You are on page 1of 393

MR Imaging of the Abdomen and Pelvis

Bernd Hamm, MD Volkmar Nicolas, MD


Professor of Radiology and Chairman Professor of Radiology and Chairman
Department of Radiology, Campus Mitte Department of Diagnostic and Interventional
Clinic of Radiology, Radiology and Nuclear Medicine
Campus Virchow-Klinikum Berufsgenossenschaftliches University Hospital
Charité – Universitätsmedizin Berlin Bergmannsheil
Berlin, Germany Bochum, Germany

Gabriel Paul Krestin, MD Matthias Taupitz, MD


Professor of Radiology and Chairman Professor of Radiology and Physicist
Department of Radiology Department of Radiology
Erasmus MC Charité – Universitätsmedizin Berlin
Rotterdam, the Netherlands Berlin, Germany

Michael Laniado, MD
Professor of Radiology and Chairman
Department of Diagnostic Radiology
Carl Gustav Carus University Hospital
Technical University of Dresden
Dresden, Germany

With contributions by
P. Asbach, D. Beyersdorf, F. Dammann, H.B. Gehl, C.R. Habermann, B. Hamm, C.M. Heyer, C. Klessen,
C. Kluener, G.P. Krestin, G. Krupski-Berdien, R.A. Kubik-Huch, M. Laniado, M. Lorenzen, W. Luboldt,
A.E. Mahfouz, U.G. Mueller-Lisse, M.R. Muehler, V. Nicolas, W. Pennekamp, P. Reimer, M. Reuter,
B. Stoever, M. Taupitz, R. Vosshenrich

1060 illustrations

Thieme
Stuttgart · New York
IV

Library of Congress Cataloging-in-Publication Data Important note: Medicine is an ever-changing science undergoing
MRT von Abdomen und Becken. English. continual development. Research and clinical experience are con-
MR imaging of the abdomen and pelvis / Bernd Hamm ... [et al.] ; tinually expanding our knowledge, in particular our knowledge of
with contributions by P. Asbach ... [et al.] ; proper treatment and drug therapy. Insofar as this book mentions
[translator, Bettina Herwig]. any dosage or application, readers may rest assured that the authors,
p. ; cm. editors, and publishers have made every effort to ensure that such
Includes bibliographical references and index. references are in accordance with the state of knowledge at the time
ISBN 978-3-13-145591-8 (alk. paper) of production of the book.
1. Abdomen--Magnetic resonance imaging. 2. Pelvis--Magnetic Nevertheless, this does not involve, imply, or express any guar-
resonance imaging. I. Hamm, Bernd, Prof. Dr. II. Title. antee or responsibility on the part of the publishers in respect to any
[DNLM: 1. Abdomen--pathology. 2. Magnetic Resonance Imaging. dosage instructions and forms of applications stated in the book.
3. Pelvis--pathology. WI 900 M9395 2009a] Every user is requested to examine carefully the manufacturers’
RC944.M6613 2009 leaflets accompanying each drug and to check, if necessary in con-
617.5'507548--dc22 sultation with a physician or specialist, whether the dosage sched-
2009018513 ules mentioned therein or the contraindications stated by the man-
ufacturers differ from the statements made in the present book. Such
This book is an authorized and revised translation of the 2nd examination is particularly important with drugs that are either
German edition published and copyrighted 2007 by Georg Thieme rarely used or have been newly released on the market. Every
Verlag, Stuttgart, Germany. Title of the German edition: MRT von dosage schedule or every form of application used is entirely at
Abdomen und Becken the user’s own risk and responsibility. The authors and publishers
request every user to report to the publishers any discrepancies or
Translator: Bettina Herwig, Berlin, Germany inaccuracies noticed. If errors in this work are found after publica-
tion, errata will be posted at www.thieme.com on the product
Illustrators: Stefanie Gay and Bert Sender, Bremen, Germany description page.

© 2010 Georg Thieme Verlag, Some of the product names, patents, and registered designs referred
Rüdigerstrasse 14, 70469 Stuttgart, Germany to in this book are in fact registered trademarks or proprietary
http://www.thieme.de names even though specific reference to this fact is not always
Thieme New York, 333 Seventh Avenue, made in the text. Therefore, the appearance of a name without
New York, NY 10001, USA designation as proprietary is not to be construed as a representation
http://www.thieme.com by the publisher that it is in the public domain.
This book, including all parts thereof, is legally protected by
Cover design: Thieme Publishing Group copyright. Any use, exploitation, or commercialization outside the
Typesetting by primustype Hurler, Notzingen, Germany narrow limits set by copyright legislation, without the publisher’s
Printed in Germany by APPL aprinta druck, Wemding consent, is illegal and liable to prosecution. This applies in particular
to photostat reproduction, copying, mimeographing, preparation of
ISBN 978-3-13-145591-8 123456 microfilms, and electronic data processing and storage.
V

Preface

Magnetic resonance imaging has developed dramatically be aware that the specific contrast media may not have
in recent years, and the technical advances have expanded been approved for all countries or continents and that
the range of diagnostic applications. In the abdomen and their approval status is subject to change.
pelvis, MRI has long developed beyond the experimental Working on this English edition has made us aware of
stage and is now the method of choice for many indica- how difficult it is to keep abreast of technical develop-
tions. With increasing experience, refined and highly spe- ments in such a dynamic field as MRI. Thus, new insights
cialized imaging techniques have emerged for the differ- at the time of publication might already have outpaced
ent organ systems, making MRI of the abdomen and pelvis the state of the art at the time of writing.
a complex field of its own. Many radiologists directly involved in the scientific
This book provides a comprehensive overview of the development of abdominal and pelvic MRI, either in co-
technically demanding, interesting, and clinically relevant operation with us or as independent researchers, have
field of abdominopelvic MRI. Each organ or organ system contributed to this book as authors or co-authors. We
is treated in a separate chapter that can be read independ- thank all of them for their dedicated, supportive, and
ently and begins with a concise description of the specific inspiring cooperation. Our thanks also go to the staff of
imaging technique. Thieme Publishers for making possible this English edi-
The individual chapters can be read as a cookbook with tion and to Bettina Herwig for the translation.
regard to the specific imaging technique and indications We hope that this book will be a useful resource to our
for MRI. The presentation of pathologic entities is lavishly colleagues interested in abdominal and pelvic MRI and
illustrated and is completed by a description of the MRI help them make use of MRI to the benefit of our patients.
findings and differential diagnoses.
Unique to MRI, especially of the hepatobiliary system, B. Hamm
is the availability of a large number of contrast agents. MRI G.P. Krestin
of the liver can be performed with different nonspecific M. Laniado
contrast media, which are available all over the world, or V. Nicolas
with one of several tissue-specific agents. Readers should M. Taupitz
VI

Contributors

Patrick Asbach, MD Claudia Kluener, MD


Assistant Professor of Radiology Department of Radiology and Neuroradiology
Department of Radiology Oldenburg Evangelical Hospital
Charité – Universitätsmedizin Berlin Oldenburg, Germany
Berlin, Germany
Gerrit Krupski-Berdien, MD
Dirk Beyersdorff, MD Professor of Radiology
Associate Professor Radiology Department of Diagnostic and Interventional Radiology
Department of Radiology Reinbek St. Adolf-Stift Hospital
Charité – Universitätsmedizin Berlin Reinbek, Germany
Berlin, Germany
Rahel A. Kubik-Huch, MD
Florian Dammann, MD Professor of Radiology
Professor of Radiology Department of Radiology
Department of Radiology Kantonsspital Baden AG
Klinik am Eichert Baden, Switzerland
Göppingen, Germany
Maren Lorenzen, MD
Hans-Bjoern Gehl, MD Radiology Practice Heegbarg
Professor of Radiology Hamburg, Germany
Department of Radiology
Bielefeld-Mitte City Hospitals Wolfgang Luboldt, MD, MSc
Bielefeld, Germany Associate Professor of Radiology and Nuclear Medicine
Physicist
Christian R. Habermann, MD Department of Radiology
Associate Professor of Radiology University Hospital Frankfurt
Diagnostic Center, Department of Diagnostic Frankfurt a. M., Germany
and Interventional Radiology
University Medical Center Hamburg-Eppendorf Ahmed-Emad Mahfouz, MD
Hamburg, Germany Professor of Radiology
Hamad Medical Corporation
Christoph M. Heyer, MD Radiology Department
Associate Professor of Radiology Doha, Quatar
Department of Diagnostic and Interventional Radiology
and Nuclear Medicine Matthias R. Muehler, MD
Berufsgenossenschaftliches University Hospital Assistant Professor of Radiology
Bergmannsheil Department of Radiology
Bochum, Germany Charité – Universitätsmedizin Berlin
Berlin, Germany
Christian Klessen, MD
Center for Diagnostic Radiology and Ullrich Gerd Mueller-Lisse, MD
Minimally Invasive Therapy Associate Professor of Radiology
The Jewish Hospital Berlin Department of Clinical Radiology
Berlin, Germany Munich University Hospital, Innenstadt
Munich, Germany
Contributors VII

Werner Pennekamp, MD Michael Reuter, MD


Assistant Professor of Radiology Professor of Radiology
Department of Diagnostic and Interventional Radiology Department of Radiology and Interventional Treatment
and Nuclear Medicine Vivantes Hospital Neukölln
Berufsgenossenschaftliches University Hospital Berlin, Germany
Bergmannsheil
Bochum, Germany Brigitte Stoever, MD
Professor of Radiology
Peter Reimer, MD Department of Pediatric Radiology
Professor of Radiology Charité – Universitätsmedizin Berlin
Department of Radiology Berlin, Germany
Karlsruhe Municipal Hospital
Academic Teaching Hospital of the University of Freiburg Rolf Vosshenrich, MD
Karlsruhe, Germany Professor of Radiology
MRI Practice Friederikenstift
Hanover, Germany
VIII

Abbreviations

1D, 2D, 3D One-dimensional, two-dimensional, three- Gd-BOPTA Gadobenic acid (relaxation-enhancing


dimensional component of the MR contrast medium
Multihance)
ACTH Adrenocorticotropic hormone Gd-DOTA Gadoterate (relaxation-enhancing compo-
ADPKD Autosomal dominant polycystic kidney nent of the MR contrast medium Dotarem)
disease Gd-DTPA Gadopentetate (relaxation-enhancing
ASSET Array spatial sensitivity encoding component of the MR contrast medium
technique Magnevist)
Gd-DTPA-BMA Gadodiamide (relaxation-enhancing com-
BPH Benign prostatic hyperplasia ponent of the MR contrast medium Om-
BCS Budd–Chiari syndrome niscan)
Gd-EOB-DTPA Gadoxetic acid (relaxation-enhancing
CCA Cholangiocarcinoma component of the MR contrast medium
CCC Cholangiocellular carcinoma Primovist)
CNR Contrast-to-noise ratio Gd-HP-DO3A Gadoteridol (relaxation-enhancing compo-
CSF Cerebrospinal fluid nent of the MR contrast medium Multi-
CSI Chemical shift imaging hance)
CT Computed tomography GI Gastrointestinal
CTA Computed tomography angiography GIST Gastrointestinal stromal tumor
CTAP Computed tomography during arterial GMR Gradient moment rephasing
portography GRASE Gradient spin echo
D&C Dilatation and curettage GRASS Gradient-recalled acquisition in a steady
state
DER Digital rectal examination GRE Gradient echo
DRG Diagnosis-related group
DSA Digital subtraction angiography HASTE Half Fourier-acquired single shot turbo spin
DWI Diffusion-weighted imaging echo
HCC Hepatocellular carcinoma
EPI Echo planar imaging HF High frequency
ERCP Endoscopic retrograde cholangiopancrea- IMH Intramural hematoma
tography IMHN Intraductal mucin-hypersecreting neopla-
ETL Echo train length sia

FAST Fourier-acquired steady state IP In-phase


FE Field echo iPAT Integrated parallel acquisition techniques
FFE Fast field echo IPMT Intraductal papillary mucinous tumor
FID Free induction decay IR Inversion recovery
FISP Fast imaging with steady state free IUD Intrauterine device
precession IV Intravenous
FLASH Fast low angle shot
FNH Focal nodular hyperplasia MEN Multiple endocrine neoplasia
FOV Field of view MFH Malignant fibrous histiocytoma
FS Fat suppression, fat-suppressed MIP Maximum intensity projection
FSE Fast spin echo Mn-DPDP Mangafodipir (relaxation-enhancing com-
ponent of the MR contrast medium Tesla-
Gd Gadolinium scan)
Abbreviations IX

MPR Multiplanar reconstruction/reformation s Second


MP-RAGE Magnetization-prepared rapid acquisition SAR Specific absorption rate
gradient echo SCT Spiral computed tomography
MPS Mononuclear phagocyte system SE Spin echo
MRA Magnetic resonance angiography SENSE Sensitivity encoding
MRC Magnetic resonance colonography SI Signal intensity
MRCP Magnetic resonance cholangiopancreatog- SIRS Systemic inflammatory response syndrome
raphy SNR Signal-to-noise ratio
MRE Magnetic resonance elastography SPGR Spoiled GRASS
MRI Magnetic resonance imaging SPIO Superparamagnetic iron oxide
MRS Magnetic resonance spectroscopy SPIR Spectral presaturation by inversion
MRSI Magnetic resonance spectroscopic imaging SR Saturation recovery
MRU Magnetic resonance urography SSD Shaded surface display
ms Millisecond SSFP Steady state free precession
MSCT Multislice spiral computed tomography SSFSE Single shot fast spin echo
NASH Nonalcoholic steatohepatitis STEAM Stimulated echo acquisition mode
NEX Number of excitations STIR Short tau inversion recovery
NHL Non-Hodgkin lymphoma
NSF Nephrogenic systemic fibrosis T Tesla
T1 w, T2 w T1-weighted, T2-weighted
OP Opposed-phase T2* Effective T2 relaxation time (T2 star)
TCC Transitional cell carcinoma
PACE Prospective acquisition correction TE Time to echo (echo time)
PAU Penetrating atherosclerotic ulcer TEE Transesophageal echocardiography
PBC Primary biliary cirrhosis TFE Turbo field echo
PBS Primary biliary sclerosis TI Time to inversion (inversion time)
PC Phase contrast TIM Total imaging matrix
PCOS Polycystic ovary syndrome TIPS Transjugular intrahepatic portosystemic
PD Proton density shunt
PET Positron emission tomography TIRM Turbo inversion recovery magnitude
PID Pelvic inflammatory disease TME Total mesorectal excision
PIN Prostatic intraepithelial neoplasm TOF Time of flight
PNET Primitive neuroectodermal tumor TR Time to repetition (repetition time)
ppm Parts per million TRUS Transrectal ultrasound
PRESS Point-resolved spectroscopy TVUS Transvaginal ultrasound
PSA Prostate-specific antigen TSE Turbo spin echo
PSC Primary sclerosing cholangitis TUR Transurethral resection
PSIF Inverted FISP TURP Transurethral resection of the prostate
PTC Percutaneous transhepatic cholangiogra-
phy UAE Uterine artery embolization
PWI Perfusion-weighted imaging US Ultrasound
USPIO Ultra-small superparamagnetic iron oxide
RARE Rapid acquisition with relaxation en-
hancement VIBE Volume-interpolated breath-hold exami-
RAS Renal artery stenosis nation
RCC Renal cell carcinoma VIP Vasoactive intestinal polypeptide
ROI Region of interest VOI Volume of interest
ROPE Respiratory ordering of phase encoding
RPF Retroperitoneal fibrosis
X

Contents

1 The Liver
M. Taupitz, P. Asbach, A.E. Mahfouz, and B. Hamm

Focal Liver Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Diffuse Liver Disease . . . . . . . . . . . . . . . . . . . . . . . . . . 34


Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 34
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . 34
MRI Appearance of Normal Anatomy . . . . . . . . . . . 11 MRI Appearance of Pathologic Entities . . . . . . . . . . 35
MRI Appearance of Pathologic Entities . . . . . . . . . . 11
Use of Tissue-Specific Contrast Media . . . . . . . . . . 27
Role of MRI in Focal Liver Lesions . . . . . . . . . . . . . . 30

2 The Bile and Pancreatic Ducts


P. Asbach and H.B. Gehl

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 MRI Appearance of Pathologic Entities . . . . . . . . . . 53


Ductal Strictures . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 53
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47
Stones . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 55
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Inflammatory Conditions . . . . . . . . . . . . . . . . . . . . . 55
Coils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 47 Primary Biliary Cirrhosis . . . . . . . . . . . . . . . . . . . . . . 55
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 48 Primary Sclerosing Cholangitis . . . . . . . . . . . . . . . . 61
Patient Preparation . . . . . . . . . . . . . . . . . . . . . . . . . . 48 Masses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 61
Recommended Imaging Protocol . . . . . . . . . . . . . . . 49
MRI Appearance of Normal Anatomy . . . . . . . . . . . 52

3 The Pancreas
P. Asbach, W. Luboldt, and H.B. Gehl

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65 MRI Appearance of Pathologic Entities . . . . . . . . . . 71


Congenital Anomalies and Diseases . . . . . . . . . . . . 71
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 65
Inflammatory Disease . . . . . . . . . . . . . . . . . . . . . . . . 72
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 Pancreatic Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . 76
Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 Differentiation of Inflammatory Pseudotumors
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 and Neoplasms . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 80
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 66 Pancreas Transplant . . . . . . . . . . . . . . . . . . . . . . . . . . 83
MRI Appearance of Normal Anatomy . . . . . . . . . . . 70
Contents XI

4 The Spleen
M. Laniado and F. Dammann

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 MRI Appearance of Pathologic Entities . . . . . . . . . . 93


Benign Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 93
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87
Malignant Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . 99
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 Infectious and Noninfectious Conditions . . . . . . . . . 102
Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 Trauma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 Splenic Infarction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 87 Diffuse Disease . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103

MRI Appearance of Normal Anatomy . . . . . . . . . . . . 91

5 The Gastrointestinal Tract


W. Luboldt and M. Laniado

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109 MRI Appearance of Pathologic Entities . . . . . . . . . . 112


Stomach . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 112
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
Small Intestine . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 109 Colon . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 119
Patient Preparation . . . . . . . . . . . . . . . . . . . . . . . . . . . 109
Functional MRI . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 110
Imaging Strategy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 111 Outlook . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 125

6 The Rectum and Anal Canal


C. Klessen and M. Laniado

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127 MRI Appearance of Normal Anatomy . . . . . . . . . . . . 128

Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127 MRI Appearance of Pathologic Entities . . . . . . . . . . 131


Rectal Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 131
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
Anal Carcinoma . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 136
Patient Preparation and Positioning . . . . . . . . . . . . . 127
Inflammatory Bowel Disease . . . . . . . . . . . . . . . . . . . 136
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
Functional Disorders . . . . . . . . . . . . . . . . . . . . . . . . . . 140
Coils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 127
Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128
Imaging Protocol . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 128

7 The Kidneys and Upper Urinary Tract


M. Taupitz and R. A. Kubik-Huch

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143 MRI Appearance of Pathologic Entities . . . . . . . . . . 150


Benign Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . . 150
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143
Malignant Renal Tumors . . . . . . . . . . . . . . . . . . . . . . 161
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143 Functional Renal Imaging . . . . . . . . . . . . . . . . . . . . . . 174
Coils . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 143 Evaluation of Living Kidney Donors . . . . . . . . . . . . . 174
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144 Renal Transplants . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 148
MRI Appearance of Normal Anatomy . . . . . . . . . . . . 148
XII Contents

8 The Adrenal Glands


M. Taupitz and G.P. Krestin

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181 Anatomy and Normal MRI Appearance . . . . . . . . . . 184

Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181 MRI Appearance of Pathologic Entities . . . . . . . . . . 184


Benign Conditions . . . . . . . . . . . . . . . . . . . . . . . . . . . 184
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181
Malignant Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . 189
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 181
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182 Rational Approach to the MRI Differentiation
Image Analysis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 182 of Adrenal Lesions . . . . . . . . . . . . . . . . . . . . . . . . . . . . 193

9 The Retroperitoneum
G. Krupski-Berdien, C.R. Habermann, and V. Nicolas

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195 Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 197

Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195 Classification of Soft-Tissue Tumors . . . . . . . . . . . . 197


MRI in Initial Diagnostic Work-up . . . . . . . . . . . . . . 200
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195
MRI in Tumor Recurrence . . . . . . . . . . . . . . . . . . . . . 206
Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 195
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 196

10 The Urinary Bladder


V. Nicolas and D. Beyersdorff

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209 MRI Appearance of Normal Anatomy . . . . . . . . . . . 210

Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209 MRI Appearance of Pathologic Entities . . . . . . . . . . 210


Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209
Inflammation. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209
Benign Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 209
Malignant Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . 211
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 210

11 The Prostate and Seminal Vesicles


V. Nicolas, D. Beyersdorff, U.G. Mueller-Lisse, W. Pennekamp, and C.M. Heyer

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 219 (1H) MR Spectroscopy . . . . . . . . . . . . . . . . . . . . . . . . 222


MR Spectroscopy of the Prostate: Biochemical
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 219
Basis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 219
MRI Appearance of Pathologic Entities . . . . . . . . . . 223
Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 219
Anomalies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 223
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220
Inflammatory Conditions . . . . . . . . . . . . . . . . . . . . . 224
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220
Benign Prostatic Hyperplasia . . . . . . . . . . . . . . . . . . 225
MRI Appearance of Normal Anatomy . . . . . . . . . . . 220 Malignant Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . 226
Contents XIII

12 The Uterus and Vagina


C. Kluener and B. Hamm

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241 MRI Appearance of Pathologic Entities . . . . . . . . . . 252


Congenital Uterine Anomalies . . . . . . . . . . . . . . . . . . 252
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241
Acquired Benign Uterine Disorders . . . . . . . . . . . . . 255
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 241 Malignant Tumors of the Uterus . . . . . . . . . . . . . . . . 262
Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 242 Vaginal Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 274
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 242 MRI Appearance after Dilatation and Curettage . . . 276
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 244 MRI Appearance after Radiotherapy. . . . . . . . . . . . . 276
General Imaging Strategy . . . . . . . . . . . . . . . . . . . . . . 244 Residual Tumor and Recurrence after
Radiotherapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 278
MRI Appearance of Normal Anatomy . . . . . . . . . . . . 245
Tumor Recurrence after Surgery . . . . . . . . . . . . . . . . 278

13 The Adnexa
M. Reuter and M. Lorenzen

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285 MRI Appearance of Pathologic Entities . . . . . . . . . . 288


Pelvic Inflammatory Disease . . . . . . . . . . . . . . . . . . . 288
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285
Ectopic Pregnancy . . . . . . . . . . . . . . . . . . . . . . . . . . . . 288
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285 Ovarian Torsion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289
Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285 Benign Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 289
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 285 Malignant Tumors . . . . . . . . . . . . . . . . . . . . . . . . . . . . 294
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 286
MRI Appearance of Normal Anatomy . . . . . . . . . . . . 287
Basic Anatomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 287
MRI Appearance . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 287

14 Magnetic Resonance Pelvimetry


M.R. Muehler

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301 Definition of Pelvic Measures . . . . . . . . . . . . . . . . . . . 302

Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 301 Imaging Technique and Findings . . . . . . . . . . . . . . . . 303

15 Magnetic Resonance Angiography of the Abdomen


R. Vosshenrich and P. Reimer

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305 Portal Venous System . . . . . . . . . . . . . . . . . . . . . . . . . 312


Abdominal and Pelvic Veins . . . . . . . . . . . . . . . . . . . 312
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305
MRI Appearance of Pathologic Entities . . . . . . . . . . 313
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 305
Abdominal and Pelvic Arteries . . . . . . . . . . . . . . . . . 313
Time-of-Flight MRA . . . . . . . . . . . . . . . . . . . . . . . . . . . 305
Portal Venous System . . . . . . . . . . . . . . . . . . . . . . . . . 321
Phase-Contrast MRA . . . . . . . . . . . . . . . . . . . . . . . . . . 306
Abdominal and Pelvic Veins . . . . . . . . . . . . . . . . . . . 325
Contrast-Enhanced MRA . . . . . . . . . . . . . . . . . . . . . . 306
MRI Appearance of Normal Anatomy . . . . . . . . . . . . 311
Abdominal and Pelvic Arteries . . . . . . . . . . . . . . . . . 311
XIV Contents

16 Intra-abdominal Lymph Nodes


M. Taupitz and D. Beyersdorff

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 331 MRI Appearance of Normal Lymph Nodes . . . . . . . 334

Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 331 MRI Appearance of Abnormal Lymph


Nodes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 336
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332
Imaging Planes . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332 Use of Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . 336
Pulse Sequences . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 332
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 333

17 Abdominal MRI in Children


B. Stoever

Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341 MRI Appearance of Pathologic Entities . . . . . . . . . . 342


Gastrointestinal Tract . . . . . . . . . . . . . . . . . . . . . . . . 342
Indications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341
Hepatobiliary System. . . . . . . . . . . . . . . . . . . . . . . . . 345
Imaging Technique . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341 Pancreas . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 348
Coils and Pulse Sequences . . . . . . . . . . . . . . . . . . . . 341 Spleen . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 350
Positioning . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341 Abdominal Vascular Malformations . . . . . . . . . . . . 350
Sedation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 341 Retroperitoneum . . . . . . . . . . . . . . . . . . . . . . . . . . . . 352
Contrast Media . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 342 Kidneys . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 352
Adrenal Glands . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 356
Contraindications . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 342
Pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 360
Systemic Neoplastic Disease . . . . . . . . . . . . . . . . . . . 363

Index . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 366
1

1 The Liver
M. Taupitz, P. Asbach, A.E. Mahfouz, and B. Hamm

Focal Liver Lesions · Evaluation of indeterminate liver lesions in patients


with cancer.
Introduction · Preoperative identification and localization of liver
metastases in candidates for surgical resection (hemi-
Continuous developments and numerous improvements hepatectomy, segmental or atypical resection) and ex-
over the last 15–20 years have made MRI a robust modal- clusion of metastases in the remaining liver.
ity for imaging of the liver. The improvements pertain to · Characterization of incidentally detected liver lesions
technical advances and the advent of new intravenous that are not definitely cystic or benign in patients with
contrast media. High-performance gradient systems and no known primary malignancy. MRI can be used as the
body or torso phased-array coils enable the use of fast second imaging test in patients with suspicious ultra-
imaging techniques with good image quality and ideally sound findings and, because it does not involve radia-
allow breath-hold imaging of the entire liver with both tion exposure, should be preferred to CT, especially in
T1- and T2-weighted sequences. In terms of contrast- younger patients.
enhanced MRI, the liver is unique because it is the only · Follow-up of malignant liver tumors.
organ for which several recently developed tissue-specific
contrast media are available besides conventional, non-
specific Gd-based agents. Thanks to these advances, MRI Imaging Technique
has evolved into a powerful imaging tool for the detection
and characterization of focal liver lesions. In this chapter Patient Preparation, Positioning, and Imaging
we first outline the major technical aspects of liver MRI Planes
and give a brief overview of contrast media for liver
imaging, then describe the MRI appearance of the most Liver MRI is performed with the patient in a comfortable
important benign and malignant focal liver lesions. We supine position. Most patients find it helpful if their knees
conclude by discussing the role of MRI in the detection are elevated with a small foam pad. Unless a body phased-
and characterization of focal liver lesions and comparing array coil is used, an abdominal belt should be employed
its performance with that of CT, its fiercest competitor. to reduce respiratory artifacts by limiting respiratory ex-
cursions if the examination is performed at high magnetic
field strength. In addition, patients in whom free-breath-
Indications ing sequences will be acquired should be carefully in-
structed to breathe shallowly and regularly to minimize
The liver is the most common site of metastatic disease respiratory motion of the abdominal wall (Fig. 1.1). Care-
from a variety of primary tumors and is therefore exam- ful breathing instructions are also important if respira-
ined in virtually all patients undergoing tumor staging. tory-triggered sequences are planned. Finally, in patients
Patients with liver metastases, especially from colorectal undergoing breath-hold imaging, the breathing com-
cancer, benefit from improved surgical approaches. Re- mands that will be given during the examination need
section of single or multiple liver metastases has been to be explained beforehand. If intravenous contrast ad-
shown to significantly improve the 5-year survival rate ministration is planned, a flexible indwelling cannula is
if all hepatic metastases are removed and enough normal inserted, preferably into an antecubital vein, before the
liver tissue is left (usually > 30 %) and patients have no patient is positioned in the magnet. The cannula is con-
additional extrahepatic metastases.1,2 On the other hand, nected via an extension tube to a saline-filled syringe or, if
up to 20 % of the general population have noncystic be- available, an MR-compatible injection pump.
nign liver tumors,3 which must be differentiated from The axial plane is the bedrock of liver MRI. Axial images
malignant lesions. MRI is highly accurate in detecting enable good evaluation and delineation of both normal
and characterizing focal liver lesions and can therefore anatomic structures and hepatic abnormalities in most
meet this challenge. The major indications for MRI of the cases, and can be directly compared with CT scans. Addi-
liver are (Table 1.1): tional coronal or sagittal images can be obtained, for
2 1 The Liver

Table 1.1 MRI techniques for different indications

Indication Sequence Plane Unenhanced/Contrast Comment


medium
Indeterminate T1w GRE IP or T1w TSE Axial Unenhanced Lesion detection
liver lesions T1w GRE OP Axial Demonstration of hepatic steatosis (diffuse or focal);
identification of intracellular lipid for differential diag-
nosis
T2w TSE Axial Unenhanced Lesion detection and characterization
Heavily T2w TSE Axial Unenhanced Single-shot technique or during breath-hold; improved
differentiation of solid tumors from cysts or heman-
giomas
T1w GRE IP or T1w 3D GRE Axial Nonspecific contrast Dynamic study after bolus injection of nonspecific
(e. g., VIBE) medium contrast medium; arterial and portal venous phase
images and additional delayed images; detection of
hypervascular lesions, characterization
Preoperative Unenhanced protocol as
evaluation above, supplemented by
T1w GRE IP or T1w TSE Axial Hepatobiliary contrast Dynamic study as described above; delayed images for
medium, injected as bolus differentiation of hepatocellular and nonhepatocellular
tumors
Hepatobiliary contrast Improved detection immediately after infusion of
medium, given as infusion contrast medium; delayed images for differentiation of
hepatocellular and nonhepatocellular tumors
T1w or T2*w GRE Axial SPIO, injected as bolusa Dynamic study as described above; delayed images for
improved detection; differentiation of tumor entities
based on Kupffer cell content
T2w TSE or T2*w GRE Axial SPIO, given as infusion Improved detection immediately after infusion; de-
layed images, see above
Follow-up T1w GRE or TSE T2w TSE Axial Unenhanced Determination of tumor number and size

Note: For all indications, additional coronal and sagittal sequences may be obtained as deemed necessary using fast imaging techniques.
IP = in-phase, OP = opposed-phase. aCurrently not commercially available.

example, to better assess the relationship of a mass to SENSE, sensitivity encoding). The gain in speed achieved
hepatic vessels or to differentiate an intrahepatic from a with parallel imaging can be used either to shorten the
subphrenic lesion. With the fast pulse sequences available acquisition time of a given T1w or T2w sequence or to
today, several slices can be obtained during one breath- improve resolution without a penalty in scan time.4–6
hold, and only little extra time is needed to acquire images However, SNR is reduced in both cases.7
in a further plane. Coronal images provide a good topo-
graphic overview and are also helpful when explaining
findings to clinical colleagues. Pulse Sequences

The standard liver protocol consists of unenhanced T1w


Coils and T2w pulse sequences. Imaging techniques and param-
eters are different for intermediate field strengths around
Nearly all manufacturers of MR imagers offer body or 0.5 T, which are rarely used today, and high field strengths
torso phased-array coils for abdominal applications. These in the range of 1.0–1.5 T.
coils provide a better signal-to-noise ratio (SNR) than the High soft-tissue contrast is crucial for the reliable iden-
integrated whole-body resonator. The higher signal yield tification and characterization of liver lesions. However,
is especially beneficial in conjunction with fast sequences. contrast must always be weighed against good image
A relative disadvantage of these coils is the very high quality, which results mainly from the absence of motion
signal intensity of subcutaneous fat, which may accentu- artifacts and high SNR. Good image quality is often equa-
ate motion artifacts when images are acquired with the ted with good visualization of anatomic detail or spatial
patient breathing freely. Phased-array coils should there- resolution (Fig. 1.2).
fore only be employed for breath-hold imaging or, if free-
breathing sequences are acquired, in combination with a T1-Weighted Imaging
fat suppression technique (see below). A phased-array T1w MR images of the liver are predominantly acquired
body coil not only improves SNR but is also necessary to using breath-hold multislice GRE sequences (e. g., FLASH,
perform parallel imaging (usually 4–8 elements; e. g., FFE), especially when imaging is performed at high mag-
Focal Liver Lesions 3

netic field strength (Table 1.2). Breath-hold GRE sequen-


ces eliminate respiratory artifacts, and the extremely 3
short echo times provide excellent T1 contrast. When a 4
1
high-performance gradient system is available, up to ca.
25 slices can be acquired during a breath-hold of 15–25 s.
The entire liver can thus be imaged with high contrast and
good image quality in 1–3 breath-holds, depending on 2
slice thickness and number of slices. Such multislice GRE
sequences are also available for lower field strengths but
will generate images with poorer SNR. Instead of a multi-
slice GRE sequence with a TR of ca. 150 ms and a TE of ca. 5
ms, one can acquire a series of single-slice sequences with
very short TRs and TEs (10–20 ms and 2–7 ms, respec-
tively). The low intrinsic contrast resulting from such
short TRs and TEs is improved by applying an inversion
pulse at the beginning of each sequence (e. g., TurboFLASH
or TFE). These 2D GRE sequences can be replaced with a
fat-suppressed 3D GRE sequence (e. g., VIBE, volume-in-
terpolated breath-hold examination).8 A 3D GRE sequence
has the advantage of enabling acquisition of thinner slices.
It is possible, for example, to reconstruct 64 2.5-mm slices
by interpolation from a set of 32 slices acquired with 5.0-
mm slice thickness. However, unenhanced 3D GRE se-
quences have a lower signal yield, resulting in poorer
contrast compared with their 2D counterparts. The 3D Fig. 1.1 Diagrammatic axial view of the upper abdomen showing
GRE technique is therefore most suitable for dynamic motion artifacts due to respiration (1), cardiac pulsation (2), vessel
contrast-enhanced studies with intravenous injection of pulsation (3), and bowel peristalsis (4) (according to Stark and
Gd-based contrast medium or delayed imaging after in- coworkers10).
travenous injection of a hepatobiliary contrast medium
(see below).
If the available equipment does not allow fast imaging supplementary information for tissue characterization. IP
with adequate image quality and good contrast, the liver and OP TEs depend on the field strength (Table 1.3). The
can be imaged in 4–8 min at intermediate field strength different effects result from the addition or subtraction of
using conventional T1w SE/TSE or GRE sequences and the signal contributions from water and fat (in general:
multiple signal averaging. Multiple averages reduce mo- lipids) within a volume element (Fig. 1.3).
tion artifacts by increasing SNR and improve contrast and The interface between tissues with different water or
image quality with good anatomic resolution.9,10 Due to fat content typically appears dark on OP images (Fig.
the short T1 relaxation times at intermediate field 1.4a, b). OP images enable sensitive detection of fatty
strengths, both TSE and GRE sequences are acquired infiltration and some lipid-containing tumors.11 Com-
with a short TR of 250–350 ms to achieve high T1 contrast. pared with IP images, fatty liver parenchyma has low
TE should be as short as possible (10–15 ms for SE and TSE, signal intensity on OP images (Fig. 1.4c, d). Note that if
5–10 ms for GRE). At higher field strength, SE or TSE images are acquired with a T1w GRE sequence, focal
sequences are acquired with longer TRs (400–500 ms) lesions in a fatty liver may be missed on OP images, and
because T1 relaxation times are longer. The number of IP images are needed for reliable detection (Fig. 1.5).
signal averages should not exceed four, corresponding to a
scan time of ca. 8 min. Again, TE should be as short as T2-Weighted Imaging
possible (10–15 ms). GRE sequences are not suitable for T2w imaging techniques are largely the same at intermedi-
conventional free-breathing imaging with multiple signal ate and high field strengths. The liver is nearly exclusively
averaging at high field strength because artifacts are ac- imaged with turbo or fast SE (TSE or FSE) pulse sequences,
centuated. If non-breath-hold pulse sequences are ac- either for classic TSE imaging with the patient breathing
quired with a body phased-array coil, use of a fat suppres- freely or single-shot imaging during breath-holding (sin-
sion technique is recommended because the very bright gle-shot TSE, e. g., HASTE). The whole liver can be imaged in
subcutaneous fat near the coil would otherwise cause 2–4 min with the breathing technique or during a single
excessive motion artifacts. breath-hold in ca. 23 s using the single-shot technique
(Table 1.2). Note, however, that lesions with only slightly
In-Phase and Opposed-Phase Imaging longer T2 relaxation times than the liver may be more
The GRE technique can be used to acquire images with in- difficult to detect on TSE images compared with standard
phase (IP) and opposed-phase (OP) echo times to obtain T2w SE images, especially when they are small.12 Imaging
4 1 The Liver

a b

c d

e f

Fig. 1.2a–g MRI anatomy of the liver and comparison of different


pulse sequences (1.5 T). a–c Images acquired with 2D T1w GRE
sequence during breath-holding illustrate good visualization of ana-
tomic detail and high T1 contrast (FLASH 199/4.1;90°; 23 slices in
21 s). Images through the liver at three different levels (from top to
bottom) show the right, middle, and left hepatic veins (a, arrows),
the right main portal branch (b), and the lower part of the right
hepatic lobe (c) (see Fig. 1.7). d Fat-suppressed 3D T1w image (VIBE
4.9/2.4;10°; 32 acquired slices, interpolated to 64 slices; scan time,
22 s. e–g T2w images acquired with single-shot TSE sequence
(HASTE ∞/80; 23 slices in 21 s), respiratory-triggered, fat-
suppressed TSE sequence (TSE 5900/77; ETL, 21; 31 slices in ca.
5 min), and echo-planar sequence (EPI ∞/59; 31 slices in 5 s).

g
Focal Liver Lesions 5

Note: The suggested parameters are only examples and have to be adjusted for use on different brands of scanners. Parallel imaging techniques can be used to shorten scan time (for sequences with one
Breath-
hold

Yes
Yes
Yes

No
No
No
  

5–7 min
4–7 min
4–8 min
20–24 s
Scan
time

23 s
23 s


Slice thick-
ness (mm)


 

 
     
   
2.5

4
7
8

7
7

Fig. 1.3 Diagram of opposed-phase (OP) and in-phase (IP) imaging.


quisitions
No. of ac-

Because water and fat protons have slightly different precession


frequencies, the amplitude of the echo in a GRE sequence is modu-
lated (“beats”) in an environment consisting of a finely dispersed
2
3
4

1
1
1

mixture of water and fat (as in hepatic steatosis). Under OP con-


ditions, the signal contributions of water and fat are subtracted in a
No. of
slices

volume element, resulting in low SI (left). Under IP conditions, the


48
21
19

23
23
64

signal contributions are added together, resulting in high SI (right).


See Fig. 1.4.
FOV (mm)

300 (75 %)
300 (75 %)
300 (75 %)

300 (75 %)
300 (75 %)
300 (75 %)

is typically performed with TEs in the range of ca. 60–110


ms; longer TEs improve the differentiation of solid liver
tumors from hemangiomas and cysts.13 Conventional TSE
168 × 320
128 × 256
128 × 256

116 × 256
116 × 256

sequences can be performed as multiecho sequences with


116 × 256
Matrix

readout of several echoes, including very late echoes.


Conventional TSE images can be acquired with a TR of
1600–2000 ms at low field strength, while a TR of at least
Yes/no

2500 ms is required at high field strength because of the


Yes
Yes
Yes
No
No
FS

longer T1 relaxation time. The fastest technique, echo-


planar imaging (EPI), is demanding on hardware and soft-
> ca. 80

ware, but most MR systems in use today have echo-planar


T1w GRE: TEs for acquisition of in-phase and opposed-phase images are given in Table 1.3.
7–15
7–15
ETL

capability. EPI is basically a T2w technique and enables




imaging of the liver in less than 5 s. Another fast sequence


for T2w imaging is based on the steady-state principle
Flip

90
10
(°)

during free precession (e. g., TrueFISP). This technique is




employed for MRI of the heart and other rapidly moving


organs but appears to be inferior to other fast techniques
TE (ms)

80–100
2.2–2.6

60–80
10–15
2.2–7

(e. g., HASTE) for T2w imaging of the liver.14 Because they
Table 1.2 Recommended pulse sequences and imaging parameters

Slice distance, 10–20 % of slice thickness (distance factor, 0.1–0.2)


80

improve liver–tumor contrast and overall image quality of


T2w images, fat suppression techniques are more impor-
ca. 170–200

tant for T2w imaging than T1w imaging. Different tech-


TR (ms)

niques of fat suppression are presented below.


signal average) but may come with a penalty in SNR.
2500
5000
500
5–7

Motion Artifacts and Artifact Reduction


Motion artifacts are a particular nuisance in liver imaging
TSE with respira-
Sequence type

3D GRE (VIBE)

and must be effectively eliminated or at least reduced to


tory trigger

obtain diagnostic images with good anatomic detail. In


SE or TSE
2D GRE

this section we therefore briefly outline the typical sour-


HASTE
TSE

ces of motion artifacts that may degrade abdominal MR


images and discuss the most important strategies cur-
rently available to control them.
(alternative)
(alternative)

Artifacts in the upper abdomen can be caused by


Weight- Plane

breathing (the liver moves up and down ca. 3–5 cm with


Axial

Axial
Axial

Axial
Axial
Axial

respiration), blood flow and vessel pulsation, cardiac pul-


sation transmitted below the diaphragm, and gastrointes-
tinal peristalsis (Fig. 1.1). Movement of anatomic struc-
ing

T2

T2
T2
T1
T1
T1

tures during the image acquisition process causes blurring


6 1 The Liver

a b

c d
Fig. 1.4a–d OP and IP imaging with a T1 w GRE sequence at 1.5 T acteristic dark lines, which occur at organ-fat and muscle-fat inter-
(TR, 199 ms; flip, 90 °) in two patients without focal liver lesions, one faces (a, arrows). In the patient with pronounced fatty liver, the liver
with fatty liver (c, d) and one without (a, b). a, c OP images acquired parenchyma is homogeneous and very hypointense (dark) on the
with a TE of 2.4 ms. b, d IP images acquired with a TE of 4.8 ms. In OP image (c). Both livers are of normal high SI on IP images (b, d).
the patient without fatty liver, only the OP image shows the char-

Table 1.3 In-phase (IP) and opposed-phase (OP) echo times at specific measures can be distinguished. Software-based
different field strengths (approximate values in ms) solutions are now available ready for use on standard
IP OP clinical MR scanners, but the radiologist needs to be fa-
miliar with them and their effects in order to choose the
0.5 T Multiple of 14 7 (plus multiple of 14)
most appropriate strategy, which is why we give a brief
1.0 T Multiple of 6.6 3.3 (plus multiple of 6.6)
outline here (see Fig. 1.2).
1.5 T Multiple of 4.4 2.2 (plus multiple of 4.4)
The simplest general measure to reduce motion arti-
facts is to increase the number of signal averages. The
most important specific measures are presaturation tech-
or ghosting in the phase-encoding direction regardless of niques, breath-hold imaging, gradient moment nulling
the direction of motion. Ghosts—e. g., a faint duplicate (also known as flow compensation), respiratory triggering
image of the high-signal-intensity abdominal wall that or gating, phase-reordering methods (e. g., respiratory
may obscure structures of interest—are due to phase mis- ordering of phase encoding—ROPE), and suppression of
registration resulting from respiratory motion during spa- the signal from fat.
tial encoding by the magnetic field gradients. Pulsation Presaturation is done by applying large presaturation
artifacts—the repeated depiction of the cross-section of bands to the vessels above and below the volume of
large vessels in the phase-encoding direction—result from interest so that spins entering the volume with the blood
blood flow in the imaging volume (Fig. 1.1). produce no signal. The blood appears black, and pulsation
A variety of hardware and software solutions exist for and inflow artifacts are eliminated. Inflow artifacts mainly
reducing motion artifacts in liver imaging. General and interfere with T1w imaging, especially when fast GRE
Focal Liver Lesions 7

a b

c d
Fig. 1.5a–d OP and IP imaging with a T1 w GRE sequence at 1.5 T single-shot T2 w TSE image because TSE sequences with long echo
(TR, 199 ms; flip, 90 °) in a patient with hepatic steatosis and a focal trains and short echo spacing exaggerate the signal from fat-con-
liver lesion. a OP image (TE, 2.4 ms) fails to demonstrate the liver taining structures. d Good visualization of the metastasis on conven-
metastasis due to low SI of fatty liver. b IP image (TE, 4.8 ms) clearly tional, fat-suppressed T2 w TSE image.
reveals the metastasis. c Liver–tumor contrast is also low on the

sequences are used after intravenous contrast adminis- Different techniques are available to reduce or elimi-
tration, which is why presaturation pulses are most ben- nate the signal from fat. Spectral fat saturation uses a
eficial in this setting. Use of presaturation pulses may frequency-selective pulse to saturate the spectral peak
result in longer TRs and thus increase scan time. of fat before imaging. Effective fat saturation relies on
Fast breath-hold sequences completely eliminate res- good separation of the spectral peaks of water and fat,
piratory artifacts but do not eliminate artifacts due to which is achieved at high field strength (1.0–1.5 T) and
transmitted cardiac pulsation, which may obscure the good magnetic field homogeneity. State-of-the-art scan-
left lobe of the liver, or artifacts due to intestinal peristal- ners have automatic programs for individual patient
sis. The latter can be eliminated by using ultrafast, sub- shimming. These programs ensure maximum magnetic
second imaging techniques (single-shot TSE, TurboFLASH, field homogeneity for uniform elimination of fat signal
or TFE). over a large volume when a fat saturation sequence is
Gradient moment nulling, or flow compensation, cor- employed. A second method is short tau inversion recov-
rects for signal loss and spatial misregistration due to ery (STIR), in which the time of inversion (TI), i. e., the time
motion, thereby also reducing ghost artifacts.15 However, between application of the 180° inversion pulse and the
the shortest possible TE is prolonged, which is why gra- start of the imaging sequence, is chosen such that the
dient moment nulling is primarily used in conjunction longitudinal magnetization of fat is at zero and no signal
with T2w imaging. Note that blood in intrahepatic vessels is obtained from fat. The inversion delay to null the fat
may appear bright on T2w images acquired with flow signal is 100–170 ms. STIR sequences are far less suscep-
compensation, and vessels depicted in cross-section may tible to magnetic field inhomogeneities and can be used at
mimic small focal lesions. all field strengths. STIR increases scan time but this draw-
8 1 The Liver

back can be compensated for, to some extent, by combin- Nonspecific Contrast Media
ing it with TSE or FSE sequences (so-called turbo inversion Nonspecific MR contrast media for intravenous injection
recovery sequence, TIR). Spectral presaturation with in- that have been in clinical use for some time are Magnevist
version recovery (SPIR) is an inversion recovery technique (Gd-DTPA) and Dotarem (Gd-DOTA). More recently, sev-
that combines elements of fat saturation and STIR. Effec- eral so-called nonionic, low-osmolar contrast media have
tive fat suppression is absolutely essential to eliminate become available, including Omniscan (gadodiamide, Gd-
motion artifacts when free-breathing T2w imaging is per- DTPA-BMA), Prohance (gadoteridol, Gd-HP-DO3A), and
formed using a body phased-array coil (Fig. 1.6a, b). Optimark (gadoversetamide). Gadovist (gadobutrol) has
Respiratory triggering is almost exclusively used for become available recently and is the only Gd-based con-
T2w imaging. It requires special equipment and a pulse trast agent with a concentration of 1.0 mmol/mL Gd (twice
sequence that allows selective data acquisition at a spe- that of the other Gd compounds). Like iodine-based X-ray
cific phase of the respiratory cycle, typically the phase of contrast media used for liver CT, nonspecific Gd chelates
least motion after expiration. With respiratory triggering, are rapidly distributed in the extracellular space and are
the examination will take at least twice as long. Several excreted by the kidneys. They act mainly by markedly
techniques are available to monitor respiratory motion. shortening T1 relaxation times, which is best appreciated
Typically, a belt with an extension sensor is placed around on heavily T1-weighted sequences.
the patient’s abdomen, or a cushion with an integrated Nonspecific Gd-based MR contrast media are typically
pressure sensor is positioned between the abdominal wall used for rapid, dynamic image acquisition after intrave-
and the anterior element of a body phased-array coil. nous bolus injection (Table 1.1). The total amount of con-
Another efficient and easy-to-handle tool is the navigator trast medium to be injected is ca. 10–20 mL when the
echo technique for monitoring diaphragmatic motion, standard dose of 0.1 mmol/kg body weight Gd is used.
which is known from cardiac imaging.16,17 If adequate Such a small amount of contrast medium is advantageous
elimination of motion artifacts and blurring is achieved for all applications requiring a bolus technique.
with respiratory triggering, the basic matrix resolution
can be increased, for instance to 320. With additional Tissue-Specific Contrast Media
administration of a spasmolytic agent, images with high Two types of tissue-specific MR contrast media are used
detail resolution of both intrahepatic and extrahepatic for liver imaging: superparamagnetic iron oxide particles
structures are obtained (Fig. 1.6c, d). Phase-ordering tech- (SPIO particles, magnetites; e.g., Endorem, Sinerem, Re-
niques (e. g., ROPE) improve image quality without a pen- sovist), which predominantly accumulate in the liver and
alty in scan time. With this technique, the data that are spleen, and paramagnetic low-molecular-weight com-
most critical for creation of the MR image are acquired pounds, which specifically target the hepatocytes. The
during the phase of least respiratory motion. latter include Teslascan (Mn-DPDP), Multihance (Gd-
Administration of an antispasmodic agent is usually BOPTA), and Primovist (Gd-EOB-DTPA). All of these con-
not necessary to reduce gastrointestinal motion artifacts trast media are in clinical use, except for Sinerem, which is
in liver MRI, especially when fast imaging techniques are in the clinical trial phase and for which approval is sought
used. However, an antispasmodic will improve image only for intravenous administration in MR lymphography.
quality, particularly in conjunction with respiratory- Magnetites are very small particles that, after intrave-
triggered sequences. nous injection, are selectively taken up by cells of the
mononuclear phagocyte system (MPS), in particular
Kupffer cells in the liver and macrophages in the spleen.
Contrast Media The particles cause marked signal loss in these tissues by
shortening their T2 relaxation times,18,19 thereby enhanc-
Contrast-enhanced MRI of the liver can be performed ing contrast between normal liver parenchyma and non-
with nonspecific contrast media or one of several tissue- hepatocellular lesions, whose signal intensity remains
specific agents that have become available more recently. unchanged because they lack MPS cells.20,21 Only very
The MR contrast media for liver imaging after intravenous small amounts of magnetites, typically between 8 and
injection belong to different classes with different proper- 15 µmol/kg body weight Fe, are needed to achieve the
ties and effects on MR signal intensities (alteration of desired effects, which persist for several hours to days
relaxation times, organ distribution, pharmacokinetics). and are most conspicuous on moderately T2-weighted
Radiologists need to be familiar with these to choose the pulse sequences, i. e., sequences with a long TR and a not
most appropriate imaging protocols and make optimal too long TE (< ca. 80 ms). In addition to their T2-shortening
use of their benefits. Contrast media development is a effects, SPIO particles also shorten T1 relaxation time while
very dynamic field, with frequent approval of new agents moving freely in blood or interstitial fluid.19 The resulting
or new indications for existing agents and the withdrawal increase in signal intensity of blood and tissues with a
of agents from the market. Before administering any intra- large blood volume is made visible on T1w images
venous contrast medium, radiologists should always acquired with very short TE. This signal-enhancing effect
check the most up-to-date information regarding appro- is especially pronounced for ultra-small SPIO particles
val status in their own country. (USPIO) such as Sinerem (see lymph node imaging, Chap-
Focal Liver Lesions 9

a b

c d
Fig. 1.6a–d Techniques for reducing motion artifacts on images tion near the coil; these artifacts are markedly reduced by fat
acquired with a free-breathing T2w sequence. a, b Role of fat suppression. c, d Effect of respiratory triggering (1.5 T). Fat-
suppression in combination with a body phased-array coil (1.5 T). suppressed T2w TSE images acquired without (c) and with (d)
T2w images without (a) and with (b) fat suppression. Pronounced respiratory triggering (navigator technique). Respiratory triggering
motion artifacts over the liver in a (arrows) due to signal accentua- markedly improves image quality and detail resolution (d vs c).

ter 16). With their long blood half-life, USPIO particles proved SPIO contrast medium that can be injected in
might be suitable as blood pool agents and cause pro- bolus form; Endorem must be given as a slow infusion.
longed signal changes in highly vascularized tumors (not Among the hepatobiliary contrast media, Primovist and
approved for clinical use).22 Multihance can be administered in intravenous bolus
Hepatocellular MR contrast media are low-molecular- form while Teslascan is infused. The contrast media that
weight compounds that accumulate in liver cells and in- can be given as a bolus enable dynamic postcontrast MR
crease the signal intensity of normal liver parenchyma by studies in addition to the acquisition of static images at
shortening T1. The signal increase persists for up to 2 h or different phases following contrast administration.
longer after intravenous injection. Hepatic lesions that do
not take up the contrast medium have unchanged signal
intensity and are thus rendered more conspicuous.23–25 MRI Protocols
However, the effect depends on hepatobiliary elimination,
which is not the same for all contrast media of this class. Unenhanced MRI
For Multihance, hepatobiliary elimination is low and The MR pulse sequences recommended for unenhanced
therefore its signal-enhancing effect in the liver is only MR assessment of focal liver lesions are listed in Tables 1.1
moderate, while Teslascan and Primovist, with ca. 50 % and 1.2.
hepatic elimination, cause a strong selective signal in-
crease in healthy liver tissue. The recommended doses Dynamic MRI
per kg body weight are 0.01 mmol Gd for Teslascan, A dynamic contrast-enhanced MRI study of the liver can
0.1 mmol Gd for Multihance, and 0.025 mmol Gd for Pri- be done with nonspecific contrast media or those hepato-
movist. biliary agents that can be given as an intravenous bolus.
Not all tissue-specific MR contrast media can be given Multiphasic imaging is performed using a T1w multislice
by intravenous bolus injection. Resovist is the only ap- IP GRE sequence or a fat-suppressed 3D GRE sequence. To
10 1 The Liver

 


15s 60 s
a b

c d

Fig. 1.7a–e a Diagrammatic representation of the temporal course


of contrast inflow into the liver via the hepatic artery (arterial phase)
and portal vein (portal venous phase). b–e Dynamic MR study
performed with a T1w volumetric 3D GRE sequence (VIBE) and
nonspecific Gd-based contrast medium: precontrast image (b); ar-
terial phase image shows enhancement only of the arteries (c);
portal venous phase image shows enhancement of the portal vein
and its branches and beginning enhancement of liver parenchyma,
but no contrast in the liver veins (d, arrow); parenchymal phase
image shows enhancement of all intrahepatic vessels and liver
parenchyma (e) (same patient as in Fig. 1.2).

capture the dual contrast inflow via the hepatic artery and formed with Resovist, the signal-enhancing effect during
portal vein (Fig. 1.7), the first acquisition begins 15 s after the blood pool phase can be exploited by obtaining a T1w
the start of bolus injection of the contrast medium into a series as with use of nonspecific Gd-based contrast me-
peripheral vein (arterial phase) and the second acquisition dium. Alternatively, a T2*w GRE sequence can be used,
at 55–60 s (portal venous phase). Delayed images (equili- which will show a temporary signal loss in highly vascu-
brium phase) can be acquired at 2.5 min and 10 min. larized tissues.
Determination of individual circulation time is not neces-
sary. An MR-compatible power injector is useful for con- Static MRI Using Tissue-Specific Contrast Media
trast injection but not a prerequisite for the success of a The relaxivity-altering effects of specific MR contrast me-
dynamic MR study. The contrast bolus should be followed dia are best depicted on postcontrast images acquired
by a 20-mL saline flush. Arterial and portal venous phase with heavily T1-weighted sequences in conjunction with
MRI is similar to biphasic spiral CT in terms of timing and hepatobiliary contrast media and with moderately T2w
image interpretation. When dynamic liver MRI is per- sequences after administration of an SPIO contrast agent.
Focal Liver Lesions 11

) ' '#% $ !" '#% $

"  %


) ' '#%  !" '#% 

 
%& $
(&&
'#% 
 

  

 

  

!" $%

Segment VII

 

  

  

!" # 

) ' # 

Fig. 1.8 Segmental anatomy of the liver.

If a hepatobiliary contrast medium is used to differentiate MRI Appearance of Pathologic Entities


hepatocellular tumors (focal nodular hyperplasia, well-
differentiated hepatocellular carcinoma), additional de- Most benign and malignant liver tumors are hypointense
layed images should be obtained no earlier than 2 h after on T1w images and hyperintense on T2w images. Cysts,
contrast injection. hemangiomas, and metastases from neuroendocrine tu-
mors are visualized with high contrast, as are intra-
tumoral necrosis and abscesses. The vast majority of other
MRI Appearance of Normal Anatomy liver metastases and cholangiocarcinoma (CCA) are less
conspicuous on both T1w and T2w images. Liver tumors
The normal liver is of uniform signal intensity, which is that are isointense or nearly isointense to normal liver
higher than that of the spleen on T1w images and lower parenchyma are focal nodular hyperplasia (FNH) as well
on T2w images. Hepatic vessels appear dark on T1w im- as an occasional adenoma or hepatocellular carcinoma
ages due to flow-related signal loss (see Fig. 1.2). They are (HCC) (Table 1.4). T1w sequences contribute little to lesion
also dark on T2w images unless gradient moment nulling characterization, except for cysts, which are clearly iden-
(flow compensation) is used, in which case intrahepatic tified as sharply demarcated lesions of very low signal
vessels are bright. The branches of the portal vein and intensity on T1w images. In all other cases, characteriza-
intrahepatic veins serve to identify the liver segments tion of focal liver lesions is primarily based on T2w se-
(Fig. 1.8). Differentiation of the liver from other structures quences, which enable good evaluation of tumor margins
in the upper abdomen is usually straightforward. and internal structures. Use of different T2 weightings,
including images generated from late echoes, allows fur-
12 1 The Liver

a b
Fig. 1.9a, b Multiple liver cysts in a patient with autosomal domi- The liver cysts are depicted as homogeneous lesions of very high SI
nant polycystic kidney disease (1.5 T). a Single-shot T2w TSE image. on the T2w image and very low SI on the T1w image. Also seen are
b T1w GRE image. Both images were acquired during breath-hold. multiple cysts in both kidneys.

Table 1.4 Signal intensities of different liver lesions relative to liver ther characterization and improves accuracy in differen-
tissue on unenhanced images. Note: opposed-phase signal inten- tiating cysts and hemangiomas from solid liver tumors.
sities (T1w OP) for patients without hepatic steatosis Intralesional hemorrhage and fatty components as well as
T1w IP T1w OP T2w melanotic liver metastases from malignant melanoma ex-
hibit atypical signal behavior with hyperintensity on both
Benign tumors
T1w and T2w images. Additional information for charac-
Cysts ↓↓↓ ↓↓↓ ↑↑↑
Hemangioma ↓↓↓ ↓↓↓ ↑↑↑
terizing focal liver lesions is provided by dynamic con-
FNH 0–(↓) 0–(↓) 0–(↑) trast-enhanced MRI, which enables the important differ-
Adenoma ↓–↑↑ ↓↓–↑↑ 0–↑ entiation of hypervascular and hypovascular lesions and
Malignant tumors reveals some typical enhancement patterns such as the
Metastases progressive centripetal enhancement characteristic of
· Melanotic melanoma ↑–↑↑ ↑–↑↑ ↑–↓ liver hemangioma (Table 1.5).
· Neuroendocrine tumors ↓↓ ↓↓ ↑–↑↑↑
Below we describe the MR appearance of the most
important benign and malignant focal liver lesions on
· Other primaries ↓↓ ↓↓ ↑–↑↑
unenhanced images and dynamic contrast-enhanced
HCC ↓↓ ↓↓ 0–↑ imaging with nonspecific Gd-based contrast media. A
CCA ↓↓ ↓↓ ↑–↑↑
separate section illustrates the use of tissue-specific MR
contrast media for selected tumor entities.
Table 1.5 List of typically hypervascular liver tumors
Benign liver tumors
FNH Benign Focal Liver Lesions
Adenoma
Malignant liver tumors Cyst
HCC
Because they contain water, cysts have long T1 and T2
Metastases relaxation times, resulting in very low signal intensity on
· Renal cell carcinoma T1w images and uniform high signal intensity on T2w
· Breast cancer (may also be hypovascular) images. A liver cyst is usually sharply demarcated from
· Neuroendocrine tumors (e. g., carcinoid, insulinoma)
the surrounding tissue but may appear blurred due to
· Melanoma
partial volume effects if the plane of section is tangential
· Sarcoma
to it (Fig. 1.9). In cases where cysts and hemangiomas
cannot be differentiated because of similar T2 signal in-
tensities, a T1w sequence or dynamic imaging will help
distinguish the two (Fig. 1.10).
MRI clearly differentiates the cyst fluid from the solid
wall and septa in echinoccocal cysts, while the character-
istic curvilinear calcifications (eggshell calcifications) are
far better revealed with CT.
Focal Liver Lesions 13

a b

c d

Fig. 1.10a–e Liver hemangioma and cyst in segment II (1.5 T).


a Axial T2w TSE image. b–e Axial T1w GRE images obtained before
(b) and 15 s (c), 2 min (d), and 10 min (e) after IV injection of Gd-
based contrast medium. Before contrast medium administration,
both lesions have very high T2 SI (a) and low T1 SI (b). On dynamic
contrast-enhanced images, the hemangioma is characterized by
initial nodular peripheral enhancement (c) with progressive fill-in
(d), resulting in complete hyperintensity of the lesion 10 min after
contrast administration (e). The cyst has unchanged low SI on all
postcontrast images.

Hemangioma from liver metastases. This is especially important in pa-


Hemangiomas are the most common benign hepatic tu- tients with multiple hemangiomas (up to 35 % of cases).
mors. They are incidentally detected in ca. 5 % of patients Hemangiomas are well-circumscribed masses of uni-
undergoing abdominal imaging for other reasons. Heman- form signal intensity on T1w and T2w images and may
giomas are mesenchymal tumors characterized by occasionally be lobular. They are moderately hypointense
densely packed, dilated vessels with an endothelial lining. on T1w images and clearly distinct from cysts, which have
Regressive changes such as scars and central hyalinization very low T1 signal intensity, while distinguishing them
may be present in large hemangiomas. Although they from other solid liver tumors is more difficult. On T2w
have no malignant potential, hemangiomas may pose a images, on the other hand, hemangiomas are of high
diagnostic challenge because they must be differentiated signal intensity and therefore at times resemble cysts
14 1 The Liver

(Fig. 1.10). Hemangiomas have long T2 values (> 80 ms), cells, and proliferating, blind-ending bile ducts and may
which are due to slow-flowing blood and correlate with have a central stellate scar.
the collective size of their constituent vascular spaces, but FNH is nearly isointense or slightly hypointense to
not with overall tumor size.26 Central thrombosis or hya- surrounding liver on T1w images and isointense or
linization is occasionally seen, especially in large heman- slightly hyperintense on T2w images (Fig. 1.12). The imag-
giomas (Fig. 1.11). Various quantitative approaches have ing appearance is attributable to the fact that FNH consists
been proposed to improve the differentiation of heman- of almost the same tissue as normal liver. T1 hypointensity
giomas and malignant tumors, including calculation of T2 is more commonly seen on GRE images obtained with a
relaxation time or contrast-to-noise ratio (CNR). However, very short TE (e. g., FLASH).31 A typical imaging feature is
none of the quantitative methods appears to be superior the extremely uniform appearance of the lesion on T1w
to visual interpretation of T2w images, taking into account images, which is observed in 57–94 % of patients.31,32 A
the morphologic features just outlined. A combination of central scar has been reported in 35–50 % of FNHs. The
moderately and heavily T2-weighted sequences has been scar is always of low signal intensity on T1w images, but is
recommended to increase diagnostic confidence in diag- revealed as a hyperintense structure on T2w imaging in
nosing hemangioma,27,28 for instance a moderately T2w only ca. 65 % of cases (Fig. 1.12).32 An occasional FNH is
TSE sequence and a single-shot TSE sequence, which has pedunculated (Fig. 1.13) with the risk of torsion and sub-
inherently stronger T2 weighting. On heavily T2-weighted sequent infarction of the tumor.
images, hemangiomas should be of high signal intensity Being hypervascular, FNH is characterized on dynamic
similar to that of cerebrospinal fluid (CSF) or fluid in the MRI by intense homogeneous enhancement in the arterial
gallbladder or stomach. MRI has an accuracy of > 90 % in phase, which rapidly fades to isointensity on later images
characterizing hemangioma.13,27 Nevertheless, there are (Figs. 1.12 and 1.13). The typical central scar is character-
still cases where accurate characterization poses a chal- ized by nonenhancement on early postcontrast images,
lenge, e. g., when confronted with an atypical heman- becoming hyperintense only after 2–4 min (Fig. 1.12).
gioma with reduced signal intensity and an inhomogene-
ous appearance due to degenerative changes, or in pa- Hepatocellular Adenoma
tients in whom hemangiomas may be confused with hep- Hepatocellular adenoma is an uncommon primary liver
atic metastases from neuroendocrine tumors, which also tumor with the risk of malignant transformation. The
have very long T2 relaxation times.29 If unenhanced imag- tumor resembles hepatocellular carcinoma in that fatty
ing fails to ascertain the presumptive diagnosis of heman- degeneration may be present (Fig. 1.14). Hemorrhage is
gioma, a dynamic MR study is done, usually with non- also quite common. The morphologic features seen on
specific contrast medium. MRI are variable because of the multifarious histologic
On dynamic contrast-enhanced imaging, most heman- composition of the tumors.33 On IP T1w images, about
giomas show initial peripheral enhancement with slow half of all hepatocellular adenomas appear heterogeneous
progressive fill-in, ultimately resulting in uniform high with hyperintensities indicating fatty degeneration or
signal intensity on delayed images (ca. 10 min after con- hemorrhage. Fatty components can be differentiated
trast administration). Nodular peripheral enhancement from hemorrhage by loss of signal on OP images
on early dynamic MR images is pathognomonic for hem- (Fig. 1.14). The T2 appearance is also predominantly het-
angioma (Figs. 1.10 and 1.11). Small and medium-sized erogeneous with areas of high and low signal intensity.
hemangiomas are usually of homogeneous high signal MRI demonstrates a peritumoral pseudocapsule in ca. 30 %
intensity on delayed images. Hemangiomas with central of cases.34 Although common in FNH, a central scar is very
thrombosis or hyalinization also show peripheral en- rare in hepatocellular adenoma. Overall, the MR appear-
hancement with centripetal progression but persistent ance of hepatocellular adenoma resembles that of hepa-
central hypointensity (Fig. 1.11). Large hemangiomas tocellular carcinoma, rarely that of FNH. Typical contrast
often undergo degeneration, seen as irregular, nonen- enhancement features are also lacking. Most hepatocellu-
hancing areas on delayed images. Very small hemangio- lar adenomas are hypervascular and the diagnosis may be
mas may show immediate uniform enhancement on ar- made with a high degree of confidence when MRI shows
terial phase images, which persists or equilibrates with an inhomogeneous hypervascular tumor with signs of
liver on later images. hemorrhage.35 However, given the diagnostic problems
and malignant potential, surgical resection may be re-
Focal Nodular Hyperplasia quired in unclear cases.
Focal nodular hyperplasia (FNH) is a relatively uncommon
benign tumor and has been associated with the use of oral
contraceptives. It is assumed that oral contraceptives pro-
mote the growth of FNH already present, which is why the
tumors become larger and are more commonly detected
in women.30 Unlike hepatocellular adenoma, FNH has no
malignant potential. It consists of hepatocytes, Kupffer
Focal Liver Lesions 15

a b

c d

Fig. 1.11a–e Hemangioma with central hyaline degeneration in


liver segment VII (1.5 T). a Axial image obtained with single-shot
T2w TSE sequence. b–e Axial T1w GRE images before (b) and 15 s
(c), 2 min (d), and 10 min (e) after IV injection of Gd-based contrast
medium. Thrombosis of the hemangioma is indicated by markedly
higher SI on T2w image (a) and markedly lower SI on T1w image (b)
relative to the periphery of the lesion. The immediate postcontrast
image shows nodular peripheral enhancement (c). Subsequent im-
ages show progressive peripheral enhancement with persistent
central hypointensity.

e
16 1 The Liver

a b

c d

Fig. 1.12a–e Focal nodular hyperplasia (FNH) in liver segments III


and IV (1.5 T). a Axial image obtained with single-shot T2w TSE
sequence. b–e Axial T1w GRE images before (b) and 15 s (c), 55 s
(d), and 10 min (e) after IV injection of Gd-based contrast medium.
Both FNHs are slightly hyperintense and homogeneous on T2w
image (arrows in a) and slightly hypointense on T1w image (b).
The central scar is seen only on the T1w image. On the arterial phase
image (c) both masses show intense enhancement sparing the
central scars. Enhancement fades rapidly, while there is delayed
enhancement of the central scars (most conspicuous in the FNH
indicated by the arrow in e).

e
Focal Liver Lesions 17

a b

c d

Fig. 1.13a–e Large pedunculated FNH of left hepatic lobe (arrow)


(1.5 T). a T2w axial single-shot TSE image. b T2w coronal single-shot
TSE image. c–e Axial T1w GRE images obtained before (c) and 15 s
(d) and 10 min (e) after IV injection of Gd-based contrast medium.
FNH is nearly isointense to surrounding liver on unenhanced images
(a–c) and shows hypervascularity on arterial phase image (d).

e
18 1 The Liver

a b

c d

e f
Fig. 1.14a–f Large liver adenoma in segment VIII (1.5 T). a Axial is suggested by moderate hyperintensity of the adenoma on IP
T2w TSE image. b IP axial T1w GRE image. c OP axial T1w GRE image (b) and marked hypointensity on OP image (c). In the dy-
image. d–f Dynamic contrast-enhanced axial T1w GRE images (IP) namic contrast-enhanced examination, high SI of the adenoma on
obtained 15 s (d), 55 s (e), and 5 min (f) after IV injection of Gd- arterial phase image (d) indicates hypervascularity. Also seen is FNH
based contrast medium. Adenoma is of slightly higher SI than in the left hepatic lobe.
surrounding liver on T2w image (a). Presence of lipid in the lesion
Focal Liver Lesions 19

a b

c d

Fig. 1.15a–e Multiple hypovascular metastases from colorectal ad-


enocarcinoma (1.5 T). a Axial single-shot T2w TSE image. b–e Axial
T1w GRE images obtained before (b) and 15 s (c), 55 s (d), and
10 min (e) after IV injection of Gd-based contrast medium. T2w
image (a) reveals multiple lesions with a hyperintense center (ne-
crosis) and less intense periphery (target sign). On T1w image (b)
the metastases are revealed as hypointense lesions with ill-defined
margins. Arterial phase image (c) of the dynamic contrast-enhanced
examination shows characteristic peripheral enhancement of large
metastases (straight arrow), while smaller lesions are obscured due
to diffuse enhancement (curved arrow). Later images show periph-
eral washout of the metastases, seen as a hypointense halo relative
to the center of the lesion and surrounding liver.

Malignant Focal Liver Lesions necrosis is present, the signal intensity of the center is
even lower than that of the surrounding viable tumor on
Metastases T1w images (doughnut sign) and higher on T2w images
The MR appearance of liver metastases is as heterogene- (target sign)36 (Fig. 1.15). This appearance strongly sug-
ous as their morphology and also varies with the type of gests metastasis, especially if multiple lesions are present.
primary tumor (see page 11 and Table 1.4). Dynamic con- Calcifications within a metastasis are low in signal inten-
trast-enhanced MR imaging differentiates hypovascular sity on both T1w and T2w MR images, but are less obvious
and hypervascularized metastases and thus provides than on CT scans. Intratumoral hemorrhage is highly con-
some clues about the primary tumor (Table 1.5). spicuous as hyperintensity on T1w images. Liver metasta-
Most liver metastases are from colorectal cancer. They ses from colorectal adenocarcinoma are usually hypovas-
have a fairly consistent MRI appearance with moderate T1 cular. In general, hypovascular metastases show thin rim
hypointensity and moderate T2 hyperintensity. If central enhancement on early-phase contrast-enhanced images
20 1 The Liver

a b

c d

Fig. 1.16a–e Hypovascular metastasis from breast cancer (straight


arrow, segments V/VI) and small hemangioma (curved arrow, seg-
ment VI). a Axial T2w TSE image. b–e Axial T1w GRE images
obtained before (b) and 15 s (c), 55 s (d), and 10 min (e) after IV
injection of Gd-based contrast medium. The metastasis is clearly
delineated from surrounding liver on both T1w and T2w images.
The dynamic contrast-enhanced examination shows slow and mild
inhomogeneous enhancement of the metastasis. Characteristic en-
hancement pattern of the small hemangioma (see Fig. 1.9).

(1–2 min), while their overall signal intensity remains ment on arterial phase dynamic images often allows de-
below that of liver (Fig. 1.15). In ca. 35 % of cases, there tection of very small lesions (Fig. 1.17). Note, however,
will be peripheral washout on delayed images (Fig. 1.15), that these tumors fade to become isointense to liver by
which has 100 % specificity for malignancy.37 Metastases the portal venous phase and will escape detection if the
from breast cancer also show moderate hypointensity on arterial phase of enhancement is missed. On unenhanced
unenhanced T1w images and moderate hyperintensity on images melanotic metastases from malignant melanoma
T2w images but may be either hyper- or hypovascular have high T1 signal intensity due to the presence of para-
(Fig. 1.16). Metastases from renal cell carcinoma, neuro- magnetic melanin and high or low T2 signal intensity,
endocrine tumors such as carcinoids, melanoma, and sar- depending on the amount of melanin present. Multiple
coma tend to be hypervascular. Their intense enhance- melanoma metastases in the liver may vary substantially
Focal Liver Lesions 21

a b

c d

Fig. 1.17a–e Hypervascular metastases from functioning neuroen-


docrine pancreatic carcinoma (1.5 T). a Axial T2w TSE image. b–e
Axial T1w GRE images obtained before (b) and 15 s (c), 55 s (d), and
5 min (e) after IV injection of Gd-based contrast medium. Only one
metastasis is seen on the unenhanced T2 and T1w images, while the
arterial phase image of the dynamic contrast-enhanced study re-
veals a second, very small metastasis (arrow in c). On portal venous
phase and delayed images, the small metastasis is obscured again
due to enhancement of the liver parenchyma (d, e).

in signal features (Fig. 1.18). Intratumoral hemorrhage can common in East Asians: it has been found in 27 % of cases
be identified by increased T1 signal intensity or the pres- in the USA,38 while Japanese investigators reported a
ence of sedimentation effects (Fig. 1.19). pseudocapsule in 42 % of HCCs.39 Internal structures
with high signal intensity on T1w images are typical of
Hepatocellular Carcinoma HCC. They have been found to be attributable to fatty
Hepatocellular carcinoma (HCC) may be expansive (uni- metamorphosis, which is present in ca. 50 % of HCCs.38
locular, multilocular) or infiltrative. Like liver adenomas, More recently, it has been proposed that such hyper-
HCCS have a variable MR appearance due to their hetero- intensities may be due to intratumoral copper.40 About
geneous morphology. HCCs may be surrounded by a 50 % of HCCs have a mosaic pattern of low and high signal
pseudocapsule, which consists largely of compressed liver intensities, which is more obvious on T2w images than
tissue and blood vessels and has low signal intensity on T1w images.41
T1w images (Figs. 1.20 and 1.21). A pseudocapsule is more
22 1 The Liver

a b
Fig. 1.18a, b Multiple metastases from malignant melanoma (1.5 T). a Axial single-shot T2w TSE image. b Axial T1w GRE image. Metastases
are of high SI on unenhanced T1w image due to presence of melanin (melanotic metastases).

a b

Fig. 1.19a, b Multiple large metastases from malignant gastrinoma intralesional hemorrhage. On T2w image, sedimentation effects are
(1.5 T). a Axial single-shot T2w TSE image. b Axial T1w GRE image. seen in part of the lesions.
Hyperintensity of some of the metastases on T1w image is due to

HCC may be hypervascular or hypovascular, with well hypovascular to moderately hypervascular. A rather typi-
differentiated HCC tending to be hypervascular and poorly cal feature is inhomogeneous high signal intensity on late-
differentiated HCC tending to be hypovascular42 (see Figs. phase images acquired after intravenous injection of non-
1.20 and 1.21). The peritumoral pseudocapsule is of low specific contrast medium.
signal intensity on early dynamic contrast-enhanced im-
ages and becomes hyperintense on later-phase images.
This pattern of enhancement is more obvious in larger Other Focal Liver Lesions
tumors, which also tend to be more inhomogeneous on
delayed postcontrast images. Hemorrhagic Liver Lesions
Hemorrhagic lesions have a typical MR pattern, which
Cholangiocarcinoma varies with the age of the hemorrhage. Following lysis of
Hepatic cholangiocarcinoma (CCA) can grow along the erythrocytes and liquefaction, hematoma has high signal
branches of the portal vein or occur in the form of a solid intensity on both T1w and T2w images. Increasing uptake
mass (see Chapter 2). The first type is difficult to identify of hemosiderin by macrophages in the periphery of a
by imaging, while the focal type has the same MR appear- hematoma is seen as a rim of low signal intensity around
ance as liver metastases (low T1 signal intensity and mod- the lesion on T2w images (see Fig. 1.19).
erately high T2 signal intensity). CCA is suggested if MRI
demonstrates an ill-defined mass, satellite lesions, and
atrophy of the affected hepatic lobe (Fig. 1.22).43 On
dynamic contrast-enhanced imaging, CCA is moderately
Focal Liver Lesions 23

a b

c d

Fig. 1.20a–e Small hypervascular HCC in liver segment IV (arrow)


(1.5 T). a Axial T2w TSE image. b–e Axial T1w GRE images obtained
before (b) and 15 s (c), 55 s (d), and 10 min (e) after IV injection of
Gd-based contrast medium. HCC is moderately hyperintense on T2w
image and hypointense on T1w image, which also reveals a low-SI
pseudocapsule. In the dynamic contrast-enhanced examination, the
hypervascular tumor is of high SI on arterial phase image (c) and
becomes isointense to liver on later images. The pseudocapsule is
seen as a thin rim of slightly higher SI. T2w image also shows small
cyst in left hepatic lobe.

e
24 1 The Liver

a b

c d

Fig. 1.21a–e Large hypovascular HCC in liver segment III (arrows)


(1.5 T). a Axial T2w TSE image. b–e Axial T1w GRE images obtained
before (b) and 15 s (c), 55 s (d), and 10 min (e) after IV injection of
Gd-based contrast medium. The HCC is only slightly higher in SI than
surrounding liver on T2w and T1w images and has a pseudocapsule
that is clearly depicted as a thin rim of low SI on T1w image. In the
dynamic contrast-enhanced examination, there is only little en-
hancement of the mass, consistent with a hypovascular lesion (c).
Delayed phase shows isointense, inhomogeneous tumor sur-
rounded by a hyperintense pseudocapsule (e).

e
Focal Liver Lesions 25

a b

Fig. 1.22a–c Cholangiocarcinoma in the left hepatic lobe (1.5 T).


a Axial T2w TSE image. b, c Axial T1w GRE images obtained before
(b) and 5 min (c) after IV injection of Gd-based contrast medium.
There is characteristic atrophy of the left hepatic lobe. Inhomoge-
neous appearance of the mass on postcontrast image.

a b

c d
Fig. 1.23a–d Multiple Candida abscesses of the liver in an immu- central portions of the lesions have high SI, which is why they appear
nosuppressed patient undergoing antimycotic treatment (1.5 T). smaller than on T2w imaging. Dynamic contrast-enhanced images
a Axial single-shot T2w TSE image. b–d Axial T1w GRE images demonstrate rim enhancement, which is very intense on delayed
obtained before (b) and 15 s (c) and 5 min (d) after IV injection image.
of Gd-based contrast medium. On the T2w image (a), only the
26 1 The Liver

a b

c d
Fig. 1.24a–d Focal fatty liver lesions and focal fatty sparing (1.5 T). infiltration is indicated by low SI relative to liver on OP image (a) and
a, b Patient with focal hepatic steatosis in segment IV. OP image, TE isointensity on IP image (b). In the patient with diffuse hepatic
= 2.4 ms (a) and IP image, TE = 4.8 ms (b) obtained with T1w GRE steatosis (c, d), focal fatty sparing is indicated by an area of high
sequence. c, d Diffuse hepatic steatosis with focal fatty sparing in SI within the low-SI fatty liver on OP image (c) (see Figs. 1.4 and
segment IV in a second patient. OP image, TE = 2.4 ms (c) and IP 1.5).
image, TE = 4.8 ms (d) obtained with T1w GRE sequence. Focal fatty

Abscess GRE images. Well-defined focal fatty lesions are uncom-


An intrahepatic abscess is hypointense on T1w images and mon and are characterized by high signal intensity on T1w
hyperintense on T2w images. The hypointense lesion seen and T2w SE sequences (without fat suppression). On TSE
on T1w images corresponds to the abscess cavity, while or FSE sequences, which exaggerate the signal from fat,
the area of hyperintensity seen on T2w images also com- such focal fatty lesions may be of very high signal inten-
prises the perifocal edema. Following initiation of medical sity and thus mimic metastases (e. g., from melanoma),
therapy, imaging will demonstrate concentric rings rep- HCC, or hemorrhagic lesions, all of which may be hyper-
resenting the surrounding granulation and connective intense on both T1w and T2w images.31,44 Both nondiffuse
tissue (Fig. 1.23) and resolution of inflammatory edema fatty infiltration in the form of geographic or focal changes
(on T2w images). and fatty sparing can be diagnosed with a high degree of
confidence by comparing OP and IP GRE images
Focal Fatty Liver Lesions (Fig. 1.24). Multifocal fatty infiltration of the liver is un-
Hepatic steatosis or fatty infiltration of the liver may be common but must be considered because the appearance
diffuse, geographic, or focal. Another pattern is focal fatty may well resemble multiple metastases on CT scans or
sparing in the setting of diffuse fatty infiltration of the when looking only at OP MR images. The true nature of
liver. Fatty liver may be caused by external factors such as the lesions will be revealed by taking into account both OP
certain foods, drugs, or toxins and is associated with por- and IP images45 (Fig. 1.25).
phyria and other metabolic disorders. Mild fatty infiltra-
tion of the liver is not seen on conventional T1w TSE or IP
Focal Liver Lesions 27

a b

Fig. 1.25a–c Multifocal hepatic steatosis (1.5 T). a Axial single-shot


T2w TSE image. b, c Axial T1w GRE images obtained with IP echo
time (TE = 4.1 ms) (b) and OP echo time (TE = 2.2 ms) (c). Fatty
lesions in the liver are moderately hyperintense on T2w image (a)
and IP T1w image (b) and hypointense on OP image (c).

Use of Tissue-Specific Contrast Media show similar enhancement patterns as after administra-
tion of nonspecific Gd-based contrast media (Fig. 1.27).
Superparamagnetic Iron Oxide Particles While nonspecific contrast media rapidly diffuse into the
extravascular space after intravenous injection, Resovist
Superparamagnetic iron oxide particles (SPIO) contrast particles have a longer blood half-life and are still intra-
media significantly increase the detection of liver meta- vascular when early dynamic images are acquired, which
stases, particularly small ones, compared with unen- is why the strong arterial phase enhancement of hyper-
hanced MRI46–48 (Fig. 1.26) and can also improve lesion vascular tumors such as FNH known from nonspecific
characterization. When Endorem (which can only be contrast media is absent when Resovist is used
given as an infusion) is used, only delayed images can (Fig. 1.28). If dynamic Resovist-enhanced imaging is per-
be acquired, and these will show a signal loss in tumors formed with a T2*-weighted sequence, highly vascular-
containing MPS cells (see Fig. 1.28). However, this infor- ized tumors will show a temporary signal loss.
mation has limited value for lesion characterization
because MPS cells are present in well-differentiated HCC
and benign tumors such as FNH or adenomatous hyper- Hepatobiliary Contrast Media
plasia. Therefore, the only possible distinction is that bet-
ween well-differentiated tumors of hepatocellular origin As with iron oxide particles, hepatobiliary contrast media
on the one hand and dedifferentiated hepatocellular tu- significantly improve the detection of small liver lesions
mors or nonhepatocellular lesions such as metastases on during the phase of hepatocellular uptake23,24,49
the other hand. SPIO formulations that can be adminis- (Fig. 1.29). Hepatobiliary contrast media accumulate in
tered as a bolus, such as Resovist, can be used for perfu- tumors of hepatocellular origin, which can thus be differ-
sion studies analogous to nonspecific contrast media. The entiated from nonhepatocellular tumors with an accuracy
signal-enhancing effect of Resovist is low in the blood pool of ca. 94 %. A hyperintense rim on delayed images is nearly
phase but usable to identify hemangiomas, which will 100 % specific for malignancy.50
28 1 The Liver

a b

c d

e f

g h
Focal Liver Lesions 29

a b

c d

e f
Fig. 1.27a–f Dynamic T1w MRI of liver hemangioma after bolus trast image (b) with progressive fill-in on later images (c and d; see
injection of iron oxide particles. a–d Axial images obtained with Fig. 1.10). At the same time, normal liver parenchyma gradually
T1w GRE sequence before (a) and 1 min (b), 5 min (c), and 10 min loses SI as a result of contrast uptake. Intravascular signal increases
(d) after IV injection of Resovist. e, f Fat-suppressed, respiratory- on postcontrast T1w images (b–d). Compare T2w images (e, f).
triggered T2w TSE images obtained before (e) and 15 min after (f) Prolonged blood pool effect of iron oxide particles markedly reduces
contrast injection. Blood pool effect of iron oxide particles results in SI of hemangioma on postcontrast T2w image (f).
nodular peripheral enhancement of hemangioma on early postcon-

v Fig. 1.26a–h Examples of improved liver lesion detection in two stases. Unenhanced T1w image for comparison (e). f–h Patient with
patients using iron oxide particles (1.5 T). a–e Patient with multiple metastasis from islet cell carcinoma. Axial T2w images obtained
metastases from colon cancer. Axial T2w images obtained with with fat-suppressed, respiratory-triggered TSE sequence before (f)
single-shot TSE sequence and fat-suppressed, respiratory-triggered and 15 min after (g) IV injection of Resovist. Precontrast image does
TSE sequence before (a, c) and 15 min after IV injection of Resovist not allow reliable detection of the liver lesion despite excellent
(b, d). Iron oxide particles improve contrast and conspicuity of liver image quality. Selective signal reduction of the liver parenchyma
metastases by selectively reducing the SI of liver parenchyma. on image enhanced with iron oxide particles improves conspicuity
Respiratory-triggered TSE sequence is superior to single-shot TSE of the very small metastasis (arrow in g). Unenhanced respiratory-
sequence in terms of image quality and conspicuity of liver meta- triggered T1w GRE image fails to demonstrate the metastasis (h).
30 1 The Liver

a b

c d

e f
Fig. 1.28a–f Dynamic T1w MRI of FNH after bolus injection of iron oxide particles produce only a negligible increase in SI of FNH on
oxide particles. a–d Axial images acquired with T1w GRE sequence arterial phase image; FNH and liver show a continual signal de-
before (a) and 15 s (b), 55 s (c), and 5 min after (d) IV injection of crease. Intravascular signal increases on T1w images (b–d). Com-
Resovist. e, f Fat-suppressed, respiratory-triggered T2w TSE images pare T2w images (e, f). There is marked signal reduction of FNH,
obtained before (e) and 15 min after (f) contrast injection. Iron indicating Kupffer cell activity.

For those hepatobiliary contrast media that can be Role of MRI in Focal Liver Lesions
administered as a bolus, the experience with dynamic
MRI using nonspecific contrast media is directly trans- Detection of Focal Liver Lesions
ferable. Hypovascular metastases will show the well-
known rim enhancement on early phase images This section discusses the role of MRI in detecting focal
(Fig. 1.29), while hemangiomas are characterized by pro- liver lesions with regard only to malignant lesions such as
gressive centripetal enhancement51 (Fig. 1.30). FNH dis- metastases and HCC. The degree of vascularization of a
plays perfusion-related enhancement in the early phase lesion determines whether it is best detected during the
and high signal intensity due to contrast uptake on de- arterial phase of a dynamic MR study after intravenous
layed images (Fig. 1.31). injection of a nonspecific Gd-based contrast medium or
during the late phase after injection of a tissue-specific
Focal Liver Lesions 31

a b

c d

Fig. 1.29a–e Liver metastases from rectal cancer on dynamic T1w


MRI with delayed imaging after IV bolus injection of hepatobiliary
contrast medium (Primovist) (1.5 T). a Axial image obtained with
fat-suppressed, respiratory-triggered T2w TSE sequence. b–e Axial
images obtained with T1w GRE sequence before (b) and 15 s (c),
55 s (d), and 2 h after (e) contrast injection. T2w and unenhanced
T1w images (a, b) reveal one large and two small metastases.
Dynamic images show peripheral enhancement of the liver lesions,
consistent with the enhancement pattern of hypovascular metasta-
ses after administration of nonspecific Gd-based contrast medium
(c, d). The two small metastases are most conspicuous on delayed
image (arrows in e) as a result of selective enhancement of liver
parenchyma (e, arrows). Variable appearance of the metastases is
due to different liver positions during free breathing (a) and breath-
holding (b–e); slice positioning optimized for visualization of the
e two small metastases in segment IV (images courtesy of Dr.
A. Huppertz, Berlin).

contrast medium (SPIO particles or hepatobiliary contrast hepatobiliary contrast media. All three hepatobiliary for-
media) (see Table 1.5). Late postcontrast images after mulations currently approved for clinical use (Multihance,
administration of a tissue-specific contrast medium ap- Teslascan, Primovist) have been shown to improve detec-
pear to be most suitable to detect hypovascular metastases tion of hypovascular metastases on delayed postcontrast
from colorectal cancer. Several studies have demonstrated images compared with both unenhanced MRI24,54,55 and
that SPIO injection significantly improves detection of dynamic contrast-enhanced MRI using nonspecific con-
hypovascular metastases on late images compared with trast media.54 The nonspecific Gd contrast media do not
both unenhanced MRI and dynamic MRI using nonspecific greatly improve detection of hypovascular metastases
contrast media.52–54 Similar results were obtained with compared with unenhanced MRI. In some cases, e. g., ex-
32 1 The Liver

a b

c d

e f
Fig. 1.30a–f Liver hemangioma on dynamic T1w MRI with delayed ment of FNH with subsequent progressive centripetal fill-in (c, d).
imaging after IV bolus injection of hepatobiliary contrast medium Complete homogeneous enhancement of hemangioma after 5 min
(Primovist) (1.5 T). a Axial image obtained with single-shot T2w TSE with loss of lesion-liver contrast due to simultaneous enhancement
sequence. b–f Axial images obtained with T1w GRE sequence before of normal liver tissue (e). Increased lesion–liver contrast on delayed
(b) and 15 s (c), 55 s (d), 5 min (e), and 15 min after (f) contrast image due to elimination of contrast medium from blood and
injection. Early dynamic images show nodular peripheral enhance- persistent enhancement of liver (f) (see Fig. 1.10).

tremely hypovascular malignant tumors, lesion–liver con- compared with unenhanced MRI. Moreover, arterial phase
trast may be improved on images acquired immediately images are at least equal, if not superior, to delayed im-
after intravenous injection. In general, however, hypovas- ages obtained after injection of a tissue-specific agent
cular liver lesions, in particular small ones, tend to be less (SPIO particles or hepatobiliary contrast media).57,58 How-
conspicuous on dynamic imaging with Gd-based agents.56 ever, most studies have investigated the detection of hy-
The situation is different for hypervascular liver lesions pervascular liver lesions in patient populations with HCC
such as metastases from carcinoids or HCC. The detection and cirrhosis. Uptake of both SPIO particles and hepato-
of these lesions is improved by arterial phase imaging biliary agents is reduced in the cirrhotic liver. Compared
after intravenous injection of nonspecific contrast media with biphasic spiral CT, delayed MR images acquired after
Focal Liver Lesions 33

a b

c d

Fig. 1.31a–e Large FNH on dynamic MRI with delayed imaging


after IV bolus injection of hepatobiliary contrast medium (Primovist)
(1.5 T). a Axial image obtained with T2w SE sequence. b–e Axial
images obtained with T1w GRE sequence before (b) and 15 s (c),
2 min (d), and 2 h (e) after contrast injection. FNH is isointense to
liver on unenhanced T2w and T1w images and becomes hyper-
intense on arterial phase image of dynamic study because it is a
hypervascular lesion (c). Subsequent uptake of contrast medium by
hepatocytes and FNH results in isointensity after 2 min (d). FNH
retains contrast medium longer, resulting in higher SI compared
with liver on delayed image (e).

administration of a liver-specific contrast medium have equal to or slightly better than that of CT during arterial
been found to be equal or even slightly superior in detect- portography (CTAP), the traditional gold standard for de-
ing both hypo- and hypervascular focal liver lesions.55,59 It tection of focal liver lesions among the cross-sectional
must be noted, however, that these studies did not use imaging modalities, and its rate of false-positive findings
state-of-the-art multislice CT scanners. In another study, was lower.60
the sensitivity of SPIO-enhanced MRI was found to be
34 1 The Liver

Characterization of Focal Liver Lesions play an important role in the routine clinical setting.
Nevertheless, MRI can often provide important clues to
Unenhanced MRI the etiology (iron storage disease) and stage (cirrhosis) of
The diagnostic information obtained with unenhanced the disease as well as to associated complications (hep-
MRI already enables good differentiation of focal liver atocellular carcinoma, cholestasis). Diagnostic imaging
lesions, particularly of nonsolid (cysts, hemangiomas) may become more important in the future in light of
and solid tumors. Solid and nonsolid lesions have different recent scientific evidence suggesting that even advanced
T2 relaxation times61 and morphologic features, which are liver fibrosis and cirrhosis may be reversible. These new
predominantly identified with T2w imaging. These fea- insights have also spurred the development of new imag-
tures were established with the advent of liver MRI and ing techniques such as liver elastography.71
are still valid today.36,62 The most common benign liver
tumors, such as hemangioma and FNH, can be differenti-
ated from metastases and malignant tumors of hepatocel- Indications
lular origin using the qualitative morphologic criteria de-
scribed in the sections on the different entities above. An overview of the underlying causes of diffuse liver
disease is given in Table 1.6. In most instances, laboratory
Contrast-Enhanced MRI tests and histologic examination are the first-line diag-
Serial dynamic imaging after administration of an extra- nostic procedures with MRI providing only supplemen-
cellular nonspecific Gd-based contrast medium such as tary information. The foremost role of MRI is to identify
Magnevist or Dotarem improves lesion characterization associated complications of diffuse liver disease, above all
by providing information on perfusion patterns. Overall, in the presence of cirrhosis. MRI is used to demonstrate
dynamic MRI has become an important component of the hepatic collateral circulation secondary to portal hyper-
diagnostic procedure in patients with indeterminate liver tension, rule out HCC, and characterize focal fatty infiltra-
lesions and significantly improves lesion characterization tion or focal fatty sparing. The latter may resemble neo-
compared with unenhanced MRI.46,63,64 plasms and their true nature may not be apparent with
The experience gained from nonspecific contrast me- other diagnostic modalities.
dia can be extended to tissue-specific contrast media ex-
cept that hypervascular tumors lack the typical “blush” in
the arterial phase after SPIO administration. In the late or Imaging Technique
accumulation phase, the tissue-specific contrast media
provide functional information on hepatocytes (hepato- Routine MRI for morphologic evaluation in patients with
biliary agents) and Kupffer cells (SPIO particles),65 thereby suspected diffuse liver disease can be performed using the
improving discrimination of well-differentiated HCC with same pulse sequences as for focal liver lesions (see Table
hepatocellular function or Kupffer cell activity from 1.2). In-phase (IP) and opposed-phase (OP) GRE images
poorly differentiated HCC and metastases.66–68 Prelimi- are an integral part of the protocol and should be obtained
nary results suggest that the hepatobiliary agent Teslascan in all patients as they enable sensitive detection of fatty
is superior to SPIO particles in this respect.69 The ability to infiltration and iron deposition. All contrast media used
assess cell function is an advantage of MRI over CT in for MRI of focal liver lesions can also be used to assess
characterizing focal liver lesions. diffuse disease (see Table 1.1), but contrast-enhanced
imaging plays only a secondary role in diffuse liver dis-
ease. Encouraging results have been obtained with more
Diffuse Liver Disease recent MR techniques, such as diffusion and perfusion
imaging, but they are not yet part of the routine diagnostic
repertoire.72,73 MR elastography (MRE)74–77 is a rapidly
Introduction developing new technique with great promise for the
diagnostic evaluation of liver fibrosis. MRE provides in-
Diffuse liver disease refers to any destructive or infiltra- formation on the stiffness of biological tissues by measur-
tive process that involves the liver parenchyma, the bile ing their shear elasticity using a time-resolved motion-
ducts, or the vascular structures.70 Although it can be sensitive MRI sequence that detects the propagation of
caused by a wide spectrum of underlying disorders rang- externally applied mechanical waves in the liver. The
ing from inflammatory, toxic, and metabolic conditions to shear elasticity of the liver has been shown to change
neoplastic disease, the reaction of the liver is rather uni- with the progression of fibrosis and can thus be exploited
form and nonspecific, mainly comprising a limited num- to grade fibrosis. MRE is noninvasive and, unlike liver
ber of changes such as fatty infiltration, fibrosis, and cho- biopsy, provides information on the entire organ.
lestasis.70,71 Diffuse liver disease is a slowly progressive
condition, and morphologic changes detectable by imag-
ing may only become apparent in advanced disease. Blood
tests and histologic examination therefore continue to
Diffuse Liver Disease 35

Table 1.6 Overview of conditions causing diffuse liver disease

Etiology Diseases Presence of Key imaging findings


fibrosis / cirrhosis
Metabolic and Diabetes/obesity/NASH Rare Fat accumulation
storage disorders Hemochromatosis Yes Signal loss of liver parenchyma most obvious on in-phase
GRE images due to iron deposition
Thalassemia
Wilson disease Yes None—copper is not ferromagnetic. Increased attenua-
tion on CT
Infectious and Acute hepatitis (autoimmune, No Increased signal intensity on T2w images
inflammatory viral, infectious)
Heterogeneous enhancement
diseases
Chronic viral hepatitis (B,C,D) Yes Expanded gallbladder fossa sign and enlargement of hilar
periportal space in early disease
Fibrous septa and regenerative nodules in advanced
disease
Sarcoidosis Rare Usually none—scattered nodules might be present
PBC/PSC Yes Biliary duct abnormalities in PSC
Cirrhosis in PBC and end-stage PSC
Toxic Alcohol Yes Fat accumulation

Medications

Radiation Enlargement of the liver (very unspecific!)

Chemicals
Vascular Budd–Chiari syndrome Possible Occluded vessels

Portal vein thrombosis Enlargement of caudate lobe in Budd–Chiari syndrome


Hepatic artery occlusion
Neoplastic Metastatic disease No Multiple focal liver lesions

Diffuse HCC/CCC
Lymphoma No Tumor infiltration may be present along portal tracts

CCC = cholangiocellular carcinoma; HCC = hepatocellular carcinoma; NASH = nonalcoholic steatohepatitis; PBC = primary biliary cirrhosis;
PSC = primary sclerosing cholangitis.

MRI Appearance of Pathologic Entities than that of the spleen on OP GRE images. Spectral fat
saturation or an inversion recovery sequence will be most
As already mentioned, the parenchymal changes occur- helpful in identifying focal fatty infiltration in an other-
ring in diffuse diseases of the liver are rather nonspecific wise normal liver or focal sparing in diffuse fatty liver.82
despite the heterogeneity of underlying etiologies (Table The aforementioned MRI techniques enable reliable char-
1.6). The remainder of this chapter is therefore organized acterization of these focal lesions, whereas they may be
by type of morphologic and structural change rather than confused with focal neoplasms on CT or ultrasonogra-
disease entity. Fibrosis and cirrhosis are of special interest phy78,82 (see Figs. 1.4, 1.24, 1.25).
because they can develop in nearly all diseases of the liver
parenchyma and are associated with high morbidity and
mortality unless proper treatment is initiated. Iron Deposition

In patients with iron storage disease, MRI can be used to


Fatty Liver detect, quantify, and follow up iron overload in the liver
and diagnose potential complications,83,84 but is limited in
Accumulation of fat in the liver is a very common finding identifying the underlying cause. The magnetic suscepti-
in a wide range of clinical conditions, including alcoholic bility of iron stored in the liver results in a decreased SI of
liver disease, diabetes mellitus, nonalcoholic steatohepa- the hepatic parenchyma on all MR pulse sequences.85,86
titis (NASH), and obesity. The mere diagnosis of fatty liver GRE sequences are more sensitive to T2* effects and are
or steatosis is of little clinical consequence. Generalized or therefore superior to SE sequences in detecting iron.86 The
focal fatty infiltration of the liver is detected using a iron overload in the liver can be quantified by calculating
combination of IP and OP GRE images78–81 (Fig. 1.32). In transverse relaxation time using a multiecho sequence.87
the presence of fatty infiltration, liver SI is markedly lower Noninvasive quantification of the iron overload by MRI is
36 1 The Liver

a b

Fig. 1.32a–c Severe geographic fatty infiltration of the liver (1.5 T).
a Axial T2w single-shot TSE image. b, c IP (b) and OP (c) T1w GRE
images. Normal appearance on T2w image (a) and IP image (b). On
OP image (c), fatty infiltration is indicated by very low SI of most of
the parenchyma of the right lobe. There is only moderate fatty
infiltration of the left lobe (see Fig. 1.4).

an alternative to biopsy86 and can be used to monitor the their storage capacity is exceeded, iron accumulates in
outcome of therapeutic phlebotomy.83 hepatocytes, the pancreas, and myocardium.89 MR signal
Iron overload of the liver occurs in many different changes in the spleen distinguish secondary hemochro-
disorders. Primary or hereditary hemochromatosis is a ge- matosis from the primary form. In primary hemochroma-
netic defect of iron metabolism characterized by excessive tosis, the spleen is usually spared, while other organs,
intestinal absorption of dietary iron (Fig. 1.33). Excess iron notably the pancreas, show signal alterations. The pres-
enters the liver, where it is taken up into hepatocytes, but ence of cirrhosis is highly indicative of primary hemochro-
not into cells of the mononuclear phagocyte system matosis.
(MPS).88 In more advanced disease, excess iron is also Paroxysmal nocturnal hemoglobinuria is characterized
stored in the joints, gonads, pancreas, pituitary gland, by intravascular hemolysis with release of hemoglobin
and myocardium and can cause joint disease, insulin- into the blood, where it initially binds to plasma proteins.
dependent diabetes mellitus, hypogonadism, and cardiac After exhaustion of the protein-binding capacity, part of
dysfunction. In primary hemochromatosis, it is of crucial the free hemoglobin is excreted in the urine and part is
importance to identify abnormal hepatic iron accumula- absorbed.90 Ceruloplasmin deficiency is a genetic disorder
tion before cirrhosis develops (precirrhotic stage) because in which the lack of ceruloplasmin, which catalyzes the
treatment by phlebotomy can prevent progression to cir- oxidation of ferrous iron to ferric iron, leads to iron de-
rhosis. In secondary hemochromatosis, the iron overload is posits in the liver.91 In porphyria cutanea tarda, disturbed
primarily due to accelerated destruction of red blood cells heme biosynthesis causes iron accumulation in periportal
(Fig. 1.34). Causes are ineffective erythropoiesis or exter- hepatocytes.92
nal factors (e. g., increased iron supply due to multiple
transfusions). The extra iron is initially stored in the
MPS cells of the liver, spleen, and bone marrow.84 Once
Diffuse Liver Disease 37

a b
Fig. 1.33a, b Hereditary hemochromatosis (1.5 T). a Axial breath-hold T2w single-shot TSE image. b Axial breath-hold T1w GRE image. The
liver has very low SI on both images due to iron deposition and shows signs of cirrhosis. The spleen is enlarged but of normal SI.

a b
Fig. 1.34a, b Secondary hemochromatosis in a man with chronic (TE, 4.6 ms) image. Low SI of the liver and spleen due to iron
renal failure and hemodialysis (1.5 T). a Axial breath-hold T2w single- deposition, which is best seen on T1w image (b). No signs of
shot TSE image (effective TE, 66 ms). b Axial breath-hold T1w GRE cirrhosis and normal SI of the pancreas.

Acute Infectious and Inflammatory Disease by an increased T2 SI of the irradiated area, which grad-
ually returns to normal after the end of radiotherapy.95,96
Acute hepatitis is characterized by the presence of edema, The main role of MRI in acute inflammation of the liver is
which is typically segmental or periportal in distribution to identify complications such as abscess formation or
but may occasionally involve the entire liver. Edema is biliary obstruction.
best identified by increased SI on T2w images. In addition, Parasitic liver infections should also be briefly men-
there will be inhomogeneous enhancement of the liver tioned. In hepatic schistosomiasis mansoni, eggs deposited
parenchyma after intravenous administration of a non- in the periportal area cause inflammation and ultimately
specific extracellular Gd-based contrast medium fibrosis, leading to portal hypertension. Affected peripor-
(Fig. 1.35). Severe acute inflammation can cause enlarge- tal areas are isointense on T1w images and hyperintense
ment of the liver and thickening of the gallbladder wall. It on T2w images and enhance intensely after injection of
has been shown that uptake of hepatobiliary contrast Gd-based contrast medium.97
media such as Mn-DPDP93 and MPS-specific contrast me-
dia such as SPIO particles94 is decreased in acute hepatitis.
However, this is not a reliable criterion for the diagnosis of
hepatitis.93 Radiation-induced hepatitis is characterized
38 1 The Liver

a b

c d
Fig. 1.35a–d Acute hepatitis (1.5 T). a Axial breath-hold T2w single- trast medium. The liver is enlarged and of high T2 SI, consistent with
shot TSE image. b–d Axial breath-hold T1w GRE images obtained intrahepatic edema. The parenchyma appears heterogeneous on
before contrast administration (b) and in the arterial (c) and portal T1w image (b) and shows heterogeneous enhancement, best seen
venous (d) phases after IV injection of nonspecific Gd-based con- in the arterial phase (c).

Fibrosis and Cirrhosis the diagnosis, but new MR techniques, most notably MRE,
have the potential to provide a noninvasive alternative in
Fibrosis and cirrhosis are characterized by the loss and the future.74–77 Definitive imaging changes will be present
regeneration of liver tissue in the setting of chronic hep- once the stage of cirrhosis has been reached. Below we
atocellular damage. Cirrhosis is the common endpoint of a outline the course of fibrosis progression from the first
variety of conditions, primarily including viral hepatitis, manifestations that can be detected by MRI to the imaging
autoimmune disorders, toxic damage, and metabolic de- features of cirrhosis, finally focusing on the development
fects. Nevertheless, the pathophysiologic mechanism of HCC in cirrhotic livers.
underlying the development of cirrhosis is fairly uniform The first MRI signs of cirrhosis are due to early atrophy
and is termed fibrosis progression.71 It must be noted that of the medial segment of the left lobe (segment IV). En-
MRI will detect changes only if there is fibrosis progres- largement of the hilar periportal space (i. e., the space
sion, and very early fibrotic changes are not detectable by anterior to the right portal vein) with fat thickness
any of the currently available MR techniques. Biopsy ≥ 1 cm is highly specific for early cirrhosis.98 Another
therefore remains the method of choice for confirming change resulting from atrophy of the left medial segment
Diffuse Liver Disease 39

a b
Fig. 1.36a, b Cirrhosis with multiple small siderotic nodules in the contour, normal-sized caudate lobe, and multiple small foci of low
liver (1.5 T). a Axial image obtained with respiratory-triggered, fat- SI. Siderotic nodules and high-SI interlobular septa are more con-
suppressed T2w TSE sequence. b Axial image obtained with breath- spicuous on T2w image (a).
hold T1w GRE sequence. T1w image (b) shows nearly normal liver

a b

Fig. 1.37a, b Cirrhosis with mild ascites (1.5 T). a Axial image hypertrophy of left lateral segment. High-SI ascites on T2w image
obtained with T2w single-shot TSE sequence. b Axial breath-hold (a). Multiple high-SI regenerative nodules are apparent on T1w
T1w GRE image. Atrophy of right lobe and left medial segment; image (b).

is the expanded gallbladder fossa sign. In the further 1.39, 1.40, 1.41; see Fig. 1.33). These features are rather
course of fibrosis progression, narrowing of the hepatic specific for cirrhosis but occur late in the course of disease.
veins occurs and the morphologic changes become more While MR contrast media are predominantly used for
conspicuous. In advanced cirrhosis, there will be addi- evaluating focal liver lesions, they may also be useful
tional atrophy of the right hepatic lobe with simultaneous when imaging diffuse liver disease.103 In cirrhosis, the
hypertrophy of the left lateral segment and the caudate heterogeneous SI of the liver parenchyma will also persist
lobe. The combination of cirrhotic changes may result in after intravenous injection of a nonspecific extracellular
nodularity of the liver surface (Figs. 1.36 and 1.37). Other Gd-based contrast medium and reflects altered perfusion
features are presence of fibrous septa and confluent intra- and a change in the profile of the interstitial space in
hepatic fibrosis (Fig. 1.38), regenerative nodules, recanal- cirrhotic livers. The uptake of cell-specific contrast media
ization of the umbilical vein in the falciform ligament, and such as SPIO particles is reduced, which was attributed to
intrahepatic portosystemic venous shunts. MRI will also structural changes that possibly alter the distribution and
show extrahepatic manifestations of cirrhosis such as ex- activity of Kupffer cells.94 Diminished uptake was also
trahepatic portosystemic venous shunts, splenomegaly, observed for hepatobiliary contrast media and attributed
iron deposits in the spleen (Gamna–Gandy bodies), as- to impairment of hepatocellular function.104
cites, and edema of the gallbladder wall77,99–102 (Figs. The characterization of focal liver lesions in the cir-
rhotic liver, most notably the diagnosis of HCC, is one of
40 1 The Liver

a b

Fig. 1.38a–c Cirrhosis with confluent fibrosis (1.5 T). a Axial breath-
hold T2w single-shot TSE image. b, c Axial breath-hold T1w GRE
images obtained before (b) and after (c) IV injection of nonspecific
Gd-based contrast medium. Confluent fibrosis extending from the
liver hilum to the capsule and retraction of the capsule. Intense
heterogeneous signal enhancement on postcontrast image (c) in-
dicates inflammatory activity of fibrosis.

Fig. 1.39 Cirrhosis with portal vein thrombosis and severe gastric
fundal varices (1.5 T). Axial image obtained with breath-hold T2w
single-shot TSE sequence. The markedly dilated fundal varices are of
low SI due to flow-induced signal loss (arrow).

the most important indications for MRI in patients with ered benign, while dysplastic lesions are regarded as
cirrhosis. HCC must always be a consideration when there either premalignant or malignant. Accurate classification
are focal lesions in the cirrhotic liver; other liver tumors, of hepatic nodules is important but not always possible by
especially metastases, are less common in the presence of MRI or histology because the lesions represent successive
cirrhosis. stages, which are not always distinct, of a carcinogenic
Advanced cirrhosis is characterized by the formation of pathway along which regenerative nodules develop into
hepatocellular nodules. Histologically, these nodular le- dysplastic nodules, high-grade HCC, and ultimately low-
sions are classified into regenerative lesions and dysplas- grade HCC. Radiologists additionally regard siderotic nod-
tic or neoplastic lesions. Regenerative lesions are consid- ules as a distinct entity. They are of low SI on T2w images
Diffuse Liver Disease 41

a b
Fig. 1.40a, b Macronodular cirrhosis with mild ascites (1.5 T). a Axial fat-suppressed respiratory-triggered T2w TSE image. b Breath-hold T1w
GRE image.

a b
Fig. 1.41a, b Cirrhosis with marked liver atrophy and severe ascites (1.5 T). Images obtained with breath-hold T2w single-shot TSE sequence.
a Axial image. b Coronal image. Air–fluid level (a) secondary to ascites puncture.

(Fig. 1.36) and are more conspicuous on GRE sequences, and Kupffer cell density (uptake of SPIO-based contrast
which are more susceptible to iron deposits and therefore medium). None of these criteria alone enables reliable
make the lesions appear larger. On T1w GRE images, the characterization.
nodules are hypointense or hyperintense (Fig. 1.36). Side- Size. The larger a lesion, the more likely it is HCC,
rotic nodules have virtually no malignant potential.105 especially if a capsule can be demonstrated. However,
In summary, the following focal lesions need to be regenerative nodules may also reach a size of several
differentiated in the cirrhotic liver105: centimeters.
· regenerative lesions: micronodular (< 3 mm) or macro- T2 signal intensity. Hyperintensity suggests a malignant
nodular (≥ 3 mm) tumor since virtually all regenerative nodules are iso-
· dysplastic lesions: low-grade and high-grade dysplas- intense or hypointense on T2w images.
tic nodules (≥ 1 mm) Vascularity. Dedifferentiation is associated with an in-
· neoplastic lesions: well, moderately, and poorly differ- crease in the proportion of arteries and a decrease in
entiated HCC. veins. Early intense enhancement on arterial-phase im-
ages after contrast administration indicates a high-grade
Several criteria have been proposed to discriminate these dysplastic nodule or HCC. If there is additional washout on
lesions: size, T2 signal intensity, vascularity, hepatocellu- portal venous and/or equilibrium phase images, HCC is
lar function (uptake of hepatocellular contrast medium), likely.106
42 1 The Liver

a b
Fig. 1.42a, b Budd–Chiari syndrome (1.5 T). a Axial breath-hold inantly in the right lobe. The hypertrophied medial areas are of
T2w single-shot TSE image. b Axial breath-hold T1w GRE image. nearly normal SI and have a tumorlike appearance with compression
Peripheral edema is indicated by high T2 SI and low T1 SI, predom- of the superior vena cava. Ascites is present.

Hepatocellular function. Regenerative nodules have vena cava with or without secondary occlusion of the
nearly normal hepatocyte function and their signal en- hepatic veins; type II is occlusion of the major hepatic
hancement following administration of a hepatocellular veins; and type III is defined as occlusion of the small
contrast medium therefore parallels that of normal liver centrilobular veins.
parenchyma. Hepatocellular function and the correspond- BCS is identified on MRI by the absence of blood flow in
ing signal enhancement decrease with progressive dedif- the occluded veins. In type II BCS, the inferior vena cava is
ferentiation at premalignant and malignant stages; well- patent but compressed by the hypertrophied caudate lobe
differentiated HCCs can have some residual hepatocellular (Fig. 1.42). Absence of blood flow is at times difficult to
function. identify on SE images because flowing blood may cause a
Kupffer cell density. Regenerative nodules have the signal void or flow-related increase in signal, depending
same density of Kupffer cells as normal liver parenchyma on the pulse sequence parameters used and the plane of
and therefore show the same signal decrease on T2w imaging relative to the direction of blood flow. Venous
images after administration of SPIO-based contrast me- thrombi have variable MR signal intensity depending on
dium. Kupffer cell density decreases with dedifferentia- age and composition. MR angiography is helpful in dem-
tion, indicated by a less pronounced signal decrease on onstrating vascular occlusion and collaterals in those
SPIO-enhanced images. A slight signal decrease can indi- cases where the cross-sectional images do not yield a
cate a well differentiated HCC with residual Kupffer cells. definitive diagnosis.107 Besides direct demonstration of
Histologically, focal HCC has been demonstrated within venous occlusion, there are numerous morphologic fea-
atypical adenomatous hyperplasia and can be seen on tures that are indicative of BCS, including compensatory
T2w images as a high-signal-intensity cancer in a low- hypertrophy of the caudate lobe, intra- and extrahepatic
signal-intensity adenomatous hyperplasia (nodule-in- systemic-portal and systemic–systemic venous anasto-
nodule). This phenomenon is especially conspicuous after moses, ascites, inhomogeneous signal intensity, and occa-
injection of SPIO contrast medium. sional intraparenchymal hemorrhage107–111 (Fig. 1.42).
MRI will also detect some rare causes of congestion such
as membranous occlusion of the inferior vena cava110 or
Vascular Disease leiomyosarcoma of the inferior vena cava.108

Budd–Chiari syndrome (BCS) is of special clinical relevance


among the vascular diseases of the liver, along with Other Diffuse Liver Diseases
thrombosis of the portal vein or hepatic artery, because
it often has a fulminant clinical cause. BSC is a congestive Wilson disease is characterized by the abnormal accumu-
liver disease caused by obstruction of hepatic venous out- lation of copper in hepatocytes. Copper toxicity leads to
flow with subsequent thrombosis of affected vessels. parenchymal necrosis and scarring of the liver with sub-
Three types of BCS are distinguished according to the sequent cirrhosis. Early stages of the disease cause no MR
site of obstruction: type I is occlusion of the inferior signal changes because copper is not ferromagnetic and
Diffuse Liver Disease 43

consequently does not affect the MR signal. Morphologic acquisition correction. Magn Reson Imaging 2005;23(9):
939–945
changes first become apparent on MRI with the onset of
17. Zech CJ, Herrmann KA, Huber A, et al. High-resolution MR-
cirrhosis.112,113 Hypertrophy of the caudate lobe, a typical imaging of the liver with T2-weighted sequences using inte-
feature of other forms of cirrhosis, has been reported to be grated parallel imaging: comparison of prospective motion cor-
absent in Wilson disease.114 rection and respiratory triggering. J Magn Reson Imaging
2004;20(3):443–450
Sarcoidosis is a chronic granulomatous inflammation 18. Saini S, Stark DD, Hahn PF, et al. Ferrite particles: a superpar-
that primarily affects mediastinal lymph nodes and the amagnetic MR contrast agent for enhanced detection of liver
lung with advanced disease occasionally involving the carcinoma. Radiology 1987;162(1 Pt 1):217–222
19. Taupitz M, Schmitz S, Hamm B. [Superparamagnetic iron oxide
liver. MRI findings include hepatomegaly and scattered particles: current state and future development]. Rofo
nodules in the liver (and spleen). Hepatic granulomas 2003;175(6):752–765
tend to occur along portal tracts and are suggested by 20. Stark DD, Weissleder R, Elizondo G, et al. Superparamagnetic
iron oxide: clinical application as a contrast agent for MR imag-
increased periportal SI on T2w images.115 Enlarged lymph ing of the liver. Radiology 1988;168(2):297–301
nodes may be demonstrated in the liver hilum. 21. Weissleder R, Elizondo G, Stark DD, et al. The diagnosis of
splenic lymphoma by MR imaging: value of superparamagnetic
iron oxide. AJR Am J Roentgenol 1989;152(1):175–180
22. Saini S, Edelman RR, Li W, Petersein J, Hahn PF. Clinical evalua-
References tion of ultrasmall superparamagnetic iron oxide particles for
liver imaging. Acad Radiol 1996;3(Suppl 2):S409–S412
1. Curley SA, Izzo F, Abdalla E, Vauthey JN. Surgical treatment of 23. Hamm B, Vogl TJ, Branding G, et al. Focal liver lesions: MR
colorectal cancer metastasis. Cancer Metastasis Rev 2004;23 imaging with Mn-DPDP – initial clinical results in 40 patients.
(1-2):165–182 Radiology 1992;182(1):167–174
2. Junginger T, Kneist W, Seifert JK. [Surgical treatment of colo- 24. Huppertz A, Balzer T, Blakeborough A, et al; European EOB Study
rectal liver metastases]. Zentralbl Chir 2003;128(11):911–919 Group. Improved detection of focal liver lesions at MR imaging:
3. Karhunen PJ. Benign hepatic tumours and tumour like condi- multicenter comparison of gadoxetic acid-enhanced MR images
tions in men. J Clin Pathol 1986;39(2):183–188 with intraoperative findings. Radiology 2004;230(1):266–275
4. Dobritz M, Radkow T, Nittka M, Bautz W, Fellner FA. [VIBE with 25. Reimer P, Rummeny EJ, Shamsi K, et al. Phase II clinical evalua-
parallel acquisition technique - a novel approach to dynamic tion of Gd-EOB-DTPA: dose, safety aspects, and pulse sequence.
contrast-enhanced MR imaging of the liver]. Rofo 2002;174(6): Radiology 1996;199(1):177–183
738–741 26. Tung GA, Vaccaro JP, Cronan JJ, Rogg JM. Cavernous hemangioma
5. Kim YK, Kim CS, Chung GH, Jeon SB, Lee JM. Feasibility of of the liver: pathologic correlation with high-field MR imaging.
application of sensitivity encoding to the breath-hold T2- AJR Am J Roentgenol 1994;162(5):1113–1117
weighted turbo spin-echo sequence for evaluation of focal hep- 27. Ito K, Mitchell DG, Outwater EK, Szklaruk J, Sadek AG. Hepatic
atic tumors. AJR Am J Roentgenol 2005;184(2):497–504 lesions: discrimination of nonsolid, benign lesions from solid,
6. Yoshioka H, Sato J, Takahashi N, et al. Dual double arterial phase malignant lesions with heavily T2-weighted fast spin-echo MR
dynamic MR imaging with sensitivity encoding (SENSE): which imaging. Radiology 1997;204(3):729–737
is better for diagnosing hypervascular hepatocellular carcino- 28. Soyer P, Dufresne AC, Somveille E, Lenormand S, Scherrer A,
mas, in-phase or opposed-phase imaging? Magn Reson Imaging Rymer R. Differentiation between hepatic cavernous heman-
2004;22(3):361–367 gioma and malignant tumor with T2-weighted MRI: compari-
7. Vogt FM, Antoch G, Hunold P, et al. Parallel acquisition techni- son of fast spin-echo and breathhold fast spin-echo pulse se-
ques for accelerated volumetric interpolated breath-hold ex- quences. Clin Imaging 1998;22(3):200–210
amination magnetic resonance imaging of the upper abdomen: 29. Lombardo DM, Baker ME, Spritzer CE, Blinder R, Meyers W,
assessment of image quality and lesion conspicuity. J Magn Herfkens RJ. Hepatic hemangiomas vs metastases: MR differ-
Reson Imaging 2005;21(4):376–382 entiation at 1.5 T. AJR Am J Roentgenol 1990;155(1):55–59
8. Rofsky NM, Lee VS, Laub G, et al. Abdominal MR imaging with a 30. Kreitner KF, Thelen M, Schild H, Heintz A, Störkel S. [Epidemio-
volumetric interpolated breath-hold examination. Radiology logical and clinical aspects of focal nodular hyperplasia of the
1999;212(3):876–884 liver. An assessment of 886 cases]. Dtsch Med Wochenschr
9. Hamm B, Fischer E, Hopfenmüller W, Sander B. [Improvement of 1987;112(22):891–896
MR tomography of the liver using a multi-slice gradient echo 31. Lee MJ, Saini S, Hamm B, et al. Focal nodular hyperplasia of the
sequence]. Rofo 1989;150(3):307–315 liver: MR findings in 35 proved cases. AJR Am J Roentgenol
10. Stark DD, Hendrick RE, Hahn PF, Ferrucci JT Jr. Motion artifact 1991;156(2):317–320
reduction with fast spin-echo imaging. Radiology 1987;164(1): 32. Shamsi K, De Schepper A, Degryse H, Deckers F. Focal nodular
183–191 hyperplasia of the liver: radiologic findings. Abdom Imaging
11. Mitchell DG. Chemical shift magnetic resonance imaging: ap- 1993;18(1):32–38
plications in the abdomen and pelvis. Top Magn Reson Imaging 33. Paulson EK, McClellan JS, Washington K, Spritzer CE, Meyers
1992;4(3):46–63 WC, Baker ME. Hepatic adenoma: MR characteristics and corre-
12. Catasca JV, Mirowitz SA. T2-weighted MR imaging of the abdo- lation with pathologic findings. AJR Am J Roentgenol
men: fast spin-echo vs conventional spin-echo sequences. AJR 1994;163(1):113–116
Am J Roentgenol 1994;162(1):61–67 34. Arrivé L, Fléjou JF, Vilgrain V, et al. Hepatic adenoma: MR find-
13. Kim YH, Saini S, Blake MA, et al. Distinguishing hepatic meta- ings in 51 pathologically proved lesions. Radiology
stases from hemangiomas: qualitative and quantitative diag- 1994;193(2):507–512
nostic performance through dual echo respiratory-triggered 35. Chung KY, Mayo-Smith WW, Saini S, Rahmouni A, Golli M,
fast spin echo magnetic resonance imaging. J Comput Assist Mathieu D. Hepatocellular adenoma: MR imaging features
Tomogr 2005;29(5):571–579 with pathologic correlation. AJR Am J Roentgenol 1995;165(2):
14. Herborn CU, Vogt F, Lauenstein TC, Goyen M, Debatin JF, Ruehm 303–308
SG. MRI of the liver: can True FISP replace HASTE? J Magn Reson 36. Wittenberg J, Stark DD, Forman BH, et al. Differentiation of
Imaging 2003;17(2):190–196 hepatic metastases from hepatic hemangiomas and cysts by
15. Haacke EM, Lenz GW. Improving MR image quality in the pres- using MR imaging. AJR Am J Roentgenol 1988;151(1):79–84
ence of motion by using rephasing gradients. AJR Am J Roent- 37. Mahfouz AE, Hamm B, Wolf KJ. Peripheral washout: a sign of
genol 1987;148(6):1251–1258 malignancy on dynamic gadolinium-enhanced MR images of
16. Asbach P, Klessen C, Kroencke TJ, et al. Magnetic resonance focal liver lesions. Radiology 1994;190(1):49–52
cholangiopancreatography using a free-breathing T2-weighted
turbo spin-echo sequence with navigator-triggered prospective
44 1 The Liver

38. Rummeny E, Weissleder R, Stark DD, et al. Primary liver tumors: 59. Hori M, Murakami T, Kim T, et al. Detection of hypervascular
diagnosis by MR imaging. AJR Am J Roentgenol 1989;152(1): hepatocellular carcinoma: comparison of SPIO-enhanced MRI
63–72 with dynamic helical CT. J Comput Assist Tomogr 2002;26(5):
39. Itoh K, Nishimura K, Togashi K, et al. Hepatocellular carcinoma: 701–710
MR imaging. Radiology 1987;164(1):21–25 60. Ba-Ssalamah A, Heinz-Peer G, Schima W, et al. Detection of focal
40. Ebara M, Watanabe S, Kita K, et al. MR imaging of small hep- hepatic lesions: comparison of unenhanced and SHU 555 A-
atocellular carcinoma: effect of intratumoral copper content on enhanced MR imaging versus biphasic helical CTAP. J Magn
signal intensity. Radiology 1991;180(3):617–621 Reson Imaging 2000;11(6):665–672
41. Kadoya M, Matsui O, Takashima T, Nonomura A. Hepatocellular 61. Fenlon HM, Tello R, deCarvalho VL, Yucel EK. Signal character-
carcinoma: correlation of MR imaging and histopathologic find- istics of focal liver lesions on double echo T2-weighted conven-
ings. Radiology 1992;183(3):819–825 tional spin echo MRI: observer performance versus quantitative
42. Vogl TJ, Stupavsky A, Pegios W, et al. Hepatocellular carcinoma: measurements of T2 relaxation times. J Comput Assist Tomogr
evaluation with dynamic and static gadobenate dimeglumine- 2000;24(2):204–211
enhanced MR imaging and histopathologic correlation. Radio- 62. Lüning M, Koch M, Abet L, et al. [The accuracy of the imaging
logy 1997;205(3):721–728 procedures (sonography, MRT, CT, angio-CT,nuclear medicine)
43. Fan ZM, Yamashita Y, Harada M, et al. Intrahepatic cholangio- in characterizing liver tumors]. Rofo 1991;154(4):398–406
carcinoma: spin-echo and contrast-enhanced dynamic MR 63. Whitney WS, Herfkens RJ, Jeffrey RB, et al. Dynamic breath-hold
imaging. AJR Am J Roentgenol 1993;161(2):313–317 multiplanar spoiled gradient-recalled MR imaging with gadoli-
44. Yates CK, Streight RA. Focal fatty infiltration of the liver simu- nium enhancement for differentiating hepatic hemangiomas
lating metastatic disease. Radiology 1986;159(1):83–84 from malignancies at 1.5 T. Radiology 1993;189(3):863–870
45. Kröncke TJ, Taupitz M, Kivelitz D, et al. Multifocal nodular fatty 64. Yamashita Y, Hatanaka Y, Yamamoto H, et al. Differential diag-
infiltration of the liver mimicking metastatic disease on CT: nosis of focal liver lesions: role of spin-echo and contrast-en-
imaging findings and diagnosis using MR imaging. Eur Radiol hanced dynamic MR imaging. Radiology 1994;193(1):59–65
2000;10(7):1095–1100 65. Jung G, Poll L, Cohnen M, et al. [Differential diagnosis of focal
46. Hamm B, Reichel M, Vogl T, Taupitz M, Wolf KJ. [Superparamag- liver lesions using contrast-enhanced MRI with SHU 555 A in
netic iron particles. The clinical results in the MR diagnosis of comparison with unenhanced MRI and multidetector spiral-CT].
liver metastases]. Rofo 1994;160(1):52–58 Rofo 2005;177(11):1571–1577
47. Kim YK, Ko SW, Hwang SB, Kim CS, Yu HC. Detection and 66. Grazioli L, Morana G, Kirchin MA, Schneider G. Accurate differ-
characterization of liver metastases: 16-slice multidetector entiation of focal nodular hyperplasia from hepatic adenoma at
computed tomography versus superparamagnetic iron oxide- gadobenate dimeglumine-enhanced MR imaging: prospective
enhanced magnetic resonance imaging. Eur Radiol 2006; study. Radiology 2005;236(1):166–177
16(6):1337–1345 67. Kacl GM, Hagspiel KD, Marincek B. Focal nodular hyperplasia of
48. Ros PR, Freeny PC, Harms SE, et al. Hepatic MR imaging with the liver: serial MRI with Gd-DOTA, superparamagnetic iron
ferumoxides: a multicenter clinical trial of the safety and effi- oxide, and Gd-EOB-DTPA. Abdom Imaging 1997;22(3):264–267
cacy in the detection of focal hepatic lesions. Radiology 1995; 68. Scharitzer M, Schima W, Schober E, et al. Characterization of
196(2):481–488 hepatocellular tumors: value of mangafodipir-enhanced mag-
49. Wang C, Ahlström H, Ekholm S, et al. Diagnostic efficacy of netic resonance imaging. J Comput Assist Tomogr 2005;
MnDPDP in MR imaging of the liver. A phase III multicentre 29(2):181–190
study. Acta Radiol 1997;38(4 Pt 2):643–649 69. Kim MJ, Kim JH, Lim JS, et al. Detection and characterization of
50. Rofsky NM, Weinreb JC, Bernardino ME, Young SW, Lee JK, Noz focal hepatic lesions: mangafodipir vs. superparamagnetic iron
ME. Hepatocellular tumors: characterization with Mn-DPDP- oxide-enhanced magnetic resonance imaging. J Magn Reson
enhanced MR imaging. Radiology 1993;188(1):53–59 Imaging 2004;20(4):612–621
51. Reimer P, Rummeny EJ, Daldrup HE, et al. Enhancement char- 70. Danet I-M, Semelka RC, Braga L. MR imaging of diffuse liver
acteristics of liver metastases, hepatocellular carcinomas, and disease. Radiol Clin North Am 2003;41(1):67–87
hemangiomas with Gd-EOB-DTPA: preliminary results with dy- 71. Friedman SL. Liver fibrosis – from bench to bedside. J Hepatol
namic MR imaging. Eur Radiol 1997;7(2):275–280 2003;38(Suppl 1):S38–S53
52. del Frate C, Bazzocchi M, Mortele KJ, et al. Detection of liver 72. Asbach P, Hein PA, Stemmer A, et al. Free-breathing echo-planar
metastases: comparison of gadobenate dimeglumine-enhanced imaging based diffusion-weighted magnetic resonance imaging
and ferumoxides-enhanced MR imaging examinations. Radiol- of the liver with prospective acquisition correction. J Comput
ogy 2002;225(3):766–772 Assist Tomogr 2008;32(3):372–378
53. Kim MJ, Kim JH, Chung JJ, Park MS, Lim JS, Oh YT. Focal hepatic 73. Hagiwara MH, Rusinek H, Lee VS, et al. Advanced liver fibrosis:
lesions: detection and characterization with combination gado- diagnosis with 3D whole-liver perfusion MR imaging – initial
linium- and superparamagnetic iron oxide-enhanced MR imag- experience. Radiology 2008;246(3):926–934
ing. Radiology 2003;228(3):719–726 74. Asbach P, Klatt D, Hamhaber U, et al. Assessment of liver viscoe-
54. Kim YK, Lee JM, Kim CS, Chung GH, Kim CY, Kim IH. Detection of lasticity using multifrequency MR elastography. Magn Reson
liver metastases: gadobenate dimeglumine-enhanced three- Med 2008;60(2):373–379
dimensional dynamic phases and one-hour delayed phase MR 75. Huwart L, Sempoux C, Salameh N, et al. Liver fibrosis: non-
imaging versus superparamagnetic iron oxide-enhanced MR invasive assessment with MR elastography versus aspartate
imaging. Eur Radiol 2005;15(2):220–228 aminotransferase-to-platelet ratio index. Radiology 2007;
55. Bartolozzi C, Donati F, Cioni D, et al. Detection of colorectal liver 245(2):458–466
metastases: a prospective multicenter trial comparing unen- 76. Klatt D, Asbach P, Rump J, et al. In vivo determination of hepatic
hanced MRI, MnDPDP-enhanced MRI, and spiral CT. Eur Radiol stiffness using steady-state free precession magnetic resonance
2004;14(1):14–20 elastography. Invest Radiol 2006;41(12):841–848
56. Hamm B, Mahfouz AE, Taupitz M, et al. Liver metastases: im- 77. Rouvière O, Yin M, Dresner MA, et al. MR elastography of the
proved detection with dynamic gadolinium-enhanced MR liver: preliminary results. Radiology 2006;240(2):440–448
imaging? Radiology 1997;202(3):677–682 78. Hamer OW, Aguirre DA, Casola G, Lavine JE, Woenckhaus M,
57. Kwak HS, Lee JM, Kim YK, Lee YH, Kim CS. Detection of hepato- Sirlin CB. Fatty liver: imaging patterns and pitfalls. Radio-
cellular carcinoma: comparison of ferumoxides-enhanced and graphics 2006;26(6):1637–1653
gadolinium-enhanced dynamic three-dimensional volume in- 79. Levenson H, Greensite F, Hoefs J, et al. Fatty infiltration of the
terpolated breath-hold MR imaging. Eur Radiol 2005;15(1): liver: quantification with phase-contrast MR imaging at 1.5 T vs
140–147 biopsy. AJR Am J Roentgenol 1991;156(2):307–312
58. Youk JH, Lee JM, Kim CS. MRI for detection of hepatocellular 80. Merkle EM, Nelson RC. Dual gradient-echo in-phase and op-
carcinoma: comparison of mangafodipir trisodium and gado- posed-phase hepatic MR imaging: a useful tool for evaluating
pentetate dimeglumine contrast agents. AJR Am J Roentgenol more than fatty infiltration or fatty sparing. Radiographics
2004;183(4):1049–1054 2006;26(5):1409–1418
Diffuse Liver Disease 45

81. Mitchell DG, Kim I, Chang TS, et al. Fatty liver. Chemical shift 98. Ito K, Mitchell DG, Gabata T. Enlargement of hilar periportal
phase-difference and suppression magnetic resonance imaging space: a sign of early cirrhosis at MR imaging. J Magn Reson
techniques in animals, phantoms, and humans. Invest Radiol Imaging 2000;11(2):136–140
1991;26(12):1041–1052 99. Itai Y, Kurosaki Y, Saida Y, Niitsu M, Kuramoto K. CT and MRI in
82. Mathieu D, Paret M, Mahfouz AE, et al. Hyperintense benign detection of intrahepatic portosystemic shunts in patients with
liver lesions on spin-echo T1-weighted MR images: pathologic liver cirrhosis. J Comput Assist Tomogr 1994;18(5):768–773
correlations. Abdom Imaging 1997;22(4):410–417 100. Mergo PJ, Ros PR, Buetow PC, Buck JL. Diffuse disease of the liver:
83. Olthof AW, Sijens PE, Kreeftenberg HG, Kappert P, van der Jagt radiologic-pathologic correlation. Radiographics 1994;14(6):
EJ, Oudkerk M. Non-invasive liver iron concentration measure- 1291–1307
ment by MRI: Comparison of two validated protocols. Eur J 101. Ohtomo K, Baron RL, Dodd GDIII, Federle MP, Ohtomo Y, Confer
Radiol 2008;19: e-pub ahead of print SR. Confluent hepatic fibrosis in advanced cirrhosis: evaluation
84. Wood JC, Ghugre N. Magnetic resonance imaging assessment of with MR imaging. Radiology 1993;189(3):871–874
excess iron in thalassemia, sickle cell disease and other iron 102. Rofsky NM, Fleishaker H. CT and MRI of diffuse liver disease.
overload diseases. Hemoglobin 2008;32(1-2):85–96 Semin Ultrasound CT MR 1995;16(1):16–33
85. Gandon Y, Guyader D, Heautot JF, et al. Hemochromatosis: diag- 103. Hughes-Cassidy F, Chavez AD, Schlang A, et al. Superparamag-
nosis and quantification of liver iron with gradient-echo MR netic iron oxides and low molecular weight gadolinium chelates
imaging. Radiology 1994;193(2):533–538 are synergistic for direct visualization of advanced liver fibrosis.
86. Guyader D, Gandon Y, Robert JY, et al. Magnetic resonance J Magn Reson Imaging 2007;26(3):728–737
imaging and assessment of liver iron content in genetic hemo- 104. Murakami T, Baron RL, Federle MP, et al. Cirrhosis of the liver:
chromatosis. J Hepatol 1992;15(3):304–308 MR imaging with mangafodipir trisodium (Mn-DPDP). Radiol-
87. Rocchi E, Cassanelli M, Borghi A, et al. Magnetic resonance ogy 1996;198(2):567–572
imaging and different levels of iron overload in chronic liver 105. Hanna RF, Aguirre DA, Kased N, Emery SC, Peterson MR, Sirlin
disease. Hepatology 1993;17(6):997–1002 CB. Cirrhosis-associated hepatocellular nodules: correlation of
88. Fillet G, Beguin Y, Baldelli L. Model of reticuloendothelial iron histopathologic and MR imaging features. Radiographics
metabolism in humans: abnormal behavior in idiopathic hemo- 2008;28(3):747–769
chromatosis and in inflammation. Blood 1989;74(2):844–851 106. Roncalli M, Roz E, Coggi G, et al. The vascular profile of regen-
89. Siegelman ES, Mitchell DG, Semelka RC. Abdominal iron depo- erative and dysplastic nodules of the cirrhotic liver: implications
sition: metabolism, MR findings, and clinical importance. Radi- for diagnosis and classification. Hepatology 1999;30(5):
ology 1996;199(1):13–22 1174–1178
90. Mathieu D, Rahmouni A, Villeneuve P, Anglade MC, Rochant H, 107. Kane R, Eustace S. Diagnosis of Budd-Chiari syndrome: compar-
Vasile N. Impact of magnetic resonance imaging on the diag- ison between sonography and MR angiography. Radiology
nosis of abdominal complications of paroxysmal nocturnal he- 1995;195(1):117–121
moglobinuria. Blood 1995;85(11):3283–3288 108. Cacoub P, Piette JC, Wechsler B, et al. Leiomyosarcoma of the
91. Logan JI, Harveyson KB, Wisdom GB, Hughes AE, Archbold GP. inferior vena cava. Experience with 7 patients and literature
Hereditary caeruloplasmin deficiency, dementia and diabetes review. Medicine (Baltimore) 1991;70(5):293–306
mellitus. QJM 1994;87(11):663–670 109. Miller WJ, Federle MP, Straub WH, Davis PL. Budd-Chiari syn-
92. Campo E, Bruguera M, Rodés J. Are there diagnostic histologic drome: imaging with pathologic correlation. Abdom Imaging
features of porphyria cutanea tarda in liver biopsy specimens? 1993;18(4):329–335
Liver 1990;10(3):185–190 110. Park JH, Han JK, Choi BI, Han MC. Membranous obstruction of
93. Tanimoto A, Kreft BP, Baba Y, et al. Evaluation of hepatocyte- the inferior vena cava with Budd-Chiari syndrome: MR imaging
specific paramagnetic contrast media for MR imaging of hep- findings. J Vasc Interv Radiol 1991;2(4):463–469
atitis. J Magn Reson Imaging 1993;3(5):786–793 111. Shapiro RS, Maldjian JA, Stancato-Pasik A, Ramos R. Hepatic
94. Elizondo G, Weissleder R, Stark DD, et al. Hepatic cirrhosis and mass in Budd-Chiari syndrome: CT and MRI findings. Comput
hepatitis: MR imaging enhanced with superparamagnetic iron Med Imaging Graph 1993;17(6):457–460
oxide. Radiology 1990;174(3 Pt 1):797–801 112. Nakakoshi T, Fujita N, Jong-Hon K, Takeichi N, Miyasaka K.
95. Unger EC, Lee JK, Weyman PJ. CT and MR imaging of radiation Influence of in vivo copper on MR images of the liver in rats. J
hepatitis. J Comput Assist Tomogr 1987;11(2):264–268 Magn Reson Imaging 1994;4(4):559–562
96. Yankelevitz DF, Knapp PH, Henschke CI, Nisce L, Yi Y, Cahill P. MR 113. Vogl TJ, Steiner P, Hammerstingl R, et al. MRT der Leber bei
appearance of radiation hepatitis. Clin Imaging 1992;16(2): Morbus Wilson. Fortschr Röntgenstr. 1994;160:40–45
89–92 114. Akpinar EO, Akhan O. Liver imaging findings of Wilson’s disease.
97. Willemsen UF, Pfluger T, Zoller WG, Kueffer G, Hahn K. MRI of Eur J Radiol 2007;61(1):25–32
hepatic schistosomiasis mansoni. J Comput Assist Tomogr 115. Warshauer DM, Lee JK. Imaging manifestations of abdominal
1995;19(5):811–813 sarcoidosis. AJR Am J Roentgenol 2004;182(1):15–28
47

2 The Bile and Pancreatic Ducts


P. Asbach and H.B. Gehl

Introduction Indications

Magnetic resonance cholangiopancreatography (MRCP) Noninvasive MRCP of the pancreatobiliary tree can con-
has evolved into an important noninvasive imaging mo- tribute valuable diagnostic information in patients with
dality for routine clinical evaluation of the pancreatobili- suspected involvement of the bile ducts or pancreatic duct
ary tree. MRCP is a very elegant imaging tool, as it is fast if the clinical symptoms and the first-line imaging test
and straightforward and has very few adverse effects. (ultrasound) do not yield a definitive diagnosis. This is
While invasive visualization of the bile ducts and pan- primarily the case in patients with suspected biliary pan-
creatic duct using conventional radiographic techniques creatitis, acute or chronic cholangitis, strictures or anoma-
requires intravenous injection of a biliary contrast me- lies of the bile ducts (e. g., Caroli disease, choledochocele,
dium (cholangiography) or direct instillation of contrast biliary atresia), anatomic variants (pancreas divisum), and
medium into the ducts (percutaneous transhepatic chol- cholangiocarcinoma (e. g., Klatskin tumor).
angiography [PTC] or endoscopic retrograde cholangio- In patients scheduled for an interventional procedure,
pancreatography [ERCP]), noninvasive MRCP exploits the preinterventional localization of strictures and stones and
very long T2 relaxation times of fluids for visualization of detection of pseudocysts are crucial for planning the ap-
the ductal system. proach. Imaging provides the clinician with detailed in-
Conventional invasive procedures carry considerable formation on the anatomic situation, thereby facilitating
risks, including the potential adverse effects of contrast interventions such as laparoscopic surgery.
administration. They are examiner-dependent and stress-
ful for the patient. The most feared complications of PTC
include bleeding and injuries to the bile ducts, while ERCP Imaging Technique
may cause duodenal perforation, pancreatitis,1,2 cholangi-
tis, and duct perforation. Complication rates between 4 %
and 11 % have been reported for ERCP.2,3 Coils
Another major advantage of MRCP is that it also pro-
vides more comprehensive diagnostic information on ad- High spatial resolution is crucial for detailed anatomic
jacent anatomic structures and organs, thus contributing visualization of the target structures (very small bile
to an earlier diagnosis. ERCP, on the other hand, is not only ducts, side branches of the pancreatic duct), which is not
a diagnostic tool but, more importantly, can also be used achieved with the integrated whole-body resonator. Sur-
to perform therapeutic interventions in the same session. face coils have the essential advantage of providing a
Noninvasive MRCP and invasive ERCP therefore supple- better signal-to-noise ratio (SNR), which improves spatial
ment each other and together are a mainstay of patient resolution and contrast while also shortening imaging
care. time (breath-hold sequences, see below). However, the
A comparative cost-benefit analysis of ERCP and MRCP most suitable coil is a multielement body or torso
concludes that primary diagnosis with MRCP is econom- phased-array surface coil (usually consisting of 4–8 ele-
ically advantageous,4 which is an important consideration ments, which, in addition to the aforementioned advan-
for health-care providers in the era of cost cutting and tages, enables use of a larger field of view (FOV) and
reimbursement based on diagnosis-related groups (DRG). reduces artifacts. When a multielement coil is used, the
entire biliary tree and pancreatic duct as well as the liver
and pancreas can be imaged in a single session without
coil repositioning. Conventional imaging of the liver and
pancreas should be part of any routine MRCP protocol.5
48 2 The Bile and Pancreatic Ducts

a b
Fig. 2.1a, b Illustration of the effect of negative oral contrast me- (arrows). The pancreatic duct appears normal. Also seen is a para-
dium in a 58-year-old man with recurrent pancreatitis and prior pelvic renal cyst causing hydronephrosis of the left kidney. Such
biliary–enteric anastomosis who underwent MRCP to rule out cho- fluid-filled structures may obscure parts of the pancreatic duct.
lestasis. a Thick-slab coronal MRCP image from T2w single-slice b Thick-slab coronal MRCP image from T2w single-slice HASTE
HASTE sequence obtained before administration of negative oral sequence acquired after negative oral contrast medium. The signal
contrast medium. Due to heavy T2 weighting, the image also from the stomach and proximal small intestine is effectively sup-
depicts the fluid-filled stomach and proximal small intestine pressed.

Pulse Sequences ures the position of the diaphragm to synchronize acquis-


ition accordingly (PACE technique: prospective acquisi-
MRCP exploits the long T2 relaxation time of fluids (sev- tion correction – Siemens) and was originally developed
eral seconds for bile) for indirect visualization of ductal for cardiac imaging. The main advantage of respiratory
structures. At the same time, signal from other tissue navigator triggering is that the longer acquisition time
structures is effectively suppressed when heavily T2- allows use of sequences with much better spatial resolu-
weighted sequences are used because the echo time (TE) tion.8
of these sequences is a multiple of the T2 relaxation time
of stationary tissues (40–100 ms in the abdomen). How-
ever, there may be overlap from other fluid-containing Patient Preparation
structures such as cysts (pancreatic pseudocysts, hepatic
and renal cysts), intestinal loops, and the renal collecting Oral Contrast Media
system and ureter.
Sequences based on the rapid acquisition with relaxa- When heavily T2w thick-slab images are acquired at var-
tion enhancement (RARE) technique,6 such as the half- ious projections along the course of the pancreatic and
Fourier acquisition single-shot turbo spin echo (HASTE) biliary ducts, there will invariably be some overlap from
sequence, are among the most widely used sequences for other fluid-filled structures, particularly the stomach and
MRCP. The examination can be performed in one of two duodenum. The signal from gastrointestinal fluids can be
complementary ways: acquisition of a single thick-slab suppressed by administering a negative oral contrast me-
projection image and 2D acquisition of a series of thin dium containing iron oxide particles. Since such contrast
slices with subsequent reconstruction using the MIP media do not distend the ducts, normal anatomy is not
(maximum intensity projection) algorithm.7 While thick- distorted.9 However, one must be aware that negative oral
slab imaging (which takes < 6 s) is well tolerated during contrast media will also obscure anatomic landmarks such
breath-hold, multislice acquisition requires a breath-hold as the descending duodenum (Fig. 2.1).
of ca. 20 s, which is beyond the capacity of some patients. There is controversy in the literature as to whether the
Alternatively, MRCP can be performed with the patient diagnostic quality of MRCP can be improved most effec-
breathing freely if acquisition is synchronized with the tively by suppressing or enhancing the gastrointestinal
respiratory cycle. Various techniques are available from (GI) signal. Positive oral contrast media cause the GI lu-
different vendors, but the equipment is cumbersome to men to appear bright, thereby improving delineation of
handle and has found little acceptance. A practical, soft- the liver and pancreas from intestinal loops if MRCP is
ware-based alternative is respiratory triggering using the supplemented by conventional axial MRI of these two
navigator echo approach. The navigator technique meas- organs. The latter is desirable in all patients undergoing
Imaging Technique 49

MRCP because it will identify possible external causes of Imaging of Upper Abdominal Organs
ductal narrowing as well as other pathology not affecting
the ducts (see below). An MRCP protocol should comprise conventional plain
Finally, the decision whether or not to use oral contrast MRI of the liver and pancreas. If these images reveal a
medium is also affected by increasing pressure to reduce lesion requiring further characterization after intravenous
health-care costs. In this context, blueberry juice, which contrast administration (Gd-based, low-molecular-weight
has the same effects on T2w images as negative oral contrast medium), MRCP is followed by a dynamic con-
contrast medium, has been proposed as an inexpensive trast-enhanced MRI study of the respective organ (for
alternative.10 Some investigators dispense with oral con- further details see the chapter on the liver or pancreas).
trast administration altogether; in this case, MRCP should Intravenous contrast media do not impair the quality of
be performed in the morning after fasting when only a the MRCP examination, and their T2-shortening effect
small amount of fluid is present in the upper GI tract. even reduces interference from overlying contrast-en-
hancing structures on thick-slab images, especially the
renal collecting systems and ureters.
Other Medication

Motion artifacts due to respiration and upper GI tract MRCP of the Bile and Pancreatic Ducts
peristalsis are a major problem for MRCP, given the small
size of some of the ductal structures. Most patients can The MRCP sequences we use are summarized in Table 2.1.
hold their breath for thick-slab imaging, which has an The examination begins with acquisition of a fast axial
acquisition time of less than 10 s. Peristalsis should be T2w multislice sequence (e. g., T2w HASTE) that covers the
suppressed by intramuscular injection of an antispas- entire upper abdomen and is used to plan the subsequent
modic at the beginning of the examination unless a pa- MRCP sequences.
tient has contraindications. Next, a coronal thick-slab projection image (120 mm) is
Visualization of the pancreatic ductal system (espe- acquired with a fast, fat-saturated T2w sequence and a
cially side branches and the accessory duct) can be im- FOV adapted to the imaging plane. A single projection
proved by secretin stimulation. Intravenous secretin in- image acquired in this way will depict the central bile
jection enhances pancreatic exocrine function, which im- ducts and most of the pancreatic duct (Fig. 2.2a). Such
proves filling of the ducts and thus allows more accurate an image has a low SNR but nevertheless provides a
evaluation of ductal morphology. In addition, pancreatic good anatomic overview of the biliary and pancreatic
exocrine function can be assessed by quantitative deter- duct systems.
mination of subsequent duodenal filling.11,12 Imaging Additional thick-slab acquisitions are then performed
5 min after intravenous injection yields the best results. with projections and slice thicknesses (30–80 mm) se-
Secretin stimulation is contraindicated in patients with lected according to the duct segments imaged. Optimal
acute pancreatitis or acute on chronic pancreatitis. orientations for targeted visualization of specific parts of
the ducts depend on the patient’s anatomy, which is why
only some very general suggestions can be made here (in
Recommended Imaging Protocol terms of a clockface): parallel to the pancreatic duct (pro-
jection between 8 and 9 o’clock); parallel to the common
General Preparation bile duct (projection at approximately 10 o’clock); parallel
to the right and left hepatic ducts (highly variable). Addi-
MRCP is best performed in the morning when secretion in tional imaging planes may be acquired as deemed neces-
the upper GI tract is minimal. Patients should fast for at sary depending on the presence of normal anatomic var-
least 6 h and abstain from even small amounts of fluid iants and site of pathology (Fig. 2.2b–d).
before the examination. Thick-slab imaging is followed by multislice, thin-slice
acquisitions (3 mm, no interslice gap) for evaluating very
small ductal structures. The individual series of thin slices
Oral Contrast Media are acquired at the same angles as the corresponding
thick-slab images. The acquisition time for one such series
We usually perform MRCP with an oral contrast medium is ca. 20–23 s. We perform thin-slice MRCP with a T2w
solution, which the patient starts drinking approximately multislice HASTE sequence (Fig. 2.3a–c). The source data
30 min before the examination (at least 300 mL; 600 mL can be reconstructed for 3D display using the MIP algo-
creates optimal imaging conditions). The contrast solution rithm (Fig. 2.3c); however, the source images are suffi-
can be mixed 1:1 with water to prevent susceptibility cient for evaluation. Figure 2.3 d shows an MIP recon-
artifacts that would result from sedimentation of iron struction of a fat-saturated T2w multislice TSE sequence
oxide particles in the immobilized GI tract. (1.5-mm slice thickness) acquired with respiratory navi-
gator triggering (PACE). This sequence has become the
mainstay of any MRCP examination because it yields
Table 2.1 Recommended pulse sequences and imaging parameters for MRCP

50
Weighting Plane Sequence type TR (ms) TE (ms) Flip (°) ETL FS Matrix No. of No. of Slice thick- Scan time Breath-
slices acquisitions ness (mm) hold

2 The Bile and Pancreatic Ducts


Scout sequence for planning subsequent MRCP acquisitions
T2 Axial Single-shot TSE with half- 800* 63 150 115 No 115 × 256 23 1 7 ca. 18 s Yes
Fourier acquisition
(e. g., HASTE)
Thick-slab MRCP overview of ductal anatomy
T2 Coronal Single-shot TSE with half- – 1100 150 256 Yes 256 × 256 1 1 120 ca. 6 s Yes
Fourier acquisition
(e. g., HASTE)
Thick-slab MRCP acquisition of multiple projections adjusted to individual ducts of interest
T2 Paracoronal Single-shot TSE with half- – 1100 150 256 Yes 256 × 256 1 1 30–80 ca. 6 s Yes
Run 3 × Fourier acquisition
(e. g., HASTE)
Multislice sequence (with MIP reconstruction as needed), same projections as for thick-slab acquisitions
T2 Paracoronal Single-shot TSE with half- 1100* 87 150 218 No 218 × 256 15 1 3 ca. 20 s Yes
Run 3 × Fourier acquisition
(e. g., HASTE)
Multislice sequence with respiratory navigator (and MIP reconstruction)
T2 Paracoronal TSE (FSE) 1910 832 180 145 Yes 384 × 384 40 1 1.5 ca. 4–8 min No

Note: Use of a multielement body or torso phased-array surface coil is recommended for all sequences.
* TR here is a technical parameter referring to the intervals between slice acquisitions; physical TR = ∞ since only one excitation pulse is applied per slice.
Imaging Technique 51

a b

c d
Fig. 2.2a–d Normal MRCP findings after negative oral contrast me- (50 mm) paracoronal MRCP (same sequence as a) aligned along
dium in a 38-year-old woman. a Thick-slab (120-mm) coronal MRCP pancreatic duct (b), common bile duct (c), and right hepatic duct
image from T2w single-slice HASTE sequence. b–d Thick-slab (d).

images with higher resolution and fewer artifacts, and the axial plane, and allow differentiation of air bubbles (lo-
data set lends itself to multiplanar reconstruction.8 cated in the nondependent portion of the duct) and small
Depending on the findings, additional axial images stones (located in the dependent portion). In patients with
may be acquired with the T2w multislice HASTE sequence. a stent, it is sometimes possible to differentiate stent
Axial images will even show very small intraductal filling obstruction (low signal intensity) from a patent stent
defects, since the ducts are nearly perpendicular to the (intraluminal fluid signal) (Fig. 2.4).
52 2 The Bile and Pancreatic Ducts

a b

c d
Fig. 2.3a–d MRCP without negative oral contrast medium in a mon bile duct (b). c MIP image created from the slab (15 slices) in a.
62-year-old woman. a, b (Para-)coronal fat-suppressed T2w multi- d Coronal MIP image from T2w multislice TSE sequence acquired
slice HASTE sequences aligned along pancreatic duct (a) and com- with respiratory navigator (PACE; 40 slices).

viduals.10,13,14 Pancreas divisum may be symptomatic and


MRI Appearance of Normal Anatomy
can cause (chronic) pancreatitis.15 While in the normal
pancreas the secretions produced in the body and tail
MRCP plays an important role in the preoperative evalua- enter the duodenum through the major papilla (papilla
tion of pancreaticobiliary ductal anatomy. Detailed ana- of Vater), pancreas divisum is drained via an accessory
tomic information is especially important prior to mini- duct (Santorini duct) that lies anteriorly in the head of
mally invasive surgery because the small incisions for pancreas and terminates in the minor papilla. The lumen
instrument insertion have to be planned beforehand and of the accessory duct and/or opening of the minor duode-
cannot easily be changed during the intervention if an nal papilla is often small, obstructing proper drainage of
unexpected anatomic variant is encountered.10 Normal pancreatic exocrine secretions, which may leak into the
anatomic variants of the pancreatic and biliary ducts are pancreatic tissue and ultimately cause chronic pancreati-
quite common, the most important being pancreas divi- tis. In some patients, pancreas divisum is associated with
sum (see Chapter 3, p. 71). Surgical and imaging studies cystic dilatation of the terminal portion of the accessory
have demonstrated pancreas divisum in 1.5–10 % of indi- duct, a condition known as santorinicele.16 A pancreatic
MRI Appearance of Pathologic Entities 53

a b

c d
Fig. 2.4a–d Caroli syndrome in a 29-year-old woman. Massive cystic HASTE sequences. There is massive dilatation of the bile ducts;
dilatation of the intra- and extrahepatic bile ducts. Patient presented the choledochal stent is seen as a hypointense round structure
with recurrent symptoms of cholestasis after stenting of the com- (arrow in b). d Axial T2w multislice HASTE sequence. Stent occlusion
mon bile duct. MRCP for evaluation of the anatomic situation and is suggested by in-stent signal void and was confirmed after stent
stent position. a Coronal MRCP image from T2w single-slice HASTE replacement.
sequence. b, c Coronal (b) and axial (c) T2w multislice (3-mm)

duct crossing the common bile duct and terminating in MRI Appearance of Pathologic Entities
the duodenum proximal to the major papilla seen on
coronal MRCP images is pathognomonic of pancreas divi-
sum (Fig. 2.5; see Fig. 2.10). For comparison, the normal Ductal Strictures
configuration is shown in Fig. 2.6, and another normal
variant with separate duodenal openings of the common One of the most common indications for MRCP of both the
bile duct and pancreatic duct in Fig. 2.7b. Other common bile ducts and the pancreatic duct is to locate strictures or
variants include an aberrant right hepatic duct, which stenoses and evaluate ductal structures proximal to the
needs to be identified in patients who undergo liver sur- narrowing. Relevant stenoses can be excluded if MR im-
gery, and variable insertion of the cystic duct. ages show a small-caliber duct without abrupt narrowing
(Fig. 2.6). The causes of strictures or stenoses (inflamma-
tion, stone, tumor) can be differentiated on conventional,
54 2 The Bile and Pancreatic Ducts

a b

c d

Fig. 2.5a–e MRCP findings 2 months after acute pancreatitis in a


53-year-old man with pancreas divisum. MRCP for evaluation of
ductal structures and pancreatic parenchyma. a Coronal MIP image
from T2w multislice TSE sequence (acquired with respiratory navi-
gator, PACE). The pancreatic duct crosses the distal common bile
duct. b Paracoronal MIP image from T2w multislice TSE sequence.
The ducts cross each other and drain separately into the duodenum.
c, d Axial T2w multislice TSE sequence (PACE). The pancreatic duct
(arrow) courses anterior to the common bile duct. e ERCP image
shows nonopacification of the pancreatic duct during cannulation of
the major papilla and normal appearance of the common bile duct.

e
MRI Appearance of Pathologic Entities 55

a b
Fig. 2.6a, b Normal MRCP findings in a 56-year-old man. a Coronal course of the cystic duct (normal appearance). The major duodenal
MIP image from T2w multislice TSE sequence (acquired with respi- papilla is not depicted on the T2w images because the sphincter of
ratory navigator, PACE). Small bile ducts and small pancreatic duct. Oddi was contracted and there was no fluid in the papilla at the time
Note incomplete coverage of the intrahepatic bile ducts in the right of imaging. This appearance is normal and must not be misinter-
lobe, which must not be mistaken for pathology. b Paracoronal MIP preted as a papillary stone, which is why the papilla should addi-
image from T2w multislice TSE sequence (PACE). Slightly tortuous tionally be evaluated on axial images.

axial or coronal, sequences (including a dynamic contrast- chronic pancreatitis (see Chapter 3, “The Pancreas”), while
enhanced series if necessary) (Figs. 2.7 and 2.8). demonstration of a communication between the cyst and
the duct may not always be possible. When evaluating a
patient for postinflammatory strictures, great care is nec-
Stones essary to differentiate true luminal narrowing from in-
complete depiction of the pancreatic duct on paracoronal
Ultrasonography is the primary imaging modality for di- images (see Fig. 2.6a). Differentiation of inflammatory
agnosing stones in the gallbladder but has limited accu- changes from a solid malignancy often presents a diag-
racy in evaluating choledocholithiasis and will miss up to nostic challenge (see Chapter 3). Imaging evaluation of the
80 % of asymptomatic stones in the common bile duct.17 In pancreatic duct may be helpful in such cases. Demonstra-
contrast, MRCP has a sensitivity of over 95 % for detecting tion of an unobstructed pancreatic duct in an area where
stones in the common bile duct18,19 (Figs. 2.9 and 2.10) or malignancy is suspected makes inflammation the more
pancreatic duct (Figs. 2.7 and 2.10) and is superior to ERCP likely cause (so-called duct-penetrating sign)21 (see Chap-
in detecting intrahepatic stones.20 ter 3, in particular Fig. 3.18). In contrast, a solid malignant
MRCP also plays a role in diagnosing gallbladder stones tumor is typically associated with complete obstruction of
in cases where small gallbladder polyps must be consid- the duct.
ered in the differential diagnosis. Gallbladder stones are
shown in Figs. 2.11 and 2.12, polyps in Fig. 2.13. A rare
differential diagnosis is adenomyomatosis of the gallblad- Primary Biliary Cirrhosis
der (Fig. 2.14). In patients who have undergone cholecys-
tectomy, stones in the cystic duct stump occasionally Primary biliary cirrhosis (PBC) is a chronic granulomatous
cause upper abdominal symptoms. The common bile inflammation of the peripheral intrahepatic bile ducts.
duct can have a diameter of up to 10 mm after cholecys- Early macroscopic changes are not seen on MRCP images,
tectomy (Fig. 2.15). which is why the indication for MRCP in suspected PBC is
to rule out other causes. Extrahepatic bile ducts are not
involved. Lymphadenopathy in the liver hilum is an indi-
Inflammatory Conditions rect, nonspecific sign of PBC. The cause of the disease is
unknown, but an autoimmune etiology is likely. It slowly
MRCP is commonly indicated for the evaluation of the progresses to liver cirrhosis, resulting in morphologic
pancreatic duct proximal to a stenosis or stricture in pa- changes of the bile ducts that are visualized on MR im-
tients with incomplete ERCP (Figs. 2.7 and 2.8). Strictures ages.
frequently occur secondary to inflammation. T2w sequen-
ces also reliably depict pseudocysts associated with
56 2 The Bile and Pancreatic Ducts

a b

c d

e f
Fig. 2.7a–f Recurrent acute pancreatitis in a 41-year-old man. creatic duct in the body of the gland (arrow). d Axial T2w multislice
a Coronal MIP image from T2w multislice TSE sequence (acquired TSE sequence (acquired with respiratory navigator, PACE). Stone in
with respiratory navigator, PACE). Cutoff of the pancreatic duct in the pancreatic duct (arrow). Inflammatory changes of the pancre-
the pancreatic body (arrow) and marked dilatation in the tail. Also atic parenchyma and fluid collections around the pancreatic head
seen in the tail are dilated side branches. b Paracoronal MIP recon- and body. e ERCP image before contrast administration already
struction from T2w TSE multislice sequence (PACE). Normal variant shows multiple calcifications projected over the pancreas. f ERCP
with separate duodenal openings of the common bile duct and image after instillation of contrast medium into the pancreatic duct
pancreatic duct. Normal appearance of intra- and extrahepatic bile confirms ductal discontinuity and stone.
ducts. c Axial T2w multislice HASTE sequence. Cutoff of the pan-
MRI Appearance of Pathologic Entities 57

a b

c d

Fig. 2.8a–e Suspected pancreatic mass in a 57-year-old man. a Axial


T1w 2 D multislice FLASH sequence. b Axial T2w multislice HASTE
sequence. There is dilatation of the pancreatic duct beginning at the
junction of the body and tail (arrow). c Coronal T2w multislice
HASTE sequence. Low-SI structure in the pancreatic duct (arrow),
consistent with intraductal detritus. d MIP image created from the
T2w multislice HASTE sequence. e MIP image from a T2w multislice
TSE sequence acquired with respiratory navigator (PACE). There is
mild dilatation of the common bile duct, central intrahepatic bile
ducts, and pancreatic duct in the head and body of the gland caused
by papillary sclerosis. The suspected pancreatic mass was not con-
firmed.

e
58 2 The Bile and Pancreatic Ducts

a b

c d
Fig. 2.9a–d Choledocholithiasis and episodes of biliary colic in a (arrow in a ). Arrow in b indicates a prepapillary stone. c, d (Para-)
55-year-old woman. a, b Axial T2w multislice TSE sequence. Stones coronal T2w multislice HASTE sequence. Numerous stones in the
are seen as round structures of low SI in the common bile duct bile duct at the level of the pancreatic head.

Fig. 2.10a–f MRCP without oral contrast administration in a pancreatic duct crosses the common bile duct (arrow) and enters
66-year-old man presenting with acute right upper abdominal the duodenum via the minor papilla (arrow). d Coronal MIP image
pain. Abdominal ultrasound evaluation was incomplete due to large generated from the T2w multislice HASTE sequence in b. The
amounts of air in the colon. Elevated cholestasis and inflammatory pancreatic duct appears normal and crosses the common bile
markers. MRCP to rule out choledocholithiasis. a Axial T2w multi- duct at the level of the stone. e, f Thick-slab coronal (e) and para-
slice HASTE sequence. There is a large stone in the distal common coronal (f) MRCP images from T2w single-slice HASTE sequence
bile duct (arrow), which was subsequently extracted during ERCP. show multiple stones in the gallbladder and cystic duct.
b, c Axial T2w multislice HASTE sequence. Pancreas divisum. The e
MRI Appearance of Pathologic Entities 59

a b

c d

e f
60 2 The Bile and Pancreatic Ducts

a b

Fig. 2.11a–c Incidental finding of gallbladder stones in a 58-year-


old woman with suspected hepatocellular carcinoma. a Axial T1w
2 D multislice FLASH sequence. b Axial T2w multislice TSE sequence
(acquired with respiratory navigator, PACE). The stone has low T1
and T2 SI. c Axial T2w multislice TSE sequence (PACE). Rounded,
2-mm structure of low SI in the dependent portion of the descend-
ing duodenum (arrow), consistent with a stone passed into the
duodenum.

a b
Fig. 2.12a, b Incidental finding of numerous small stones in the HASTE sequence. b Axial T2w multislice TSE sequence (acquired
dependent portion of the gallbladder in a 75-year-old man who with respiratory navigator, PACE).
underwent MRI work-up of a focal liver lesion. a Axial T2w multislice
MRI Appearance of Pathologic Entities 61

c d
Fig. 2.13a–d Small lesions contiguous with the gallbladder wall IV contrast bolus injection (0.1 mmol/kg Gd). The gallbladder con-
noted on ultrasound in a 52-year-old man. MRI for differential tains numerous rounded lesions attached to the wall and up to
diagnosis—gallbladder polyps vs cholesterol sediments. a Axial 2 mm in size. Enhancement of the lesions after contrast injection
T2w multislice HASTE sequence. b Coronal T2w multislice HASTE establishes the diagnosis of polyps.
sequence. c, d T1w multislice 2 D FLASH sequence (VIBE) 55 s after

Primary Sclerosing Cholangitis wall irregularities of the intra- and extrahepatic bile ducts
as the disease progresses22 (Fig. 2.16).
Primary sclerosing cholangitis (PSC) is an idiopathic
chronic inflammation of the bile ducts, leading to choles-
tasis and, in advanced disease, secondary biliary cirrho- Masses
sis.22 There is a close association with chronic inflamma-
tory bowel disease, in which case the condition is called Compression by a tumor should be considered in the
secondary sclerosing cholangitis. PSC is considered a risk differential diagnosis of nearly all cases of luminal nar-
factor for the development of cholangiocarcinoma. MRCP rowing or (sub-)total occlusion of a duct. Since tumors are
will show a “beaded” appearance of the central bile ducts best excluded in the axial plane, additional axial images
due to strictures alternating with normal or dilated ductal should be obtained whenever MRCP images show ductal
segments in early disease and multifocal strictures and discontinuity. MRCP allows excellent evaluation of the
62 2 The Bile and Pancreatic Ducts

a b

Fig. 2.14a–e Diffuse adenomyomatosis of the gallbladder (hyper-


plastic cholecystosis) in a 43-year-old man presenting with colicky
symptoms. a Axial T2w multislice HASTE sequence. b Axial fat-sup-
pressed T2w multislice HASTE sequence. There is characteristic
thickening of the gallbladder wall (due to overgrowth of the mucosa
and hypertrophy of the muscular layer). Increased intraluminal
pressure leads to formation of intramucosal fluid collections resem-
bling diverticula known as Rokitansky–Aschoff sinuses, which are
pathognomonic of adenomyomatosis of the gallbladder. c Axial T1w
2 D multislice FLASH sequence 15 s after IV contrast bolus injection
(0.1 mmol/kg Gd). Marked uniform mucosal enhancement. d Co-
ronal T2w multislice HASTE sequence. e Thick-slab coronal MRCP
image from T2w single-slice HASTE sequence. The etiology of ad-
enomyomatosis of the gallbladder is unknown; the pattern of in-
volvement may be diffuse (as in the case presented here), segmen-
tal, or localized. Segmental adenomyomatosis is considered a pre-
e malignant stage of carcinoma of the gallbladder.
MRI Appearance of Pathologic Entities 63

a b
Fig. 2.15a, b MRCP in a 62-year-old woman presenting with acute a Coronal T2w multislice HASTE sequence after negative oral con-
upper abdominal pain 8 years after cholecystectomy for sympto- trast medium. b MIP image created from T2w multislice TSE se-
matic cholecystolithiasis. Ultrasound suggested a stone in the com- quence (acquired with respiratory navigator, PACE). Normal appear-
mon bile duct. The patient was scheduled for ERCP but underwent ance after cholecystectomy. The common bile duct has a maximum
MRCP for further work-up. MRCP did not confirm cholelithiasis. A diameter of 10 mm. No remnant of the cystic duct is seen. No
stomach ulcer was finally diagnosed as the cause of abdominal pain. intrahepatic cholestasis. Small pancreatic duct.

a b c

Fig. 2.16a–c Primary sclerosing cholangitis in a 26-year-old woman; (acquired with respiratory navigator, PACE). Beaded appearance of
advanced disease with multiple strictures of the bile ducts. a Axial the intra- and extrahepatic ducts due to strictures alternating with
T2w multislice HASTE sequence. b Coronal T2w multislice HASTE dilated segments.
sequence. c MIP image from coronal T2w multislice TSE sequence

degree of outflow obstruction (also after stent placement, Klatskin tumors are staged according to the Bismuth clas-
see Fig. 2.4). sification, which distinguishes four types: intraluminal
MRCP is especially useful in evaluating the extent of tumor below the bifurcation of the common hepatic
cholangiocarcinoma in the bifurcation of the common duct (type I); tumor at the level of the bifurcation (type
hepatic duct, a cholangiocellular carcinoma known as II); tumor extending into the right or left hepatic duct
Klatskin tumor. This tumor spreads intraluminally along (type IIIa and IIIb, respectively); and tumor extending
the duct wall (Fig. 2.17b) with secondary infiltration of into both hepatic ducts (type IV). In these patients, the
the liver parenchyma at the liver hilum (Fig. 2.17a, c). MRCP findings are also useful for intervention planning.23
64 2 The Bile and Pancreatic Ducts

a b c
Fig. 2.17a–c Klatskin tumor (Bismuth type IV) in a 72-year-old man. Gd). Coronal image shows intraductal extent in the hepatic bifurca-
a Axial T2w multislice TSE sequence (acquired with respiratory tion (arrow, b). Infiltration of the liver (arrow, c) is best appreciated
navigator, PACE). b Coronal T2w multislice HASTE sequence. c T1w on the contrast-enhanced parenchymal phase image.
VIBE sequence 5 min after IV contrast bolus injection (0.1 mmol/kg

References ministration: image quality and diagnostic accuracy. AJR Am J


Roentgenol 2002;179(1):121–129
13. Kim HJ, Kim MH, Lee SK, et al. Normal structure, variations, and
1. Freeman ML, DiSario JA, Nelson DB, et al. Risk factors for post-
anomalies of the pancreaticobiliary ducts of Koreans: a nation-
ERCP pancreatitis: a prospective, multicenter study. Gastroint-
wide cooperative prospective study. Gastrointest Endosc
est Endosc 2001;54(4):425–434
2002;55(7):889–896
2. Murray B, Carter R, Imrie C, Evans S, O’Suilleabhain C. Diclofenac
14. Morgan DE, Logan K, Baron TH, Koehler RE, Smith JK. Pancreas
reduces the incidence of acute pancreatitis after endoscopic
divisum: implications for diagnostic and therapeutic pancrea-
retrograde cholangiopancreatography. Gastroenterology
tography. AJR Am J Roentgenol 1999;173(1):193–198
2003;124(7):1786–1791
15. Warshaw AL, Simeone JF, Schapiro RH, Flavin-Warshaw B. Eval-
3. Loperfido S, Angelini G, Benedetti G, et al. Major early compli-
uation and treatment of the dominant dorsal duct syndrome
cations from diagnostic and therapeutic ERCP: a prospective
(pancreas divisum redefined). Am J Surg 1990;159(1):59–64,
multicenter study. Gastrointest Endosc 1998;48(1):1–10
discussion 64–66
4. Carlos RC, Scheiman JM, Hussain HK, Song JH, Francis IR, Fen-
16. Manfredi R, Costamagna G, Brizi MG, et al. Pancreas divisum and
drick AM. Making cost-effectiveness analyses clinically relevant:
“santorinicele”: diagnosis with dynamic MR cholangiopancrea-
the effect of provider expertise and biliary disease prevalence
tography with secretin stimulation. Radiology 2000;217(2):
on the economic comparison of alternative diagnostic strat-
403–408
egies. Acad Radiol 2003;10(6):620–630
17. Stott MA, Farrands PA, Guyer PB, Dewbury KC, Browning JJ,
5. Takehara Y, Ichijo K, Tooyama N, et al. Breath-hold MR cholan-
Sutton R. Ultrasound of the common bile duct in patients under-
giopancreatography with a long-echo-train fast spin-echo se-
going cholecystectomy. J Clin Ultrasound 1991;19(2):73–76
quence and a surface coil in chronic pancreatitis. Radiology
18. Laubenberger J, Büchert M, Schneider B, Blum U, Hennig J,
1994;192(1):73–78
Langer M. Breath-hold projection magnetic resonance-cholan-
6. Hennig J, Nauerth A, Friedburg H. RARE imaging: a fast imaging
gio-pancreaticography (MRCP): a new method for the examina-
method for clinical MR. Magn Reson Med 1986;3(6):823–833
tion of the bile and pancreatic ducts. Magn Reson Med
7. Tang Y, Yamashita Y, Arakawa A, et al. Pancreaticobiliary ductal
1995;33(1):18–23
system: value of half-Fourier rapid acquisition with relaxation
19. Topal B, Van de Moortel M, Fieuws S, et al. The value of magnetic
enhancement MR cholangiopancreatography for postoperative
resonance cholangiopancreatography in predicting common
evaluation. Radiology 2000;215(1):81–88
bile duct stones in patients with gallstone disease. Br J Surg
8. Asbach P, Klessen C, Kroencke TJ, et al. Magnetic resonance
2003;90(1):42–47
cholangiopancreatography using a free-breathing T2-weighted
20. Kim TK, Kim BS, Kim JH, et al. Diagnosis of intrahepatic stones:
turbo spin-echo sequence with navigator-triggered prospective
superiority of MR cholangiopancreatography over endoscopic
acquisition correction. Magn Reson Imaging 2005;23(9):
retrograde cholangiopancreatography. AJR Am J Roentgenol
939–945
2002;179(2):429–434
9. Petersein J, Reisinger W, Mutze S, Hamm B. [Value of negative
21. Ichikawa T, Sou H, Araki T, et al. Duct-penetrating sign at MRCP:
oral contrast media in MR cholangiopancreatography (MRCP)].
usefulness for differentiating inflammatory pancreatic mass
Rofo 2000;172(1):55–60
from pancreatic carcinomas. Radiology 2001;221(1):107–116
10. Neuhaus H, Ungeheuer A, Feussner H, Classen M, Siewert JR.
22. Vitellas KM, Keogan MT, Freed KS, et al. Radiologic manifesta-
[Laparoscopic cholecystectomy: ERCP as standard preoperative
tions of sclerosing cholangitis with emphasis on MR cholangio-
diagnostic technique]. Dtsch Med Wochenschr 1992;117(49):
pancreatography. Radiographics 2000;20(4):959–975, quiz
1863–1867
1108–1109, 1112
11. Fukukura Y, Fujiyoshi F, Sasaki M, Nakajo M. Pancreatic duct:
23. Hintze RE, Abou-Rebyeh H, Adler A, Veltzke-Schlieker W, Felix
morphologic evaluation with MR cholangiopancreatography
R, Wiedenmann B. Magnetic resonance cholangiopancreatogra-
after secretin stimulation. Radiology 2002;222(3):674–680
phy-guided unilateral endoscopic stent placement for Klatskin
12. Hellerhoff KJ, Helmberger HIII, Rösch T, Settles MR, Link TM,
tumors. Gastrointest Endosc 2001;53(1):40–46
Rummeny EJ. Dynamic MR pancreatography after secretin ad-
65

3 The Pancreas
P. Asbach, W. Luboldt, and H.B. Gehl

modality in the acute setting (acute pancreatitis, trauma)


Introduction
because it is faster and more readily available than MRI.
One of the most challenging tasks for radiologists is to
The pancreas has two very different functions in the reg- differentiate pancreatic malignancy from benign lesions,
ulation of metabolism, which is why functional disorders in particular chronic inflammatory changes with a mass
present with a variety of clinical symptoms. Treatment is effect. The distinction can be made with a high degree of
complex and may include pancreas transplant as a final accuracy by using a combination of MR strategies (axial
option in some patients. imaging, MRCP, MR angiography).5 In patients with
Insofar as specialized cells (grouped in the islets of chronic pancreatitis, MRI is useful in assessing and follow-
Langerhans) secrete several important hormones—insu- ing up the extent of the disease process and possible
lin, glucagon, somatostatin, and pancreatic polypep- effects on adjacent structures (splenic vein thrombosis,
tide—the pancreas is an endocrine organ. It is also an perforation of pseudocysts into neighboring organs). In
exocrine organ, producing several purely serous secre- contrast, CT is still superior in identifying pancreatic cal-
tions with important digestive functions in the gastro- cifications and abscess-related air inclusions.
intestinal tract: proteases (trypsin, chymotrypsin, and As open MR scanners are becoming more widely avail-
others), esterases (including lipase), carbohydrases, and able, the option of performing interventional procedures
nucleases. The pancreas is therefore made up of glandular (biopsy, drainage, celiac plexus block) under real-time
tissue and a system of ducts. It is embedded between the multiplanar MRI guidance is also expected to expand the
liver, stomach, and duodenum (Fig. 3.1) and is a highly therapeutic applications of pancreatic MRI.
vascularized organ with multiple blood supply. Since the
pancreas lacks a capsule and is in close vicinity to the
vessels and organs of the upper abdomen, pancreatic dis-
ease often involves these structures. The clinical presen-
tation is chronic to hyperacute.

Vena cava
Indications Portal vein

The high intrinsic soft-tissue contrast justifies the use of Celiac


MRI as the primary imaging modality in the diagnosis and trunk
staging of pancreatic tumors (including identification of
nodal and distant metastases) and evaluation of patients
for normal anatomic variants (Table 3.1). MRI using fast
breath-hold sequences with high spatial resolution has
been shown to be superior to CT and ultrasound in the
detection of pancreatic lesions.1–3 Moreover, MRI offers a
wider range of diagnostic options because it enables non- Superior mesenteric artery
invasive 3D imaging of the pancreatic duct system using
MR cholangiopancreatography (MRCP; see Chapter 2) in
the same session. By contrast, initial results suggest that
multiplanar reconstruction of multislice spiral CT data
does not greatly increase the sensitivity of CT in detecting
pancreatic tumors.4 However, results are expected to im-
prove given the ongoing rapid development of multislice Fig. 3.1 Anatomic relationships and lymphatic drainage of the pan-
spiral CT technology. CT is currently the preferred imaging creas.
66 3 The Pancreas

Table 3.1 Indications and imaging techniques for MRI of the pancreas

Indication Sequence Plane Comment


Pancreas divisum Single-shot TSE with half-Fourier Axial and Additional MRCP, T2-positive oral contrast
acquisition (e. g., HASTE) coronal medium (e. g., water) if necessary to
delineate the duodenum
Annular pancreas Single-shot TSE with half-Fourier Axial and With positive oral contrast medium to
acquisition coronal delineate the duodenum
(e. g., HASTE)
Hemochromatosis (primary T2w TSE, T2*w GRE Axial Should include full coverage of the liver
and secondary) and spleen
Pancreatitis (> 72 h) Single-shot TSE with half-Fourier Axial Without/with fat suppression; additional
acquisition (e. g., HASTE); dynamic MRCP; MR angiography if necessary to
contrast-enhanced MRI (3D GRE, evaluate for vascular complications
e. g., VIBE)
Pancreatic tumors Dynamic contrast-enhanced MRI Axial Additional planes on an individual basis;
(3D GRE, e. g., VIBE) liver staging if necessary

staltic artifacts because of the longer acquisition time.


Imaging Technique
Since the high signal intensity of fat improves the conspi-
cuity of the pancreatic contours (Fig. 3.2b), a fat-suppres-
High spatial resolution and good soft-tissue contrast are sion technique is not applied unless peripancreatic fluid
essential when imaging the pancreas. Therefore, a high collections are suspected (Fig. 3.2c). Additional axial (co-
signal-to-noise ratio (SNR) is needed. This can be achieved ronal slices if necessary) T1w and T2w thin-slice sequen-
by imaging at high field strength (at least 1 T) and using a ces (3 mm) should be acquired for evaluation of ductal
body or torso phased-array surface coil.6 Fat saturation structures and identification of very small parenchymal
techniques are also more effective at higher field lesions (Fig. 3.2 d, e).
strengths. Motion artifacts can be minimized by using A dynamic MR examination after intravenous bolus
fast breath-hold sequences, which require high-perform- injection of Gd-based contrast medium (e. g., Omniscan,
ance gradients, or by using respiratory triggering.7 Respi- Magnevist) is recommended for more detailed morpho-
ratory-triggered sequences take much longer to acquire logic evaluation of the pancreatic parenchyma. Arterial
but improve spatial resolution and are therefore an inte- phase images obtained 15 s after the contrast bolus (at a
gral part of pancreatic MRI. Application of presaturation standard dose of 0.1 mmol/kg body weight Gd) are most
bands above and below the field of view (FOV) is recom- useful. Additional images should be acquired at 55 s,
mended to reduce artifacts from inflowing blood. 2 min, and 5 min. The dynamic study is best performed
using a thin-slice T1w 3D GRE sequence with high spatial
resolution, such as a VIBE sequence (volume-interpolated
Imaging Planes breath-hold examination) (Fig. 3.2 f–j). Postcontrast im-
ages obtained with this GRE sequence at the above times
Axial images through the pancreas are usually sufficient to are well suited for detecting pancreatic lesions6,8,9 and can
establish a diagnosis. An additional coronal or sagittal replace imaging with conventional T1w sequences, which
sequence may help delineate the pancreatic head from are inferior in terms of spatial resolution and slice thick-
the duodenum and predict the resectability of pancreatic ness.
cancer. Since MR cholangiopancreatography (MRCP; see Chap-
ter 2) is fast to perform and often provides useful addi-
tional information, it should be done routinely in all pa-
Pulse Sequences tients undergoing MRI of the pancreas.
Dynamic contrast-enhanced MRI can be dispensed
An MRI protocol for the pancreas is presented in Table 3.2. with in favor of MR angiography to rule out splenic vein
We start by obtaining a three-plane localizer of the upper thrombosis or vascular infiltration in patients with a pan-
abdomen using a breath-hold GRE sequence. Next, fast creatic tumor or severe pancreatitis.
axial multislice breath-hold sequences (e. g., T1w FLASH,
T2w HASTE; Fig. 3.2a, b) are acquired of the pancreas, the
entire liver, the spleen, and the upper kidney poles (each Contrast Media
within one breath-hold, acquisition time < 23 s). Alterna-
tively, T2w images can be obtained without breath-hold- Dynamic contrast-enhanced MRI for evaluating perfusion
ing using a respiratory-triggered TSE sequence (e. g., of the pancreas at different times can be performed after
PACE)7 (Fig. 3.2c). The non-breath-hold sequence has intravenous injection of a nonspecific, Gd-based contrast
higher spatial resolution but is more susceptible to peri- medium (e. g., Magnevist, Omniscan) at a dose of
Table 3.2 Recommended pulse sequences and imaging parameters for MRI of the pancreas

Weighting Plane Sequence type TR (ms) TE (ms) Flip (°) ETL FS Matrix No. of No of Slice thick- Scan time Breath-hold
slices acquisitions ness (mm)
T1 Axial 2D GRE (e. g., FLASH) 199 4.1 90 - No 115 × 256 23 1 7 ca. 23 s Yes
T1 Axial 2D GRE (e. g., FLASH) 192 4.38 90 - No 115 × 256 17 1 3 ca. 22 s Yes
T2 Axial Single-shot TSE with 800* 63 150 115 No 115 × 256 23 1 7 ca. 18 s Yes
half-Fourier acquisi-
tion (e. g., HASTE)
T2 Axial Single-shot TSE with 800* 66 150 115 No 115 × 256 23 1 3 ca. 18 s Yes
half-Fourier acquisi-
tion (e. g., HASTE)
T2 Axial TSE (FSE) 2340 80 180 21 Yes 168 × 320 42 2 4 ca. 6–9 min No**
T2 Coronal*** Single-shot TSE with 800* 63 150 115 Yes/no 115 × 256 23 1 7 ca. 18 s Yes
half-Fourier acquisi-
tion (e. g., HASTE)
Dynamic contrast-enhanced MRI 15 s, 55 s, 2 min, 5 min after IV contrast bolus (0.1 mmol/kg Gd)
T1 Axial 3D GRE (e. g., VIBE) 5.2 2.59 10 – Yes 115 × 256 64 1 2.5 ca. 22 s Yes
MR angiography (optional for improved vascular assessment, especially to evaluate for vascular involvement in tumor staging)
T1 Coronal 3D GRE (e. g., FLASH) 3.67 1.21 20 – Yes 250 × 512 56 1 2 ca. 24 s Yes

* TR as a technical parameter referring to the interval between slice acquisitions; physical TR = ∞ since only one excitation pulse is applied per slice.
** Acquisition with respiratory triggering using the navigator echo technique (PACE, prospective acquisition correction).
*** Optional to improve assessment in complex anatomic situations (e. g., pancreas divisum, annular pancreas).

Imaging Technique
67
68 3 The Pancreas

a b

c d

f
e

Fig. 3.2a–j Illustration of normal findings obtained with standard saturated T2w multislice TSE sequence (acquired with respiratory
protocol for MRI of the pancreas (see Table 3.2). a T1w 2D multislice navigator, PACE). d Thin-slice (3-mm) T1w 2D multislice FLASH
FLASH sequence. b T2w multislice HASTE sequence. c Axial fat- sequence. e Thin-slice (3-mm) T2w multislice HASTE sequence.

0.1 mmol/kg body weight (see above). As with CT,10 arte- ing in patients with reduced cardiac output. Since para-
rial phase images (15 s after the contrast bolus) are most magnetic contrast media are low-molecular-weight sub-
suitable for parenchymal evaluation and tumor detec- stances with rapid distribution in the extracellular space,
tion.8 Determination of individual circulation time after focal pancreatic lesions may be obscured on equilibrium
administering a test bolus (2 mL) may be advisable to phase images.11 Current knowledge suggests that Gd-
optimize timing of the scan delay for arterial phase imag- based contrast media are not likely to adversely affect
Imaging Technique 69

g h

i j
Fig. 3.2a–j f–j T1w 3D GRE sequences (VIBE) before (f) and 15 s (g), 55 s (h), 2 min (i), and 5 min (j) after IV contrast bolus (0.1 mmol/kg
Gd).

the course of acute pancreatitis and can therefore be ad- needed to distinguish between free and endoluminal
ministered at the standard dose.12 fluids. Negative contrast media include blueberry juice,
Timing of postcontrast image acquisition is less critical which is rich in manganese,15 and iron oxide particles.16
when tissue-specific contrast media are used. A tissue- Use of negative oral contrast medium is recommended
specific contrast medium approved for use in MRI of the especially when additional MRCP is performed (see Chap-
pancreas is mangafodipir trisodium (MnDPDP; Teslascan, ter 2).
GE Healthcare). It is administered as a short intravenous One must be aware that T1-positive oral contrast me-
infusion, and images are acquired with a delay of ca. 15 dia, much like fat, exacerbate motion artifacts and should
min. MnDPDP was originally developed for liver imaging only be used in conjunction with breath-hold sequences.
but can also be used to detect focal pancreatic lesions as it Oral contrast media on the basis of superparamagnetic
markedly enhances the signal intensity of normal pan- iron oxide particles17 will eliminate this problem but may
creas on T1w GRE images.13 lead to susceptibility artifacts on GRE images if the con-
Oral contrast media14 are helpful to differentiate the centration is too high or agglutination occurs.18
pancreatic head from the duodenum or free fluid from The oral contrast solution (300–600 mL) should be
fluid in the intestine (Fig. 3.3). Tap water acts as a positive ingested over a period of 30 min before the examination.
contrast medium on T2w sequences and is sufficient to On the scanner table, the patient can be briefly turned into
improve delineation of the pancreas from the duodenum. the left lateral position to improve contrast filling of the
A negative oral contrast medium, which reduces or elimi- duodenum. Peristaltic artifacts can be reduced by intra-
nates the signal from the bowel lumen on T2w images, is muscular injection of a spasmolytic.
70 3 The Pancreas

a b
Fig. 3.3a, b Chronic pancreatitis with an acute episode 2 weeks (a descending part, b horizontal part), while the free peripancreatic
earlier in a 41-year-old man. MRI with negative oral contrast me- fluid (straight arrows) is seen as a thin rim of high SI around the head
dium. T2w multislice TSE sequence (acquired with respiratory nav- of the pancreas (a) and immediately below the head (b).
igator, PACE). The duodenal content has low SI (curved arrow)

a b
Fig. 3.4a, b Incidental finding of extensive lipomatosis of the pan- multislice HASTE sequence. Lipomatosis is seen throughout the
creas in a 71-year-old woman who presented with repeated episodes pancreas, and it is very difficult to distinguish the gland from
of acute upper abdominal complaints and underwent MRI for evalu- surrounding fatty tissue (arrows).
ation of the biliary tract. a T1w 2D multislice FLASH sequence. b T2w

artery and vein with the right transverse colon and gastro-
MRI Appearance of Normal Anatomy
duodenal artery lying anterior to it. Posterior to the body
of the pancreas are the aorta and the celiac and superior
The pancreas is located in the retroperitoneum at the level mesenteric arteries arising from it, the superior mesen-
of the first and second lumbar vertebrae. It consists of a teric and splenic veins, the left renal vessels, the hilum of
head with the uncinate process (which hooks behind the the left kidney, and the left adrenal gland; anterior to the
superior mesenteric artery), body, and tail. The head is body lie the transverse mesocolon and the omental bursa
supplied by the gastroduodenal artery (arising from the with the posterior gastric wall.
common hepatic artery) and the superior mesenteric ar- The normal pancreatic parenchyma is hyperintense to
tery and its pancreaticoduodenal branches. The body and liver on fat-suppressed T1w SE sequences and isointense
tail are supplied by the pancreatic branches of the splenic on T1w GRE sequences (Fig. 3.2a). It shows a marked and
artery. The veins draining the pancreas empty into the early signal increase on contrast-enhanced arterial phase
splenic vein or directly into the portal vein. The most images, which rapidly returns to almost precontrast in-
important lymph node stations are located in the porta tensities (Fig. 3.2 g–j). Partial or complete fatty replace-
hepatis, along the celiac trunk, and at the mesenteric root ment (lipomatosis) of the pancreas is common in older
(Fig. 3.1). Most of the pancreatic head is surrounded by persons and is characterized by prominent lobulation and
the duodenum, the so-called duodenal C-loop. Posterior a decrease in anteroposterior diameter (Fig. 3.4).
to the head run the inferior vena cava and the right renal
MRI Appearance of Pathologic Entities 71

a b
Fig. 3.5a, b Primary hemochromatosis in a 34-year-old woman. caused by iron deposits in affected organs is best appreciated on
a T1w 2D multislice FLASH sequence. b T2w multislice HASTE T2*w images. In primary (congenital) hemochromatosis, iron does
sequence. There is marked hypointensity of the parenchyma of not accumulate in the spleen but in the pancreas, which is spared in
the liver and pancreas on the T2w image. The MR signal reduction secondary (acquired) hemochromatosis.

MRI Appearance of Pathologic Entities Pancreatic Cysts

Congenital Anomalies and Diseases Pancreatic cysts (which are true cysts and must not be
confused with pseudocysts, see below) typically occur in
association with cysts in the liver, kidneys, or cerebellum
Pancreas Divisum and in patients with von Hippel–Lindau disease. They are
clearly identified by their high signal intensity on T2w
Pancreas divisum results when the dorsal and ventral images and, unlike cystic tumors, do not enhance after
pancreatic anlagen fail to fuse and there is persistence of contrast administration.
two separate ductal systems that do not communicate.19
In affected individuals, the secretions produced in the
body and tail of the pancreas drain through the accessory Cystic Fibrosis
pancreatic duct (duct of Santorini), which courses in the
anterior part of the pancreatic head and enters the duo- Cystic fibrosis (mucoviscidosis) is an autosomal recessive
denum through the minor papilla. Pancreas divisum has a disease causing fibrosis in the pancreas and lungs. Three
reported prevalence of 1.5–10 %.19–21 Although pancreas distinct patterns of pancreatic involvement have been
divisum is a normal anatomic variant, affected individuals noted27:
may suffer from recurrent episodes of pancreatitis due to · Lobulated, enlarged pancreas with complete replace-
functional stenosis obstructing the outflow of exocrine ment by fatty tissue
juices through the minor papilla.22,23 Improvement can · Small atrophic pancreas with partial fatty replacement
be achieved by sphincteroplasty, sphincterotomy, or · Diffuse atrophy without fatty replacement.
stenting.24 In approximately 42 % of patients with pan-
creas divisum, the pancreatic head is enlarged and can All three patterns can be distinguished by MRI. The degree
sometimes mimic a tumor.25 MRCP may be helpful in of fatty replacement can be estimated by comparing T1w
diagnosing pancreas divisum (see Chapter 2, Fig. 2.5). images acquired without and with fat saturation.

Annular Pancreas Primary Hemochromatosis

Annular pancreas is an extremely uncommon congenital Primary (hereditary, idiopathic) hemochromatosis is an au-
anomaly characterized by a ring of normal pancreatic tosomal recessive disorder of iron storage. Excessive ab-
tissue encircling and obstructing the descending duode- sorption of ingested iron in the jejunum and a limited
num. To diagnose this condition, administering oral con- capacity of the mononuclear phagocyte system (MPS) to
trast medium and acquiring coronal images to supple- cope with the excess iron lead to deposition of hemosid-
ment the standard axial sequence is recommended.26 erin in tissue, particularly in the liver, heart, gonads, skin,
and pancreas (Fig. 3.5). The iron overload causes the islet
cells to atrophy and can ultimately result in endocrine
72 3 The Pancreas

tumors obstructing the pancreatic duct. The underlying


pathophysiologic mechanism is premature, intrapancre-
atic activation of proteolytic enzymes (particularly tryp-
sin) with subsequent autodigestion.30
There are two forms of acute pancreatitis—edematous
and necrotizing. Edematous pancreatitis is the more com-
mon and less severe form, accounting for 85 % of cases.
The remaining 15 % of patients develop systemic inflam-
matory response syndrome (SIRS) with fulminant necrot-
izing pancreatitis, ultimately leading to partial or com-
plete necrosis of the organ.30
The diagnosis of acute pancreatitis is based on clinical
and laboratory findings. Cross-sectional imaging is indi-
cated if no improvement is seen 72 h after initiation of
Fig. 3.6 Acute edematous pancreatitis secondary to alcohol abuse conservative treatment.31 Since acute inflammatory and
in a 39-year-old man. Axial T2w multislice TSE sequence (acquired normal pancreatic tissue have similar MR signal inten-
with respiratory navigator, PACE). The pancreatic head is enlarged sities, the MR diagnosis primarily relies on morphologic
and shows subtle diffuse hyperintensities. criteria, but these are not always specific in edematous
pancreatitis (Fig. 3.6). An enlarged gland with loss of def-
inition of its normal boundaries suggests interstitial
edema and inflammation of the surrounding tissue. Peri-
dysfunction (clinically manifesting as bronze diabetes). pancreatic fluid collections occur in 40 % of patients with
Stored iron has higher susceptibility (i. e., is more readily acute pancreatitis and are best appreciated on T2w images
magnetized) and thus distorts the magnetic field, short- (Fig. 3.3). However, free fluid is often difficult to differ-
ening T2 and T2* relaxation times and reducing signal entiate from endoluminal fluid. A negative oral contrast
intensity on T2w and T2*w images (Fig. 3.5b). The signal medium may help make the distinction.
reduction is best appreciated on T2*w GRE images. SE The peripancreatic fluid contains proteolytic enzymes,
sequences are less sensitive in detecting iron because which induce an inflammatory reaction in the retroper-
stored iron interacts directly with the nuclear spins and itoneal fatty tissue. Ascites and thickening of the fascial
magnetic field inhomogeneities are compensated for by plane, especially of the Gerota fascia, indicate more severe
the 180° refocusing pulse. inflammation. Collections of exudative fluid can extend as
far as the true pelvis. The pancreatic contour may become
indistinguishable since inflammatory strands and fluid in
Secondary Hemochromatosis the peripancreatic fat may have the same signal intensity
as the pancreas. Differentiating uninvolved pancreatic
In secondary (acquired) hemochromatosis (also known as tissue from necrotic areas on unenhanced MR images
hemosiderosis), the iron overload is due to increased ery- may also be difficult at this stage. Such cases are absolute
throcyte breakdown and accumulation in the phagocytos- indications for dynamic contrast-enhanced imaging after
ing system (e. g., Kupffer cells in the liver). Causes may be intravenous contrast administration.
internal (ineffective or hypoplastic erythropoiesis) or ex- The complications of acute pancreatitis include pseu-
ternal (increased iron intake, e. g., through repeat trans- docysts (Fig. 3.7), fistulas to adjacent organs, splenic vein
fusion). The pancreas is usually spared in secondary he- thrombosis, pseudoaneurysm of the splenic artery with a
mochromatosis and retains its normal signal intensity, 37 % risk of bleeding, autodigestion of arterial walls with
while the liver shows the same iron-related signal resultant blood leaks, and bacterial superinfection of ne-
changes as in primary hemochromatosis.28 crotic tissue and fluid collections.32 Superinfection is the
most severe complication.
Since CT is more readily available and easier to per-
Inflammatory Disease form, it remains the method of choice, especially when
following up ICU patients. However, CT does not detect
Acute Pancreatitis small areas of intrapancreatic necrosis and requires ad-
ministration of iodine-based contrast medium, which
Acute pancreatitis is a common condition with an inci- could potentially harm the kidneys. MRI, on the other
dence of 5–10 cases per 100 000 population and a peak hand, being highly sensitive to paramagnetic contrast
between 40 and 60 years. The most common causes are media, enables good differentiation of unperfused (ne-
cholelithiasis (60–70 %) and alcohol abuse (20–30 %). Less crosis) and hyperperfused (abscess) areas.12 The paramag-
common causes include autoimmune diseases, genetic netic effects of blood breakdown products also result in
defects,29 trauma (including ERCP), drugs, metabolic dis- improved hemorrhage detection by MRI (Fig. 3.8). Finally,
orders, normal anatomic variants (pancreas divisum), and T2w imaging is superior to CT in differentiating between
MRI Appearance of Pathologic Entities 73

a d

c f
Fig. 3.7a–f Chronic pancreatitis and recurrent acute episodes in a renal compartment. c–e Axial T2w multislice TSE sequence (ac-
55-year-old man. a Axial T2w multislice HASTE sequence. The pan- quired with respiratory navigator, PACE). f MRCP. MIP image from
creatic duct is dilated due to compression by a large pseudocyst in T2w TSE multislice sequence (PACE). There is marked dilatation of
the pancreatic head (string of pearls appearance). There are also the pancreatic duct with normal appearance of the intra- and
multiple pseudocysts in the right renal compartment (some within extrahepatic biliary ducts. Also seen are several pseudocysts in
the anterior perirenal space). b Coronal T2w multislice HASTE se- the pancreatic head.
quence. Right-sided pseudocysts below the diaphragm and in the
74 3 The Pancreas

a b

c d
Fig. 3.8a–d Hemorrhagic pseudocyst in the body of the pancreas in contains areas of low and high SI on T1w and T2w images, reflecting
a 45-year-old man. a Axial T1w 2 D multislice FLASH sequence. different stages of intralesional hemorrhage (arrow). There is a
b, c Axial T2w multislice HASTE sequence. d Axial T2w multislice second, small, nonhemorrhagic pseudocyst in the pancreatic tail.
TSE sequence (acquired with respiratory navigator, PACE). The cyst

fluid collections (edema) and solid tissue (necrotic fatty the pancreas is common. Imaging typically shows dilata-
tissue). This differentiation is important in patients with tion of the main pancreatic duct with branch duct ectasia,
bacterial infections because it may affect treatment: while yielding a “chain of lakes” or “string of pearls” appearance
infected fluid collections are amenable to percutaneous (Figs. 3.7 and 3.9). Calcium deposits resulting from the
drainage in most cases, infected necrotic tissue requires precipitation of proteins with calcium in acini and termi-
surgical débridement.31,33 nal ducts are present in 50 % of patients with chronic
To identify vascular complications, such as pseudo- pancreatitis,36 but usually only in late stages.37 Another
aneurysm of the splenic artery or splenic vein thrombosis, finding is obstruction of the pancreatic and/or bile duct by
full MRI evaluation of acute pancreatitis should include stones (see Chapter 2, Fig. 2.7). Pseudocysts develop in ca.
contrast-enhanced MR angiography with a fast 3D GRE 30 % of cases. Other complications of chronic pancreatitis
sequence.34 are abscess formation and splenic vein thrombosis.
Fibrosis results in less intense enhancement compared
with normal pancreatic tissue on fat-suppressed T1w SE
Chronic Pancreatitis and GRE sequences acquired after intravenous contrast
administration. MRI therefore appears to be more sensi-
About 70 % of patients with chronic pancreatitis have a tive than CT in evaluating pancreatic fibrosis, although
history of alcohol abuse and recurrent episodes of acute quantitative data to confirm this observation are still lack-
pancreatitis.35 Chronic damage to acini results in paren- ing. CT, however, has the advantage of directly visualizing
chymal destruction and pancreatic autodigestion with calcifications (Fig. 3.10). With MRI, calcifications are sug-
subsequent fibrous replacement of the acinar tissue and gested only indirectly by signal voids on all sequences and
loss of both exocrine and endocrine function. Atrophy of therefore remain difficult to detect, even on T2*w GRE
MRI Appearance of Pathologic Entities 75

a b

c d

e f
Fig. 3.9a–f MRI findings 2 weeks after an acute episode of pancrea- respiratory navigator, PACE) at the level of the head (e) and body (f)
titis in a 41-year-old man with a history of chronic pancreatitis. of the pancreas. The pancreas is enlarged (pancreatic head measur-
a, b Axial T1w 2D multislice FLASH sequences acquired at the level ing 5 cm in axial diameter) with inhomogeneous T1 and T2 SI of the
of the head (a) and body (b) of the pancreas. c, d Axial T2w multi- parenchyma. The pancreatic duct is dilated and appears irregular
slice HASTE sequences at the level of the head (c) and body (d) of (arrow) in the tail of the pancreas. There is a small peripancreatic
the pancreas. e, f Axial T2w multislice TSE sequences (acquired with fluid collection persisting after an episode of acute pancreatitis.

sequences, where the signal voids appear larger than the Pseudocysts
actual calcifications (long TE).
An advantage of MRI in patients with chronic pancrea- About 30–50 % of pseudocysts develop from fluid collec-
titis is that it enables noninvasive evaluation of the ductal tions arising in the setting of pancreatitis (Figs. 3.7 and
system and will confirm or rule out dilatation of the pan- 3.8). If such fluid collections persist, they may develop a
creatic duct with high sensitivity (MRCP, see Chapter 2). capsule over a period of 4 weeks or longer due to inflam-
matory reactions. Pancreatic pseudocysts can contain
proteinaceous fluid or blood.38 Unlike retention cysts,
76 3 The Pancreas

a b
Fig. 3.10a, b Acute cholangitis developing after replacement of a spiral CT (4-mm reconstructed slice thickness). Multiple calcifica-
common bile duct stent in a 50-year-old man with a several-year tions in the head and tail of the pancreas.
history of chronic pancreatitis. CT scans obtained using multislice

Fig. 3.11a, b Pancreatic head carcinoma in a 61-year-old woman. SI compared with the normal surrounding parenchyma. Following
Axial T1w 2D multislice FLASH sequence before (a) and 15 s after (b) contrast injection, the tumor becomes more conspicuous due to
IV bolus injection of contrast medium (0.1 mmol/kg Gd). On the intense parenchymal enhancement and is seen to be directly con-
precontrast image, the 2-cm tumor (arrow) is of homogeneous low tiguous with the duodenal wall.

pseudocysts do not have an epithelial lining.39 The cysts Pancreatic Neoplasms


can lead to compression of the splenic vein or common
bile duct, formation of fistulas to adjacent organs, infec- Pancreatic Cancer
tion, or obstruction of lymphatic drainage. Rupture of a
pseudocyst can cause peritonitis. Pseudocysts can occur Adenocarcinoma is the most common pancreatic neo-
anywhere in the abdomen (Fig. 3.7) but rarely outside the plasm, accounting for 95 % of malignant tumors of the
abdomen (e. g., in the mediastinum). pancreas. Ninety percent are ductal carcinomas arising
The cyst fluid is best appreciated on T2w MR images. from the epithelium of small pancreatic ducts and 10 %
Pseudocysts do not enhance after intravenous contrast originate in the acinar epithelium (acinar carcinomas).
administration. Negative oral contrast medium is helpful Adenocarcinomas typically occur in the pancreatic head
to reliably differentiate suspected pseudocysts from fluid (60 %) (Fig. 3.11), less commonly in the body (15 %) or tail
in the duodenum. (5 %) (Fig. 3.12). About 20 % are diffuse tumors involving
the entire pancreas.37 Pancreatic head tumors are defined
MRI Appearance of Pathologic Entities 77

as tumors located to the right of the left border of the Table 3.3 T classification of pancreatic and ampullary cancer
superior mesenteric vein (the uncinate process is part of
Pancreatic cancer Ampullary cancer
the head), tumors of the body lie between the left border
of the superior mesenteric vein and the left border of the T1 Tumor limited to the pan- Tumor limited to the ampulla
creas, ≤ 2 cm in greatest of Vater or sphincter of Oddi
aorta, and tumors of the tail are those to the left of the left
dimension
border of the aorta. While tumors located in the head of
T2 Tumor limited to the pan- Tumor invades the duodenal
the gland tend to present early with symptoms of com- creas, > 2 cm in greatest wall
mon bile duct obstruction, most pancreatic carcinomas dimension
are diagnosed at an advanced stage and are unresectable T3 Tumor extends beyond Tumor invades the pancreas
because of liver and/or lymph node metastases, vascular the pancreas (but does not
invasion, or peritoneal or retroperitoneal infiltration.40 involve the celiac trunk or
Complete surgical resection is the only potentially cura- superior mesenteric ar-
tery)
tive treatment but is only possible if the tumor is confined
T4 Tumor invades the celiac Tumor invades peripancreatic
to the pancreas (T classification in Table 3.3).
trunk or superior mesen- soft tissues and/or other ad-
Most pancreatic carcinomas have lower signal inten- teric artery jacent organs or structures
sity than normal pancreatic tissue on T1w SE and GRE
images, which reflects the low protein content of malig-
nant tissue. On T2w images, they are of variable signal
intensity, typically slightly hyperintense to normal glan-
dular tissue (Fig. 3.12). tumor resectability,3 for which it has a positive predictive
Unlike endocrine tumors, adenocarcinomas are hypo- value well over 80 %.1 Nevertheless, exploratory laparot-
vascular because of their desmoplastic, fibrotic composi- omy is necessary to assess resectability in all critical
tion, which is why they have lower signal intensity than cases.41
normal pancreas on dynamic contrast-enhanced images
(Fig. 3.12 d–g).
Depending on its location, pancreatic carcinoma will Ampullary Cancer
cause dilatation of the pancreatic and/or bile duct.41 Duc-
tal dilatation can be confirmed or ruled out using T2w Because of its more favorable prognosis, ampullary cancer
thin-slice HASTE sequences (axial and coronal), MRCP, or (carcinoma of the ampulla of Vater) must be differentiated
contrast-enhanced GRE sequences. from tumors arising in the pancreatic head. Other peri-
The lack of a pancreatic capsule allows early spread of ampullary neoplasms to be considered in the differential
cancer to local tissues and invasion of the large vessels, diagnosis are tumors of the terminal pancreatic and com-
particularly the superior mesenteric artery and vein and mon bile ducts. While, histologically, they are also adeno-
the portal vein. Patients with vascular invasion have a carcinomas, true ampullary carcinomas have a better
poorer prognosis, as have patients with perineural and 5-year survival rate after Whipple operation. A separate
lymphatic invasion. More than 50 % of patients with pan- T classification system exists for ampullary cancer
creatic cancer have lymph node metastases at the time of (Table 3.3).
surgery. A distinction is made between involvement of Ampullary cancer presents early with obstructive jaun-
lymph nodes near the pancreas and involvement of a dice. MRCP may be helpful in distinguishing ampullary
second nodal group along the superior mesenteric, gastro- cancer from pancreatic head masses. Usually, the cancer is
duodenal, common hepatic, and splenic arteries and celiac most conspicuous on contrast-enhanced GRE images. Use
trunk (see Fig. 3.1). Because the lymphatics are very short, of negative oral contrast medium is indicated to facilitate
there is also early invasion of para-aortic, paracaval, and differentiation from the duodenum.
porta hepatis nodes (see Fig. 3.1).
Pancreatic cancer initially spreads to the liver (66 % of
cases) and lymph nodes (22 % of cases). Lung metastases Cystic Pancreatic Neoplasms
occur relatively late. Other metastatic sites are the bones,
intestine, and peritoneal cavity. Advanced pancreatic can- Although very rare, cystic neoplasms present a challenge
cer is characterized by contiguous invasion of adjacent for imaging because they may be confused with pseudo-
structures including the duodenum, inferior vena cava, cysts or congenital cysts of the pancreas.38,45 The primary
splenic vein, stomach, colon, spleen, adrenal, and kidney. role of imaging is to differentiate cystic neoplasms from
Surgical resection is an option in patients without hepatic these cysts because, unlike cysts, most cystic tumors re-
or nodal metastases or vascular encasement.42 Vascular quire resection or at least histologic confirmation. Four
encasement is suggested by loss of surrounding fat planes, major types of cystic neoplasms can be distinguished
which is more obvious on T1w MR images43 than on CT.44 (Table 3.4): serous cystadenoma (micro- and macrocystic
MRA using a GRE sequence is helpful for evaluating the forms) and mucinous cystadenoma/cystadenocarcinoma,
lumen of the superior mesenteric vein and the hepatic which are most common, and the less common intraduc-
portal system. MRI is slightly better than CT in assessing tal papillary mucinous tumor (IPMT).46,47 Very rarely,
78 3 The Pancreas

a b

c d

e f

Fig. 3.12a–g Pancreatic tail carcinoma (arrow) incidentally de-


tected at MRI in a 64-year-old woman with focal liver lesions and a
history of breast cancer. The liver lesions are most likely metastases
from the pancreatic carcinoma. a Plain axial T1w 2D multislice
FLASH sequence. b Axial T2w multislice HASTE sequence. c–g Dy-
namic MRI using a thin-slice T1w 3D FLASH sequence (VIBE). Images
acquired before (c) and 15 s (d), 55 s (e), 2 min (f), and 5 min (g)
after IV contrast bolus injection (0.1 mmol/kg Gd). The tumor is
most conspicuous in the arterial phase due to intense enhancement
of normal parenchyma.

g
MRI Appearance of Pathologic Entities 79

a b
Fig. 3.13a, b Microcystic serous cystadenoma at the junction of the body and tail of the pancreas. a Axial T1w 2D multislice FLASH
sequence. b Axial T2w multislice HASTE sequence. Images show multiple clustered cysts (< 2 cm). Also seen is cirrhosis of the liver.

Table 3.4 Cystic pancreatic neoplasms

Neoplasm M:F Peak age Cyst architecture Differential diagnosis Management


ratio (years)
Serous 1:4 65 Microcystic serous Cystic neuroendocrine tumor Histologic confirmation (biopsy)
cystadenoma (82 % > 60)
Macrocystic serous Mucinous cystadenoma/ Histologic confirmation (biopsy)
cystadenocarcinoma
Mucinous 1:9 40–60 Macrocystic Macrocystic serous Surgical resection
cystadenoma/ mucinous cystadenoma
cystadeno-
carcinoma
IPMT M>F ? Macrocystic Mucinous cystadenoma/ Histologic confirmation (biopsy)
mucinous cystadenocarcinoma
Cystic neuro- M=F 30–60 Microcystic Microcystic serous Surgical resection
endocrine tumor cystadenoma

neuroendocrine pancreatic tumors may have cystic com- and their imaging features may resemble a mucinous
ponents (see “Islet Cell Tumors” below).48 cystadenoma/cystadenocarcinoma.
Serous cystadenomas have a predilection for the pan- Mucinous cystadenomas/cystadenocarcinomas typically
creatic head. There are basically two variants, microcystic arise in the pancreatic body or tail (Fig. 3.15). The tumors
and macrocystic cystadenomas. Some authors assign the produce proteinaceous mucus and always exhibit a
macrocystic variant to the group of mucinous cystadeno- macrocystic pattern.45 Mucinous cystadenomas have
mas and use microcystic cystadenoma synonymously high malignant potential (mucinous cystadenocarcino-
with serous cystadenoma. However, because treatment mas). They have irregular borders, a capsule, and septa;
is different, we recommend distinguishing between mi- peripheral calcification is quite common.
crocystic and macrocystic serous adenomas and separat- Intraductal papillary mucinous tumors (IPMT) are usu-
ing these from mucinous cystadenomas. The microcystic ally found in the pancreatic head (uncinate process). They
form is characterized by a grapelike cluster of multiple arise in the pancreatic duct or one of its main branches
small cysts (< 2 cm) (Fig. 3.13) with nodular margins. A and are characterized by a macrocystic appearance and
central scar with calcifications is common. The cyst fluid excessive intraductal mucus production,45 which may ob-
may contain blood, resulting in high signal intensity on struct the pancreatic duct and cause recurrent pancreati-
T1w images.49 Microcystic serous cystadenomas are con- tis. Differentiation of IPMT from chronic pancreatitis is
sidered benign tumors that do not encase vessels;50 how- difficult, unless there is clear evidence of a mucous plug.
ever, they cannot be reliably differentiated from the very In patients without signs of pancreatitis, IPMT is also
rare cystic neuroendocrine tumors solely on the basis of difficult to distinguish from mucinous cystadenoma/cyst-
their imaging appearance (Fig. 3.14). Macrocystic serous adenocarcinoma.
cystadenomas consist of clusters of larger cysts (> 2 cm),
80 3 The Pancreas

a b
Fig. 3.14a, b Well-differentiated cystic neuroendocrine carcinoma multiple clustered cysts (< 2 cm). The cyst walls enhance, and no
of the pancreas. a Axial T2w multislice HASTE sequence. b Axial T1w solid tumor components are seen. This tumor cannot be reliably
3D multislice FLASH sequence (VIBE) 2 min after IV bolus injection distinguished from microcystic serous cystadenoma using morpho-
of contrast medium (0.1 mmol/kg Gd). As in Fig. 3.13, there are logic imaging criteria.

Islet Cell Tumors ized, gastrinomas enhance only moderately compared


with insulinomas.
With an incidence of 0.5 per 100 000 population, pancre- Glucagoma, somatostatinoma56 (Fig. 3.17), and VIPoma
atic islet cell tumors are fairly uncommon. The majority, (vasoactive intestinal polypeptide) are very rare, usually
60–85 %, are functioning islet cell tumors51 and present malignant, tumors that tend to metastasize to the liver.57
early with symptoms of hormone overproduction, making Unlike insulinomas and gastrinomas, these islet cell tu-
the diagnosis straightforward. Nonfunctioning tumors mors are so rare that they are unlikely to be encountered
only become apparent once they have reached a certain in the routine clinical setting.
size and cause biliary or intestinal obstruction. MRI has evolved into an important imaging modality
Islet cell tumors are hypointense to normal pancreatic for evaluating patients with islet cell tumors: preopera-
tissue on T1w images and markedly hyperintense on T2w tively for precise tumor localization and exclusion of hep-
images.52,53 Being hypervascular, they enhance intensely atic or nodal metastases and postoperatively for early
on dynamic contrast-enhanced arterial phase images,52,53 detection of tumor recurrence, which is seen in 50 % of
as do liver metastases from these tumors.52–54 Short tau patients with gastrinoma.
inversion recovery (STIR) sequences are also helpful in
highlighting islet cell tumors,54,55 but the improved con-
spicuity is accompanied by a penalty in spatial resolution. Differentiation of Inflammatory Pseudotumors
Most islet cell tumors are insulinomas, which are usu- and Neoplasms
ally benign (> 90 %), and only half of them produce insulin.
They are hypervascular tumors and are therefore best Patients with recurrent pancreatitis often have areas of
detected by dynamic imaging. Large insulinomas, as well focal enlargement in the gland, which are very difficult to
as their liver and lymph node metastases, are character- characterize. Differentiating these so-called pseudo-
ized by rim enhancement.52 tumors from malignant tumors remains an interdiscipli-
Gastrinomas are gastrin-producing tumors of the pan- nary challenge. Neither the patient’s history nor labora-
creas (80 %) or duodenum (20 %). They secrete large tory tests (tumor markers) provide a definitive diagnosis
amounts of gastrin, resulting in chronic overproduction because the tumor marker CA 19-9 may be elevated in
of gastric acid (Zollinger–Ellison syndrome). Thirty per- both conditions.58 Similarly, morphologic imaging criteria
cent of gastrinomas occur in conjunction with other en- fail to provide a reliable diagnosis. Focal enlargement of
docrine neoplasms (pituitary and parathyroid tumors) in the pancreas favors the diagnosis of neoplasm in the
patients with multiple endocrine neoplasia type 1 absence of classic signs of inflammation such as exuda-
(MEN 1). Most gastrinomas are malignant and typically tion, peripancreatic fascial thickening, or beading of the
larger and less well vascularized than insulinomas. Gas- pancreatic duct. There is more intense and longer en-
trinomas are hypointense to normal pancreatic tissue on hancement of the parenchyma in pancreatitis compared
fat-suppressed T1w SE images and, regardless of their with carcinoma.59 The duct-penetrating sign60 may also
size, always have high signal intensity on fat-suppressed be helpful in establishing the differential diagnosis
T2w SE sequences49 (Fig. 3.16). Being less well vascular- (Fig. 3.18)—if narrowing of the pancreatic duct within
MRI Appearance of Pathologic Entities 81

a b

c d

e f
Fig. 3.15a–f Macrocystic mucinous cystadenoma in a 78-year-old e, f Single-slice MRCP (e) and MIP image (f) from T2w multislice
woman. a Axial T2w multislice HASTE sequence. b Axial T2w multi- TSE sequence (PACE). The characteristic septa of the macrocystic
slice TSE sequence (acquired with respiratory navigator, PACE). mass are most conspicuous on the MRCP images. The postcontrast
c, d Axial T1w 3D FLASH sequence (VIBE) 15 s (c) and 2 min (d) sequences show enhancement of the septa (d) and absence of
after IV bolus injection of contrast medium (0.1 mmol/kg Gd). hypervascular areas within the mass (c).
82 3 The Pancreas

a b

c d

e f

Fig. 3.16a–g Gastrinoma. a Axial T1w SE sequence. b Axial T2w fat-


suppressed SE sequence. c–f Dynamic MRI with T1w GRE sequence
before (c) and 15 s (d), 55 s (e) and 3 min (f) after IV contrast bolus
injection (0.1 mmol/kg Gd). g Delayed postcontrast axial T1w fat-
suppressed SE sequence.

g
MRI Appearance of Pathologic Entities 83

a b

Fig. 3.17a–c Somatostatinoma. a, b Axial T1w SE images obtained


before (a) and after (b) contrast administration (0.1 mmol/kg Gd).
c Contrast-enhanced spiral CT scan for comparison.

the mass is minimal, inflammation is the more likely Pancreas Transplant


cause. Absence of the duct-penetrating sign is highly in-
dicative of malignancy. In addition, the appearance of the Patients with diabetic nephropathy often receive a pan-
pancreatic duct can also serve to distinguish a malignant creas transplant in combination with renal transplanta-
tumor from an inflammatory process. Gradual narrowing tion. MRI is therefore the preferred imaging modality for
of the duct suggests inflammation, while abrupt obstruc- evaluating pancreas grafts since Gd-based contrast media
tion indicates a stone or neoplasm. The duct is best eval- pose little risk29 compared with CT and use of a contrast
uated by performing an additional MRCP study. Intact medium that is potentially harmful to the kidneys. Dy-
perivascular fat planes are more common in focal pan- namic contrast-enhanced MRI with acquisition of images
creatitis, while vascular encasement is more likely in pan- in different phases of perfusion (arterial, parenchymal,
creatic cancer. Note, however, that edema of the fat plane and interstitial) is most suitable for detecting postopera-
around the mesenteric artery and vein in acute pancrea- tive complications such as venous thrombosis or abscess.
titis may mimic vascular encasement.61 Complete replace- MR angiography allows excellent assessment of the vas-
ment of the fatty tissue in chronic fibrotic pancreatitis cular status and can replace conventional digital subtrac-
may also be mistaken for vascular encasement. tion angiography (DSA).62
Because of the difficulties just outlined, histologic ex-
amination remains the diagnostic standard for differenti-
ating an inflammatory pseudotumor from pancreatic can-
cer with secondary obstructive pancreatitis, despite on-
going advances in CT and MRI.
84 3 The Pancreas

a b

c d

Fig. 3.18a–e Chronic pancreatitis in a 41-year-old man. There is


enlargement of the head of the pancreas (5.5 cm in axial diameter)
with inhomogeneous T1 and T2 SI. a Axial T1w 2D multislice FLASH
sequence. b Axial T2w multislice HASTE sequence. c Axial T2w
multislice TSE sequence (acquired with respiratory navigator,
PACE). d Axial T1w 2D multislice FLASH sequence 15 s after IV
contrast bolus injection (0.1 mmol/kg Gd). The pancreatic head
has low SI relative to the body. Carcinoma confined to the head
cannot be excluded. e MIP image created from T2w multislice TSE
sequence (acquired with respiratory navigator, PACE). There is no
compression of the pancreatic duct in the head (arrow), which
would be expected if malignancy were present. Carcinoma was
ruled out by histologic examination of the pancreatic head after
Whipple resection.

e
MRI Appearance of Pathologic Entities 85

References (pancreas divisum redefined). Am J Surg 1990;159(1):59–64,


discussion 64–66
24. Lans JI, Geenen JE, Johanson JF, Hogan WJ. Endoscopic therapy in
1. Fischer U, Vosshenrich R, Horstmann O, et al. Preoperative local
patients with pancreas divisum and acute pancreatitis: a pro-
MRI-staging of patients with a suspected pancreatic mass. Eur
spective, randomized, controlled clinical trial. Gastrointest En-
Radiol 2002;12(2):296–303
dosc 1992;38(4):430–434
2. Ichikawa T, Haradome H, Hachiya J, et al. Pancreatic ductal
25. Zeman RK, McVay LV, Silverman PM, et al. Pancreas divisum:
adenocarcinoma: preoperative assessment with helical CT ver-
thin-section CT. Radiology 1988;169(2):395–398
sus dynamic MR imaging. Radiology 1997;202(3):655–662
26. Lecesne R, Stein L, Reinhold C, Bret PM. MR cholangiopancrea-
3. Schima W, Függer R, Schober E, et al. Diagnosis and staging of
tography of annular pancreas. J Comput Assist Tomogr
pancreatic cancer: comparison of mangafodipir trisodium-en-
1998;22(1):85–86
hanced MR imaging and contrast-enhanced helical hydro-CT.
27. Tham RT, Heyerman HG, Falke TH, et al. Cystic fibrosis: MR
AJR Am J Roentgenol 2002;179(3):717–724
imaging of the pancreas. Radiology 1991;179(1):183–186
4. Prokesch RW, Chow LC, Beaulieu CF, et al. Local staging of
28. Yoon DY, Choi BI, Han JK, Han MC, Park MO, Suh SJ. MR findings
pancreatic carcinoma with multi-detector row CT: use of curved
of secondary hemochromatosis: transfusional vs erythropoietic.
planar reformations initial experience. Radiology 2002;225
J Comput Assist Tomogr 1994;18(3):416–419
(3):759–765
29. Haustein J, Niendorf HP, Krestin G, et al. Renal tolerance of
5. Lopez Hänninen E, Amthauer H, Hosten N, et al. Prospective
gadolinium-DTPA/dimeglumine in patients with chronic renal
evaluation of pancreatic tumors: accuracy of MR imaging with
failure. Invest Radiol 1992;27(2):153–156
MR cholangiopancreatography and MR angiography. Radiology
30. Mitchell RM, Byrne MF, Baillie J. Pancreatitis. Lancet 2003;
2002;224(1):34–41
361(9367):1447–1455
6. Semelka RC, Ascher SM. MR imaging of the pancreas. Radiology
31. Balthazar EJ, Freeny PC, vanSonnenberg E. Imaging and inter-
1993;188(3):593–602
vention in acute pancreatitis. Radiology 1994;193(2):297–306
7. Klessen C, Asbach P, Kroencke TJ, et al. Magnetic resonance
32. Fishman EK, Soyer P, Bliss DF, Bluemke DA, Devine N. Splenic
imaging of the upper abdomen using a free-breathing T2-
involvement in pancreatitis: spectrum of CT findings. AJR Am J
weighted turbo spin echo sequence with navigator triggered
Roentgenol 1995;164(3):631–635
prospective acquisition correction. J Magn Reson Imaging
33. Fernández-del Castillo C, Rattner DW, Makary MA, Mostafavi A,
2005;21(5):576–582
McGrath D, Warshaw AL. Débridement and closed packing for
8. Gabata T, Matsui O, Kadoya M, et al. Small pancreatic adenocar-
the treatment of necrotizing pancreatitis. Ann Surg 1998;
cinomas: efficacy of MR imaging with fat suppression and ga-
228(5):676–684
dolinium enhancement. Radiology 1994;193(3):683–688
34. Leung DA, McKinnon GC, Davis CP, Pfammatter T, Krestin GP,
9. Semelka RC, Kroeker MA, Shoenut JP, Kroeker R, Yaffe CS, Mic-
Debatin JF. Breath-hold, contrast-enhanced, three-dimensional
flikier AB. Pancreatic disease: prospective comparison of CT,
MR angiography. Radiology 1996;200(2):569–571
ERCP, and 1.5-T MR imaging with dynamic gadolinium enhance-
35. Etemad B, Whitcomb DC. Chronic pancreatitis: diagnosis, clas-
ment and fat suppression. Radiology 1991;181(3):785–791
sification, and new genetic developments. Gastroenterology
10. Lu DS, Vedantham S, Krasny RM, Kadell B, Berger WL, Reber HA.
2001;120(3):682–707
Two-phase helical CT for pancreatic tumors: pancreatic versus
36. Luetmer PH, Stephens DH, Ward EM. Chronic pancreatitis: re-
hepatic phase enhancement of tumor, pancreas, and vascular
assessment with current CT. Radiology 1989;171(2):353–357
structures. Radiology 1996;199(3):697–701
37. Clark LR, Jaffe MH, Choyke PL, Grant EG, Zeman RK. Pancreatic
11. Brailsford J, Ward J, Chalmers AG, Ridgway J, Robinson PJ. Dy-
imaging. Radiol Clin North Am 1985;23(3):489–501
namic MRI of the pancreas—gadolinium enhancement in nor-
38. Kim YH, Saini S, Sahani D, Hahn PF, Mueller PR, Auh YH. Imaging
mal tissue. Clin Radiol 1994;49(2):104–108
diagnosis of cystic pancreatic lesions: pseudocyst versus non-
12. Johnson CD, Stephens DH, Sarr MG. CT of acute pancreatitis:
pseudocyst. Radiographics 2005;25(3):671–685
correlation between lack of contrast enhancement and pancre-
39. Boeve WJ, Kok T, Tegzess AM, et al. Comparison of contrast
atic necrosis. AJR Am J Roentgenol 1991;156(1):93–95
enhanced MR-angiography-MRI and digital subtraction angio-
13. Gehl HB, Urhahn R, Bohndorf K, et al. Mn-DPDP in MR imaging
graphy in the evaluation of pancreas and/or kidney transplan-
of pancreatic adenocarcinoma: initial clinical experience. Radi-
tation patients: initial experience. Magn Reson Imaging 2001;
ology 1993;186(3):795–798
19(5):595–607
14. Brown JJ. Gastrointestinal contrast agents for MR imaging. Magn
40. Tsuchiya R, Noda T, Harada N, et al. Collective review of small
Reson Imaging Clin N Am 1996;4(1):25–35
carcinomas of the pancreas. Ann Surg 1986;203(1):77–81
15. Papanikolaou N, Karantanas A, Maris T, Gourtsoyiannis N. MR
41. Freeny PC, Traverso LW, Ryan JA. Diagnosis and staging of pan-
cholangiopancreatography before and after oral blueberry juice
creatic adenocarcinoma with dynamic computed tomography.
administration. J Comput Assist Tomogr 2000;24(2):229–234
Am J Surg 1993;165(5):600–606
16. Jacobsen TF, Laniado M, Van Beers BE, et al. Oral magnetic
42. Megibow AJ, Zhou XH, Rotterdam H, et al. Pancreatic adenocar-
particles (ferristene) as a contrast medium in abdominal mag-
cinoma: CT versus MR imaging in the evaluation of resectabili-
netic resonance imaging. Acad Radiol 1996;3(7):571–580
ty—report of the Radiology Diagnostic Oncology Group. Radiol-
17. Rogers J, Lewis J, Josephson L. Use of AMI-227 as an oral MR
ogy 1995;195(2):327–332
contrast agent. Magn Reson Imaging 1994;12(4):631–639
43. Sironi S, De Cobelli F, Zerbi A, Balzano G, Di Carlo V, DelMaschio
18. Briggs RW, Wu Z, Mladinich CR, et al. In vivo animal tests of an
A. Pancreatic carcinoma: MR assessment of tumor invasion of
artifact-free contrast agent for gastrointestinal MRI. Magn Reson
the peripancreatic vessels. J Comput Assist Tomogr 1995;19:
Imaging 1997;15(5):559–566
739–744
19. Warshaw AL. Pancreas divisum—really. Surgery 2000;128(5):
44. Vellet AD, Romano W, Bach DB, Passi RB, Taves DH, Munk PL.
832–833
Adenocarcinoma of the pancreatic ducts: comparative evalua-
20. Kim HJ, Kim MH, Lee SK, et al. Normal structure, variations, and
tion with CT and MR imaging at 1.5 T. Radiology 1992;183(1):
anomalies of the pancreaticobiliary ducts of Koreans: a nation-
87–95
wide cooperative prospective study. Gastrointest Endosc
45. Sahani DV, Kadavigere R, Saokar A, Fernandez-del Castillo C,
2002;55(7):889–896
Brugge WR, Hahn PF. Cystic pancreatic lesions: a simple imag-
21. Morgan DE, Logan K, Baron TH, Koehler RE, Smith JK. Pancreas
ing-based classification system for guiding management. Radio-
divisum: implications for diagnostic and therapeutic pancrea-
graphics 2005;25(6):1471–1484
tography. AJR Am J Roentgenol 1999;173(1):193–198
46. Lichtenstein DR, Carr-Locke DL. Mucin-secreting tumors of the
22. Ohshima Y, Tsukamoto Y, Naitoh Y, et al. Function of the minor
pancreas. Gastrointest Endosc Clin N Am 1995;5(1):237–258
duodenal papilla in pancreas divisum as determined by duode-
47. Procacci C, Graziani R, Bicego E, et al. Intraductal mucin-pro-
noscopy using indigo carmine dye and a pH sensor. Am J Gastro-
ducing tumors of the pancreas: imaging findings. Radiology
enterol 1994;89(12):2188–2191
1996;198(1):249–257
23. Warshaw AL, Simeone JF, Schapiro RH, Flavin-Warshaw B. Eval-
uation and treatment of the dominant dorsal duct syndrome
86 3 The Pancreas

48. Imaoka H, Yamao K, Salem AA, et al. Pancreatic endocrine neo- 56. Tjon A Tham RT, Jansen JB, Falke TH, Lamers CB, Lamers CB.
plasm can mimic serous cystadenoma. Int J Gastrointest Cancer Imaging features of somatostatinoma: MR, CT, US, and angio-
2005;35(3):217–220 graphy. J Comput Assist Tomogr 1994;18(3):427–431
49. Minami M, Itai Y, Ohtomo K, Yoshida H, Yoshikawa K, Iio M. 57. Tjon A Tham RT, Jansen JB, Falke TH, et al. MR, CT, and ultrasound
Cystic neoplasms of the pancreas: comparison of MR imaging findings of metastatic vipoma in pancreas. J Comput Assist
with CT. Radiology 1989;171(1):53–56 Tomogr 1989;13(1):142–144
50. Fuhrman GM, Charnsangavej C, Abbruzzese JL, et al. Thin-sec- 58. Chung YS, Ho JJ, Kim YS, et al. The detection of human pancreatic
tion contrast-enhanced computed tomography accurately pre- cancer-associated antigen in the serum of cancer patients. Can-
dicts the resectability of malignant pancreatic neoplasms. Am J cer 1987;60(7):1636–1643
Surg 1994;167(1):104–111, discussion 111–113 59. Sittek H, Heuck AF, Fölsing C, Gieseke J, Reiser M. [Static and
51. Klöppel G, Heitz PU. Pancreatic endocrine tumors. Pathol Res dynamic MR tomography of the pancreas: contrast media ki-
Pract 1988;183(2):155–168 netics of the normal pancreatic parenchyma in pancreatic car-
52. Liessi G, Pasquali C, D’Andrea AA, Scandellari C, Pedrazzoli S. cinoma and chronic pancreatitis]. Rofo 1995;162(5):396–403
MRI in insulinomas: preliminary findings. Eur J Radiol 60. Ichikawa T, Sou H, Araki T, et al. Duct-penetrating sign at MRCP:
1992;14(1):46–51 usefulness for differentiating inflammatory pancreatic mass
53. Semelka RC, Cumming MJ, Shoenut JP, et al. Islet cell tumors: from pancreatic carcinomas. Radiology 2001;221(1):107–116
comparison of dynamic contrast-enhanced CT and MR imaging 61. Luetmer PH, Stephens DH, Fischer AP. Obliteration of periarte-
with dynamic gadolinium enhancement and fat suppression. rial retropancreatic fat on CT in pancreatitis: an exception to the
Radiology 1993;186(3):799–802 rule. AJR Am J Roentgenol 1989;153(1):63–64
54. Tjon A Tham RT, Falke TH, Jansen JB, Lamers CB, Lamers CB. CT 62. Klöppel G, Maillet B. Pseudocysts in chronic pancreatitis: a
and MR imaging of advanced Zollinger-Ellison syndrome. J Com- morphological analysis of 57 resection specimens and 9 autopsy
put Assist Tomogr 1989;13(5):821–828 pancreata. Pancreas 1991;6(3):266–274
55. Kier R, Kinder B. Insulinomas: MR imaging with STIR sequences
and motion suppression. [letter] AJR Am J Roentgenol 1992;
158(2):457–458
87

4 The Spleen
M. Laniado and F. Dammann

with the alignment light of the scanner centered at the


Introduction
level of the xiphoid process.

The spleen is a lymphatic organ that can be regarded as a


large lymph node integrated into the blood circulatory Imaging Planes
system. At the same time, with its special vascular archi-
tecture, the spleen also affects the nonlymphatic cells in The axial plane is the backbone of a dedicated examina-
the blood. As a functionally complex organ, the spleen tion of the spleen (Fig. 4.1). Additional coronal imaging is
thus has a central, though not vital, role in adult life, which helpful if the patient’s breath-hold capacity and the MR
is why many disease processes involve the spleen, while equipment allow acquisition of good-quality images dur-
primary splenic disease is fairly uncommon.1,2 ing breath-hold (Fig. 4.2). The spleen is imaged with a
slice thickness of 6–8 mm and an interslice gap of 2 mm.

Indications
Pulse Sequences

There are no established indications for MRI of the spleen The basic protocol consists of unenhanced T1w and T2w
because ultrasound and CT allow excellent diagnostic sequences. T1w images are acquired with an SE or TSE
evaluation of this organ. Relative indications for MRI exist sequence but preferably with a 2D GRE sequence during
in the staging of lymphoproliferative disease (Hodgkin breath-hold. All of these sequences are acquired with the
and non-Hodgkin lymphoma) and characterization of fo- shortest possible TE to optimize image contrast. Unen-
cal splenic lesions. MRI is also a suitable imaging modality hanced T2w imaging is performed with a breath-hold
for planning infradiaphragmatic radiotherapy in patients single-shot TSE sequence (e. g., HASTE). Because these
with lymphoproliferative disease as coronal sequences 2D sequences have short acquisition times, basic imaging
give an excellent overview of the vascular anatomy in in the axial plane can be supplemented by a coronal
the splenic hilum. Another relative indication is the sequence, or even sagittal images if needed, with only a
follow-up of posttraumatic splenic hematoma in pediatric minimum of additional time. A free-breathing TSE se-
patients with inconclusive sonographic findings after quence with fat suppression (e. g., inversion recovery
nonsurgical treatment. technique, spectral fat saturation) may improve image
quality but takes longer to acquire. The image quality of
free-breathing T2w sequences can be improved by using
respiratory gating (respiratory bellows, navigator echo
Imaging Technique
technique), which will markedly reduce motion artifacts.
(Tables 4.1 and 4.2).
Before the examination, the patient is given a general
explanation of the procedure (e. g., duration of breath-
holds) including information about placement of an intra- Contrast Media
venous line for contrast injection—either Gd-based ex-
tracellular contrast medium or SPIO particles (superpara- Intravenous bolus injection of extracellular Gd-based con-
magnetic iron oxide)—and the need for administering an trast medium (e. g., Magnevist, Dotarem) with dynamic
antispasmodic drug (e. g., butylscopolamine or glucagon). acquisition of serial contrast-enhanced T1w images is
Oral contrast is not required for MRI examinations of the recommended to detect and characterize focal lesions in
spleen. Coil selection depends on the equipment available the spleen. The dynamic images are acquired with a GRE
(e. g., torso or body phased-array coil). Scanning is per- sequence during breath-holds before and 15 s, 45 s, 90 s,
formed with the splenic hilum in the isocenter of the and ca. 3 min after injection of the contrast medium at a
magnet. To this end, the patient is positioned supine dose of 0.1 mmol Gd per kg body weight. Immediate
88 4 The Spleen

a b

c d

e f

Fig. 4.1a–f Normal MR appearance of the spleen at 0.2 T (a, b) and hyperintense on T2w image (FSE 2000/128; turbo factor, 23) (d).
1.5 T (c–f). a, b At 0.2 T, the spleen has lower SI than the liver on e On T2w HASTE image, the SI difference between spleen and liver is
T1w image (SE 450/15) (a), while it is hyperintense on T2w image less pronounced (HASTE ∞/90). f On fat-suppressed T2w image, the
(FSE 3000/102; turbo factor, 13) (b). A solid tumor of low SI is seen spleen has markedly higher SI than the liver (FSE 2000/128; turbo
in the upper pole of the right kidney. c, d At 1.5 T, the spleen is again factor, 23).
hypointense to the liver on T1w image (GRE 126/5;75°) (c) and
Imaging Technique 89

Fig. 4.2 Coronal T2w image acquired with HASTE sequence at 1.0 T
(HASTE ∞/43). Using this technique, the normal spleen is nearly
isointense to liver. Bowel is seen in the splenic hilum.

Table 4.1 Recommended pulse sequences and imaging parameters for MRI of the spleen

Weighting Sequence type TR TE Flip ETL FS No. of No. Scan Breath-


(ms) (ms) (°) slices of ac- time hold
quisi-
tions
T1 Unenhanced GRE (e. g., FLASH) 127–199 4.1 75–90 – No/(yes) 15–23 1 15–23 s Yes
and dynamic
Gd-enhanced
T1 Alternative SE 600 15 – – No 19 3 5–8 min No
(unenhanced) (16–20)
T2 Single-shot TSE 87 180 No < 20 1 < 20 s Yes
(e. g., HASTE)
T2 Alternative TSE (or FSE) 2000– 128 – 15–28 No + yes 6 (3–8) 1 12–28 min Yes
2500
T2 Alternative FSE (or TSE); may ca. 3500 90 – 3–7 No 19 2 6–9 min No
be performed (16–20)
with respiratory
gating (belt or
navigator echo)
T2 Alternative IR (e. g., TIRM, ca. 3500 60–90 – 5–9 Yes 19 2 6–9 min No
STIR) (16–20)
PD TSE double-echo > 3500 22, 90 – 3–7 No 19 2 6–9 min No
(16–20)
T1 Dynamic 3D GRE 5.2 2.5 10 – Yes 64 1 23 s Yes
Gd-enhanced (e. g., VIBE)
T2* GRE 141 18 30 – No 6 (3–8) 1 16 Yes
(e. g., FLASH) (77–196) (16–23) s

Use of a torso or body phased-array coil is recommended; matrix, 192 × 256; FOV, 300–400 mm; rectangular FOV, 75 %; slice thickness,
5–8 mm; distance factor, 0.2–0.3; planes – axial, coronal (optionally), sagittal (rarely).
Note: All recommendations for imaging at 1.0–1.5 T.
The suggested parameters are only examples and have to be adjusted for use on different brands of scanners. Parallel imaging techniques
can be used to shorten scan time but may come with a penalty in SNR.

postcontrast T1w GRE images allow sensitive detection of acquired with a 3D GRE sequence (e. g., VIBE), which has
focal splenic lesions3,4 (Fig. 4.3). Additional late postcon- higher spatial resolution and produces an angiographic
trast images should be acquired after ca. 6–10 min using a effect while slightly reducing soft tissue contrast.
fat-suppressed SE or TSE sequence or fat-suppressed GRE Instead of an extracellular Gd-based contrast medium,
sequence. Alternatively, the dynamic T1w series can be an SPIO preparation can be infused or injected. Examples
90 4 The Spleen

a b

Fig. 4.3a–c Splenic lesion in a 28-year-old man on chemotherapy


for Hodgkin disease. Unenhanced and dynamic postcontrast images
obtained immediately and 5 min after injection of Gd-based con-
trast medium (0.1 mmol/kg Gd). a Unenhanced T1w image does
not allow reliable differentiation of the splenic lesion. b Early post-
contrast image clearly reveals the lesion within the inhomogene-
ously enhancing normal spleen. c Lesion conspicuity is reduced
again on 5-min postcontrast image (1.0 T; GRE 64/5;70°).

Table 4.2 Recommended sequence protocol for MRI of the spleen

Sequence Plane Breath-hold Indication


a) T1w GRE Axial Yes Basic protocol
b) T2w HASTE Axial Yes Basic protocol
c) T2w TSE -/+ fat suppression, may be Axial No Basic protocol; improves image quality
performed with respiratory gating compared with (b)
Optional T1w GRE with dynamic Gd-enhanced Axial Yes (Suspected) focal lesion
series with delayed images
Optional T1w SE or TSE Axial No If (a) not possible
Optional TIRM Axial No If (c) not possible
d) Post-Gd T1w GRE Axial Yes Basic protocol
Optional Post-Gd T1w GRE + fat Axial Yes For example in patients with extrasplenic
saturation disease extension or suspected pathology of
surrounding structures
Optional Post-SPIO Axial No Improved characterization of focal and dif-
T2w HASTE, TSE fuse changes

Note: Axial images can be replaced or supplemented by other planes (primarily coronal) depending on the anatomic situation.

of commercially available SPIO preparations are Endorem istration. The pre- and postcontrast PD images are ideally
and Resovist (Europe) and Feridex (e. g., USA), which are acquired with a double-echo TSE sequence, producing a
approved for liver imaging and can therefore be used in T2w image with the second echo.
patients whose spleen is imaged as part of an MRI exami-
nation of the liver (see Chapter 1, Contrast Media, p. 8 ff.).
In this case, the precontrast protocol is supplemented by a
proton density (PD) sequence.5,6 Identical T2w, PD, and
T1w sequences are obtained before and after SPIO admin-
MRI Appearance of Normal Anatomy 91

of similar signal intensity when fast T2w techniques are


MRI Appearance of Normal Anatomy
used (Fig. 4.4). After bolus injection of Gd-based contrast
medium, the spleen shows early heterogeneous enhance-
The spleen has longer T1 and T2 relaxation times than the ment (arciform, mottled, or peripheral) and within a few
liver, resulting in lower signal intensity on T1w images minutes becomes uniformly hyperintense 4,9–12 (Fig. 4.5).
and higher signal intensity on T2w images compared with Occasionally, there may be immediate uniform enhance-
the liver7,8 (see Fig. 4.1). However, the two organs may be ment.4,10 Following SPIO injection, ca. 10 % of the dose

a b
Fig. 4.4a, b Effects of imaging parameters on T2 contrast illustrated is of high SI similar to that of the liver metastasis. b On breath-hold
in a 53-year-old woman with central liver metastasis (segments III/ image (FSE 2500/138; turbo factor, 29), the spleen and liver are
IVa) and subcapsular liver cyst (segment IVa) but normal spleen (1.0 isointense.
T). a On T2w FSE image (TR/TE 3000/90; turbo factor, 5), the spleen

a b

Fig. 4.5a–c Normal dynamic contrast-enhanced MRI of the spleen


in a 63-year-old man with portal vein thrombosis (1.0 T). a Shadow-
ing in the unenhanced T1w image is due to the use of a phased-array
body coil. b Immediately after bolus injection of Gd-based contrast
medium (0.1 mmol/kg Gd), there is arciform enhancement of the
spleen. c Uniform enhancement of the spleen after 1 min (GRE 106/
5;70°).

c
92 4 The Spleen

a b

c d

e f
Fig. 4.6a–f Normal spleen before (a–c) and after (d–f) administra- contrast PD (d) and T2w (e) images, there is marked signal reduc-
tion of SPIO contrast medium (Resovist, 8 µmol/kg Fe) in a 45-year- tion of the spleen and liver (70 min after SPIO). f Postcontrast T1w
old woman with focal nodular hyperplasia in liver segment VII image obtained with identical window/center settings shows mark-
(1.0 T). a–c On precontrast PD image (SE 2500/45) (a) and T2w edly reduced SI in the liver and slightly decreased SI in the spleen.
image (SE 2500/90) (b), the spleen is hyperintense to the liver while
on T1w image (c) it is hypointense (GRE 150/5;70°). d, e On post-

reaches the spleen, resulting in a marked signal decrease The neonatal spleen is isointense or slightly hypo-
on PD and T2w images.5 On SPIO-enhanced T1w GRE intense relative to the liver on T2w images in the first
images, the spleen is slightly hypointense or hyperintense week of life and then gradually becomes hyperintense
compared with precontrast images (Fig. 4.6). until 8 months of age. On T1w images, the spleen is iso-
intense or slightly hypointense to the liver during the first
2 weeks of life, only later becoming more markedly hypo-
intense.13
MRI Appearance of Pathologic Entities 93

MRI Appearance of Pathologic Entities contrast administration14 (Fig. 4.7). Only intracystic septa,
which are common in hydatid cysts, may increase in
signal intensity on postcontrast images.15 Calcifications
Benign Tumors can occur in hydatid, posttraumatic, and epidermoid cysts
and are characterized by uniform low signal intensity on
The two most common benign tumors of the spleen are all pulse sequences. When the cyst fluid has a high cell or
cysts and hemangiomas. Less common are lymphangio- protein content or contains blood, signal intensity is
mas, hamartomas, and inflammatory pseudotumors. Note higher on T1w images (Fig. 4.8), which may help differ-
that MR data on these entities are still limited because entiate secondary from primary cysts.
only case reports have been published on the MR appear- While common in the liver, hemangiomas are very rare
ances of most of the benign splenic lesions presented in the spleen but constitute the majority of primary
below. splenic tumors. The most common type in the spleen is
Most splenic cysts are pseudocysts secondary to trauma cavernous hemangioma, which often has cystic spaces
or splenic infarction (80 % of all splenic cysts), epidermoid containing serous or hemorrhagic fluid.16 Capillary he-
cysts (true congenital cysts with an epithelial lining), and mangioma of the spleen is rare. Spontaneous splenic rup-
hydatid (echinococcal) cysts (splenic echinococcosis ture occurs in up to 25 % of patients. If the entire splenic
< 2 %). In rare cases, splenic pseudocysts may arise in parenchyma is replaced by multiple hemangiomas, the
patients with pancreatitis. Cysts appear as well-defined condition is referred to as hemangiomatosis and may be
lesions with low signal intensity on T1w images and high a sign of generalized angiomatosis (Klippel–Trenaunay–
signal intensity on T2w images and do not enhance after Weber syndrome). Hemangiomas are characterized by

a b

c d
Fig. 4.7a–f Epidermoid cyst in a 34-year-old woman (1.5 T). a, b On 5000/108). e, f There is no signal enhancement of the cyst after
T1w images, the cyst has lower SI than the spleen (GRE 126/5;75°). injection of Gd-based contrast medium (0.1 mmol/kg Gd; GRE 126/
c On the breath-hold T2w image, the cyst is seen as a well circum- 5;75°). Note wraparound artifacts in c and f.
scribed lesion of uniform high SI (FSE 2500/138; turbo factor, 23). Fig. 4.7e, f e
d The cyst is even more conspicuous on fat-suppressed image (FSE
94 4 The Spleen

e f
Fig. 4.7e, f

a b

c d
Fig. 4.8a–e Splenic cyst after septic embolism in a 62-year-old show inhomogeneities within the cyst, probably due to cell debris.
woman (1.0 T). a On unenhanced T1w image, the cyst has higher The low SI of the spleen on PD and T2w images suggests iron
SI than the spleen (GRE 112/5;70°). b–d PD (SE 3000/22) (b) and storage in the MPS.
T2w images (SE 3000/90; FSE 2500/128; turbo factor, 15) (c, d) Fig. 4.8e e
MRI Appearance of Pathologic Entities 95

Fig. 4.8 e There is no enhancement of the cyst after injection of Gd-


based contrast medium (0.1 mmol/kg Gd; GRE 112/5;70°).

a b

c d
Fig. 4.9a–d Hemangiomas in the spleen of a 59-year-old man not visible on the unenhanced T1w image (SE 600/15). d Delayed
(1.5 T). a, b Three hyperintense lesions are revealed on PD image image after injection of Gd-based contrast medium shows intense,
(SE 2500/15) (a) and T2w image (SE 2500/90) (b). c The lesions are uniform enhancement of the hemangiomas (SE 600/15).

uniform high signal intensity on T2w images and typically dynamic images acquired after injection of extracellular
have smooth margins17–19 (Fig. 4.9). An inhomogeneous Gd-based contrast medium, hemangiomas characteristi-
appearance suggests the presence of cystic and solid com- cally show peripheral enhancement with progression to
ponents (e. g., hemangiomatosis) or infarction within a uniform enhancement, resulting in hyperintensity rela-
large hemangioma17,19,20 (Fig. 4.10). On T1w images, tive to the spleen on late images (Fig. 4.9).20 Other en-
they have the same or lower signal intensity compared hancement patterns are immediate and persistent homo-
with the spleen but may be hyperintense in the presence geneous enhancement and initial peripheral enhance-
of intralesional hemorrhage.20–22 On contrast-enhanced ment with centripetal progression but persistent nonen-
96 4 The Spleen

a b

Fig. 4.10a–c Splenic hemangiomatosis in a 63-year-old woman


(1.5 T). a T2w image shows an inhomogeneous spleen with both
hypointense and hyperintense lesions. The sediment-fluid level in
one of the two hyperintense lesions in the posterior aspect of the
spleen is due to sedimentation after hemorrhage (SE 2100/90).
b Only the hyperintense hemorrhagic lesion is seen on unenhanced
T1w image (SE 600/15). c Delayed image obtained after injection
of Gd-based contrast medium (0.1 mmol/kg Gd) reveals multiple
lesions in the spleen (SE 600/15).

hancement of the center on delayed images, consistent mas are rather small, but larger ones can occur and may be
with a central fibrous scar. Mixed high and low signal associated with hypersplenism. Splenic hamartomas are
intensity is seen in hemangiomatosis19,23 (Fig. 4.10) and isointense on T1w images and usually markedly hyper-
littoral cell angioma, an extremely rare vascular tumor of intense on T2w images. Their appearance is heterogene-
the spleen24,25 (Fig. 4.11). ous, and they may contain areas of fibrosis and calcifica-
Lymphangiomas of the spleen resemble hemangiomas tion, which are hypointense on T2w images.27 On post-
in that they also have epithelium-lined spaces, which, contrast images following administration of Gd-based
however, contain lymph fluid rather than blood.16 Capil- contrast medium, hamartomas are characterized by slow
lary, cavernous, and cystic lymphangiomas are distin- enhancement with a clear signal increase on more de-
guished.26 Splenic lymphangiomas are single or multiple layed images, which may be inhomogeneous.18,20
(lymphangiomatosis) and can occur alone or in associa- Inflammatory pseudotumor is another very rare splenic
tion with hemangiomas and lymphangiomas in other or- mass. Histologically, the tumor is composed of a fibroblas-
gans, so-called systemic cystic angiomatosis, which is a tic stroma and contains inflammatory cells. Its MR signal
progressive condition with a poor prognosis. Lymphan- pattern is not uniform. Inflammatory pseudotumor has
giomas have the same MR appearance as proteinaceous been reported to be isointense to the spleen on T1w
cysts.16 images and heterogeneously hypointense on T2w images
Hamartomas are very rare benign splenic tumors that with delayed enhancement after contrast administra-
are composed of an anomalous mixture of normal red tion.28 However, the tumor may also show early, intense
pulp elements with or without pulp cells. Most hamarto- enhancement (Fig. 4.12).
MRI Appearance of Pathologic Entities 97

a b

c d

e f
Fig. 4.11a–f Littoral cell angioma in a 51-year-old woman (1.0 T). based contrast medium (0.1 mmol/kg Gd) depicts numerous hypo-
a, b T2w images show multiple focal lesions of high SI in the spleen intense lesions (GRE 63/5;70°). e The lesions are poorly demarcated
(FSE 2500/128; turbo factor, 32). c Only some of the lesions are seen from the surrounding spleen ca. 2 min after contrast injection (GRE
as hypointense foci on unenhanced T1w image (GRE 112/5;70°). 63/5;70°). f On 10-min postcontrast image, the lesions are hyper-
d Immediate postcontrast image obtained after injection of Gd- intense to the spleen (GRE 112/5;70°).
98 4 The Spleen

a b

c d
Fig. 4.12a–e Inflammatory pseudotumor in a 72-year-old woman (0.1 mmol/kg Gd), there is intense enhancement of the tumor
(1.5 T). a T1w image shows the tumor with slightly lower SI than the (GRE 127/4;80°). d The tumor becomes isointense to the spleen
spleen (GRE 127/4;80°). b On T2w image, the tumor is slightly within 1 min (GRE 127/4;80°).
hyperintense and inhomogeneous (TrueFISP 4/2;80°). c Immedi- Fig. 4.12e e
ately after bolus injection of Gd-based contrast medium
MRI Appearance of Pathologic Entities 99

Malignant Tumors

Lymphoma is the most common malignancy of the spleen.


When first diagnosed with the disease, 23–34 % of patients
with Hodgkin lymphoma and 30–40 % of those with non-
Hodgkin lymphoma have splenic involvement. Splenic
lymphoma can manifest as diffuse involvement without
circumscribed masses, small focal lesions (< 2 cm), or large
tumor nodes. If there is necrosis, cystic components will be
present. Rare primary splenic lymphoma without nodular
manifestation (accounting for 1 % of non-Hodgkin lympho-
mas, more common in AIDS-associated lymphoma) can
extend through the capsule and infiltrate adjacent organs.
Diffuse infiltration of the spleen and lesions < 1 cm
(45–70 % of cases) are difficult to detect by MRI and may
only be suggested by splenomegaly. However, absence of
the signal loss normally observed after SPIO administra-
tion has been reported to be a sensitive predictor of
diffuse splenic lymphoma.6 Alternatively, diffuse involve-
e
ment can be identified as patchy enhancement of the
Fig. 4.12 e The pseudotumor remains isointense on delayed image spleen on dynamic MRI after administration of extracel-
with fat saturation (GRE 86/4;60°). There are two small cysts in the
lular Gd-based contrast medium4 (Fig. 4.13). Even some
left kidney.
larger focal lesions may be difficult to detect with unen-

a b

Fig. 4.13a–c Micronodular non-Hodgkin lymphoma of the spleen in


a 58-year-old woman (1.5 T). a T1w image reveals splenomegaly and
a lymphoma in the splenic hilum (GRE 105/5;75°). b T2w image
depicts multiple small lesions that are slightly hypointense (FSE
3800/90; turbo factor, 5). c The small nodules are more conspicuous
following injection of Gd-based contrast medium (0.1 mmol/kg Gd)
(GRE 105/5;75°).

c
100 4 The Spleen

a b

Fig. 4.14a–c Focal non-Hodgkin lymphoma of the spleen in a


48-year-old man (1.0 T). a Unenhanced T1w image shows an en-
larged spleen with small foci of low SI (GRE 127/5;70°). b On T2w
image, the lesions also have low SI but more lesions are visible (FSE
2000/138; turbo factor, 29). c Injection of Gd-based contrast me-
dium (0.1 mmol/kg Gd) leads to marked heterogeneous enhance-
ment of the spleen and numerous focal lesions are revealed (GRE
127/5;70°).

hanced sequences because contrast to surrounding spleen mediately after bolus injection of extracellular Gd-based
is minimal due to similar T1 and T2 relaxation times contrast medium. Splenic metastases from melanotic mel-
(Fig. 4.14).8,16,22,29 Such lesions are easier to identify if anoma may be sensitively detected on unenhanced T1w
they contain necrotic areas, which have higher signal images as a result of their high signal intensity. On T2w
intensity than the spleen on T2w images.8 Focal lesions images they may have low signal intensity relative to the
are much more conspicuous on dynamic MR images.4 spleen30 (Fig. 4.16). Hemorrhagic metastases from other
Experience suggests that the use of an SPIO contrast me- primary tumors may have the same signal characteris-
dium will also improve detection of focal splenic lym- tics.31
phoma compared with unenhanced pulse sequences. Angiosarcoma is a very rare splenic neoplasm but con-
Metastases in the spleen are seen in approximately 7 % stitutes the most common nonlymphoid primary tumor of
of patients with metastatic tumors. The most common the spleen. Metastatic spread is typically to the liver, and
primary tumor spreading to the spleen is melanoma patients are at risk of spontaneous splenic rupture. Le-
(50 %); less common are metastases from cancer of the sions are single or multiple and may be made up of cystic
breast, lungs, colon, ovaries, endometrium, and prostate. and solid components. Thorotrast storage has been shown
Splenic metastases have low signal intensity on T1w im- to induce hepatic angiosarcoma but there is no evidence
ages and increased signal intensity on T2w images8 that it also causes splenic angiosarcoma. If intratumoral
(Fig. 4.15). SPIO contrast media improve the detection of hemorrhage is present, angiosarcoma is hypointense to
splenic metastases on PD and T2w images.5 Metastases the spleen on T1w and T2w images.32,33
are also more conspicuous on T1w images obtained im-
MRI Appearance of Pathologic Entities 101

a b

c d
Fig. 4.15a–d Multiple liver metastases and a single splenic metas- factor, 23). c On fat-suppressed T2w image, the splenic metastasis
tasis from breast cancer in a 61-year-old woman (1.0 T). a Unen- is poorly delineated because it has the same high SI as the spleen
hanced T1w image reveals metastases in the liver but not the (FSE 3142/22; turbo factor, 5). d Contrast-enhanced T1w image
metastasis in the low-SI spleen (GRE 127/5;70°). b T2w image obtained 2 min after injection of Gd-based contrast medium
demonstrates both the hyperintense metastases in the liver and (0.1 mmol/kg Gd) clearly reveals the splenic metastasis, while the
the hyperintense metastasis in the spleen (FSE 2500/128; turbo small liver metastases are difficult to see (GRE 127/5;70°).

a b
Fig. 4.16a–c Metastases from melanotic melanoma in the liver and image and are clearly delineated only in the spleen because of its
spleen of a 64-year-old man (1.0 T). a Unenhanced T1w image higher normal SI compared with the liver (FSE 2500/128; turbo
reveals multiple high-SI metastases in the liver and both metastases factor, 23).
in the spleen (GRE 112/5;70°). b The metastases have low SI on T2w Fig. 4.16c e
102 4 The Spleen

Fig. 4.16 c Following injection of Gd-based contrast medium


(0.1mmol/kg Gd), the metastases in the liver and spleen are less
conspicuous but still demarcated from the enhancing surrounding
tissue as slightly hyperintense lesions (GRE 127/5;70°).

Infectious and Noninfectious Conditions Sarcoidosis is a multiorgan granulomatous disease that


can also involve the spleen. In splenic sarcoidosis, the
Histoplasmosis, tuberculosis, and echinococcosis are the spleen has heterogeneous low SI, and/or hypointense le-
most common nonviral infections involving the spleen in sions are seen on T2w images36 (Fig. 4.17).
immunocompetent individuals. Viral infections are most In Niemann–Pick disease, a rare lipidosis due to a con-
commonly caused by Epstein–Barr virus, varicella, and genital enzyme defect with autosomal recessive inheri-
cytomegalovirus and result in splenomegaly. Immuno- tance, there is generalized abnormal accumulation of
compromised patients have an increased risk of splenic sphingomyelin in various organs including the spleen.
infection with Candida albicans, Aspergillus fumigatus, and The lipid deposits cause a slight increase in splenic signal
Cryptococcus neoformans (multiple microabscesses); My- intensity on T1w and T2w images. Localized lesions are
cobacterium tuberculosis (usually in a miliary form); My- characterized by delayed uptake of extracellular Gd-based
cobacterium avium-intracellulare (MAI); and Pneumocystis contrast medium and are markedly hyperintense on T2w
carinii (characterized by early disseminated calcifica- images.37 Focal splenic lesions of variable size and signal
tions). intensity (typically isointense on T1w images and hypo-
There are five mechanisms leading to formation of intense on T2w images) in an enlarged spleen may also be
splenic abscesses: seen in patients with Gaucher disease (19–30 % of cases).
· hematogenous dissemination (e. g., endocarditis, sep-
sis)
· direct spread from adjacent organs (e. g., pancreatitis, Trauma
perinephric abscess)
· superinfection secondary to thromboembolic splenic Injury to the spleen can result from blunt or penetrating
infarction abdominal trauma or be caused iatrogenically (by surgical
· trauma or other medical procedures). Acute hematoma has low
· immunocompromised states. signal intensity on T1w images and high signal intensity
on T2w images and, by day 7, becomes hyperintense on
A pyogenic abscess has variable signal intensity on T1w T1w images as well. At higher field strength (e. g., 1.5 T),
and T2w images. It is hypointense to normal spleen on chronic hematoma is characterized by a low-signal-inten-
T1w images but may also be hyperintense (pus containing sity rim, which is due to hemosiderin deposits and is best
many granulocytes). On contrast-enhanced images, a appreciated on T2w images.38 Calcifications in older hem-
splenic abscess is visualized as an irregular, cystic lesion. atomas have low signal intensity with all sequences. A
Multiple microabscesses due to fungal infection of the posttraumatic pseudocyst has the same signal character-
spleen are seen as rounded lesions with diminished signal istics as cysts of other origin. Splenic hematomas do not
intensity on T1w images and increased signal intensity on enhance.
T2w images.22,34 Even very small abscesses are sensitively
detected by dynamic MRI.34 The fact that small fungal
abscesses are clearly visualized even in patients with
storage of excess iron in the mononuclear phagocyte sys-
tem (MPS) of the spleen35 indicates that administration of
SPIO contrast medium will improve the detection of mi-
croabscesses by MRI.
MRI Appearance of Pathologic Entities 103

a b

c d
Fig. 4.17a–d Sarcoidosis involving the spleen in a 44-year-old are even more conspicuous on the fat-suppressed image (FSE 2000/
woman (1.0 T). a Unenhanced T1w image depicts the spleen with 128; turbo factor, 23). d Marked enhancement of the splenic gran-
uniform, low SI (GRE 139/7;70°). b T2w image reveals hypointense ulomas 3 min after injection of Gd-based contrast medium
lesions in the spleen (FSE 2000/128; turbo factor, 23). c The lesions (0.1 mmol/kg Gd) (GRE 139/7;70°).

Splenic Infarction histiocytosis), hematologic disorders (e. g., polycythemia


vera, myelofibrosis, leukemia), inflammatory conditions
Splenic infarction is most commonly caused by throm- (e. g., infectious mononucleosis), and neoplastic disease
boembolism in patients with endocarditis, atrial fibrilla- (e. g., lymphoma, leukemia). Some causes of splenomegaly
tion, or left ventricular thrombus (ischemic infarction). can be diagnosed by MRI (e. g., portal hypertension with
Venous infarction can occur as a result of thrombosis in fundal varices). In most cases, however, the underlying
the splenic sinusoids due to reduced blood flow in mas- condition is suggested by the clinical findings (Fig. 4.20).
sive splenomegaly. Complications of splenic infarction are A very small spleen is seen in thorotrastosis and the
subcapsular hematoma, splenic rupture, and superinfec- end stage of splenic atrophy in homozygous sickle cell
tion. The morphologic appearance and signal intensity of anemia (autosplenectomy).22 In patients with sickle cell
splenic infarcts vary with the stage. In acute infarction, the anemia, hemosiderin deposits and calcifications in the
infarcted area is typically wedge-shaped (Fig. 4.18). Sub- spleen result in low signal intensity of the organ on T1w
acute infarcts may be seen as cystlike lesions (Fig. 4.19), and T2w images.7 Low signal intensity on all pulse se-
while the presence of fibrosis determines the MR appear- quences is also seen when there is extensive fibrosis in
ance in chronic infarction.16,22 thorotrastosis.
Splenic Iron Deposition. The two most common causes of
iron storage in the spleen are acute sequestration of red
Diffuse Disease blood cells in the spleen, e. g., in patients having received
multiple transfusions (extravascular hemolysis), and por-
Splenomegaly. Many conditions can cause enlargement of tal hypertension. A less common cause is rhabdomyolysis.
the spleen. These include venous outflow obstruction In the setting of rhabdomyolysis and extravascular hemol-
(e. g., portal hypertension, splenic vein occlusion or throm- ysis, there is diffuse iron deposition in the MPS of the
bosis), infiltrative conditions (e. g., Gaucher disease, spleen, while portal hypertension is associated with focal
104 4 The Spleen

a b
Fig. 4.18a, b Acute splenic infarction in a 37-year-old man (1.0 T). Gd), the lesions are seen as perfusion defects, some of which are
a The lesions in the spleen are not visible on unenhanced T1w image wedge-shaped (GRE 128/5;70°).
(GRE 128/5;70°). b On contrast-enhanced T1w image (0.1 mmol/kg

a b

c d
Fig. 4.19a–d Splenic infarction with hemorrhage in a 6-year-old boy 3000/22) (b) and T2w (SE 3000/90) (c) images, the infarcted area
with cirrhosis and splenomegaly (1.0 T). a Unenhanced T1w image has markedly increased SI. The presumed hemorrhagic rim has low
shows a slightly hyperintense, arciform area in the enlarged spleen, SI, consistent with hemosiderin deposits. d There is no enhance-
which likely corresponds to a hemorrhagic rim. There is hypointense ment of the infarcted area after injection of Gd-based contrast
ascites in the right paracolic gutter (SE 6000/12). b, c On PD (SE medium (0.1 mmol/kg Gd) (SE 600/12).
MRI Appearance of Pathologic Entities 105

hemosiderin deposition in so-called Gamna–Gandy


bodies, which are made up of thickened collagen bundles.
Congenital (autosomal recessive) and acquired hemo-
chromatosis (e. g., in sideroblastic anemia) with excess
iron absorption in the intestine is characterized by iron
deposits in hepatocytes, pancreas, endocrine glands, and
heart, while the MPS cells of the liver and spleen are
spared. Paroxysmal nocturnal hemoglobinuria (intravas-
cular hemolysis) is another condition in which excess iron
is stored in other organs (liver, kidneys) but not in the
spleen. When excess iron is stored in the MPS, the spleen
has the same MR signal characteristics as after adminis-
tration of SPIO-based contrast medium (Fig. 4.21). The
resulting diffuse signal reduction is most sensitively de-
tected using PD and T2*w GRE sequences.7,37 Large

Fig. 4.20 Marked splenomegaly in a 41-year-old man with cirrhosis w


(1.0 T; coronal plane; GRE 128/5;70°).

a b

c d
Fig. 4.21a–d Iron storage in the MPS of the spleen in a 23-year-old image shows not only hypointensity of the spleen but also reduced
man with autoimmune hemolysis (1.5 T). a On unenhanced T1w SI of the liver (GRE 96/18;30°). d Postcontrast image after injection
image, the spleen is markedly hypointense relative to the liver (GRE of Gd-based contrast medium (0.1 mmol/kg Gd) with fat saturation
75/5;72°). b The hypointensity of the spleen is even more pro- reveals only little enhancement of the spleen (GRE 73/5;60°).
nounced on T2w image (FSE 3000/138; turbo factor, 28). c T2*w
106 4 The Spleen

a b

Fig. 4.22a–c Normal SI of the spleen and hypointensity of the liver


due to iron accumulation in hepatocytes in a 76-year-old man with
hemochromatosis and cirrhosis, hepatocellular carcinoma (not
shown), and splenomegaly (0.2 T). a T1w image demonstrates
abnormally low SI of the liver and isointensity of the spleen (SE
520/15). b, c On PD image (FSE 3500/26; turbo factor, 5) (b) and
T2w image (FSE 3500/106; turbo factor, 5) (c), the enlarged spleen
has normal high SI, while liver SI is reduced. The hypointensity to the
left of the spleen represents the hypertrophic left hepatic lobe.

amounts of iron also cause signal voids on T1w GRE im- References
ages. In patients with hemochromatosis, the signal inten-
1. Dachman AH, Friedman AC. Radiology of the Spleen. St. Louis:
sity is reduced in the cirrhotic liver, while the spleen may Mosby; 1993
be enlarged but has normal signal intensity (Fig. 4.22). 2. Semelka RC, Shoenut JP. The spleen. In: Semelka RC, JP Shoenut.
Gamna–Gandy bodies, or siderotic nodules, are typi- MRI of the Abdomen with CT Correlation. New York: Raven
Press; 1993: pp. 53–58
cally diffusely distributed throughout the spleen. The nod- 3. Mirowitz SA, Brown JJ, Lee JK, Heiken JP. Dynamic gadolinium-
ules are small, with a diameter of a few millimeters. They enhanced MR imaging of the spleen: normal enhancement
are most conspicuous as lesions of low signal intensity on patterns and evaluation of splenic lesions. Radiology 1991;
179(3):681–686
GRE images acquired at high field strength.40–42 On T1w
4. Semelka RC, Shoenut JP, Lawrence PH, Greenberg HM, Madden
images, the lesions are more conspicuous after adminis- TP, Kroeker MA. Spleen: dynamic enhancement patterns on
tration of Gd-based contrast medium.40 When SPIO par- gradient-echo MR images enhanced with gadopentetate dime-
glumine. Radiology 1992;185(2):479–482
ticles are used, the nodules become isointense to the
5. Weissleder R, Hahn PF, Stark DD, et al. Superparamagnetic iron
spleen or remain visible (Fig. 4.23). Gamna–Gandy bodies oxide: enhanced detection of focal splenic tumors with MR
are most commonly caused by portal hypertension and imaging. Radiology 1988;169(2):399–403
6. Weissleder R, Elizondo G, Stark DD, et al. The diagnosis of
portal or splenic vein thrombosis or are idiopathic. Rarely,
splenic lymphoma by MR imaging: value of superparamagnetic
they occur in the setting of hemolytic anemia, leukemia, iron oxide. AJR Am J Roentgenol 1989;152(1):175–180
and lymphoma. 7. Adler DD, Glazer GM, Aisen AM. MRI of the spleen: normal
appearance and findings in sickle-cell anemia. AJR Am J Roent-
genol 1986;147(4):843–845
8. Hahn PF, Weissleder R, Stark DD, Saini S, Elizondo G, Ferrucci JT.
MR imaging of focal splenic tumors. AJR Am J Roentgenol
1988;150(4):823–827
9. Hamed MM, Hamm B, Ibrahim ME, Taupitz M, Mahfouz AE.
Dynamic MR imaging of the abdomen with gadopentetate di-
meglumine: normal enhancement patterns of the liver, spleen,
stomach, and pancreas. AJR Am J Roentgenol 1992;158(2):
303–307
MRI Appearance of Pathologic Entities 107

a b

c d
Fig. 4.23a–d Gamna–Gandy bodies in the enlarged spleen of a d T1w image (GRE 150/5;70°) obtained 40 min after injection of
35-year-old man with cirrhosis and hepatocellular carcinoma in SPIO contrast medium (Resovist, 8 µmol/kg Fe) shows improved
the right hepatic lobe (1.0 T). a–c T1w (GRE 150/5;70°) (a), PD lesion conspicuity (arrows).
(SE 2500/45) (b), and T2w (SE 2500/90) (c) images before contrast
administration show multiple hypointense lesions in the spleen.

10. Ito K, Mitchell DG, Honjo K, et al. Gadolinium-enhanced MR 19. Peene P, Wilms G, Stockx L, Rigauts H, Vanhoenacker P, Baert AL.
imaging of the spleen: artifacts and potential pitfalls. AJR Am J Splenic hemangiomatosis: CT and MR features. J Comput Assist
Roentgenol 1996;167(5):1147–1151 Tomogr 1991;15(6):1070–1072
11. Ito K, Mitchell DG, Honjo K, et al. MR imaging of acquired 20. Ramani M, Reinhold C, Semelka RC, et al. Splenic hemangiomas
abnormalities of the spleen. AJR Am J Roentgenol 1997;168(3): and hamartomas: MR imaging characteristics of 28 lesions.
697–702 Radiology 1997;202(1):166–172
12. Mirowitz SA, Gutierrez E, Lee JK, Brown JJ, Heiken JP. Normal 21. Harris RD, Simpson W. MRI of splenic hemangioma associated
abdominal enhancement patterns with dynamic gadolinium- with thrombocytopenia. Gastrointest Radiol 1989;14(4):
enhanced MR imaging. Radiology 1991;180(3):637–640 308–310
13. Donnelly LF, Emery KH, Bove KE, Bissett GSIII. Normal changes 22. Rabushka LS, Kawashima A, Fishman EK. Imaging of the spleen:
in the MR appearance of the spleen during early childhood. AJR CT with supplemental MR examination. Radiographics 1994;
Am J Roentgenol 1996;166(3):635–639 14(2):307–332
14. Shirkhoda A, Freeman J, Armin AR, Cacciarelli AA, Morden R. 23. Teufl F, Duda SH, Horny HP, Xiac JC, Busch FW, Schareck W.
Imaging features of splenic epidermoid cyst with pathologic Hämangiomatose der Milz. Erscheinungsbild in der Magnet-
correlation. Abdom Imaging 1995;20(5):449–451 resonanztomographie. Radiol Diagn (Berl) 1992;33:193–196
15. von Sinner WN, Stridbeck H. Hydatid disease of the spleen. 24. Oliver-Goldaracena JM, Blanco A, Miralles M, Martin-Gonzalez
Ultrasonography, CT and MR imaging. Acta Radiol 1992;33(5): MA. Littoral cell angioma of the spleen: US and MR imaging
459–461 findings. Abdom Imaging 1998;23(6):636–639
16. Urrutia M, Mergo PJ, Ros LH, Torres GM, Ros PR. Cystic masses of 25. Schülen V, Horny P, Busch F-W. Two cases of vascular tumors of
the spleen: radiologic-pathologic correlation. Radiographics the spleen; imaging results with pathologic correlation. Ra-
1996;16(1):107–129 diologie 1994;14:61–62
17. Disler DG, Chew FS. Splenic hemangioma. AJR Am J Roentgenol 26. Ito K, Murata T, Nakanishi T. Cystic lymphangioma of the spleen:
1991;157(1):44 MR findings with pathologic correlation. Abdom Imaging
18. Ohtomo K, Fukuda H, Mori K, Minami M, Itai Y, Inoue Y. CT and 1995;20(1):82–84
MR appearances of splenic hamartoma. J Comput Assist Tomogr 27. Pinto PO, Avigado P, Garcia H, Alves EC, Marques C. Splenic
1992;16(3):425–428 hamartoma: a case report. Eur Radiol 1995;5:93–95
108 4 The Spleen

28. Irie H, Honda H, Kaneko K, et al. Inflammatory pseudotumors of 36. Kessler A, Mitchell DG, Israel HL, Goldberg BB. Hepatic and
the spleen: CT and MRI findings. J Comput Assist Tomogr splenic sarcoidosis: ultrasound and MR imaging. Abdom Imag-
1996;20(2):244–248 ing 1993;18(2):159–163
29. Hess CF, Griebel J, Schmiedl U, Kurtz B, Koelbel G, Jaehde E. Focal 37. Omarini LPA, Frank-Burkhardt SE, Seemayer TA, Mentha G, Ter-
lesions of the spleen: preliminary results with fast MR imaging rier F. Niemann-Pick disease type C: nodular splenomegaly.
at 1.5 T. J Comput Assist Tomogr 1988;12(4):569–574 Abdom Imaging 1995;20(2):157–160
30. Premkumar A, Sanders L, Marincola F, Feuerstein I, Concepcion 38. Hahn PF, Saini S, Stark DD, Papanicolaou N, Ferrucci JTJr. Intra-
R, Schwartzentruber D. Visceral metastases from melanoma: abdominal hematoma: the concentric-ring sign in MR imaging.
findings on MR imaging. AJR Am J Roentgenol 1992;158(2): AJR Am J Roentgenol 1987;148(1):115–119
293–298 39. Siegelman ES, Mitchell DG, Rubin R, et al. Parenchymal versus
31. Torres GM, Terry NL, Mergo PJ, Ros PR. MR imaging of the spleen. reticuloendothelial iron overload in the liver: distinction with
Magn Reson Imaging Clin N Am 1995;3(1):39–50 MR imaging. Radiology 1991;179(2):361–366
32. Ha HK, Kim HH, Kim BK, Han JK, Choi BI. Primary angiosarcoma 40. Minami M, Itai Y, Ohtomo K, et al. Siderotic nodules in the
of the spleen. CT and MR imaging. Acta Radiol spleen: MR imaging of portal hypertension. Radiology 1989;
1994;35(5):455–458 172(3):681–684
33. Kaneko K, Onitsuka H, Murakami J, et al. MRI of primary spleen 41. Roubidoux MA. MR of the kidneys, liver, and spleen in parox-
angiosarcoma with iron accumulation. J Comput Assist Tomogr ysmal nocturnal hemoglobinuria. Abdom Imaging 1994;19(2):
1992;16(2):298–300 168–173
34. Semelka RC, Shoenut JP, Greenberg HM, Bow EJ. Detection of 42. Sagoh T, Itoh K, Togashi K, et al. Gamna-Gandy bodies of the
acute and treated lesions of hepatosplenic candidiasis: compari- spleen: evaluation with MR imaging. Radiology 1989;172(3):
son of dynamic contrast-enhanced CT and MR imaging. J Magn 685–687
Reson Imaging 1992;2(3):341–345
35. Cho J-S, Kim EE, Varma DGK, Wallace S. MR imaging of hepato-
splenic candidiasis superimposed on hemochromatosis. J Com-
put Assist Tomogr 1990;14(5):774–776
109

5 The Gastrointestinal Tract


W. Luboldt and M. Laniado

Introduction Indications

For many decades, imaging of the gastrointestinal (GI) MR enteroclysis1–6 has been used since 1997 to evaluate
tract was the domain of radiographic procedures, notably and follow up complications of Crohn disease that require
double-contrast techniques. Today, with endoscopy hav- surgery. MR colonography (MRC) is still under investiga-
ing evolved into a serious competitor, even the small tion for colorectal screening7–12 (Table 5.1). MRI is also a
intestine is no longer the undisputed territory of radio- promising modality for diagnosing appendicitis in cases
graphic techniques. New perspectives are also opened up where ultrasound findings are inconclusive and imaging
by the advances made in CT, which offers good visual- does not delay surgery. Finally, MRI enables functional
ization of the bowel wall and provides more diagnostic assessment in esophageal reflux, gastric emptying disor-
information than conventional X-ray examinations and ders, adhesions, pelvic floor hernias, and defecation dis-
endoscopy because it also allows direct evaluation of the orders.
tissues outside the GI tract. MRI, the other major cross-
sectional imaging modality, was of little use for GI imaging
in its early years because of long acquisition times. The Imaging Technique
situation has changed with the development of fast MR
pulse sequences and parallel imaging techniques. Never-
theless, CT is still preferred to MRI for most diagnostic Patient Preparation
applications in the GI tract because it is superior in terms
of speed, resolution, multiplanar image reformation, Fasting for 12 h is sufficient before MRI of the stomach or
imaging of the entire abdomen in a single scan, and ab- small intestine, but active bowel preparation is needed for
sence of artifacts. On the other hand, MRI has the crucial imaging of the colon. Bowel cleansing for MR colonogra-
advantage of not involving ionizing radiation and is there- phy is the same as for colonoscopy: using, for example, a
fore generally preferred in young persons and pregnant polyethylene glycol electrolyte solution (PEG-ES; Golytely,
women, for follow-up examinations, and in dynamic stud- Klean-Prep).13 For adequate cleansing, patients should
ies. With its high intrinsic contrast, MRI has great poten- start drinking the solution at 3 p. m. on the day before
tial for evaluating inflammatory and neoplastic processes the examination and restrict themselves to clear liquids.
of the bowel. The question of whether less strict bowel preparation or
dietary measures alone may be sufficient before intestinal
MRI7 needs to be investigated in further studies. An ad-

Table 5.1 Indications for MRI of the GI tract

Indication (examination) Sequence (planes) Comment


Crohn disease (MR enteroclysis) HASTE, TrueFISP (?), contrast-enhanced VIBE To evaluate complications
(abdomen: coronal; pelvis: axial) (see Table 5.3)
Colorectal screening HASTE, TrueFISP (?), contrast-enhanced VIBE Under investigation
(MR colonography) (abdomen: coronal; pelvis: axial)
Appendicitis HASTE, HASTE-IRM, contrast-enhanced VIBE (?) If clinical findings are unclear and
(identification of the appendix with axial and coronal MRI does not delay surgery
HASTE and HASTE-IRM; if still inconclusive, use additional
focused contrast-enhanced axial VIBE for MPR)

Start VIBE (volume-interpolated breath-hold examination) sequence ca. 40 s after IV administration of spasmolytic and contrast medium
and repeat sequence 2–4 times to have alternative images for interpretation in case of peristalsis artifacts. If peristalsis artifacts are
encountered, reduce scan time by decreasing number of slices and increasing slice thickness.
110 5 The Gastrointestinal Tract

a b c
Fig. 5.1a–c Mechanical ileus due to residual mesenteric lymphoma quence (a). Adjunct TrueFISP sequence (b) acquired in the same
(arrow). a T2w HASTE used as fast and robust screening sequence. plane confirms the obstruction. Postcontrast VIBE sequence (c)
b TrueFISP. c T1w 3D GRE (VIBE) after IV injection of Gd-based yields a high-resolution image of the gastrointestinal wall and differ-
contrast medium. The site of obstruction is revealed indirectly by entiates contrast-enhancing viable tissue from scars and residual
prestenotic dilatation and water-filled bowel on the screening se- stool.

vantage of MRI over unenhanced CT is that evaluation of Spasmolysis


the intestinal wall is not degraded by residues of the
cleansing solution. Unless butylscopolamine is contraindicated, intravenous
spasmolysis with 20 mg of Buscopan is recommended to
maximize bowel distention and minimize peristalsis-
Oral/Rectal Contrast Media related artifacts. The maximum effect of butylscopol-
amine occurs as early as 1 min after intravenous injection
Evaluation of the GI tract is possible only after adequate and persists for only a few minutes. Butylscopolamine
distention (see Fig. 5.2). Although water alone is sufficient should therefore be saved for bolus administration imme-
for distention and delineation of the gastric or intestinal diately before the scan for which effective suppression of
wall, 2.5 % mannitol needs to be added to prevent prema- peristalsis is most important. Imaging should then start
ture osmotic absorption of the water when the small 1 min after bolus injection and should be completed in
bowel is examined. Alternatively, small bowel loops can less than 10 min.
be distended and delineated with PEG-ES, as used for If butylscopolamine is not approved in a country or is
bowel lavage before colonoscopy.6 When PEG-ES is used, contraindicated in a patient (prostatic hyperplasia, nar-
the MRI scans must be timed such that enough of the row angle glaucoma, tachyarrhythmia, myasthenia
solution is retained in the small bowel without inducing gravis), an unenhanced VIBE sequence can be acquired
a desire to defecate. If the contrast solution is adminis- to estimate the extent of peristaltic artifacts. If reduction
tered through a nasojejunal tube (MR enteroclysis), filling of persistaltic artifacts is deemed necessary, the patient
of the small bowel can be evaluated in a dynamic MR should be given 1 mg of glucagon.
study.5 Contrast administration through a nasal tube is
more efficient, but oral intake is also possible, since the
tube cannot be positioned under MRI guidance and some Pulse Sequences
patients refuse intubation.
For MR colonography, a rectal water enema adminis- Abdomen
tered with a bag suspended 1 m above the patient is
theoretically superior to air insufflation because water As abdominal imaging should be performed with breath-
results in better delineation of the bowel wall on HASTE holding, there are basically three sequences that can be
sequences than air (Fig. 5.1) and possibly also better dis- used: HASTE, TrueFISP, and 3D GRE (VIBE) (see Fig. 5.1).
tention (Fig. 5.2). However, as with CT colonography, air The HASTE sequence can also be obtained with the patient
insufflation is more convenient and is preferred as long as breathing freely and is therefore well suited for orienta-
there is no clear evidence of its disadvantages. tion and the initial search for pathology. A TrueFISP se-
quence allows evaluation of vessel patency and differen-
tiation of vessels and lymph nodes. Moreover, it can serve
Imaging Technique 111

a b
Fig. 5.2a, b Pitfall. Coronal T2w HASTE images obtained with in- mimics a tumor, which is shown to be a fold on the image obtained
adequate rectal air insufflation (a) and after adequate air insuffla- after adequate distention (b).
tion (b). With poor colonic distention (a), a nondistended segment

to identify infiltration of adjacent organs by exploiting Imaging Strategy


chemical shift effects that occur at interfaces between
soft tissue and fat. Presence of this effect indicates an Gastrointestinal imaging is performed with the patient in
intact fat plane between two adjacent organs. A VIBE a comfortable supine position using a surface coil com-
sequence should be started ca. 1 min after butylscopol- bined with the coil elements integrated in the table.
amine administration and 40 s after intravenous contrast As with CT, an overview of the abdomen and pelvis
injection (nonspecific Gd-based contrast medium at a should be obtained in the axial plane, for which a HASTE
dose of 0.1 mmol Gd per kg body weight; e. g., Magnevist sequence is used. While coronal imaging is preferred for
or Dotarem). Recommended practice is to repeat the se- further evaluation of the abdominal portion of the GI tract,
quence immediately to have a second data set in case the the pelvic part is primarily imaged in the axial plane.
first one is degraded by motion artifacts. As with CT, the Double angulation along the terminal ileum is helpful in
3D data set can be used for multiplanar reconstruction. In patients with colitis involving this bowel segment. Data
the abdomen, images should be acquired in the coronal sets acquired with a VIBE sequence allow multiplanar
plane for three reasons: reconstruction images to be retrospectively generated in
· It is the most suitable for following the intestine. any desired plane. If peristaltic artifacts are present and it
· Long, continuous segments of the bowel wall can be is not possible to reduce the scan volume, the number of
evaluated. slices can be reduced by increasing the slice thickness
· The regular pattern of opposing haustra in the coronal (1.5–2 mm).
plane facilitates identification of polyps. Since there is not much motion in the pelvic region,
spatial resolution can be improved by acquiring the VIBE
sequence during shallow breathing. Higher resolution im-
Pelvis proves multiplanar reconstruction for image interpreta-
tion; the rectum can then be evaluated on sagittal recon-
Artifacts due to respiratory motion are usually less severe structions instead of performing primary sagittal imaging
in the pelvis, and breath-hold imaging is not necessary in of this region. To maintain adequate SNR, the number of
most instances. The pelvis can therefore be imaged using a acquisitions should also be increased if the slice thickness
TSE or SE sequence with scan times longer than 25 s. STIR is decreased (minimum of 1 mm) and the matrix in-
imaging is the method of choice for evaluating fistulas. creased.
With the improved coils available today, most diagnostic When a VIBE sequence is used, intravenous contrast
questions can be answered using a fast T2w sequence, administration is needed to evaluate the bowel wall (see
which markedly reduces scan time and does not require Fig. 5.1). Timing of postcontrast imaging is not very crit-
contrast administration (see Fig. 5.1). The rectum and ical as signal enhancement of colorectal masses persists
sigmoid colon are best evaluated on axial images. for a few minutes. However, there should be a delay of at
112 5 The Gastrointestinal Tract

least 40 s after the start of contrast administration to berg tumor). TNM staging of gastric cancer is summarized
ensure that the contrast medium has reached the target in Table 5.2.
site when the central k-space lines are sampled. It is good
practice to repeat the VIBE sequence as a dynamic series Gastric Lymphoma. The stomach is the most common site
to have backup images if others are degraded by artifacts. of lymphoma in the GI tract (especially in non-Hodgkin
lymphoma), with gastric lymphoma accounting for 3–5 %
of malignant stomach tumors. While there may be iso-
lated lymphoma of the stomach, concomitant manifesta-
MRI Appearance of Pathologic Entities
tion in other parts of the GI tract is more common. Since
lymphoma is primarily submucosal, it may be difficult to
Stomach diagnose by endoscopy. Gastric lymphoma can directly
infiltrate perigastric fat and adjacent organs, be associated
Adenocarcinoma. Adenocarcinoma is the most common with regional lymphadenopathy, and/or disseminate into
malignant tumor of the stomach. Nearly half of all gastric the peritoneal cavity. Unlike adenocarcinoma, lymphoma
carcinomas occur in the region of the gastroesophageal often involves the entire stomach and may be confined to
junction. Three growth patterns are distinguished: local- the wall, even if the wall is > 4 cm thick.
ized, circular, and diffusely infiltrating (linitis plastica,
“leather bottle” stomach). Thickening of the gastric wall Leiomyosarcoma. This rare tumor accounts for 1–3 % of
may be minimal to very pronounced (> 4 cm) and corre- malignant gastric neoplasms. The primary tumor is usu-
lates with transmural tumor extension. A wall thickness ally large and round to ellipsoid in shape. In contrast to
> 2 cm is highly indicative of extragastric spread. Proximal other gastric tumors, wall thickening may be absent be-
cancer spreads along the gastrosplenic ligament to the left cause the bulk of the tumor is often outside the stomach.
lobe of liver, the diaphragm, and the spleen, while distal Leiomyosarcomas metastasize by contiguous extension to
cancer may invade the pancreas. Lymph node metastases adjacent organs, peritoneal seeding, or hematogenous
occur in perigastric, celiac trunk, hepatoduodenal liga- spread (liver, lungs, bone). Metastasis to perigastric and
ment, retropancreatic, mesenteric root, and para-aortic para-aortic lymph nodes is uncommon.
nodes. Advanced disease is characterized by tumor spread
to the major omentum, peritoneum, and ovaries (Kruken- Gastric Metastasis. The most common primaries are ma-
lignant melanoma, breast cancer, and lung cancer. Gastric
Table 5.2 TNM staging system for gastric cancer metastases from breast cancer occasionally manifest as
diffuse wall thickening, which cannot be differentiated
Invasion level Lymph node meta- Distant
from primary adenocarcinoma. Squamous cell carcinoma
stases metastases
of the distal esophagus involves the cardia in 15 % of cases.
T1 Lamina propria or N1: 1–6 regional M1* Cancer of the transverse colon and pancreas can directly
submucosa lymph nodes
invade the stomach wall along the gastrocolic and gastro-
T2 Muscularis propria or N2: 7–15 regional
splenic ligament, respectively.
subserosa lymph nodes
T3 Serosa (visceral N3: > 15 regional
peritoneum) lymph nodes Leiomyoma. This is the most common benign tumor of the
T4 Adjacent structures stomach and arises in the submucosa. It is usually asymp-
tomatic. Leiomyomas > 5 cm frequently undergo ulcera-
* E.g., liver (45–55 %), lung (6–30 %), peritoneum, ovaries.
tion and hemorrhage. They can then be diagnosed on T1w
images by the presence of high-signal-intensity blood
(between 2 days and 4 weeks) or susceptibility artifacts
produced by iron-containing blood products such as he-
mosiderin. Other conditions that can cause thickening of
the gastric wall are Ménétrier disease (typically of the
fundus and corpus) and Crohn disease (typically of the
antrum).

MRI
The patient is asked to drink as much water as possible
5 min before the examination and is given an intravenous
injection of butylscopolamine to ensure maximum dis-
tention of the stomach. Most gastric cancers are hyper-
intense relative to the stomach wall on T2w images
(Fig. 5.3). However, they may also be isointense, which
Fig. 5.3 Gastric carcinoma. The tumor has high SI (arrow) on T2w is why a contrast-enhanced study is recommended in
TSE image. patients with suspected gastric cancer (Fig. 5.4). Chemical
MRI Appearance of Pathologic Entities 113

shift imaging appears well suited for local cancer staging


(Fig. 5.5). The destructive interaction between fat and
water signals on opposed-phase (OP) images, which are
obtained at specific TEs (2.1 ms or an odd-numbered
multiple at 1.5 T), produces a dark line at the interface
between the gastric wall and surrounding fat. Interruption
of this line on OP images is a fairly reliable indicator of
tumor extension to adjacent organs (Fig. 5.5).

Small Intestine

Tumors of the small intestine are rare, accounting for ca.


6 % of gastrointestinal neoplasms. One-third are found in
the duodenum, and most of the remaining two-thirds are
located in the terminal ileum. The most common benign
tumors of the small intestine are leiomyomas, adenomas, a
and lipomas. Malignant small-bowel tumors include ad-
enocarcinoma, leiomyosarcoma, lymphoma, neurofibro-
sarcoma, carcinoids, gastrointestinal stromal tumors
(GIST), and metastases (e. g., from the lungs, breasts, or
malignant melanomas). Neoplasms of the small intestine
may cause intussusception.

Leiomyoma and Leiosarcoma. These are highly vascular


tumors, which often undergo central necrosis and com-
monly present with profuse bleeding. Since their growth
is eccentric, they typically have an extraluminal compo-
nent. Leiomyomas and leiosarcomas are often difficult to
distinguish on the basis of their imaging appearance.

Adenocarcinoma and Lymphoma. These tumors cause


concentric thickening of the bowel wall. While adenocar-
cinomas have a propensity for the proximal small intes-
tine (50 % occur in the duodenum) and are associated with b
clinical signs of obstruction, lymphomas (20 % of all small-
bowel tumors) are most frequently found in the terminal
ileum with concomitant para-aortic or mesenteric lym-
phomas. Mesenteric lymphomas are common in non-
Hodgkin disease (50 %) and rare in Hodgkin disease
(4 %). Carcinoid is the most common primary tumor of
the small bowel (ileocecal region) and appendix. Regional
lymph node enlargement is associated with stellate re-
traction of the mesentery.

Gastrointestinal Stromal Tumor. A rare entity, gastrointes-


tinal stromal tumor (GIST) arises from the wall of the
small intestine (20–35 %) or stomach (39–70 %). Rarely,
the tumor originates in the large bowel (5–15 %), omen-
tum or mesentery (9 %), or esophagus (< 5 %). GIST was
defined as a new tumor entity in 1998 based on the
expression of a CD117 (c-kit proto-oncogene) receptor
on the cell surface.14 The mutation of this receptor is c
associated with constant activation of tyrosine kinase, Fig. 5.4a–c Gastric cancer. a T2w HASTE. b STIR. c T1w GRE image
which in turn results in uncontrolled cell proliferation after IV injection of Gd-based contrast medium. The tumor shows
low SI on T2w and STIR images (a, b) and marked enhancement on
and protection from apoptosis. The diagnosis of GIST has
the postcontrast image (c).
important therapeutic implications because the tumor
can be effectively treated by selective inhibition of tyro-
114 5 The Gastrointestinal Tract

a b

c d
Fig. 5.5a–d Gastric cancer. a T2w HASTE. b T2w TSE. c T2w HASTE. d OP GRE. The tumor is of low SI on T2w images (arrows in a–c). On the
OP image (d), loss of the fat plane indicates invasion of the pancreas (arrowhead).

sine kinase (imatinib, currently at a dose of 400 mg/day). proximal to the stricture (Fig. 5.7). Extraintestinal mani-
GISTs are typically large, well-circumscribed, and hetero- festations comprise fistula and abscess formation, phleg-
geneous lesions with central necrosis.15 Despite their size mons, lymph node enlargement, and excess mesenteric
and metastatic spread to the liver, GISTs are not associated fat. Currently, the patient’s prognosis and choice of opti-
with obstruction (Fig. 5.6). GISTs have an increased glu- mal therapy are primarily determined on the basis of
cose metabolism, which can be exploited to monitor ther- clinical and laboratory findings, while MRI is used to
apy using 18F-FDG PET/CT. Given the excellent response corroborate indications for surgery (Table 5.3) and localize
rate, tumor size alone appears to be an adequate para- pathology. The role of MRI remains to be defined, either as
meter to monitor the response to therapy. a competing diagnostic tool or a supplementary proce-
dure. Available data suggest that MRI findings appear to
Crohn Disease. Crohn disease is the most important in- correlate with the Crohn Disease Activity Index (CDAI)
flammatory condition of the small intestine. Although the (http://www.ibdjohn.com/cdai/). This index comprises
disease can involve any part of the small bowel, it has a the following items: number of liquid or very soft stools/
propensity for the terminal ileum. There is characteristic week, abdominal pain, general well-being, associated
thickening of the bowel wall involving all layers and re- conditions (arthritis/arthralgia, iritis/uveitis, erythema
sulting in luminal narrowing with or without dilatation nodosum, pyoderma gangrenosum, aphthous stomatitis,
MRI Appearance of Pathologic Entities 115

Fig. 5.6 Mesenteric GIST. The inherent bright blood effect of the TrueFISP sequence permits evaluation of vascular invasion. In the patient
shown, the large tumor encases long segments of the mesenteric vessels. No thrombosis in the portal vein and confluence.

anal fissures, fistulas, abscess, fever), intake of medica- HASTE imaging without fat suppression since inflamma-
tions for diarrhea, hematocrit, and body weight. tory processes are less conspicuous on T2w images when
a bright-lumen contrast medium such as water is used
Other Small-Intestinal Pathology. A much less common rather than a dark-lumen negative contrast medium, and
cause of postinflammatory wall thickening of the small since wall thickness is difficult to evaluate when the wall
bowel is radiation enteritis. Other small-bowel conditions is not outlined by fat. Non-fat-suppressed sequences thus
potentially amenable to assessment by MRI include duo- help identify wall thickening or at least the terminal ileum
denal diverticula, which are typically found on the medial as the preferred site of Crohn disease. Coronal and axial
side of the duodenal C-loop or in the papillary region and contrast-enhanced VIBE sequences can then be acquired
may cause dilatation of the pancreatic and bile ducts. to continue the search or to assess the severity of inflam-
mation (Fig. 5.8). With its better resolution and high con-
MRI trast of the bowel wall after intravenous contrast admin-
The search for an inflammatory process should begin with istration, the T1w VIBE sequence is superior to T2w HASTE
a coronal fat-suppressed HASTE sequence (Fig. 5.8). This and TrueFISP sequences in both the colon and the small
initial sequence can be supplemented by axial and coronal intestine (see Fig. 5.1) as long as artifacts due to bowel
116 5 The Gastrointestinal Tract

Table 5.3 Surgical indications for complications of Crohn disease

Complication Surgical indication


Fistula Interenteric In patients with functional short bowel syndrome (bypass); in all other cases only in the setting of
surgery performed for other reasons
Enterocutaneous For “high” enterocutaneous fistulas with skin irritation; limited indication for distal enterocuta-
neous fistulas
Blind-ending Absolute surgical indication because a blind-ending fistula may lead to severe, insidious sepsis,
which is typically not controllable
Enterovesical Absolute surgical indication in all patients with proven or strongly suspected enterovesical fistula
(e. g., recurrent urinary tract infection)
Enterovaginal In patients with severe symptoms (daily secretions, recurrent vaginal infection, recurrent urinary
tract infection)
Abscess Interventional drainage of all intra-abdominal abscesses; surgical drainage if not amenable to
intervention or very superficial
Stricture Stricture causing postprandial pain; subileus not responding to conservative management (in-
cluding endoscopic dilatation); and colonic stricture including asymptomatic stricture of unclear
etiology
Dysplasia Proven diagnosis of dysplasia and repeat work-up required to rule out ulcerative colitis
Fulminant Bleeding cannot be stopped by conservative measures and > 2 units of erythrocyte concentrate
episode are required per day; patient does not respond to intensified immunosuppressive therapy

a b

c d
Fig. 5.7a–f Acute episode of Crohn disease. a CT after IV contrast narrowing, prestenotic dilatation, distancing of bowel loops, and
administration. b T2w HASTE. c–f T1w GRE images obtained before hyperemia (strong enhancement after IV contrast) of the affected
and at various time points after IV injection of Gd-based contrast bowel wall (see Table 5.4).
medium. Characteristic findings are present: free fluid (b), homoge- Fig. 5.7e, f e
neous (edematous) thickening of long wall segments with luminal
MRI Appearance of Pathologic Entities 117

e f
Fig. 5.7e, f

motion can be effectively suppressed by administration of Table 5.4 MRI criteria for assessing severity in inflammatory bowel
an antispasmodic.2 disease5
The presence of edema and contrast enhancement can MRI criterion Inflammatory activity
help differentiate inflammatory stricture from stricture
Mild Moderate Severe
due to scar formation, which is important because the
latter may require surgery. The length of involvement, Wall thickening 4–5 mm 5–10 mm > 10 mm
mural thickening, and postcontrast enhancement can be Length of diseased < 5 cm – –
quantified and serve as objective measures of inflamma- segment
tory activity16,17 (Table 5.4). However, the optimal thera- Contrast enhancement < 50 % ≤ 100 % > 100 %
peutic regimen is currently prescribed on the basis of
clinical and laboratory findings. A STIR sequence is the
sequence of choice for the pelvis, especially for evaluating
fistulas (Fig. 5.8).

a b
Fig. 5.8a–j Crohn disease with enterocutaneous fistula. a, b Percu- ness; e, f) or STIR sequence (4-mm slice thickness; g, h). 3D GRE
taneous (retrograde) fistulography combined with Sellink. c–j On images after IV injection of Gd-based contrast medium (1.2-mm
MRI the fistula opening is marked with a nifedipine capsule. Search slice thickness; i, j) show concomitant inflammation of fatty tissue
for inflammatory changes with a fat-saturated HASTE sequence and edematous wall thickening (target sign).
(c, d). Affected bowel segments are then further evaluated using Fig. 5.8c–j e
higher-resolution breath-hold TrueFISP sequence (2-mm slice thick-
118 5 The Gastrointestinal Tract

c d

e f

g h

i j
Fig. 5.8c–j
MRI Appearance of Pathologic Entities 119

a b

Fig. 5.9a–c Small-bowel lymphoma. a Axial T1w GRE image. b Axial


T2w fat-suppressed TSE image. c Sagittal T2w TSE image. There is
marked homogeneous wall thickening, which is characteristic of
small-bowel lymphoma.

Lipoma can be diagnosed with a high degree of accu- Colon


racy using MRI. It is suggested by high signal intensity on
T1w images with a typical signal drop on fat-suppressed Carcinoma
images. Most other small-bowel tumors are not depicted
by T1w sequences unless intravenous contrast medium is Colorectal cancer is the second most common malignant
given. Lymphomas show only moderate enhancement tumor in men and women.19 About 70–95 % of colorectal
and are primarily identified as wall thickening (Fig. 5.9) tumors arise from adenomas.20 The typical growth pat-
in association with enlarged mesenteric lymph nodes. No tern is circumferential (“apple core” appearance), ulti-
data are available in the literature on the T2 signal inten- mately resulting in bowel obstruction. About 50 % of all
sities of small-bowel tumors except for lymphomas, colorectal carcinomas are found in the rectum, 20 % in the
which are isointense to fat and hyperintense to muscle sigmoid colon, 6 % in the descending colon, 8 % in the
on T2w images.18 transverse colon, 6 % in the ascending colon, and 10 % in
the cecum (Fig. 5.10). Multiple colorectal carcinomas are
seen in 2–5 % of patients.
The TNM staging system for colorectal cancer is sum-
marized in Table 5.5. Colorectal tumors spread locally to
perirectal or pericolic fat, via the lymphatics, and through
the bloodstream if there is vascular invasion. Primary
spread is lymphatic in most cases. Resection of draining
lymph nodes along the supplying blood vessels is crucial
120 5 The Gastrointestinal Tract

a b

Fig. 5.10a–c Malignant polyp (stage 1 cancer) in the proximal transverse colon.
MR colonography with water enema. a T2w HASTE. b TrueFISP. c T1w 3 D GRE
(VIBE) after IV injection of Gd-based contrast medium. This example clearly
illustrates that the HASTE sequence is less susceptible to artifacts than the
TrueFISP sequence. On the postcontrast VIBE image (c), enhancement of the
suspected lesion indicates vascularization and permits differentiation from re-
sidual stool.

Table 5.5 TNM staging system for colorectal cancer for preventing local recurrence and secondary distant
Invasion level Lymph node Distant
metastases.
metastases metasta- The lymphatic drainage of the colon follows its arterial
ses supply along the ileocolic artery, the right colic artery, the
two branches of the middle colic artery, and the short
T1 Submucosa N1: 1–3 regional M1*
lymph nodes trunk of the inferior mesenteric artery with the left colic
T2 Muscularis propria N2: ≥ 4 regional artery and the sigmoid arteries (Fig. 5.10).
lymph nodes In contradistinction to other parts of the colon, the
T3 Subserosa, nonperito- rectum has relatively sparse lymphatic drainage, which
nealized pericolic/peri- is why lymphatic metastatic spread does not occur until a
rectal tissues rectal tumor has invaded the muscularis mucosae and
T4 Adjacent structures/vis- submucosa. These tumors may then spread through the
ceral peritoneum
lymphatics following the superior rectal artery to the
* Colon cancer: liver (69–80 %), lung (12–37 %), peritoneum inferior mesenteric artery and the inferior rectal arteries
(17–32 %), bones, adrenals, brain. and internal iliac vessels to the pelvic sidewall. Spread to
Rectal cancer: liver (59–66 %), lung (19–47 %), peritoneum (12 %), distal and inguinal lymph nodes, as in anal cancer, occurs
bones, adrenals, brain.
only in case of very low rectal tumors extending to the
level of the levator ani muscle or if proximal lymphatic
MRI Appearance of Pathologic Entities 121

drainage is blocked. Metastatic distal lymph nodes are raphy with imaging of the breast or prostate might be
usually not more than 2–3 cm away from the tumor exploited in the screening setting. However, MR colonog-
margin. raphy is a relatively new technique and is limited by the
If gelatinous peritoneal carcinosis is present, the differ- fact that it is still difficult to visualize the entire colon with
ential diagnosis includes mucinous adenocarcinoma of high resolution and no artifacts.
the colon and ovarian cancer but also the rare pseudomyx-
oma peritonei (PMP, “jelly belly”), which typically arises as MR Colonography (MRC)
a mucinous tumor of the appendix that ruptures into the After bowel preparation, water or air is introduced rec-
peritoneum. tally according to the individual patient’s tolerance. Ad-
equacy of colonic distention is monitored by acquisition of
a coronal HASTE sequence with thick slices and corre-
Distant Metastatic Disease sponding interslice gaps. An axial HASTE sequence is ac-
quired to determine the anteroposterior extent of the
Since the venous drainage of the colon and upper rectum colon. The coronal and axial HASTE images serve to pre-
empties into the hepatic portal system, the liver is the first scribe the scan volume for the subsequent HASTE and
and most common site of organ metastases from colo- VIBE sequences. The FOV must be large enough to encom-
rectal cancer (Table 5.5). Second in frequency are pulmo- pass the entire colon and planning must therefore take
nary metastases. The lungs may also be the primary site of into account that water filling in conjunction with a spas-
metastatic spread, especially in low rectal carcinoma with molytic may further expand the colon. All subsequent
drainage via the pelvic and paravertebral veins. Less com- sequences are acquired during breath-holds. The breath-
mon are metastases to the bones, adrenals, and brain. In hold intervals, slice thickness, and number of slices are
advanced disease, there will be peritoneal seeding, possi- tailored to the individual colon size. Next, an intravenous
bly with ovarian metastases. bolus of 20 mg of butylscopolamine is given, followed by
The likelihood of synchronous and metachronous adjustment of the hydrostatic pressure to the patient’s
metastases is determined by different features of the pri- tolerance level by varying the height at which the enema
mary tumor. The incidence increases not only with the bag is hung from the IV stand (50-cm water column). A
T and N stages but also with decreasing tumor differen- coronal HASTE sequence and three successive postcon-
tiation. Other contributory but less well-established fac- trast VIBE sequences are acquired 40 s after a bolus of Gd-
tors are ploidy status, growth fraction, and loss of adhe- based contrast medium (0.2 mmol per kg body weight)
sion molecules. (Fig. 5.10). Since the maximum effect of intravenous bu-
Colorectal cancer typically recurs locoregionally. Re- tylscopolamine is reached ca. 1 min after administration,
currence at the anastomotic site is especially common the contrast medium for the subsequent VIBE sequence
after low anterior resection of tumors of the proximal can already be given during acquisition of the HASTE
rectum or distal sigmoid. Locally recurrent tumors may sequence. TrueFISP images can be acquired before the
involve the abdominal wall, pancreas, ureters, and pelvic VIBE sequence, but their diagnostic benefit remains to
bones. Presacral recurrence of rectal carcinoma typically be determined (Figs. 5.10 and 5.11). The T2 signal inten-
involves the piriform muscle and may also invade the sity of colorectal carcinomas is very low. It is highest on
sciatic nerve. Colorectal cancer recurs in up to 50 % of STIR images (Fig. 5.11), but abdominal STIR sequences are
patients, depending on the tumor stage at diagnosis. very susceptible to motion artifacts, especially when ac-
centuated by water as positive T2 contrast medium. If the
colon cannot be imaged in its entirety in a single acqui-
MRI in Colon Cancer sition due to coil or magnetic field limitations, two scans
Since surgical resection is the method of choice regardless can be obtained, one to image the abdomen in the coronal
of the T stage, there is no need for preoperative T staging plane and one to image the pelvis in the axial plane
of colon cancer by imaging. CT is more accurate than MRI (Fig. 5.12).
in detecting enlarged lymph nodes due to its higher spa-
tial resolution, which improves the quality of multiplanar
reconstruction. Screening for distant metastases is also Inflammatory Disease
more practical with CT because it can cover the lungs
and abdomen with one 10-s scan and is superior to MRI Diverticulitis secondary to diverticulosis, ulcerative colitis,
in detecting pulmonary metastases. and Crohn disease are the most common inflammatory
PET/CT is superior to MRI in searching for a primary conditions affecting the colon. Much less common are
tumor or ruling out a tumor. CT colonography and endos- radiation-induced changes of the colon and rectum. While
copy appear to be equally suitable for detecting clinically Crohn disease is characterized by transmural involve-
relevant colorectal adenomas.21 Because of the radiation ment, ulcerative colitis predominantly involves the mu-
exposure involved, CT is limited as a screening test, and cosa but may nevertheless cause marked wall thickening
MR colonography may be considered as an alternative for in severe inflammation. Ulcerative colitis typically begins
this indication.11,12 The option of combining MR colonog- in the rectum and continuously progresses to involve
122 5 The Gastrointestinal Tract

Fig. 5.11a–d Carcinoma of the ascending colon. MR


colonography after air insufflation. a T2w HASTE.
b T2w TrueFISP. c STIR. d T1w 3D GRE (VIBE) after IV
injection of Gd-based contrast medium. The colon
tumor (arrow in a) has rather low SI on HASTE, True-
FISP, and STIR images. The contrast-enhanced VIBE
image (d) allows good tumor delineation 40–50 s after
contrast administration.

a b

c d

a c
Fig. 5.12a–c Sigmoid carcinoma. 3D GRE images (VIBE) obtained serial acquisitions for evaluation of the tumor in different planes.
after IV injection of Gd-based contrast medium in coronal (a) and Note prestenotic dilatation in an otherwise fully distended colon as
axial (b, c) planes. There is pronounced signal enhancement of the an indirect sign of cancer.
tumor (arrows). Enhancement persists for at least 5 min and enables
MRI Appearance of Pathologic Entities 123

a b
Fig. 5.13a, b Acute ulcerative colitis in the sigmoid colon. T1w SE rectum is typical of ulcerative colitis. Wall thickening, the length
images before (a) and after (b) IV injection of Gd-based contrast of the involved colon segment, and signal enhancement indicate
medium. Contiguous extension of the disease process from the the severity of inflammation. No prestenotic dilatation.

a b
Fig. 5.14a, b Radiation enteritis in the sigmoid colon. T1w GRE administration and is confined to the mucosa and submucosa (dis-
images before (a) and after (b) IV injection of Gd-based contrast tinguishing it from Crohn disease). No prestenotic dilatation.
medium. The inflammatory process is revealed only after contrast

more proximal colon segments. In Crohn disease, on the MRI in Inflammatory Disease
other hand, the inflammation is discontinuous and can MR colonography (see above) can also be used for assess-
produce skip lesions throughout the bowel. Fistulas, ab- ing inflammatory disease of the colon. In ulcerative colitis,
scesses, and locoregional lymph node enlargement char- imaging will show loss of haustra. The colon wall (mucosa
acterize Crohn disease, but they are rare in ulcerative and submucosa) has increased signal intensity on T1w and
colitis, though sigmoidovesical fistulas do occur. Divertic- T2w images.22 In inactive ulcerative colitis, the disease is
ulosis, which is found in the sigmoid colon in two thirds of more likely to be recognized by thickening of the colon
cases, will also cause wall thickening as the disease wall. MRI is not superior to endoscopy in differentiating
evolves. Diverticulitis may be complicated by strictures, Crohn disease and ulcerative colitis.23 Transmural en-
peridiverticular infiltration of fatty tissue, covered perfo- hancement and skip lesions that involve the terminal
rations, abscesses, and fistula formation. ileum but spare the rectum are characteristic findings in
Acute appendicitis occurs in ca. 6 % of the population. Crohn disease, whereas a disease process extending con-
Uncomplicated appendicitis is associated with wall thick- tinuously from the rectum suggests ulcerative colitis
ening, inflammatory changes in surrounding fat (fluid (Fig. 5.13). Whereas Crohn disease is characterized by
collection around the appendix; 58–88 %), and fecaliths enhancement of all wall layers on postcontrast GRE im-
(appendicoliths; in up to 23 % of cases). The reported ages, the serosa usually does not enhance in chronic ulcer-
incidence of perforated acute appendicitis is 25 %. Perfo- ative colitis or unspecific enteritis (Fig. 5.14). Submucosal
rated appendicitis may be associated with phlegmons or thickening due to edema and lymphangiectasia is seen as
perityphlitic abscesses. Appendicoliths are much more rather low T1 signal intensity and occurs in chronic ulcer-
common than in uncomplicated appendicitis. ative colitis already after one year.
124 5 The Gastrointestinal Tract

a b
Fig. 5.15a, b Sigmoid diverticulitis. a T2w TSE. b 3D GRE image tion with the clinical findings, thus helps identify those patients who
(VIBE) obtained after IV injection of Gd-based contrast medium. MRI require surgical management. But MRI cannot exclude perforation,
provides information on the extent of diverticulitis and, in conjunc- for which CT is the imaging modality of choice.

a b
Fig. 5.16a, b Sigmoidovesicular fistula. a Fat-suppressed T2w HASTE. b 3D GRE image (VIBE) after 1 % Gd and water enema. The fistula is
revealed as a hyperintense structure (arrow in b) after rectal contrast medium has entered the tract.

Complications of Crohn disease are fistulas, abscesses, be more sensitive in identifying inflammation of sur-
strictures, and conglomerate tumors (Table 5.3), whereas rounding fat (peridiverticulitis). However, MRI can equally
ulcerative colitis may be complicated by bleeding and well be used to diagnose diverticulitis (Fig. 5.15) and
toxic megacolon. Patients with ulcerative colitis have a spares the patient an intravenous contrast injection,
higher risk of developing colorectal cancer than those which may be necessary with CT. Fat-suppressed T2w
with Crohn disease, in whom cancer is a very rare late HASTE images allow evaluation of the inflammatory proc-
complication. The risk of carcinoma development corre- ess and exclusion of abscess. A VIBE sequence acquired
lates with the extent of colonic involvement and disease after a 2 % Gd and water enema will identify fistulas
duration (40 % in patients with involvement of the entire between the sigmoid and the urinary bladder either di-
colon and a 25-year history of disease), which must be rectly (Fig. 5.16) or indirectly by the presence of contrast
borne in mind in the follow-up of patients with inflam- medium in the bladder. However, contrast medium in the
matory bowel disease. bladder can serve as indirect evidence only in patients
CT is preferred to MRI in suspected diverticulitis be- who have not received intravenous Gd-based contrast
cause it will demonstrate free air as a sign of perforation. medium.
Moreover, with its higher spatial resolution, CT appears to
Outlook 125

Intense enhancement of the appendix wall on fat-sup-


pressed T1w images after intravenous contrast adminis-
tration was found to be a sensitive and specific sign of
appendicitis,24 as was marked hyperintensity of the lu-
men, a slightly hyperintense, thickened wall (Fig. 5.17),
and marked hyperintensity of surrounding tissue on T2w
TSE images.25 These are preliminary results, but they
suggest that MRI may also have the potential to diagnose
appendicitis.

Functional MRI

MRI is very well suited for functional studies because it


does not involve radiation exposure and thus allows re-
peated sequential imaging. Hence, MRI can be used to
quantify esophageal reflux26 and gastric motility and
emptying.27 Causes of defecation disorders such as recto-
cele or rectal invagination (enteroceles with or without
prolapse of the urinary bladder, vagina, uterus, or colon)
can be identified and evaluated by means of dynamic MR Fig. 5.17 Appendicitis. Coronal T2w TrueFISP image acquired in an
defecography.28 Dynamic MRI requires rectal filling. If open 0.2-T scanner during breath-holding (25 s). Appendicits (ar-
water is used, in the form of either ultrasound gel or a row) is suggested by wall thickening and high SI. At 1.5 T the HASTE-
IRM sequence should be used to quickly identify the appendix by
cellulose mixture, imaging can be performed with a True-
periappendiceal inflammatory stranding and free fluid. Once the
FISP or HASTE sequence. If volumetric analysis is neces- appendix has been found the examination can be supplemented by
sary, imaging can be performed using a 3D GRE sequence an axial 3D contrast-enhanced VIBE sequence if the results are still
after a 1 % Gd and water enema. inconclusive. This VIBE sequence allows optimal angulation in the
multiplanar reconstruction mode.

Outlook
movement. Ga-68-DOTATOC-PET/CT using the somato-
statin analogue DOTATOC as tracer to replace somatosta-
In the gastrointestinal tract, MRI competes not only with tin receptor scintigraphy (octreotid-scan) is emerging as
other cross-sectional imaging modalities (CT, ultrasound) the standard of reference for the detection of gastro-
and conventional projection radiography (double-con- enteropancreatic neuroendocrine tumors (GEP-NETs).
trast barium enema, Sellink) but also with endoscopy
and PET/CT imaging. Unlike colonoscopy, both CT and
MRI yield digital volume data, which are a prerequisite References
for using computer-aided diagnosis (e. g., CT-density- and/
1. Umschaden HW, Szolar D, Gasser J, Umschaden M, Haselbach H.
or shape-based algorithms in colorectal cancer screen-
Small-bowel disease: comparison of MR enteroclysis images
ing29). At present, CT is preferred to MRI for gastrointes- with conventional enteroclysis and surgical findings. Radiol-
tinal imaging because it is fast, combines high spatial ogy 2000;215(3):717–725
2. Gourtsoyiannis N, Papanikolaou N, Grammatikakis J, Maris T,
resolution with a minimum of artifacts, and allows the
Prassopoulos P. MR enteroclysis protocol optimization: compar-
combination of lung and abdominal imaging for staging in ison between 3 D FLASH with fat saturation after intravenous
less than 20 s. MRI, on the other hand, theoretically offers gadolinium injection and true FISP sequences. Eur Radiol
some advantages such as high soft-tissue contrast, a 2001;11(6):908–913
3. Gourtsoyiannis N, Papanikolaou N, Grammatikakis J, Prassopou-
higher sensitivity to contrast media, the absence of radi- los P. MR enteroclysis: technical considerations and clinical
ation exposure, the possibility of dispensing with contrast applications. Eur Radiol 2002;12(11):2651–2658
administration, and the option of performing kinematic 4. Low RN, Sebrechts CP, Politoske DA, et al. Crohn disease with
endoscopic correlation: single-shot fast spin-echo and gadoli-
imaging for functional assessment. PET/CT is increasingly nium-enhanced fat-suppressed spoiled gradient-echo MR
being recommended as the baseline staging modality for imaging. Radiology 2002;222(3):652–660
oncologic imaging (except for hepatocellular and pancre- 5. Rohr A, Rohr D, Kühbacher T, Schreiber S, Heller M, Reuter M.
[Radiological assessment of small bowel obstructions: Value of
atic carcinoma) and can be considered the standard of conventional enteroclysis and dynamic MR-enteroclysis]. Rofo
reference for GIST and possibly colorectal cancer, although 2002;174(9):1158–1164
it is supposed to be inferior to MRI in the detection of 6. Laghi A, Borrelli O, Paolantonio P, et al. Contrast enhanced
magnetic resonance imaging of the terminal ileum in children
small liver metastases due to poorer contrast and addi- with Crohn’s disease. Gut 2003;52(3):393–397
tional blurring by partial volume effects caused by liver
126 5 The Gastrointestinal Tract

7. Luboldt W, Bauerfeind P, Steiner P, Fried M, Krestin GP, Debatin 19. Surveillance: Epidemiology and End Results (SEER). http://seer.
JF. Preliminary assessment of three-dimensional magnetic res- cancer.gov/csr/1973_1999/sections.html
onance imaging for various colonic disorders. Lancet 1997; 20. Vogelstein B, Fearon ER, Hamilton SR, et al. Genetic alterations
349(9061):1288–1291 during colorectal-tumor development. N Engl J Med 1988;
8. Luboldt W, Bauerfeind P, Wildermuth S, Marincek B, Fried M, 319(9):525–532
Debatin JF. Colonic masses: detection with MR colonography. 21. Pickhardt PJ, Choi JR, Hwang I, et al. Computed tomographic
Radiology 2000;216(2):383–388 virtual colonoscopy to screen for colorectal neoplasia in asymp-
9. Luboldt W, Luz O, Vonthein R, et al. Three-dimensional double- tomatic adults. N Engl J Med 2003;349(23):2191–2200
contrast MR colonography: a display method simulating dou- 22. Giovagnoni A, Misericordia M, Terilli F, Brunelli E, Contucci S,
ble-contrast barium enema. AJR Am J Roentgenol 2001; Bearzi I. MR imaging of ulcerative colitis. Abdom Imaging
176(4):930–932 1993;18(4):371–375
10. Luboldt W, Fletcher JG, Vogl TJ. Colonography: current status, 23. Shoenut JP, Semelka RC, Magro CM, Silverman R, Yaffe CS, Mic-
research directions and challenges. Update 2002. Eur Radiol flikier AB. Comparison of magnetic resonance imaging and en-
2002;12(3):502–524 www.screening.info doscopy in distinguishing the type and severity of inflammatory
11. Luboldt W, Hoepffner N, Holzer K, et al. [Early detection of bowel disease. J Clin Gastroenterol 1994;19(1):31–35
colorectal tumors: CT or MRI?]. Radiologe 2003;43(2):136–150 24. Incesu L, Coskun A, Selcuk MB, Akan H, Sozubir S, Bernay F.
www.screening.info Acute appendicitis: MR imaging and sonographic correlation.
12. Lauenstein TC, Goehde SC, Ruehm SG, Holtmann G, Debatin JF. AJR Am J Roentgenol 1997;168(3):669–674
MR colonography with barium-based fecal tagging: initial clin- 25. Hörmann M, Paya K, Eibenberger K, et al. MR imaging in chil-
ical experience. Radiology 2002;223(1):248–254 dren with nonperforated acute appendicitis: value of unen-
13. Ell C, Fischbach W, Keller R, et al; Hintertux Study Group. A hanced MR imaging in sonographically selected cases. AJR Am
randomized, blinded, prospective trial to compare the safety J Roentgenol 1998;171(2):467–470
and efficacy of three bowel-cleansing solutions for colonoscopy 26. Knippig C, Fass R, Malfertheiner P. Tests for the evaluation of
(HSG-01*). Endoscopy 2003;35(4):300–304 functional gastrointestinal disorders. Dig Dis 2001;19(3):
14. Hohenberger P, Reichardt P, Stroszczynski C, Schneider U, Hoss- 232–239
feld DK. Gastrointestinale Stromatumoren–Tumorentität und 27. Schwizer W, Fox M, Steingötter A. Non-invasive investigation of
Therapie mit Imatinib. Dtsch Arztebl 2003;100:A1612–A1618 gastrointestinal functions with magnetic resonance imaging:
15. Burkill GJ, Badran M, Al-Muderis O, et al. Malignant gastrointes- towards an “ideal” investigation of gastrointestinal function.
tinal stromal tumor: distribution, imaging features, and pattern Gut 2003;52(Suppl 4):iv34–iv39
of metastatic spread. Radiology 2003;226(2):527–532 28. Bertschinger KM, Hetzer FH, Roos JE, Treiber K, Marincek B,
16. Koh DM, Miao Y, Chinn RJ, et al. MR imaging evaluation of the Hilfiker PR. Dynamic MR imaging of the pelvic floor performed
activity of Crohn’s disease. AJR Am J Roentgenol 2001;177(6): with patient sitting in an open-magnet unit versus with patient
1325–1332 supine in a closed-magnet unit. Radiology 2002;223(2):
17. Pauls S, Kratzer W, Rieber A, et al. [Quantifying the inflamma- 501–508
tory activity in Crohn’s disease using CE dynamic MRI]. Rofo 29. Luboldt W, Tryon C, Kroll M, et al. Automated mass detection in
2003;175(8):1093–1099 contrast-enhanced CT colonography: an approach based on
18. Negendank WG, al-Katib AM, Karanes C, Smith MR. Lympho- contrast and volume. Eur Radiol 2005;15(2):247–253 www.
mas: MR imaging contrast characteristics with clinical-patho- screening.info
logic correlations. Radiology 1990;177(1):209–216
127

6 The Rectum and Anal Canal


C. Klessen and M. Laniado

Introduction Imaging Technique

With the advent of powerful gradients and high-resolu- Patient Preparation and Positioning
tion surface and endorectal coil systems, MRI is increas-
ingly used to evaluate inflammatory and neoplastic dis- Before the examination, a careful explanation of the pro-
eases of the rectum and anal canal. MRI is superior to cedure is given, and patients are informed about the risks
endoscopic and endosonographic techniques in that it of administration of an antispasmodic agent and asked
enables noninvasive evaluation of the rectal lumen and about possible contraindications. A venous cannula for
wall and additionally provides detailed information on contrast injection is placed before image acquisition in
surrounding structures in the true pelvis. Accurate infor- those cases where additional contrast-enhanced pulse
mation on the extent of a disease process and possible sequences need to be acquired.
involvement of adjacent structures is crucial for tailoring Unless contraindicated, an antispasmodic agent (bu-
surgical or medical treatment to the individual patient’s tylscopolamine or glucagon) should be given to reduce
needs. The superior tissue contrast provided by MRI is an artifacts caused by bowel motion. Antispasmodics have
advantage over CT, but ongoing technical developments very short half-lives and an intravenous injection should
may redefine the role of CT in assessing the local extent of therefore be given immediately before the start of image
rectal tumors. Evaluation for nodal and distant metastases acquisition.
in patients with colorectal cancer is still the domain of CT. The patient should be in a comfortable supine position,
with the knees supported by a foam pad if necessary.
Before the examination, the patient is instructed to lie still
during acquisitions.
Indications

Currently, MRI has the following indications in the diag- Contrast Media
nostic assessment of the rectum, anal canal, and pelvic
floor: Most MRI examinations of the rectum can be performed
· Determination of the activity and extent of acute and without giving an enteral contrast medium. Some authors
chronic inflammatory bowel disease in the rectum and advocate the use of a positive or negative enteral contrast
anal canal and involvement of surrounding organs. agent, but there appears to be general agreement in the
· Evaluation of the extent and course of perianal and current literature that this is not necessary. No intralumi-
perirectal fistulas and abscesses, either in isolation or nal contrast is needed for MRI in patients with inflamma-
as a complication of chronic inflammatory bowel dis- tory rectal disease.
ease, for devising the most suitable therapeutic strat- Some clinical indications require intravenous injection
egy. of an extracellular, Gd-based contrast medium such as
· Tumor staging in patients with anorectal malignancy, Magnevist (Gd-DTPA) or Dotarem (Gd-DOTA). The stan-
especially if an advanced tumor stage (T3, T4) is sus- dard dose is 0.1 mmol Gd per kg body weight, and the
pected on clinical grounds or endosonography is in- contrast medium is automatically injected during the ex-
conclusive or not tolerated by the patient due to pain. amination.
· Detection of recurrent tumor after surgical, conserva-
tive, or combined treatment, especially in patients with
suspected extraluminal or presacral tumor extension. Coils
· Morphologic and functional assessment of the pelvic
floor in patients with fecal incontinence or other def- Ideally, phased-array surface coils should be used because
ecation disorders. they provide a much better signal-to-noise ratio (SNR).1
The coils are positioned according to the target region and
128 6 The Rectum and Anal Canal

kept in place with belts. When first introduced, endorectal Contrast-enhanced MRI is performed using T1w SE or
coils appeared promising, but they have failed to establish TSE sequences with spectral fat saturation.
themselves for imaging of the rectum and anal canal The pelvic lymph nodes are best imaged with axial T1w
because they are cumbersome to handle, expensive (dis- or PD sequences, covering the entire area from the aortic
posable systems), and have a limited field of view (FOV). bifurcation to the pelvic floor (see Chapter 16).
Parallel imaging techniques (SENSE, iPAT) can be used
to shorten acquisition time,3 but this is accomplished at
Imaging Planes the expense of SNR.
Several recent studies suggest that certain diffusion
Following the usual three-plane localizer, sequences in and perfusion parameters may predict the response to
the sagittal and axial planes are best suited for imaging radiochemotherapy, which is why the use of diffusion-
the rectum and anal canal and evaluating their relation- and perfusion-weighted imaging (DWI and PWI sequen-
ship to surrounding structures in the true pelvis. When ces) is under clinical investigation.4–6
MRI is performed for suspected fistula, additional coronal Details of the recommended pulse sequences and
images should be obtained, and sagittal images may not imaging parameters are summarized in Tables 6.1 and 6.2.
be needed (depending on the site of the fistula). In pa-
tients with rectal cancer, imaging in an oblique axial plane
perpendicular to the lumen of the affected bowel segment
MRI Appearance of Normal Anatomy
is necessary to evaluate the wall and identify invasion into
perirectal fat. Additional coronal images will improve
identification of possible involvement of the anal sphinc- The rectum is ca. 12–15 cm in length and extends from the
ter in patients with low rectal cancer. level of the third sacral vertebra, where the mesentery of
the sigmoid colon ends, to the anus (Fig. 6.1). Unlike the
colon, the rectum has no teniae, haustra, or omental ap-
Imaging Protocol pendices. When viewed laterally, the rectum has two
bends—the upper sacral flexure with posterior convexity
After a three-plane localizer, fast breath-hold sequences and the lower anorectal flexure with anterior convexity.
in at least two planes (e. g., T2w HASTE) should be ob- The rectum can be divided into the pelvic rectum or rectal
tained to define the exact area involved and plan the ampulla, a contractile reservoir, and the perineal rectum
subsequent sequences. These sequences have extremely or anal canal. The latter is ca. 3 cm long and extends from
short acquisition times and are fairly insensitive to motion the levator ani muscle to the anus. Surgeons typically refer
artifacts. to the anal canal as the portion of the rectum below the
In patients with inflammatory bowel disease, an inver- pectinate or dentate (anorectal) line, which marks the
sion recovery sequence with a short inversion time (e. g., transition from the columnar epithelium of the rectal
TIRM, STIR) is acquired next for detection of fluid in ab- mucosa to the squamous epithelium of the anoderm.
scess cavities and fistula tracts, making such a sequence Fistulas in this area are therefore designated as perianal
especially useful when looking for perianal and perirectal fistulas in the radiologist’s report. A second line, the ano-
fistulas. cutaneous line, demarcates the transition from the hair-
Unenhanced images for assessment of local tumor ex- less skin of the anal canal to the perianal skin. The normal
tent in patients with rectal cancer are obtained using wall layers of the rectum are depicted diagrammatically in
high-resolution T2w TSE sequences, which provide a bet- Fig. 6.2a.
ter contrast-to-noise ratio (CNR) and markedly higher The anterior and lateral surfaces of the upper two
spatial resolution than T2w HASTE sequences, but acqui- thirds of the ampulla are covered by peritoneum. The
sition times are much longer and they are more suscep- part of the rectum above the middle transverse rectal
tible to motion artifacts. It is especially with these sequen- fold (Kohlrausch fold) is retroperitoneal, while the portion
ces that imaging quality can be markedly improved by below is extraperitoneal. The rectal fascia constitutes a
placement of saturation bands over the anterior subcuta- cylindrical sheath surrounding the rectum down to the
neous fat and administration of an antispasmodic agent pelvic floor and is referred to as the mesorectal fascia in
(see above). the clinical and surgical literature7 (Fig. 6.3). Posteriorly,
In patients with rectal inflammatory disease, intrave- the mesorectal fascia is thickened and overlies the parietal
nous contrast medium will improve evaluation of disease pelvic fascia, which covers the sacrum. So-called total
activity and delineation of anorectal fistula tracts and mesorectal excision (TME) of rectal cancer is the en bloc
abscesses. Though we present some examples of con- resection of the tumor-bearing rectum within its envelop-
trast-enhanced images, investigators seem to agree that ing fascia including lymphatics, lymph nodes, and meso-
no intravenous contrast medium is needed for initial rectal fat, while preserving the parietal pelvic fascia and
imaging of rectal cancer.2 Intravenous contrast may be pelvic splanchnic nerves (nervi erigentes).
helpful, though, in patients with suspected tumor recur- Closure of the anal canal is ensured by the external and
rence. internal anal sphincters and levator ani muscle in the wall
MRI Appearance of Normal Anatomy 129

Table 6.1 Recommended pulse sequences and imaging parameters for MRI of rectal carcinoma

Weight- Plane Sequence type TR TE Flip ETL FS Matrix No. of Slice thick- Breath-
ing (ms) (ms) (°) acquisi- ness (mm) hold
tions
PD Axial TSE (FSE) 1980 10 150 3 – 219 × 512 3 5 –
T2 Axial Single-shot TSE 800* 63 150 115 115 × 256 1 5 Yes
with half-Fourier
acquisition, e. g.,
HASTE
T2 Sagittal Single-shot TSE 800* 63 150 115 – 115 × 256 1 5 Yes
with half-Fourier
acquisition, e. g.,
HASTE
T2** Axial TSE (FSE) 3550 68 180 19 – 179 × 256 5 3 –
T2** Sagittal TSE (FSE) 3760 68 180 19 – 179 × 256 5 3 –
T1*** Axial TSE (FSE) 575 11 150 3 + 230 × 256 3 3 –
T1*** Sagittal TSE (FSE) 575 11 150 3 + 230 × 256 3 3 –

Note: Use of a surface phased-array multicoil is recommended. The imaging parameters are only examples and have to be adjusted for use
on different brands of scanners.
* TR: used here as a technical parameter referring to the intervals between slice acquisitions; physical TR = infinite since only one slice is
acquired per excitation.
** FOV: 180 × 180, centered on the tumor.
*** Fat-suppressed T1w sequences after IV contrast administration. Rarely necessary for this indication (see text).

Table 6.2 Recommended pulse sequences and imaging parameters for MRI of anorectal fistulas and abscesses

Weight- Plane Sequence type TR TE Flip ETL FS Matrix No. of Slice thick- Breath-
ing (ms) (ms) (°) acquisi- ness (mm) hold
tions
PD Axial TSE (FSE) 2360 8.5 150 5 – 192 × 512 2 5 –
IR Axial IR (TI, 150 ms), 7770 30 150 7 IR 192 × 512 1 5 –
e. g., TIRM
IR Coronal IR (TI, 150 ms), 4990 30 150 7 IR 256 × 512 1 4 –
e. g., TIRM
T1* Axial TSE (FSE) 901 8.5 150 5 + 192 × 512 2 5 –
T1* Coronal TSE (FSE) 901 8.5 150 5 + 256 × 512 2 5 –

Note: Use of a surface phased-array multicoil is recommended. The imaging parameters are only examples and have to be adjusted for use
on different brands of scanners.
* Fat-suppressed T1w sequences after IV contrast administration.

of the anal canal. Muscular closure is supported by the


anal cushions (corpora cavernosa recti) (Figs. 6.4 and 6.5).
The rectum above the anal canal is supplied by the
superior rectal artery, which is the continuation of the
inferior mesenteric artery. The paired middle rectal ar-
teries arising from the internal iliac or internal pudendal
artery course laterally through the paraproctium to sup-
ply the anal canal and lower portion of the ampulla.
At least three layers of the rectal wall can be distin-
guished on high-resolution T2w MR images: an inner
layer of high signal intensity comprising the mucosa and

Fig. 6.1 Normal MR appearance of the rectum in a male on a


sagittal T2w TSE image. Sacral flexure (1) anorectal flexure (2),
anal canal (3), sacrum (4), urinary bladder (5), prostate (6), and
pubic symphysis (7).
130 6 The Rectum and Anal Canal

a b
Fig. 6.2a, b Rectal anatomy. a Diagram of microscopic anatomy. b the mucosa and submucosa are depicted as a high-SI band (white
MR anatomy. Intestinal lumen (1), mucosa (2), submucosa (3), arrows), and the muscularis propria appears as a thin line of low SI
muscular layer (muscularis propria) consisting of inner circular (4), (open arrows) surrounded by the high-SI mesorectal fat (*).
and outer longitudinal layers (5). On the corresponding MR image,

v Fig. 6.3 Normal appearance on axial T2w TSE image. Note good
delineation of the mesorectum (*) and mesorectal fascia (arrow-
heads). Stool is present in the rectum (arrow).

a b
Fig. 6.4a, b Normal anatomy. a Coronal TSE image. b Axial PD TSE The coronal image (a) clearly depicts the levator ani muscle on both
image. Curved arrows indicate the ischiorectal fossa, open arrows sides (arrowheads).
the para-anal space, and straight arrows the subcutaneous space.
MRI Appearance of Pathologic Entities 131

a b

Fig. 6.5a–c Normal MR appearance of the anal sphincter complex.


a Coronal PD TSE image. b Axial PD TSE image. c Axial fat-suppressed
T2w TSE image. The external anal sphincter muscle (arrowhead) is
of the same SI as skeletal muscle, while the internal anal sphincter is
markedly hyperintense (arrow). c Contrast is improved on the fat-
suppressed image.

submucosa; a middle layer of low signal intensity, which MRI Appearance of Pathologic Entities
corresponds to the muscularis propria; and an outer layer
of high signal intensity representing the perirectal fat
(Fig. 6.2b). Under optimal conditions, with the bowel re-
Rectal Carcinoma
laxed and empty, the mucosa is seen as a thin line of low
signal intensity. The mesorectal fascia is consistently de- Colorectal cancer is the third most common cancer world-
picted as a thin, hypointense line surrounding the rectum wide. In the United States, ca. 145 000 new cases and
and perirectal fatty tissue. On contrast-enhanced T1w 56 000 deaths were estimated for 2005.8 In all European
images, the mucosa and muscularis mucosae enhance countries, the incidence of malignant colorectal tumors is
early and intensely, differentiating these two layers from on the rise. While colon cancer affects both sexes nearly
the nonenhancing muscularis propria. Perirectal fat has equally, rectal cancer is more common in men. The inci-
high signal intensity on non-fat-suppressed T1w images dence of rectal cancer doubles every decade after the age
(Fig. 6.5). of 40, reaching a peak in the sixth to seventh decade.
Nearly all children and young adults who are diagnosed
with colon cancer have a predisposing condition. About
90 % of colorectal cancers arise via the so-called
132 6 The Rectum and Anal Canal

Table 6.3 TNM staging system for colorectal carcinoma the groin or pass through the pelvic floor to terminate in
the sacral and internal iliac nodes.
Stage Invasion
T1 Submucosa
T2 Muscularis propria
Distant Metastasis
T3 Subserosa, pericolic/perirectal tissue
T4 Other organs or structures/visceral peritoneum
Blood from the rectum above the anal canal drains
N1 Metastasis in 1–3 regional lymph nodes (of at
through the superior rectal and inferior mesenteric veins
least 12 sampled)
into the portal venous system. The middle and inferior
N2 Metastasis in 4 or more regional lymph nodes (of
at least 12 sampled) rectal veins drain into the inferior vena cava via the in-
ternal iliac vein.
Since venous drainage is through the portal system, the
Table 6.4 UICC stage grouping of rectal carcinoma liver is the first and most common site of organ metasta-
Stage 0 Tis N0 M0 ses from rectal tumors. Another common site is the lung,
Stage I particularly in patients with low rectal cancer. Next in
T1 N0 M0
frequency are metastases to the bones, adrenals, and
T2 N0 M0
brain. Advanced rectal cancer may be associated with
Stage II A T3 N0 M0 peritoneal seeding.
Stage II B T4 N0 M0
Stage III A T1, T2 N1 M0
MRI
Stage III B T3, T4 N1 M0
Stage III C Any T N2 M0 Although MRI may not allow exact T staging, the contrast
Stage IV Any T Any N M1 resolution it affords enables precise definition of tumor
spread in relation to the mesorectal fascia, which forms
the boundary of the surgical excision plane in total meso-
rectal excision (TME), the standard surgical approach for
adenoma–carcinoma sequence. Individuals with benign resection of tumors involving the middle or lower third of
adenomas have a 2–3 times higher risk of developing the rectum in combination with neoadjuvant or adjuvant
colorectal cancer than the normal population. The risk of therapy.10,11 MRI is currently the only imaging modality
malignant transformation increases with adenoma size, that is able to reliably predict whether a tumor-free cir-
especially in individuals with the villous type of adenoma. cumferential resection margin (CRM) is likely to be
Invasive carcinoma is present in 1 % of all adenomas < 1 cm achieved, thus providing information which is of para-
in diameter, 10 % of those 1–2 cm in size, and 30–50 % of mount importance to selecting the most effective thera-
adenomas > 2 cm. Rectal cancer is defined as a tumor peutic approach, especially in patients with advanced
located within 16 cm of the anal verge by rigid sigmoido- rectal cancer.12–19 The radiologist’s report must describe
scopy. The fact that 50 % of colorectal carcinomas arise in the relationship of the tumor to the mesorectal fascia in
the rectum underlines the importance of early detection detail.
and accurate tumor staging in this region. Staging is now Since, as already mentioned, MRI does not reveal the
mostly done using the TNM and UICC9 staging systems, mucosa and submucosa as distinct layers in most cases, it
which have largely replaced the older Duke classification is often not possible to discriminate T1 and T2 tumors.
(Tables 6.3 and 6.4). Rectal cancer spreads locally through Stage T2 rectal cancer is characterized by invasion of the
the rectal wall into the perirectal tissue (mesorectum). muscularis propria with loss of the interface between the
Initial metastatic spread is predominantly through the submucosa and circular muscle layer of the rectum, while
lymphatic system. the outer boundary between the muscle layer and peri-
rectal fat is intact (Fig. 6.6).
The most important feature distinguishing T3 tumors
Lymph Node Metastasis from T2 tumors is transmural extension into the meso-
rectum, seen as obliteration of the interface between
Because the rectum has only sparse lymphatic drainage muscle and perirectal fat. A problem facing MRI is that
compared with other colonic segments, lymph node inflammatory changes such as desmoplastic reaction, wall
metastases do not occur unless a tumor has infiltrated edema, and hypervascularization can lead to overstaging
the muscularis mucosae and submucosa. of T2 tumors. Therefore, the only reliable criterion for T3
Lymphatic vessels from the proximal rectum drain into rectal cancer is nodular extension of tumor into perirectal
the inferior mesenteric and presacral nodes. The mid- fat (Figs. 6.7 and 6.8). The accurate identification of early
rectum, which is above the pelvic floor, drains into the T3 tumors, in which either tumor tissue or just fibrous
internal iliac and sacral nodes. Lymphatic vessels from the tissue due to desmoplastic reaction extends into the mes-
perianal skin drain into the superficial inguinal nodes in orectum, has little impact on patient management.
MRI Appearance of Pathologic Entities 133

a
Fig. 6.6a, b Rectal carcinoma, stage T1/2. a Axial T2w TSE image.
b Sagittal T2w TSE image. Tumor (arrows) with a broad-based at-
tachment to the left rectal wall. There is no evidence of tumor
extension through the wall. b

a b
Fig. 6.7a, b Rectal carcinoma, stage T3. a Axial T2w TSE image. heads). Subtotal intestinal occlusion due to large intraluminal tumor
b Axial T1w fat-suppressed image after IV bolus administration of mass. Intense enhancement of the tumor on postcontrast image
Gd-based contrast medium (0.1 mmol/kg body weight). There is (b). A lymph node is seen in the mesorectal fatty tissue on the right
nodular extension of the tumor into the mesorectal fat (arrows), but (open arrow).
the tumor does not extend as far as the mesorectal fascia (arrow-

T4 tumors invade the visceral peritoneum, surrounding Recent data suggest that, with use of high-resolution
pelvic organs, or the muscle layer of the pelvic sidewall pulse sequences, signal intensity and border contour
(Fig. 6.9). may be more reliable predictors of nodal status than
Despite advances in MRI, identification of metastatic size. Metastatic lymph nodes tend to have mixed signal
perirectal lymph nodes remains a problem (Fig. 6.10). intensity and an irregular border.20
134 6 The Rectum and Anal Canal

b
Fig. 6.8a, b Rectal carcinoma, stage T3. a Axial T2w TSE image.
b Axial T1w fat-suppressed image after IV bolus administration of
Gd-based contrast medium (0.1 mmol/kg body weight). The tumor
(arrows) arises from the right circumference of the rectum. Tumor
streaks extending into the perirectal fat correspond to a desmo-
plastic reaction. In addition, there is nodular extension into the
a mesorectum (open arrow). The tumor enhances intensely on the
postcontrast image. A suspicious mesorectal lymph node is present
(arrowhead).

a b

Fig. 6.9a–c Low rectal carcinoma, stage T4. a Axial T2w TSE image.
b, c Axial (b) and sagittal (c) T1w fat-suppressed images after IV
bolus administration of Gd-based contrast medium (0.1 mmol/kg
body weight). The ulcerating tumor (arrows) invades the external
and internal anal sphincter muscles, vagina, and anal canal. There is
subtotal intestinal occlusion.

c
MRI Appearance of Pathologic Entities 135

Tumor Recurrence

Local recurrence is defined as regrowth of tumor in or


around the tumor bed after radical surgical excision (R0
resection) and includes regrowth within the regional lym-
phatics, surgical scars, and drain sites. A distinction is
made between intraluminal recurrence at the anasto-
motic sites and extraluminal recurrence (Fig. 6.11). Recur-
rent rectal cancer in the presacral area often involves the
piriform muscle and may invade the sacral bone and
ischiadic nerve. Rectal cancer has a recurrence rate of up
to 50 %, depending on the tumor stage at diagnosis.
It may be very difficult to distinguish postoperative or
radiation-induced scars from recurrent tumor. Recurrent
rectal cancer is of high signal intensity on T2w images and
enhances after contrast administration. Fig. 6.10 Mesorectal lymph nodes in a man with rectal carcinoma.
Axial PD image. There is good delineation of two enlarged lymph
nodes (arrows) within the mesorectal fatty tissue. MRI provides no
reliable criteria for deciding whether these lymph nodes are meta-
static or not.

a b

c d
Fig. 6.11a–g Two cases of rectal carcinoma recurrence. a–d Recur- to the right pelvic sidewall and invasion of the right ureter and the
rent rectal carcinoma. Axial T2w TSE images (a, c); axial T1w fat- vagina. A stent is present in the ureter (open arrow). The more
suppressed images (b, d) after IV bolus administration of Gd-based proximal slices (c, d) show a tumor cavity (*) containing liquefied
contrast medium (0.1 mmol/kg body weight). There is extraluminal tumor tissue.
tumor growth on the right side (arrows) with extension (arrowhead) Fig. 6.11e–g e
136 6 The Rectum and Anal Canal

e f

Fig. 6.11e–g Recurrent mucinous rectal carcinoma. Axial (e) and


sagittal (f) T2w TSE images. Axial (g) T1w fat-suppressed image
after IV bolus administration of Gd-based contrast medium (0.1
mmol/kg body weight). The extraluminal tumor on the left side
(arrows) is of high SI on the T2w images due to its high mucinous
content. Strong peripheral enhancement of the tumor on the post-
contrast image.

Anal Carcinoma is radiochemotherapy; radiotherapy alone may be ad-


equate in patients with small anal tumors. The TNM stag-
Anal carcinomas account for approximately 1–2 % of all ing system for anal carcinoma is summarized in Table 6.5.
colorectal carcinomas. The annual incidence is ca. 1 per
100 000 population. A distinction is made between tu-
mors of the anal canal and perianal tumors. The median Inflammatory Bowel Disease
age at diagnosis is ca. 60 years, and women are affected
more commonly. Risk factors are chronic inflammation Patients with Crohn disease of the small intestine have a
resulting from benign anal lesions, such as fistulas, fis- 32 % risk of developing perianal complications such as
sures, and abscesses, and viruses transmitted by anal fistulas and abscesses. The risk for these complications
intercourse. Histologically, the vast majority are squa- increases to 56 % in patients with additional colonic in-
mous cell carcinomas (ca. 90 %), which, unlike colorectal volvement (Fig. 6.12) and is as high as 70 % in isolated
cancer, do not arise in adenomatous polyps. Anal carci- Crohn disease of the colon. In 5 % of cases, perianal fistulas
noma is characterized by local infiltrative growth. Tumors and abscesses are the first manifestation of Crohn disease.
arising in the upper portion of the anal canal typically Other conditions associated with perianal fistulas are tu-
metastasize to perirectal, iliac, and mesenteric lymph no- berculosis and ulcerative colitis. Fistulas and abscesses in
des. Distant metastasis is rare. Lower tumors tend to in- Crohn disease differ from their conventional, simple coun-
vade inguinal lymph node groups. The standard treatment terparts in that they often form complex branching net-
MRI Appearance of Pathologic Entities 137

works of tracts and tend to recur. It is mainly in the Table 6.5 TNM staging system for anal carcinoma
preoperative evaluation of such complex branching fistu-
Primary tumor Lymph node Distant
las that MRI can provide important supplementary infor- size metastasis metastasis
mation on the exact extent and course.21–24
T1 ≤ 2 cm N1 – perirectal nodes M1*
As a rule, no rectal contrast medium is needed. The MRI
T2 > 2–5 cm N2 – unilateral internal iliac/
protocol primarily consists of IR sequences (STIR, TIRM)
inguinal node(s)
and fat-suppressed T1w sequences after intravenous con- T3 > 5 cm N3 – perirectal and inguinal
trast administration in coronal and axial planes. Addi- nodes; bilateral internal iliac/
tional sagittal sequences may be required if rectovaginal, inguinal nodes
rectovesical, or rectourethral fistulas are suspected. T4 Organ
The aim of preoperative MRI is to accurately character- invasion
ize fistulous tracts and their relationship to the sphincter * E.g., liver (50 %), pelvis and peritoneum (25 %), lung (15 %)
complex.25 The types of perianal fistulas that are distin-
guished on the basis of their course are summarized in
Table 6.6. The radiologist’s report should provide informa-
Table 6.6 Anatomic classification of perianal fistulas
tion on the internal and external openings of any fistulous
tract and its course in relation to the internal and external Fistula Course
anal sphincters and the levator ani muscle. In more ex- Sub- Courses from the dentate line to exit the skin in the
tensive fistulous disease, the relationship to adjacent pel- cutaneous perianal area, bypassing the sphincter mechanism
vic organs (uterus, uterine tubes, ovaries, vagina, prostate, Inter- Passes from the dentate line through the internal
seminal vesicles, urethra) and their possible involvement sphincteric sphincter and intersphincteric space to exit the
in the inflammatory process are described. skin in the perianal area
Active fistulous tracts are high in signal intensity on Trans- Extends from the dentate line through the internal
sphincteric and external sphincters, then continues para-anally
fat-suppressed T2w or IR images because they contain
or through the ischiorectal fossa to exit the skin in
fluid, while they are isointense to fat on non-fat-sup- the perianal area
pressed T2w images. On T1w imaging, fistulas are of low Ischiorectal Extends from the skin into the ischiorectal fossa,
signal intensity and enhance after contrast administra- does not communicate with the sphincter or anal
tion. Perianal abscesses, which are defined as lesions canal, often has branching tracts
> 1 cm in size, have the same signal characteristics. A Supra- Extends into the supralevator space above the le-
subcutaneous fistula arises low in the anal canal and levator vator ani muscle, opens into the anal canal or
traverses the internal anal sphincter to then track down rectum

a b
Fig. 6.12a, b Crohn disease with rectal involvement. Axial (a) and to severe inflammation (arrows) and enhances intensely. Thickening
coronal (b) T1w fat-suppressed images after IV bolus administration causes subtotal occlusion of the intestinal lumen (*). Perirectal fat
of Gd-based contrast medium (0.1 mmol/kg body weight). The wall stranding (open arrow) is consistent with an accompanying inflam-
of the rectum and rectosigmoid junction is markedly thickened due matory response.
138 6 The Rectum and Anal Canal

a b

c d
Fig. 6.13a–d Subcutaneous fistula tract in Crohn disease. a Axial therefore shown with high SI on the IR image (arrowhead in a).
fat-suppressed IR image. b–d Axial (b, c) and coronal (d) T1w fat- There is inflammatory soft-tissue edema (* in a) in the area of the
suppressed images after IV bolus administration of Gd-based con- gluteal fold on the left. The internal opening is at ca. 3 o’clock (open
trast medium (0.1 mmol/kg body weight). The cutaneous opening arrow in c). Nearly the entire course of the fistula is visualized on the
of the fistula seen at the 6 o’clock position contains fluid and is coronal T1w fat-suppressed image (arrows in d).

the intersphincteric space to the skin (Fig. 6.13). A fistula


that arises at a higher level, or a distal fistula that exclu-
sively or additionally courses upward initially, passes
through the intersphincteric space, where an abscess
may develop (intersphincteric abscess). More complicated
fistulas traverse both layers of the sphincter and extend
into the para-anal space (Fig. 6.14), or even further into
the ischiorectal fossa, and are often associated with para-
anal or ischiorectal abscess formation (Fig. 6.15). An inter-
sphincteric fistula can traverse the levator ani muscle and
give rise to a supralevator abscess (Fig. 6.16) and/or track
through the levator plate from above (supralevator, trans-
levator fistula, Fig. 6.17). In this way, the inflammatory
process spreads to the ischiorectal fossa, where an abscess
and/or additional fistulous tracts may form. Scars are of
Fig. 6.14 Transsphincteric fistula on the left (arrow). Axial T2w TSE low signal intensity on T1w and T2w images but may have
image. The transsphincteric fistula opens into a pararectal abscess slightly higher signal intensity than fat on fat-suppressed
on the left. There is an additional, interspincteric abscess anterior to T2w images.
the anal canal.
MRI Appearance of Pathologic Entities 139

a b

c d
Fig. 6.15a–d Para-anal horseshoe abscess. Axial (a) and coronal (b) is of high SI on the IR images. On the postcontrast fat-suppressed
fat-suppressed IR images. Axial (c) and coronal (d) T1w fat-sup- T1w images, the liquid has low SI while there is marked enhance-
pressed images after IV bolus administration of Gd-based contrast ment of the abscess membrane.
medium (0.1 mmol/kg body weight). The large para-anal abscess (*)

a b
Fig. 6.16a, b Supralevator abscess. a, b Axial (a) coronal (b) T1w abscess (arrow) above the left levator ani muscle. Low SI in the
fat-suppressed images after IV bolus administration of Gd-based abscess cavity. Intense enhancement of the abscess membrane. A
contrast medium (0.1 mmol/kg body weight). There is a small utricular cyst is present (open arrow).
140 6 The Rectum and Anal Canal

duced into the rectum for bowel opacification. In contrast


to conventional defecography, opacification of the bladder
and vagina is usually not required because of the high
intrinsic contrast of MRI, nor is it necessary to use intra-
venous contrast medium.
Performing MR defecography in an open-configura-
tion, low-field MR imager, which is normally used for
research and interventional procedures, appears to offer
some advantages over conventional, closed MR scanners
because it allows examining the patient in a natural sitting
position.26
In a closed MR system, defecography is performed with
the patient in the supine position. Before positioning the
Fig. 6.17 Supralevator (translevator) fistula. Axial T1w fat-sup- patient, the table is protected with an absorbent cover and
pressed image after IV bolus administration of Gd-based contrast a waterproof sheet. The examination should start with a
medium (0.1 mmol/kg body weight). The fistula tract (open arrow) fast three-plane T2w sequence (e. g., HASTE) to obtain an
extends through the right levator ani muscle. anatomic overview and rule out other pathology in the
true pelvis. The localizer is followed by a TrueFISP cine
sequence for acquisition of images in the midsagittal
Functional Disorders plane at rest and with the patient performing stool evac-
uation and holding maneuvers. In patients with a sus-
Functional disorders of the pelvic floor are a common pected lateral rectocele or pelvic floor hernia, the dynamic
clinical problem and can severely impair a patient’s qual- sequence is repeated in the axial plane.
ity of life because they may be associated with anal in- MR defecography will reveal anterior and lateral rec-
continence, stress incontinence, obstipation, organ pro- toceles (Fig. 6.18), invaginations, and rectal prolapse.27
lapse, or incomplete defecation. MR defecography is supe- Hernias of the pelvic floor can be identified and their
rior to conventional radiographic defecography because it severity assessed.
involves no radiation exposure and affords superior soft- Anatomic landmarks for identifying abnormalities are
tissue contrast and enables direct image acquisition in any the anorectal angle (angle formed between the central
plane. axis of the anal canal and a line parallel to the posterior
Bowel cleansing with an enema is advisable before MR wall of the distal rectum) and the pubococcygeal line (line
defecography. Immediately before the MRI examination, a extending from the inferior border of the pubic symphysis
contrast medium—most often ultrasound gel—is intro- to the last coccygeal joint).

a b
Fig. 6.18a, b MR defecography in a 65-year-old woman after hys- other anatomic structures of the true pelvis. During defecation,
terectomy. Sagittal TrueFISP cine sequences. a At rest. b During there is prolapse of the pelvic floor (arrows) and a large anterior
defecation. The ultrasound gel introduced using a rectal tube and rectocele becomes apparent (open arrows).
bladder syringe allows good delineation of the rectum (*) from the
MRI Appearance of Pathologic Entities 141

References 14. Beets-Tan RG, Beets GL. Rectal cancer: review with emphasis on
MR imaging. Radiology 2004;232(2):335–346
15. Brown G, Radcliffe AG, Newcombe RG, Dallimore NS, Bourne
1. Beets-Tan RG, Beets GL, van der Hoop AG, et al. High-resolution
MW, Williams GT. Preoperative assessment of prognostic factors
magnetic resonance imaging of the anorectal region without an
in rectal cancer using high-resolution magnetic resonance
endocoil. Abdom Imaging 1999;24(6):576–581, discussion
imaging. Br J Surg 2003;90(3):355–364
582–584
16. Brown G, Richards CJ, Newcombe RG, et al. Rectal carcinoma:
2. Vliegen RF, Beets GL, von Meyenfeldt MF, et al. Rectal cancer: MR
thin-section MR imaging for staging in 28 patients. Radiology
imaging in local staging—is gadolinium-based contrast material
1999;211(1):215–222
helpful? Radiology 2005;234(1):179–188
17. Cawthorn SJ, Parums DV, Gibbs NM, et al. Extent of mesorectal
3. Oberholzer K, Junginger T, Kreitner KF, et al. Local staging of
spread and involvement of lateral resection margin as prognos-
rectal carcinoma and assessment of the circumferential resec-
tic factors after surgery for rectal cancer. Lancet 1990;
tion margin with high-resolution MRI using an integrated par-
335(8697):1055–1059
allel acquisition technique. J Magn Reson Imaging 2005;
18. Klessen C, Rogalla P, Taupitz M. Local staging of rectal cancer:
22(1):101–108
the current role of MRI. Eur Radiol 2007;17(2):379–389
4. Devries AF, Griebel J, Kremser C, et al. Tumor microcirculation
19. Laghi A, Ferri M, Catalano C, et al. Local staging of rectal cancer
evaluated by dynamic magnetic resonance imaging predicts
with MRI using a phased array body coil. Abdom Imaging
therapy outcome for primary rectal carcinoma. Cancer Res
2002;27(4):425–431
2001;61(6):2513–2516
20. Brown G, Richards CJ, Bourne MW, et al. Morphologic predictors
5. DeVries AF, Kremser C, Hein PA, et al. Tumor microcirculation
of lymph node status in rectal cancer with use of high-spatial-
and diffusion predict therapy outcome for primary rectal carci-
resolution MR imaging with histopathologic comparison. Radi-
noma. Int J Radiat Oncol Biol Phys 2003;56(4):958–965
ology 2003;227(2):371–377
6. Dzik-Jurasz A, Domenig C, George M, et al. Diffusion MRI for
21. Beets-Tan RG, Beets GL, van der Hoop AG, et al. Preoperative MR
prediction of response of rectal cancer to chemoradiation.
imaging of anal fistulas: Does it really help the surgeon? Radi-
Lancet 2002;360(9329):307–308
ology 2001;218(1):75–84
7. Grabbe E, Lierse W, Winkler R. The perirectal fascia: morphology
22. Laniado M, Makowiec F, Dammann F, Jehle EC, Claussen CD,
and use in staging of rectal carcinoma. Radiology 1983;149(1):
Starlinger M. Perianal complications of Crohn disease: MR imag-
241–246
ing findings. Eur Radiol 1997;7(7):1035–1042
8. Jemal A, Murray T, Ward E, et al. Cancer statistics, 2005. CA
23. Maccioni F, Colaiacomo MC, Stasolla A, Manganaro L, Izzo L,
Cancer J Clin 2005;55(1):10–30
Marini M. Value of MRI performed with phased-array coil in
9. Sobin LH, Wittekind C. International Union Against Cancer
the diagnosis and pre-operative classification of perianal and
(UICC). TNM Classification of Malignant Tumours. New York:
anal fistulas. Radiol Med (Torino) 2002;104(1–2):58–67
Wiley; 2002
24. Myhr GE, Myrvold HE, Nilsen G, Thoresen JE, Rinck PA. Perianal
10. Swedish Rectal Cancer Trial. Improved survival with preopera-
fistulas: use of MR imaging for diagnosis. Radiology 1994;
tive radiotherapy in resectable rectal cancer. N Engl J Med
191(2):545–549
1997;336(14):980–987
25. Parks AG, Gordon PH, Hardcastle JD. A classification of fistula-in-
11. Kapiteijn E, Marijnen CA, Nagtegaal ID, et al; Dutch Colorectal
ano. Br J Surg 1976;63(1):1–12
Cancer Group. Preoperative radiotherapy combined with total
26. Roos JE, Weishaupt D, Wildermuth S, Willmann JK, Marincek B,
mesorectal excision for resectable rectal cancer. N Engl J Med
Hilfiker PR. Experience of 4 years with open MR defecography:
2001;345(9):638–646
pictorial review of anorectal anatomy and disease. Radio-
12. Bartram C, Brown G. Endorectal ultrasound and magnetic reso-
graphics 2002;22(4):817–832
nance imaging in rectal cancer staging. Gastroenterol Clin North
27. Hilfiker PR, Debatin JF, Schwizer W, Schoenenberger AW, Fried
Am 2002;31(3):827–839
M, Marincek B. MR defecography: depiction of anorectal anat-
13. Beets-Tan RG, Beets GL, Vliegen RF, et al. Accuracy of magnetic
omy and pathology. J Comput Assist Tomogr 1998;22(5):
resonance imaging in prediction of tumour-free resection mar-
749–755
gin in rectal cancer surgery. Lancet 2001;357(9255):497–504
143

7 The Kidneys and Upper Urinary Tract


M. Taupitz and R. A. Kubik-Huch

· Identification of the cause of urinary obstruction, e. g.,


Introduction
vascular compression of the ureteropelvic junction.
· Evaluation for renal artery stenosis as a cause of hyper-
MRI no longer merely provides morphologic information tension (discussed in Chapter 15).
on the kidneys and ureters but has evolved into a versatile · Evaluation of potential living kidney donors.
imaging technique for use in patients with renal or ure- · Post-transplant evaluation for suspected vascular com-
teral tumors and for detailed assessment of the renal plications, urinary obstruction, parenchymal perfusion
vasculature. Moreover, it also allows an insight into the defects, or tumor.
excretory function of the kidneys. A comprehensive MRI
protocol with use of intravenous contrast medium com-
bines multiplanar soft-tissue evaluation and qualitative
Imaging Technique
assessment of tissue perfusion with arterial and venous
MR angiography (MRA) and also includes excretory MR
urography (MRU). In particular, MRI can serve as a “one- Renal MRI is performed with the patient in a comfortable
stop shop” modality, replacing the classic combination of supine position; a knee support can be offered to improve
cross-sectional imaging, intravenous urogram, and con- comfort. As renal MRI regularly comprises sequences in
ventional angiography in the preoperative evaluation of the coronal plane with a left-to-right phase-encoding di-
renal and ureteral tumors. Such an MRI protocol can also rection, the patient’s arms may cause wraparound arti-
be used for assessing patients with renal and ureteral facts. Such artifacts can be avoided by placing cushions
anomalies. Two notable advantages—the absence of radi- underneath the arms to elevate them above kidney level.1
ation exposure and the lower nephrotoxicity of MRI due to The arms must not be placed on the patient’s abdomen as
the need for smaller amounts of contrast material—make this will cause wraparound on axial images. Patients are
this method suitable for younger patients and also for carefully instructed to breathe shallowly and regularly
patients with nonmalignant disease. MRI yields the during acquisition of non-breath-hold sequences to avoid
same diagnostic information as CT in patients who have excessive breathing motion of the abdominal wall. Careful
reduced kidney function or do not tolerate iodine-based breathing instructions are also necessary if respiratory-
contrast media. The only disadvantage of MRI compared triggered acquisition is planned. Finally, it is important
with CT is its poor visualization of urinary calculi, that the breathing commands to be given for breath-hold
although it nevertheless allows excellent evaluation of imaging are explained beforehand. For contrast-enhanced
the urinary obstruction secondary to urolithiasis. imaging, a flexible cannula should be placed, ideally in an
antecubital vein, before positioning the patient in the
magnet, and connected to a saline-filled syringe or, if
available, an MR-compatible injection pump via extension
Indications
tubing.

Thanks to its technical versatility, MRI enables evaluation


of the renal parenchyma, the arteriovenous system, and Coils
the renal collecting system and ureters, resulting in a
broad spectrum of indications for renal MRI: Body or torso phased-array coils for abdominal imaging
· Characterization of incidentally detected renal tumors are available from nearly all manufacturers and should be
if ultrasound or CT findings cannot exclude malig- used to improve the signal-to-noise ratio (SNR), especially
nancy. when fast pulse sequences are acquired2. Phased-array
· Comprehensive evaluation of surgical renal lesions (ex- coils (with 4–8 elements) are also needed to employ
tent, lymphadenopathy, intra-abdominal metastases) parallel imaging techniques such as sensitivity encoding
for surgical planning, which includes assessment of (SENSE), which can be used to shorten scan time or to
renal vascular anatomy and of the upper urinary tract. acquire higher-resolution images with both T1w and T2w
144 7 The Kidneys and Upper Urinary Tract

sequences.3–5 However, this gain may come with a pen- Precontrast Imaging
alty in SNR.6
At our institution, we acquire a localizer followed by a
T2w single-shot TSE sequence (e. g., HASTE) in axial, sagit-
Pulse Sequences tal, and coronal planes. The sagittal images are used to
angle the coronal sequence to the long axis of the kidney.
The renal MRI protocol can be tailored to different clinical An additional respiratory-triggered, fat-suppressed high-
indications (Table 7.1). The basic protocol for soft-tissue resolution T2w TSE sequence should be acquired in pa-
evaluation comprises T2w and T1w sequences in multiple tients with a small tumor7 (see “T2-Weighted Imaging” in
planes and should include a T1w sequence acquired with Chapter 1) (Fig. 7.1). An axial 2D T1w GRE sequence (e. g.,
in-phase (IP) and opposed-phase (OP) echo times (TEs) 2D FLASH) acquired with IP and OP TEs (see Table 1.3) is
(see Chapter 1). Static MRU of the renal collecting systems required for identification of lipid-containing renal tu-
and ureters is performed by acquiring a heavily T2w se- mors such as angiomyolipoma.1 If available, IP and OP
quence in the coronal plane (comparable to that em- images can be acquired using a double-echo sequence.
ployed for MRCP; see Chapter 2). The contrast-enhanced The 2D T1w GRE sequence can be replaced or supple-
series is acquired using a coronal 3D MRA sequence and mented by an axial or coronal fat-suppressed 3D GRE
includes an arterial and venous phase for vascular assess- sequence (e. g., VIBE) (Fig. 7.1). The 3D GRE sequence
ment (see Chapter 15). The protocol is completed by ac- improves spatial resolution because thinner slices can be
quiring a delayed axial T1w sequence identical to the acquired compared with its 2D counterpart; however, this
corresponding precontrast sequence. To obtain an excre- is achieved at the expense of soft-tissue contrast on non-
tory MR urogram, the 3D MRA sequence is repeated 5 min enhanced images.
and 10 min after intravenous contrast injection as well as
at later times if contrast medium excretion is delayed.
Details of the sequences used for the three main portions Contrast-Enhanced Imaging
of the renal MRI protocol are summarized in Table 7.2.
If contrast-enhanced MR images are primarily needed for
optimal soft-tissue visualization, and vessel contrast is
less important, an axial or coronal 3D GRE sequence em-

Table 7.1 MRI techniques for different indications

Indication Sequence Plane Unenhanced/ Comment


Contrast medium
Soft-tissue evaluation T2w single-shot TSE Axial, sagittal, Unenhanced Localization, extent, and characterization of
for characterization of coronal renal tumors; breath-hold acquisition
renal tumors and
assessment of tumor T1w GRE IP and OP Axial Localization, extent, and characterization;
extent breath-hold acquisition
T2w TSE, respiratory- Axial or Unenhanced Adjunct high-resolution images; free-breathing
triggered coronal acquisition
Renal vasculature T1w 3D GRE MRA Coronal Nonspecific contrast Arterial and venous phases for MRA and evalu-
(MRA) sequence medium ation of renal perfusion; tumor characterization
(hypovascular versus hypervascular); aberrant
vessels; anomalies
Improved contrast-en- T1w 3D GRE Axial or Nonspecific contrast Cortical, parenchymal, and excretory phases
hanced soft-tissue eval- (e. g., VIBE) coronal medium for evaluation of tissue perfusion; tumor char-
uation (instead of MRA) acterization (hypovascular versus hypervascu-
lar)
T1w GRE IP Axial Delayed images Detection of small tumors, characterization
after contrast
administration
Visualization of the Heavily T2w TSE Coronal Unenhanced Without or with furosmide; morphology of the
collecting systems and collecting system; anomalies
ureters (MRU)
T1w 3D GRE Coronal Nonspecific contrast Without or with furosemide; excretion and
sequence (same as medium (adminis- outflow, anomalies
for MRA) tered for MRA)
Follow-up T1w GRE, T2w TSE Axial, coronal Unenhanced Number and size of tumors

Note: Preoperative evaluation of renal tumors is performed using all three portions of the renal protocol (soft-tissue evaluation, MRA, and
MRU).
Table 7.2 Recommended pulse sequences and imaging parameters

Weighting Plane Sequence type TR TE Flip ETL FS Matrix FOV (mm) No. of No. of Slice thick- Scan time Breath-
(ms) (ms) (°) slices acquisi- ness (mm) hold
tions
T2 Axial, sagittal, HASTE ∞ 60–80 Fixed Yes/no 116 × 256 300 (75 %) 23 1 7 23 s Yes
coronal
T2 (supple- Axial TSE, respiratory- ca. 2500 80 – 7–15 Yes 168 × 320 300 (75 %) 48 2 4 5–7 min No
mentary T2w) triggered
T1 Axial 2D GRE ca. 2.2–7.0 90 – No 116 × 256 300 (75 %) 23 1 7 23 s Yes
170–200
T1 post- Axial or 3D GRE (VIBE) 5–7 2.2–2.6 10 – Yes 116 × 256 300 (75 %) 64 1 2.5 20–24 s Yes
contrast, coronal
soft tissue
T1 post- Coronal 3D GRE MRA 10–15 – – No 128 × 256 300 (75 %) 19 4 8 4–8 min No
contrast,
vessels
T2, collecting Coronal, thin HASTE ∞ 91 – 218 Yes 218 × 256 400 (100 %) 35 1 3 40 s Yes, mul-
systems slices tiple
T2, collecting Coronal, thick RARE 2800 1100 – 256 Yes 256 × 256 500 (100 %) 1 1 120 5s Yes
systems slab
T2, collecting Coronal TSE, respiratory- 2000 740 – 129 Yes 384 × 384 380 (100 %) 52 1 1.5 5–7 min No
systems triggered
T1, contrast Axial, coro- HASTE ∞ 60–80 Fixed Yes/no 116 × 256 300 (75 %) 23 1 7 23 s Yes
medium nal, sagittal
excretion

Slice distance, 10–20 % of slice thickness (distance factor, 0.1–0.2).


T1w GRE: TEs for acquisition of in-phase and opposed phase images, see Table 1.3.
FOV may have to be adjusted based on body habitus.
Note: The suggested parameters are only examples and have to be adjusted for use on different brands of scanners. Parallel imaging techniques can be used to shorten scan time (for sequences with one
signal average) but may come with a penalty in SNR.

Imaging Technique
145
146 7 The Kidneys and Upper Urinary Tract

a b

c d

e f
Fig. 7.1a–f Renal protocol in normal kidneys. Soft-tissue evaluation different time points after IV injection of Gd-based contrast me-
using unenhanced axial and coronal images and contrast-enhanced dium: at 15 s (d), 1 min (e), and 3 min (f). This renal protocol
axial images. a Axial T2w TSE image acquired with respiratory provides high-resolution postcontrast images for optimal soft tissue
triggering. b Coronal breath-hold T2w TSE image (HASTE). c–f evaluation with excellent corticomedullary differentiation in the
Dynamic contrast-enhanced series comprising axial fat-suppressed arterial phase (d) and characteristic tiger-stripe pattern of the
breath-hold T1w 3D GRE images (VIBE) acquired before (c) and at spleen.
Imaging Technique 147

a b

c d
Fig. 7.2a–d Renal protocol with coronal contrast-enhanced MRA quired 10 min after contrast injection to generate an excretory
sequence (3D GRE sequence) instead of the soft-tissue sequence MRU. This variant of the renal protocol yields postcontrast images
illustrated in Fig. 7.1. a, b MRA images were acquired 15 s (a) and of the renal parenchyma, images for evaluation of renal vessels, and
1 min (b) after IV contrast injection. c MIP reconstruction of a to images of the renal collecting systems and ureters for evaluation of
generate an arteriogram. d MIP reconstruction of a sequence ac- urinary outflow.

phasizing soft tissue (e. g., VIBE) should be used. Dynamic phase and 1 min after bolus injection of the contrast
contrast-enhanced imaging is performed during the arte- medium (Fig. 7.2). The MRA dataset serves to generate
rial/cortical phase (15 s), venous/corticomedullary phase multiplanar reformations (MPR) or maximum intensity
(1 min), and early excretory phase (at ca. 3 min) (Fig. 7.1). projections (MIP) of the target vessels and at the same
If the contrast-enhanced series is performed for vascular time provides detailed information on renal perfusion.
evaluation, a coronal 3D MRA sequence is acquired with a Finally, the precontrast 2D or 3D GRE sequence is repeated
field of view completely including the aorta and vena cava to obtain delayed images emphasizing soft tissues. To
as well as the kidneys. The sequence is angled to the obtain an excretory MR urogram, the 3D MRA sequence
longitudinal axis of the kidney using the sagittal T2w is repeated ca. 10 min after contrast injection (Fig. 7.2).
precontrast sequence (see above). Following a timing
run, the MRA sequence is acquired during the arterial
148 7 The Kidneys and Upper Urinary Tract

MR Urography vist), or Gd-DOTA (Dotarem). These are only examples,


and contrast media development is a very dynamic field,
This can be performed in one of two ways:8,9 which is why radiologists should always check the most
· T2w static MRU up-to-date information regarding approval status in their
· T1w excretory MRU. own country before administering any intravenous con-
trast medium. The nonspecific Gd-based agents rapidly
T2w Static MR Urography. This technique involves the use distribute in the extracellular space after intravenous in-
of heavily T2-weighted TSE sequences initially developed jection and are eliminated via the kidneys. Their elimina-
for MRCP and yielding images on which stagnant fluid is tion is thus comparable to that of iodine-based X-ray
depicted with a bright signal (hydrography). The slices are contrast media. Soft-tissue evaluation and MRU are per-
acquired in coronal planes angled to the kidneys and formed with administration of the standard dose of
ureters using a sagittal localizer. One way to obtain a static 0.1 mmol Gd per kg body weight. A dose of 0.2 mmol/kg
MR urogram is to acquire thick slabs in multiple projec- Gd is administered if the protocol also includes MRA.
tions during short breath-holds of ca. 3–5 s using a single- Especially when the higher dose is injected, the high
shot T2w TSE sequence (e. g., HASTE, RARE). These have urinary concentration can cause signal voids in the col-
limited detail resolution and merely serve to gain a quick lecting system on delayed images. Note that static T2w
overview or as an additional planning scan. Better image MRU cannot be performed after intravenous contrast in-
quality is obtained by acquiring multiple thin slices during jection.
a 20-s breath-hold using a T2w single-shot TSE sequence. Patients with severely compromised renal function
The thin-slice datasets can be postprocessed using MPR or have a small risk of developing nephrogenic systemic
MIP algorithms. Image quality can be further improved by fibrosis (NSF) after intravenous injection of Gd-based con-
respiratory-triggered acquisition of T2w 3D TSE sequen- trast medium. Radiologists should therefore use such
ces;10 however, the scan time is several minutes (Fig. 7.3). agents with great caution in these patients, taking into
Static MR urograms provide no functional information but account the most recent official guidelines and man-
allow evaluation of the collecting system in patients with ufacturers’ recommendations. In general, patients with
no or only little excretory function. severe renal impairment should not receive Gd doses
exceeding 0.1 mmol/kg and should not undergo repeated
T1w Excretory MR Urography. This technique is based on contrast-enhanced MRI at short intervals.
the renal excretion of an intravenously injected MR con-
trast medium and its detection with a heavily T1-weighted
coronal 3D GRE sequence identical to that employed for
MRI Appearance of Normal Anatomy
MRA. Images are acquired at similar time points as with
conventional intravenous urography (Fig. 7.3). However,
adequate contrast filling may be delayed in patients with The kidneys are paired organs located in the lumbar fos-
severely dilated collecting systems and ureters or reduced sae in the retroperitoneum. Grossly, the renal parenchyma
excretory function. This limits the use of excretory MRU in is composed of the renal medulla and the renal cortex.
the routine clinical setting as it may not be feasible to With MRI, the corticomedullary differentiation is best
repeat imaging at later time points. Both techniques of appreciated on unenhanced and early contrast-enhanced
MRU can be performed with administration of a diuretic T1w images (Fig. 7.1). The kidney has a firm capsule,
(0.05–0.1 mg furosemide) for dilatation and improved which is not usually seen on imaging, and an outer adi-
visualization of the collecting systems and ureters. Furo- pose capsule (or perirenal fat). The kidney, adrenal gland,
semide improves overall image quality of excretory MRU and adipose capsule are enclosed by the renal fascia. The
by enhancing the elimination of the contrast medium and fascia is most conspicuous on MR images when it is thick-
its mixing with the urine.8 ened, e. g., due to inflammation.11

Contrast Media

Renal MRI including MRA and MRU is performed using a


nonspecific Gd-based contrast medium such as Gd-DTPA
(Magnevist), gadoteridol (Prohance), gadobutrol (Gado-
MRI Appearance of Normal Anatomy 149

a b

c d
Fig. 7.3a–d Illustration of normal collecting system on static MRU gering. b–d Coronal 3D GRE images (MRA sequence) acquired
(hydrography) and excretory MRU. a MIP reconstruction of coronal 1 min (b), 7 min (c), and 15 min (d) after IV injection of Gd-based
heavily T2w multislice TSE sequence acquired with respiratory trig- contrast medium (augmented by IV injection of 5 mg furosemide).
150 7 The Kidneys and Upper Urinary Tract

MRI Appearance of Pathologic Entities matic injury because it is less well protected than a kidney
in normal location.12
Ectopic insertion of a ureter results from abnormal mi-
Benign Conditions gration of a ureteral bud. An ectopic ureter opening into
the bladder typically inserts lower than a normal ureter.
Anomalies Other ectopic insertions are the urethra, the vagina, and
the uterus in females and the posterior urethra, the semi-
An ectopic kidney, such as a pelvic kidney, results from nal vesicles, the ejaculatory duct, and the vas deferens in
failure of the developing kidney to ascend to its normal males. An ectopic ureter inserting below the continence
position. The multiplanar capability of MRI, in particular mechanism causes urinary incontinence, which is the case
the coronal plane, is helpful for defining the exact position in ca. 50 % of ectopic ureters. About 70 % of ectopic ureteral
of an ectopic kidney, and an MRA sequence can be per- openings are associated with a duplex kidney and a bifid
formed to assess its blood supply. An ectopic kidney is ureter.13 It is important to identify such anomalies as early
typically supplied by aberrant arteries arising from the as possible; however, the diagnosis is sometimes delayed
aorta or pelvic arteries. until adulthood. MRI with the option of static T2w uro-
A horseshoe kidney (Fig. 7.4) is the fusion of the inferior graphy is the ideal imaging modality for this purpose
poles of the two kidneys by an isthmus of fibrous tissue or because it will also depict a nonfunctioning or poorly
renal parenchyma. An ectopic or horseshoe kidney typi- functioning renal moiety (Fig. 7.5).14
cally has normal function but is more susceptible to trau-

a b

c
Fig. 7.4a–d Horseshoe kidney without associated anomalies.
a, b Axial T1w (a) and T2w (b) images through the renal hilum.
c Axial fat-suppressed T2w TSE image acquired through the paren-
chymal isthmus at a lower level. d MIP reconstruction of a contrast-
enhanced MRA showing the parenchymal vessels and beginning
excretion of the contrast medium (from test bolus injection) into
the renal caliceal system.
d
MRI Appearance of Pathologic Entities 151

a b
Fig. 7.5a, b Ectopic insertion of left ureter draining the upper markedly dilated ureter draining the upper moiety inserts into the
moiety in duplex kidney. a Coronal T2w HASTE image. b Coronal urethra (curved arrow), and there is high-grade stenosis of the
heavily T2w thick-slab TSE image (projection technique). The rudi- ureteral orifice.
mentary upper moiety shows hydronephrotic changes (arrow); the

Trauma Inflammation/Abscess

Abdominal trauma such as that associated with traffic Imaging modalities are typically used in patients with
accidents often causes renal contusion or renal vascular acute pyelonephritis to evaluate for complications such
injury. Kidneys with prior damage (e. g., due to hydro- as pyonephrosis or abscess. Renal inflammation is seen on
nephrosis) or in an ectopic position are more susceptible MRI as swelling of the kidney, altered signal intensities
to traumatic injury. The role of MRI in emergencies is due to accompanying edema, blurring of renal contours,
limited because monitoring of severely injured patients and loss of corticomedullary differentiation. There may be
is generally not possible. Multislice CT is the method of inflammatory stranding of perirenal fat and thickening of
choice in acute situations because it enables simultaneous perirenal fasciae, best appreciated on unenhanced T1w
evaluation of the renal parenchyma and renal vessels. images. Severe inflammation may be associated with focal
Apart from accidents, intra- or perirenal hematoma can perfusion defects on contrast-enhanced images. A full-
be caused by extracorporeal shockwave lithotripsy, diag- blown abscess is a lesion with a central fluid collection
nostic puncture, clotting disorders, arteriovenous malfor- of high T2 signal intensity surrounded by a wall that will
mations, renal artery aneurysms, renal cell carcinoma, or enhance after contrast administration.15
rupture of a renal cyst. In this setting, MRI will detect Both solitary renal cysts and cysts in patients with
small hemorrhage and contributes to the identification polycstic kidney disease can become infected. An infected
of the underlying cause and is also useful for follow-up. cyst resembles an abscess with a central fluid signal sur-
The T1 and T2 signal intensities of hemorrhagic lesions rounded by a thickened wall showing intense enhance-
vary with the age of the hemorrhage (Fig. 7.6). ment on postcontrast T1w images (Fig. 7.7).16
Perirenal hematoma must be differentiated from uri- Renal atrophy is usually due to chronic inflammation.
noma, which—just like urine in the bladder—has low sig- MRI may be indicated for example if a tumor is suspected.
nal intensity on T1w images and high signal intensity on Atrophied kidneys are only seen otherwise on MRI if the
T2w images. If injury of the pelvicaliceal system is sus- examination is performed for other purposes (Fig. 7.8).
pected in the acute setting, a postcontrast T1w series will
demonstrate leakage of contrast medium and thereby of
urine (see Figs. 7.33 and 7.34).
152 7 The Kidneys and Upper Urinary Tract

a b

Fig. 7.6a–c Older perirenal hematoma following puncture of the


left kidney. Axial breath-hold T1w GRE image (a) and breath-hold
T2w TSE images in axial (b) and sagittal (c) planes. Intralesional area
of high SI on T1w image and low-SI margin on T2w sequence
indicate different stages of hematoma organization with marginal
hemosiderin deposits (arrow).

a
Fig. 7.7a–d Infected renal cyst in the right kidney in bilateral cystic
kidney disease. a, b Axial (a) and coronal (b) breath-hold T2w TSE
images. c Precontrast axial breath-hold T1w GRE image. d Fat-sup-
pressed axial breath-hold T1w GRE image after IV contrast injection.
The fluid in the infected cyst appears homogeneous on the unen-
hanced images and has a thickened wall, which enhances intensely
on the postcontrast image.
b
Fig. 7.7c, d e
MRI Appearance of Pathologic Entities 153

c d
Fig. 7.7c, d

Fig. 7.8a–d Pyelonephritic atrophy of both kidneys. a, b Breath-


hold axial (a) and (b) coronal T2w TSE images. c, d Breath-hold axial
T1w GRE images before (c) and 2 min after (d) IV contrast injection.
There is marked atrophy of both kidneys with only a little perfused
residual parenchyma. d
154 7 The Kidneys and Upper Urinary Tract

(Figs. 7.9 and 7.10). Chronic obstruction can be congenital


or acquired. Causes of acquired obstruction are tumors of
the urinary bladder, prostate, uterine cervix, or retroper-
itoneum, ureteral strictures, and benign prostatic hyper-
plasia. If the underlying cause cannot be identified by
ultrasound, MRU performed as part of a renal soft tissue
and vascular MRI protocol should be preferred to conven-
tional intravenous urography or CT. The absence of radi-
ation exposure is especially important in younger pa-
tients.

Renal Cysts

Fig. 7.9 Small caliceal stone in the middle caliceal group of the left Simple cysts (Fig. 7.11), the most common renal lesions,
kidney. Respiratory-triggered, fat-suppressed T2w TSE image. The
are found in ca. 50 % of adults after the age of 50. They are
stone causes a signal void within the slightly dilated calix (arrow).
Also present is a cyst in the lower pole of the right kidney. typically benign and detected incidentally. On MRI they
are seen as sharply demarcated lesions of low T1 signal
intensity and high T2 signal intensity which do not en-
hance on T1w images following intravenous contrast me-
dium administration.1 Parenchymal, cortical, and parapel-
vic renal cysts are distinguished by location. Parapelvic
cysts can mimic dilatation of the pelvicaliceal system on
ultrasound and unenhanced T1w and T2w MR images.
Unclear cases can be resolved by a contrast-enhanced
T1w study including an excretory MR urogram (Fig. 7.12).
Complicated cysts are due to inflammation or hemor-
rhage and contain proteinaceous material or blood. They
typically have higher signal intensity on T1w images and
lower signal intensity on T2w images; the signal intensity
of hemorrhagic cysts varies with the age of the blood
(Figs. 7.13 and 7.14). Septa, wall thickening, and calcifi-
cations are common. Differentiation of a complicated cyst
from a neoplasm may occasionally pose a problem based
merely on the MRI appearance. It has been reported that
cancer is present in up to 30 % of kidneys with a hemor-
rhagic cyst. If imaging findings are inconclusive, surgical
exposure of the kidney and histologic examination are
needed for a definitive diagnosis.17
Autosomal dominant polycystic kidney disease (ADPKD)
is the adult form of polycystic kidney disease with symp-
toms usually developing after the age of 40. There is an
Fig. 7.10 Urinary obstruction due to a stone in the right ureter. MIP association with cysts in other organs, such as the liver,
image of excretory MRU performed with a coronal 3D GRE sequence and cerebral artery aneurysms. Unlike contrast-enhanced
ca. 10 min after IV contrast injection. Dilatation of the right collect-
CT, MRI can also be performed in patients with renal
ing system and ureter down to the level of the stone at the iliac
vessel crossing (arrow).
insufficiency.18 The typical MRI finding is that of massively
enlarged kidneys containing multiple cysts of varying size
and signal intensity (Fig. 7.14). MRI is typically performed
to exclude superinfection (see Fig. 7.7) or renal cell carci-
Urinary Obstruction noma in patients presenting with fever or pain. However,
differentiation between a complicated hemorrhagic cyst
Dilatation of the renal collecting systems and ureters oc- and inflammation or cancer may pose a considerable
curs secondary to acute or chronic obstruction. The most challenge, even with MRI. Hilpert and coworkers19 have
common causes of acute obstruction are stones or blood shown that hemorrhagic cysts in patients with polycystic
clots, pregnancy, and ureteral edema developing after kidney disease can often be distinguished from cancer by
iatrogenic instrumentation, e. g., for stone extraction the presence of visible fluid–hemosiderin levels.
MRI Appearance of Pathologic Entities 155

b
Fig. 7.11a–c Simple renal cyst. a, b Axial images acquired with
breath-hold T2w TSE sequence (a) and T1w GRE sequence (b).
c Parasagittal reconstruction of a 3D GRE MRA sequence acquired
1 min after IV injection of Gd-based contrast medium. The cyst is
seen as a smoothly demarcated lesion of uniform high SI on T2w
image (a) and uniform low SI on T1w image (b). No enhancement of
the lesion on postcontrast image (c).

Benign Renal Tumors cytomas are rather large, measuring on average 5–8 cm,
and have an excellent long-term prognosis. However,
Benign tumors of the kidney are usually small and asymp- oncocytomas have been reported to contain focal malig-
tomatic and are often incidentally detected by ultrasound, nant areas.22 Despite their size, about half of all renal
CT, or MRI. They are of epithelial or mesenchymal origin oncocytomas cause no symptoms. In the other cases,
(Table 7.3). Oncocytoma and renal cell adenoma are of hematuria is the most common symptom.
epithelial origin. Benign mesenchymal tumors comprise The CT and MRI appearance of renal oncocytoma is
angiomyolipomas and less common neoplasms such as characterized by a central stellate scar in an otherwise
hemangioma, lymphangioma, leiomyoma, lipoma, and homogeneous lesion. The scar is present in ca. 50 % of all
juxtaglomerular tumors (reninoma). oncocytomas, but has also been reported in renal cell
Oncocytoma is composed of large eosinophilic cells and carcinoma.23 A spoke-wheel-like pattern of enhancement,
is among the more common benign renal tumors. They known from conventional angiography, may be seen on
are 1.6–2.5 times more common in men and occur at early dynamic contrast-enhanced images24 (Figs. 7.15 and
slightly higher ages than classic adenomas.20,21 Onco- 7.16).
156 7 The Kidneys and Upper Urinary Tract

a b

c d
Fig. 7.12a–d Bilateral parapelvic cysts. a, b Breath-hold axial T2w present, which appear as a septated mass within the dilated renal
TSE image (a) and breath-hold sagittal T2w TSE image of the right sinus, in particular on the T2w images, and may be misinterpreted
side (b). c Breath-hold axial T1w GRE image. d MIP reconstruction of as dilatation of the collecting system. MIP image depicts thin cal-
a 3D GRE MRA sequence acquired 10 min after IV injection of Gd- iceal necks, and only the upper caliceal group on the right is slightly
based contrast medium (MRU). Multiple large parapelvic cysts are dilated because the necks are compressed by the cysts.

Fig. 7.14a–d Polycystic kidney disease. a Axial breath-hold T1w GRE image. b–d Axial (b), coronal (c), and sagittal (d) breath-hold T2w TSE w
images. Both kidneys are massively enlarged and completely replaced by cysts. High SI of some cysts on T1w image (a) and fluid-hemosiderin
levels indicate hemorrhage.
MRI Appearance of Pathologic Entities 157

a b
Fig. 7.13a, b Hemorrhagic cortical cyst next to an uncomplicated cyst. a Axial breath-hold T2w TSE image. b Axial breath-hold T1w GRE
image. The hemorrhagic cyst (arrow) reverses the SI of the simple cyst with low T2 SI and moderately high T1 SI.

a b

c d
158 7 The Kidneys and Upper Urinary Tract

a b

c d

Fig. 7.15a–e Oncocytoma. a Axial breath-hold T2w image (True-


FISP). b–e Axial breath-hold T1w GRE images acquired before (b)
and 15 s (c), 1 min (d), and 2 min (e) after IV contrast injection. The
tumor shows typical early and nearly completely homogeneous
enhancement, consistent with a hypervascular tumor such as onco-
cytoma. This MRI examination does not exclude RCC (images cour-
e tesy of Dr. B. Sander, Berlin).

Table 7.3 Overview of benign renal tumors

Common Rare
· Oncocytoma · Hemangioma
· Angiomyolipoma · Leiomyoma
· Multilocular cystic nephroma · Lymphangioma
· Lipoma
· Juxtaglomerular tumor (reninoma)
MRI Appearance of Pathologic Entities 159

a b

c d

e f
Fig. 7.16a–f Oncocytoma. a Unenhanced axial T1w SE image. b Fat- images as it is nearly isointense to surrounding renal parenchyma.
suppressed axial T2w TSE image. c–f Dynamic breath-hold coronal The dynamic contrast-enhanced images show a sharply marginated
GRE images before (c) and immediately (d), 1 min (e), and 3 min (f) lesion with spoke-wheel enhancement, consistent with an onco-
after IV injection of contrast medium. Mass in the center of the right cytoma.
kidney (arrows). The lesion is not very conspicuous on T1w and T2w
160 7 The Kidneys and Upper Urinary Tract

a b

Fig. 7.17a–c Angiomyolipoma. a, b Unenhanced axial T1w GRE


images acquired with IP (a) and OP (b) TEs (see Chapter 1 for details
of IP/OP imaging). c Axial T2w HASTE image. Tumor in the right
kidney (arrow in a) with high SI on IP image and loss of signal on OP
image, resulting in a dark line around the tumor. The IP/OP signal
characteristics suggest a large fatty component of the tumor, in
keeping with an angiomyolipoma. The T2w features contribute no
diagnostic information.

Renal angiomyolipoma is a hamartoma consisting of fat, location of liposarcoma.28,29 In rare instances, an angio-
smooth muscle, and abnormal blood vessels. Also com- myolipoma is predominantly composed of muscle tissue
mon are intralesional hemorrhage and necrosis. Angio- with only very little macroscopic fat; this tumor is difficult
myolipomas are rare, accounting for only 0.3 % of all renal to distinguish from renal carcinoma or other tumors
tumors.25 About 50–80 % of patients with renal angiomyo- based on imaging features.
lipomas suffer from tuberous sclerosis, and these patients On the whole, multilocular cystic nephroma is a rare
usually have smaller, multiple, and bilateral tumors.20,26 tumor of the metanephric blastema, though it is one of the
An angiomyolipoma may become as large as 20 cm. Symp- more common benign renal tumors. It appears to be a
tomatic patients typically present with a palpable ab- benign variant of Wilms tumor and has a biphasic age and
dominal mass, flank pain, microhematuria, or retroperi- sex distribution, affecting boys < 4 years of age and
toneal bleeding. Malignant behavior, including invasive women aged 40–60 years.30,31 The tumor is usually large
local growth, regional lymphadenopathy, and inferior (ca. 10 cm on average) and consists of multiple noncom-
vena cava thrombosis, has occasionally been observed. municating cysts separated by thin septa with a thick
However, renal angiomyolipomas are usually benign and capsule.
definitive control is achieved by surgical resection.20 A The clinical behavior is usually benign, with a rare
confident diagnosis of an angiomyolipoma can usually multilocular cystic nephroma undergoing malignant
be made by MRI. Fatty tumor components have high transformation to nephroblastoma in children or sarcoma
signal intensity on T1w images and can be confirmed by in adults. There are no CT or MRI criteria to reliably differ-
an additional fat-suppressed sequence, which clearly dis- entiate multilocular cystic nephroma from malignant
tinguishes fat from intralesional hemorrhage.27 On OP cystic tumors such as cystic Wilms tumor or cystic renal
images, there may be a loss of signal intensity of intra- cell carcinoma. For this reason surgical excision is indi-
tumoral fatty areas, or the signal loss is confined to an cated in all cases.30
interface between fat and normal renal tissue (Figs. 7.17 Rare benign tumors of the kidneys include heman-
and 7.18). gioma, lymphangioma, leiomyoma, and juxtaglomerular
Angiomyolipoma must be differentiated from liposar- tumors (reninoma). Except for lipoma, the MRI appear-
coma of the perirenal fatty tissue. Here, the multiplanar ance of these tumors is nonspecific and the diagnosis
capability of MRI is helpful in showing the extrarenal must be histologically confirmed.
MRI Appearance of Pathologic Entities 161

a b

c d
Fig. 7.18a–d Small angiomyolipoma. a, b Unenhanced axial T1w like loss of SI on OP image. The T2 SI is high without fat suppression
GRE images acquired with IP (a) and OP (b) TEs (see Chapter 1 for and low with fat suppression. This constellation of SIs suggests a
details of IP/OP imaging). c Axial T2w HASTE image. d Axial fat- tumor with a large fatty component and is consistent with the
suppressed T2w TSE image. Small tumor in the parenchyma of the diagnosis of angiomyolipoma.
left kidney (arrow) with high SI on IP image and characteristic ring-

In the past, the term renal adenoma was used to refer Malignant Renal Tumors
to solid tumors up to 2 cm in size, which are even difficult
to differentiate histologically from malignant adenocarci- Primary Renal Tumors
nomas. Therefore, it has been proposed that what used to
be referred to as renal adenoma is simply an early, non- An overview of primary and secondary renal malignancies
metastatic stage of malignant adenocarcinoma.20 A small is given in Table 7.4.
vascularized solid tumor without features of an angio- Renal cell carcinoma (RCC) is the most common malig-
myolipoma (fatty component) should be classified as a nancy of the kidneys but accounts for only 2 % of all adult
small renal cell carcinoma (RCC). tumors. RCC is more common in men, with an age peak in
Small solid tumors < 2 cm in diameter without patho- the fifth and sixth decades. About 1 % of RCCs are bilateral,
logic, histologic, or imaging features of malignancy or and multiple tumors in one kidney are present in ca. 5 % of
aggressive behavior are found in 4–22 % of all autop- cases. The signs and symptoms are unspecific and typi-
sies.32 Since no definitive imaging criteria exist to distin- cally occur late. Only ca. 20 % of RCCs present with the
guish between benign and malignant lesions, all lesions, classic triad of flank pain, hematuria, and a palpable
including small ones, incidentally detected by MRI or mass.33
another imaging modality should be regarded as poten- Exact pretherapeutic determination of the tumor ex-
tially malignant and closely monitored or surgically re- tent is important because radical surgical resection is the
moved. MR imaging in multiple planes provides detailed only curative treatment option. RCC not extending beyond
information on the site and extent of a renal tumor, which the renal capsule (stages T1 and T2) is treated by radical
is especially important in patients scheduled for surgical nephrectomy, supplemented by thrombectomy with ve-
enucleation or partial kidney resection rather than ne- nous graft repair as needed for tumors extending into the
phrectomy. renal vein and inferior vena cava.
162 7 The Kidneys and Upper Urinary Tract

Table 7.4 Overview of primary and secondary malignant renal The Robson classification is widely accepted for staging
tumors RCC in the USA, whereas the TNM classification system is
Primary malignant renal tumors more widely used in Europe.34 The staging accuracy re-
ported for multislice CT ranges between 70 % and 91 %,
Common with that for MRI being comparable or slightly better.35–37
· Renal cell carcinoma (hypernephroma, renal adenocarcino- Both CT and MRI are highly accurate in staging RCC with
ma) tumor thrombus in the inferior vena cava.38 With regard
· Transitional cell carcinoma (TCC) to tumor characterization, MRI is slightly better than CT in
· Wilms tumor (nephroblastoma)
correctly identifying cystic lesions.39
Rare Like other solid renal tumors, RCC is typically iso-
· Leiomyosarcoma intense to surrounding tissue on unenhanced T1w images
· Rhabdomyosarcoma and can only be suspected if the tumor distorts the renal
· Angiosarcoma contour. The T2 appearance is variable. Liquid areas due to
· Liposarcoma
necrosis and intralesional hemorrhage are present in
· Fibrosarcoma
ca. 15 % of RCCs and have high signal intensity on T2w
Secondary malignant renal tumors images. Both detection and characterization of RCC can
· Metastases be improved by administration of intravenous contrast
· Lymphoma medium.27,40
Even small tumors can be detected and characterized
using the high-resolution sequences available today. Im-
ages obtained 1–2 min after administration of contrast
medium are an integral part of the renal protocol (Figs.
7.19 and 7.20). Also important is the multiplanar capabil-

a b

c d
Fig. 7.19a–d Small RCC in the right kidney, stage T1. a Fat-sup- of the right kidney (arrow). The tumor has no cystic components on
pressed, respiratory-triggered axial T2w TSE image. b–d Dynamic T2w image and shows a moderate SI increase on contrast-enhanced
contrast-enhanced, breath-hold axial T1w 2D GRE images acquired image. These features suggest a solid, vascularized tumor and are
before (b) and 15 s (c) and 2 min (d) after IV injection of Gd-based highly indicative of malignancy.
contrast medium. Small parenchymal tumor in the anterior aspect
MRI Appearance of Pathologic Entities 163

a b

Fig. 7.20a–c Small RCC in the right kidney, stage T1, incidentally
detected in an evaluation of a potential renal donor. a Breath-hold
axial T2w TSE image. b Breath-hold axial T1w GRE image. c Coronal
reconstruction of a 3D GRE MRA sequence acquired 1 min after IV
contrast injection. Only focal contour distortion is seen on the
unenhanced images. A malignant tumor is suggested by the inho-
mogeneous SI increase seen in this area on the postcontrast image
(arrow in c).

ity of MRI, which affords accurate assessment of tumor Transitional cell carcinoma (TCC) of the renal pelvis
extent with good delineation of the mass from surround- accounts for 7 % of all renal neoplasms. Risk factors include
ing organs on sagittal and coronal images (Figs. 7.21, 7.22, urinary bladder cancer, analgesic abuse, and exposure to
7.23, 7.24). carcinogenic agents (aniline dyes, cyclophosphamide, to-
Venous invasion is present in ca. 20 % of patients with bacco smoke).
RCC at the time of diagnosis and is best detected by a TCC tends to be multicentric with ca. 8–40 % of TCC
venous phase 3D MRA sequence (MR venogram) patients having a synchronous or metachronous tumor of
(Fig. 7.23). At the same time, contrast-enhanced T1w im- the lower urogenital tract or on the contralateral side.41,42
ages enable differentiation of a vascularized tumor throm- The diagnostic role of MRI is limited and small tumors that
bus from an appositional thrombus. do not dilate the pelvicaliceal system may be overlooked
The high susceptibility of MRI to the effects of contrast because they are typically isointense to surrounding tis-
media, in conjunction with the high resolution afforded sues. However, TCC usually enhances early on postcon-
by state-of-the-art techniques, most notably 3D MRA se- trast images.43 Imaging cannot differentiate advanced TCC
quences, allows good evaluation of delicate structures invading the renal parenchyma from RCC; and vascular
enhanced by contrast administration and facilitates the invasion, though less common than in RCC, has also been
separation of complicated benign cysts and cystic RCC reported for TCC44 (Figs. 7.26 and 7.27). If a tumor cannot
(Fig. 7.25). be reliably classified as RCC, the radiologist’s report
Above a size threshold of 1–1.5 cm, a lymph node is should mention a TCC as a possible differential diagnosis.
assumed to be metastatic; however, this criterion is un- This is important because the surgical approach is differ-
reliable and false positive results due to reactive lymph ent: nephrectomy for RCC vs nephrectoureterectomy for
node enlargement and false negative results due to micro- TCC.
scopic metastasis in normal-sized lymph nodes are not
uncommon (Fig. 7.24).
164 7 The Kidneys and Upper Urinary Tract

a b

c d
Fig. 7.21a–f RCC, stage T1. MRI to plan organ-sparing surgical fat. Slices acquired in different planes and during different perfusion
resection. a, b Breath-hold axial (a) and sagittal (b) T2w TSE im- phases enable highly accurate definition of tumor extent, especially
ages. c, d Breath-hold T1w GRE images before (c) and 2 min after (d) its relationship to the structures of the renal sinus (including the
IV injection of Gd-based contrast medium. e, f Contrast-enhanced pelvicaliceal system). In the case shown, the MRA sequence of the
3D GRE MRA sequence reconstructed as an MIP image at 15 sec (e) renal protocol revealed three arteries supplying the right kidney.
and as a coronal MPR at 1 min (f). Tumor in the upper aspect of the The tumor was laparoscopically removed and the kidney preserved.
right kidney causing contour distortion without invasion of perirenal
Fig. 7.21e, f e
MRI Appearance of Pathologic Entities 165

e f
Fig. 7.21e, f

a b
Fig. 7.22a–e RCC of the right kidney, stage T3b. a–c Breath-hold signs of extension to the Gerota fascia. The tumor invades the renal
axial (a), coronal (b), and sagittal (c) T2w TSE images. d, e Breath- sinus and a small tumor thrombus extends through the renal vein
hold T1w GRE images before (d) and 2 min after (e) IV injection of into the inferior vena cava (arrow in e).
Gd-based contrast medium. Large tumor in the upper half of the
right kidney causes marked contour distortion while there are no Fig. 7.22c–e e
166 7 The Kidneys and Upper Urinary Tract

c d

Fig. 7.22c–e

Fig. 7.23a–e RCC of the right kidney, stage T3c. a–c Breath-hold
axial (a), coronal (b), and sagittal (c) T2w TSE images. d Coronal
breath-hold 3D GRE MRA sequence acquired 1 min after IV contrast
injection with reconstruction of coronal slice for evaluation of the
tumor. e Coronal breath-hold thin-slice MIP image for evaluation of
the tumor thrombus. Tumor in the upper third of the right kidney
with contour distortion; no invasion of the perirenal fat but large
tumor thrombus in the inferior vena cava with the tip extending into
the right atrium (arrow in e).

Fig. 7.23b–e e

a
MRI Appearance of Pathologic Entities 167

b c

d
Fig. 7.23b–e

e
168 7 The Kidneys and Upper Urinary Tract

a
Fig. 7.24a, b RCC of the right kidney, stage T4. a Breath-hold axial
T1w GRE image. b 3D GRE MRA sequence acquired 1 min after IV
contrast injection with reconstruction of coronal slice. The tumor
appears small on the axial image, while extensive infiltration of the
liver is seen on the coronal image. The axial image also reveals b
numerous enlarged retroperitoneal lymph nodes. Histology demon-
strated these to be nonmetastatic.

a c

d
Fig. 7.25a–e Cystic RCC of the right kidney, stage T1. a, b Breath-
hold axial (a) and coronal (b) T2w TSE images. c, d Breath-hold axial
T1w GRE images obtained before (c) and 2 min after (d) IV injection
of Gd-based contrast medium. e Coronal reconstruction of 3D GRE
MRA sequence acquired 1 min after IV injection of contrast me-
b dium. Predominantly cystic tumor with some septa and small solid
areas, which enhance after contrast administration.
Fig. 7.25e e
MRI Appearance of Pathologic Entities 169

v Fig. 7.25e

a b

c d
Fig. 7.26a–d TCC. Breath-hold dynamic coronary GRE images ob- (arrows) in the left ureteropelvic junction with obstruction and
tained before (a) and immediately (b), 1 min (c), and 3 min (d) after dilatation of the pelvicaliceal system.
IV injection of Gd-based contrast medium. Small enhancing mass
170 7 The Kidneys and Upper Urinary Tract

a b

c d

e f

Fig. 7.27a–g TCC of the left kidney. a Precontrast axial T1w SE


image. b Fat-suppressed axial fast T2w SE image. c–f Breath-hold
coronal dynamic GRE images obtained before (c) and immediately
(d), 1 min (e), and 3 min (f) after IV injection of Gd-based contrast
medium. g Fat-suppressed contrast-enhanced axial T1w SE image.
Mass in the left renal pelvis (arrow) of the same signal intensity as
the renal parenchyma on the unenhanced T1w and T2w images (a,
b). The tumor is revealed on the contrast-enhanced images because
it enhances less intensely than the surrounding parenchyma (arrow
in c–f, g). Small simple cyst in the right renal cortex (d).

g
MRI Appearance of Pathologic Entities 171

Nephroblastoma, or Wilms tumor, is a malignant em-


bryonic tumor that occurs predominantly in children aged
2.5–3 years, affecting boys and girls equally. It is the most
common abdominal malignancy of the first 8 years of life
and is associated with urogenital anomalies, aniridia, and
Beckwith–Wiedemann syndrome.20 The signal intensity
is typically inhomogeneous due to the presence of ne-
crosis and hemorrhage and does not allow differentiation
from other renal tumors. Nevertheless, MRI may be useful
for preoperative planning by differentiating tumor tissue
from normal renal tissue and surrounding structures45,46
(Fig. 7.28).
Leiomyosarcoma, rhabdomyosarcoma, liposarcoma, an-
giosarcoma, and fibrosarcoma are rare primary renal ma-
a
lignancies. Most of these tumors have nonspecific MRI
findings and the final diagnosis is based on histology.

Secondary Renal Tumors

Although renal metastases are detected in 2–20 % of all


autopsies, they have only a small role in imaging as they
are typically asymptomatic and are detected late or not at
all.47 Renal metastases tend to be multifocal (Fig. 7.29).
Despite the nonspecific MR findings, the diagnosis is ob-
vious in patients with multiple solid lesions in both kid-
neys who have a known primary tumor or additional
nonrenal metastases. However, large solitary renal meta-
stases may occur in patients with cancer of the lung, b
breast, or colon, and these cannot be distinguished from
RCC based on their MRI appearance alone.
Primary renal lymphoma is very rare, but renal involve-
ment through continuous extension from retroperitoneal
lymph nodes or hematogenous spread in patients with
systemic lymphoma is more common. Renal lymphoma is
either diffuse or focal in the form of multiple or solitary
lesions. Diffuse renal involvement is associated with en-
largement of the kidney.48,49 Lymphoma nodules are usu-
ally hypovascular, making them conspicuous relative to
the intensely enhancing normal renal parenchyma on
early arterial phase contrast-enhanced T1w images
(Figs. 7.30 and 7.31). MRI findings in diffuse renal lym-
phoma are loss of the corticomedullary differentiation,
diffuse renal enlargement, and associated lymphadenop-
athy.24

Fig. 7.28a–c Nephroblastoma in an 18-month-old girl. a Axial T2w


TSE image. b Axial contrast-enhanced T1w SE image. c Coronal
contrast-enhanced T1w SE image. The tumor is of inhomogeneously
high SI on the T2w image and poorly demarcated from the renal
parenchyma (a). It enhances less intensely than surrounding normal
parenchyma, and its extent can be accurately determined by eval-
uation in two planes (b, c). c
172 7 The Kidneys and Upper Urinary Tract

a b

Fig. 7.29a–c Metastases from squamous cell carcinoma (ENT) in


the left kidney. a Breath-hold axial T2w TSE image. b, c Breath-hold
axial T1w GRE images obtained before (b) and 2 min after (c) IV
injection of Gd-based contrast medium (image quality slightly de-
graded by ghosting artifacts). The metastases are markedly hyper-
intense on T2w image and hypointense on postcontrast image.
Hypointensity indicates necrosis, which is typical of metastases
from squamous cell carcinoma.

a b
Fig. 7.30a–d Lymphoma in the left kidney (solitary kidney). a, b Breath-hold axial (a) and coronal (b) T2w TSE images.
Fig. 7.30c, d e
MRI Appearance of Pathologic Entities 173

c
Fig. 7.30c, d
c Unenhanced breath-hold axial T1w GRE image. d Coronal recon-
struction of a 3D GRE MRA sequence obtained 15 s after IV injection
of Gd-based contrast medium. Tissue of nearly the same SI as renal
tissue is present in the renal sinus and obstructs outflow from the
calices (b). Reduced perfusion, predominantly in the upper third of d
the kidney (d). Patient had non-Hodgkin lymphoma. The imaging
appearance is also consistent with TCC of the renal pelvis.

a b

c d
Fig. 7.31a–d Lymphoma in both kidneys. Breath-hold dynamic co- kidneys are enlarged and contain multiple hypovascular, rounded
ronal T1w GRE images before (a) and immediately (b), 1 min (c), and parenchymal lesions.
3 min (d) after IV injection of Gd-based contrast medium. Both
174 7 The Kidneys and Upper Urinary Tract

Functional Renal Imaging

With its high spatial resolution and good temporal reso-


lution, MRI provides not only morphologic information on
renal pathology but also an insight into renal function.
Several conditions including glomerulonephritis, intersti-
tial nephritis, renal involvement in diabetes mellitus, and
chronic urinary obstruction are associated with global im-
pairment of renal function, whereas extracorporeal shock-
wave lithotripsy can cause segmental functional impair-
ment.50 MR contrast media, unlike the iodinated X-ray
contrast media used in radiography and CT, are not
nephrotoxic because only very small amounts are needed,
and they can therefore also be used in patients with mildly
impaired renal function without the risk of additional
renal damage.27,51,52 For contrast medium administration
in patients with severely compromised renal function, see
the Contrast Media section earlier in this chapter.
Gd-based contrast media are completely filtered in the a
renal glomeruli and then concentrated in the Henle loops
and collecting tubes of the medulla by water reabsorption.
Sequences acquired with a high temporal resolution, such
as dynamic contrast-enhanced GRE or echo-planar se-
quences, are well suited to track the passage of the con-
trast medium as concentration-dependent changes in re-
laxation times. Patients with delayed elimination of the
contrast medium due to impaired renal function show a
less pronounced decrease in signal intensity than individ-
uals with normal renal function. In patients with severely
impaired renal function and a creatinine clearance
< 30 mL/min, the typical contrast reversal in the medulla,
which is due to the high concentration of Gd and the
resulting predominance of the T2-shortening effect, may
even be completely absent.24,44 Quantification of renal
function by serial measurement of signal intensities after
intravenous injection of contrast medium, using special
pulse sequences such as inversion-prepared or saturation-
prepared fast sequences in conjunction with an appropri-
ate analysis algorithm, has been proposed. However, the b
error rate in determining local contrast medium concen- Fig. 7.32a, b Evaluation of a potential living kidney donor. MIP
tration is high, and the technique does not yet allow reconstructions of a 3D GRE sequence acquired 15 s after IV in-
reliable determination of renal function parameters.53,54 jection of Gd-based contrast medium. a Left anterior oblique pro-
jection. b Right anterior oblique projection. There are two renal
arteries on the left and two renal veins on the right (arrows).

Evaluation of Living Kidney Donors


used in the past to map vascular anatomy in potential
Kidneys from living donors are increasingly used to meet kidney donors; however, these are healthy individuals
the demand of waiting recipients. Laparoscopic donor and the risks of an invasive diagnostic test should be
nephrectomy is minimally invasive and can promote liv- avoided. Several studies have shown that MRA is equiv-
ing kidney donation.55 Careful evaluation of potential alent to conventional angiography in identifying relevant
kidney donors and their kidneys contributes to the tech- arterial anomalies and even superior in detecting venous
nical success of renal transplants and minimizes the peri- variants (Fig. 7.32).57,58
and postoperative risk for the donor. Renal vascular anat- Moreover, the different MRI techniques for renal imag-
omy is important in selecting the side of donor nephrec- ing enable a more comprehensive morphologic evaluation
tomy. Ideally, the kidney to be donated should have a and exclusion of anomalies of the kidneys and urinary
single artery and a single vein. Vascular renal anatomy is tract in potential kidney donors. In very rare instances,
highly variable, with a 40 % rate of arterial and 20 % venous kidney donor MRI may even detect an incidental malig-
anomalies.56 This is why catheter-based angiography was nant renal tumor (see Fig. 7.20).
MRI Appearance of Pathologic Entities 175

a b

Fig. 7.33a–c Urinoma in a renal transplant recipient. a, b Fast T1w


GRE images before (a) and 10 min after (b) IV injection of Gd-based
contrast medium. c Coronal reconstruction of a 3D GRE sequence
performed ca. 5 min after injection of a test bolus for determination
of circulation time and before the actual MRA sequence for vascular
evaluation was acquired. Postcontrast images (b and c) show leak-
age of contrast medium from the ureter, which collects posterior to
the kidney, consistent with urinoma (arrow in c).

Renal Transplants tional complications such as ureteral leaks causing uri-


noma (Fig. 7.33). Vascular complications such as throm-
Several complications can occur in renal transplant recip- bosis of the transplant renal vein can be detected with a
ients including postoperative hematoma, urinoma or lym- venous phase MRA sequence (for further details see Chap-
phocele, urinary obstruction, infarction, acute tubular ne- ter 15). As with all operations, bleeding with hematoma
crosis, toxicity of cyclosporine and other drugs, and acute formation may also occur after kidney transplant. Active
or chronic rejection.59,60 MRI has gained an increasing role bleeding is occasionally seen on contrast-enhanced im-
in evaluating complications in renal transplant recipients, ages (Fig. 7.34).
not least because of technical refinements. MRI enables Rejection of a kidney transplant may be associated
assessment of renal transplants in terms of morphology, with loss of corticomedullary differentiation, which is
function, and perfusion.59,60 best appreciated on T1w images. However, this is a non-
The MRI protocol for kidney graft recipients includes specific sign and may also occur in association with cyclo-
fast T2w sequences (e. g., HASTE) in all three orthogonal sporine toxicity, congestion, and other complications.59,60
planes and an axial T1w GRE sequence in conjunction Renal infarction and cortical necrosis are characterized by
with a contrast-enhanced 3D MRA sequence and a de- increased signal intensity on T2w images and markedly
layed T1w sequence. This protocol may be supplemented reduced perfusion on dynamic contrast-enhanced se-
by a static or excretory MRU (see Tables 7.1 and 7.2). An quences (Fig. 7.35).
excretory MRU will detect postoperative or postinterven-
176 7 The Kidneys and Upper Urinary Tract

Fig. 7.34a–e Evaluation of a kidney graft recipient with bleeding


from a parenchymal lesion. a Axial breath-hold T2w TSE image. b, c
Axial breath-hold T1w GRE images obtained before (b) and 2 min
after (c) IV injection of Gd-based contrast medium. d, e Coronal
reconstruction (d) and MIP image (e) of a 3D MRA sequence
acquired 15 s after contrast injection. Images depict a large hema-
toma lateral to and compressing the transplant kidney (arrows). In
(c) and (d), active bleeding is indicated by leakage of contrast
medium from the parenchyma.

b c

d e
MRI Appearance of Pathologic Entities 177

a b

c d

f
Fig. 7.35a–f Vascular rejection in a transplanted kidney. a–d
Breath-hold dynamic coronal T1w GRE images obtained before (a)
and immediately (b), 1 min (c), and 3 min (d) after IV injection of
Gd-based contrast medium. e MIP image of the arterial phase.
f Explanted kidney. There is no perfusion of the renal cortex (arrows
in a–d). The main branch of the transplant renal artery (arrow in e)
and its segmental branches appear normal, while no peripheral
perfusion is seen. The histologic diagnosis was cortical necrosis
secondary to vascular rejection.

e
178 7 The Kidneys and Upper Urinary Tract

References 22. Tikkakoski T, Päivänsalo M, Alanen A, et al. Radiologic findings


in renal oncocytoma. Acta Radiol 1991;32(5):363–367
23. Harmon WJ, King BF, Lieber MM. Renal oncocytoma: magnetic
1. Israel GM, Bosniak MA. How I do it: evaluating renal masses.
resonance imaging characteristics. J Urol 1996;155(3):863–867
Radiology 2005;236(2):441–450
24. Krestin GP. Morphologic and Functional MRI of the Kidneys and
2. Helmberger T, Holzknecht N, Lackerbauer CA, et al. [Phased-
Adrenal Glands. Philadelphia: Field & Wood; 1990
array superficial coil and breath holding technique in MRI of the
25. Stanley RJ. Benign renal neoplasm. In: McClennan BL, ed. Syl-
liver. Comparison of conventional spin echo sequences with
labus: A Categorial Course in Genitourinary Radiology: RSNA,
rapid fat suppressing gradient echo and turbo-spin sequen-
1994
ces]. Radiologe 1995;35(12):919–924
26. Hajdu SI, Foote FWJr. Angiomyolipoma of the kidney: report of
3. Dobritz M, Radkow T, Nittka M, Bautz W, Fellner FA. [VIBE with
27 cases and review of the literature. J Urol 1969;102(4):
parallel acquisition technique - a novel approach to dynamic
396–401
contrast-enhanced MR imaging of the liver]. Rofo 2002;174(6):
27. Semelka RC, Hricak H, Stevens SK, Finegold R, Tomei E, Carroll
738–741
PR. Combined gadolinium-enhanced and fat-saturation MR
4. Kim YK, Kim CS, Chung GH, Jeon SB, Lee JM. Feasibility of
imaging of renal masses. Radiology 1991;178(3):803–809
application of sensitivity encoding to the breath-hold T2-
28. Friedman AC, Hartman DS, Sherman J, Lautin EM, Goldman M.
weighted turbo spin-echo sequence for evaluation of focal hep-
Computed tomography of abdominal fatty masses. Radiology
atic tumors. AJR Am J Roentgenol 2005;184(2):497–504
1981;139(2):415–429
5. Yoshioka H, Sato J, Takahashi N, et al. Dual double arterial phase
29. Vas W, Wolverson MK, Johnson F, Sundaram M, Salimi Z. MRI of
dynamic MR imaging with sensitivity encoding (SENSE): which
an angioyolipoma. Magn Reson Imaging 1986;4:485–488
is better for diagnosing hypervascular hepatocellular carcino-
30. Madewell JE, Goldman SM, Davis CJJr, Hartman DS, Feigin DS,
mas, in-phase or opposed-phase imaging? Magn Reson Imaging
Lichtenstein JE. Multilocular cystic nephroma: a radiographic-
2004;22(3):361–367
pathologic correlation of 58 patients. Radiology 1983;146(2):
6. Vogt FM, Antoch G, Hunold P, et al. Parallel acquisition techni-
309–321
ques for accelerated volumetric interpolated breath-hold ex-
31. Rha SE, Byun JY, Jung SE, et al. The renal sinus: pathologic
amination magnetic resonance imaging of the upper abdomen:
spectrum and multimodality imaging approach. Radiographics
assessment of image quality and lesion conspicuity. J Magn
2004;24(Suppl 1):S117–S131
Reson Imaging 2005;21(4):376–382
32. Harrison RB, Dyer R. Benign space-occupying conditions of the
7. Asbach P, Klessen C, Kroencke TJ, et al. Magnetic resonance
kidneys. Semin Roentgenol 1987;22(4):275–283
cholangiopancreatography using a free-breathing T2-weighted
33. Riches EW, Griffiths IH, Thackray AC. New growths of the kidney
turbo spin-echo sequence with navigator-triggered prospective
and ureter. Br J Urol 1951;23(4):297–356
acquisition correction. Magn Reson Imaging 2005;23(9):
34. Wittekind Ch, Sobin LH. TNM Classification of Malignant Tu-
939–945
mours. New York: Wiley-Liss; 2002
8. Nolte-Ernsting C, Staatz G, Wildberger J, Adam G. [MR-urogra-
35. Ergen FB, Hussain HK, Caoili EM, et al. MRI for preoperative
phy and CT-urography: principles, examination techniques, ap-
staging of renal cell carcinoma using the 1997 TNM classifica-
plications]. Rofo 2003;175(2):211–222
tion: comparison with surgical and pathologic staging. AJR Am J
9. Memarsadeghi M, Riccabona M, Heinz-Peer G. [MR urography:
Roentgenol 2004;182(1):217–225
principles, examination techniques, indications]. Radiologe
36. Hallscheidt PJ, Bock M, Riedasch G, et al. Diagnostic accuracy of
2005;45(10):915–923
staging renal cell carcinomas using multidetector-row com-
10. O’Malley ME, Soto JA, Yucel EK, Hussain S. MR urography: eval-
puted tomography and magnetic resonance imaging: a prospec-
uation of a three-dimensional fast spin-echo technique in pa-
tive study with histopathologic correlation. J Comput Assist
tients with hydronephrosis. AJR Am J Roentgenol 1997;168(2):
Tomogr 2004;28(3):333–339
387–392
37. Kamel IR, Hochman MG, Keogan MT, et al. Accuracy of breath-
11. Semelka RC, Kelekis N. Kidneys. In: Semelka RC, Ascher PM,
hold magnetic resonance imaging in preoperative staging of
Reinhold C, eds. MRI of the Abdomen and Pelvis. New York:
organ-confined renal cell carcinoma. J Comput Assist Tomogr
Wiley-Liss; 1997: pp. 397–470
2004;28(3):327–332
12. Pollack HM, Wein AJ. Imaging of renal trauma. Radiology
38. Hallscheidt PJ, Fink C, Haferkamp A, et al. Preoperative staging of
1989;172(2):297–308
renal cell carcinoma with inferior vena cava thrombus using
13. Berrocal T, López-Pereira P, Arjonilla A, Gutiérrez J. Anomalies of
multidetector CT and MRI: prospective study with histopatho-
the distal ureter, bladder, and urethra in children: embryologic,
logical correlation. J Comput Assist Tomogr 2005;29(1):64–68
radiologic, and pathologic features. Radiographics 2002;22(5):
39. Kreft BP, Müller-Miny H, Sommer T, et al. Diagnostic value of MR
1139–1164
imaging in comparison to CT in the detection and differential
14. Staatz G, Rohrmann D, Nolte-Ernsting CC, et al. Magnetic reso-
diagnosis of renal masses: ROC analysis. Eur Radiol 1997;7(4):
nance urography in children: evaluation of suspected ureteral
542–547
ectopia in duplex systems. J Urol 2001;166(6):2346–2350
40. Eilenberg SS, Lee JK, Brown J, Mirowitz SA, Tartar VM. Renal
15. Aerts P, Van Hoe L, Bosmans H, Oyen R, Marchal G, Baert AL.
masses: evaluation with gradient-echo Gd-DTPA-enhanced dy-
Breath-hold MR urography using the HASTE technique. AJR Am J
namic MR imaging. Radiology 1990;176(2):333–338
Roentgenol 1996;166(3):543–545
41. Browne RF, Meehan CP, Colville J, Power R, Torreggiani WC.
16. Chicoskie C, Chaoui A, Kuligowska E, Dember LM, Tello R. MRI
Transitional cell carcinoma of the upper urinary tract: spectrum
isolation of infected renal cyst in autosomal dominant polycys-
of imaging findings. Radiographics 2005;25(6):1609–1627
tic kidney disease. Clin Imaging 2001;25(2):114–117
42. Yousem DM, Gatewood OM, Goldman SM, Marshall FF. Synchro-
17. Marotti M, Hricak H, Fritzsche P, Crooks LE, Hedgcock MW,
nous and metachronous transitional cell carcinoma of the uri-
Tanagho EA. Complex and simple renal cysts: comparative eval-
nary tract: prevalence, incidence, and radiographic detection.
uation with MR imaging. Radiology 1987;162(3):679–684
Radiology 1988;167(3):613–618
18. Schuhmann-Giampieri G, Krestin G. Pharmacokinetics of Gd-
43. Barentsz JO, Ruijs SH, Strijk SP. The role of MR imaging in
DTPA in patients with chronic renal failure. Invest Radiol
carcinoma of the urinary bladder. AJR Am J Roentgenol
1991;26(11):975–979
1993;160(5):937–947
19. Hilpert PL, Friedman AC, Radecki PD, et al. MRI of hemorrhagic
44. Krestin GP. Magnetic resonance imaging of the kidneys: current
renal cysts in polycystic kidney disease. AJR Am J Roentgenol
status. Magn Reson Q 1994;10(1):2–21
1986;146(6):1167–1172
45. Belt TG, Cohen MD, Smith JA, Cory DA, McKenna S, Weetman R.
20. Leder LD, Richter HP. Pathology of renal and adrenal neoplasms.
MRI of Wilms’ tumor: promise as the primary imaging method.
In: Lohr EL, Leder LD, eds. Renal and Adrenal Tumors. New York:
AJR Am J Roentgenol 1986;146(5):955–961
Springer; 1987: pp.1–68
46. Müller MF, Krestin GP, Willi UV. [Abdominal tumors in children.
21. Romis L, Cindolo L, Patard JJ, et al. Frequency, clinical presenta-
A comparison between magnetic resonance tomography (MRT)
tion and evolution of renal oncocytomas: multicentric experi-
and ultrasonography (US)]. Rofo 1993;158(1):9–14
ence from a European database. Eur Urol 2004;45(1):53–57,
discussion 57
MRI Appearance of Pathologic Entities 179

47. Choyke PL, White EM, Zeman RK, Jaffe MH, Clark LR. Renal 54. Levin YS, Chow LC, Pelc NJ, Sommer FG, Spielman DM. Estima-
metastases: clinicopathologic and radiologic correlation. Radi- tion of renal extraction fraction based on postcontrast venous
ology 1987;162(2):359–363 and arterial differential T1 values: an error analysis. Magn Reson
48. Hauser M, Krestin GP, Hagspiel KD. Bilateral solid multifocal Med 2005;54(2):309–316
intrarenal and perirenal lesions: differentiation with ultraso- 55. Giessing M, Deger S, Schönberger B, Türk I, Loening SA. Laparo-
nography, computed tomography and magnetic resonance scopic living donor nephrectomy: from alternative to standard
imaging. Clin Radiol 1995;50(5):288–294 procedure. Transplant Proc 2003;35(6):2093–2095
49 Reznek RH, Mootoosamy I, Webb JA, Richards MA. CT in renal 56. Kadir P. Atlas of normal and variant angiographic anatomy.
and perirenal lymphoma: a further look. Clin Radiol Philadelphia: WB Saunders Company; 1991
1990;42(4):233–238 57. Giessing M, Kroencke TJ, Taupitz M, et al. Gadolinium-enhanced
50. Krestin G, Fischbach R, Vorreuther R, von Schlthess GK. Alter- three-dimensional magnetic resonance angiography versus
ations in renal morphology and functionafter ESWL therapy: conventional digital subtraction angiography: which modality
evaluation with dynamic contrast-enhanced MRI. Eur Radiol is superior in evaluating living kidney donors? Transplantation
1993;3:227–233 2003;76(6):1000–1002
51. Haustein J, Niendorf HP, Krestin G, et al. Renal tolerance of 58. Israel GM, Lee VS, Edye M, et al. Comprehensive MR imaging in
gadolinium-DTPA/dimeglumine in patients with chronic renal the preoperative evaluation of living donor candidates for lap-
failure. Invest Radiol 1992;27(2):153–156 aroscopic nephrectomy: initial experience. Radiology 2002;
52. Rofsky NM, Weinreb JC, Bosniak MA, Libes RB, Birnbaum BA. 225(2):427–432
Renal lesion characterization with gadolinium-enhanced MR 59. Hanna S, Helenon O, Legendre C, et al. MR imaging of renal
imaging: efficacy and safety in patients with renal insuffi- transplant rejection. Acta Radiol 1991;32(1):42–46
ciency. Radiology 1991;180(1):85–89 60. Hélénon O, Attlan E, Legendre C, et al. Gd-DOTA-enhanced MR
53. Buonocore MH, Katzberg RW. Estimation of extraction fraction imaging and color Doppler US of renal allograft necrosis. Radio-
(EF) and glomerular filtration rate (GFR) using MRI: consider- graphics 1992;12(1):21–33
ations derived from a new Gd-chelate biodistribution model
simulation. IEEE Trans Med Imaging 2005;24(5):651–666
181

8 The Adrenal Glands


M. Taupitz and G.P. Krestin

Introduction Imaging Technique

Despite their small size and total weight of only 11 g, the See the respective sections in Chapter 1 for patient prep-
adrenal glands are complex hormone-producing organs. aration, positioning, and coils. The usual axial sequences
As such, they are affected by dysregulation of the endo- should be supplemented by a coronal sequence to define
crine system, resulting in clinically manifest hormonal the relationship to the diaphragmatic crura. An additional
disorders and morphologic changes that can be detected sagittal sequence may be necessary to separate an adrenal
by imaging. In addition, several nonfunctioning benign lesion from the upper renal poles.
and malignant tumors can arise in the adrenal glands.
Previously undetected adrenal adenomas are identified
in 2–10 % of the population, and up to 26 % of patients Pulse Sequences
with advanced extra-adrenal primary malignancies have
adrenal metastases. Adrenal masses that can be demon- If the adrenal glands are to be included in an MRI exami-
strated by imaging are present in ca. 9 % of individuals.1,2 nation of an upper abdominal organ (e. g., kidneys, pan-
Unsurprisingly, adrenal incidentalomas are common find- creas, liver), it is important to acquire both in-phase (IP)
ings on abdominal imaging studies performed for other and opposed-phase (OP) T1w GRE images (Fig. 8.1).
reasons. Characterization of such incidental adrenal Otherwise, the pulse sequences used for MRI of the liver
masses is especially important in patients with a known or the kidneys (see the respective sections in Chapters 1
extra-adrenal malignancy as it is likely to affect their and 7) are also suitable for adrenal MRI. The respiratory-
further management. triggered, fat-suppressed axial T2w TSE sequence sug-
gested for upper abdominal MRI also yields images with
excellent detail of the adrenal glands. Additional coronal
and sagittal images should be acquired with a single-shot
Indications
T2w TSE sequence (e. g., HASTE), which is characterized
by short scan times and robustness to artifacts (Fig. 8.2,
The adrenal glands are visualized and evaluated in all MRI Table 8.1).
examinations of the abdomen or upper abdomen. Scruti-
nizing the adrenal glands for the presence of metastasis is
especially important in patients who undergo MRI for a
suspected or known malignancy.
A dedicated MRI examination of the adrenal glands is
indicated in the following situations:
· Known extra-abdominal malignancy and indetermi-
nate adrenal mass detected by other imaging modal-
ities.
· Characterization of renal incidentaloma. p
· Diagnostic work-up of patients in whom an adrenal
mass is suspected on clinical grounds, e. g., hyperaldos-
teronism, Cushing syndrome, or hypertension. Fig. 8.1 Principle of opposed-phase (OP) and in-phase (IP) imaging.
Because water and fat protons have slightly different precession
frequencies, the amplitude of the echo in a GRE sequence is modu-
lated (“beats”) in an environment consisting of a finely dispersed
mixture of water and fat (as in a typical adrenal adenoma). Under OP
conditions, the signal contributions of water and fat are subtracted in
a volume element, resulting in low SI (left). Under IP conditions, the
signal contributions are added together, resulting in high SI (right).
182 8 The Adrenal Glands

To further characterize a very small suspicious adrenal

Note: The suggested parameters are only examples and have to be adjusted for use on different brands of scanners. Parallel imaging techniques can be used to shorten scan time (for sequences with one
mass, a set of T1w and T2w sequences with a slice thick-
Breath-
ness not exceeding 3–5 mm and a maximum interslice
hold

Yes
Yes

Yes
Yes
Yes

No

No
No
gap of 20 % should be acquired. The resolution in the
phase-encoding and frequency-encoding directions

4–8 min

4–7 min
5–7 min
20–24 s
should be less than 1.5 mm, which is typically achieved
Slice thick- Scan
ness (mm) time

23 s

23 s
23 s
23 s

using a field of view (FOV) between 28 and 36 cm, accord-


ing to patient habitus, and a 192 × 256 matrix.
The acquisition of IP and OP images for identifying
intracellular lipid is frequently referred to as chemical
3–5
3–5

2.5

shift imaging (CSI) and must not be confused with spa-


6

5
5
7
4
tially resolved MR spectroscopy, which is also designated
as CSI. The latter is not used for MRI of the adrenal glands.
quisitions
No. of ac-

IP and OP images can be acquired with two successive


sequences or simultaneously using a double-echo se-
1
4

1
1
3
1
1

quence, which is available on newer scanners. Compari-


son of IP and OP signal intensities is especially important
No. of
slices

for evaluation of adrenal masses because it allows detec-


64
19

23

21
19
23
23

48

tion of finely dispersed intracellular lipid, which is highly


300 (100 %)

characteristic of adrenal adenoma and rules out a malig-


FOV (mm)

300 (75 %)
300 (75 %)

300 (75 %)
300 (75 %)
300 (75 %)
300 (75 %)

300 (75 %)

nant tumor with a high degree of likelihood.3–5


The TEs given for acquiring IP and OP 2D GRE images are valid for 1.5 T; TEs for other field strengths are listed in Table 1.3.

Contrast Media
116 × 256
128 × 256

116 × 256
192 × 256
128 × 256
116 × 256
116 × 256

168 × 320
Matrix

The precontrast sequences can be supplemented by a


dynamic series performed after intravenous injection of
nonspecific Gd-based contrast medium (e. g., Dotarem,
Yes/no
Yes/no

Magnevist) at a standard dose of 0.1 mmol Gd per kg


Yes

Yes
Yes
No
No
No
FS

body weight. For details on nonspecific MR contrast media


and the dynamic study protocol see the respective sec-
Fixed
Fixed
7–15
7–15

tions in Chapter 1. The postcontrast series is acquired


ETL

using a conventional T1w GRE sequence with an IP echo





time. Alternatively, the dynamic series can be performed


Flip

10
90
90
(°)

using a 3D GRE sequence (e. g., VIBE). Images are acquired




at the usual postcontrast time points for upper abdominal


TE (ms)

80–100
2.2–2.6
2.2–2.4
4.4–4.8

10–15

60–80
60–80

MRI: arterial phase at 15 s, portal venous phase at 55–60 s,


80

and delayed phases at 2 and 5 min, optionally also at 10


min. If a double-echo T1w GRE sequence is available for
Table 8.1 Recommended pulse sequences and imaging parameters

Slice distance, 10–20 % of slice thickness (distance factor, 0.1–0.2)

IP/OP imaging, it can also be used for the dynamic series.


ca. 170–200
ca. 170–200

Lipid-containing tumors such as adrenal adenoma may


TR (ms)

fail to enhance or even decrease in signal intensity on


5000
2500

OP images acquired after contrast administration,6 while


500
5–7

signal average) but may come with a penalty in SNR.



they increase in signal intensity on IP images. This para-


TSE, respiratory-

doxical phenomenon is attributed to the fact that the


3D GRE (VIBE)

contrast medium predominantly distributes in the watery


Sequence

triggered
SE or TSE

compartment, resulting in a shift in signal contributions


2D GRE
2D GRE

HASTE
HASE

from fatty and watery compartments on OP images. No


type

TSE

diagnostic benefit of this effect is known.


Axial (optional)
(alternative)

(alternative)

Image Analysis
Coronal
Plane

Axial
Axial

Axial

Axial
Axial
Axial

Determination of signal intensities on IP and OP images as


well as on T2w images plays an important role in the MRI
Weight-

characterization of adrenal masses. Various quantitative


T1 OP
T1 FS
T1 IP

methods have been proposed for region of interest (ROI)


ing

T1

T2
T2
T2

T2

measurements in adrenal masses and, depending on the


Imaging Technique 183

a b

c d
Fig. 8.2a–d Normal adrenal glands. a, b Breath-hold axial (a) and coronal (b) T2w HASTE images. c, d IP (c) and OP (d) images acquired
simultaneously using a breath-hold axial T1w double-echo GRE sequence (1.5 T). Both adrenal glands are depicted as delicate structures.

method, in an adjacent reference tissue.4 Quantitative nal intensity is to calculate the percentage signal differ-
analysis is time-consuming and the results depend on ence (SI%) between OP and IP images:
the magnetic field strength and other technical parame-
SI% = 100 – (SIOP × 100/SIIP).
ters; published results and cut-off values for differentiat-
ing adenoma from malignant adrenal tumors may there- An SI difference < 5 % calculated according to this equation
fore not be directly applicable to every situation. More- is assumed to rule out a significant lipid component in an
over, regressive changes and hemorrhage can alter the adrenal mass; a difference > 25 % is taken as positive evi-
signal intensities of both benign and malignant tumors. dence that a lesion contains lipid. Other SI ratios were
Quantitative approaches were primarily pursued and fa- investigated by Fujiyosji and coworkers and found to be of
vored in the early era of adrenal MRI, but are no longer little diagnostic value.4
considered to be superior to simple visual analysis. Some Other techniques use T2w signal intensities to separate
of the formulas proposed are briefly outlined below. benign and malignant adrenal lesions.8,9 One approach is
The ROIs used for measuring signal intensity are placed to relate the signal intensity of an adrenal tumor on fat-
in a homogeneous, solid area of an adrenal lesion and suppressed T2w images (SIT) to that of a comparable area
should be as large as possible while excluding partial in the back muscle (SIM), the spleen (SIS), or the liver (SIL).
volume effects and motion artifacts. Relative signal intensity can thus be calculated for inter-
Tsushima et al. proposed an index of signal intensities individual comparison (e. g., SIrel = SIT/SIM). Because MR
(SI) calculated from IP and OP images as follows7: signal intensities of the liver and spleen are often altered
by diffuse conditions (steatosis) or storage diseases (he-
Index = ([SIIP – SIOP]/SIIP) × 100 %.
mosiderosis), and because the fat signal is reduced to
An index > 5 % is assumed to indicate a significant lipid variable degrees when a fat suppression technique is
component. A more straightforward way to quantify sig- used, SIrel should be calculated in relation to muscle. An
184 8 The Adrenal Glands

SIrel cut-off value of 3.5 was found to be highly sensitive On all conventional pulse sequences, a normal adrenal
and specific for the identification of adrenal adenomas. gland is of uniform low to intermediate signal intensity,
If dynamic contrast-enhanced images are used to char- slightly above that of paravertebral muscles and slightly
acterize an adrenal mass, signal intensities are deter- below that of the liver and renal cortex. As the adrenal
mined at different time points after contrast administra- gland contains fat, it loses signal intensity on OP images
tion (SIt) and compared with the precontrast signal inten- compared with IP images.5 Following administration of
sity (SIpre). Dynamic contrast ratios (SIdyn = SIt/SIpre) can nonspecific Gd-based contrast medium, the adrenal
thus be plotted over time. According to Krestin and co- glands enhance early and washout within ca. 5 min.11
workers,10 an early and persistent signal increase (SIdyn
> 2) characterizes a malignant adrenal mass, whereas
moderate enhancement (SIdyn < 2) with complete wash-
MRI Appearance of Pathologic Entities
out after 10 min indicates a benign lesion. The cut-off
values for this method vary with the field strength, scan-
ner, and sequence used. The first sign of a pathologic process of an adrenal gland is
With some experience and training, every radiologist a pronounced contour distortion. Small adrenal lesions
can acquire the skill to analyze images qualitatively and (< 1 cm) can be detected by MRI using surface coils and
achieve the same results as with a quantitative analysis. breath-hold acquisition to eliminate artifacts.
The presumptive diagnosis of a benign tumor can be Adrenal tumors can arise in the cortex or medulla and
established if an adrenal mass or most of it appears mark- cause no overt clinical symptoms if they are nonfunction-
edly hypointense on OP images compared with the IP ing. Functioning masses become apparent due to clinical
images. On T2w images, very high signal intensity is sug- manifestations associated with hormonal hypersecretion
gestive of a malignant adrenal tumor. On dynamic con- or hyposecretion. Primary or secondary functioning adre-
trast-enhanced images, a moderate increase in signal in- nal masses can be diagnosed with clinical tests. MRI is not
tensity, which drops again within a few minutes, suggests a first line modality in this setting but may occasionally
a benign mass, whereas intense and persistent signal provide useful findings for further treatment.
enhancement indicates a malignant process. Characterizing a nonfunctioning adrenal mass is a com-
plex task. Such lesions are incidentally detected on ab-
dominal CT scans in ca. 0.6–1.3 % of patients.12 At autop-
sies, incidentalomas are detected in 1.4–64.5 % of cases.13
Anatomy and Normal MRI Appearance
They can range in size from 0.5 to 6.0 cm and are typically
nonfunctioning adenomas. In patients with a known
The adrenal glands are located lateral to the vertebral metastatic tumor such as lung cancer, it is important to
bodies at the level of the 11th to 12th rib and are enclosed establish the benign character of an incidentally detected
by the upper portion of the Gerota fascia. They have the adrenal mass and rule out a metastasis.
shape of an inverted Y or T. Embedded in perirenal fat, the
adrenals are clearly demarcated from surrounding struc-
tures. The right adrenal gland lies above the upper renal Benign Conditions
pole, medial to the posterior contour of the right hepatic
lobe, and lateral to the right crura of the diaphragm. Adrenocortical Insufficiency
Anteriorly, it borders on the inferior vena cava. The left
adrenal gland comes to lie anteromedial to the upper pole Adrenocortical insufficiency, or Addison disease, is either
of the left kidney, lateral to the left crura of the diaphragm, a primary condition or occurs secondary to an imbalance
posterolateral to the aorta, and posteromedial to the of the hypothalamic axis. It is now widely believed that
splenic vessels and pancreas. the underlying mechanism is an idiopathic autoimmune
On MRI, the adrenal glands are clearly demarcated process in which the adrenal glands are normal or almost
from surrounding high-signal-intensity retroperitoneal normal in size.14 Destruction of the adrenal cortex can be
fat on non-fat-suppressed T1w and T2w images. In most due to inflammatory diseases such as tuberculosis or his-
patients, the two glands can be easily identified on MRI. toplasmosis, metastases, hemorrhagic infarction, and stor-
When little or no intra-abdominal fat is present, as in very age diseases.15 If the underlying cause is a mass (tuber-
slim or cachectic patients, identifying the adrenal glands culosis, metastasis), the adrenal gland is enlarged in the
may be difficult. They may also be difficult to detect in shape of that mass. Adrenal insufficiency becomes clini-
extreme hepatomegaly or when an adjacent mass such as cally apparent if at least 90 % of the adrenal tissue is lost.15
a renal tumor is present. In patients with portal hyper-
tension, a dilated left diaphragmatic vein may mimic
thickening at the anterior border of the left adrenal. The Inflammatory Conditions
true nature of vascular structures is revealed when flow-
related signal loss can be demonstrated, which is most Before the era of tuberculostatic therapy, adrenal tuber-
obvious on single-shot TSE sequences. culosis was a common cause of adrenal insufficiency. In-
flammatory involvement of the adrenal glands has again
MRI Appearance of Pathologic Entities 185

become more common as there are now more immuno-


compromised individuals. The most common pathogens
are Mycobacterium tuberculosis and Histoplasma capsula-
tum; adrenal infection with Blastomyces and Cryptococcus
is seen occasionally. Concomitant involvement of other
organs is common.16
Adrenal inflammation is usually symmetric and in-
volves both glands. Inflammatory lesions typically appear
inhomogeneous with a central area of liquefaction (ab-
scess). Because they contain no intracellular lipid (identi-
cal signal intensities on IP and OP images), they cannot be
distinguished from adrenal malignancies based on their
MRI appearance. Solid components typically have low
signal intensity on T2w images (SIrel < 3.5 compared
with paravertebral muscle). On contrast-enhanced dy-
namic series, inflammatory lesions tend to enhance early a
and wash out rapidly.

Adrenocortical Hyperplasia and Hypersecretion

Adrenocortical hyperplasia is difficult to diagnose on the


basis of morphologic appearance, as no adrenal changes
are apparent in most cases. The condition is suggested if
there is diffuse enlargement with preservation of the
normal adreniform shape (Fig. 8.3). Imaging is indicated
only to confirm or rule out an adenoma; however, macro-
nodular hyperplasia (which is primarily seen in hyper-
aldosteronism) cannot always be distinguished from a
small adenoma. In such cases, functional scintigraphy or
venous blood sampling is necessary.
Endogenous hypercortisolism (Cushing syndrome) is
caused by excessive ACTH secretion due to dysregulation b
of the hypothalamus–pituitary–adrenal axis in 80 % of
cases and is associated with bilateral adrenal hyperplasia.
Fewer than 20 % of patients have ectopic paraneoplastic
ACTH secretion in the setting of an extra-adrenal primary
tumor (lung cancer, breast cancer, melanoma). About 20 %
of adult patients have the ACTH-independent form of
Cushing syndrome, caused by a cortisol-producing tumor
of the adrenal cortex, which is malignant in one third of
cases (adrenal carcinoma).
Primary hyperaldosteronism is caused by an aldoster-
one-producing adenoma of the adrenal cortex in 80 % of
affected patients. The remaining 20 % of cases are ac-
counted for by hyperplasia of the zona glomerulosa. Car-
cinoma is very rare (< 1 %). Adenoma is usually unilateral c
and more common in women and typically occurs be-
Fig. 8.3a–c Bilateral adrenal hyperplasia. a Breath-hold coronal T2w
tween 30 and 50 years of age.15 Adrenocortical hyper-
HASTE image. b, c IP (b) and OP (c) images acquired simultaneously
plasia is bilateral and has no sex predilection. An autono- using a breath-hold axial T1w double-echo GRE sequence (1.5 T).
mous adenoma is usually treated surgically, while hyper- Normal adreniform shape is barely preserved and the adrenal limbs
plasia is amenable to medical treatment. are thickened with additional nodular appearance of the left adre-
Excess androgen production typically occurs on the nal. Signal drop of both adrenal glands on the OP image (c) com-
basis of congenital bilateral adrenocortical hyperplasia pared with the IP image (b).
secondary to an enzyme defect of steroid synthesis.
Twenty percent of patients have an autonomous adrenal
tumor, which can occur at any age and affects men and
women alike. The majority of adenomas are benign,
although up to 25 % can be malignant.
186 8 The Adrenal Glands

Cysts

Adrenal cysts are rare lesions that may occur at any age,
with a female-to-male ratio of 3:1.17 They are of variable
size and both adrenals are affected in 15 % of cases. Four
histologic types are distinguished. The most common are
endothelial cysts, accounting for 45 % of adrenal cysts.
They are thought to be due to obstructed lymphatic drain-
age. About 39 % are pseudocysts, which represent residues
of hemorrhage or degenerated adrenal neoplasms. Epi-
thelial cysts (9 %) are rare and comprise cystic adenomas.
The last group are parasitic cysts (7 %), which are caused
by echinococcal infection.
At MRI, adrenal cysts are characterized by low signal
intensity on T1w images and high intensity on T2w im-
a ages15 (Fig. 8.4), and they do not enhance on dynamic
contrast-enhanced sequences. Unlike renal cysts, adrenal
cysts often have thickened walls.

Adrenocortical Adenoma

Adrenocortical adenomas are benign tumors that arise


from adrenocortical cells. Histologically, they are predom-
inantly composed of lipid-laden spongiocytes arranged in
trabecular fashion or as solid clusters. They have a fibrous
capsule and are clearly separated from the surrounding
adrenal gland. MRI depicts adrenal adenomas as homoge-
neous masses ranging in size from < 1 cm to 8 cm. The
majority of nonfunctioning adenomas are < 3 cm.
While nonfunctioning adenomas have relaxation times
comparable to those of the normal adrenal gland and
liver,18,19 some hormonally active adenomas, in particular
b
those producing aldosterone, have a moderately in-
creased signal intensity on T2w images.14 However, there
are also functioning tumors that are isointense to liver and
nonfunctioning adenomas that are hyperintense to liver. A
higher signal intensity is usually due to hemorrhagic in-
farction and necrosis.15 Hence, MRI does not enable reli-
able differentiation of functioning and nonfunctioning
adrenal adenomas.
Most adrenal adenomas can be differentiated from
malignant tumors on T2w images. Regardless of whether
an adenoma is functioning or nonfunctioning, SIrel relative
to muscle is typically < 3.5. Using IP/OP imaging, adeno-
mas can be identified with a high degree of accuracy.
Because of their lipid content, adrenal adenomas display
c the expected decrease in signal intensity of > 25 % on OP
Fig. 8.4a–c Cyst of the left adrenal gland. a, b Breath-hold axial (a) images compared with IP images4,5,7,20 (Fig. 8.5). After
and coronal (b) T2w HASTE images. c Breath-hold axial T1w GRE contrast administration, adenomas enhance early and
image (1.5 T). The adrenal cyst is depicted as a smoothly delineated wash out rapidly.10 Larger adrenal adenomas may appear
mass anterosuperior to the left upper kidney pole. The cyst is of inhomogeneous on T2w images, OP images, and contrast-
homogeneously high T2 SI and low T1 SI. enhanced images. Identification of an intralesional area
clearly containing lipid on the basis of the OP signal in-
tensity establishes the diagnosis of an adenoma (Fig. 8.6).
MRI Appearance of Pathologic Entities 187

a b

c d

e f
Fig. 8.5a–f Typical MRI appearance of a nonfunctioning adrenal based contrast medium. The markedly lower SI of the adrenal mass
adenoma on the left. a, b Breath-hold axial (a) and coronal (b) on unenhanced T1w OP image (d) compared with the IP image (c) is
T2w HASTE images. c–f IP and OP images acquired simultaneously consistent with intracellular lipid and is typical of adrenal adenoma.
using a breath-hold axial T1w double-echo GRE sequence (1.5 T): IP The lack of high-SI areas on the T2w images indicates absence of
(c) and OP (d) images acquired before contrast administration and regressive changes. The mass shows only little enhancement on
IP (e) and OP (f) images acquired 1 min after IV injection of Gd- postcontrast IP (e) and OP (f) images (see Fig. 8.10).
188 8 The Adrenal Glands

a b

c d
Fig. 8.6a–d Atypical, nonfunctioning adrenal adenoma. a Breath- with IP image (b), consistent with a mass containing only little lipid
hold axial T2w HASTE image. b, c IP (b) and OP (c) images acquired (arrow in c). Contrast-enhanced image shows inhomogeneous,
simultaneously using an axial T1w double-echo GRE sequence strong enhancement of the mass, sparing rounded intralesional
(1.5 T). d Fat-suppressed T1w GRE image obtained 2 min after IV areas (arrow in d). The histologic diagnosis was adrenal adenoma
injection of Gd-based contrast medium (1.5 T). T2w image shows with numerous intralesional hemorrhagic foci. Images also show
inhomogeneous mass with areas of high and low SI. Nonenhanced patchy hepatic steatosis and a liver cyst.
T1w OP image (c) shows only small areas of signal loss compared

Myelolipoma Hemangioma

Myelolipoma is a rare adrenal tumor that is composed of Adrenal hemangioma is rare and often an incidental find-
mature fatty tissue and hematopoietic tissue in variable ing. A cavernous hemangioma can cause clinical signs and
proportions. It is usually detected incidentally. Large adre- symptoms based on size, which may be up to 25 cm.21
nal myelolipomas can cause abdominal signs and symp- Adrenal hemangiomas are of uniform high signal intensity
toms and may be complicated by spontaneous hemor- on T2w images and have the same signal intensity on IP
rhage. The MRI appearance is determined by the large and OP images. In a dynamic contrast-enhanced study,
component of pure fatty tissue, resulting in very high progressive centripetal enhancement, as in liver heman-
signal intensity on non-fat-suppressed T1w and T2w se- gioma, can occur, especially in larger hemangiomas. Con-
quences and low signal intensity on the corresponding fident characterization by MRI poses a challenge because
fat-suppressed sequences. Because of their large fatty adrenal hemangiomas lack two criteria of benign adrenal
component, myelolipomas are of very high signal inten- tumors—rather low T2 signal intensity and signal loss on
sity on OP images. A myelolipoma containing connective OP images (Fig. 8.8).
tissue or a larger component of hematopoietic tissue ap-
pears inhomogeneous (Fig. 8.7).3
MRI Appearance of Pathologic Entities 189

a b

c d

Fig. 8.7a–e Myelolipoma of the right adrenal gland. a, b Breath-


hold axial (a) and coronal (b) T2w HASTE images. c, d IP (c) and OP
(d) images acquired simultaneously using an axial T1w double-echo
GRE sequence. e Breath-hold, fat-suppressed axial T1w GRE image
(1.5 T). The mass is predominantly composed of fat, indicated by
high SI on the non-fat-suppressed images (a–d). On the OP image,
only the intralesional areas that still contain some residual nonfatty
tissue (arrow in d) show a loss of SI compared with the IP image (c).
The fat-suppressed image (e) shows nearly complete loss of signal of
the lesion.

Malignant Tumors
The MRI appearance varies with size and vasculariza-
tion. Small tumors (< 5 cm in diameter) tend to appear
Primary Adrenocortical Carcinoma uniform, larger ones often have areas of necrosis and
hemorrhagic infarction (Fig. 8.9). Infiltration of adjacent
With an incidence of ca. 1 per 1 million population, adre- organs is common. Vascular invasion, especially of the
nocortical carcinoma is a rare tumor.15 The mean age at vena cava, is best demonstrated on flow-sensitive GRE
presentation is 50 years, but the tumor can occur at all sequences or an MRA sequence (see Chapter 15).
ages. Over 90 % of adrenocortical carcinomas reported had Adrenocortical carcinomas typically have high signal
a size of > 6 cm. Involvement of the left adrenal gland is intensity on T2w images (SIrel relative to muscle > 3.5).
more common, and 10 % of adrenocortical carcinomas are Unlike adenoma, an adrenocortical carcinoma contains no
bilateral. About half are functioning carcinomas (hyper- lipid, and therefore the decrease in signal intensity on OP
corticoidism, virilization).22 images vs IP images is less than 5 %. Because of their
190 8 The Adrenal Glands

a b

c d
Fig. 8.8a–d Hemangioma of the left adrenal gland (arrow) in a markedly hypointense on the precontrast T1w images, without any
patient with a large renal cell carcinoma of the right kidney (curved difference between IP (b) and OP (c) intensities. Uniform high SI of
arrow). a Breath-hold axial T2w HASTE image. b, c IP (b) and OP (c) the adrenal hemangioma on postcontrast image (d). Despite the
images acquired simultaneously using a breath-hold axial T1w typical MRI findings of an adrenal hemangioma, the left adrenal
double-echo GRE sequence. d T1w IP image acquired 2 min after gland was removed because of the rarity of this lesion and sus-
IV injection of Gd-based contrast medium (1.5 T). The adrenal pected metastasis in this patient with a large renal cell carcinoma.
hemangioma is markedly hyperintense on the T2w image (a) and

hypervascularity, adrenocortical carcinomas show intense Lymphoma


enhancement within 1 min of intravenous injection of
nonspecific contrast medium and persistent high signal Adrenal involvement is more common in non-Hodgkin
intensity for > 10 min.23 lymphoma compared with Hodgkin lymphoma. Primary
adrenal lymphoma is rare.16 Most patients have concom-
itant retroperitoneal lymphomatosis. Lymphoma rarely
Metastases causes adrenal insufficiency, although the condition typ-
ically involves both glands.15
The adrenals are a common site of metastatic disease. MRI cannot distinguish adrenal lymphoma from other
Primary tumors that tend to metastasize to the adrenal malignant tumors of the adrenal glands. The lesions have
glands are lung and breast cancer, melanoma, gastrointes- increased T2 signal intensity24 with marked and pro-
tinal tumors, medullary thyroid carcinoma, and pancre- longed signal enhancement on postcontrast images.10
atic cancer.15 In an autopsy study, up to 27 % of patients
with a malignant tumor were found to have adrenal
metastases.16 Pheochromocytoma
Containing no intracellular lipid, metastases have sim-
ilar signal intensities on IP and OP images (Fig. 8.10). Pheochromocytoma is a functional chromaffinoma of the
adrenal medulla, and patients may present with signs and
symptoms of excessive catecholamine secretion (hyper-
MRI Appearance of Pathologic Entities 191

a b

Fig. 8.9a–c Adrenocortical carcinoma. a Breath-hold axial T2w


HASTE image. b, c Breath-hold axial T1w GRE images acquired
before (b) and 2 min after (c) IV injection of Gd-based contrast
medium (1.5 T). Giant mass in the left upper abdomen (arrows).
Central necrotic areas of high SI on T2w image without enhance-
ment on postcontrast image.

a b

Fig. 8.10a–c Metastasis in the right adrenal gland (from transitional


cell carcinoma). a Breath-hold axial T2w HASTE image. b, c IP (b) and
OP (c) images acquired simultaneously using a breath-hold axial T1w
double-echo GRE sequence (1.5 T). Smoothly demarcated mass in
the right adrenal gland of uniform SI on all pulse sequences and
identical SI on IP and OP images indicate that the mass contains no
lipid (see Fig. 8.5).

c
192 8 The Adrenal Glands

a b

c d
Fig. 8.11a–d Pheochromocytoma in the right adrenal gland. echo GRE sequence (1.5 T). Smoothly demarcated mass in the right
a Breath-hold axial T2w HASTE image. b Respiratory-triggered, fat- adrenal gland of uniform SI on all pulse sequences (typical high T2 SI
suppressed axial T2w TSE image. c, d IP (c) and OP (d) images and low T1 SI) and identical SI on IP and OP images indicate that the
acquired simultaneously using a breath-hold axial T1w double- mass contains no lipid.

tension). The diagnosis can be established by the demon- cystic areas (Fig. 8.12).15,19 Most pheochromocytomas lack
stration of catecholamines or their metabolites in urine or fat and are therefore indistinct from other adrenal masses
serum. not containing cytoplasmic lipids on IP/OP images. Some
Pheochromocytomas tend to occur in certain familial pheochromocytomas with a fatty component have been
syndromes including multiple endocrine neoplasia (MEN) reported in the literature and these have been misinter-
2A and 2B, neurofibromatosis, and von Hippel–Lindau preted as adenomas on fat-sensitive sequences.27
disease.25 About 65–100 % of patients with MEN 2A or The contrast enhancement of pheochromocytomas re-
2B have pheochromocytomas, typically in both adrenal sembles that of malignant adrenal tumors with an intense
glands (80 %), and ca. 10 % of those with neurofibromato- early signal increase and slow washout. Pheochromocy-
sis. tomas have been reported to enhance even more in-
Approximately 15 % of pheochromocytomas are lo- tensely than malignant adrenal tumors.23
cated outside the adrenal gland and are termed paragan- MRI is comparable to CT and superior to MIBG scinti-
gliomas. All pheochromocytomas occurring in the setting graphy in detecting adrenal pheochromocytoma (MRI has
of an endocrine syndrome are intra-adrenal. Most pheo- a higher sensitivity but lower specificity). MRI and MIBG
chromocytomas are benign, only ca. 13 % are malignant.15 scintigraphy are comparable regarding paragangliomas.
Malignant transformation is more common in extra-adre-
nal pheochromocytomas.
A pheochromocytoma is typically depicted as a well- Neuroblastoma
defined round or oval mass. The tumors have an average
size of 5 cm and compress adjacent tissue (Fig. 8.11). Neuroblastoma is the second most common tumor in
Pheochromocytomas tend to be hypervascular and often childhood, accounting for 7–8 % of all neoplastic cases in
hemorrhagic26 (Fig. 8.12). this age group (see Chapter 17). It is derived from neural
The MR signal intensity on T2w images is higher than crest cells in the sympathetic ganglia26 and typically arises
that of muscle and the liver (Fig. 8.11). The appearance in the adrenal medulla or in the sympathetic chain.28 Most
tends to be inhomogeneous due to necrosis with central neuroblastomas secrete catecholamines or their less ac-
Rational Approach to the MRI Differentiation of Adrenal Lesions 193

a b

c d
Fig. 8.12a–d Pheochromocytoma with intralesional hemorrhage in hold axial T1w double-echo GRE sequence (1.5 T). Mass in the left
the left adrenal gland. a Breath-hold axial T2w HASTE image. adrenal gland with liquid areas and sedimentation, consistent with
b Respiratory-triggered, fat-suppressed axial T2w TSE image. c, d intralesional hemorrhage. IP and OP signal intensities rule out a lipid-
IP (c) and OP (d) images acquired simultaneously using a breath- containing mass.

tive precursors, which can be detected in urine. Neuro- with regard to their potential to provide information for
blastoma tends to metastasize extensively and early and characterizing adrenal masses.4,5,7,9,10,19,20,29–31 Published
often presents with symptoms of metastatic disease. data on their sensitivities and specificities are variable.
Neuroblastomas are isointense or hyperintense to Acquisition of IP and OP images with evaluation of the
muscle on T1w images and typically hyperintense on signal change on OP images compared with IP images has
T2w images. The tumors have an unchanged signal inten- shown to be highly sensitive and specific for the demon-
sity on fat-saturated compared with non-fat-saturated stration of cytoplasmic lipid and establishes the diagnosis
sequences or on OP images compared with IP images of adrenal adenoma. IP and OP images will therefore also
because they contain no fat. After contrast injection, allow differentiation of benign from malignant adrenal
they enhance early and intensely. Approximately masses in most cases. In the group of non-fat-containing
40–50 % of neuroblastomas contain calcifications and tumors, only inflammatory lesions can be classified as
these are difficult to detect by MRI. However, the multi- benign on T2w images and dynamic contrast-enhanced
planar capability of MRI affords accurate definition of series; for all other adrenal lesions, further differentiation
tumor extent and is helpful for staging. by MRI is not possible (including metastases, primary
adrenal carcinoma, lymphoma, pheochromocytoma).
The following MRI approach is therefore recommended
Rational Approach to the MRI Differentia- for the characterization of adrenal lesions (Fig. 8.13):
Based on the reported 100 % sensitivity of IP/OP imaging,
tion of Adrenal Lesions
one may confidently establish the diagnosis of an adrenal
adenoma if intracellular lipid is demonstrated using this
The aim of MRI is to narrow the diagnosis of an adrenal technique, and the examination can end here. If no lipid is
lesion. Numerous pulse sequences have been investigated demonstrated in a lesion, a T2w sequence (SIrel in relation
194 8 The Adrenal Glands

8. Gruss LP, Newhouse JH. Eight echo T2 measurements of adrenal


masses: limitations of differential diagnosis by relaxation time
Adrenal lesion determination. J Comput Assist Tomogr 1996;20(5):792–797
9. Slapa RZ, Jakubowski W, Januszewicz A, et al. Discriminatory
power of MRI for differentiation of adrenal non-adenomas vs
adenomas evaluated by means of ROC analysis: can biopsy be
In-phase (IP) and opposed- obviated? Eur Radiol 2000;10(1):95–104
phase (OP) imaging 10. Krestin GP, Freidmann G, Fishbach R, Neufang KF, Allolio B.
Evaluation of adrenal masses in oncologic patients: dynamic
contrast-enhanced MR vs CT. J Comput Assist Tomogr 1991;
Lipid+ Lipid−
15(1):104–110
11. Krestin GP, Steinbrich W, Friedmann G. Adrenal masses: evalu-
ation with fast gradient-echo MR imaging and Gd-DTPA-en-
Inflammation hanced dynamic studies. Radiology 1989;171(3):675–680
Adenoma Pheochromocytoma 12. Thompson NW, Cheung PS. Diagnosis and treatment of func-
Malignant tumor tioning and nonfunctioning adrenocortical neoplasms including
incidentalomas. Surg Clin North Am 1987;67(2):423–436
13. Commons R, Callaway R. Adenomas of the adrenal cortex. Arch
Intern Med 1948;81:37–41
T2w imaging 14. Baker ME, Blinder R, Spritzer C, Leight GS, Herfkens RJ, Dunnick
Dynamic NR. MR evaluation of adrenal masses at 1.5 T. AJR Am J Roent-
contrast-enhanced study genol 1989;153(2):307–312
15. Dunnick NR. The adrenal gland. In: Taveras JM, et al., eds.
T2+ T2– Radiology: Diagnosis, Imaging, Intervention. Philadelphia: Lip-
CM+ +/– CM– pincott; 1988
16. Moulton JS, Moulton JS. CT of the adrenal glands. Semin Roent-
genol 1988;23(4):288–303
Malignant tumor 17. Cheema P, Cartagena R, Staubitz W. Adrenal cysts: diagnosis and
Pheochromocytoma Biopsy Inflammation treatment. J Urol 1981;126(3):396–399
18. Chang A, Glazer HS, Lee JK, Ling D, Heiken JP. Adrenal gland: MR
imaging. Radiology 1987;163(1):123–128
Fig. 8.13 Flowchart for the MRI evaluation of adrenal lesions. If the 19. Reinig JW, Stutley JE, Leonhardt CM, Spicer KM, Margolis M,
fat-sensitive pulse sequences demonstrate intracellular lipid within Caldwell CB. Differentiation of adrenal masses with MR imag-
ing: comparison of techniques. Radiology 1994;192(1):41–46
an adrenal lesion, the diagnosis of adenoma is confirmed. If no fat
20. Zimmermann GG, Debatin JF, Krestin GP. The differentiation of
can be demonstrated, the combination of T2w and dynamic con- adrenal gland tumors: an improvement in accuracy by a combi-
trast-enhanced sequences allows further differentiation of inflam- nation of fat-sensitive, T2-weighted and contrast-enhanced MR
matory lesions from malignant tumors and pheochromocytoma. sequences. [Article in German] Rofo 1997;167:153–159
CM = contrast medium. 21. Yamada T, Ishibashi T, Saito H, et al. Two cases of adrenal
hemangioma: CT and MRI findings with pathological correla-
tions. Radiat Med 2002;20(1):51–56
to muscle < 3.5) and contrast-enhanced dynamic images 22. Bodie B, Novick AC, Pontes JE, et al. The Cleveland Clinic expe-
rience with adrenal cortical carcinoma. J Urol 1989;141(2):
(enhancement with rapid washout) can identify an in-
257–260
flammatory condition with a high degree of confidence. 23. Ichikawa T, Ohtomo K, Uchiyama G, Fujimoto H, Nasu K. Con-
All other adrenal masses must be considered malignant trast-enhanced dynamic MRI of adrenal masses: classification of
characteristic enhancement patterns. Clin Radiol 1995;50(5):
tumors or pheochromocytomas until proven otherwise.
295–300
24. Lee MJ, Mayo-Smith WW, Hahn PF, et al. State-of-the-art MR
imaging of the adrenal gland. Radiographics 1994;14(5):
References 1015–1029, discussion 1029–1032
25. Mathieu E, Despres E, Delepine N, Taieb A. MR imaging of the
adrenal gland in Sipple disease. J Comput Assist Tomogr 1987;
1. Dunnick NR, Korobkin M, Francis I. Adrenal radiology: distin- 11(5):790–794
guishing benign from malignant adrenal masses. AJR Am J 26. Leder LD, Richter HP. Pathology of renal and adrenal neoplasms.
Roentgenol 1996;167(4):861–867 In: Lohr EL, Leder LD, eds. Renal and Adrenal Tumors. New York:
2. Glazer HS, Weyman PJ, Sagel SS, Levitt RG, McClennan BL. Non- Springer; 1987, pp.1–68
functioning adrenal masses: incidental discovery on computed 27. McLoughlin RF, Bilbey JH. Tumors of the adrenal gland: findings
tomography. AJR Am J Roentgenol 1982;139(1):81–85 on CT and MR imaging. AJR Am J Roentgenol 1994;163(6):
3. Elsayes KM, Mukundan G, Narra VR, et al. Adrenal masses: mr 1413–1418
imaging features with pathologic correlation. Radiographics 28. Brady TM, Gross BH, Glazer GM, Williams DM. Adrenal pseudo-
2004;24(Suppl 1):S73–S86 masses due to varices: angiographic-CT-MRI-pathologic corre-
4. Fujiyoshi F, Nakajo M, Fukukura Y, Tsuchimochi S. Character- lations. AJR Am J Roentgenol 1985;145(2):301–304
ization of adrenal tumors by chemical shift fast low-angle shot 29. Haider MA, Ghai S, Jhaveri K, Lockwood G. Chemical shift MR
MR imaging: comparison of four methods of quantitative eval- imaging of hyperattenuating (> 10 HU) adrenal masses: does it
uation. AJR Am J Roentgenol 2003;180(6):1649–1657 still have a role? Radiology 2004;231(3):711–716
5. Mitchell DG, Crovello M, Matteucci T, Petersen RO, Miettinen 30. Korobkin M, Lombardi TJ, Aisen AM, et al. Characterization of
MM. Benign adrenocortical masses: diagnosis with chemical adrenal masses with chemical shift and gadolinium-enhanced
shift MR imaging. Radiology 1992;185(2):345–351 MR imaging. Radiology 1995;197(2):411–418
6. Mitchell DG, Stolpen AH, Siegelman ES, Bolinger L, Outwater EK. 31. Schwartz LH, Panicek DM, Koutcher JA, Heelan RT, Bains MS,
Fatty tissue on opposed-phase MR images: paradoxical suppres- Burt M. Echoplanar MR imaging for characterization of adrenal
sion of signal intensity by paramagnetic contrast agents. Radi- masses in patients with malignant neoplasms: preliminary eval-
ology 1996;198(2):351–357 uation of calculated T2 relaxation values. AJR Am J Roentgenol
7. Tsushima Y, Ishizaka H, Matsumoto M. Adrenal masses: differ- 1995;164(4):911–915
entiation with chemical shift, fast low-angle shot MR imaging.
Radiology 1993;186(3):705–709
195

9 The Retroperitoneum
G. Krupski-Berdien, C.R. Habermann, and V. Nicolas

This chapter discusses MRI of those retroperitoneal


Introduction
tumors and diseases that are not addressed in the organ-
specific chapters.
In recent years MRI has evolved into a powerful imaging
tool. The technical innovations that are most relevant in
the setting of retroperitoneal disease include parallel
Indications
imaging techniques and improved gradient echo sequen-
ces for 3D volume acquisition (e. g., VIBE).1 These advan-
ces have been made possible by the advent of high-per- MRI is indicated in patients with a retroperitoneal mass
formance gradient systems (30–40 mT/m), ultrafast se- suggested by clinical findings, palpation, ultrasound, or CT
quences that can be acquired during breath-holding, and or in patients with suspected diffuse disease such as retro-
better techniques for magnetization preparation. Of in- peritoneal fibrosis. It is estimated that more than half of all
creasing importance are optimized body coils and combi- retroperitoneal MRI examinations are performed for soft-
nations of several surface coils for imaging of the entire tissue tumors. CT tends to be the preferred method in
retroperitoneum in a single acquisition (e. g., total imaging patients with inflammatory disease and abscess formation
matrix— TIM, Siemens). Taken together, these new tech- because it can also be used for interventional procedures.
niques enable full retroperitoneal evaluation in a short However, MRI is preferred for the evaluation of retro-
time while virtually eliminating artifacts. MRI is now the peritoneal fistulas, which may occur as a rare complica-
modality of choice for imaging benign soft-tissue tumors tion of Crohn disease.
throughout the body because it enables evaluation of a set
of malignancy criteria and identification of several specific
tissues (e. g., well-differentiated liposarcoma). Further-
Imaging Technique
more, MRI allows excellent definition of local tumor ex-
tent, providing crucial information for biopsy guidance
and subsequent resection of tumors thought to be malig- All retroperitoneal MRI examinations are performed with
nant on the basis of clinical behavior (e. g., growth) and the patient in the supine position. Intravenous access is
imaging appearance. This information is important for established before imaging so that a contrast-enhanced
predicting the prognosis of patients with soft-tissue tu- dynamic study can be performed and an antispasmodic
mors, which is mainly determined by the tumor-free re- agent (butylscopolamine or glucagon) can be injected if
section margin and the histologic subtype.2 necessary. In general, the retroperitoneum is imaged
Precise evaluation of tumor extent in the retroperito- using a combination of spinal and abdominal phased-
neum by MRI requires imaging in two planes, which array surface coils. Phased-array multicoils can be com-
should show the long and short axis of the tumor and bined with fast pulse sequences and parallel imaging
take into account known patterns of spread of retroper- techniques and are preferable to the whole-body resona-
itoneal soft-tissue tumors—these tend to grow in natural tor.3,4 Infants are often examined using a multichannel
spaces such as muscle compartments and extend along head coil, knee coil, or flexible surface coil.5
anatomic pathways such as vessels or nerve sheaths.
Use of standardized imaging protocols is especially
important in the retroperitoneum to ensure adequate Imaging Planes
interpretation of follow-up findings obtained on the
same or a different MR scanner. In addition, MR images The examination usually begins with a coronal sequence
should show anatomic landmarks such as typical bone to estimate the craniocaudal extent of a disease process
structures, joints, and unchanging soft-tissue structures and its topographic relationship to the iliopsoas muscle,
(e. g., vessel bifurcations, muscles), which can help iden- the kidneys, and the adrenals. Axial images are useful for
tify the site of a disease process on serial MR studies, comparison with CT scans. The volume to be imaged and
especially after surgical resection. slice thickness are tailored to the specific clinical question.
196 9 The Retroperitoneum

Table 9.1 Recommended pulse sequences and imaging parameters for MRI of the retroperitoneum (parameters for imaging at 1.5 T, gradient strength of 30 mT/m, phased-array coils, parallel imaging) As a rule of thumb, a slice thickness of 4–10 mm (with no

Note: Alternatively, T1w images can be acquired using a TSE sequence and adjusting parameters accordingly. The suggested parameters are only examples and have to be adjusted for use on different
Breath--
interslice gap) is chosen, depending on tumor size.

hold


+
+
+





Pulse Sequences
Scan time

4.14 min
2.11 min
3.45 min

3.10 min
A T2w HASTE sequence acquired during breath-hold al-
22 s
12 s
40 s
23 s

34 s
lows rapid documentation of tumor extent in the retro-
peritoneum. Breath-hold imaging minimizes artifacts and
will improve conformity with the prescribed slice loca-
Slice thick-
ness (mm)

tions. However, fast pulse sequences accentuate the fat


signal compared with conventional sequences, making it
6–8

6–8
6–8
6–8
6–8

6–8

more difficult to differentiate between fat and fluid. This


8

2
6
problem can be overcome by using a fat suppression
technique, which enables good separation of retroperito-
acquisitions

neal fat and fluid (e. g., inversion recovery sequence or


No. of

T2w sequence with spectral fat saturation).


Provided that the necessary equipment is available,
1

1
1

1
1
1

1
1
3

T1w imaging before and after contrast administration


should be performed with a gradient echo (GRE) sequence
No. of
slices

(e. g., 2D FLASH), which allows acquisition of larger slabs


19

21
19

23
19
19

19
36
21

during a breath-hold of less than 30 s. GRE sequences are


not only faster than spin echo (SE) sequences but also
(mm)

allow good identification of heterotopic ossification or


FOV

350

350
450
350

360
350

360
360
360

hemorrhage as sources of artifacts distorting field homo-


geneity. Most indications for retroperitoneal MRI require
intravenous contrast administration for improved delin-
128 × 256

384 × 512
128 × 256

280 × 512
180 × 256
196 × 256

300 × 512
182 × 256
330 × 512

eation of tumor borders and internal architecture. For


Matrix

comparability, postcontrast imaging should be performed


with the same parameters as the precontrast T1w series
(Table 9.1). If a 2D FLASH sequence is used, it can be
TE (ms) FS

repeated with fat suppression after contrast administra-






+

+
+

tion, typically with acquisition of two phases. Alterna-


4.76
2.47

1.81

tively, a 3D GRE sequence (VIBE) can be used, which


101

14
15
55

13

99

combines fast acquisition with high resolution, but, owing


to inherent fat saturation, provides no information on the
TR (ms)

5.12
4860
3200

5540
601
183
208
653

840

presence of fat.
If T1w imaging during breath-hold is precluded for
technical reasons, an SE or GRE sequence can be used,
3D FLASH (VIBE)
Sequence type

whereas T2w images should always be acquired with a


fast SE (FSE or TSE) sequence. A T2*w sequence may be
2D FLASH
2D FLASH

useful in patients with a rapidly growing tumor and sus-


HASTE

TIRM
TSE

TSE

pected intralesional hemorrhage or to confirm a sus-


SE
SE

pected hematoma. These pulse sequences can also be


used for imaging below the iliac crest, where artifacts
Axial/coronal
Axial/coronal

Axial/coronal

due to respiratory motion are negligible. Details of the


Coronal

imaging parameters are summarized in Table 9.1.


Plane

Axial
Axial
Axial
Axial

Axial

Contrast Media
Fat suppression: T1 post IV

or optional T1 (see text)


T1 with fat suppression

An MRI examination for suspected retroperitoneal path-


Optional T2 (see text)

ology is not complete without intravenous administration


brands of scanners.
T1 ± IV contrast

of contrast medium (e. g., Magnevist, Dotarem) at a stand-


ard dose of 0.1 mmol Gd per kg body weight. Newer
Weighting

contrast

contrast agents, in particular ultra-small superparamag-


netic iron oxide particles (USPIO), have not yet proven
T2
T2

T1
T2

beneficial in this setting, except for lymph node imaging.


Classification of Soft-Tissue Tumors 197

Using the techniques described above the radiologist is deep fibromatosis. The very detailed classification pre-
can fully exploit the advantages of MRI, i. e., its exquisite sented in Table 9.2 provides an overview of the large
soft-tissue contrast and multiplanar capability, and pro- group of soft-tissue tumors.
vide important information to improve planning of pre- The staging classification of the American Joint Com-
operative chemotherapy and/or radiotherapy in patients mittee on Cancer, which is based on the TNM system, is
with retroperitoneal disease. most widely used in the clinical setting. The TNM staging
system for soft-tissue sarcomas is presented in Table 9.3.
The second important factor for therapeutic decision-
making is the histologic tumor grade, which describes
Anatomy
the degree of differentiation. Well-differentiated G1 tu-
mors do not require adjuvant postoperative treatment if
The retroperitoneum is the connective tissue space be- R0 resection has been achieved, but nearly all patients
hind the peritoneal cavity. Posteromedially, the lumbar with dedifferentiated G3 tumors, which have a high re-
spine and the psoas muscles on either side protrude into currence rate, are candidates for postoperative radiother-
this space. Medially within the retroperitoneal space lie apy and/or adjuvant chemotherapy.
the abdominal aorta, the inferior vena cava, the ascending Soft-tissue tumors are rare, and it is almost impossible
lumbar vein, portions of the sympathetic trunk, networks to give exact frequency data. Especially for benign tumors,
of vegetative nerves, and the chyle cistern. Lateral to the the incidence can only be estimated: a figure of ca. 300 per
paired psoas muscle, the retroperitoneum widens to en- 100 000 individuals has ben proposed.6 Statistical data on
close the renal compartments. Through the posterolateral malignant neoplasms are more reliable, since one may
border of the retroperitoneum pass the lumbar plexus safely assume that all malignant soft-tissue tumors will
nerve, the subcostal nerve, and the segmental blood ves- come to clinical attention sooner or later and are then
sels and lymphatics. The retroperitoneum is bounded biopsied. For the USA, it has been estimated that a total of
posterosuperiorly by the fascial sheath of the diaphragm 486 000 malignant tumors occurred in1990, among them
and inferiorly by the peritoneal reflection onto the rectum 5700 soft-tissue sarcomas with ca. 3100 sarcoma-related
and inguinal ligament. At its largest extent in the upper deaths. Based on these estimates, soft-tissue sarcomas
abdomen, the retroperitoneal space is subdivided into constitute 1 % of all malignant tumors. The incidence re-
three compartments: the anterior pararenal space be- ported in the literature is 1.35 to 1.4 per 100 000 popula-
tween the peritoneum and the anterior renal fascia (Ger- tion,6 and it is assumed that the incidence of soft-tissue
ota fascia), the perinephric space between the anterior sarcomas of the extremities is higher in old age (up to 8
renal fascia and the posterior renal fascia (Zuckerkandl per 100 000 in those over 80).7 Important epidemiologic
fascia), and the posterior pararenal space between the data are summarized in Table 9.4.
posterior renal fascia and the fascial sheath of the autoch- Some soft-tissue tumors have a predilection for specific
thonous back muscles arising from the transversalis fas- sites—leiomyosarcomas constitute nearly half of all retro-
cia. The fascia are very accurate anatomic boundaries but peritoneal, intra-abdominal, and visceral tumors. Next in
are not consistently visualized by MRI in healthy indivi- frequency in the retroperitoneum are liposarcomas and
duals, while they are often clearly delineated in the pres- schwannomas.4 Common tumors in the extremities are
ence of inflammation. liposarcoma (26 %) and malignant fibrous histiocytoma (or
the “newer” entities derived from these) (24 %).
The classic histologic categorization (leiomyosarcoma,
liposarcoma, malignant fibrous histiocytoma, etc.) is in-
Classification of Soft-Tissue Tumors
creasingly being abandoned in favor of a more refined
classification based on immunohistochemical and molec-
Soft-tissue tumors are neoplasms of mesenchymal origin ular biological properties.8,9 At the same time these prop-
that arise in the soft tissues of the extremities or in any erties have the potential to serve as targets for new thera-
other organ. Since connective tissue cells retain their abil- pies: gastrointestinal stromal tumor (GIST), a variant of
ity to divide, these tumors can differentiate into various sarcoma, was established as a separate tumor entity quite
types of mesenchymal tissue elements (e. g., connective recently. On the molecular level, it is characterized by
tissue, fat, muscle, cartilage, bone, nerve tissue, synovial partially excessive c-kit expression, making the tumor
tissue). The most widely used classification of soft-tissue amenable to chemotherapeutic treatment with imatinab
tumors is the one by Enzinger and Weiss,6 which is based (Glivec/Gleevec), a tyrosine kinase inhibitor.
on the different mesenchymal tissue types imitated by
these tumors. This classification distinguishes benign, ma-
lignant, and indeterminate soft-tissue tumors on the basis
of their biological behavior. A fourth class consists of
tumorlike lesions, defined as nonneoplastic disease pro-
cesses that mimic tumors. Like tumors, they can recur, but
they have not been observed to metastasize. An example
198 9 The Retroperitoneum

Table 9.2 Classification of soft-tissue tumors (according to Enzinger and Weiss, Salzer and Kuntschik)

Tissue of Tumorlike Benign Intermediate Malignant


origin
Fat · Lipomatosis and variants · Lipoma and variants · Atypical lipoma · Liposarcoma
· Lipoblastomatosis – spindle cell lipoma – well-differentiated
– pleomorphic – lipomalike
lipoma – sclerosing
– angiolipoma – inflammatory
· Lipoblastoma – myxoid
· Hibernoma – round cell
– pleomorphic
– dedifferentiated
Fibroblas- · Fibromatosis · Fibroma with subtypes · Atypical fibroxanthoma · Fibrosarcoma with subtypes
tic tissue – fascial · Nasopharyngeal · Dermatofibrosarcoma · Congenital and infantile
– musculoaponeurotic angiofibroma protuberans fibrosarcoma
· Infantile myofibromatosis · Giant cell fibro- · Bednar tumor · Malignant fibrous histio-
– solitary blastoma · Plexiform fibrohistiocytic cytoma
– multicentric · Intranodal myofibro- tumor (PFT) – storiform
· Infantile and juvenile fibro- blastoma – pleomorphic
matosis with subtypes · Fibrous histiocytoma – myxoid
· Myofibromatosis · Juvenile xanthogranu- – giant cell
– congenital/acquired loma – inflammatory
· Nodular fasciitis – angiomatoid
· Proliferative fasciitis
· Proliferative myositis
· Elastofibroma
· Keloid
· Fibrous hamartoma of
infancy
· Calcifying aponeurotic
fibroma
· Fibromyxoid inflammatory
pseudotumor
· Xanthoma
· Generalized eruptive histio-
cytoma
· Reticulohistiocytoma
– localized
– multicentric
Smooth · Leiomyomatosis · Leiomyoma with · Leiomyosarcoma with
muscle – intravenous subtypes subtypes
– perit