traum atic hem atom as or other uid collections. These will usually have a characteristic “m olar tooth” con guration. Intraperitoneal pelvic uid collections (Figure 17-2) can occasionally have a sim ilar m olar tooth con guration, but intraperitoneal collections displace the bladder in eriorly rather than posteriorly and m edially and in addition the “root” portions o the collection are higher in the pelvis (above the bladder). The perivesical space is sm all and perivesical uid is typically not seen in the absence o prevesical uid. The rectal extraperitoneal space is divided into the inner p rir c al and outer parar c al spaces by a sleeve-like ascia. This ascia m ay prevent com m unication o the perirectal and pararectal spaces, but the pararectal space com m unicates with the vesical extraperitoneal spaces. Most rectal extraperitoneal abnorm alities are related to rectal pathology.

is de ned superiorly and m edially by the levator ani and the external sphincter m uscles. The levator ani separates the ossa rom the extraperitoneal space o the pelvis (supralevator space). The ossa is de ned laterally by the obturator

Pe r In e u m The perineum lies below the pelvic diaphragm , which is com posed o the levator ani anteriorly and the coccygeus posteriorly (Figure 17-3). The rectum , urethra, and vagina pass through the pelvic diaphragm . The m ost prom inent structure in the perineum is the ischior c al ossa or ischioa al spac . The ischiorectal ossa

Figure 17-3 Perineum Coronal E, Extraperitoneal (supralevator) space; IF, ischiorectal ossa; L, levator ani; O, obturator internus m uscle; P, peritoneal cavity; R, rectum; ES, external sphincter.

Chapter 17 Pelvis

243

internus m uscle and ascia, posteriorly by the gluteus m axim us m uscle and sacrotuberous ligam ent, and anteriorly by the transverse perineal m uscles.

Fe m a l e Pe l v IS The broad li am is a double old o peritoneum which extends rom the lateral uterine m argins to the pelvic sidewalls. It com pletely divides the true pelvis in anterior and posterior com partm ents. The largest area o the broad ligam ent is the m esentery o the uterus (m esom etrium ). The allopian tubes are enclosed in the superior aspect o the broad ligam ent (m esosalpinx). The ovaries are connected to the broad ligam ent by the m esovarium . As the m esovarium attaches to the posterior layer o the broad ligam ent, the ovary, i not in the adnexal region, is generally in the posterior pelvic com partm ent or above or posterior to the uterine undus. The ovaries typically do not lie in the anterior cul-de-sac or between the urinary bladder and uterus. The suspensory ligam ent (between the ovary and posterolateral pelvic wall) and utero–ovarian ligam ent also suspend the ovaries. The ro d li am s o the uterus unction to m aintain anteversion. They originate rom the uterine horns and extend through the inguinal canals to the labia m ajora. Other uterine ligam ents include the uterosacral, cardinal, and pubocervical ligam ents. These extend to the sacrum , ischial spines, and pubic sym physis, respectively. The param ri m is the connective tissue and at around the cervix, extending laterally between the leaves o the broad ligam ent. The param etrium contains the allopian tubes, uterine and ovarian vessels and lym phatics, pelvic ureters, and the round ligam ents.

Figure 17-4 Indirect Inguinal Hernia An indirect inguinal hernia is noted passing lateral to the in erior epigastric vessels (arrow). This distinguishes it rom direct and em oral hernias, which pass m edial to the in erior epigastric vessels. Fem oral vein com pression would di erentiate em oral hernias rom direct hernias.

F moral h r ias (Figure 17-5) have a prevalence less than one-tenth than that o inguinal hernias, and are m uch m ore com m on in em ales. Coronal im ages are help ul in diagnosing em oral hernias. The em oral triangle is bordered laterally by the sartorius m uscle, m edially by the adductor longus, and superiorly by the inguinal ligam ent (m nem onic SAIL). Fem oral hernias pass through the potential space o the em oral canal m edial to the em oral

In g u In a l r e g Io n (H e r n Ia S) CT is help ul in di erentiation o direct inguinal hernias, indirect inguinal hernias, and emoral hernias. Femoral hernias are the most likely to strangulate, whereas direct inguinal hernias are the most benign. Femoral and indirect inguinal hernias are typically surgically repaired, whereas direct inguinal hernias may be managed more conservatively. I dir c i i al h r ias (Figure 17-4) are ve tim es m ore com m on than direct inguinal hernias. They are m uch m ore com m on in m en. Direct and indirect hernias can be di erentiated based on the relationship to the in erior epigastric vessels. Indirect hernias exit superolateral to the in erior epigastric vessels, and then are directed lateral to the m edial ollowing the course o the inguinal canal. Indirect hernias appear to contain the usual inguinal canal contents which are not com pressed. Dir c i i al h r ias protrude through the Hesselbach triangle, above the inguinal ligam ent and anterior and m edial to the in erior epigastric vessels. They occur m ore com m only in m en. The inguinal canal contents will be com pressed and displaced laterally by the hernia.

Figure 17-5 Femoral Hernia A em oral hernia (large arrow) is noted in a characteristic location lateral and posterior to the pubic tubercle. A em oral hernia will not lie m edial to the tubercle, although an inguinal hernia can lie lateral to the tubercle. Com pression o the em oral vein (small arrow) is an additional sign which di erentiates a em oral rom an inguinal hernia.

244

Body CT: The Essentials

A

B

Figure 17-6 Ovarian Torsion A. Coronal CT im age dem onstrates an enlarged torsed ovary in a m idline location, with in ltration o the periadnexal at and

engorged vessels. B. CT in a di erent patient dem onstrates an enlarged torsed right ovarian m ass ( brothecom a) (arrowhead) with deviation o the uterus (arrow) to the involved side.

vein. I the inguinal ligam ent is visualized, em oral hernias pass posterior to the ligam ent whereas inguinal hernias pass anterior to the ligam ent. Like direct inguinal hernias, em oral hernias pass m edial to the in erior epigastric vessels. However, em oral hernias are m uch m ore likely to com press the em oral vein. The pubic tubercle is another help ul landm ark in distinguishing hernias. Fem oral hernias will lie lateral and m ostly posterior to the tubercle. I a hernia sac is m edial to the tubercle, it is inguinal, whereas a hernia sac lateral to the tubercle could be inguinal or em oral. Fem oral vein com pression suggests a em oral hernia.

Pelvic In ammatory Disease/ Tubo– Ovarian Abscess

a c u t e Fe m a l e Pe l v Ic DISe a Se Adnexal Torsion Ultrasound is the prim ary im aging m odality in patients suspected to have adnexal torsion. Although CT ndings are not speci c or torsion, a constellation o ndings can raise the suspicion or torsion. CT ndings o adnexal torsion (Figure 17-6 ) include: Enlarged adnexal structure (> 5 cm ) with sm ooth border, sm ooth cystic wall thickening (> 3 m m ) Hemorrhage, lack o enhancement, or gas in the torsed lesion Misplacem ent o the torsed structure (to the m idline or contralateral side) Deviation o the uterus to the involved side In ltration o the periadnexal at Tubal thickening Twisted vascular pedicle with engorged vessels Ascites

CT has limited sensitivity or the diagnosis o pelvic in ammatory disease. The most sensitive CT nding is mid-pelvic at stranding. The most speci c nding is tubal thickening. Other ndings (Figure 17-7) include enlarged and abnormally enhancing ovaries (sometimes with a polycystic appearance), abnormally enhancing and dilated endometrial and endocervical cavities, pyosalpinx, loss o normal at planes, thickened uterosacral ligaments, and para-aortic adenopathy at the level o the renal hila. A tubo–ovarian abscess may resemble pelvic abscesses rom other etiologies, but the previously noted ndings (in particular pyosalpinx) as well as satellite lesions and anterior displacement o the broad and round ligaments can be help ul in di erentiation. Associated ndings include bowel ileus and obstruction, renal obstruction, and perihepatitis (Fitz-Hugh–Curtis syndrome).

o v a r Ia n l e SIo n S Identi ying Ovarian Origin A lesion which is potentially o ovarian origin should be di erentiated rom nonovarian lesions such as iliac lym ph nodes and subserosal uterine lesions. The intraperitoneal ovaries are located anterior or anterom edial to the ureters (Figure 17-8), whereas the extraperitoneal iliac nodes are located lateral or posterolateral to the ureters. Thus ovarian m asses should displace the ureter posteriorly or posterolaterally, whereas iliac nodal enlargem ent will displace the ureter m edially and anterom edially.

Chapter 17 Pelvis

A

245

B

Figure 17-7 Tubo–Ovarian Abscess A. Dilated and thickened allopian tubes secondary to pyosalpinx and a dilated endom etrial canal (arrow) are noted in a patient

with bilateral tubo–ovarian abscesses. B. Coronal CT in a di erent patient dem onstrates right-sided hydronephrosis secondary to a right tubo–ovarian abscess.

However, uterine m asses can also displace the ureter posteriorly or posterolaterally. An ovarian m ass can be di erentiated rom other pelvic m asses by tracking the ovarian veins or suspensory ligam ent to the region o the m ass (Figure 17-9 ). The s sp sory li am is a peritoneal old which suspends the ovary rom the posterolateral pelvic wall. The suspensory ligam ent transm its the ovarian artery and vein. I the ligam ent is identi ed by CT it will appear as a linear band thicker than the ovarian vein leading into it. The ovarian veins will o ten course along the lateral and dorsal border

o an ovarian m ass, but will o ten show abrupt term ination at the lateral m argin o a uterine m ass. The ovary is also im m ediately posterior to the broad ligam ent, but the broad ligam ent is typically not well visualized without ascites.

Figure 17-8 Intraperitoneal versus Extraperitoneal Because o the lack o parenchym al contrast enhancem ent, it is dif cult to determ ine whether the indicated pelvic structures (arrows) represent the ovaries. However, these are lateral to the contrast- lled ureters and are thus extraperitoneal and cannot represent the ovaries. The intraperitoneal ovaries are located anterior or anterom edial to the ureters, whereas extraperitoneal structures are located lateral or posterolateral to the ureters.

Figure 17-9 Identi ying Ovarian Origin Sagittal CT dem onstrates the le t ovarian vein (medium arrow) draining into the le t renal vein (long arrow). In eriorly, the ovarian vein runs in the suspensory ligam ent (short arrow) which carries the ovarian artery and vein to the ovary (arrowhead).

246

Body CT: The Essentials

A

B

Figure 17-10 Mature Cystic Teratoma A le t ovarian m ature cystic teratom a (derm oid cyst), contains a at– uid level as well as intracystic protrusions (Rokitansky

nodules or derm oid plugs) com posed o a tooth (A) and so t tissue (B).

Di erential Diagnosis

mors (Figure 17-12), and the etiology is as Kr k b r typically retrograde lym phatic spread rather than direct seeding. Features which suggest a malignant ovarian tumor are larger size, vegetations in a cystic lesions, wall and septal thickness greater than 3 mm, necrosis in a solid lesion, and ascites.

Ovarian lesions are usually better evaluated by ultrasound or MRI. A com m on ovarian lesion is a s ro s cys ad oma. This is unilocular or m ultilocular, with thin walls and septa and hom ogeneous attenuation. These are typically dif cult to di erentiate rom physiological cysts in prem enopausal wom en. The serous tum ors are m ore o ten bilateral than m ucinous tum ors. M ci o s cys ad omas are less com m on. These are alm ost always m ultilocular and m ay contain uid o di erent attenuations. The benign serous and m ucinous lesions o ten have no endocystic or exocystic vegetations. Mature ra omas (Figure 17-10 ) are the m ost com m on benign ovarian tum or in wom en less than 45 years old. Mature teratom as have a range o appearances, including purely cystic, predom inately at, and m ixed m asses containing com ponents o all three germ cell layers. The presence o at attenuation in an ovarian m ass is highly speci c or a teratom a. A typical protuberance into the cyst cavity known as a Roki a sky od l can som etim es be seen, and calci cation, bone, and teeth can be seen in these nodules. Calcif ca io s are m ost com m only seen in teratom as, serous epithelial tum ors, Sertoli–Leydig cell tum ors, cystadeno brom a, and strum a ovarii. Hi hly ha ci solid por io s have been described in Sertoli–Leydig cell tumors, cystadeno brom as (Figure 17-11), sclerosing stromal tum or, and strum a ovarii. Bila ral ovaria mass s should raise the suspicion or m etastases and serous epithelial tum ors. Colon, stom ach, breast, and lung are the m ost com m on sources o ovarian m etastases. Ovarian m etastases are also known

Figure 17-11 Ovarian Cystadenof broma A le t ovarian cystic lesion with enhancing solid com ponents is noted. The appearance is not speci c or a speci c lesion, and enhancing solid com ponents have been described in a variety o lesions including Sertoli–Leydig cell tum ors, cystadeno brom as, and sclerosing strom al tum or.

Chapter 17 Pelvis

A

247

B

Figure 17-12 Ovarian Metastases A. CT demonstrates bilateral solid ovarian lesions consistent with ovarian metastases in a patient with gastric cancer. B. PET/ CT

in the sam e patient dem onstrates that the etiology o the ovarian m etastases (arrowheads) is retrograde lym phatic spread (arrows).

Nonovarian Cystic Lesions

tive mesothelial proli eration o peritoneal cells. These cysts occur almost exclusively in premenopausal woman with active ovaries, pelvic adhesions, and impaired absorption and are related to prior peritoneal insults such as prior surgery, trauma, pelvic in ammatory disease, and endometriosis. Fluid- lled cysts are noted con orming to the pelvic cavity; the ovaries are surrounded by, but separate rom the cysts. A paraovaria cys arises rom the m esosalpinx. These arise in a wide age range but are m ost com m on in the third to ourth decades o li e. They have a wide size range but the average size at diagnosis is 8 cm . They appear as a round or oval cystic structure near but separate rom the ovary.

Other cystic-appearing lesions in the emale pelvis include peritoneal inclusion cysts, hydrosalpinx, and paraovarian cysts. The p ri o al i cl sio cys (also known as benign cystic mesothelioma) (Figure 17-13) is a nonmalignant reac-

Staging Ovarian Cancer

Figure 17-13 Peritoneal Inclusion Cyst Coronal CT dem onstrates a m ulticystic pelvic lesion in a prem enopausal wom an status post total-abdom inal hysterectom y and bilateral salpingo-oophorectom y. This is consistent with a peritoneal inclusion cyst, or benign cystic m esotheliom a. This nding suggests that ovarian rem nant tissue is present as these cysts typically develop in wom en with active ovaries.

Com puted tom ography is the prim ary im aging m odality or staging ovarian cancer. Ovarian cancer can spread by direct extension to the surrounding pelvic tissues. Tum or can spread outside the pelvis via intraperitoneal seeding, lym phatic invasion, and hem atogenous dissem ination. Intraperitoneal spread is the m ost com m on m ode o tum or spread and approxim ately 70 % o patients have peritoneal m etastasis at staging laparotom y. Tum or spreads via the standard pathways o peritoneal spread (see Chapter 15). The peritoneal sur aces should be exam ined or calci cation (Fi r 15-16 ) as approxim ately one-third o m etastatic serous cystadenocarcinom as produce calci cation. Mucinous m etastases can also calci y. One o the m ajor

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Body CT: The Essentials

lim itations o CT in staging ovarian cancer is the inability to detect sm all (< 5 m m ) peritoneal im plants, especially when ascites is not present. There are three pathways o lym phatic drainage rom the ovaries. Nodal m etastases m ost com m only ascend along the gonadal vessels to the retroperitoneal nodes at the level o the renal hilum . Iliac and obturator adenopathy can also result rom spread along the broad ligam ent. Occasionally, inguinal adenopathy can be seen rom spread through the round ligam ent. Hem atogenous m etastases are the least com m on m ode o spread. The m ost com m on location is the liver, ollowed by the lung. There are two staging system s or ovarian m alignancy. The m ost com m only used is the surgically based system proposed by the International Federation o Obstetrics and Gynecology (FIGO). A TNM (tum or, node, m etastasis) system also exists. Although the FIGO system is surgically based, im aging can be com plem entary to surgical staging. In stage IA and IB disease, the tum or is lim ited to one or both ovaries, but m alignant ascites can be present in the pelvis in stage IC. The presence o ascites has a positive predictive value o 72% to 80% as a sign o peritoneal m etastasis. Peritoneal m etastases identi ed outside the pelvis are stage III disease. Stage II disease is characterized by local extension o tum or con ned to the pelvis. Tum or can extend into the uterus, allopian tubes, uterus, iliac vessels, bowel, or bladder. Pelvic side wall invasion is typically present when the tum or is less than 3 m m rom the pelvic side wall.

In stage III disease there is peritoneal spread outside the pelvis and/ or regional lym ph nodes. In stage IV disease there are distant m etastases outside the peritoneal cavity. Di erentiation between stage III and IV disease impacts patient management. Stage III disease is treated by primary surgical debulking whereas stage IV disease is treated with chemotherapy and cytoreduction. There are some pit alls in diagnosing potential stage IV disease by CT. Pleural e usions in patients with ovarian cancer can be benign or malignant. The presence o pleural thickening and nodularity suggests malignancy, but thoracentesis is o ten necessary. Peritoneal implants over the liver (stage III) (Figure 17-14) may sometimes be dif cult to di erentiate rom hematogenous liver metastases (stage IV).

Figure 17-14 Serosal Metastases Serosal m etastases (arrows) rom ovarian cancer are noted involving the liver and spleen, including serosal lesions arising rom tumor extension into the ssure or ligamentum venosum. In patients with ovarian cancer it is important to distinguish peritoneal implants (stage III) rom hematogenous liver metastases (stage IV). The peripheral location o the lesions and association with adjacent peritoneal disease are help ul in identi ying the serosal origin, as is review o multiple imaging planes.

Cervical Cancer

u t e r In e l e SIo n S Leiomyomas Leiom yom as usually appear as uterine enlargem ent with a contour de orm ity. They are o ten o sim ilar density to the norm al uterus, but low attenuation can result rom necrosis and degeneration. Calci cation is a m ore speci c nding which can occur in up to 10 % o leiom yom as. Leiom yom as should be distinguished rom ovarian lesions, adenom yom as, uterine sarcom as, and endom etrial carcinom as. Pedunculated leiom yom as with areas o low attenuation can m im ic ovarian lesions; the previously discussed criteria or identi ying ovarian origin are help ul in di erentiation. Ad omyomas are o ten not detected by CT and can be better di erentiated rom leiom yom as by MRI. Adenom yom as typically have less m ass e ect relative to the size o the lesion and an elliptical (rather than rounded) conguration paralleling the endom etrium . Dilated vessels at the m yom etrial inter ace suggest a leiom yom a rather than adenom yom a. Leiomyomas can som etim es appear as an intracavitary m ass and m im ic endom etrial carcinoma, endom etrial strom al sarcoma, or m ixed m ullerian tumor. Endometrial carcinom as usually enhance less than the myometrium whereas leiomyom as o ten have similar enhancement. The uterine sarcom as m ay enhance substantially but tend to have in ltrative m argins in contrast to the well-de ned m argin o a leiomyom a. Leiomyom as usually cannot be di erentiated rom l iomyosarcomas (Figure 17-15) in the absence o m etastases but leiom yosarcom as tend to be larger, m ore irregular, and have larger areas o necrosis.

Prim ary cervical tum ors can be isodense or hypodense to norm al cervical parenchym a a ter contrast adm inistration. CT is lim ited in depiction o cervical cancer as 50 % o tumors are isodense. I the primary tumor is visible, it o ten has low-attenuation areas secondary to necrosis, ulceration or decreased vascularity. Greater degrees o cervical enlargem ent are associated with poorer outcom e.

Chapter 17 Pelvis

Figure 17-15 Uterine Leiomyosarcoma Coronal CT dem onstrates a heterogeneous uterine mass. This cannot be di erentiated rom a leiomyoma based upon the uterine ndings alone; however, a bone metastasis (arrow) is present.

The role o im aging in staging cervical cancer is to evaluate or invasion o the param etrium , pelvic wall and adjacent organs, and to diagnosis nodal and distant m etastases. MRI is o ten pre erred to CT or local staging. The param etrium is the connective tissue separating the cervix rom the bladder, extending between the leaves o the broad ligam ent laterally. The lateral m argin is the pelvic sidewall. An important distinction in staging is between stage IIA disease with no param etrial involvement and stage IIB disease in which the param etrium is involved. Patients with tum ors less than or equal to stage IIA can be treated

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with surgery or radiation whereas patients with stage IIB or higher-stage disease are treated with radiation only. CT has a reported accuracy o 76 % to 80 % in the detection o param etrial invasion. MRI has a reported accuracy o 77% to 9 6 %. Speci c signs o param etrial invasion on CT include a param etrial so t tissue m ass and encasem ent o the ureter. I hydronephrosis is present, the patient has stage III disease. Other signs include periuterine vascular encasem ent and thickening o the uterosacral ligam ents. Increased attenuation and stranding o the param etrial at is less speci c (Figure 17-16 ) and m ay be secondary to in am m ation. Invasion o the pelvic sidewall (obturator internus and piri ormis m uscles) is stage III disease and can be suggested when the tumor is less than 3 mm rom the sidewall. More direct signs include encasem ent o the iliac vessels, direct invasion o the sidewall m uscles, and bony destruction. Although nodal disease is not assessed in the clinical FIGO staging system it a ects prognosis. There are three lym phatic drainage pathways rom the cervix: the lateral and hypogastric routes along the external iliac and internal iliac vessels, respectively and the presacral route along the uterosacral ligam ents. In the absence o m etastases to these sites, m ore cranial (e.g., para-aortic) nodal involvem ent is rare. Both CT and MRI have com parable accuracy in detecting lym ph node involvem ent. However both techniques have relatively low sensitivity and PET/ CT m ay be m ore use ul or detecting nodal disease. Invasion o the bladder and rectum and distant metastases are stage IV disease. Distant metastases are typically seen in the liver, lung, peritoneum, bone, and extrapelvic nodes.

Endometrial Cancer

Figure 17-16 Cervical Cancer A heterogeneous cervical m ass is present consistent with cervical carcinom a. Stranding in the le t param etrium (arrow) is not speci c or param etrial involvem ent (stage 2B) as it can also be noted secondary to in am m ation.

Endom etrial cancer is staged surgically and im aging is not included in the standard FIGO staging o endom etrial cancer. However, pretreatm ent im aging can be help ul in patients who are not surgical candidates, and in determ ining the type and extent o surgery and/ or radiation treatm ent. In particular, im aging can be help ul in determ ining the depth o m yom etrial invasion, tum or extent, and lym phadenopathy. On contrast-enhanced CT, endom etrial cancers (Figure 17-17) are usually o lower attenuation than the m yom etrium . However, CT is o lim ited accuracy or the assessm ent o m yom etrial and cervical invasion, and MRI is pre erred or this purpose. CT is m ore help ul in assessm ent o advanced disease, such as local invasion o the bladder or rectum , and distant m etastases. Distant m etastases are m ost com m only seen in the extrapelvic lym ph nodes and peritoneum . Endom etrial cancer can directly m etastasize to the para-aortic nodes (particularly on the le t side) in the absence o pelvic lym phadenopathy. Tum ors in the proxim al body and undus o the uterus drain to com m on iliac and para-aortic nodes whereas tum ors in the m iddle and in erior uterus drain to param etrial and obturator nodes.

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Body CT: The Essentials 8. Jung SI, Kim KJ, Park H S, Jeon H J, Jeong KA. Acute pelvic in am m atory disease: diagnostic per orm ance o CT. J Obstet Gynaecol Res. 20 0 1;37(3):228–235. 9 . Sam JW, Jacobs JE, Birnbaum BA. Spectrum o CT ndings in acute pyogenic pelvic in am m atory disease. Radiographics. 20 0 2;22:1237–1334. 10 . Potter AW, Chandrasekhar CA. US and CT evaluation o acute pelvic pain o gynecologic origin in nonpregnant prem enopausal patients. Radiographics. 20 0 8;28:16 45–16 59 . 11. Saksouk FA, Johnson SC. Recognition o the ovaries and ovarian origin o pelvic m asses. Radiographics. 20 0 4;24:S133–S146 . 12. Asayam a Y, Yoshim itsu K, Aibe H , et al. MDCT o the gonadal veins in em ales with large pelvic m asses: value in di erentiating ovarian versus uterine origin. AJR Am J Roentgenol. 20 0 6 ;186 :440 –448. 13. Jung SE, Lee JM, Rha SE, Byun JY, Jung JI, Hahn ST. CT and MR im aging o ovarian tum ors with em phasis on di erential diagnosis. Radiographics. 20 0 2;22(6 ):130 5–1325. 14. Sohaib SA, Sahdev A, Van Trappen P, Jacobs IJ, Reznek RH . Characterization o adenexal m asses on MR im aging. AJR Am J Roentgenol. 20 0 3;180 :129 7–130 4.

Figure 17-17 Endometrial Cancer An endom etrial m ass is present consistent with endom etrial carcinom a. Endom etrial carcinom a is typically less dense than the m yometrium . Loss o m ucosal enhancem ent (arrow) is suspicious or m yom etrial invasion which was present. However, MRI is better suited to evaluate or possible m yom etrial invasion.

15. H ricak H , Chen M, Coakley FV, et al. Com plex adenexal m asses: detection and characterization with MR im aging – m ultivariate analysis. Radiology. 20 0 0 ;214:39 –46 . 16 . Moyle PL, Katoakoa MY, Nakai A, Takahata A, Reinhold C, Sala E. Nonovarian cystic lesions o the pelvis. Radiographics. 20 10 ;20 :9 21–9 38. 17. Bell DJ, Pannu H K. Radiological assessm ent o gynecological m alignancies. Obstet Gynecol Clin N Am. 20 11;38:45–6 8. 18. Moyle P, Addley H C, Sala E. Radiological staging o ovarian carcinom a. Semin Ultrasound CT MR. 20 10 ;31(5):388–39 8.

Su g g e St e D Re ADIn g S 1. Chen N, Min PQ, Liu ZY, Wu B, Yang KQ, Lu CY. Radiological and anatom ic study o the extraperitoneal space associated with the rectum . AJR Am J Roentgenol. 20 10;19 4:6 42–6 52. 2. O’Connell AM, Duddy L, Lee C, Lee MJ. CT o the pelvic extraperitoneal spaces: an anatom ic study in cadavers. Clin Radiol. 200 7:6 2(5):432–438. 3. Llauger J, Palm er J, Perez C Monill J, Ribé J, Moreno A. The norm al and pathologic ischiorectal ossa at CT and MR im aging. Radiographics. 19 9 8;18(1):6 1–82. 4. Burkhardt JH , Arshankiy Y, Munson JL, Scholz FJ. Diagnosis o inguinal region hernias with axial CT: the lateral crescent sign and other key ndings. Radiographics. 2011;31(2):E1–E12. 5. Suzuki S, Furui S, Okinaga K, et al. Di erentiation o em oral versus inguinal hernia: CT ndings. AJR Am J Roentgenol. 20 0 7;189 :W78–W83. 6 . Kitam i M, Takase K, Tsuboi M, et al. Di erentiation o em oral and inguinal hernias on the basis o anteroposterior relationship to the inguinal ligam ent on m ultidim ensional com puted tom ography. J Comput Assist Tomogr. 20 0 9 ;33(5):6 78–6 81. 7. Rha SE, Byun JY, Jung SE, et al. CT and MR im aging eatures o adenexal torsion. Radiographics. 20 02;22:283–29 4.

19 . Woodward PJ, Hosseinzadeh K, Saenger JS. From the archives o the AFIP: radiological staging o ovarian carcinom a with pathological correlation. Radiographics. 20 0 4;24:225–246 . 20 . Coakley FV, Choi PH , Gougoutas CA, et al. Peritoneal m etastases: detection with spiral CT in patients with ovarian cancer. Radiology. 20 0 2;223:49 5–49 9 . 21. Mironov S, Akin O, Pandit-Taskar N, Hann LE. Ovarian cancer. Radiol Clin North Am. 20 0 7;45(1):149 –16 6 . 22. Togashi K, Ozasa H , Konishi I, et al. Enlarged uterus: di erentiation between adenom yosis and leiom yom a with MR im aging. Radiology. 19 89 ;171(2):531–534. 23. Sahdev A, Sohaib SA, Jacobs I, Shepherd JH , Oram DH , Reznek RH . MR im aging o uterine sarcom as. AJR Am J Roentgenol. 20 0 1;177:130 7–1311. 24. Pannu H K, Corl FM, Fishm an EK. CT evaluation o cervical cancer: spectrum o disease. Radiographics. 20 0 1;21:1155–116 8. 25. Sohaib SA, Verm a H , Attygalle AD, Ind TE. Im aging o uterine m alignancies. Semin Ultrasound CT MR. 20 10 ;31(5):377–387. 26 . Akin O, Mironov S, Pandit-Taskar N, Hann LE. Im aging o uterine cancer. Radiol Clin North Am. 20 0 7;45(1):16 7–182. 27. Kim SH , Choi BI, Kim JK, et al. Preoperative staging o uterine cervical carcinom a: com parison o CT and MRI in 9 9 patients. J Comput Assist Tomogr. 19 9 3;17:6 33–6 40 .

Ch a p t e r

18

T Claudia T. Sadro, MD Claire K. Sandstrom, MD Stephanie Cheng, MD

I. TRAUMA II. CT TECHNIQUE a. Thorax b. Abdomen and Pelvis III. THORACIC TRAUMA a. Rib Fractures b. Sternal Fractures c. Scapulothoracic Dissociation d. Pneumothorax e. Pulmonary Contusion and Laceration f. Tracheobronchial Injury g. Esophageal Injury h. Diaphragmatic Rupture i. Acute Traumatic Aortic Injuries

Tr a u m a Major traum a to the torso is m ost o ten due to m otor vehicle crashes, m otorcycle crashes, pedestrians struck by vehicles, alls rom a height, athletic injuries, and crush injuries. Geriatric patients m ay experience m ajor torso traum a rom relatively m inor injuries such as a ground level all particularly i they are osteoporotic, have a rigid spine, are on anticoagulants, or have pre-existing health conditions such as cancer or liver disease. Penetrating traum a rom gunshot wounds and stabbings also accounts or m ajor traum a to the torso. Traum a patients are assessed by the traum a team and have a traum a radiograph series consisting o rontal chest and pelvic radiographs. Patients with penetrating traum a to the abdom en will also have an abdom inal radiograph. Select patients will have portable extrem ity x-rays and lateral cervical spine x-rays. Many patients require a CT head to evaluate or head injury, a CT cervical spine to evaluate or cervical spine injury and a CT chest, abdom en, and pelvis with reconstructions o the thoracolum bar spine to evaluate or torso traum a and thoracolum bar spine

IV. ABDOMINAL AND PELVIC TRAUMA a. Hemoperitoneum b. Active Hemorrhage c. Hemodynamic Shock d. Solid Organ Injuries e. Gastrointestinal Injuries i. Splenic injury ii. Liver injury iii. Gall bladder injury iv. Pancreatic and duodenal injuries v. Bowel and mesenteric injuries f. Genitourinary Injuries i. Renal and ureteral injuries ii. Bladder injury iii. Adrenal injury iv. Pregnancy and abdominopelvic trauma

injury. Hem odynam ically unstable patients m ay go to the angiography interventional suite or operating room be ore being evaluated with CT.

CT Te Ch n iq u e Thorax When there is concern or traumatic aortic injury or m ajor vascular injury to the subclavian vessels based on clinical assessm ent or the traum a chest x-ray, a CT angiogram (CTA) chest is per orm ed. CTA chest requires a timing bolus centered on the descending thoracic aorta. The scan tim e delay is peak plus 8 seconds. For the timing bolus, 20 mL o intravenous contrast is used. For the scan, 80 m L intravenous iodinated contrast is in used at a rate o 4 m L/ s through an intravenous access catheter placed in the antecubital ossa that is 20 gauge or higher. The scanning eld o view is rom the thoracic inlet to L1 at 2.5 mm with a pitch o 1.375 and a scan interval o 1.25 m m . Also, 10-m m oblique sagittal m aximal intensity projection (MIP) im ages are per orm ed 251

252 Body CT: The Essentials through the aortic arch at 2.5-mm intervals. Coronal and sagittal 2.5-mm thick sections are also per ormed. When there is no concern or traum atic aortic injury but there is concern or chest traum a, a venous phase CT chest is added to the CT abdomen and pelvis.

Abdomen and Pelvis In traum a patients placement o a nasogastric tube or gastric decom pression decreases the risk o aspiration and reduces streak arti act. I a Foley catheter has been placed, it is tem porarily clam ped during the scan to distend the bladder. Oral contrast is not routinely used in patients with blunt abdom inal traum a. In patients with penetrating abdom inal or pelvic injury, water-soluble oral contrast and rectal contrast are adm inistered to evaluate or bowel injury. Obese patients should be strapped to the CT table so that their bodies are as round as possible. This m inim izes arti acts and also reduces radiation dose to those body parts that would otherwise be outside the bowtie lter o the scanner. Except in patients with a history o severe contrast reaction, intravenous iodinated contrast is routinely used or CT o traum a patients to diagnose parenchym al injuries and to evaluate or vascular injuries. In patients with im paired renal unction in whom the index o suspicion or visceral injury is low such as a geriatric patient with all rom standing, intravenous contrast m ay not be necessary. However, this determ ination should be made in consultation with the trauma team in advance o the scan. Intravenous contrast o 100 to 170 m L is administered at an injection rate o 3 to 4 mL/ s depending on patient size with higher dose and higher ow rates or larger patients. Imaging is per orm ed in the portal venous phase a ter a 70-second delay. For pediatric patients, the dose o intravenous contrast is 2 mL/ kg at an injection rate o 1 to 2 mL/ s. Intravenous access should be at the antecubital ossa or more central with at least a 20-gauge intravenous access catheter. I the only intravenous access is through the oot, the m axim al ow rate o 3 mL/ s precludes a high-quality CTA examination. Trauma CT is per ormed on m ultidetector CT scanners with 3.75-mm collimation and a pitch o 1.375 at 2.5-m m intervals. Coronal and sagittal reconstructions o 2.5 mm are sent to PACS or review with the axial im ages. For obese patients, 5-mm collimation is used to decrease noise and to reduce the radiation dose. The entire abdom en and pelvis is im aged rom the top o the diaphragm s to the ischial tuberosities in all traum a patients. The radiologist should review the im ages on the scanner. I there is evidence o renal injury or perinephric uid, a 10-m inute delayed scan is per orm ed through the kidneys, ureters, and bladder to evaluate or collecting system rupture. The delayed scan should be per ormed with low-radiation dose technique and 5-m m collimation. Delayed scans at 5 to 10 minutes m ay also be per ormed when there is suspicion or active hemorrhage with contrast extravasation or pseudoaneurysm . The delayed scan should be ocused on the region o interest and does not need to re-im age the entire abdom en and pelvis.

CT cystography is per orm ed when there is suspicion or bladder injury. Bladder injury is considered in patients with (1) m icroscopic hem aturia and pelvic racture or acetabular racture involving the obturator ring or penetrating traum a to the pelvis, or (2) gross hem aturia and stranding around the bladder. Iodinated contrast o 50 m L is diluted in a 50 0 -m L bag o warm ed norm al saline. A ter the bladder has been em ptied 300 m L o the diluted contrast is instilled into the bladder via Foley catheter under gravity ow and then CT through the pelvis per orm ed. CT cystography m ay be per orm ed at the sam e tim e as the 10-m inute delayed scan through the kidneys, ureters, and bladder.

Th o r a CiC Tr a u m a Rib Fractures Rib ractures commonly occur ollowing blunt chest trauma and in isolation are not li e threatening although the pain associated with them may lead to hypoxemia, particularly in elderly patients. The presence o multiple rib ractures, however, is associated with more serious injuries. Fracture o the rst through third ribs indicates a high-energy mechanism o injury and is associated with traumatic injury to the brachial plexus and great vessels. Fractures o the lower ribs can be associated with injury to the liver, spleen, and kidneys. Any rib ractures can result in pneumothorax, hemothorax, and pulmonary contusion or laceration (Figure 18-1). CT has a higher sensitivity or detecting rib ractures than chest radiographs and can also aid in the diagnosis o associated injuries. Flail chest can occur when three or m ore consecutive ribs are each ractured in at least two places and occurs in the setting o high-energy traum a. In this condition the contiguous ractured rib ragm ents orm a ail segm ent that m oves paradoxically during respiration. A ail sterum occurs when three contiguous bilateral anterior ribs are ractured. Patients usually require surgical treatm ent and prolonged m echanical ventilation.

Sternal Fractures Sternal ractures can occur when the sternum is crushed against the steering wheel during m otor vehicle crashes. Sagittal re orm ations o the sternum are use ul to diagnose these injuries that m ay be m issed on axial CT scans. It is especially im portant to evaluate the sternum i one observes a retrosternal hem atoma on axial CT im ages. Sternal ractures are associated with cardiac and aortic injuries. Cardiac injuries include myocardial contusion, hemopericardium , and m yocardial rupture usually o the anterior right atrium or ventricle (Figure 18-2). Hemopericardium can lead to cardiac tam ponade and requires emergency decom pression. Myocardial contusion requires ECG m onitoring. Nondisplaced sternal ractures are managed like rib ractures. Sternoclavicular dissociation m ay be associated with injuries to the trachea, esophagus, subclavian vessels, and brachial plexus when the clavicle is dislocated posteriorly.

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Figure 18-3 Right Scapulothoracic Dissociation Contrast-enhanced CT o the chest in a 57-year-old m ale a ter a m otorcycle collision dem onstrating asym m etrically increased distance between the right scapula and thoracic cage (asterisk) and contrast extravasation rom an injured right axillary artery (black arrow).

Scapulothoracic Dissociation

Figure 18-1 Rib Fracture with Pulmonary Contusion Chest CT in a 43-year-old m ale a ter m otor vehicle collision dem onstrates a displaced posterior rib racture (black arrow) with adjacent pulm onary contusion (white arrow). Associated subcutaneous em physem a and sm all pneum othorax (black arrowhead) are present.

Scapulothoracic dissociation occurs when there is separation o the scapula rom the chest wall (Figure 18-3). It m ay be associated with ractures o the clavicle or scapula or sternoclavicular separation. These injuries are orequarter am putations and are associated with vascular injury to the subclavian and axillary vessels and traum atic avulsion o the brachial plexus. They m ay be suspected on chest radiograph when the scapula is asym m etrically o set rom the chest wall. One should evaluate the distance rom the m edial border o the scapula to the thoracic spine and com pare both sides. The diagnosis is readily m ade on CT.

Pneumothorax

Figure 18-2 Sternal Fracture with Hemopericardium Contrast-enhanced chest CT in a 47-year-old m ale a ter m otor vehicle collision dem onstrating a sternal racture (white arrow) with a sm all am ount o hemopericardium (arrowheads).

Pneum othorax can occur rom penetrating or blunt traum a. In blunt traum a, pneum othorax results rom alveolar rupture due to increased intrathoracic pressure or by dam age caused by ractured ribs. Because m ost traum a patients are im aged in supine position the diagnosis o pneum othorax by radiography is challenging. In a supine patient, radiographic ndings o pneum othorax include increased lucency at the involved lung base, accentuation o the lateral costophrenic angle (deep sulcus sig ), and abnorm ally sharp de nition o the m ediastinal contours. CT has high sensitivity and speci city or detection o pneum othorax. In an individual patient the decision to treat a pneum othorax o ten depends on their sym ptom s and physiologic status. Treatm ent consists o placem ent o a chest tube into the pleural space. A te sio p eumothorax requires im m ediate treatm ent and occurs when the pneum othorax leads to increased intrapleural pressure so that venous return to the heart is im paired with resultant hem odynam ic collapse. Findings suggestive o tension pneum othorax include m ediastinal shi t to the side opposite the pneum othorax, attening or inversion o the ipsilateral hem idiaphragm , and hyperexpansion o the ipsilateral chest.

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Pulmonary Contusion and Laceration Pulmo ary co tusio occurs when injury to pulm onary alveoli causes hem orrhage without signi cant alveolar disruption. Contusions can occur with blunt or penetrating traum a although they are usually sm aller and clinically inconsequential in the setting o penetrating traum a. On both CT and radiographs, contusions will m ani est as illde ned patchy airspace opacities in a nonsegm ental distribution (Figure 18-4). They typically occur at the site o im pact, although contrecoup injury in a portion o the lung opposite rom the site o injury m ay occur. Consolidation will o ten spare the outer 1to 2 m m o the lung (subpleural spari g). Pulm onary contusion is im m ediately visible on CT but m ay take up to 6 hours to be evident on radiography. The appearance o ocal lung opacities greater than 24 hours a ter injury is m ore likely to result rom pneum onia or aspiration. Pulm onary contusions typically resolve in 3 to 10 days. Pulmo ary laceratio s occur when there is disruption o the lung parenchym a. A round or oval cavity orm s due to the inherent elastic recoil o the lung tissue. The cavity m ay be lled with air (pneum atocele), blood (hem atocele), or both (hem atopneum atocele) and is usually surrounded by

Figure 18-4 Pulmonary Contusion and Laceration Contrast-enhanced chest CT in a 41-year-old m ale a ter a all o 15 eet. Pulm onary laceration in the right lower lobe (black arrows) contains both air and blood (hematopneum atocele). Several areas o pulm onary contusion (white arrows) and a trace pneum othorax (black arrowhead) are also present.

contusion, which m ay obscure the ndings on radiography. Four di erent types o pulm onary lacerations have been described on the basis o their CT appearance and m echanism o action: (1) compressio rupture—the m ost com m on type and occurs deep in the lung parenchym a; (2) compressio shear i jury occurs in the paraspinal regions due to injury against the spine; (3) rib pe etratio is a peripheral injury associated with rib racture and pneum othorax; (4) adhesio tears are rare and caused by shearing related to a pre-existing pleuropulm onary adhesion. Unlike contusions, lacerations m ay take several m onths to heal. They are m ore com m only seen in children and young adults due to greater chest wall com pliance, which m akes them m ore susceptible to lung injury with blunt traum a.

Tracheobronchial Injury Tracheobronchial injuries are serious injuries that occur in 3% o blunt chest traum a (Figure 18-5). In 80% o cases the injury is intrathoracic and located within 2.5 cm o the carina. Up to 80% o patients with tracheobronchial injury die within the rst 2 hours ollowing their injury. Injuries associated with tracheobronchial disruption include esophageal per oration, rst and second rib ractures, aortic injury, and pseudoaneurysm o the pulm onary artery. Tracheal disruptio is usually a longitudinally oriented disruption that occurs at the junction o the cartilaginous and membranous portions o the trachea. Bro chial laceratio s are m ore com mon than tracheal lacerations and most requently a ect the right m ainstem bronchus. On CT tracheobronchial disruption m ay result in subcutaneous emphysema, pneumom ediastinum , or pneum othorax. Additional ndings o tracheobronchial injury include the alle lu g sig which results rom com plete transection o a bronchus and occurs when the ipsilateral lung alls away dependently rom the pulm onary hilum (usually posterolaterally in a

Figure 18-5 Tracheal Rupture Contrast-enhanced chest CT in a 12-year-old em ale a ter an ATV accident. Although exact site o the tracheal disruption could not be identi ed on CT, a tracheal injury was correctly suspected due to the extensive subcutaneous air and pneum om ediastinum .

Chapter 18 Trauma

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supine patient). Persistent pneum othorax despite adequate treatment with chest tube placem ent should raise suspicion or a bronchial injury. Although tracheobronchial injury is one cause o pneum omediastinum , air in the mediastinum can also result rom alveolar disruption with visible air dissecting along the bronchovascular lung interstitium into the mediastinum (Mackli ef ect). Tracheal diverticula are a comm on incidental nding that occur at the m embranous portion o the trachea, near the junction with the cartilaginous portion. They can range in size rom 1 to 15 m m and occur more requently on the right side. They are characteristically located at the thoracic inlet and should not be m istaken or a tracheal injury. In patients with suspected tracheobronchial injury con rm atory bronchoscopy is per ormed and injuries treated surgically.

Esophageal Injury Esophageal injuries m ay occur rom blunt or penetrating traum a and are rare. The cervical and upper thoracic esophageal segm ents are the m ost com m only injured, and there is an association with tracheal injuries. Injuries can range rom m ucosal lacerations and intram ural lacerations to ull-thickness per oration with contained or reeowing leakage o contents. Im aging ndings associated with esophageal injury include gas or uid in the m ediastinum , pleural e usion, and extravasation o oral contrast. Mediastinitis and abscess orm ation m ay be present on delayed im aging. In patients with suspected esophageal injury rom blunt traum a, an esophagram with water-soluble contrast is per orm ed. I is it negative, then barium contrast should be used as it is reported to have greater sensitivity or detection o sm all leaks. In patients with suspected esophageal injury resulting rom penetrating traum a, CT is usually per orm ed rst due to the high likelihood o vascular injuries and ollowed by an esophagram . Patients with m ucosal lacerations or contained transm ural per orations m ay be m anaged conservatively. Uncontained esophageal per oration is considered a surgical em ergency.

Diaphragmatic Rupture Diaphragm atic rupture occurs in up to 8% o patients with blunt traum a with up to 9 0 % occurring in young m en in high speed m otor vehicle collisions. Patients with diaphragm atic rupture com m only have other injuries, which m ay include hepatic and splenic injuries, thoracic aortic and nonaortic injuries, and pelvic ractures. Tears typically involve the posterolateral sur ace o the hem idiaphragm and occur m uch m ore requently on the le t than on the right, which m ay be due to a protective e ect o the liver or underdiagnosis. Herniation o visceral organs into the chest m ay dem onstrate the collar sig with orm ation o a narrowed waist-like area o viscera as it passes through the disrupted diaphragm (Figure 18-6 ). Another nding on CT is the depe de t viscera sig in which the abdom inal viscera are no longer supported posteriorly by the diaphragm and

Figure 18-6 Left Diaphragmatic Rupture Coronal im age rom a contrast-enhanced CT o the chest and abdom en in a 44-year-old m ale a ter high-speed motor vehicle collision. Intra-abdom inal contents including the distal stom ach and splenic exure o the colon have herniated into the le t chest with a “collar sign” or a waist as the stomach extends through the diaphragm atic de ect (arrows). A nasogastric tube delineates the esophagus and esophageal hiatus (arrowhead).

all dependently through the de ect to contact the posterior chest wall. With a right side injury the upper liver will be positioned adjacent to the posterior right ribs and with le t side injury stom ach and bowel will abut the posterior le t ribs. When diaphragm atic injury occurs in the setting o penetrating injury, the de ect is usually sm all and diagnosis m ay be delayed. With the use o coronal and sagittal re orm ations, CT can o ten dem onstrate even sm all areas o diaphragm atic discontinuity without herniation. Mim ics o traum atic diaphragm atic disruption include posterolateral diaphragm atic de ects rom congenital Bochdalek hernias, which occur in 6 % o individuals and are m ore com m on on the le t side. A ocal contour de orm ity or eventration o the diaphragm can m im ic a tear. Use o coronal and sagittal re orm ats is help ul to di erentiate a diaphragm atic eventration rom a disruption.

Acute Traumatic Aortic Injuries Acute traum atic aortic injury (ATAI) encom passes a variety o entities that can range rom an intram ural hem atom a to com plete aortic transection (Figure 18-7). ATAI is im m ediately atal in up to 80% to 9 0% o patients with very high early m ortality even am ong patients who do survive long enough to reach m edical attention. ATAI requently occurs

256

Body CT: The Essentials

A

B

Figure 18-7 Traumatic Aortic Injury Axial (A) and m ultiplanar re orm at (B) rom a CT angiography o the chest in a 24-year-old em ale a ter a m otor vehicle crash. Axial im age (A) dem onstrates an intim al dissection ap (arrow) in the descending aorta with surrounding m ediastinal hem orrhage contacting the aorta and a le t hemothorax

(arrowheads). Multiplanar re orm at im age (B) dem onstrates a pseudoaneurysm distal to the le t subclavian artery which orm s acute m argins with the aortic wall (arrow). A norm al ductus diverticulum could be seen at this location; however, it would have a sm ooth contour with gentle obtuse angles continous with the aortic wall.

rom rapid deceleration, which causes torsion or shearing orces in areas where the aorta is relatively im m obile. The m ost com m on level o injury is at the aortic isthm us near the ligam entum arteriosum , with less requent involvem ent at the origins o the great vessels, the aortic root, and the diaphragm atic hiatus. Another potential m echanism o injury is the “osseous pinch” or aortic com pression between the chest wall anteriorly and the thoracic spine posteriorly. Approxim ately 75% to 80 % o ATAI result rom high-speed m otor vehicle collisions. Other etiologies include a all rom a height. Risk actors associated with ATAI include patient age greater than 50 years, being unrestrained, hypotension, thoracic injury, abdom inopelvic injury requiring em ergent laparotom y, long-bone ractures, and m ajor head injury. ATAI alm ost never occurs in patients under 10 years o age. Chest radiograph is requently used as an initial screening exam ination to look or signs o m ediastinal hem atom a indicating potential underlying vascular injury. Findings o m ediastinal hem atom a on chest radiographs include (i) loss o the norm al aortic contour; (ii) m ediastinal widening greater than 8 cm or 25% o the thoracic width; (iii) rightward tracheal or esophageal deviation; (iv) depression o the le t m ainstem bronchus; and (v)

presence o a le t apical cap. Because m any types o injuries can result in m ediastinal hem atom a including bleeding rom sm all arteries and veins and bleeding rom ractured bones, chest radiographs have a low speci city o 5% to 10 % or ATAI. Furtherm ore, som e patients with ATAI have little or no m ediastinal hem orrhage with a near-norm al m ediastinum on chest radiograph. Generally patients with abnorm al chest radiographs or with risk actors or ATAI are evaluated with CT angiography (CTA) with m ultiplanar re orm ations. CTA has a sensitivity approaching 10 0% and speci city o 80% to 9 0% or ATAI. Direct ndings o aortic injury on CTA include pseudoaneurysm , abnorm al aortic contour, intim al ap, intram ural hem atom a, and rarely active extravasation. Mediastinal hem orrhage requently occurs in the setting o traum atic aortic injury but the m ediastinal blood usually does not arise rom the aortic lum en. Rather it arises rom injury to sm all veins or the vasa vasorum . I a m ediastinal hem atom a contacts the aorta, one should look closely or direct signs o aortic injury. However, i direct signs are not present on a good quality study, the cautious approach m ight be to per orm a ollow-up CTA a ew days later. CT can also better evaluate or other causes or a m ediastinal hem atom a including ractures o the sternum , ribs, or vertebrae or active

Chapter 18 Trauma contrast extravasation rom other vessels such as the internal m am m ary arteries. It should be noted that with the signi cant im provem ents in CT technology, sm all intim al tears are increasingly being diagnosed. Although these ndings should be described, the natural history and clinical signi cance o these “m inim al aortic injuries” has not yet been determ ined. Throm bus can develop on these intim al aps and em bolize distally warranting intervention. Norm al anatom ic variants or arti actual ndings m ay m im ic aortic injury on CT and should be recognized to prevent m isdiagnosis. A ductus diverticulum is a ocal convex outpouching in the region o the aortic isthm us that is thought to be a rem nant o the ductus arteriosus. As the aortic isthm us is a com m on site or traum atic pseudoaneurysm , it is im portant to be able to distinguish between the two. A ductus diverticulum is avored i the area has a sm ooth contour that orm s obtuse m argins continuous with the aortic wall. In contrast, a traum atic pseudoaneurysm typically has an irregular contour and orm s an acute m argin with the aortic wall. Calci cation in a ductus rem nant is requently seen and occasionally one m ay observe a patent ductus arteriosus. Norm al enhancem ent within collapsed lung adjacent to the aorta can m im ic the appearance o an intim al ap; however, pulm onary vessels and bronchi can usually be seen entering the collapsed segm ent. Cardiac pulsation arti act is m ost prevalent near the aortic root and can also give the appearance o an intim al ap. The pulsation arti act is o ten at the 2- and 7-o’clock positions and o ten the apparent intim al ap will extend out into the m ediastinal at and also be present in the pulm onary arteries. However, i ndings are equivocal, cardiac-gated CTA, transesophageal echocardiography, or conventional aortography m ay be necessary. Acute traum atic aortic injuries are considered surgical em ergencies. Treatm ent options include surgical repair and placem ent o an endovascular stent gra t. There is increasing use o endovascular stents in these patients particularly or intim al tears and sm all pseudoaneurysm s although there is little data on long-term outcom es and com plications in patients treated with endovascular techniques. Treatm ents also include blood pressure control and anticoagulation i there is evidence o throm bus and distal em bolization.

a b d o m in a l a n d Pe l v iC Tr a u m a Hemoperitoneum In blunt traum a, hem operitoneum or low-density ree uid without solid organ injury indicates bowel or bladder injury until proven otherwise. In penetrating traum a, hem operitoneum indicates violation o the peritoneal cavity. Due to the presence o hem orrhage, the attenuation o hem operitoneum is typically 30 to 45 H U but in anem ic patients the attenuation m ay be lower and closer to that o sim ple uid (< 20 H U). Layering hem orrhage within peritoneal uid m ay result in a visible hem atocrit level. The presence o a

257

hyperdense (45–70 H U) se ti el clot adjacent to an injured organ can be a use ul clue in identi ying the source o hem orrhage. Peritoneal uid will collect in dependent portions o the peritoneal space including the hepatorenal pouch (Morrison pouch), around the spleen, in the paracolic gutters, and in the rectovesical pouch or rectouterine pouch (pouch o Douglas). The m ost com m on cause o hem operitoneum in blunt abdom inal traum a is injury to the liver or spleen (Figure 18-8). In cases o bowel or bladder injury the intraperitoneal uid m ay have water attenuation (0–15 H U). The presence o uid within the bowel m esentery uid should raise concern or bowel and m esenteric injury (Figure 18-15). Another potential cause or ree uid in traum a patients is diag ostic perito eal lavage (DPL), which is a procedure per orm ed at som e traum a centers in which isotonic uid is instilled into the peritoneal space and then aspirated as a m eans o detecting hem orrhage. On CT there will be surgical clips at the um bilicus and bubbles o intraperitoneal air in patients who have undergone DPL. Most patients who undergo DPL are hem odynam ically unstable. Patients in which DPL reveals gross hem operitoneum usually bypass CT and are taken or exploratory surgery. The presence o blood or uid in the retroperitoneal spaces should result in a search or traum atic injury to retroperitoneal organs. Blood or uid in the anterior pararenal space m ay result rom injury to the duodenum or pancreas. Blood or uid in the perirenal spaces m ay result rom renal or adrenal gland injuries. Retroperitoneal hem atom as m ay also be due to injury o the abdom inal aorta or other vessels, or injury to the posterior bare area o the liver. Tests such as DPL and ocused abdomi al ultrasou d or trauma (FAST US) that evaluate the peritoneal space are not sensitive or detection o uid or hem orrhage in the retroperitoneal space.

Active Hemorrhage Whenever a hem atom a is observed on CT, it is im portant to evaluate or extravasation o contrast rom vessels (Figure 18-8) that indicates active hem orrhage. Extravasated contrast will appear as a dense am orphous collection o contrast that is sim ilar or greater than blood pool (85–350 H U) on portal venous phase. On delayed scans extravasated contrast rem ains dense while the blood pool decreases in density and extravasated blood will tend to dissipate or di use within a surrounding hem atom a. This distinguishes active contrast extravasation rom a pseudoa eurysm in which the contrast density will ollow that o the blood pool (within 10 H U) and will m aintain the sam e shape and con guration on delayed im ages (Figures 18-9 and 18-10 ). The presence o active arterial hem orrhage is a m edical em ergency that requires em ergent endovascular or surgical treatm ent. Patients with active hem orrhage rom veins are usually treated conservatively, but the presence o active hem orrhage should be com m unicated with the traum a team .

258 Body CT: The Essentials

A

B

Figure 18-8 Grade III Splenic Hematoma with Active Contrast Extravasation A–B. Selected axial im ages are shown rom portal venous phase contrast-enhanced abdom inopelvic CT in a 42-year-old m an ollowing assault. Intraparenchym al hem atom a (black

arrowheads in A) lls a large splenic laceration (> 3 cm ). Contrast extravasating (white arrows in A and B) rom the posterior splenic capsule extends around the le t peritoneal space and greater gastric curve and accounts or hem operitoneum (labeled H ).

Hemodynamic Shock There are several signs on abdom inal CT that m ay indicate a patient is in hemodynam ic shock. The most com mon is attening o the IVC, in which the AP diameter o the IVC m easures less than 9 m m at the level o the le t renal vein. In patients with greater volume depletion the caliber o the abdom inal aorta and m esenteric arteries will dim inish. H ypotensive patients may dem onstrate thick-walled sm all bowel loops with m ucosal hyperenhancement and subm ucosal edem a (Figure 18-11) term ed shock bowel that results rom splanchnic vasoconstriction. The pathophysiology o the nding is not known but is thought to be due to increased mucosal perm eability. Other signs that may be observed in the hypoper usio complex include prolonged renal enhancem ent, hyperenhancing adrenal glands, diminished spleen enhancem ent, and variable pancreatic enhancement with peripancreatic edem a.

Solid Organ Injuries

Figure 18-9 Traumatic Renal Pseudoaneurysm Axial im ages rom portal venous phase abdom inopelvic CT in a 27-year-old m an shot in the right ank dem onstrate two pseudoaneurysms (black arrows) in the upper pole o the right kidney. On 10 m inute delayed CT the pseudoaneurysm s were unchanged in size and had same density as blood pool (not shown).

Solid organ injuries are graded according to the Orga I jury Scali g (OIS) Committee o the America Associatio or the Surgery o Trauma (AAST). Under this system , the greater the grade o organ injury the greater the severity and the greater the likelihood that patient will require intervention which can range rom interventional procedures to surgery. General patterns o injury or solid organs range rom contusion, subcapsular and intraparenchym al hem atomas, ruptured hem atom as, lacerations, and

Chapter 18 Trauma

259

A

B

Figure 18-10 Grade V Juxtavenous Hepatic Laceration with Active Arterial and Venous Extravasation Axial im ages rom portal venous (A) and 10 -m inute delayed (B) phases o an abdom inopelvic CT in a 40 -year-old m an ollowing m otor vehicle crash dem onstrate large hepatic

laceration (labeled L) extending to the retrohepatic IVC. Two oci o intraparenchym al active arterial extravasation (white arrows) increase in size on delayed im ages (open arrows). Active extravasation rom the IVC (black arrowheads) is best seen on delayed im ages.

devascularization. Intraparenchym al hematomas are ovoid and mass-like areas o clotted blood within an organ that have high attenuation (40–6 0 H U) even on unenhanced CT. Subcapsular hematomas are intraparenchym al hem atomas located along the periphery o an organ and abutting

the capsule that will usually result in m ass-like compression o the adjacent organ parenchyma. Hem atomas can rupture through a capsule into the tissues surrounding the organ, resulting in a sentinel clot. Co tusio s are ill-de ned areas o dim inished attenuation. Laceratio s are well-de ned

A

B

Figure 18-11 Hypoperfusion Complex Due to Hemorrhagic Shock A and B. Selected axial images are shown rom contrastenhanced abdom inopelvic CT in a 75-year-old wom an hit by a

car. Findings include collapsed IVC, (circled in B) peripancreatic uid (large open arrowheads), and di use bowel wall thickening, and mucosal hyperenhancem ent.

260

Body CT: The Essentials

linear or branching areas o low attenuation. Traumatic i arcts present as subcapsular wedge-shaped areas o diminished enhancem ent that may be due to traum atic injury or dissection o a major or sm all vessel o the involved organ. Other injury patterns m ay be relevant to a speci c organ such as collecting system rupture or renal injuries. A shortcoming o the OIS injury grading system is that som e types o vascular injuries such as active hemorrhage, pseudoaneurysm , and arteriovenous stula, and biliary injuries are not orm ally included in the grading system s, but do in uence management and intervention.

Gastrointestinal Injuries Splenic injury The spleen is the most com monly injured solid organ in the abdom en ollowing blunt traum a. Injury to the spleen may be associated with adjacent le t rib ractures and injury to the liver and other abdom inal organs. Isolated splenic injury occurs and is more likely i there is splenom egaly. Delayed splenic rupture discovered several days a ter traum a m ay occur in patients with splenic injuries m anaged conservatively and in patients with undiagnosed splenic injury. The AAST grading schem e or splenic injury is shown in Table 18-1. It is im portant to di erentiate norm al splenic T

18-1. AAST Spleen Injury Grading System

Grade I h o Lc ion

Subc sul C sul

Grade II h o Lc

Subc In 1–3 c

ion

Grade III h o

Lc

c nc y

ld

sul 10%–50% su c nc y l < 5 c di nc y d no involving nc y l v ss l

Subc sul > 50% su c o x nding r u u d subc sul o nc y l o In nc y l o > 5c > 3c nc y l d o involving b cul v ss ls

ion

Grade IV

Lc ion o s g n l o il v ss ls oducing jo d v scul iz ion (> 25% o s l n)

Grade V Lc ion V scul a dv nc on g d

< 10% su < 1c

Co l ly s ds l n h il v scul inju y w ic d v scul iz d s l n o

ul i l inju i s o s

og nu

o G d III.

cle ts and lobulations rom lacerations. Unlike lacerations, splenic cle ts have rounded m argins and m ay contain invaginated at. Because the spleen is an essential organ in m aintaining im m une com petence, there is a trend away rom splenectom y and toward conservative m anagem ent o splenic injuries. AAST grade III and higher splenic injuries and those with a large hem operitoneum are at greater risk or ailed nonoperative m anagem ent. The only absolute indication or surgery in any patient with splenic injury is hem odynam ic instability. Most ailures o conservative therapy occur during the rst 24 hours a ter injury. Although not taken into account by the AAST classi cation patients with active hem orrhage into the peritoneal cavity usually require surgical intervention (Figure 18-8). Hem odynam ically stable patients with active contrast extravasation con ned to the splenic parenchym a m ay be m anaged with endovascular em bolization. Traum atic pseudoaneurysm s and arteriovenous stulas require therapy due to the risk o delayed rupture.

Liver injury The liver is the second m ost com m only injured solid organ ollowing blunt traum a and is the m ost com m only injured solid organ in the abdom en when blunt traum a and penetrating traum a are com bined. The right hepatic lobe is m ore likely to be injured than the le t hepatic lobe. Le t hepatic lobe injuries m ay be associated with injuries to the pancreas and duodenum . The AAST grading schem e or liver injury is shown in Table 18-2. Most liver injuries are m anaged conservatively. Major vascular injury occurs when the laceration involves portal veins, hepatic veins, IVC, or when there is active contrast extravasation (Figure 18-10 ). Injury to the retrohepatic IVC or hepatic veins is associated with high m ortality due to high risk o bleeding and dif cult surgical access. Active contrast extravasation into the peritoneal cavity usually requires surgery. Delayed hem orrhage can result rom pseudoaneurysm s. Pseudoaneurysm s and arteriovenous stula are m ost requently m anaged with endovascular treatm ent. Liver lacerations that extend to the porta hepatis or liver hilum m ay result in biliary injury leading to developm ent o bilom a or bile peritonitis. Treatm ents or bile duct injuries include placem ent o biliary stents, percutaneous drainage, and surgery. Periportal edema is a nding that can be present in patients with blunt abdom inal traum a. On CT low-density uid is seen tracking alongside portal vein branches within the liver. Unlike dilated bile ducts which are usually only on one side o a portal vein, periportal edem a is present on both sides o a portal vein branch. Periportal edem a m ay be present in patients with liver injuries, but is not speci c or liver injury and is o ten in patients who have undergone volum e resuscitation. Periportal edem a m ay also occur in patients with pre-existing liver disease. Because the bare area o the liver does not com m unicate with the peritoneal space, injuries to this portion o the

Chapter 18 Trauma T

Subc sul , < 10% su C sul , < 1c

Grade II h o

c nc y

ld

h

o

m ino con usion wi ou duc inju y

Lc

ion

Su

f ci l l c

ion wi ou duc inju y

Grade II Subc sul , 10%–50% su c in nc y l < 10 c in di 1–3 c nc y d , < 10 c in l ng

ion

Grade III h o

Lc

18-3. AAST Pancreas Injury Grading System

Grade I

Grade I h o Lc ion

Lc

T

18-2. AAST Liver Injury Grading System

261

;

Subc sul > 50% su c o x nding; u u d subc sul o nc y l o ; in nc y l o > 10 c di o x nding

ion

> 3c

nc y

in

ld

h

o

m jo con usion wi ou duc inju y

Lc

ion

m jo l c issu loss

ion wi ou duc inju y o

Grade III

Dis l ns c ion o wi duc inju y

Grade IV

p oxi l ns c ion o nc y l inju y involving ull o bil duc

Grade V

m ssiv dis u ion o d

a dv nc on g d

o

ul i l inju i s u

nc y

nc

l inju y

ic

o g d III.

Grade IV Lc

ion

p nc y l dis u ion involving 25%–75% o ic lob o 1–3 Couin ud s g n s wi in singl lob

Grade V

p nc y l l c ion involving > 75% o ic lob o > 3 Couin ud s g n s wi in singl lob Jux ic v nous inju i s ( .g., o ic v n c v o c n l jo ic v ins)

Grade VI

h

a dv nc on g d

o

ic vulsion ul i l inju i s u

o g d III.

liver m ay be associated with a right retroperitoneal hem atom a and injury to the right adrenal gland or kidney rather than hem operitoneum . Incidental liver m asses such as a hem angiom a should not be con used with intraparenchym al hem atom a or contusion. The presence o peripheral nodular discontinuous enhancem ent in the portal venous phase that lls in with an attenuation near that o blood pool on a 5- to 10 -m inute delayed scan distinguishes a hem angiom a rom a liver injury.

Gall bladder injury Gall bladder wall contusion, rupture, and avulsion are rare com plications o traum a usually diagnosed at surgery.

Pancreatic and duodenal injuries Pancreatic injuries are uncom m on but are associated with high m orbidity and m ortality. The m ost com m on m echanism o pancreatic injury in blunt traum a is anterior–posterior com pression o the pancreas against the vertebral

colum n. Exam ples o this injury include seat belt injuries in m otor vehicle collision, a child alling over the handlebars o a bike, and child abuse. Most pancreatic injuries involve the pancreatic body. Patients with pancreatic injury requently have associated injuries o the le t liver, spleen, duodenum , or stom ach. Pancreatic injuries are associated with elevated serum am ylase levels; however, am ylase levels m ay be norm al in the rst 48 hours a ter traum a. CT can be alsely negative or underestim ate the severity o pancreatic injury in the rst 12 hours ollowing traum a. There ore, in patients at risk o pancreatic injury based on their m echanism o traum a and in those with elevated serum am ylase, repeat im aging 12 to 24 hours ollowing injury be necessary. The AAST scoring system is used to grade pancreatic injuries (Table 18-3). Findings o pancreas injury on CT include contusions, hem atom as, lacerations, and transections (Figure 18-12). Hem atom as are requently located between the splenic vein and the pancreatic parenchym a. Pancreatic injuries are categorized as distal i they are to the le t o the superior m esenteric vein (SMV) and proxim al i they are to the right o the SMV. Pancreatic lacerations that involve greater than 50 % the AP dim ension o the pancreas are likely to involve the m ain pancreatic duct which is im portant because injury o the pancreatic duct requires treatm ent with surgery or rarely stenting. Distal pancreatic duct injuries m ay be treated surgically with distal pancreatectom y or Puestow procedure i the central pancreas is involved. Treatm ent o proxim al pancreatic duct injuries m ay require surgical treatm ent with Whipple procedure. Com plications o pancreatic injury include pancreatitis, pancreatic stulas, and pseudocysts. Duodenal injuries are requently associated with pancreatic injuries. The second or third segm ents o the duodenum are m ost com m only a ected. Duodenal injuries

262 Body CT: The Essentials can include contusion, wall hem atom a, per oration, and bowel transection (Figure 18-13). Wall contusions and hem atom as are m anaged conservatively. Per oration or discontinuity o the bowel is treated surgically. Duodenal injury is o ten accom panied by retroperitoneal uid adjacent to the injury.

Bowel and mesenteric injuries

Figure 18-12 Pancreatic Laceration Axial im age rom contrast-enhanced abdom inopelvic CT in a 21-year-old m an shot in the abdom en shows transection o the pancreatic tail (arrows) with intrapancreatic and retroperitoneal hem atom a. Patient was treated with distal pancreatectom y and splenectom y.

Bowel and m esenteric injuries are relatively uncom m on ollowing blunt traum a being present in 5% o patients who undergo surgery or blunt abdom inal traum a. They are m ore com m on in penetrating traum a. The m ost com m on sites o bowel injury in blunt traum a are the proxim al jejunum near the ligam ent o Treitz and the distal ileum near the ileocecal junction because the bowel is xed at these locations and prone to injury due to shearing orces that develop with rapid deceleration. Com pression injuries o the duodenum and transverse colon can occur in a seat belt injury or in the case o a child who alls over the handlebars o a bike or child abuse. Rectal injuries m ay occur with pelvic ractures. Signi cant bowel and m esenteric injuries require surgery because o the risk o hem orrhage, bowel ischem ia, per oration, and in ection. The m ost com m on sign o bowel injury on CT is a segm ental thick-walled loop o bowel (Figure 18-13). Other signs o bowel injury include discontinuity o the bowel wall, extravasated oral contrast, extralum inal air, hyperdense hem orrhage in the bowel wall, and dim inished enhancem ent o the bowel wall (Figure 18-14). Free uid

A

B

Figure 18-13 Duodenal Hematoma and Abdominal Aortic Injury Selected axial im ages are shown rom contrast-enhanced abdom inopelvic CT in a 21-year-old m an ollowing m otor vehicle crash. Injuries consistent with seat belt injury include

intram ural hem atom a (white arrows in A) at the third portion o the duodenum and traum atic abdom inal aortic injury with intim al aps and pseudoaneurysm (open arrowheads in B).

Chapter 18 Trauma

263

A

B

Figure 18-14 Bowel Injury with Free Intraperitoneal Fluid A. Axial im age is shown rom contrast-enhanced abdom inal CT in a 41-year-old wom an with seat belt sign ollowing m otor vehicle crash. Findings were lim ited to a sm all volum e o ree intraperitoneal uid (white arrows) and segm ental thickening o a proxim al loop o jejunum (black arrows). B. Progressive

abdominal pain prom pted repeat CT with intravenous and enteric contrast 24 hours later. In addition to m arked increase in ree uid throughout the abdomen and some pneumoperitoneum (open arrowheads), enteric contrast (asterisk) extravasates rom an abnormal jejunal bowel loop (white arrowheads). Full-thickness tear o the jejunum was con rmed at surgery.

is a m ore com m on nding than pneum operitoneum in patients with bowel injury. Mesenteric injury presents as stranding or a hem atom a within the m esentery. The m esenteric vessels m ay be narrowed with a beaded con guration or an abrupt cuto , and there m ay be active contrast extravasation into a m esenteric

hem atom a (Figure 18-15). Mesenteric injury m ay be associated with devascularization o bowel loops that can result in bowel wall thickening or dim inished enhancem ent. Minor bowel and m esenteric injuries such as an isolated bowel wall hem atom a, isolated segm ental bowel wall thickening, or isolated m esenteric hem atom a without

A

B

Figure 18-15 Mesenteric Hematoma with Active Extravasation Axial im ages are shown rom portal venous (A) and 5-m inute delayed (B) phases o an abdom inopelvic CT in a 72-year-old wom an ollowing m otor vehicle crash. Foci o active contrast

extravasation (black arrows) into a le t m esenteric hem atoma dissipate and decrease in density with delay (open arrows). Pneum operitoneum (white arrowheads) was due to additional bowel injury (not shown).

264

Body CT: The Essentials

active contrast extravasation do not necessarily require surgery. However, i m ultiple m inor injuries occur together, the likelihood o serious injury and need or surgical exploration increases. Hem operitoneum or greater than physiologic am ounts o ree uid in the absence o solid organ injury indicates bowel injury until proven otherwise, and surgical exploration is warranted in m ost patients. Discontinuity o the bowel wall, extravasated oral contrast, dim inished enhancement o the bowel wall, and active contrast extravasation into a m esenteric hematom a indicate serious injury that requires surgery. In blunt trauma, the presence o extralum inal air is a speci c sign or bowel injury and warrants surgical exploration. However, in the setting o penetrating trauma, extraluminal air m ay be introduced by the injury rather than a bowel per oration. For this reason, water-soluble oral and rectal contrast are used or CT in patients with penetrating abdom inal traum a. Free air may also be seen in patients ollowing DPL, as a complication o severe chest traum a, or in patients with intraperitoneal bladder rupture and a Foley catheter.

Genitourinary Injuries

T

18-4. AAST Renal Injury Grading System

Grade I Con usion h

o

Grade II h

o

Lc

ion

Lc

ion

nc y l d > 1c coll c ing sys u u x v s ion

wi ou o u in y

Grade IV Lc

ion

V scul

p

nc y l l c ion x nding oug n l co x, dull nd coll c ing sys wi coll c ing sys u u o u in x v s ion m in n l y o v in inju y wi con in d o g

Grade V Lc ion V scul a dv nc on g d

Figure 18-16 Grade IV Traumatic Renal Devascularization Axial image rom portal venous phase abdominal CT in a 30-yearold m an status post skiing accident. Abrupt term ination o contrast within the right renal artery (white arrows) rom traumatic injury results in devascularization o the right kidney. Small hematoma is seen in the expected region o the distal right renal artery (asterisk) and is likely related to vascular injury.

Non x nding i n l o conf n d o n l o i on u nc y l d o n l < 1c co x wi ou u in x v s ion

Grade III

Renal and ureteral injuries Blunt renal injury m ay occur rom m otor vehicle crashes, or a direct blow to the back rom sports-related injuries or a all rom a height. Renal injuries include contusion, hem atom a, laceration, and collecting system rupture. Shearing injuries to the renal artery or vein m ay lead to intim al tears and post-traum atic throm bosis (Figure 18-16 ). Penetrating traum a to the back caused by stabbing or gunshot accounts

m ic osco ic o g oss ui o u ologic s udi s no l Subc sul non x nding wi ou nc y l l c ion

Co l ly s d kidn y a vulsion o n l ilu w ic d v scul iz s kidn y o bil

l inju i s u

o g d III.

or 10 % o renal injuries. Most patients with renal traum a will have hem aturia. However, patients with injuries o the renal hilum involving the vascular pedicle or ureteropelvic junction (UPJ) disruption m ay not have hem aturia. The AAST renal injury grading schem e is shown in Table 18-4. Renal injuries are usually m anaged conservatively unless there is a vascular pedicle injury with hem orrhage or UPJ disruption. When a renal injury or perinephric uid is observed on CT, delayed scans at 10 m inutes are per orm ed to evaluate the collecting system . Grade IV injuries with collecting system rupture are identi ed on delayed scans when hyperdense contrast in the collecting system extravasates, usually into a subcapsular location or in the perinephric space. Som e grade IV injuries m ay be undergraded as grade III injuries on the initial CT because disruption o the collecting system m ay be m asked by clotted blood which prevents the contrast rom extravasating rom the collecting system . Eventually urine urokinase will lyse the blood clot and a ollow-up CT reveals the collecting system rupture (Figure 18-17). Minor grade IV lacerations

Chapter 18 Trauma

265

A

B

Figure 18-17 Renal Laceration with Delayed Urine Leak A. Axial im age rom portal venous phase abdom inal CT in a 12-year-old boy status post all shows m ultiple deep lacerations o the right kidney (white arrows) and large perinephric hem atom a (open arrowheads). No urinary contrast extravasation was detected

on delayed im ages at the initial evaluation, consistent with grade III renal lacerations. B. CT per orm ed 4 days later; however, shows contrast-opaci ed urine leaking posterior to the kidney (open circle), upgrading the renal injury to grade IV.

m ay resolve without intervention. More serious grade IV lacerations are treated with ureteral stent placem ent. Grade V renal injuries include the shattered kid ey that is separated into at least three ragm ents, traumatic thrombosis o the renal artery, and UPJ disruptio . In UPJ disruption, contrast that extravasates rom the collecting system collects in erior m edial to the renal pelvis. Delayed hemorrhage may occur in renal injuries greater than grade III due to a ruptured pseudoaneurysm (Figure 18-9) or arteriovenous stula. These vascular complications are treated with endovascular therapy. Delayed hemorrhage typically occurs within 12 days o the initial trauma. Congenital anom alies such as hydronephrosis rom UPJ obstruction or a horseshoe kidney are risk actors or renal injury.

55% o bladder injuries are extraperitoneal, 40% are intraperitoneal, and 5% are combined intraperitoneal and extraperitoneal. Extraperito eal bladder rupture is almost always associated with a pelvic racture. At CT cystography, contrast rom the bladder leaks into the anterior retropubic extraperitoneal space (o Retzius) and the extraperitoneal at on either side o the bladder resembling a “molar tooth” (Figure 18-18). With more severe injuries and disruption o the urogenital diaphragm, the extravasated contrast may extend into the scrotum. I traperito eal bladder rupture occurs due to raised intravesical pressure in patients who sustain trauma with a ull bladder. At CT cystography, extravasated contrast leaks through a usually large de ect in the bladder dome into the paracolic gutters and around loops o bowel (Figure 18-19). Intraperitoneal bladder rupture is a potential cause or ree uid in the absence o solid organ injury. Patients with intraperitoneal bladder rupture always have gross hematuria. Extraperitoneal bladder rupture m ay be treated conservatively with a Foley catheter in m ost cases. Large com plex ruptures and ruptures that involve the bladder neck are treated surgically. Extraperitoneal bladder rupture is also treated surgically in patients undergoing orthopedic surgery or their pelvic ractures. Intraperitoneal bladder rupture is always treated surgically. I one observes extraperitoneal bladder rupture on delayed scans o a CT abdom en and pelvis, it is still necessary to per orm a CT cystogram to determ ine i there is a com bined intraperitoneal com ponent since that would necessitate surgical

Bladder injury Bladder injuries occur as a result o blunt or penetrating traum a. More than 80% o bladder injuries are associated with a pelvic racture. On the other hand, only 10% o patients with a pelvic racture have a bladder injury. Bladder injuries are diagnosed with CT cystography in at-risk patients with hem aturia. At-risk patients include those with m icroscopic hem aturia (3+ hem aturia on dipstick) and pelvic racture or acetabular racture involving the obturator ring, or patients with gross hem aturia and stranding around the bladder.

266

Body CT: The Essentials intervention. CT cystography m ay be alsely negative or intraperitoneal rupture when an associated large extraperitoneal de ect prevents the bladder rom being adequately distended.

Adrenal injury

Figure 18-18 Extraperitoneal Bladder Rupture CT cystogram is shown in a 55-year-old m an su ering open-book pelvic ractures in a m otorcycle crash. Axial im age through the bladder dem onstrates extravasation o contrast through a de ect in the right anterolateral bladder wall (open arrowhead), lling the space o Retzius (asterisk) and tracking along the pelvic sidewalls bilaterally (black arrows), giving the “m olar tooth” appearance o extraperitoneal contrast. Contrast also opaci es packing m aterial on the skin (white arrow), having leaked through a de ect in the anterior abdominal wall (not shown).

Adrenal injuries usually occur in the setting o high-injury injuries to other organs although isolated right adrenal gland hem atom as ollowing blunt traum a have been described. They are usually unilateral, and the right adrenal gland is a ected m ore com m only than the le t due to its location between the liver and spine. Adrenal injuries include adrenal gland hem atom as, hem orrhage obscuring the adrenal gland, enlargem ent o the adrenal gland, and active hem orrhage into the adrenal gland. There is o ten edem a in the periadrenal at. Adrenal gland hem atom as are usually 2 to 5 cm in size with a hom ogeneous attenuation o 40 to 6 0 H U. In m ost cases, there are associated injuries to ipsilateral organs in the abdom en, retroperitoneum , and chest (Figure 18-20 ). Bilateral adrenal injuries are uncom m on but could lead to li e-threatening adrenal insuf ciency requiring steroid replacem ent.

Pregnancy and abdominopelvic trauma Traum a is the leading cause o nonobstetric m aternal m ortality and is a signi cant cause o etal loss. Both m ajor and m inor traum as in pregnancy are associated with an increased risk o etal loss. Maternal death alm ost always

A

B

Figure 18-19 I traperito eal Bladder Rupture CT cystogram in a 45-year-old m an hit by a car. (A) Axial and (B) coronal im ages dem onstrate contrast rom the urinary bladder owing reely through the peritoneal cavity, including in the

rectovesical pouch (asterisk) and m esenteric leaves (black arrows). The de ect in the bladder dom e is best seen on coronal im ages (open arrowhead in B).

Chapter 18 Trauma

Figure 18-20 Adrenal Hematoma Axial im age rom contrast-enhanced abdom inal CT in a 51-yearold m an status post m otor vehicle collision dem onstrates right adrenal hem atom a (labeled H ), sm all peripheral liver laceration (black arrow), and sm all pericaval hem atom a (white arrowheads).

results in etal death, and the best chance or etal survival is m aternal survival. In serious traum a when there is concern or m aternal injuries, CT is rst-line im aging m odality in the pregnant traum a patient as it is in nonpregnant traum a victim s. The risk o ionizing radiation rom CT to the etus is sm all com pared to the risk o delayed or m issed diagnosis o traum a to the m other, and CT should be perorm ed without delay. A single-pass CT scan through the gravid uterus results in a etal dose o approxim ately 25 m Gy (16 –31 m Gy). There is no risk o teratogenic e ects to the etus at doses less than 50 to 100 m Gy. There is a risk o teratogenic e ects at doses in excess o 10 0 m Gy between 2 and 15 weeks post conception. There is a sm all increased risk o childhood cancer death rom in utero exposure to ionizing radiation particularly at doses above 10 m Gy that is in the order o 0.0 6 % or 10 m Gy, or one cancer death in every 170 0 cancer deaths, or a relative risk o 1.4 given that the background risk o childhood cancer death is 0.14%. The risk o childhood cancer ollowing in utero exposure to ionizing radiation is relatively low at diagnostic levels. Intravenous iodinated contrast is an FDA category B agent with no known adverse e ects in pregnancy and is adm inistered to pregnant traum a patients or CT. When a CT abdom en and pelvis is per orm ed in a pregnant traum a patient, it is im portant to avoid m ultiple passes and scan overlap. However, i delayed scans are necessary to diagnose collecting system rupture, bladder injury, or active hem orrhage they should be per orm ed. A m edical physicist should calculate the etal dose rom all im aging studies and provide a dose

267

estim ate while the patient is in hospital. The patient will be counseled about the risks o ionizing radiation to the pregnancy once she is stabilized. Pregnant traum a patients are at risk or the sam e spectrum o injuries encountered in nonpregnant traum a patients. Because the ovarian veins enlarge in pregnancy, there is increased risk o retroperitoneal hem orrhage rom ovaria vei i jury. Pelvic ractures are associated with an increased risk o etal loss due to hem orrhage resulting in etal exsanguination. The m ost com m on injury to the gravid uterus ollowing blunt traum a is place tal abruptio . Although the diagnosis o placental abruption m ay be m ade on CT, the m ost sensitive test to diagnose placental abruption is external etal m onitoring with devices that m easure uterine tone and contractility and etal heart rate. CT is not per orm ed speci cally to diagnose placental abruption. Serious uterine injuries including uterine laceration and rupture and etal traum a are rare but m ay be diagnosed on CT. In uteri e rupture, the uterus is em pty and there is a ree- oating etus surrounded by am niotic uid and blood. Fetal traum a is rare because the etus is protected by the m aternal body wall and am niotic uid. When etal traum a occurs, it is usually in late third trim ester pregnancies when the volum e o am niotic uid relative to the volum e o the etus is low. The m ost com m on etal injury is a etal skull racture a d head i jury that occurs when the etus is in cephalic presentation in the setting o a pelvic racture. Uterine rupture and etal head injury are alm ost universally atal to the etus. SUGGESTED READIn GS 1. Angel E, Wellnitz CV, Goodsitt MM, et al. Radiation dose to the etus or pregnant patients undergoing m ultidetector CT im aging: Monte Carlo sim ulations estim ating etal dose or a range o gestational age and patient size. Radiology. 20 0 8;249 :220 –227. 2. Avery LL, Schein eld MH . Im aging o m ale pelvic traum a. Radiol Clin North Am. 20 12;50 :120 1–1217. 3. Boscak A, Shanm uganathan K. Splenic traum a: what is new? Radiol Clin North Am. 20 12;50 :10 5–122. 4. Bro m an N, Atri M, Hanson JM, Grinblat L, Chughtai T, Brennem an F. Evaluation o bowel and m esenteric blunt traum a with m ultidetector CT. Radiographics. 20 0 6 ;26 :1119 –1131. 5. Burks DW, Mirvis SE, Shanm uganathan K. Acute adrenal injury a ter blunt abdom inal traum a: CT ndings. AJR Am J Roentgenol. 19 9 2;158:50 3–50 7. 6 . Dang C, Schlater T, Bui H , Oshita T. Delayed rupture o the spleen. Ann Emerg Med. 19 9 0 ;19 :39 9 –40 3. 7. Gupta A, Stuhl aut JW, Flem ing KW, Lucey BC, Soto JA. Blunt trauma o the pancreas and biliary tract: a m ultim odality imaging approach to diagnosis. Radiographics. 20 0 4;24:1381–139 5. 8. Lee YJ, Oh SN, Rha SE, Byun JY. Renal traum a. Radiol Clin North Am. 20 0 7;45:581–59 2, ix 9 . Linsenm aier U, Wirth S, Reiser M, Korner M. Diagnosis and classi cation o pancreatic and duodenal injuries in em ergency radiology. Radiographics. 20 0 8;28:159 1–16 0 2. 10 . Lowderm ilk C, Gavant ML, Qaisi W, West OC, Goldm an SM. Screening helical CT or evaluation o blunt traum atic injury in

268 Body CT: The Essentials the pregnant patient. Radiographics. 19 9 9 ;19 (Spec No):S243–255; discussion S256 –S258 11. Lozano JD, Munera F, Anderson SW, Soto JA, Menias CO, Caban KM. Penetrating wounds to the torso: evaluation with triple-contrast m ultidetector CT. Radiographics. 20 13;33: 341–359 . 12. Lubner M, Dem ertzis J, Lee JY, Appleton CM, Bhalla S, Menias CO. CT evaluation o shock viscera: a pictorial review. Emerg Radiol. 200 8;15:1–11. 13. Lubner M, Menias C, Rucker C, et al. Blood in the belly: CT ndings o hem operitoneum . Radiographics. 20 07;27:10 9 –125. 14. Marm ery H , Shanm uganathan K. Multidetector-row com puted tom ography im aging o splenic traum a. Semin Ultrasound CT MR. 20 06 ;27:404–419 . 15. Miller LA, Shanm uganathan K. Multidetector CT evaluation o abdom inal traum a. Radiol Clin North Am. 20 05;43:10 79 –10 9 5, viii 16 . Moore EE, Cogbill TH , Jurkovich GJ, Shack ord SR, Malangoni MA, Cham pion H R. Organ injury scaling: spleen and liver (19 9 4 revision). J Trauma. 19 9 5;38:323–324.

17. Moore EE, Malangoni M, Jurkovich G, Cham pion H . Traum a Source: The Am erican Association o the Surgery o Traum a. In: Moore EE, ed. Scaling System or Organ Specif c Injuries. 20 13:http:/ / www.aast.org/ library/ traum atools/ injuryscoringscales.aspx - htm lBody, last accessed June 26 , 20 14. 18. Sadro C, Bernstein MP, Kanal KM. Im aging o traum a: part 2, Abdom inal traum a and pregnancy–a radiologist’s guide to doing what is best or the m other and baby. AJR Am J Roentgenol. 20 12;19 9 :120 7–1219 . 19 . Sinelnikov AO, Abujudeh H H , Chan D, Novelline RA. CT m ani estations o adrenal traum a: experience with 73 cases. Emerg Radiol. 20 0 7;13:313–318. 20 . Titton RL, Gervais DA, Hahn PF, Harisinghani MG, Arellano RS, Mueller PR. Urine leaks and urinom as: diagnosis and im aging-guided intervention. Radiographics. 20 0 3;23:1133–1147. 21. Yam auchi FI, Ortega CD, Blasbalg R, Rocha MS, Jukem ura J, Cerri GG. Multidetector CT evaluation o the postoperative pancreas. Radiographics. 20 12;32:743–76 4. 22. Yoon W, Jeong YY, Kim JK, et al. CT in blunt liver traum a. Radiographics. 20 0 5;25:87–10 4.

Index Note: Page num bers ollowed by and t represent f gures and tables respectively.

A AAST. See Am erican Association or the Surgery o Traum a (AAST) Abdom inal aorta, 231–234 aneurysms (See Aneurysms, abdominal aortic) aortoenteric f stulas, 233–234, 233 Abdom inopelvic traum a, 26 6 –26 7 active hem orrhage, 257, 258 , 259 gastrointestinal injuries (See Gastrointestinal injuries) genitourinary injuries (See Genitourinary injuries) hem odynam ic shock, 258, 259 hem operitoneum , 257, 258 solid organ injuries, 258–26 0 Aberrant le t subclavian artery (ALSCA), 9 6 Aberrant right subclavian artery (ARSCA), 96, 97 ABPA. See Allergic bronchopulm onary aspergillosis (ABPA) Absorbed dose, CT radiation, 8 Acalculous cholecystitis, 125 ACC. See Adenoid cystic carcinom a (ACC); Adrenocortical carcinom as (ACC) Accessory duct, 132 Accessory f ssures, 71 Achalasia, 27, 28 Acinar cell carcinom a, 142 Acquired cystic kidney disease, 16 5–16 6 ACR. See American College o Radiology (ACR) ACTH. See Adrenocorticotropic hormone (ACTH) Actinomyces, 83 Actinom ycosis, 83, 83 Acute aortic dissection, 9 8–9 9 , 9 9 Acute aortic syndrom e acute aortic dissection, 9 8–9 9 , 9 9 def ned, 9 8 intram ural hem atom a, 9 9 , 10 0 penetrating atherosclerotic ulcer, 9 9 , 10 0 Acute cholecystitis, 124–125, 124 Acute eosinophilic pneum onia (AEP), 35 Acute interstitial pneum onia (AIP), 37 Acute m arginal branch, RCA, 88 Acute pancreatitis. See Pancreatitis Acute pulm onary throm boem bolism , 50 , 50 Acute pyelonephritis, 158–159 , 159 Acute respiratory distress syndrom e (ARDS), 37, 37 Acute traum atic aortic injury (ATAI), 255–257, 256 Adenoid cystic carcinom a (ACC), 58, 59 Adenom yom as, 248 Adenom yom atosis, 125, 126 Adhesion tears, 254

Adnexal torsion, 244, 244 ADPKD. See Adult polycystic kidney disease (ADPKD) Adrenal adenom as absolute percentage washout, 174 endocrine abnorm alities due to, 176 lipid-poor, 173–174, 175 lipid-rich, 173, 174 relative percentage washout, 174 Adrenal aplasia, 173 Adrenal calcif cations, 180 t Adrenal cysts, 179 –180 , 180 parasitic, 180 Adrenal glands adrenal adenom as (See Adren al adenom as) anatom y, 173, 174 collision tum ors, 178 discoid, 173, 174 granulom atous disease o , 180 incidentalom as, 181–182, 181 lym phom a, 178 m etastases, 177–178, 178 m yelolipom as, 177, 177 , 177t neoplasm s, 173–179 neuroblastic tum ors, 178–179 nonneoplastic m asses, 179 –180 pheochrom ocytom as, 176 –177, 176 variants, 173 Adrenal hem orrhage, 179 , 180 Adrenal injuries, 26 6 , 26 7 Adrenal pseudocysts, 179 –180 Adrenocortical carcinomas (ACC), 177, 178 , 178t Adrenocorticotropic hormone (ACTH ), 176 , 179 Adult polycystic kidney disease (ADPKD), 10 9 AEP. See Acute eosinophilic pneum onia (AEP) AIDS-cholangiopathy, 127 AIP. See Acute interstitial pneum onia (AIP) Airways disease in ections, 6 1 tracheobronchom alacia, 56 –57, 58 AJCC. See Am erican Joint Com m ittee on Cancer (AJCC) Alert value (AV), 13 Allergic bronchopulm onary aspergillosis (ABPA), 6 4–6 5, 6 4 ALSCA. See Aberrant le t subclavian artery (ALSCA) Am ebic abscesses, 10 8, 10 8 Am erican Association or the Surgery o Traum a (AAST) grading schem e or splenic injury, 26 0t

liver injury grading system , 26 0 , 26 1t OIS Com m ittee, 258 pancreas injury grading system , 26 1t renal injury grading system , 26 4t Am erican College o Radiology (ACR), 114 Am erican Joint Com m ittee on Cancer (AJCC), 143 Am iodarone, 10 7 AML. See Angiom yolipom a (AML) Androgenital syndrom e, 176 Aneurysm al dilatation, 20 6 , 20 6 Aneurysm s, abdom inal aortic, 231–232 in am m atory, 233 m ycotic, 232–233 rupture, 232, 232 , 233 Angiom yolipom a (AML), 16 5–16 6 , 16 6 , 239 Angiosarcom a, 9 3, 9 3 , 188 Angular m odulation, 11 Annular pancreas, 132, 132 Annuloaortic ectasia, 9 8 Anom alous pancreaticobiliary junction, 133 Anterior m ediastinum anatom y, 19 ectopic parathyroid tissue in, 24, 25 germ cell tumors (See Germ cell tumor (GCT)) lym phom a, 21, 22 m asses in, 21t m ediastinal at necrosis, 24, 25 , 26 m ediastinal lipom atosis, 24, 25 thym ic carcinoid, 22–23, 22 thym ic cysts, 22, 22 thym ic hyperplasia, 23, 23 thym olipom a, 22 thym om a, 21, 22 thym us, 19 , 21 thyroid m asses, 24, 24 Anterior pararenal space, 149 , 231 Aortic aneurysm , 9 8, 9 8 Aortic coarctation, 9 7 Aortic hypoplasia, 9 7 Aortitis def ned, 9 9 giant cell arteritis, 10 0 , 10 1 Takayasu arteritis, 9 9 –10 0 Aortoenteric f stulas, 233–234, 233 Appendicitis, 20 8 CT f ndings, 20 7 per orated, 20 7–20 8, 20 8 signs o , 20 7 tip, 20 8, 20 8 Appendix m ucocele o , 20 8–20 9 , 20 8 size and appearance, 20 7

269

270

Index

ARDS. See Acute respiratory distress syndrom e (ARDS) ARPKD. See Autosom al recessive polycystic kidney disease (ARPKD) “Arrowhead” sign, 209 ARSCA. See Aberrant right subclavian artery (ARSCA) Arterial enhancem ent, 15–16 injection rate e ect on, 16 , 16 iodine concentration e ect on, 16 , 16 Aspergillosis, 6 1, 6 1 Aspergillus umigatus, 6 4 Aspiration bronchiolitis, 38 Asplenia, 184 ATAI. See Acute traum atic aortic injury (ATAI) Atelectasis, 47 classif cation o , 43 Atherosclerosis, 9 8, 16 1 Atrioventricular (AV) nodal artery, 89 Atypical hem angiom as, 110 Autoim m une pancreatitis, 138 Autosom al dom inant polycystic kidney disease (ADPKD), 16 5 Autosom al recessive polycystic kidney disease (ARPKD), 16 5 AV. See Alert value (AV) AVM. See Pulm onary arteriovenous m al orm ation (AVM) Axilla, 79 Azygos f ssure, 71–72, 72

B Back projection (BP), 4 Bacterial acute cholangitis, 127, 127 Bare area liver, 221, 221 spleen, 183, 223, 223 β-catenin–m utated adenom as, 112 B-cell lym phom a, 21 Beam hardening, 2–3 Bear paw sign, 16 0 Behçet disease, 51 Benign cystic neoplasm , 186 Benign cysts, 139 –140 Beta-blockers, 86 Biapical subpleural nodules, 44 Bilateral adrenal hyperplasia, 179 , 179 t Bilateral m ultinodular hyperplasia, 179 Bilateral ovarian m asses, 246 Bilateral renal agenesis, 153 Bile ducts cholangitis, 127, 127 drug- and toxin-induced cholangiopathies, 128 IgG4 cholangiopathy, 128 ischem ic cholangiopathy, 127 prim ary sclerosing cholangitis, 126 –127 Biliary cystadenom a, 129 , 129 Biliary ham artom as, 123, 123 Biliary hilum , cholangiocarcinoma at, 129 , 129 Biliary system anatom y, 120–122 bile ducts (See Bile ducts) biliary cystadenom a, 129 , 129 biliary ham artom as, 123, 123 cholangiocarcinom a, 128–129 , 129 choledochal cysts, 122–123, 122 cholelithiasis, 123–124, 124t

gallbladder (See Gallbladder) periam pullary carcinom a, 130 , 130 Biological E ects o Ionizing Radiation (BEIR) VII report, 10 Biphasic injection, 17 Bism uth shielding, 12 Bladder, 16 8–171 adenocarcinom a o , 170 –171 anom alies, 155–156 cystitis, 171 endom etriom as o , 171, 171 injuries, 26 5–26 6 , 26 6 nonneoplastic m asses, 171 stones, 158 TCC o , 170 , 170 traum a, 26 5–26 6 , 26 6 variants, 155–156 wall thickening, 170 , 170 t, 171t Bladder exstrophy, 155 Bladder lum en, gas in, 171, 171t Blastomyces dermatitidis, 34 Bochdalek hernias, 77, 78 Body weight, and contrast adm inistration, 16 Bolus tracking, 15 Bone kernel, 4 Borderline resectable category, or ductal adenocarcinom a, 145 Bosniak classif cation system , 16 2–16 5, 16 3t, 16 4 , 16 5t Bowel wall attenuation, 19 2 enhancem ent, 19 3, 19 3 hyperdensity in, 19 2 pneum atosis intestinalis, 19 3–19 4, 19 3 , 19 4 , 19 4t thickening, 19 2 Bow-tie f lter, 11 BP. See Back projection (BP) Branch duct IPMN, 140 –141 Brem sstrahlung, 2 Broad ligam ent, 243 Bronchi anatom y o , 6 1, 6 2–6 3 bronchial atresia, 6 3, 6 4 bronchiectasis, 6 3–6 5 cardiac bronchus, 6 1, 6 3 dilated, 6 3–6 4 endobronchial lesions, 6 5–6 6 tracheal bronchus, 6 1, 6 3 Bronchial atresia, 6 3, 6 4 Bronchial dilation, 6 3–6 4 def ned, 6 3 Bronchial lacerations, 254 Bronchiectasis allergic bronchopulm onary aspergillosis and, 6 4–6 5, 6 4 causes o , 6 4t cystic f brosis and, 6 4, 6 4 def ned, 6 3 dyskinetic cilia syndrom e and, 6 5, 6 5 in ections and, 6 3 Bronchioles, 6 6 –6 9 anatom y o , 6 6 bronchiolitis (See Bronchiolitis) Bronchiolitis, 6 6 causes o , 6 7t cellular, 6 6 –6 7 constrictive, 6 7, 6 9 , 6 9

di use aspiration, 6 7, 6 8 di use panbronchiolitis, 6 9 ollicular, 6 8, 6 8 and hypersensitivity pneumonitis, 67–68, 68 in ectious, 6 7, 6 7 respiratory, 6 8, 6 8 types o , 6 7t Bronchogenic carcinom a, 27, 27 Bronchogenic cysts, 26 , 27 Broncholiths, 6 5, 6 6 Bronchopleural f stula, 74–75, 74 Bronchopneum onia, 34–35

C Capillary hem angiom as, 110 , 112 Carcinoid tum ors, sm all bowel, 20 6 , 206 Cardiac bronchus, 6 1, 6 3 Cardiac com puted tom ography, 85–86 Cardiac output, and contrast adm inistration, 16 –17 Caroli disease, 123, 123 Castlem an disease, 27 Cavernous hem angiom as, 110 , 111 CB. See Constrictive bronchiolitis (CB) CD. See Crohn disease (CD) “Cecal arrowhead” sign, 20 8 “Cecal bar” sign, 20 8 Cecal polyp, 216 Cecal volvulus, 214, 215 Cellular bronchiolitis, 6 6 –6 7 “Central dot” sign, 210 Centrilobular em physem a, 48–49 , 48 Centrilobular pattern, Nodules, 37–38 CEP. See Chronic eosinophilic pneum onia (CEP) Cervical aortic arch, 9 7 Cervical cancer, 248–249 , 249 CF. See Cystic f brosis (CF) Chagas disease, 27 Charcot triad, 127 Chem odectom as, 30 Chest, com puted tom ography o , 33–34 Chest radiograph, 256 Chest wall anatom y, 79 –80 , 79 –80 in ections, 82–83 m asses (See Masses, chest wall) Cholangiocarcinom a, 128–129 , 129 at biliary hilum , 129 , 129 Cholangitis bacterial acute, 127 recurrent pyogenic, 127 Cholecystitis acalculous, 125 acute, 124–125, 124 em physem atous, 125 gangrenous, 124 , 125 hem orrhagic, 125 Choledochal cysts, 122–123, 122 caroli disease, 123, 123 extrahepatic, 123 Choledocholithiasis, 124, 124 Cholelithiasis, 123–124, 124t and acute pancreatitis, 134 Chondrosarcom a, 80 , 82 Chrom ophobe RCC, 16 7 Chronic atrophic pyelonephritis, 16 0 Chronic cholecystitis, 125, 125

Index 271 Chronic eosinophilic pneum onia (CEP), 35, 35 Chronic pancreatitis, 138, 138 caused by cystic f brosis, 138 com plications o , 138–139 Chronic throm boem bolic pulm onary hypertension (CTEPH ), 50 –51, 51 Churg-Strauss syndrom e (CSS), 52 Chylothorax, 73 Circum caval ureter. See Retrocaval (circum caval) ureter Cirrhosis, 10 5–106 , 105 causes o , 10 5 Classic Potter sequence, 153 Clear cell RCC, 16 6 –16 7 Closed-loop obstruction, 20 2–20 3, 20 3 Clostridium dif cile, 213 Coal worker’s pneum oconiosis (CWP), 38 Cobra head sign, 155 Cobweb sign, 9 9 , 9 9 “Co ee bean” sign, 214, 215 Collar sign, 255 Collecting duct carcinom a, 16 7 Collecting system . See Intrarenal collecting system Collision tum or, 177, 178 Colon, 20 7–217 anatom y, 207 appendicitis (See Appendicitis) cecal volvulus, 214, 215 colorectal cancer, 215–216 diverticulitis, 209 –210 , 210 , 210 t epiploic appendagitis, 210 , 210 in ectious colitis, 212–213 in am m atory bowel disease, 211–212 ischem ic colitis, 211, 211 lipom a, 214–215, 215 lym phom a, 215 m easurem ents, 20 7 om ental in arctions, 211, 211 sigm oid volvulus, 213–214, 214 toxic m egacolon, 213, 213 Colorectal cancer (CRC), 215–216 Colum ns o Bertin, 149 “Com b” sign, 212 Com et-tail sign, 158 Com m on iliac lym ph nodes, 236 Com pound calyx, 150 Com pression rupture, 254 Com pression shear injury, 254 Com pressive atelectasis, 43 Com puted tom ography (CT), 1 cardiac, 85–86 o chest, 33–34 com ponents, 2 contrast-enhanced, or acute pyelonephritis, 158–159 generational scanners, 2 inspiratory, 57, 58 liver, 104–10 5 m ultidetector, 3 oversight o , 13 protocol, 13 technique, to evaluate kidneys, 150 –151, 152 technique, to evaluate pancreas, 134 technique, to evaluate stom ach, 19 4 work ow, 1 Computed tomography dose index (CTDI), 9, 9 Congenital adrenal hyperplasia, 179

Congenital bladder diverticula, 156 Congenital lobar overin ation, 50 Congenital lung disease congenital pulm onary airway m al orm ations, 50 , 50 pulm onary sequestration, 49 –50 , 49 Congenital m egacalyces, 155 Congenital (prim ary) m egaureter, 155 Congenital pulm onary airway m al orm ation (CPAM), 50 , 50 Congenital UPJ obstruction, 16 9 , 16 9 Conn syndrom e, 176 Consolidation, lung causes o , 34t in ection and, 34–35 and pneum onia (See Pneum onia) Constrictive bronchiolitis (CB), 6 7, 6 9 , 6 9 Contrast adm inistration, 15–17 arterial enhancem ent, 15–16 , 16 body weight and, 16 cardiac output and, 16 –17 enhancem ent duration, 15 parenchym al organ and venous enhancem ent, 16 saline ush and, 17 scan delay, 15 scan duration, 15 tim e to peak enhancem ent, 15 voltage and, 17 Contrast m aterial arrival tim e, 15 Conus artery, 88, 89 COP. See Cryptogenic organizing pneum onia (COP) Coronary arteries anatom y, 87–89 anom alies, 89 –9 1 codom inant system , 87, 88 f stulas, 9 0 , 9 1 le t dom inant system , 87, 87 right dom inant system , 87, 87 Coronary CT angiography (CCTA) indications, 86 –87 Coronary dom inance, 87 Coronary ligam ents, 221 Cortical nephrocalcinosis, 156 Cortical rim sign, 159 , 16 2 Couinaud classif cation, 10 4, 10 4 CPAM. See Congenital pulm onary airway m al orm ation (CPAM) C-RADS. See CT Colonography Reporting and Data System (C-RADS) Crazy-paving, 43, 43t causes o , 43t def ned, 43 CRC. See Colorectal cancer (CRC) “Crescent” sign, 232 Crista term inalis, 88, 9 0 Crohn disease (CD), 211, 212 bowel wall thickening in, 212 distribution, 212 Crossed used ectopy, 154 Cryptogenic organizing pneum onia (COP), 35–36 , 35 Cryptosporidium parvum, 127 CSS. See Churg-Strauss syndrom e (CSS) CT. See Com puted tom ography (CT) CT angiography (CTA), 11, 251, 256 –257 CT colonography (CTC), 216 –217

CT Colonography Reporting and Data System (C-RADS), 217 CT cystogram , 151 CT cystography, 252 CTDI. See Com puted tom ography dose index (CTDI) CT enterography, or sm all bowel evaluation, 19 8–19 9 , 19 9 CTEPH . See Chronic throm boem bolic pulm onary hypertension (CTEPH ) CT-KUB, 150 –151 CT radiation dose and cardiac CT, 86 com m on term inology, 7–8, 7 e ective, estim ation o , 10 actors a ecting, 10 –12 indicators, 7–10 m anaging, 12–13 m etrics, 10t reduction in, 11–12 size-specif c estim ation, 9 –10 specif c term inology, 8–10 CT rim sign, 124 CT Severity Index (CTSI) or acute pancreatitis, 135–136 , 137t CTSI. See CT Severity Index (CTSI) CT urography (CTU), 150 , 16 9 Cushing syndrom e, 23, 176 CWP. See Coal worker’s pneumoconiosis (CWP) Cystadenof brom as, 246 , 246 Cystic f brosis (CF), 140 and bronchiectasis, 6 4, 6 4 chronic pancreatitis caused by, 138 Cystic peritoneal m asses, 227t di erential diagnosis o , 227 pseudom yxom a peritonei, 227–228, 228 Cystic retroperitoneal lesions, 239 , 239 t Cystitis, 171 Cystitis cystica, 171 Cystitis glandularis, 171 Cysts adrenal, 179 –180 , 180 bronchogenic, 26 , 27 causes o , 41t choledochal, 122–123, 122 def ned, 41 esophageal duplication, 27, 27 honeycom b, 40 intrapulm onary bronchogenic, 50 liver, 10 9 , 110 t lym phangioleiom yom atosis, 42, 42 lym phoepithelial, 140 lym phoid interstitial pneum onia, 42, 42 nonneoplastic, 185–186 , 185 pancreas (See Pancreatic cysts) paraovarian, 247 pericardial, 9 5, 9 5 peritoneal inclusion, 247, 247 pulm onary Langerhans’ cell histiocytosis, 41–42, 42 renal (See Renal cysts) thym ic, 22, 22

D DAB. See Di use aspiration bronchiolitis (DAB) Deep (m usculoaponeurotic) f brom atosis/ desm oid, 82

272 Index Delayed attenuation value (DA), 174 Delayed/ striated nephrogram s, 159 t Dependent viscera sign, 255 Desm oplastic sm all round cell tum or, 227 Detection process, in CT scanner, 3 Determ inistic e ects, radiation exposure, 7 Diagnostic peritoneal lavage (DPL), 257 Diagnostic re erence levels (DRL), 13 Diaphragm anatom y, 77–79 eventration, 77, 78 hernias, 77, 78 , 79 , 79 Diaphragm atic hernias, 77, 78 , 79 , 79 Diaphragm atic rupture, 255, 255 DICOM (digital im aging and com m unications in m edicine), 5 Di erential diagnosis cystic splenic lesions, 185, 185t Di use alveolar dam age, 37 Di use aspiration bronchiolitis (DAB), 6 7, 6 8 Di use autoim m une pancreatitis, 138, 139 Di use ocal narrowing, 56 , 56 t Di use idiopathic pulm onary neuroendocrine cell hyperplasia (DIPNECH ), 6 9 Di use nodules, 38 Di use panbronchiolitis (DPB), 6 9 Di use solid peritoneal disease, 226 –227, 226t Di use tracheal diseases, 58 granulom atosis with polyangiitis, 59 , 6 0 in ections, 6 1 in am m atory bowel disease, 6 1 relapsing polychondritis, 59 , 6 0 sarcoidosis, 6 1 tracheobronchial am yloidosis, 6 0 , 6 1 tracheobronchopathia osteochondroplastica, 6 1 Dilated esophagus, 27 DIPNECH . See Di use idiopathic pulm onary neuroendocrine cell hyperplasia (DIPNECH ) DIR. See Dose Index Registry (DIR) Direct inguinal hernias, 243 Disconnected duct, 138 Distal Pancreatectom y, 146 –147 Diverticulitis com plications o , 209 right colonic, 209 , 20 9 vs. colon cancer, 20 9 , 210 , 210 t DKS. See Dyskinetic cilia syndrom e (DKS) DLP. See Dose-length product (DLP) DoseCheck so tware, 13 Dose Index Registry (DIR), 13 Dose-length product (DLP), 9 Double aortic arch, 9 6 Double duct sign, 143, 143 “Double halo” sign, 19 2, 19 2 DPB. See Di use panbronchiolitis (DPB) DPL. See Diagnostic peritoneal lavage (DPL) DRL. See Diagnostic re erence levels (DRL) Drom edary hum p, 151, 153 Dropping lily sign, 155 Dual-energy CT, 12 Ductal adenocarcinom a, 142–145, 143 unresectable, 145 Duct o Santorini, 132 Duct o Wirsung, 132 Duodenal injuries, 26 1–26 2, 26 2 Duodenum , 20 0

Dyskinetic cilia syndrom e (DKS), 6 5, 6 5 Dysplastic nodules, 10 6

E Echinococcus granulosus, 108–10 9 , 186 Echinococcus multilocularis, 108, 186 Ectasia, 9 8 annuloaortic, 9 8 Ectopic pancreas, 132 Ectopic parathyroid tissue, 24, 25 EDAC. See Excessive dynam ic expiratory collapse (EDAC) E ective dose, CT radiation, 8 def ned, 10 estim ation o , 10 , 10 t EH E. See Epithelioid hem angioendotheliom a (EH E) Ehlers–Danlos syndrom e, 9 8 Elastof brom a dorsi, 82, 82 Em physem a centrilobular, 48, 48 def ned, 48 panlobular, 48, 48 paracicatricial, 48, 49 Em physem atous cholecystitis, 125 Em physem atous cystitis, 171, 171 Em physem atous pyelitis, 159 –16 0 Em physem atous pyelonephritis, 159 , 16 0 Em pyem a, 74, 74 Em pyem a necessitatis, 82 Endobronchial aspergillosis, 6 1 Endobronchial carcinoid, 6 5, 6 5 Endobronchial tuberculosis, 6 1 Endom etrial cancer, 249 , 250 Endom etriom as, o bladder, 171, 171 Endoscopic ultrasound (EUS), 19 6 Enhanced attenuation value (EA), 174 Entameba histolytica, 10 8 Eosinophilic pneum onia, 35, 35 Epiploic appendagitis, 210 , 210 Epithelioid hem angioendotheliom a (EH E), 116 , 117 Equivalent dose, CT radiation, 8 Escherichia coli, 171 Esophageal carcinom as, 28, 28 Esophageal duplication cysts, 27, 27 Esophageal injuries, 255 Esophageal varices, 28, 29 Esophagus, dilated, 27 EUS. See Endoscopic ultrasound (EUS) Eventration, diaphragm , 77, 78 Ewing am ily o sarcom as, 80 –81 Excessive dynam ic expiratory collapse (EDAC), 57, 58 Exophytic cysts, 16 2 External iliac lym ph nodes, 237 Extralobar pulm onary sequestration, 49 Extram edullary hem atopoiesis, 30 , 30 Extraperitoneal bladder rupture, 265–266, 266 Extraperitoneal space, pelvis, 241–242 Extrarenal pelvis, 150 Extrinsic ocal narrowing, 56

F Falci orm ligam ent, 221, 221 Fallen lung sign, 254

FAST US. See Focused abdom inal ultrasound or traum a (FAST US) Fat-containing retroperitoneal lesions, 239, 239t “Fat halo” sign, 19 2, 19 2 “Fat notch” sign, 20 0 , 20 1 Fat replacem ent, o pancreas, 133, 133 Fatty liver, 10 6 –10 7, 10 6 , 10 6 t FB. See Follicular bronchiolitis (FB) FBP. See Filtered back projection (FBP) Fem ale pelvis, 243 adnexal torsion, 244, 244 cystic-appearing lesions in, 247 em oral hernias, 243, 243 ovarian lesions (See Ovarian lesions) pelvic in am m atory disease, 244 tubo–ovarian abscess, 244, 245 Fem oral hernias, 243, 243 Fibroepithelial polyps, 16 9 Fibrolam ellar hepatocellular carcinom a (FLC), 110 , 116 Fibrom uscular dysplasia (FMD), 16 1, 16 1 Fibrothorax, 77, 77 Field o view (FOV), 5 FIGO. See International Federation o Obstetrics and Gynecology (FIGO) Filtered back projection (FBP), 4, 12 First-generation CT scanners, 1, 2 Flail chest, 252 Flash-f lling hem angiom as, 110 , 113 FLC. See Fibrolam ellar hepatocellular carcinom a (FLC) Fleischner Society guidelines, or ollow-up o incidentally detected solid lung nodules, 44t guidelines, or ollow-up o incidentally detected subsolid nodules, 45t “Floating lily” sign, 186 FMD. See Fibrom uscular dysplasia (FMD) FNH . See Focal nodular hyperplasia (FNH ) Focal autoim m une pancreatitis, 138 Focal nodular hyperplasia (FNH ), 110 , 113 Focal xanthogranulom atous pyelonephritis, 16 0 –16 1, 16 0 Focused abdom inal ultrasound or traum a (FAST US), 257 Follicular bronchiolitis (FB), 6 8, 6 8 Foram en o Winslow, 222 Foreign bodies, 6 5, 6 6 Fourth-generation CT scanners, 2 FOV. See Field o view (FOV) Fractures rib, 252, 253 sternal, 252, 253 Fungal abscesses, 10 8 Fungal in ection, o urinary tract, 16 1 Fusi orm ascending aortic aneurysm , 9 8, 9 8

G Gallbladder acalculous cholecystitis, 125 acute cholecystitis, 124–125, 124 adenom yom atosis, 125, 126 chronic cholecystitis, 125, 125 injury, 26 1 m etastases to, 128 neoplasm s, 128, 128 porcelain, 128 wall thickening, 124, 124t

Index 273 Gallbladder per oration, 124, 125 Gallstone ileus, 125, 126 Gallstones. See Cholelithiasis Ganglioneuroblastom as, 30 , 178 Ganglioneurom as, 30, 178–179 , 179 Gangrenous cholecystitis, 124 , 125 Gastric adenocarcinom a, 19 6 , 19 6 Gastric lym phom a, 19 8 Gastric volvulus, 19 5 Gastrinom as, 145 Gastritis, 19 5–19 6 Gastrocolic ligam ent, 223, 223 Gastrohepatic ligam ent, 221–222, 221 Gastrointestinal injuries bowel and m esenteric injuries, 26 2–26 4 gall bladder injury, 26 1 liver injury, 26 0 –26 1, 26 1t pancreatic and duodenal injuries, 26 1–26 2, 26 2 spleen injury, 26 0 , 26 0t Gastrointestinal stromal tumor (GIST), 196–197 advanced, 19 7–19 8 appearances, 19 7, 19 7 treatm ent response, 19 8, 19 8 Gastrointestinal tract, 19 1–217 bowel wall (See Bowel wall) colon (See Colon) sm all bowel (See Sm all bowel) stom ach (See Stom ach) GCA. See Giant cell arteritis (GCA) GCT. See Germ cell tum or (GCT) Genitourinary injuries adrenal injuries, 26 6 bladder injuries, 26 5–26 6 , 26 6 pregnancy and abdom inopelvic traum a, 26 6 –26 7 renal and ureteral injuries, 26 4–26 5 Germ cell tum or (GCT), 23 m alignant, 24, 24 teratom a, 23–24, 23 Giant cell arteritis (GCA), 51, 10 0 , 10 1 Giant hem angiom as, 110 GIST. See Gastrointestinal stromal tumor (GIST) Gluconom as, 145–146 Granulom atosis with polyangiitis (GPA), 51, 52 , 59 , 6 0 Granulom atous disease, 180 Greater om entum , 223, 223 Groove (paraduodenal) pancreatitis, 138 Ground-glass opacity acute respiratory distress syndrom e and, 37, 37 causes o , 36 , 37t def ned, 36 di erential diagnosis, 36 pneumocystis jiroveci pneum onia and, 37, 37

H Haemophilus in uenzae, 34, 35 Ham artom as, 188 H CC. See Hepatocellular carcinom a (H CC) Heart rate, and cardiac CT, 86 Helical CT, 4 Helicobacter pylori, 19 8 Hem angiom as, 10 9 , 188, 188 atypical, 110 capillary, 110 , 112

cavernous, 110 , 111 ash-f lling, 110 giant, 110 Hem angiom atosis, 110 Hem atom as, 259 , 26 1 Hem odynam ic shock, 258, 259 Hem opericardium , 9 3–9 4, 9 5 , 252 Hem operitoneum , 225–226 , 225 , 257, 258 Hem orrhage adrenal, 179 , 180 liver, 118, 118 Hem orrhagic cholecystitis, 125 Hem osiderosis, 10 7, 10 7 Hem othorax, 73, 73 Hepatic angiosarcom a, 116 Hepatic arterial bu er response, 10 4 Hepatic in arctions, 119 Hepatitis B, 10 7 Hepatitis C, 10 7 Hepatitis D, 10 7–10 8 Hepatoblastom a, 116 Hepatocellular adenom a, 110 β-catenin–m utated adenom as, 112 H NF-1 α –m utated (steatotic) adenom as, 111–112 in am m atory/ teleangiectatic adenom as, 111 Hepatocellular adenom atosis, 112, 114 Hepatocellular carcinom a (H CC), 10 5, 112–116 , 115 growth patterns, 113 inf ltrative, 114, 115 m etastases, 114 Hepatoduodenal ligam ent, 222 Hepatorenal ossa, 220 Hernias bochdalek, 77, 78 diaphragm atic, 77, 78 , 79 , 79 em oral, 243, 243 hiatal, 28–29 , 29 , 79 , 19 4–19 5 inguinal (See Inguinal hernias) internal, 20 2, 20 4–20 5, 20 4 m orgagni, 77, 79 , 79 Petersen, 20 4 Hiatal hernias, 28–29 , 29 , 79 , 19 4–19 5 High density liver, 10 7, 10 7 , 10 7t High-resolution com puted tom ography (H RCT), 33 Histoplasm osis, 44 H NF-1 α –m utated (steatotic) adenom as, 111–112 Hodgkin disease (H D), 21, 22 , 186 Honeycom b cysts, 40 Honeycom bing, 40 Horseshoe kidney, 154, 154 Hounsf eld units (H U), 4 H P. See H ypersensitivity pneum onitis (H P) H PV. See Hum an papillom a virus (H PV) H RCT. See High-resolution com puted tom ography (H RCT) H U. See Hounsf eld units (H U) Hum an papillom a virus (H PV), 58 H ydatid disease, 186 H ydronephrosis, 157, 158, 158t H ydroureter, causes o , 158t “H yperattenuating ring” sign, 210 H ypereosinophilic syndrom e, def ned, 35

H ypersensitivity pneum onitis (H P), 40 , 6 7–6 8, 6 8 chronic/ f brotic, 41, 41 H ypertrophy, 10 5 H ypoper usion com plex, 258

I Idiopathic pulm onary f brosis (IPF), 40 IEP. See Interstitial edem atous pancreatitis (IEP) IgG4 cholangiopathy, 128 Ileum, 20 0 Im ages, CT orm ats, 5 processing o , 4–5 properties, 5–6 reconstruction m ethods, 12 resolution o , 5 storage, 5–6 Im atinib, 19 7–19 8 IMH . See Intram ural hem atom a (IMH ) Incidentalom as, adrenal, 181–182, 181 Indinavir, 157 Indirect inguinal hernias, 243, 243 In antile hem angioendotheliom a, 116 In ections airway, 6 1 and bronchiectasis, 6 3 chest wall, 82–83 liver, 10 7–10 9 and lung consolidation, 34–35 renal, 158–16 1 Streptococcus pneumoniae, 35 In ectious bronchiolitis, 6 7, 6 7 In ectious colitis, 212–213 In erior accessory f ssure, 71, 72 In erior pulm onary ligam ent, 72, 73 In erior vena cava (IVC) azygous continuation o , 234, 234 congenital abnorm alities, 234 double, 234 le t-sided, 234 pseudolipom a o , 234, 234 retrograde contrast opacif cation o , 234, 235 throm bosis, 234–235, 235 In am m atory aneurysm s, 233 In am m atory bowel disease, 6 1, 211–212 In am m atory pseudotum ors, 112, 171 In am m atory/ teleangiectatic adenom as, 111 In ram esocolic com partm ent, 219 abdom inal, 220 sigm oid m esocolon and, 224, 224 In undibulum , 150 Inguinal hernias direct, 243 indirect, 243, 243 Injection duration, 15 Injection rate, 16 , 16 Inner m edulla, 173 Insulinom as, 145 Intercostal m uscles, 80 Inter ascial space, 231 Internal hernias, 20 2, 20 4–20 5, 20 4 Internal iliac lym ph nodes, 237 International Federation o Obstetrics and Gynecology (FIGO), 248 Interstitial edem atous pancreatitis (IEP), 135, 135

274

Index

Intraductal papillary m ucinous neoplasm s (IPMN), 140 branch duct/ side branch, 140 –141 com bined, 141, 141 m ain duct, 141, 141 Intralobar pulm onary sequestration, 49 , 49 Intram ural hem atom a (IMH ), 9 9 , 10 0 Intraperitoneal space, pelvis, 241, 242 Intrapulm onary bronchogenic cysts, 50 Intrapulm onary lym ph nodes, 44 Intrarenal collecting system , 150 , 16 8–171 benign m asses o , 16 9 congenital UPJ obstruction, 16 9 , 16 9 contrast f lling de ects in, 16 8t duplicated, 154, 154 papillary necrosis, 16 8–16 9 , 16 8 stones in, 157 TCC in, 170, 170 and ureters, 154–155 Intussusception, 205, 205 Iodine concentration, 16 , 16 Iodine ux, 15 IPF. See Idiopathic pulm onary f brosis (IPF) IPMN. See Intraductal papillary m ucinous neoplasm s (IPMN) Ischem ic cholangiopathy, 127 Ischem ic colitis, 211, 211 Ischioanal space, 242–243 Ischiorectal ossa, 242–243 Islets o Langerhans, 131

J Jejunum , 200

K Kartagener syndrom e, 6 5 Kidneys acute pyelonephritis, 158–159 , 159 anatom y, 149 –150, 150 angiom yolipom a, 16 5–16 6 , 16 6 anom alies and variants, 151, 153 benign prim ary m asses, 16 5–16 6 bilateral enlarged, 153, 154t bilateral sm all, 153t chronic atrophic pyelonephritis, 16 0 CT technique, 150–151, 152 cysts (See Renal cysts) em physem atous pyelonephritis, 159 , 16 0 f brom uscular dysplasia o , 16 1, 16 1 horseshoe, 154, 154 m alignant prim ary m asses, 16 6 –16 7 m alignant secondary m asses, 16 7–16 8 m etastases to, 16 8 nephrocalcinosis, 156 oncocytom as, 16 6 pelvic, 153–154 pyonephrosis, 16 0 renal abscess, 159 , 159 renal tuberculosis, 16 1, 16 1 sizes, variation in, 151, 153 Takayasu arteritis, 16 1–16 2 unilateral enlarged, 153, 153t unilateral sm all, 153t urolithiasis, 156 –158 vascular disease, 16 1–16 2 xanthogranulom atous pyelonephritis, 16 0–16 1, 16 0

Klebsiella pneumoniae, 34, 6 1, 157 Krukenberg tum ors, 19 6 , 246 , 247

L LAD. See Le t anterior descending artery (LAD) Large vessel vasculitis, 51 Lateral conal ascia, 231 LCA. See Le t coronary artery (LCA) Le t anterior descending artery (LAD), 87, 89 Le t circum ex artery, 87–88 Le t coronary artery (LCA), 9 0 anom alous, 9 0 Le t m ain coronary artery, 87, 88 Le t supram esocolic space, 222–223 Legionella pneumophila, 34 Leiom yom as, 16 9 , 248, 249 Leiom yosarcom as, 16 7, 237, 248, 249 Lesser om entum , 221 Lesser sac, 222, 222 Ligam ents, 219 broad, 243 coronary, 221 alci orm , 221, 221 gastrocolic, 223, 223 gastrohepatic, 221–222, 221 hepatoduodenal, 222 le t-sided, 219 round, 243 suspensory, 245 Ligam entum teres, 221 LIH S. See Lipom atous hypertrophy o the interatrial septum (LIH S) Linguine sign, 10 9 , 10 9 LIP. See Lymphoid interstitial pneumonia (LIP) Lipid-poor adrenal adenom a, 173–174, 175 Lipid-rich adrenal adenom a, 173, 174 Lipoid pneum onia, 36 , 36 Lipom as, 80 , 80 , 214–215, 215 Lipom atosis, o pancreas, 133, 133 Lipom atous hypertrophy o the interatrial septum (LIH S), 9 3, 9 3 Liposarcom as, 236 –237, 238 . See also specif c types LI-RADS reporting system . See Liver Im aging Reporting and Data System (LI-RADS) reporting system Liver am ebic abscesses, 10 8, 10 8 anatom y, 10 3–10 4, 10 4 bare area, 221, 221 blood supply, 10 3 cirrhosis, 10 5–10 6 , 10 5 CT technique, 10 4–10 5 cysts, 10 9 , 110 t echinococcal in ection, 10 8–10 9 epithelioid hem angioendotheliom a, 116 , 117 f brolam ellar hepatocellular carcinom a, 116 ocal nodular hyperplasia, 110 , 113 unctions o , 10 3 ungal abscesses, 10 8 hem angiom as, 10 9 –110 hem orrhage, 118, 118 hepatic angiosarcom a, 116 hepatic in arctions, 119 hepatoblastom a, 116 hepatocellular adenom a (See Hepatocellular adenom a) hepatocellular carcinom a, 112–116 , 115

high density, 10 7, 10 7 , 10 7t in antile hem angioendotheliom a, 116 in am m atory pseudotum ors, 112 injury, 26 0 –26 1, 26 1t lym phatic drainage o , 10 4 lym phom a, 116 –117 m etastases, 117–118, 117 peliosis hepatis, 119 –120 , 121 physiology, 10 3–10 4 polycystic disease, 10 9 , 10 9 portosystem ic shunt, 119 , 120 pyogenic liver abscesses, 10 8, 108 schistosom iasis, 10 9 steatosis, 10 6 –10 7, 10 6 , 10 6 t transient hepatic attenuation di erence, 118–119 , 118 viral hepatitis, 10 7–10 8 Liver Im aging Reporting and Data System (LI-RADS) reporting system , 114–115 Lobar pneum onia, 34, 35 Lobster claw, 16 8 Localized renal cystic disease, 16 5 Loe er syndrom e, 35 Long com m on channel, 122, 133 Longitudinal m odulation, 11 Lum bar triangle, 231 Lung cancer, 45–48 adenocarcinom a, 46 , 46 em physem a, 48–49 , 48–49 histopathology, 46 –47 m etastatic, 48 non–sm all cell, 46 sm all cell, 27, 27 , 46 , 47, 47 squam ous cell carcinom as, 46 –47, 46 staging system or, 47–48, 47–48 TNM staging system or, 47–48, 47–48t Lung consolidation. See Consolidation, lung Lung diseases, patterns o atelectasis, 43, 44 congenital (See Congenital lung disease) consolidation, 34–36 crazy-paving, 43, 43t cysts, 41–42 (See also Cysts) ground-glass opacity, 36 –37, 37t lung cancer (See Lung cancer) m osaic attenuation, 42–43 nodular pattern, 37–39 (See also Nodules, lung) pulm onary vascular disease (See Pulm onary vascular disease) reticular pattern, 40 –41 septal pattern, 39 –40 Lung edem a, 39 , 39 Lung neoplasm s, 6 5 Lying down adrenal gland, 153 Lym phadenopathy, 26 –27, 26 Lym phangioleiom yom atosis, 42, 42 , 73 Lym phangiom as, 185 Lym phangitic carcinom atosis, 39 –40, 40 Lym ph nodes anatom y, 236 , 236 , 237 calcif cation, 235, 235 com m on iliac, 236 density, 235–236 , 236 , 236 t external iliac, 237 internal iliac, 237 m etastases, 248 size, 235, 235t

Index 275 Lym phoepithelial cysts, 140 Lym phoid interstitial pneum onia (LIP), 42, 42 Lym phoid thym ic hyperplasia, 23 Lym phom a, 21, 22 , 36 , 36 , 76 , 76 , 116 –117 adrenal glands, 178 colon, 215–216 pancreatic, 146 renal, 16 7–16 8, 16 8 retroperitoneal, 236 , 237 sm all bowel, 205–20 6 , 20 6 Lym phom atosis, peritoneal, 227

M Macklin e ect, 255 Macrocystic (oligocystic) serous cystadenom a, 141 Macronodular cirrhosis, 105, 10 5 Main duct IPMN, 141, 141 Main pancreatic duct, 132 Malacoplakia, 171 Malignant f brous histiocytom a, 237 Malignant peripheral nerve sheath tum ors, 29 , 29 , 30 MALTom as. See Mucosa-associated lym phoid tissue (MALT) lym phom as (MALTom as) m A m odulation technique, 11 Masses, chest wall lipom a, 80 , 80 m etastases, 80, 81 neurogenic tum ors, 80 , 81 plasm acytom a, 81, 82 prim ary m alignancies, 80 –81 Mass- orm ing, growth pattern o cholangiocarcinom a, 128–129 Maxim um intensity projection (MIP), 4 MCKD. See Medullary cystic kidney disease (MCKD) Medial f broplasia, 16 1 Mediastinal at necrosis, 24, 25 , 26 Mediastinal lipom atosis, 24, 25 Mediastinitis, 30 , 30 Mediastinum , 19 –31, 20 anterior (See Anterior m ediastinum ) m iddle (See Middle m ediastinum ) posterior (See Posterior m ediastinum ) superior, 19 Medical Im aging and Technology Alliance (MITA), 13 Medullary cystic kidney disease (MCKD), 16 5 Medullary nephrocalcinosis, 156 Medullary sponge kidney disease (MSK), 156 , 156 Megacalycosis, 155 MEN I. See Multiple endocrine neoplasia type I (MEN I) Mercedes Benz sign, 123 Mesenteric f brom atosis, 230 , 230 Mesenteries, 219 Mesenteroaxial volvulus, 19 5 Mesocolic window, 20 4–20 5 Mesotheliom a, 75, 75 Metastases, 39 adrenal glands, 177–178, 178 chest wall, 80 , 81 to gallbladder, 128

hem atogenous, 248 hepatocellular carcinom a, 114 to kidneys, 16 8 liver, 117–118, 117 nodal, 248 pancreatic, 146 pleural, 75–76 , 76 sm all bowel, 20 7 splenic lesions, 186 , 186 , 187, 187 Metastatic papillary thyroid carcinom a, 39 Metoprolol, 86 Meyer–Weigert rules, 154–155 MIB. See Mirror im age branching (MIB) Microcystic serous cystadenom as, 141, 142 Micronodular cirrhosis, 10 5, 10 5 Microscopic polyangiitis (MPA), 52, 52 Middle m ediastinum anatom y, 26 bronchogenic carcinom a, 27, 27 bronchogenic cysts, 26 , 27 esophageal duplication cysts, 27, 27 lym phadenopathy, 26 –27, 26 m asses, 26 t Midgut m alrotation, 20 3, 20 3 Miliary tuberculosis, 39 , 39 Minim um intensity projection (MinIP), 4 MinIP. See Minim um intensity projection (MinIP) MIP. See Maxim um intensity projection (MIP) Mirizzi syndrom e, 124 Mirror im age branching (MIB), 9 6 MITA. See Medical Im aging and Technology Alliance (MITA) MLCN. See Multilocular cystic nephrom a (MLCN) Molar tooth, 26 5, 26 6 Morgagni hernias, 77, 79 , 79 Morison pouch, 220 Mosaic attenuation, 42–43 Mounier-Kuhn syndrom e, 56 , 57 MPA. See Microscopic polyangiitis (MPA) MSK. See Medullary sponge kidney disease (MSK) Mucinous carcinom atosis, 227 Mucinous cystadenom as, 246 Mucinous cystic neoplasm s, 141, 141 Mucocele, o appendix, 20 8–20 9 , 20 8 Mucosa-associated lym phoid tissue (MALT) lym phom as (MALTom as), 36 , 19 8 Mucous pseudotum or, 6 6 , 6 6 Multicystic dysplastic kidney disease, 16 5 Multi ocal autoim m une pancreatitis, 138 Multilocular cystic nephrom a (MLCN), 16 6 Multilocular cystic RCC, 16 7 Multiphasic injection, 17 Multiple endocrine neoplasia type I (MEN I), 145 Myasthenia gravis, 23 Mycobacterium bovis, 39 Mycobacterium tuberculosis, 34, 83, 16 1 Mycotic aneurysm s, 232–233 Myelolipom as, 177, 177 , 177t, 239 Myocardial ischem ia, 9 1, 9 2 Myocardium angiosarcom a, 9 3, 9 3 lipom atous hypertrophy o the interatrial septum , 9 3, 9 3

m yocardial ischem ia, 9 1, 9 2 m yxom as, 9 2, 9 2 papillary f broelastom a, 9 2, 9 2 Myxoid liposarcom as, 236 Myxom as, 9 2, 9 2

N NAFLD. See Nonalcoholic atty liver disease (NAFLD) Narrowing, o trachea di use ocal, 56 , 56 extrinsic ocal, 56 intrinsic ocal, 56 postintubation stenosis, 56 , 57 saber-sheath trachea, 56 , 56 NASH . See Nonalcoholic steatohepatitis (NASH ) National Lung Screening Trial (NLST), 45 Neck, pancreas segm ent, 131, 132 Nephroblastom a, 16 7 Nephrocalcinosis cortical, 156 def ned, 156 m edullary, 156 Nephrogram s, delayed/ striated, 158t Neuroblastom a, 30 , 179 Neuroendocrine tum ors, 145–146 , 146 Neurof brom a, 80 Neurof brom as, 29 , 30 Neurogenic neoplasm s paragangliom as, 30 peripheral nerves, 29 –30 sym pathetic ganglia, 30 Neutropenic colitis, 213 NH L. See Non-Hodgkin lym phom a (NH L) NLST. See National Lung Screening Trial (NLST) Nocardia asteroides, 34, 83 Nocardiosis, 83 Nodules, liver dysplastic, 10 6 siderotic, 10 6 Nodules, lung biapical subpleural, 44 centrilobular pattern o , 37–38 di use, 38 m etastasis, 39 , 39 m iliary pattern o , 38, 39 , 39 in perilym phatic distribution, 38 random pattern, 38 solitary (See Solitary lung nodule) subsolid, 45 Nonalcoholic atty liver disease (NAFLD), 10 7 Nonalcoholic steatohepatitis (NASH ), 107 Non-Hodgkin lym phom a (NH L), 21, 186 , 215 Nonneoplastic cysts, 185–186 , 185 Non-sm all cell lung carcinom a (NSCLC), 46 Nontuberculous m ycobacterial in ection, 67 “Northern exposure” sign, 213, 214 Notif cation value (NV), 13 NSCLC. See Non-sm all cell lung carcinom a (NSCLC) NSIP (nonspecif c interstitial pneum onia) pattern, f brosis, 40 , 41 NV. See Notif cation value (NV)

276

Index

O Obesity, 24 Obstructive atelectasis, 43 Obstructive pneum onia, 47 Oligocystic serous cystadenom a. See Macrocystic (oligocystic) serous cystadenom a Om enta, 219 Om ental in arctions, 211, 211 Oncocytom as, 16 6 OP. See Organizing pneum onia (OP) Organ dose, CT radiation, 8 Organ Injury Scaling (OIS) Com m ittee, AAST, 258 Organizing pneum onia (OP), 35–36 Organoaxial volvulus, 19 5 Organs o Zuckerkandl, 239 Orthotopic ureterocele, 155, 155 Ovarian cancer, 247–248 Ovarian cystadenof brom as, 246 , 246 Ovarian lesions, 244–248 di erential diagnosis, 246 Ovarian origin, identi ying, 244–245, 245 Over-beam ing, 11

P Pancreas anatom y, 131–132, 132 annular, 132, 132 CT technique, 134 cystic lesion o (See Pancreatic cysts) divisum , 132–133 ductal adenocarcinom a, 142–145, 143 , 145 ducts, 132 ectopic, 132 lipom atosis o , 133, 133 lym phom a, 146 m etastases, 146 neuroendocrine tum ors, 145–146 , 146 pancreatitis (See Pancreatitis) postoperative, 146 –147 pseudom asses, 133–134 solid neoplasm s, 142–146 , 144t Pancreatic ascites, 138 Pancreatic cysts, 139 t acinar cell carcinom a, 142 benign, 139 –140 im aging eatures o , 140 intraductal papillary m ucinous neoplasm s (See Intraductal papillary m ucinous neoplasm s (IPMN)) m anagem ent o , 142 m ucinous cystic neoplasm s, 141, 141 serous cystadenom as, 141, 142 solid pseudopapillary tum ors, 141–142 Pancreatic f stula, 138 Pancreatic injuries, 26 1 AAST scoring system , 26 1t Pancreaticobiliary junction, 121 Pancreatic pleural e usion, 138 Pancreatic pseudocysts, 30 –31, 31 Pancreatitis acute necrotizing, 135–136 , 136 , 138 acute peripancreatic uid collections, 136 autoim m une, 138 chronic, 138, 138 com plications o , 136 –138

CT Severity Index or, 135–136 , 137t groove (paraduodenal), 138 interstitial edem atous, 135, 135 peripancreatic collections in, 136 –137, 137t revised Atlanta classif cation, 136 , 137t tropical, 138 Pancreatoduodenectom y, 146 Panlobular em physem a, 48, 48 PAP. See Pulmonary alveolar proteinosis (PAP) Papilla, renal, 149 Papillary f broelastom a, 9 2, 9 2 Papillary necrosis, 16 8–16 9 , 16 8 Papillary RCC, 16 7 Paracicatricial atelectasis, 43 Paracicatricial em physem a, 48, 49 Paraduodenal, 20 4 Paragangliom as, 30 , 237, 239 “Parallel beam” arrangem ent, 1 Param etrium , 243 Paraovarian cyst, 247 Parapelvic cysts, 16 2 Parasitic adrenal cysts, 180 Parietal pleura, 71 Partial scan reconstruction, 86 Passive atelectasis, 43 Patient positioning, during scanning, 3 PAU. See Penetrating atherosclerotic ulcer (PAU) PDA. See Posterior descending artery (PDA) PE. See Pulm onary em bolism (PE) Peak tube voltage (kVp), 10 Peliosis hepatis, 119 –120 , 121 Pelvicaliectasis causes o , 158t def ned, 157 Pelvic in am m atory disease, 244 Pelvic kidney, 153–154 Pelvis, 241–250 CT technique or evaluation, 252 extraperitoneal space, 241–242 em ale (See Fem ale pelvis) inguinal hernias, 243–244 intraperitoneal space, 241, 242 ovarian lesions (See Ovarian lesions) perineum , 242–243, 242 uterine lesions (See Uterine lesions) Penetrating atherosclerotic ulcer (PAU), 99, 100 Peptic ulcer disease, 19 6 , 19 6 Per orated appendicitis, 20 7–20 8, 20 8 Per orated ulcer, 19 6 , 19 6 Periam pullary carcinom a, 130 , 130 Pericardial cysts, 9 5, 9 5 Pericardial diverticulum , 9 5 Pericardial e usion, 9 3, 9 5 Pericardial m esotheliom a, 9 5 Pericardial thickening, 9 4–9 5, 9 5 Pericardium anatom y, 9 3, 9 3 cysts, 9 5, 9 5 e usion, 9 3, 9 5 hem opericardium , 9 3–9 4, 9 5 neoplasm s, 9 5 Perilym phatic lung nodules, 38 coal worker’s pneum oconiosis and, 38 in sarcoidosis, 38, 38 silicosis and, 38, 38 Perineum , 242–243, 242 Peripancreatic collections, in acute pancreatitis, 136 –137, 137t

Peripelvic cysts, 16 2, 16 2 Peripheral nerves, neoplasm s o , 29 –30 Periportal edem a, 26 0 Perirenal space, 149 , 231 Peritoneal cavity divisions o , 219 –220 , 220 (See also In ram esocolic com partm ent; Supram esocolic com partm ent) Peritoneal inclusion cyst, 247, 247 Peritoneum anatom y, 219 –224 calcif cation, 226 , 226 , 226 t carcinom atosis, 226 cystic m asses (See Cystic peritoneal m asses) desm oplastic sm all round cell tum or, 227 di use solid peritoneal disease, 226 –227, 226 t enhancem ent, 225, 225 uid distribution, 225, 225 gastrocolic ligam ent, 223, 223 greater om entum , 223, 223 hem operitoneum , 225–226 , 225 lym phom atosis, 227 m alignant m esotheliom a, 227 m esenteric f brom atosis, 230 , 230 sarcom atosis, 227 serous sur ace papillary carcinom a, 227 sigm oid m esocolon, 224, 224 sm all bowel m esentery, 224, 224 solid m esenteric m asses (See Solid m esenteric m asses) spaces, 219 –220 , 220 supram esocolic com partm ent (See Supram esocolic com partm ent) transverse m esocolon, 223–224, 223 tuberculosis, 226 –227, 226 Persistent etal lobations, 151 Petersen hernia, 20 4 Pheochrom ocytom as, 30 , 176 –177, 176 Phrenicocolic ligam ent, 223 PI. See Pneum atosis intestinalis (PI) Pixel, 5 PJP. See Pneumocystis jiroveci pneum onia (PJP) Plasm acytom a, 81, 82 PLCH . See Pulm onary Langerhans’ cell histiocytosis (PLCH ) Pleom orphic liposarcom as, 237 Pleura, 71–77 anatom y, 71–75 bronchopleural f stula, 74–75, 74 chylothorax, 73 em pyem a, 74, 74 hem othorax, 73, 73 lym phom a, 76 , 76 m esotheliom a, 75, 75 m etastases, 75–76 , 76 neoplasm , 75–76 parietal, 71 pleuroparenchym al/ pleuropulm onary f stula, 74–75, 74 pneum othorax, 74, 74 solitary f brous tum or o , 75, 75 splenosis, 77, 77 visceral, 71 Pleural e usions, 72–73, 73 Pleural f ssures, 71, 72 Pleural plaques, 76 , 76

Index 277 Pleural space, 71 Pleural thickening, 76 –77 Pleuroparenchym al/ pleuropulm onary f stula, 74–75, 74 PMC. See Pseudom em branous colitis (PMC) PMF. See Progressive m assive f brosis (PMF) Pneum atosis intestinalis (PI), 19 3–19 4, 19 3 , 19 4 , 19 4t Pneum obilia, 124t Pneumocystis jiroveci, 180 Pneumocystis jiroveci pneum onia (PJP), 37, 37 Pneum onia bronchopneum onia, 34–35 diagnosis o , 34 eosinophilic, 35, 35 lipoid, 36 , 36 lobar, 34, 35 obstructive, 47 organizing, 35–36 pneumocystis jiroveci, 37, 37 postobstructive, 6 6 round, 35 Pneum othorax, 74, 74 , 253 Polyarteritis nodosa, 16 2 Polycystic liver disease, 10 9 , 10 9 Polysplenia, 184 Porcelain gallbladder, 128 Portosystem ic shunt, 119 , 120 Posterior descending artery (PDA), 87, 89 Posterior m ediastinum , 27 esophagus, 27–29 extram edullary hem atopoiesis, 30 , 30 m asses, 27t m ediastinitis, 30, 30 neurogenic neoplasm s, 29 –30 pancreatic pseudocysts, 30 –31, 31 Posterior pararenal space, 149 , 231 Posterolateral le t ventricular branch, 89 Postintubation stenosis, 56 , 57 Postobstructive pneum onia, 6 6 Posttraum atic cysts, 185 Pouch o Douglas, 220, 241 Pregnancy, traum a in, 26 6 –26 7 Prevesical space, 241–242, 241 Prim ary hem ochrom atosis, 10 7 Prim ary sclerosing cholangitis (PSC), 126 –127 Prim ary tracheal m alignancies, 57 Progressive m assive f brosis (PMF), 38 Prom inent colum n o Bertin, 151 Prospective triggering vs. retrospective gating, 86 Protocol, CT review o , 13 PSC. See Prim ary sclerosing cholangitis (PSC) Pseudoaneurysm s, 137, 257 Pseudocoarctation, o thoracic aorta, 9 7–9 8, 98 Pseudocysts, 136 , 138, 139 Pseudoenhancem ent, 16 3 Pseudolipom a, o IVC, 234, 234 Pseudom asses, pancreatic, 133–134 Pseudom em branous colitis (PMC), 213, 213 Pseudomonas aeruginosa, 83, 157 Pseudom yxom a peritonei, 227–228, 228 Pseudosequestrations, 49 –50 Puestow procedure, 147 Pulm onary agenesis, 49 Pulm onary alveolar proteinosis (PAP), 43, 43

Pulm onary aplasia, 49 Pulm onary arteriovenous m al orm ation (AVM), 52–53, 52 Pulm onary artery sarcom a, 51, 51 Pulm onary contusion, 254, 254 Pulm onary em bolism (PE), 50 Pulm onary f brosis hypersensitivity pneum onitis, 40 –41, 41 idiopathic, 40 NSIP pattern o , 40 , 41 sarcoidosis and, 41 UIP pattern o , 40 , 40 Pulmonary hamartomas/ mesenchymomas, 45 Pulm onary hypoplasia, 49 Pulm onary lacerations, 254, 254 Pulm onary Langerhans’ cell histiocytosis (PLCH ), 41–42, 42 Pulm onary sequestration, 49 –50 , 49 Pulm onary vascular disease acute pulm onary thromboembolism , 50 , 50 chronic throm boem bolic pulm onary hypertension, 50 –51, 51 pulm onary arteriovenous m al orm ation, 52–53, 52 pulm onary artery sarcom a, 51, 51 vasculitis (See Vasculitis) Putty kidney, 16 1, 16 1 Pyelosinus extravasation, 158 Pylorus-sparing Whipple procedure, 146 Pyogenic liver abscesses, 10 8, 10 8 Pyonephrosis, 16 0

R Radiation dose. See CT radiation dose Radiation exposure, e ects o , 7 Ram us interm edius artery, 87 Random pattern, perilym phatic distribution, 38 Rate o injection, 16 , 16 RB. See Respiratory bronchiolitis (RB) RB-associated interstitial lung disease (RBILD), 6 8 RB-ILD. See RB-associated interstitial lung disease (RB-ILD) RCA. See Right coronary artery (RCA) Reconstruction m ethodologies, im ages, 12 Rectouterine pouch, 220 Recurrent pyogenic cholangitis, 127 Re ux nephropathy, 16 0 , 16 0 Relapsing polychondritis (RPC), 56 , 59 , 6 0 Renal abscess, 159 , 159 Renal agenesis, 153 bilateral, 153 unilateral, 153 Renal calcif cation, causes o , 157t Renal cell carcinom a (RCC), 16 6 , 16 7 chrom ophobe, 16 7 clear cell, 16 6 –16 7 collecting duct carcinom a, 16 7 at-containing, 16 6 t leiom yosarcom as, 16 7 m ultilocular cystic, 16 7 papillary, 16 7 renal m edullary carcinom a, 16 7 Wilm s’ tum or, 16 7 Renal cysts, 16 2 Bosniak classif cation system , 16 2–16 5, 16 3t, 16 4 , 16 5t

diseases, 16 5 exophytic, 16 2 parapelvic, 16 2 peripelvic, 16 2, 16 2 Renal ectopy, 153–154 Renal hilum , 149 Renal in arctions, 16 2, 16 2 Renal injury, 26 4–26 5 AAST grading system , 26 4t Renal lym phom a, 16 7–16 8, 16 8 Renal m edullary carcinom a, 16 7 Renal papilla, 149 Renal parenchym a, 149 Renal pyram id, 149 , 151 Renal sinus, 149 Renal tuberculosis, 16 1, 16 1 Respiratory bronchiolitis (RB), 6 8, 6 8 Respiratory papillom atosis, 58, 59 Reticulation, 40 Retractile m esenteritis, 229 Retrocaval (circum caval) ureter, 155, 155 Retrograde contrast opacif cation, IVC, 234, 235 Retrom esenteric/ anterior inter ascial space, 231 Retroperitoneal m asses cystic lesions, 239 , 239 t at-containing lesions, 239 , 239 t f brosis, 239 –240 , 240 leiom yosarcom as, 237 liposarcom as, 236 –237, 238 m alignant f brous histiocytom a, 237 neurogenic tum ors, 237–239 , 238 sarcom as, 236 –237 Retroperitoneum anatom y, 231, 232 m asses (See Retroperitoneal m asses) Retrorenal/ posterior inter ascial space, 231 Retrospective gating, prospective triggering vs., 86 Retrouterine pouch, 241 Rib ractures, 252, 253 Rib penetration, 254 Right aortic arch, 9 6 , 9 7 Right colonic diverticulitis, 20 9 , 209 Right coronary artery (RCA), 87, 87 , 88–89 , 89 , 9 0 anom alous, 9 1 Right in erior accessory f ssure, 71, 72 Right ventricular m arginal arteries, 88 Rim sign, 157, 158 Rokitansky–Ascho sinuses, 125 Rokitansky nodule, 246 Round cell liposarcom a, 237 Rounded atelectasis, 43, 44 Round ligam ents, 243 Round pneum onia, 35 Roux-en-Y gastric bypass, 20 4, 20 4 RPC. See Relapsing polychondritis (RPC) “Rule o 10 ,” 176

S Saber-sheath trachea, 56 , 56 SAIL. See Superiorly by the inguinal ligam ent (SAIL) Saline ush, 17 SA node, 88 Sarcoidosis, 26 , 38, 38 , 41, 6 1, 187, 187

278

Index

Sarcom as, retroperitoneal, 236 –237 Sarcom atosis, peritoneal, 227 SBO. See Sm all bowel obstruction (SBO) Scan delay, 15 Scan duration, 15 Scanning process, CT, 3–4 Scapulothoracic dissociation, 253, 253 SCC. See Squam ous cell carcinom a (SCC) Schistosoma japonicum, 10 9 Schistosoma mansoni, 10 9 Schistosom iasis, 10 9 Schwannom as, 29 –30 , 29 , 80 , 81 , 237 Scim itar syndrom e, 49 SCLC. See Sm all cell lung carcinom a (SCLC) Sclerosing m esenteritis, 228–230 , 229 Scout. See Topogram / scout Sebaceous cysts, 82 Secondary hem ochrom atosis, 10 7, 10 7 Second-generation CT scanners, 2 Septal pattern, lung disease lung edem a, 39 , 39 lym phangitic carcinom atosis, 39 –40 , 40 Septal per orators, 87 Serous cystadenom as, 141, 142 , 246 Serous sur ace papillary carcinom a, o peritoneum , 227 Sessile polyp, 216 SFT. See Solitary f brous tum ors (SFT) Shock bowel, 258 Shunt sign, 9 0 Side branch IPMN, 140–141 Siderotic nodules, 10 6 Sigm oid m esocolon, 224, 224 Sigm oid volvulus, 213–214, 214 Silicosis, 38, 38 Sim ple pulm onary eosinophilia, 35 Sinoatrial (SA) nodal artery, 88, 89 Sinuses o Valsalva, 9 5, 9 6 , 9 8, 9 8 Slip ring m echanism , 3 Sm all bowel adenocarcinom as, 205, 20 5 anatom y, 19 9 –200 carcinoid tum ors, 20 6 , 20 6 CT enterography or evaluation, 19 8–19 9 , 19 9 intussusception, 20 5, 20 5 ischem ia, 200 –20 1, 20 0 lym phom a, 20 5–20 6 , 20 6 m easurem ents, 20 0 m etastases, 20 7 neoplasm s, 205–207 obstruction (See Sm all bowel obstruction (SBO)) “Sm all bowel eces” sign, 20 1–20 2, 20 2 Sm all bowel intram ural hem orrhage causes o , 19 2 Sm all bowel m esentery, 224, 224 Sm all bowel obstruction (SBO), 19 8, 20 1–20 5 diagnosis o , 201 Sm all cell lung carcinom a (SCLC), 27, 27 , 46 , 47, 47 Sm all vessel vasculitis, 51–52 “SMV rotation” sign, 20 3, 20 3 So t tissue sarcom a, 80 , 81 Solid m esenteric m asses, 228t di erential diagnosis, 228 eatures o , 229 sclerosing m esenteritis, 228–230 , 229

Solid organ injuries, 258–26 0 Solid pseudopapillary tum ors, 141–142 Solid serous cystadenom a, 141 Solitary f brous tum ors (SFT), 75, 75 Solitary lung nodule def ned, 44 Space o Retzius, 241 Spiral CT, 4 Spleen, 183–189 asplenia, 184 bare area o , 183, 223, 223 density, 183 in arcts, 188–189 , 189 injury, 26 0 , 26 0 t lesions (See Splenic lesions) polysplenia, 184 size, 183 splenosis, 184, 185 variants, 183–184, 184 “wandering,” 184 Splenic lesions, 184 benign cystic neoplasm , 186 cystic, 185–186 di erential diagnosis, 185, 185t m etastases, 186 , 186 , 187, 187 nonneoplastic cysts, 185–186 , 185 sarcoidosis, 187, 187 solid, nonvascular, 186 –188, 186 t vascular, 188 Splenic recess, o lesser sac, 222 Splenom egaly, 183 Splenosis, 77, 77 , 184, 185 Splenules, 133–134, 183–184 in pancreatic tail, 184 “Split-bolus” technique, CT, 151 “Split wall” sign, 213, 214 Squam ous cell carcinom a (SCC), 46 –47, 46 , 57–58, 59 , 6 5, 170 Staghorn calculi, 157, 157 Staphylococcus aureus, 35, 83 Staphylococcus epidermidis, 83 Steatosis, 10 6 –10 7, 10 6 , 10 6 t Sternal ractures, 252, 253 Stochastic e ects, radiation exposure, 7 Stom ach, 219 anatom y, 19 4 CT technique, 19 4 gastric adenocarcinom a, 19 6 , 19 6 gastric lym phom a, 19 8 gastric volvulus, 19 5 gastric wall thickening, 19 5–19 6 gastritis, 19 5–19 6 gastrointestinal strom al tum or, 19 6 –19 8, 19 7–19 8 hiatal hernias, 19 4–19 5 peptic ulcer disease, 19 6 , 19 6 Storage, o CT im ages, 5–6 Streptococcus pneumoniae, 34, 35, 35 Striated nephrogram s. See Delayed/ striated nephrogram s String o pearls sign, 125, 16 1 Subcapsular hem atom as, 259 Subhepatic space, 220 Subperitoneal space, 219 Subphrenic space, 220 Subpleural sparing, 254 Subsolid lung nodules, 45 Superiorly by the inguinal ligament (SAIL), 243

Superior m ediastinum , def ned, 19 Superior recess, o lesser sac, 222 Supracolic ligam ent. See Gastrocolic ligam ent Supram esocolic com partm ent, 219 , 220 –223 le t, 222–223 lesser sac, 222, 222 right, 220 –222 Suspensory ligam ent, 245 Swyer–Jam es–MacLeod syndrom e, 6 9 Sym pathetic ganglia, neoplasm s o , 30 System ic arterial supply, lung, 50

T TA. See Takayasu arteritis (TA) Tail, pancreas segm ent, 131, 132, 132 Takayasu arteritis (TA), 51, 9 9 –10 0, 16 1–16 2 “Target” sign, 19 2, 19 2 TBM. See Tracheobronchom alacia (TBM) TCC. See Transitional cell carcinom a (TCC) Teleangiectatic adenom as. See In am m atory/ teleangiectatic adenom as Tem poral resolution, cardiac CT, 85–86 Tension pneum othorax, 253 Teratom as, 23–24, 23 , 239 , 239 , 246 , 246 Test bolus, 15 Tetralogy o Fallot (TOF), 9 6 TH AD. See Transient hepatic attenuation di erence (TH AD) Third-generation CT scanners, 2 Thoracentesis, 73 Thoracic aorta aberrant right subclavian artery, 9 6 , 9 7 acute aortic syndrom e, 9 8–9 9 anatom y, 9 5–9 6 , 9 6 aortic coarctation, 9 7 aortic hypoplasia, 9 7 aortitis (See Aortitis) cervical aortic arch, 9 7 double aortic arch, 9 6 pseudocoarctation o , 9 7–9 8, 9 8 right aortic arch, 9 6 , 9 7 Thoracic aortic aneurysm , 9 8, 9 8 Thoracic traum a acute traum atic aortic injury, 255–257, 256 diaphragm atic rupture, 255, 255 esophageal injuries, 255 pneum othorax, 253, 253 pulm onary contusion, 254, 254 pulm onary lacerations, 254, 254 rib ractures, 252, 253 scapulothoracic dissociation, 253, 253 sternal ractures, 252, 253 tracheobronchial injuries, 254–255, 255 Thorax, CT technique or evaluation, 251–252 Throm bocytopenia, 110 Throm bus, 9 1 Thym ic carcinoid, 22–23, 22 Thym ic cysts, 22, 22 Thym ic hyperplasia, 23 lym phoid, 23 true, 23 Thym olipom a, 22 Thym om a, 21, 22 Thym us, 19 , 21, 21 Thyroid carcinom a, 24 Thyroiditis, 24 Thyroid m asses, 24, 24

Index 279 Tim e to peak enhancem ent, 15 Tip appendicitis, 20 8, 20 8 TIPSS. See Transjugular intrahepatic portosystem ic shunt (TIPSS) TNM staging system , or lung cancer, 47–48, 47–48t TNM (tum or, node, m etastasis) system , 248 TO. See Tracheobronchopathia osteochondroplastica (TO) Todani classif cation system , 122–123 TOF. See Tetralogy o Fallot (TOF) Topogram / scout, 3 Total iodine dose, 16 Toxic m egacolon, 213, 213 Trachea anatom y o , 55 di use diseases (See Di use tracheal diseases) dilation, 56 excessive dynam ic expiratory collapse, 57, 58 narrowing o (See Narrowing, o trachea) tracheobronchom alacia, 56 –57, 58 tum ors (See Tracheal neoplasm s) Tracheal bronchus, 6 1, 6 3 Tracheal disruption, 254 Tracheal neoplasm s m alignant, 57–58 respiratory papillom atosis, 58, 59 Tracheobronchial am yloidosis, 6 0 , 6 1 Tracheobronchial injuries, 254–255, 255 Tracheobronchom alacia (TBM), 56 –57, 58 Tracheobronchom egaly. See Mounier-Kuhn syndrom e Tracheobronchopathia osteochondroplastica (TO), 56 , 6 1 Transient hepatic attenuation di erence (TH AD), 118–119 , 118 conditions associated with, 119 t Transitional cell carcinom a (TCC), 16 9 –170 in intrarenal collecting system , 170 , 170 Transjugular intrahepatic portosystem ic shunt (TIPSS), 119 Transverse m esocolon, 131, 223–224, 223 Traum a, 251–26 7 abdom inal, 257–26 7 CT technique, 251–252 pelvic, 257–26 7 thoracic traum a (See Thoracic traum a) Tree-in-bud opacities, 38, 6 5 Tropical pancreatitis, 138 True pancreatic cyst, 139

True thym ic hyperplasia, 23 Trypanosoma cruzi, 27 Tube current (m A), 11 Tuberculosis, 6 7 , 83 peritoneal, 226 –227, 226 renal, 16 1, 16 1 Tube rotation tim e, 11 Tuberous sclerosis, 16 5 Tubo–ovarian abscess, 244, 245 Tum oral pseudocapsule, 229 Type A aortic dissections, 9 9 , 9 9 Type B aortic dissections, 9 9 , 9 9 Typhlitis, 213

U UC. See Ulcerative colitis (UC) UIP (usual interstitial pneum onia) pattern, f brosis, 40 , 40 Ulcerative colitis (UC), 211, 212 bowel wall thickening in, 212 distribution, 212 Ulcers, per orated, 19 6 , 19 6 Ultrasound, 128 endoscopic, 19 6 Uncinate process, 131, 132 Unilateral adrenal agenesis, 173 Unilateral renal agenesis, 153 Uniphasic injection, 17 UPJ. See Ureteropelvic junction (UPJ) UPJ disruption, 26 5 Urachal cyst, 156 Urachal diverticulum , 155–156 , 156 Urachal rem nant anom aly, 155, 156 Urachal sinus, 155 Urachus, 155 Ureterocele, 155 Ureteropelvic junction (UPJ) congenital obstruction, 16 9 , 16 9 Ureterovesicle junction (UVJ), 150 Ureters, 150 , 16 8–171 intrarenal collecting system and, 154–155 retrocaval/ circum caval, 155, 155 transitional cell carcinom a o , 16 9 –170 Urinary bladder, 150 Urinary tract ungal in ection o , 16 1 Urolithiasis, 156 –158 Uterine lesions cervical cancer, 248–249 , 249 endom etrial cancer, 249 , 250 leiom yom as, 248, 249 UVJ. See Ureterovesicle junction (UVJ)

V Vasculitis large vessel, 51 sm all vessel, 51–52 Venous occlusion, 138–139 Venous throm boem bolism , 137 Vessel penetration sign, 117 VH L. See von Hippel-Lindau disease (VH L) VIPom as, 146 Viral hepatitis, 10 7–10 8 Visceral pleura, 71 Voltage, and contrast adm inistration, 17 Volvulus, 20 2, 20 3–20 4, 20 3 cecal, 214, 215 sigm oid, 213–214, 214 von Hippel-Lindau disease (VH L), 139 –140, 16 5 von Meyenburg com plexes, 123 Voxel, 5

W “Wandering” spleen, 184 “Water halo” sign, 19 2, 212 Well-di erentiated liposarcom as, 236 Whipple procedure. See Pancreatoduodenectom y “Whirl” sign, 20 2, 20 2 Wilm s’ tum or, 16 7

X Xanthogranulom atous pyelonephritis (XGN), 16 0 ocal, 16 0 –16 1, 16 0 “X m arks the spot” sign, 213, 214 XR-25, MITA standard, 13 X-ray generation, in scanner, 1–2 X-ray tube, 1–2 XR-25 CT DoseCheck standard, 13

Z Z-axis m odulation, 11 Zollinger–Ellison (ZE) syndrom e, 145, 19 5–19 6 Zona asciculata, 173 Zona glom erulosa, 173 Zona reticularis, 173 Zygom ycosis, 6 1