MRI Manual of Pelvic Cancer, Second Edition

Second Edition About the editors Pelvic cancers usually require MR imaging and the revised and updated MRI Manual of P...

Author: Soo Mak | Paul A. Hulse | B. M. Carrington

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Second Edition

About the editors

Pelvic cancers usually require MR imaging and the revised and updated MRI Manual of Pelvic Cancer Second Edition contains chapters covering all the major pelvic cancers. There are also chapters dealing with basic pelvic anatomy, staging, and imaging techniques. The use of advanced MR techniques such as diffusion weighted imaging, dynamic contrast enhancement, and magnetic resonance spectroscopy is integrated appropriately.

Soo Y. S. K. Mak MBChB, MRCP(UK), FRCR is a Consultant Radiologist at The Christie NHS Foundation Trust, Manchester, UK. She is an oncological radiologist specializing in cross-sectional imaging and PET CT.

The extensive use of high quality MR images makes this book an invaluable bench reference for all those required to be familiar with or report MRI pelvic cancer examinations. New to the Second Edition: • new imaging techniques as applicable to a number of pelvic cancers including cervical, endometrial, ovarian, and vaginal cancer • imaging findings post chemoradiation for cervical, rectal, bladder, and anal cancer • imaging findings in brachytherapy for prostate cancer • new penile cancer chapter A highly useful resource, this guide: • presents a comprehensive set of top-quality images of pelvic cancers • introduces pelvic cancer staging, MRI technique, and pelvic anatomy • provides a short account of each disease and a set of images demonstrating the tumor, node, and metastasis stages • contains illustrations of recurrent disease and appearances following chemoradiotherapy • discusses imaging before exenterative surgery and the imaging of metastatic disease within the pelvis

Bernadette M. Carrington MBChB, MRCP(UK), FRCR is a Consultant Radiologist at The Christie NHS Foundation Trust, Manchester, UK and an Honorary Lecturer at the University of Manchester UK. She has vast oncology cross-sectional and PET CT experience and has written widely on oncology imaging topics.

Second Edition

• has a consistent format with the extensive use of high quality MR images of pelvic cancer to aid diagnosis

Paul A. Hulse B.Med.Sci. (Hons), BMBS, MRCP(UK), FRCR is a Consultant Radiologist at The Christie NHS Foundation Trust, Manchester, UK. Dr Hulse is an experienced oncoradiologist specializing in cross-sectional and PET CT imaging.

MRI Manual of Pelvic Cancer

About the book

Mak Hulse Carrington


MRI Manual of Pelvic Cancer Second Edition

Edited by

Soo Y. S. K. Mak Paul A. Hulse Bernadette M. Carrington

[gajendra][D:/informa_Publishing/Hulse-Mak_2400075/z_3B2_3D_files/978-1-8418-4676-7_CH0000_O.3d] [12/9/ 011/18:32:11] [1–12]




MRI Manual of Pelvic Cancer Second Edition

Edited by Soo Y. S. K. Mak Consultant Radiologist Christie NHS Foundation Trust, Manchester, UK Paul A. Hulse Consultant Radiologist Christie NHS Foundation Trust, Manchester, UK Bernadette M. Carrington Consultant Radiologist Christie NHS Foundation Trust, Manchester, UK


First edition published in 2004 by Martin Dunitz, an imprint of the Taylor and Francis Group This edition published in 2012 by Informa Healthcare, Telephone House, 69-77 Paul Street, London EC2A 4LQ, UK. Simultaneously published in the USA by Informa Healthcare, 52 Vanderbilt Avenue, 7th Floor, New York, NY 10017, USA. Informa Healthcare is a trading division of Informa UK Ltd. Registered Office: 37–41 Mortimer Street, London W1T 3JH, UK. Registered in England and Wales number 1072954. #2012 Informa Healthcare, except as otherwise indicated No claim to original U.S. Government works Reprinted material is quoted with permission. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, unless with the prior written permission of the publisher or in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1P 0LP, UK, or the Copyright Clearance Center, Inc., 222 Rosewood Drive, Danvers, MA 01923, USA (http://www.copyright.com/ or telephone 978-750-8400). Product or corporate names may be trademarks or registered trademarks, and are used only for identification and explanation without intent to infringe. This book contains information from reputable sources and although reasonable efforts have been made to publish accurate information, the publisher makes no warranties (either express or implied) as to the accuracy or fitness for a particular purpose of the information or advice contained herein. The publisher wishes to make it clear that any views or opinions expressed in this book by individual authors or contributors are their personal views and opinions and do not necessarily reflect the views/opinions of the publisher. Any information or guidance contained in this book is intended for use solely by medical professionals strictly as a supplement to the medical professional’s own judgement, knowledge of the patient’s medical history, relevant manufacturer’s instructions and the appropriate best practice guidelines. Because of the rapid advances in medical science, any information or advice on dosages, procedures, or diagnoses should be independently verified. This book does not indicate whether a particular treatment is appropriate or suitable for a particular individual. Ultimately it is the sole responsibility of the medical professional to make his or her own professional judgements, so as appropriately to advise and treat patients. Save for death or personal injury caused by the publisher’s negligence and to the fullest extent otherwise permitted by law, neither the publisher nor any person engaged or employed by the publisher shall be responsible or liable for any loss, injury or damage caused to any person or property arising in any way from the use of this book. A CIP record for this book is available from the British Library. ISBN-13: 9781841846767 Orders may be sent to: Informa Healthcare, Sheepen Place, Colchester, Essex CO3 3LP, UK Telephone: +44 (0)20 7017 5540 Email: [email protected] Website: http://informahealthcarebooks.com/ Library of Congress Cataloging-in-Publication Data MRI manual of pelvic cancer / edited by Soo Y.S.K. Mak, Paul A. Hulse, and Bernadette M. Carrington. – 2nd ed. p. ; cm. Includes bibliographical references and index. ISBN 978-1-84184-676-7 (hb : alk. paper) 1. Pelvis–Cancer–Magnetic resonance imaging. I. Mak, Soo Y. S. K. II. Hulse, Paul. III. Carrington, Bernadette M. [DNLM: 1. Pelvic Neoplasms–diagnosis–Atlases. 2. Magnetic Resonance Imaging–methods. WE 17] RC946.M75 2011 616.99’4736–dc23 2011017123

For corporate sales please contact: [email protected] For foreign rights please contact: [email protected] For reprint permissions please contact: [email protected] Typeset by MPS, a Macmillan company, Printed and bound in the United Kingdom


This book is dedicated to Cuong, Joshua, and Alex Claire, Max, Felix, and Maxi Paddy, Rachel, and Helen


Contents

Contributors . . . . . . . . . . . vii Preface. . . . . . . . . . . viii Acknowledgment . . . . . . . . . . . ix Abbreviations . . . . . . . . . . . x 1. Diagnosis, staging, and follow-up of pelvic tumors: The role of MR imaging . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 Bernadette M. Carrington 2. MR imaging techniques in pelvic cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 3 Andrew P. Jones, Rohit Kochhar, and Alison Kilburn 3. Anatomy of the pelvis . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 16 James O’Connor and Paul A. Hulse 4. Cervical cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 38 Bernadette M. Carrington 5. Endometrial cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 77 Maryna Brochwicz-Lewinski 6. Ovarian cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 97 Soo Y. S. K. Mak and Prakash Manoharan 7. Vaginal cancer M. Ben Taylor

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118

8. Vulval cancer. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 135 Maryna Brochwicz-Lewinski and Jane Hawnaur 9. Rectal cancer Mike Dobson

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152

10. Anal cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 178 Rohit Kochhar and Paul A. Hulse 11. Bladder cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201 Suzanne Bonington 12. Prostate cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 220 Claire Barker 13. Penile cancer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 236 Rohit Kochhar and M. Ben Taylor 14. Pelvic metastases Fenella Wong

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15. MRI of residual and recurrent tumor before pelvic clearance surgery . . . . . . . . 288 Bernadette M. Carrington Index . . . . 315


Contributors

Claire Barker

Christie NHS Foundation Trust, Manchester, UK

Suzanne Bonington


Maryna Brochwicz-Lewinski Trust, Stockport, UK Bernadette M. Carrington Mike Dobson Preston, UK

Stepping Hill Hospital, Stockport NHS Foundation


Lancashire Teaching Hospitals NHS Foundation Trust,

Jane Hawnaur Central Manchester and Manchester Children’s University Hospitals NHS Foundation Trust, Manchester, UK Paul A. Hulse

Christie NHS Foundation Trust, Manchester, UK Christie NHS Foundation Trust, Manchester, UK

Andrew P. Jones Alison Kilburn


Rohit Kochhar


Soo Y. S. K. Mak


Prakash Manoharan


James O’Connor School of Cancer and Enabling Sciences, University of Manchester, Manchester, UK M. Ben Taylor Fenella Wong

Christie NHS Foundation Trust, Manchester, UK Christie NHS Foundation Trust, Manchester, UK


Preface

Magnetic resonance imaging continues to be an invaluable imaging tool in the staging of pelvic malignancy. In the second edition of this book, the chapters have been extensively revised and incorporate the 2010 UICC/AJCC staging system. A new chapter deals with penile cancer. The evidence for and sensible use of advanced MR techniques such as diffusion-weighted imaging, dynamic contrast enhancement, and magnetic resonance spectroscopy are discussed. There are sections which deal with pitfalls in pelvic cancer MR imaging interpretation. Our intention is that this book will remain a useful bench reference for radiographers who image and radiologists who report pelvic MR examinations as well as being of interest to all those involved in the clinical management of pelvic cancer. Soo Y. S. K. Mak Paul A. Hulse Bernadette M. Carrington


Acknowledgment

Once again a tremendous amount of team work has contributed to this book. In particular, we thank our secretaries Kami Ramnarain, Liz Stockton, Angela Squire, and Jackie Nevins for their work in helping us prepare our manuscripts and images, Kath Westwell our CRIS manager for performing many word searches, and our MR radiographers for constant high-quality imaging. Finally, we should like to acknowledge our contributors for their extremely hard work and patience in both writing and revising their chapters and we also acknowledge contributions of the following from the first edition: Rhidian Bramley, Neelam Dugar, Jeremy Lawrance, Sue Roach and Susan Todd.


Abbreviations ADC AFP AIN AJCC APR BLADE BPH CA-125 CEA Cho Ci CIN Cr CRT CSI CT DCE DRE DTPA DWI ERC EBRT EGFR EMVI EORTC EPI EUA FAME 5-FU FDG PET-CT FFE FIESTA FIGO FISP FOV FS FSE Gd GE GEPDI GI HCG HIV HNPCC

Apparent diffusion coefficient Alpha-fetoprotein Anal intraepithelial neoplasia American Joint Committee on Cancer Abdominoperineal resection Periodically rotated overlapping parallel lines with enhanced reconstruction Benign prostatic hypertrophy Cancer/carbohydrate antigen-125 Carcinoembryonic antigen Choline Citrate Cervical intraepithelial neoplasia Creatine Chemoradiotherapy Chemical shift imaging Computed tomography Dynamic contrast enhancement/enhanced Digital rectal examination Diethylenetriamine pentaacetic acid Diffusion-weighted imaging Endorectal coil External beam radiotherapy Extracellular growth factor receptors Extramural vascular invasion European Organisation for Research and Treatment of Cancer Echo planar imaging Examination under anesthesia Three-dimensional fast SPGR pulse sequence 5-Fluorouracil 18-Fluorodeoxyglucose positron emission tomography and computed tomography Fast field echo Fast imaging employing steady state acquisition Federation Internationale Gynecologie et Oncologie Fast imaging steady state precession Field of view Fat saturation Fast spin echo Gadolinium Gradient echo Gradient echo proton density image Gastrointestinal Human chorionic gonadotrophin Human immunodeficiency virus Hereditary nonpolyposis colorectal cancer


ABBREVIATIONS

HPV HRT IVC IAF IOG JSM KRAS gene LAVA MIP MR MRS MSAD NICE PACS PA p53 PIN PROPELLER PSA Rb RF ROC ROI SCC SNP SPAIR SPIO SPIR STIR SV T1WI T2WI TEs THRIVE Tis TME TNM TR TRUS TSE TURP UICC UKCCR US USPIOs VAIN VIBE VIN

Human papillomavirus Hormone replacement therapy Inferior vena cava Ischioanal fossa Improving outcomes guidance Jewett-Strong-Marshall v-Ki-ras2 Kirsten rat sarcoma viral oncogene homolog Liver acquisition with volume acceleration Maximum intensity projection Magnetic resonance MR spectroscopy Maximum short axis diameter National Institute for Health and Clinical Excellence Picture archiving and communication system(s) Polyamine Protein 53 gene Prostatic intraepithelial neoplasia Periodically rotated overlapping parallel lines with enhanced reconstruction (Siemens) Prostate-specific antigen Retinoblastoma tumor suppressor gene Radiofrequency Receiver operating characteristics Region of interest Squamous cell carcinoma Single nucleotide polymorphism Spectral adiabatic inversion recovery Super-paramagnetic iron oxide Spectral presaturation with inversion recovery Short tau inversion recovery Seminal vesicle T1-weighted image(s) T2-weighted image(s) Echo times Ultrafast spoiled gradient echo Carcinoma in situ Total mesorectal excision Tumor node metastasis Repetition time Transrectal ultrasound Turbo spin echo Transurethral resection of the prostate Union Internationale Contre le Cancer United Kingdom Coordinating Committee on Cancer Research Ultrasound Ultrasmall paramagnetic iron oxide Vaginal intraepithelial neoplasia Modified three-dimensional fast gradient echo sequence Vulval intraepithelial neoplasia

xi


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1 Diagnosis, staging, and follow-up of pelvic tumors: The role of MR imaging Bernadette M. Carrington

INTRODUCTION Cancer is due to an abnormal proliferation of cells which are resistant to normal regulatory mechanisms and which have the propensity to infiltrate the host organ, to invade locally and to activate mechanisms which allow more widespread dissemination through the body via blood vessels or lymphatics. Critical initial steps in cancer management are tumor confirmation by histological diagnosis and determination of extent by staging. This fundamental information is central to all management decisions and provides prognostic information. Accurate stratification of patients by tumor type and stage is also a prerequisite of cancer research, enabling valid comparison of outcomes between treatment groups. Objective assessment of treatment response is required to facilitate further management decisions and accurately evaluate the efficacy of treatment regimens. MR imaging plays an important part in pelvic cancer staging and treatment response assessment. Functional MR imaging offers sophisticated tumor analysis and permits more individualized prognostic information, treatment planning and response evaluation.

TUMOR DIAGNOSIS Tissue confirmation of malignancy is required wherever possible. This may be achieved by cytological analysis of surface accessible lesions, via needle biopsy of deeper masses (often image-guided) or by excision or incision biopsy, which involves resection of all or part of the tumor respectively. Excision biopsy is ideal since it allows accurate histopathological staging of the primary tumor and offers a potential cure. Most pelvic tumors are diagnosed by clinical examination and biopsy at the time of cystoscopy, colposcopy, or rigid sigmoidoscopy. Occasionally, examination under anesthesia is required. MR imaging is then used to locally stage the tumor, and computed tomography (CT) of the thorax and abdomen is performed to look for disseminated metastases. Ultrasound, either transabdominal or transrectal, can be used for primary tumor assessment but is inferior to MRI in depiction of local spread and the detection of regional lymph node metastases.

MR imaging allows multiplanar assessment of tumor extent within and beyond the organ of origin. Two- to threemillimeter thin-section (“high-resolution”) turbo spin echo T2weighted sequences are needed, usually in the orthogonal planes but occasionally utilizing off-axis imaging perpendicular to the tumor. The intramuscular injection of smooth muscle relaxants such as hyoscine butylbromide (Buscopan1) has been shown to improve image quality and diagnostic confidence in pelvic cancer imaging. In addition to imaging the true pelvis, it is recommended that at least one MR imaging sequence be performed through the abdomen to allow evaluation of the retroperitoneal nodal stations and visualization of the lumbar skeleton and kidneys. Machine time constraints do not usually permit full MR imaging of the liver, and small volume omental and mesenteric disease may not be identified without increased patient scan time and the use of intravenous contrast media. Moreover, the lungs are suboptimally assessed by MR imaging. Therefore, it is often necessary to image the thorax and abdomen using CT to provide as accurate an imaging tumor stage as possible. Additional need for extrapelvic imaging to stage patients will be included in the chapters dealing with individual malignancies. The MR examination should be correlated with clinical, biochemical, surgical, and pathological findings to improve image interpretation and provide the patient with as accurate a tumor stage as possible.

TUMOR STAGING SYSTEMS Tumor staging systems are internationally agreed graduated classifications of tumor spread. All the tumor staging systems incorporate common principles: l

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TUMOR STAGING Tumor staging requires the accurate identification of local tumor spread and the detection of lymph node or systemic metastases. It can be estimated from the patient’s symptoms, clinical examination findings, and the level of biochemical tumor markers. The histological type and grade of the tumor also correlate with the propensity for extraorgan spread and the early development of metastases.

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There is a gradation from “early” confined tumors, which are given low numbers in the classification systems, to “late” more widespread tumors, which are given higher numbers. The presence and number or size of lymph node metastases are treated similarly. Visceral and bone metastases are grouped in a general metastasis category but are not quantified. Each primary tumor has an individual staging classification tailored to its pattern of spread. The difference between tumor extent for each step is clearly demarcated. The systems must be easily and consistently applicable, forming a shorthand summary of the tumor extent which is understood within the national and international cancer community. The precise information supplied must be of relevance to therapeutic decision making.


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MRI MANUAL OF PELVIC CANCER

The staging systems are an indicator of likely prognosis since each step within the system correlates with a worse prognosis.

In oncology practice, additional benefits accrue from cancer staging systems: l

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The efficacy of new treatments can be assessed in similarly staged, and therefore standardized, populations. The performance of cancer centers can be compared nationally and internationally. The exchange of information is facilitated between different cancer organizations.

The most commonly used staging system is the Tumor Node Metastasis (TNM) classification, which has common stratification groups for each tumor type. The TNM cancer staging classifications are reviewed regularly by the International Union against Cancer (Union Internationale Contre le Cancer, UICC) with contributions from associated national and international organizations. The American classification is the “AJCC Cancer Staging Manual” produced by the American Joint Committee on Cancer and it correlates exactly with the TNM classification. For gynecological malignancy, there is also the Federation Internationale Gyne´cologie et Obste´trique (FIGO) classification and for bladder cancer there is the Jewitt– Strong–Marshall classification, which is principally used in the United States. Colorectal cancer may be staged using the Dukes’ classification, principally in the United Kingdom.

STAGE MIGRATION (STAGE SHIFT) Two factors contribute to the phenomenon of stage migration. The first is the periodic amendments all cancer staging systems undergo, which may lead to tumors being up- or downstaged in the new system. The second is the impact of cross-sectional imaging, which generally upstages more tumors than it downstages when compared to clinical staging. This results in fewer patients categorized as having early stage disease and more patients categorized as having later stage disease, with an overall apparent improvement in survival, stage for stage, compared with nonimaged patients. This is because the patients who are radiologically upstaged usually have a smaller volume of disease than those who are clinically categorized as belonging to the same stage. The upstaged patients are likely to improve the overall survival rate for the higher stage group and may also result in better tumor response rates. In addition, the early stage disease group is less confounded by inaccurate clinical staging of patients with more advanced tumors, and so this group too will appear to have improved tumor response rates and survival. The stage migration phenomenon should be remembered when interpreting modern clinical trial results and comparing them to historical controls. In this situation, stage migration may contribute to spurious increased efficacy of the new therapies.

PRINCIPLES OF ONCORADIOLOGICAL PRACTICE IN TUMOR DIAGNOSIS AND STAGING The aims of cancer imaging are to l

select the optimal imaging modality for the tumor to be assessed;

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design imaging protocols that take account of pathways of tumor spread; differentiate between tumor and benign conditions that can mimic tumor; provide the means to obtain histological confirmation of cancer by image-guided biopsy, which should not compromise the chance of cure; allocate a tumor stage on the basis of imaging findings; provide any additional information which will inform clinical decision making, for example, the likelihood of a tumor-free resection margin; maintain a common imaging modality and imaging protocol before and after treatment to allow assessment of response.

Each oncological staging report needs to incorporate standard information including an accurate description of tumor size, local extent, the presence of enlarged lymph nodes together with their location and maximum short-axis diameter, and the presence of any distant metastases. This information should be summarized using an appropriate staging system, which is clearly understood by the clinicians involved in the patient’s care. Where there is uncertainty about the exact stage, then this should be recorded, for example, “the MR stage of this patient’s prostate tumor is either T2b N0 M0 or T3a N0 M0.” If the staging assessment incorporates information obtained from clinical or pathological examination, this should be noted. It is also necessary to identify important normal structures, for example unobstructed kidneys, and to mention any comorbid conditions that may have an implication for patient treatment such as severe diverticular disease in a patient who may require pelvic radiotherapy.

FUNCTIONAL MR IMAGING Functional MR imaging enables information about tumor physiological parameters such as vascularity, oxygenation, metabolism, and diffusion to be quantified. The results are used to guide treatment decisions and identify treatment response, particularly with newer therapeutic agents which may be effective without altering tumor size. MRI can provide similar tumor-specific information to PET CT and may be preferable since it is readily available and does not require manufacture and administration of radiopharmaceuticals. Where published research supports the use of functional MR imaging in a particular pelvic cancer, then information will be included in the relevant chapter.

FURTHER READING Edge SB, Byrd DR, Compton CC, et al. AJCC Cancer Staging Manual. 7th ed. New York: Springer, 2010. International Federation of Gynecology and Obstetrics. Staging Announcement. FIGO staging of gynaecologic cancers; cervix and vulva. Int J Gynecol Obstet 1995; 5:319. Payne GS, Schmidt M, Morgan VA, et al. Evaluation of magnetic resonance diffusion and spectroscopy measurements as predictive biomarkers in stage 1 cervical cancer. Gynecol Oncol 2010; 116: 246–252. Wittekind C, Greene FL, Hutter RVP, et al. TNM Atlas Illustrated Guide to the TNM/pTNM Classification of Malignant Tumours. 5th ed. (2nd printing, corrected 2007). Berlin, Heidelberg, New York: Springer-Verlag, 2005. Zahra MA, Hollingsworth KG, Sala E, et al. Dynamic contrast-enhanced MRI as a predictor of tumour response to radiotherapy. Lancet Oncol 2007; 8:63–74.


2 MR imaging techniques in pelvic cancer Andrew P. Jones, Rohit Kochhar, and Alison Kilburn

MR IMAGING EQUIPMENT Superconducting 1.5-T MR scanners have now become the standard for clinical imaging. While there are options for lower-field open systems and a growing trend toward widerbore, shorter-length superconducting magnets, the horizontal bore 1.5-T magnet with the latest multiple-receiver technology generally provides the optimal specification for pelvic MR imaging in oncology. Higher-field 3-T imaging is emerging as a platform for research and, although some technical barriers still remain, these machines may become the systems of choice for MR body imaging. Three-Tesla systems offer higher signal-tonoise and contrast-to-noise ratios resulting in shorter-image acquisition times or improved resolution for some pelvic applications. Changes in T1 and T2 relaxation times, increased sensitivity to magnetic susceptibility, and radio frequency (RF) energy deposition have required the implementation of sequence and hardware adaptations to realize the full benefits of 3-T imaging. Also, within the abdomen and pelvis, RF field inhomogeneity resulting from dielectric effects within tissues has been a problem when using larger fields of view and can lead to standing wave effects and large local variations in signal intensity. The most recent application of parallel transmission techniques or multitransmit coil designs have addressed these problems with significant improvements in image quality for body imaging at 3 T. Many issues surrounding MR device compatibility and safety have yet to be fully addressed at 3 T mainly due to a lack of information and testing data for many devices. In comparison to a 1.5-T system, 3-T systems are more expensive to buy and operate, which has prevented widespread uptake in the clinical setting. Recent technical advances in equipment have resulted in a stabilized magnetic field gradient specification, an escalation in the number of independent receive channels and an improved range of multielement receiver coils. Standard magnetic field gradient performance with maximum amplitudes of approximately 30 mT/m and slew rates of 125 T/m/sec provide satisfactory imaging performance for pelvic imaging where very small field of views (FOVs) are not required and appropriate b-values for diffusion-weighted imaging (DWI) can easily be achieved. Higher-level gradients of maximum amplitudes of approximately 45 mT/m and slew rates of 250 T/m/ sec can provide advantages for better optimized echo times and echo train lengths. The latest receiver technology utilizing multiple receive channels and multielement receiver coils provides significant benefits for pelvic imaging, which requires maximum signal-to-noise ratio for large FOVs. Systems using 16- to 18-channel receivers offer performance that matches the requirements of the majority of multielement body coils used in pelvic imaging and allow the use of parallel imaging techni-

ques. Increased receiver channels of 32 and greater may establish a role for combined pelvic and abdominal imaging or emerging whole body applications. Modern MR systems conventionally have multielement body coils for imaging the pelvis. An array or matrix of coil elements positioned anteriorly are matched with a paired matrix positioned posteriorly or with the matrix of coils in the spine coil. Endorectal coils can provide an increase in signal-to-noise ratio for small FOV applications, for instance in prostate imaging, but physical tissue distortion of the wall of the rectum and signal flaring directly adjacent to the coil can impact on image interpretation.

MR IMAGING PROTOCOLS Patient Preparation and Care The interaction between the patient and the radiographic/ technological staff is essential in ensuring a successful examination. Most patients with cancer will be motivated to cooperate but could have difficulty complying due to pain, claustrophobia, or psychological stress. With careful explanation and sympathetic handling, patients are often able to cooperate fully. Time spent in making them as comfortable as possible before the examination, assisting them during the examination, and praising their efforts afterwards may ensure that the current examination is satisfactory and, importantly, that the patient is happy to undergo follow-up MR examinations. For all pelvic cancers, a standardized imaging protocol should be agreed so as to l

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ensure that imaging covers all the potential regions of tumor spread within the pelvis; keep scan times to the minimum necessary for patient comfort and efficient use of the MR equipment; allow comprehensive interpretation of the examination; ensure reproducibility of subsequent MRI examinations.

The administration of Buscopan1 (hyoscine-N-butylbromide) to reduce bowel peristalsis can provide significant benefits in some pelvic imaging applications where involuntary bowel motion degrades image quality. Accepted practice involves the use of orthogonal plane T1-weighted (T1W) and T2-weighted (T2W) sequences with off-axis planes or additional sequences being used for welldefined indications.

T1W Sequences (Spin Echo or Gradient Echo) T1W sequences give an overview of the abdomen and pelvis for detection of lymph node enlargement, bone marrow metastases, and hydronephrosis and hydroureter (Fig. 2.1). They allow


4


evaluation of tumor bulk, extension into pelvic fat, and provide some tissue-specific information, for example, the presence of hemorrhage and water. They are most commonly performed in the coronal and transaxial planes (Figs. 2.2–2.7).

T2W Sequences (Fast or Turbo Spin Echo) T2W sequences demonstrate the zonal anatomy of the pelvic viscera and nearly always clearly identify the primary tumor and its local extent. They are usually performed in three orthogonal planes.

Chemical Fat Saturation Chemical- or frequency-selective fat saturation techniques rely on the difference in resonant frequencies of water and fat and their resultant chemical shift of 3.5 ppm (220 Hz at 1.5 T). A saturation pulse centered only over the frequency for fat can selectively remove the signal contribution of fat from the image (Fat Sat and SPIR). The fat saturation pulse is normally delivered for each repetition period (TR) which leads to an increased TR and longer acquisition times. The impact of fat saturation varies with sequence type. Nonuniformity of the RF pulse may cause incomplete fat suppression, but this can be improved by SPAIR sequence, particularly in difficult body regions where there are tissue/air/bone boundaries. The sequence requires extended TEs, so is usually employed in T2-weighted fat suppression. The chemical shift between water and fat can also be exploited by using a frequency-selective excitation pulse at the water frequency (water excitation), resulting in the selective excitation of only water with no contribution from fat in the resulting images. In general, fat saturation techniques can be applied to both T1W and T2W sequences (Fig. 2.8). They are useful to delineate primary tumor extension into fat and to distinguish fat within lesions (e.g., ovarian masses).

Imaging Protocols for Specific Cancer Types DWI and dynamic contrast-enhanced imaging (DCE) are increasingly being applied to a variety of imaging protocols within the pelvis. However, because these techniques are relatively new in terms of routine application, they have not been included in the basic imaging protocol descriptions given below. These techniques are discussed in more detail later in this chapter. All the following examination protocols will require the T1W overview sequences detailed in Table 2.1 plus the T2W/ other sequences specified in Table 2.2.

ARTIFACTS AND STRATEGIES FOR REDUCTION The main artifacts encountered in MR pelvic imaging are motion and flow related. Motion within the pelvis can arise from respiratory movement, although in most patients this is minimal. Bowel peristalsis produces the more significant artifact of ghosting, which is blurring propagated in the phase encoding direction. Pulsatile flow artifacts arising from arterial blood are most noticeable on STIR sequences and postcontrast T1W images where the dominant high-signal structure on the image is blood. Chemical shift artifacts, arising from the differing resonant frequencies of water and fat, historically caused problems

in pelvic imaging. Currently, utilization of higher receiver bandwidths to achieve rapid signal sampling means that chemical shift artifacts are negligible. Standard techniques such as the application of saturation bands, choice of phase encoding direction, and the use of multiple signal averages can reduce the impact of artifacts from respiratory motion and blood flow. Parallel imaging techniques allow change of phase encoding direction and include phase oversampling to avoid aliasing with no increase of scan time. Similarly, where signal-to-noise ratio is sufficient, the use of parallel imaging factors of 2 and greater enable multiple signal averages to be included to reduce the impact of flow and respiratory motion with only limited impact on scan times. Potential problems with motion artifacts in non-breath-hold techniques can be minimized using free-breathing approaches. These new data acquisition strategies are generally either continuous, with retrospective selection and reordering of phase-encoding steps, or prospective using navigator echo techniques to selectively gate the acquisition according to respiratory motion. Nearly all such acquisition techniques, which involve the selective acquisition of data, require an increase in scan time. They are most applicable to imaging the upper abdomen and are not usually required for pelvic MR imaging. Techniques originally designed for head imaging such as BLADE and PROPELLER have now been very successfully used throughout the body to allow compensation for some motion artifacts. They use an incremented set of radial segments of k-space lines, which produce data filling within k-space with overlapping spokes of a wheel. The effective repeat sampling of the central region of k-space where the “blades” or “propellers” overlap results in a reduction of the effects of primarily in-plane motion. Overall acquisition times can be slightly greater, but good-quality T2W or proton density images are often obtained in uncooperative or difficult patients. As with all MR imaging, effective preparation of the patient and good positioning, so that he or she is comfortable and relaxed, reduce the likelihood of generalized patient movement.

CONTRAST ENHANCEMENT TECHNIQUES Intravenous injection of a gadolinium-based contrast agent is not routinely employed in pelvic imaging for malignancy. This is largely due to l

l

the inherent contrast differences between tumors and pelvic organs and tissues on T2W images; the enhancement of both tumors and normal pelvic organs, which can decrease tumor conspicuity.

However, a contrast agent injection may be valuable in certain instances: 1.

2.

Nondynamic injection l To clarify the composition of complex ovarian tumors l To determine the extent of sarcoma spread l To delineate the extent of disease or treatment effect within muscle groups l To predict or identify response to treatment Dynamic injection of a contrast bolus l To identify the tumor site in prostate cancer l To assess the depth of myometrial and bladder wall involvement in patients with endometrial or bladder cancer

2

0

0

2

0

TR 3.5 TE 1.32 258

2

0

TR 4100 TE 82 TR 4300 TE 88 TR 5.98 TE 2.76 108

2

Not used routinely

17

TR 5000 TE 102 908, 1508

Not used routinely

Not used routinely

17

17

2

0

2

7

2

None

0

1

Parallel imaging factor

TSE factor (ETL)

TR 5030 TE 102 908, 1508

TR 20 TE 5 408 TR 669 TE20 908, 1508 TR 400 TE 12 908, 1808 TR 208 TE 476 708, 1808 TR 5390 TE 102 908, 1508

Typical TE (ms), TR (ms), Flip angle

1

1

5

4

2

2

3

1

1

6

1

Signal averages

5

2.5

6

6

3

3

3

5.5

5

6

10

Slice thickness (mm)

R-L

A-P

A-P

A-P

R-L

R-L

A-P

A-P

R-L

R-L

A-P

Phase encoding direction

56

8

0

0

100%

100%

20%

0%

25%

30%

0%

Phase oversampling (%)

Abbreviations: ETL, echo train length; DWI, diffusion-weighted imaging. VIBE, volume interpolated breath-hold examination.

T2W Transaxial (oblique for cervix and rectum) T2W Coronal (oblique for prostate) DWI Transaxial DWI Transaxial T1 3D Gradient echo (VIBE or equivalent) Sagittal T1 3D Gradient echo (VIBE or equivalent) Transaxial

T1W Transaxial Pelvis T1W Transaxial Abdomen T2W Sagittal

T1W 3 planes (scout) T1W Coronal

Sequence Weighting Plane

Table 2.1 Basic Imaging Parameters for Staging Pelvic Cancers Matrix size (phase frequency) 128 256 256 512 256 512 109 256 210 256

210 256

210 256

156 192 156 192 146 256

101 192

Field of view, frequency (cm) phase (%) 49 100% 49 100% 38.3 100% 38 68.8% 20 100%

20 100%

20 100%

38 81.3% 38 81.3% 38 81.3%

32 75%

Temporal resolution 3 sec 100 measurements

Temporal resolution 30 sec 5 measurements

b-values = 0(50), 100, 300, 600 b-value = 1000

Fat Sat used occasionally

1 presaturation band to cover anterior abdominal wall Parallel presaturation band superior to slice block Inferior and superior presaturation bands parallel to slice block Presaturation band positioned over anterior pelvic wall fat and superior to slice block Inferior and superior presaturation bands parallel to slice block

To plan subsequent slice positions

Comments


MR IMAGING TECHNIQUES IN PELVIC CANCER 5


6


Table 2.2 Examination Protocols for Pelvic Cancers Examination protocol Vulva

Vagina Endometrium

Sequences

Comment

T2W T2W T2W T2W T2W T2W T2W

T2W sequences in all three orthogonal planes

sagittal transaxial coronal sagittal transaxial sagittal transaxial

Cervix uteri

T2W sagittal T2W transaxial

Ovary

T2W transaxial

Prostate

Bladder

Rectum

Sigmoid colon

Pelvic floor, urethra, and anus Penis

T2W T2W T2W T2W T2W T2W

coronal sagittal sagittal transaxial coronal sagittal

T2W T2W T2W T2W T2W T2W T2W T2W T2W T2W T2W T2W

transaxial coronal sagittal transaxial coronal transaxial sagittal coronal sagittal transaxial coronal sagittal

T2W coronal

Bone metastases Pelvic lymph node metastases Recurrent tumor Pelvic clearance

T2W transaxial STIR coronal T1W transaxial T2W transaxial T2W T2W T2W T2W

sequences sagittal transaxial coronal

Sequence to cover vagina Two blocks to include cervix uteri down to introitus Midline to cover endometrium and vagina. Use to plan transaxial sequences To cover whole of the endometrium. One block perpendicular to the endometrium and a second block parallel to the endometrium Sequence to include corpus uteri down to introitus One block positioned over cervix uteri and angled 908 to the endocervical canal, the second block positioned over the cervix uteri and variably angled perpendicular to the plane that needs to be assessed, e.g., posterior bladder/anterior rectum One or two blocks to include all of disease. May need to increase slice thickness up to 6 mm to include the whole area of interest May need to increase slice thickness to encompass whole of disease May be useful in some circumstances To include seminal vesicles to apex of prostate from perineum up Oblique sequence to include seminal vesicles, position parallel to prostatic urethra T2W sequences in all three orthogonal planes to cover whole bladder. May need to increase slice thickness up to 6 mm depending on distension of the bladder From perineum up to include whole bladder Start with sagittal sequence to enable planning further T2W sequences Transaxial oblique positioned perpendicular to the lesion and coronal blocks positioned on the sagittal images to include rectum Start with transaxial sequence to enable planning further T2W sequences Sagittal and coronal blocks positioned on the transaxial images T2W sequences in all three orthogonal planes positioned to include disease, ensure FOV is positioned low when scanning the anus Midline to include penis and sacrum. May need a larger FOV for coverage. No anterior saturation band To cover front of penis anteriorly and back of bladder posteriorly. May need to increase slice thickness for coverage One or two blocks to cover penis and scrotum inferiorly to above the bladder To cover from iliac crests to below symphysis pubis One or two overlapping blocks to cover from bifurcation of the aorta to below symphysis pubis Follow site-specific T2W sequences as suggested T2W sequences in all three orthogonal planes to include pelvic side walls, and from sacral promontory down to symphysis pubis

T1W (three-plane) scout sequence and T1W coronal and T1W transaxial are performed for all protocols in addition to the specific sequences listed. Abbreviation: FOV, field of view.

l

l

To obtain physiological information about tumor perfusion, oxygenation, and angiogenesis To differentiate tumor from inflammation or posttreatment fibrosis in bladder cancer

Dynamic Contrast Enhancement Dynamic postcontrast imaging is usually achieved using specialized 3D sequences. These 3D volume fat saturated gradient echo sequences use short TEs and TRs, along with k-space

interpolation techniques, to minimize acquisition times. Such rapid 3D volume acquisition times enable multiple volume acquisitions during the arterial, venous, and delayed phases of contrast circulation. Dynamic contrast enhancement (DCE) techniques can be used to assess tumor perfusion, oxygenation, and angiogenesis, employing modifications of methods first developed in cerebral studies usually based on dynamic T1 contrast enhancement. Signal enhancement curves obtained are mathematically fitted using a variety of pharmacokinetic models, and promising


MR IMAGING TECHNIQUES IN PELVIC CANCER

results have been published, for example, in the study of carcinoma of the cervix and carcinoma of the prostate. Figure 2.9A–E shows data for DCE analysis of posttreatment bladder cancer. The signal-intensity time curves from areas of residual tumor and fibrosis are shown to be quite different. Areas of residual tumor demonstrate a rapid increase in signal intensity (Fig. 2.9E) due to the increased permeability (leakiness) of tumor capillaries compared to areas of fibrosis that demonstrate intermediate signal increase.

NEW EMERGING TECHNIQUES Diffusion-Weighted Imaging DWI is an established technique for body imaging. Improvements in magnetic field homogeneity and sequence optimization using automated phase maps to optimize the magnetic field homogeneity over the imaging volume have resulted in good-quality DWI techniques. Faster imaging sequences, generally using echo planar imaging (EPI) signal readout, permit the use of multiple signal averages (typically 6–10) in combination with parallel imaging to reduce motion effects and permit acquisitions times of two to three minutes. The use of parallel imaging techniques reduces the echo train length of the DWI sequence EPI readout and hence the effective TE, producing a decreased sensitivity to magnetic field inhomogeneities, which can greatly affect image quality within the pelvis. DWI still remains very sensitive to susceptibility effects that arise from metallic objects or biomedical implants within or close to the imaging volume, as well as hemorrhage where there is a breakdown of blood products containing iron. Both cause signal voids and distortion within the DWI images. In some circumstances, it may be possible to alter image slice positions or orientation to minimize the impact of this susceptibility artifact. DWI produces an image contrast that results from inherent differences in the restriction of movement of water molecules. Pelvic cancers have been shown to have significantly lower apparent diffusion coefficient (ADC) values compared with normal tissue, with ADC values showing promise as a biomarker for treatment response. In general, DWI is helpful in staging known malignancies, differentiating benign from malignant lesions, and assessing treatment response or identifying disease recurrence (Fig. 2.10). In clinical practice, DWI normally acquires images at three or more different b-values to allow calculation of the ADC. These b-values always include one or more low b-values (0 or 50 sec/mm2) and a high-b-value (usually about 600–1000 sec/mm2). The choice of the b-values influences both the image appearance of lesions with restricted diffusion on the DWIs and

7

the accuracy of the calculated ADC values and ADC maps. Unfortunately, there is no absolute value of ADC which can be used to identify cancer in the pelvis, as several normal tissues such as lymph nodes, endometrium, and bowel, along with fibrosis, can have low ADC values. DWI data sets can be combined and fused with conventional MR images to correlate information. High-b-value images showing tumors of high cellularity as high signal can be fused with T2W images to improve the visualization of the depth of tumor invasion, for example, providing enhanced detail compared to T2W images alone. 1

H MR Spectroscopy

Multivoxel 1H spectroscopy or chemical shift imaging (CSI) has been applied to the brain for some time. However, CSI techniques have more recently been used for examination of prostate cancer (Fig. 2.11). 1H spectra show changes in creatine (Cr) and choline (Cho) signals in the presence of tumor and a metabolite signal from citrate (Ci), which is present only in normal healthy tissue. In prostate cancer, spectral changes have been reported as being present, despite normal imaging appearances. The spectroscopy provides important information on disease spread in the peripheral zone and in the neurovascular bundle and can be used to guide biopsies, monitor response to treatment, and for the assessment of possible recurrence. Recently, reductions in CSI voxel size have improved the resolution of the CSI data, although best results are reported for endocavity coils rather than pelvic-phased array coils. A number of studies have produced numerical data for [Cho + Cr]/[Ci] ratios in malignancy versus normal tissue or in benign prostatic hyperplasia (BPH). However, a number of problems still exist with this approach because citrate is a strongly coupled resonance and the spectral shape of this resonance depends on magnetic field strength and pulse sequence timing. Therefore, variations are seen in quantification of the citrate peak between different MR systems. The use of ratios for the metabolites also seems to be more robust in the peripheral zone because of regional variations of citrate within normal prostate. It is now widely recognized that polyamine (PA) resonances, predominantly from spermine, feature in prostate MRS and appear between choline and creatine. Hence, numbers that are quoted as [Cho + Cr]/[Ci] are actually [Cho + PA + Ci]/[Cr]. There is also evidence that polyamine is reduced in malignancy so that at the very least this may be a confounding factor in many earlier published studies. It is important to appreciate that all the other imaging techniques, including DWI, will in the future contribute to the complete examination.


8


Figure 2.1 Coronal T1WI of the abdomen and pelvis demonstrating lymph node metastases (arrows).

Figure 2.3 (A) Transaxial T2WI with phase encoding direction anterior to posterior with ghosting artifact (arrows). (B) Transaxial T2WI with phase encoding direction left to right showing greatly reduced ghosting artifact.

Figure 2.2 Transaxial T1WI of the pelvis showing the corpus uteri (intermediate signal intensity, straight arrow) and low signal intensity adnexal cysts (curved arrows).



9

Figure 2.4 (A) Sagittal T2WI of the female pelvis showing image degradation as a result of peristalsis (arrows). (B) Sagittal T2WI of the female pelvis post administration of an antispasmodic agent. The cervical tumor and its relationship with the bladder wall (straight arrow) and rectum (curved arrow) are more clearly visualized.

Figure 2.5 (A) Sagittal T2WI of the female pelvis showing the plane of transaxial oblique slices perpendicular to the endocervical canal (white line). (B) Transaxial oblique T2WI of the female pelvis along the plane illustrated in A. The intact fat plane between the cervix uteri and the bladder is clearly visualized (arrows).


10


Figure 2.6 (A) Sagittal T2WI showing the plane of transaxial oblique slices parallel to the endocervical canal (white line). (B) Transaxial oblique T2WI of the female pelvis along the plane illustrated in A, showing infiltration of cervical tumor into the rectal wall (arrows).

Figure 2.7 (A) Sagittal T2WI showing the plane of coronal oblique slices through the prostate (white line) and the reduced signal from fat in the abdominopelvic wall due to positioning of a presaturation band (arrows). (B) Coronal oblique T2WI of the male pelvis along the plane illustrated in A, showing disease extending into the bladder from the base of the prostate (arrows).



11

Figure 2.8 Example of a small field of view transaxial T2W of the male pelvis with fat saturation. Note the loss of signal from fat (arrows) which allows clear visualization of the prostate (curved arrow) and abnormal low signal in the peripheral zone posteriorly (arrowheads) consistent with prostatic cancer.

Figure 2.9 Example images and data from a DCE (dynamic contrast enhanced) MR obtained post treatment for two patients with bladder carcinoma for the assessment of residual tumor and treatment response. Thickening in the bladder wall is seen in both patients on transaxial T2W TSE images. The patient shown in A (T2W) and B (dynamic) was found to have residual tumor post treatment (arrowed). The patient shown in C (T2W) and D (dynamic) was found to have evidence of fibrosis post treatment (arrowed). Graphs in E illustrate an example of DCE concentration-time curves obtained from ROIs defined in residual tumor (triangles), posttreatment fibrosis (circles), and normal bladder wall (crosses) for the two patients. The signal-intensity time curves from areas found to be residual tumor and fibrosis are shown to be quite different. Areas of residual tumor demonstrate a rapid increase in signal intensity due to the increased permeability (leakiness) of tumor capillaries compared to areas of fibrosis which demonstrate intermediate signal increase. (Continued)


12


Figure 2.9 (Continued)



13

Figure 2.10 Fifty-eight-year-old female with rectal carcinoma planned for radical pelvic surgery post radiochemotherapy. (A) Sagittal and (B) transaxial T2WI images demonstrating a large lobulated recurrent mass (T) involving the upper and mid rectum (arrows in A). The mass infiltrates the mesorectum and abuts the left levator ani (arrowheads in B). In addition there is possible anterior extension to infiltrate the cervix (curved arrow in B); however, it is difficult to differentiate how much of this is due to post-treatment inflammatory change as opposed to disease. Diffusion-weighted imaging performed using (C) b100, (D) b600, and (E) b1000 demonstrate progressively increasing high signal in the rectal tumor mass (T) and in the nodular anterior extension infiltrating the cervix with corresponding low signal on the ADC map (F) in keeping with restricted diffusion confirming locally infiltrative tumor (curved arrows in C–F). (Continued)


14


Figure 2.10 (Continued)

Figure 2.11 1H spectroscopic chemical shift imaging of the prostate. The position of the voxels is shown in the left image and the measured spectrum for each voxel is demonstrated on the right. Citrate occurs only within normal healthy tissue. Areas of malignant tissue are characterized by a decrease in citrate signal and an increase in the choline signal.



FURTHER READING Brown MA, Martin DR, Semelka RC. Future directions in MR imaging of the female pelvis. Magn Reson Imaging Clin N Am 2006; 14 (4):431–437. A review of probable future applications for MR of the female pelvis. Chang KJ, Kamel IR, Macura KJ, et al. 3.0-T MR imaging of the abdomen: comparison with 1.5 T. Radiographics 2008; 28:1983– 1998. Paper discussing and comparing MR applications in the abdomen at 1.5-T and 3-T magnetic field strengths. Elster AD, Burdette JH. Questions and Answers in Magnetic Resonance Imaging. 2nd ed. St Louis, Missouri: Mosby, 2001. Thorough but easy to read physics text providing practical answers on specific topics of benefit to all involved in MRI. Husband J, Reznek RJ. Imaging in Oncology (2 volume set). 3rd ed. London, UK: Informa Healthcare, 2010. A very comprehensive and detailed clinical text book which is an excellent source of reference for clinical imaging in oncology. Johnson W, Taylor MB, Carrington MB, et al. The value of hyoscine butylbromide in pelvic MRI. Clin Radiol 2007; 11(62):1087–1093. Paper describing the benefits and practical regimen for using Buscopan in specific routine pelvic MR imaging applications. Lomas DJ. Review: optimization of sequences for MRI of the abdomen and pelvis. Clin Radiol 1997; 52(6):412–428. Physics based review of

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MR sequences and artifacts encountered in abdomen and pelvic MR imaging. Loncaster JA, Carrington BM, Sykes JR, et al. Prediction of radiotherapy outcome using dynamic contrast enhanced magnetic resonance imaging of carcinoma of the cervix. Int J Radiat Oncol Biol Phys 2002; 54(3):759–767. Paper describing method and correlation between clinical outcome and dynamic contrast-enhanced MRI. McRobbie DW, Moore EA, Graves MJ, et al. MRI from Picture to Proton. 2nd ed. UK: Cambridge University Press, 2007. Excellent comprehensive MR physics text book that allows the reader to learn about MR at both a practical level and at a more detailed physics level. O’Connor JP, Jackson A, Parker GJ, et al. DCE-MRI biomarkers in the clinical evaluation of antiangiogenic and vascular disrupting agents. Br J Cancer 2007; 96:189–195. Paper describing the potential role of dynamic contrast-enhanced MR techniques. Shukla-Dave A, Hedvig H, Moskovitz C, et al. Detection of prostate cancer with MR spectroscopic imaging: an expanded paradigm incorporating polyamines. Radiology 2007; 245(2):499–506. Paper assessing the usefulness of 1H MR spectroscopy in prostate cancer. Whittaker CS, Coady A, Culver L, et al. Diffusion-weighted MR imaging of female pelvic tumours: a pictorial review. Radiographics 2009; 29:759–778. Pictorial review of DWI in pelvic oncology.


3 Anatomy of the pelvis James O’Connor and Paul A. Hulse

MUSCULOSKELETAL MORPHOLOGY The pelvic cavity is divided into the false (greater) pelvis above and the true (lesser) pelvis below by an imaginary plane passing from the sacral promontory posteriorly around the arcuate lines laterally and anteriorly onto the symphysis pubis. The true pelvis is a bowl-shaped structure that contains and protects the lower portions of the urinary and intestinal tracts, and the internal reproductive organs. The bony pelvis forms an articulated ring consisting of the paired hip bones (composed of the fused iliac, ischial, and pubic bones), the sacrum, and the coccyx. The pelvic sidewalls are composed of a horseshoe-shaped muscular sling covered with pelvic fascia. The iliopsoas muscles form the walls of the false pelvis, while the obturator internus and piriformis muscles form the walls of the true pelvis. The pelvic floor is a fibromuscular diaphragm formed from the paired levator ani muscles anteriorly and the paired coccygeal muscles posteriorly. The levator ani muscle arises from the superior and posterior aspects of the pubis, the pelvic fascia covering the obturator internus muscle and the inner surface of the ischial bone and ischial spine. It inserts into the perineal body, coccyx, and the anococcygeal body. The levator ani is divided into three groups of muscles. The anterior group (levator prostate or sphincter vaginae) forms a sling around the prostate and vagina and inserts into the perineal body. The middle group (puborectalis) forms a sling around the junction of the rectum and anal canal and blends with the external anal sphincter. The posterior group (pubococcygeus and iliococcygeus) inserts into the anococcygeal body. The paired coccygei muscles form the posterior part of the pelvic floor. These arise from the ischial spines and attach to the coccyx posterior to the levator ani muscles. The groups of muscles are not resolved separately on MR imaging. Lying centrally in the pelvic floor is the perineal body, a fibromuscular mass that gives attachment to the anal sphincter, bulbospongiosus, transverse perineal, and levator ani muscles. Lying posteriorly between the anus and coccyx is the anococcygeal body, a fibromuscular mass that gives attachment to levator ani and fibers from the anal sphincter. The pelvic floor divides the pelvic cavity above from the perineum and ischiorectal fossae below.

PELVIC FASCIA, VISCERAL LIGAMENTS, AND PERITONEAL REFLECTIONS The pelvis has a two-layered covering of fascia. The parietal fascia covers the walls and floor and is continuous superiorly with the iliacus and transversalis fascia. It is thickened over the obturator internus and is more conspicuous on MR imaging. The visceral fascia covers the bladder, uterus, and rectum. Fascial condensations form a bilateral band running from

pubis to sacrum. These form supporting ligaments around the urethra and at the bases of the prostate, bladder, rectum, and uterus, attaching each respective organ to the pelvic wall. The urethropelvic and parapelvic ligaments support the urethra. The pubovesical and puboprostatic ligaments support the bladder and prostate. The posterior ligaments support the rectum. The lateral cervical (cardinal) and pubocervical ligaments support the cervix and uterus. The sacrogenital ligaments pass around the side of the rectum to attach to the prostate in the male and the vagina in the female. A fascial condensation anterior to the sacrum forms the presacral fascia. The uterosacral and sacroprostatic ligaments and presacral fascia are normally demonstrated on MR imaging although the other visceral ligaments are not seen unless pathologically thickened. The pelvic cavity can be divided into intra- and extraperitoneal compartments. The peritoneum forms a sack, which, in the pelvis, is draped over the pelvic organs to form a number of intraperitoneal recesses. The largest is the rectovesical space. Within the male rectovesical space, the opposing layers of peritoneum between the prostate and rectum fuse to form Denonvilliers fascia. In the female, the rectovesical space is divided by the uterus into the small vesicouterine recess anteriorly and the larger rectouterine space (pouch of Douglas) posteriorly. The apposing peritoneal layers between the vagina and rectum fuse to form the rectovaginal septum. The rectovesical space is continuous laterally with the pararectal fossae. The sigmoid colon usually indents the left pararectal fossa so that the left pararectal fossa is smaller than the right. The pararectal fossae are continuous anteriorly with the paravesical and supravesical spaces. The paravesical spaces are indented by the lateral and medial umbilical ligaments formed from the peritoneal coverings of the inferior epigastric vessels and obliterated umbilical arteries, respectively. Lying between the transversalis fascia of the anterior abdominal wall anteriorly and the umbilicovesical fascia posteriorly is the extraperitoneal prevesical space. This is limited inferiorly in the male by the puboprostatic ligament and in the female by the pubovesical ligament. The paravesical connective tissues form the lateral border. It extends superiorly to the level of the umbilicus. It is indented anteriorly in the midline by the median umbilical ligament, which contains the urachus; this runs from the apex of the bladder to the umbilicus. The peritoneal reflection and umbilical ligament are consistently demonstrated on MR imaging.

PELVIC VISCERA Urinary Bladder The urinary bladder is a muscular organ that has a maximum capacity of around 800 mL when distended with urine. It lies


ANATOMY OF THE PELVIS

below the peritoneal reflection and rests on the pelvic floor. It is separated from the pubic bones anteriorly by the retropubic space. The vagina in the female and the seminal vesicles and vasa deferentia in the male lie posteriorly. The bladder is pyramidal in shape when empty with an apex, body, base (fundus), and neck. The apex lies anteriorly and points to the symphysis pubis. The base forms the posterior wall. The body lies between the apex and base and is formed from the inferolateral surfaces. These converge with the base at the bladder neck. When full, the bladder has an ovoid shape with the superior surface rising out of the pelvis and into the lower abdomen. The trigone is a smooth triangular area of internal mucous membrane lying between the ureteric and internal urethral orifices. When fully distended the bladder wall thickness should not exceed 5 mm. MR Appearance On T1WI, the bladder wall has intermediate signal intensity slightly higher than urine in the adjacent lumen. The wall is best demonstrated on T2WI because of contrast between its lowsignal muscle layer, high-signal urine, and high/intermediatesignal perivesical fat. On MR imaging of the bladder wall, the adventitia is variably identified, the deep and superficial muscle layers cannot be consistently distinguished, and the mucosa is only defined clearly when inflamed. Occasionally, the inner mucosal layer can be identified particularly following intravenous gadolinium-diethylenetriamine penta-ecetic acid (DTPA), which results in delayed enhancement of the wall (Fig. 3.6B).

17

into a small cul-de-sac, the prostatic utricle. The ejaculatory ducts open onto the orifice of the prostatic utricle. On either side of the urethral crest is the prostatic sinus into which the prostatic ductules open. The membranous urethra is 1.5 cm long and continuous with the prostatic urethra. It is the portion that passes through the external urethral sphincter within the urogenital diaphragm. Consequently, it is the narrowest and least distensible part of the urethra. The spongy urethra is 15.0 to 16.0 cm long and extends from the membranous urethra to the external urethral orifice. It is divided into bulbous and penile portions. The bulbous urethra lies in the bulb of the penis where it is expanded to form the intrabulbar fossa. This contains the orifices of the bulbourethral glands (Cowper’s glands). The penile urethra is dilated within the glans penis to form the navicular fossa. Multiple minute openings of the mucus-secreting urethral glands open along the length of the spongy urethra. MR Appearance The proximal prostatic urethra and the spongy urethra are not usually demonstrated on MR imaging unless a Foley catheter is in situ. On T2WI transaxial images, the membranous urethra appears as a low–signal intensity ring surrounded by high– signal intensity epithelium. The female urethra is 4.0 cm long and passes from the bladder neck to the vaginal vestibule, opening directly anterior to the vaginal orifice and behind the clitoris. It lies anterior to and describes a course parallel to the axis of the vagina. It passes with the vagina through the urogenital diaphragm. The ducts of multiple paraurethral glands open onto the vestibule on each side of the external urethral orifice.

Ureters The ureters are retroperitoneal structures, which enter the pelvis passing over the pelvic brim close to the bifurcation of the common iliac artery. They pass posteroinferiorly onto the lateral pelvic walls anterior to the internal iliac arteries. Subsequently, they curve anteromedially superior to the levator ani to enter the bladder where they describe an oblique course through the bladder wall. In the male, the ureter lies posterolateral to the ductus deferens and enters the bladder just superior to the seminal vesicles. In the female, the ureter passes medial to the origin of the uterine artery (a branch of the anterior division of the internal iliac artery). At the level of the ischial spine, the ureter runs in the broad ligament of the uterus and parametrium lateral to the cervix and just above the lateral fornices of the vagina, where it is crossed superiorly by the uterine artery. MR Appearance The ureters can be identified on high-resolution T1WI and T2WI in the pelvis by the low signal intensity in their thin walls. They are most easily identified on T2WI when they are obstructed in their distal course so that they become distended with high–signal intensity urine.

Urethra The male urethra is divided into four parts. The preprostatic urethra is 1.0 to 1.5 cm long and extends from the neck of the bladder to the superior aspect of the prostate. The prostatic urethra is 3.0 to 4.0 cm long; on its posterior wall it has a median ridge, the urethral crest. In the middle of the crest is the seminal colliculus (verumontanum), which has a slit-like orifice that opens

MR Appearance On T2WI the female urethra appears as four concentric rings of alternating signal intensity. An outer low-signal ring corresponds to the striated muscle layer, a middle high-signal ring corresponds to the smooth muscle layer and submucosa, and the inner two rings correspond to mucosa lined by stratified squamous epithelium and lumen (Figs. 3.7B, 3.9B, and 3.17).

Prostate The prostate is a pyramidal structure approximately 3.0 to 4.5 cm long composed of glandular and fibromuscular tissue. It is enclosed by a 2- to 3-mm band of concentrically orientated fibromuscular stromal tissue, inseparable from the prostate gland that forms a false capsule. This is deficient at the apex allowing a route of extracapsular tumor spread. A fibrous prostatic sheath that is continuous with the puboprostatic ligaments surrounds the capsule. Between the prostatic capsule and sheath is the prostatic venous plexus. The prostate is broader superiorly with a base closely related to bladder neck. Inferiorly, the apex rests on the urogenital diaphragm in contact with fascia of the urethral sphincter and deep perineal muscles. Its anterior surface is separated from the symphysis pubis by loose areolar tissue in the retropubic space, which contains the puboprostatic ligament and part of the prostatic venous plexus. Inferolaterally, the prostate rests on the levator ani muscles. The seminal vesicles and ejaculatory ducts lie posterosuperiorly. Posteriorly, the surface of the prostate is separated from the adjacent rectum by Denonvillier’s fascia. The nonglandular anterior fibromuscular band extends over the anterolateral surface of the prostate. Above the level of the ejaculatory ducts the small


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transitional zone surrounds the urethra. This is covered posterolaterally by the horseshoe-shaped central zone through which the ejaculatory ducts pass. This in turn is surrounded on its posterior, inferior, and lateral surfaces by the peripheral zone. MR Appearance On T1WI, the prostate, seminal vesicles, and periprostatic veins are of uniform intermediate to low signal. On T2WI, the zonal anatomy is clearly demonstrated. The central zone and transitional zone, commonly termed the central gland, have low signal compared to the high–signal intensity peripheral zone. The anterior fibromuscular band has low signal on T1WI and T2WI and is contrasted with the relatively high signal from fat in the retropubic space. The verumontanum is often visualized on T2WI as a high–signal intensity structure. The prostatic capsule is consistently identified as a low–signal intensity structure on T1WI. Following intravenous gadolinium-DTPA, gland enhancement is variable. The periurethral region enhances during the early phase and subsequently the whole gland enhances homogeneously (Figs. 3.8 and 3.26). Zonal anatomy changes with increasing age. The central zone shrinks as the transitional zone enlarges due to benign prostatic hypertrophy. This causes compression of the peripheral zone and creates a low–signal intensity band (surgical pseudocapsule) between it and the hypertrophied transitional zone (Figs. 3.22 and 3.25).

Seminal Vesicles, Vas Deferens, and Ejaculatory Ducts The seminal vesicles are lobulated sacks 5 cm long with a terminal duct positioned inferiorly within the retroperitoneum. They lie obliquely behind the bladder and converge toward the midline. The superior parts of the seminal vesicles lie posterior to the ureters and extend above the level of the peritoneal reflection within the rectovesical space, separated from the rectum by a double layer of peritoneum. The inferior part of each seminal vesicles lies below the peritoneal reflection and is separated from the rectum by Denonvilliers’ fascia. The duct of the seminal vesicle joins the vas deferens to form the ejaculatory ducts. The vas deferens originates in the tail of the epididymis, ascends in the spermatic cord, and passes through the inguinal canal to enter the pelvis crossing the external iliac vessels. It traverses the pelvic sidewall lying external to the peritoneum and then passes medially behind the bladder anterior to and above the ureter and medial to the seminal vesicles where it is dilated to form an ampulla. The paired ejaculatory ducts arise adjacent to the neck of the bladder and run in close proximity passing anteroinferiorly through the prostate where they converge and open onto the prostatic utricles. MR Appearance On T1WI, the seminal vesicles are of intermediate signal intensity similar to muscle contrasted with the high signal intensity present within pelvic fat. On T2WI, the walls appear of low signal intensity and the contents return high signal intensity. A clear fat plane should be present in the angle between the anterior surface of the seminal vesicle and the posterior surface of the bladder (Figs. 3.22–3.24).

Vagina This is a musculomembranous tube, which extends from the vulva posterosuperiorly to surround the cervix of the uterus. It is normally collapsed, with its anterior and posterior walls apposed. It broadens superiorly to form a continuous recess around the cervix divided into the shallow anterior fornix and the deeper posterior and lateral fornices. The anterior wall is approximately 1.5 cm shorter than the posterior wall. The vagina is arbitrarily divided into thirds, the important division being between the upper two-thirds and the lower third, demarcated anteriorly by the junction of the bladder and urethra at the bladder neck. Anteriorly, the vagina is closely related to the base of the bladder and the urethra. Posteriorly, the upper third of the vagina at the level of the vaginal fornices is related to the peritoneal reflection in the pouch of Douglas, the middle third is related to the ampulla of the rectum, and the lower third to the perineal body and anal canal. In postmenopausal women, the vagina shrinks and the cervix is less prominent so that the vaginal fornices are virtually effaced. MR Appearance Layered anatomy of the vagina can be recognized on MR imaging. Mucus secretions within the lumen and the inner mucosal layer maybe seen as low signal on T1WI and high signal on T2WI. The surrounding layers of submucosa, collagen, longitudinal, and circular smooth muscle have low signal on T1WI and T2WI. The surrounding adventitia that contains the vaginal venous plexus appears of high signal intensity on T2WI (Figs. 3.17 and 3.18). Following intravenous gadolinium-DTPA the vaginal muscle wall and submucosa enhance. A central low–signal intensity line, which probably represents the vaginal lumen, is occasionally identified (Figs. 3.6 and 3.7). The vaginal appearances vary with the phase of the menstrual cycle. The wall is thicker in the proliferative phase than the secretory phase. Vaginal secretions are most prominent in the late proliferative and early to mid secretory phase. In the postmenopausal woman, the vaginal wall is thin and of low signal intensity on T1WI and T2WI.

Uterus and Uterine Tubes The uterus is a pear-shaped muscular organ lying centrally in the pelvis between the bladder anteriorly and the rectum posteriorly. It is divided into the fundus, which lies above the level of the uterine tube orifices, the body, and the isthmus, which constricts inferiorly to form the cervix. The cervix is divided into supravaginal and infravaginal parts. The fundus, body, and isthmus of the uterus are predominantly muscular, whereas the cervix is predominantly fibrous in composition. The uterine cavity communicates superolaterally with the uterine (fallopian) tubes and inferiorly with the cervical canal at the internal os. The cervical canal communicates with the vagina via the external os. Anterior and posterior reflections of the peritoneum pass over the uterine tubes to form the broad ligaments. These also enclose the round ligaments of the uterus, the ovarian ligament, and the uterine vessels. The round ligament arises anteroinferiorly to the origin of the uterine tube from the body of the uterus and passes through the inguinal canal to insert into the labia majora. The ovarian ligament arises posteroinferior to the origin of the uterine tubes and passes in the mesovarium to attach to the ovary.



The uterine tubes extend from the uterine cornua to open into the peritoneal cavity close to the ovaries. They run in the mesosalpinx formed by the free edges of the broad ligament. They have an infundibulum, a funnel-shaped distal end, which extends beyond the broad ligament to overhang the ovary with its fimbriae; an ampulla forming the widest and longest parts of the uterine tube and an isthmus that is continuous with the interstitial portion lying within the uterine wall. MR Appearance On MRI the demarcation between the uterine body and cervix is denoted by a waist in the uterine contour and the entrance of the uterine blood vessels at the level of the internal os. On T1WI, the uterus appears of low to intermediate signal intensity. On T2WI, three separate layers are distinguished—the endometrium, junctional zone, and myometrium. The endometrium lies centrally and appears of high signal. Its thickness varies with the phase of the menstrual cycle, being thinnest after menstruation and thickest during the mid-secretory phase. The outer layer of myometrium is of intermediate signal intensity that increases through the menstrual cycle to a maximum intensity in the mid-secretory phase. Between the endometrium and myometrium is the junctional zone that appears of low signal intensity. Uterine appearances also vary under the influence of oral contraceptives with the myometrium appearing of high signal intensity on T1WI and T2WI. The cervix is of variable composition consisting of an outer zone of smooth muscle, which appears of intermediate signal on T2WI; an inner zone of fibrous stroma, which appears of low signal on T2WI; and a central area of high signal intensity due to epithelium and mucus in the cervical canal (Fig. 3.15). In the shrunken uterus of the postmenopausal woman, the zonal anatomy is not well distinguished, the endometrium is thin, and the myometrium is of lower signal intensity. Following intravenous gadolinium-DTPA zonal anatomy can be displayed on T1WI. The myometrium and endometrium enhance, but the junctional zone remains of low signal intensity. The paracervical tissues (paracolpos) and inner cervical epithelium enhance, but the cervical stroma remains of low signal intensity.

Parametrium The parametrium is the extraperitoneal connective tissue that lies adjacent to the uterine body (parametrium), the cervix (paracervix), and vagina (paracolpos), which together are termed the parametrium clinically. The parametrium is rich in vascular and lymphatic tissue and contains the ureters, which pass lateral to the supravaginal part of the cervix. The floor of the parametrium is formed from the lateral cervical (cardinal) ligaments and divides the paracervical parametria from the paracolpos. The uterovesical ligaments demarcate the lateral margin of the parametrial tissues. MR Appearance The parametrium appears of heterogeneous intermediate signal intensity on T1WI and heterogeneous high signal intensity on T2WI (Fig. 3.16). The parametrial tissues enhance following intravenous gadolinium-DTPA (Fig. 3.6).

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Ovary The ovaries are almond shaped structures usually located in the ovarian fossae close to the lateral pelvic sidewall. Their size varies with age. In the adult, the ovary measures up to 3.0 cm in its longest dimension, but atrophies following the menopause reducing to a dimension of less than 2.0 cm. Considerable variation is seen in their anatomical position. The ovary is attached to the posterior surface of the broad ligament by a double fold of peritoneum, the mesovarium. Further support is given by the ovarian ligament proper and the suspensory ligament of the ovary that is continuous with the broad ligament attaching to the pelvic sidewall and in which the ovarian vessels and lymphatics run. Each adult ovary contains approximately 70,000 follicles. With each menstrual cycle some of these develop into Graafian follicles, one of which matures and releases an ovum at ovulation, leaving the corpus luteum. Therefore, the ovarian cortex contains immature follicles, Graafian follicles, and corpora lutea. MR Appearance The adult ovary appears of intermediate signal intensity on T1WI. On T2WI, the central stroma is of low signal intensity with hyperintense follicles identified in the high–signal intensity peripheral cortex (Fig. 3.16). Following intravenous gadolinium-DTPA, the central ovarian stroma enhances and contrasts with the low-signal ovarian follicles. Sometimes the ovaries can be difficult to locate on MR imaging. If the round ligament is identified and traced posteriorly, the ovaries lie in close proximity to it, attached to it by the ovarian ligament. Peripherally located follicular cysts and surrounding small vessels help to differentiate the ovaries from adjacent bowel. Occasionally, the ovaries are transposed from the pelvis, using the ovarian vessels as a pedicle, to an intraperitoneal paracolic or retrocecal location in order to remove them from a pelvic radiation field. Knowledge of this is important to avoid confusion with metastatic disease.

Rectum The rectum describes an S-shape in the sagittal plane formed by the rectosigmoid junction superiorly and the indentation of the puborectalis muscle of the pelvic floor (the anorectal flexure) inferiorly. In the coronal plane, there are three lateral flexures caused by internal mucosal folds, which overlie thickenings of the circular muscle layer of the rectal wall (valves of Houston). The terminal part of the rectum is dilated to form an ampulla that is supported by the pelvic floor and anococcygeal ligaments. The rectum has no mesentery and is only partially invested by peritoneum. In its upper third, peritoneum covers the anterior and lateral surfaces; in the middle third, only the anterior surface; and in the lower third, there is no peritoneal covering. Above the level of the levator ani and below the peritoneal reflection, a loose layer of connective tissue comprising the perirectal fat, blood vessels, nerves, and lymphatics encloses the rectum. The visceral and parietal layers of perirectal fascia surround this. The rectum and tissues enclosed by the visceral layer of perirectal fascia, also termed the mesorectal fascia, form a distinct anatomical entity, the mesorectum. This is important because radical removal of the rectum is achieved at total mesorectal excision surgery by dissecting along the plane that


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separates the visceral (mesorectal) from the parietal layers of perirectal pelvic fascia. MR Appearance The bowel wall appears of low signal on T1WI and intermediate signal on T2WI. When distended, the wall thickness of the rectosigmoid and anal canal should not exceed 5 mm and 10 mm, respectively. As the bowel wall thickens in the lower rectum, four concentric layers can be discerned. An outside low–signal intensity ring represents the outer muscular layer (muscularis propria), within this a layer of higher signal intensity represents the submucosa; this encloses a layer of low signal intensity corresponding to the muscularis mucosa and lamina propria, and centrally lies a high–signal intensity layer representing the mucosa. On postcontrast T1WI, the submucosal and mucosal layers enhance, but the intervening layer of muscularis mucosa and outer muscular layer do not, permitting differentiation between the layers.

Anal Canal The anal canal begins at the narrowing of the rectal ampulla formed by the indentation of the puborectalis portion of the levator ani and ends at the anal verge, a term that describes the transitional zone between the mucosa of the anal canal and the perianal skin. The upper part of the anal canal is lined with transitional (urothelial type) or rectal glandular mucosa. The lower part of the anal canal is lined with squamous mucosa. The line of demarcation (pectinate line, dentate line) between the two parts lies 2.5 to 3.0 cm proximal to the anal verge and is visible macroscopically but not on MR imaging. It forms a transitional area of squamous and nonsquamous mucosa and indicates the watershed for arterial supply and venous and lymphatic drainage. Above the pectinate line the anal canal is supplied by the superior rectal artery a branch of the inferior mesenteric artery and drained by the superior rectal vein into the portal venous systems. Below the pectinate line, blood supply is from the inferior rectal artery, a branch of the internal iliac artery, and venous drainage is via the inferior rectal veins to the systemic venous system. At the level of the pectinate line, arterial supply and venous drainage passes in both directions via anastomoses formed by the middle rectal arteries and veins. Lymphatic drainage above the level of the pectinate line is to the internal iliac lymph nodes and below the level of the pectinate line to the superficial inguinal lymph nodes. The anal canal has a larger voluntary external sphincter formed from striated muscle, which blends superiorly with the puborectalis muscle. The internal anal sphincter is involuntary and is formed from a thickening of the circular smooth muscle layer, which invests the upper two-thirds of the anal canal. Between the internal and external sphincters lies a continuation of the longitudinal muscle layer of the rectum, which inserts via a fascial extension into the pectinate line. MR Appearance On MRI the upper and lower parts of the anal canal are identified and appear different. The upper part contains the internal anal sphincter, the longitudinal muscle layer, and the puborectalis muscle. The lower part contains the internal anal sphincter, the longitudinal muscle layer, and the external anal sphincter. The longitudinal muscle layer lies in a slit-like space between the internal anal sphincter, the external anal sphincter, and puborectalis muscle—the intersphincteric space.

On T2WI, all the muscles except the internal sphincter, which has intermediate signal intensity, have low signal intensity (Fig. 3.28).

PERINEUM The perineum lies below the pelvic diaphragm. It is a diamondshaped space, which is bounded anterolaterally by the ischiopubic rami, laterally by the ischial tuberosities and posterolaterally by the lower borders of the sacrotuberous ligaments. A line drawn between the ischial tuberosities passes just anterior to the anus and divides the perineum into the urogenital triangle anteriorly and the anal triangle posteriorly.

Urogenital Triangle This compartment contains the urogenital diaphragm, which is a triangular double layer of fascia, which spans the pubic arch and attaches to the ischiopubic rami. The inferior fascial layer of the urogenital diaphragm forms the perineal membrane, which gives attachment to the bulb and crura of the penis or clitoris. It is pierced by the urethra in both sexes and the vagina in the female. Below the urogenital diaphragm lies the superficial perineal pouch. The muscles of the superficial perineal pouch are analogous in both sexes but smaller in the female. In the male, the bulbospongiosus muscles cover the corpus spongiosum, which encloses the urethra, to form the bulb of the penis. The corpus spongiosum extends anteriorly to form the glans penis. The ischiocavernosus muscles arise from the ischial rami to cover the corpora cavernosa and fuse anteriorly together and with the bulb of the penis to form the body of the penis. Thus, the penis is composed of three cylindrical structures: the paired dorsolateral corpora cavernosa and the single, ventral midline corpus spongiosum. Three layers of connective tissue cover the penile corpora. The innermost fibrous tissue layer is the tunica albuginea, surrounding the corpora cavernosa and the corpus spongiosum. The intermediate layer is the deep fascia of the penis (known as Buck’s fascia) which surrounds the corpora cavernosa and separates them from the corpus spongiosum. The outermost layer is a loose layer of subcutaneous connective tissue separated from the overlying skin by the dartos fascia. In the female, the bulbospongiosus muscles cover the vestibular bulbs. The bulbs arise from the perineal membrane, are united anteriorly by a median commissure, and lie each side of the vestibule. The vestibule contains the openings of the vagina, urethra, and ducts of the greater vestibular (Bartholins) glands, which lie at the posterior border of each vestibular bulb. The glans clitoris is a small round tubercle of spongy tissue analogous to the glans penis often covered by a prepuce. Two corpora or crura lie laterally formed by the paired ischiocavernosus muscles. The vulva is the collective term for the external female genitalia that includes the labia majora and minora, clitoris, bulb of the vestibule, vestibule of the vagina, greater and lesser vestibular glands, and the opening of the vagina. The superficial transverse perineal muscle is a slender muscle that runs along the posterior border of the perineal membrane and attaches to the perineal body and ischial rami. Deep to the perineal membrane lies the deep perineal pouch, bounded superiorly by the superior layer of the urogenital diaphragm. This principally consists of the deep transverse perineal



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muscles and the sphincter urethrae. In the male, it contains the bulbourethral (Cowper’s) glands and ducts, and in the female, it is pierced by the vagina.

flow voids, although veins with slow flowing blood may appear as high signal intensity on T2WI.

MR Appearance The three corpora are of intermediate signal on T1WI and high signal on T2WI. The penile bulb normally has higher T2W signal intensity than the corpora cavernosa due to differences in blood flow. Both the tunica albuginea and the Buck’s fascia are depicted on both T1WI and T2WI as a single inseparate hypointense band.

LYMPH NODES

Anal Triangle This contains the anus, anal sphincters, levator ani, and wedgeshaped ischiorectal and ischioanal fossae. The ischiorectal and ischioanal fossae lie between the ischium and rectum and anal canal, respectively. They are bounded superiorly by the posterior fibers of levator ani and inferiorly by the perineal skin. The fossae communicate with each other around the anal canal but are separated by the anococcygeal body, the anal canal, and the perineal body.

ARTERIES The abdominal aorta bifurcates at the L4 level to form the common iliac arteries. These pass inferolaterally to divide at the level of the pelvic brim into the external and internal iliac arteries. They lie anterior to the common iliac veins. The external iliac artery follows the iliopsoas muscle to pass under the inguinal ligament. It gives origin to the deep circumflex iliac and inferior epigastric arteries, which supply the anterior abdominal wall. It lies anterolateral to the external iliac vein. The internal iliac artery supplies the pelvic viscera, buttocks, medial thighs, and perineum. It passes posteromedially into the pelvis dividing into anterior and posterior divisions at the superior edge of the greater sciatic foramen. The anterior division gives rise to the umbilical, obturator, vesical, middle rectal, vaginal, uterine, internal pudendal, and inferior gluteal arteries. The posterior division gives rise to the superior gluteal, iliolumbar, and lateral sacral arteries.

VEINS The venous drainage of the pelvic viscera is mainly via a network of interconnecting veins, which form the pelvic venous plexuses (rectal, vesical, prostatic, uterine, vaginal). These principally drain to the internal iliac veins but also drain via the superior rectal vein to the inferior mesenteric vein and through the lateral sacral veins to the internal vertebral venous plexus. The internal and external iliac veins join to form the common iliac veins, which unite to form the inferior vena cava at the level of the L5 vertebra. The left common iliac vein describes a more horizontal course than the right so that it may appear quite large and elongated on transaxial cross-sectional imaging.

The pelvic lymph nodes are arranged in chains and usually named according to the artery, which they accompany. Unlike the abdominal organs, the pelvic viscera do not possess a hilum. Lymphatic drainage, therefore, occurs along the nodal chains on both sides of the pelvis and not to hilar nodes of each individual organ.

Inguinal Lymph Nodes These lie outside of the pelvis below the inguinal ligament but drain to the external iliac lymph nodes within the pelvis. They are divided into superficial and deep groups. The superficial inguinal nodes receive lymphatic drainage from the lower limb, the anterior abdominal wall below the umbilicus, the gluteal region, the anus and perianal skin, the perianal genitalia, the glans penis, the lower third of the vagina below the hymen, the uterine fundus, and the round ligaments of the uterus. The deep inguinal lymph nodes are located medial to the femoral vein and receive lymphatic drainage from the superficial inguinal nodes, the glans penis, and the clitoris.

External Iliac Nodes These consist of 9 to 10 nodes arranged in three distinct chains surrounding the external iliac artery. They receive lymphatic drainage from the bladder, the membranous urethra, the prostate, the cervix, and the upper part of the vagina. They drain to the common iliac nodes.

Internal Iliac Nodes These receive lymphatic drainage from the rectum, anal canal, bladder, lower ureter, body and cervix of the uterus, upper part of the vagina, seminal vesicles, prostate, and vas deferens. These drain to the common iliac nodes and the surgical obturator nodes.

Obturator Nodes These are divided into proximal (surgical) obturator nodes and the distal (anatomical) obturator nodes. The surgical obturator nodes receive lymphatic drainage from the internal iliac nodes and drain to the external iliac nodes. They are located adjacent to the obturator nerve and vessels proximal to their entry into the obturator canal and are seen posterior to the iliopsoas muscle on transaxial imaging. The anatomical obturator nodes are part of the internal iliac group and lie within the obturator canal itself (see Diagram 3.1).

Sacral Lymph Nodes These are part of the internal iliac group and receive a similar lymphatic drainage. They drain to the lateral aortic lymph nodes. They are located along the medial and lateral sacral vessels.

MR Appearance Blood vessels can be distinguished from lymph nodes on MRI because of their different signal characteristics. Patent vessels usually appear as low signal on spin echo images because of

Common Iliac Lymph Nodes Around four to seven nodes receive lymphatic drainage from the internal and external iliac nodes and drain to the lumbar nodes.


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Diagram 3.1 Schematic representation and T1W images of lower pelvis illustrate the location of pelvic side wall lymph nodes.

Lumbar Nodes These are composed of right and left lateral aortic chains and preaortic and retroaortic chains. The lateral aortic chains receive lymphatic drainage from the legs, pelvic viscera, and lower abdominal wall via the common iliac and sacral nodes. They also receive direct drainage from the ovary and testis. The preaortic nodes receive drainage from the rectum, anal canal, colon, and anterior abdominal wall. The retroaortic nodes receive drainage from the posterior abdominal wall. MR Appearance Lymph nodes appear of intermediate signal intensity on T1WI and variable signal intensity on T2WI, although usually greater than the signal intensity of muscle. In malignant nodes, the fatty hilum is lost and the morphology may appear rounded or have irregular edges, the latter suggesting capsular penetration. Lymph nodes enhance to a variable degree following intravenous gadolinium-DTPA, but this does not help to differentiate malignant from hyperplastic lymph nodes. Pelvic lymph nodes greater than 1.0 cm in short-axis diameter and inguinal nodes greater than 1.5 cm in short-axis diameter are considered enlarged (Table 3.1), although size has also been shown to be

a poor predictor of nodal status. Lymph nodes in the perirectal, paracervical, and presacral spaces are not normally seen, so that their identification on MRI is a good indicator that they are abnormal.

NERVES The pelvis is innervated by the sacral and coccygeal plexi. The sacral plexus lies on the anterior surface of the piriformis muscle just beneath the sacroiliac joint. It gives rise to the sciatic and pudendal nerves. The sciatic nerve leaves the pelvis through the greater sciatic foramen and enters the posterior thigh lateral to the ischial tuberosity. The pudendal nerve also leaves the pelvis through the greater sciatic foramen between the piriformis and coccygeus muscles, hooks around the ischial spine and sacrospinous ligament, and enters the perineum via the lesser sciatic foramen. Passing through the pelvis are the femoral and obturator nerves which originate from the lumbar plexus. The femoral nerve lies in the groove between the iliacus and psoas muscles. The obturator nerve runs along the medial border of the psoas, across the pelvic sidewall, to exit through the obturator foramen.

Table 3.1 Upper Limit of Normal-Sized Pelvic Lymph Nodes Location Inguinal Common iliac Internal iliac Obturator Presacral, paracervical, perirectal

Short-axis diameter (mm) 15 9 7 8 Not normally identified

MR Appearance Nerves appear as low/intermediate signal on T1WI and have a speckled appearance on T2WI, with low signal axons and high signal myelin and other supporting connective tissue. Only the sacral plexus and sciatic and femoral nerves are usually identified on MRI.



Figure 3.1 Transaxial T1WI at level of L5 vertebra.

Figure 3.3 Transaxial T1WI at level of mid sacrum.

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Thecal sac L5 nerve root Cecum Descending colon Urachus Psoas muscle Iliacus muscle Rectus abdominus muscle Gluteus maximus muscle Erector spinae muscle Right common iliac artery Right common iliac vein Left common iliac artery Left common iliac vein L5 vertebral body Iliac blade

Sigmoid colon Small intestine Internal oblique muscle Rectus abdominus muscle Iliopsoas muscle Gluteus minimus muscle Gluteus medius muscle Gluteus maximus muscle Piriformis muscle Inferior epigastric vessels External iliac artery External iliac vein Superior gluteal artery Branches of internal iliac artery and vein

Figure 3.4 Transaxial T1WI at level of acetabular roof. Figure 3.2 Transaxial T1WI at level of S1 vertebra. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Cecum Gluteus minimus muscle Gluteus medius muscle Gluteus maximus muscle Iliopsoas muscle Rectus abdominus muscle External iliac artery External iliac vein Internal iliac artery Internal iliac vein Body of sacrum Sacral ala Ilium

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.

Uterus (retroverted) Rectum Rectus abdominus muscle Internal oblique muscle Sartorius muscle Iliopsoas muscle Gluteus minimus muscle Gluteus medius muscle Gluteus maximus muscle Piriformis muscle Obturator internus muscle Left ovary Inferior epigastric vessels External iliac vein External iliac artery Deep circumflex iliac vessels Acetabular roof

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Figure 3.5 Transaxial T1WI at level of femoral head. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.

Urinary bladder Vagina Rectum Obturator externus muscle Iliopsoas muscle Rectus femoris muscle Tensor fascia lata muscle Sartorius muscle Gluteus maximus muscle Piriformis muscle Obturator internus muscle Levator ani muscle Obturator vessels and nerve Common femoral vein Common femoral artery Femoral nerve Deep inguinal lymph node Superior pubic ramus Ischium Head of femur Ischiorectal/anal fossa

Figure 3.6 Transaxial T1WI of female pelvis at level of femoral heads (A) before and (B) after intravenous gadolinium-DTPA. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Bladder Bladder mucosa Vagina Vagina muscle wall Vagina submucosa Vagina-lumen Paracolpos Rectum Obturator internus muscle Blood vessels in paracolpos



Figure 3.7 Transaxial T1WI of female pelvis at level of symphysis pubis (A) before and (B) after intravenous gadolinium-DTPA. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.

Urethra Urethra striated muscle layer Urethra-smooth muscle layer and submucosa Urethra-lumen Vagina Vagina muscle wall Vagina-lumen Anal canal Anococcygeal body Levator ani muscle Obturator internus muscle

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Figure 3.8 Transaxial T1WI of male pelvis at level of symphysis pubis (A) before and (B) after intravenous gadolinium-DTPA. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Prostate Prostate—periurethral region Prostate—central and peripheral zone Anal canal Levator ani muscle Obturator internus muscle Anococcygeal raphe Coccyx Natal cleft Symphysis pubis


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Figure 3.9 Transaxial T1WI of male pelvis at level of perineum (A) before and (B) after intravenous gadolinium-DTPA. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Deep dorsal vein of penis Urethra Urethra striated muscle layer Urethra-smooth muscle layer and submucosa Urethra-lumen Perineal body Anal canal Ischioanal fossa Ischial tuberosity Inferior pubic ramus

Figure 3.10 Transaxial T1WI at level of symphysis pubis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

Anal canal Ischioanal fossa Pectineus muscle Obturator externus muscle Obturator internus muscle Sartorius muscle Rectus femoris muscle Tensor fascia lata muscle Iliopsoas muscle Vastus lateralis muscle Gluteus maximus muscle Gemellus muscle Body of pubis Neck of femur Greater trochanter of femur Ischial tuberosity



Figure 3.11 Coronal T1WI of female posterior abdomen and pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

Liver Spleen Right kidney Thecal sac Sigmoid colon Retroverted uterus Psoas muscle Quadratus lumborum muscle Gluteus maximus muscle Piriformis muscle Levator ani muscle Inferior gluteal artery and vein Ischioanal fossa Ilium Sacral ala Body of sacrum

Figure 3.12 Coronal T1WI of female mid-abdomen and pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

Liver Ascending colon Descending colon Uterus Psoas muscle Illiacus muscle Gluteus maximus muscle Obturator internus muscle Obturator externus muscle Adductor brevis muscle Adductor longus muscle Right renal artery Abdominal aorta Left renal artery Right common iliac vein Right common iliac artery Left common iliac artery Iliac blade Acetabulum Head of femur

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Figure 3.13 Coronal T1WI of male mid abdomen and pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22.

Liver Urinary bladder Prostate Transversus abdominus muscle Internal oblique muscle External oblique muscle Psoas muscle Iliacus muscle Gluteus medius muscle Inferior vena cava Right renal artery Left renal artery Abdominal aorta Left renal vein Left testicular artery Left testicular vein Ilium Acetabulum Head of femur Superior pubic ramus Body of pubis Symphysis pubis

Figure 3.14 Coronal T1WI of female anterior abdomen and pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.

Liver Transverse colon Small intestine Urinary bladder Iliacus muscle Gluteus medius muscle Gluteus minimus muscle Acetabulum Rectus femoris muscle Adductor longus muscle External iliac vessels Ilium Superior pubic ramus Symphysis pubis



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Figure 3.16 Transaxial T2WI of female pelvis at level of acetabular roof. Figure 3.15 Sagittal T2WI of female pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.

Urinary bladder Urethra Muscular layer of bladder wall Outer myometrium Junctional zone Endometrium Plane of uterocervical junction Cervical lumen Cervical mucosa Cervix (fibromuscular layer) Cervix (outer layer) Ectocervical mucosa Posterior vaginal fornix Nabothian cyst Vaginal lumen containing secretions Vaginal wall (submucosal and muscle layers) Vaginal adventitia and venous plexus Rectovaginal septum Rectum Rectouterine space (pouch of Douglas) containing small volume of fluid Prevesical space Retropubic space Introitus Anal canal Rectus abdominus muscle Pubic bone and symphysis Sacrum

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

Uterus Parametrium Ovarian follicular cyst Cecum Rectum Perirectal fat Perirectal fascia Peritoneum Round ligament of ovary Rectus abdominus muscle External oblique muscle Iliopsoas muscle Piriformis muscle Gluteus medius muscle Gluteus maximus muscle Internal iliac vessels External iliac vein External iliac artery Sacrum Acetabular roof


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Figure 3.17 Transaxial T2WI of female pelvis at level of symphysis pubis.

Figure 3.18 Transaxial T2WI of female pelvis below symphysis pubis.

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.

Urethra striated muscle layer Urethra-smooth muscle layer and submucosa Urethra-mucosal layer Urethra—lumen Vagina—mucus secretions and inner mucosal layer Vagina—submucosa and smooth muscle layer Vagina—adventitia and venous plexus Pubourethral and periurethral ligaments Rectum Anococcygeal ligament Ischiorectal/anal fossa Levator ani muscle Sartorius muscle Rectus femoris muscle Iliopsoas muscle Pectineus muscle Adductor longus muscle Adductor brevis muscle Obturator externus muscle Obturator internus muscle Gluteus maximus muscle Deep dorsal vein of clitoris Common femoral vessels Symphysis pubis Body of pubis Femur Ischium

Clitoris Corpus cavernosum Urethra Parapelvic ligament Urethropelvic ligament Vagina—mucus secretions and inner mucosal layer Vagina—submucosa and smooth muscle layer Vagina—adventitia and venous plexus Anal canal—internal sphincter Anal canal—external sphincter and longitudinal muscle layer Ischioanal fossa Levator ani muscle—puborectalis portion Sciatic nerve Inferior gluteal vessels Pudendal vessels Inferior pubic ramus Ischium



Figure 3.19 Coronal T2WI of female mid-pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20.

Cervical lumen Cervical mucosa Cervix (fibromuscular layer) Cervix (outer layer) Nabothian cyst Paracervix containing venous plexus Bladder Peritoneum Rectosigmoid junction Posterior wall of vagina and vaginal adventitia Ischioanal fossa Sacral nerve root component of sciatic nerve Gluteus medius muscle Piriformis muscle Obturator internus muscle Levator ani muscle Internal iliac vessels Sacral ala Ilium Ischium

Figure 3.20 Coronal T2WI of female anterior pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.

Endometrium Uterus—junctional zone Outer myometrium Ovarian follicular cyst Bladder Broad ligament of uterus Sigmoid colon Small intestine Urethra Peritoneum Psoas muscle Iliacus muscle Obturator internus muscle Obturator externus muscle Adductor magnus muscle Acetabulum Head of femur

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Figure 3.21 Coronal T2WI of female pelvis through symphysis pubis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.

Crura of clitoris Body of clitoris Vestibule Labia majora Bladder Endometrium Uterus—junctional zone Outer myometrium Psoas muscle Iliacus muscle Obturator externus muscle Adductor brevis muscle Pectineus muscle External iliac vessels Acetabulum Femoral head

Figure 3.22 Sagittal T2WI image of male pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.

Prostate with benign prostatic hypertrophy in central zone Peripheral zone Seminal vesicle Bladder Bladder trigone Retropubic space Urogenital diaphragm Anal canal External sphincter Anococcygeal body Anococcygeal ligament Rectum Corpus cavernosum Corpus spongiosum Symphysis pubis Sacrum Sacral canal Coccyx



Figure 3.24 Transaxial T2WI of male pelvis. Figure 3.23 Transaxial T2WI of male pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.

Rectum Fat in perirectal space Perirectal fascia enclosing mesorectum Seminal vesicle Vas deferens Urinary bladder Perivesical venous plexus Wound scar Rectus abdominus muscle Obturator internus muscle Gluteus maximus muscle Common femoral vein Common femoral artery Femoral nerve Obturator vessels and nerve in obturator foramen Head of femur Acetabulum Sacrum

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.

Rectum Fat in perirectal space Seminal vesicle Bladder Scar Rectus abdominus muscle Obturator internus muscle Levator ani muscle Gluteus maximus muscle Sciatic nerve Superficial inguinal lymph node Common femoral artery Common femoral vein Inferior gluteal vessels Head of femur Acetabulum Sacrum

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Figure 3.26 Transaxial T2WI of male pelvis at level of prostate gland.

Figure 3.25 Transaxial T2WI of male pelvis at level of prostate gland showing benign prostatic hypertrophy. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

Rectum Denonvilliers fascia Prostate—peripheral zone Urethra Surgical pseudocapsule Prostate—transitional zone with benign prostatic hypertrophy Prostatic capsule (see text) Vesicoprostatic venous plexus Bladder Pectineus muscle Obturator internus muscle Muscular slips of levator ani muscle Gluteus maximus muscle Common femoral vein Common femoral artery Obturator vessels and nerve Head of femur Acetabulum Sacrum

1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

Anorectum Denonvilliers fascia Prostate—peripheral zone Prostate—central gland Prostatic capsule (see text) Prostate—fibromuscular band Bladder base Ischioanal fossa Spermatic cord Rectus abdominus muscle Pectineus muscle Obturator internus muscle Gluteus maximus muscle Levator ani—puborectalis portion Obturator nerve and vessels Common femoral vein Common femoral artery Head of femur Acetabulum



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Figure 3.27 Transaxial T2WI of male pelvis at level of symphysis pubis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15.

Anococcygeal body Anal canal Urethra Retropubic space Ischioanal fossa Sciatic nerve Levator ani—puborectalis portion Pectineus muscle Obturator externus muscle Obturator internus muscle Gluteus maximus muscle Common femoral vein Common femoral artery Pubic symphysis Ischial tuberosity

Figure 3.28 Transaxial T2WI of male pelvis at level of perineal body. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

Anal canal Internal sphincter Longitudinal muscle layer in intersphincteric space External sphincter Anococcygeal body Perineal body Ischioanal fossa Bulb of penis Crus of penis Corpus cavenosum Urethra Pectineus muscle Adductor longus muscle Adductor brevis muscle Obturator externus muscle Gluteus maximus muscle Common femoral vessels Ischial tuberosity Inferior pubic ramus


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Figure 3.29 Coronal T2WI of posterior male pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.

Seminal vesicle Ductus deferens Ampulla of rectum Anal canal External anal sphincter Levator ani muscle Psoas muscle Iliacus muscle Obturator internus muscle Common iliac vessels Ilium Ischium Head of femur

Figure 3.30 Coronal T2WI of male pelvis. 1. Prostate—central gland (transitional zone with benign prostatic hypertrophy, see text) 2. Prostate—peripheral zone 3. Prostatic capsule (see text) 4. Urinary bladder 5. Perineal body 6. Ischiocavernosus muscle 7. Levator ani muscle 8. Obturator internus muscle 9. Psoas muscle 10. Iliacus muscle 11. Acetabulum 12. Head of femur 13. Ischium

Figure 3.31 Coronal T2WI of anterior male pelvis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.

Bulb of penis Crus of penis Urogenital diaphragm Prostate—peripheral zone Prostate—central gland Prostatic capsule (see text) Prostatic venous plexus Urinary bladder Ischiocavernosus muscle Levator ani muscle—levator prostate portion Obturator internus muscle Obturator externus muscle Psoas muscle Iliacus muscle Ilium Acetabulum Head of femur Ischium



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Figure 3.32 Coronal T2WI of male pelvis through symphysis pubis. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

Prostate—fibromuscular band Bladder Suspensory ligament of penis Urethra Corpus spongiosum Corpus cavernosum Obturator externus External iliac vessels Body of pubis Symphysis pubis

FURTHER READING

Figure 3.33 Coronal T2WI of the body of the penis. 1. 2. 3. 4. 5. 6.

Corpus cavernosum Corpus spongiosum Bucks fascia and tunica albuginuea Central artery of corpus cavernosum Urethra Dorsal vein of penis

Barentsz JO, Sager GJ, Witjes JA. MR imaging of the urinary bladder. Magn Reson Imaging Clin North Am 2000; 8(4):853–867. Useful review. Coakley FV, Hricak H. Radiologic anatomy of the prostate gland: a clinical approach. Radiol Clin North Am 2000; 38(1):15–30. Useful review. Debatin JF, Patak MA. MRI of the small and large bowel. Eur Radiol 1999; 9(8):1523–1534. Useful review. Hricak H, Carrington BM. MRI of the Pelvis: A Text Atlas. London: Martin Dunitz, 1991. ISBN 1-85317–027-S. Definitive text atlas of pelvic pathology. Hussain SM, Stoker J, Lame´ris JS. Anal sphincter complex: Endoanal MR imaging of normal anatomy. Radiology 1995; 197:671–677. Lengele´ B, Scalliet P. Anatomical bases for the radiological delineation of lymph node areas. Part III: Pelvis and lower limbs. Radiother Oncol 2009; 92(1):22–33. Useful recent review of lymph node anatomy. Moore KL, Dalley AF. Clinically Oriented Anatomy. 4th ed. Baltimore: Lippincott, Williams and Wilkins, 1999. ISBN 0-683-06141-0. Wellillustrated clinical anatomy text. Netter FH. Atlas of human anatomy. Ciba-Geigy, Summit, 1989. ISBN 0-914168-19-3. Invaluable bench reference. Ryu J, Kim B. MR imaging of the male and female urethra. Radiographics 2001; 21:1169–1185. Useful review. Siegelman ES, Outwater EK, Banner MP, et al. High resolution MR imaging of the vagina. Radiographics 1997; 17:1183–1203. Useful review. Vinnicombe SJ, Husband JE. In: Butler P, Mitchell AMW, Ellis H, eds. Applied Radiological Anatomy. The pelvis. Cambridge: Cambridge University Press, 1999. ISBN 0-S21-48110-4. Valuable overview of radiological anatomy.


4 Cervical cancer Bernadette M. Carrington

BACKGROUND INFORMATION Epidemiology Worldwide, cervical cancer is the second most common cancer among women with 493,000 new cases and 273,000 deaths per year. There is a high incidence of up to 40 per 100,000 women in developing countries. In developed countries, cervical cancer is the third most common gynecological malignancy with an estimated annual incidence of 8.4 per 100,000 women in the United Kingdom and 7 per 100,00 women in the United States. The peak incidence is between 30 and 40 years with a second peak in women over 70. Since 1975, there has been a decreasing incidence due to national screening programs for cervical cancer and for cervical intraepithelial neoplasia (CIN), its precursor. Etiological factors implicated in the pathogenesis of CIN and cervical cancers are multiple and include smoking, immunosuppression, and sexual activity with exposure to human papillomavirus particularly types 16 and 18. Vaccination has been introduced against these types of human papillomavirus, and the incidence of cervical cancer is likely to fall further over the next 10 to 20 years.

Histopathology Approximately 80% of cervical carcinomas are of squamous cell origin, 15% being adenocarcinomas or adenosquamous carcinomas, and 5% poorly specified carcinomas. There is some evidence that the relative incidence of adenocarcinoma is increasing. Rare cervical malignancies include malignant melanoma, sarcoma, lymphoma, and small cell carcinoma. Squamous carcinomas usually arise from the squamocolumnar junction, the position of which varies with age. Before puberty and after the menopause, it is situated inside the endocervical canal. At puberty, estrogen-influenced cervical eversion occurs, followed by squamous cell metaplasia, which has the potential to dedifferentiate into squamous cell carcinoma. Adenocarcinomas arise within the endocervical canal and are more likely to remain occult, delaying clinical presentation. There is a histopathological grading system for cervical cancer incorporating four grades, from 1 (well differentiated) to 4 (undifferentiated).

Patterns of Tumor Spread Cervical cancer spreads through the cervical stroma and into the parametrium. With increasing infiltration of the pericervical connective tissue and ligaments, disease may reach the pelvic sidewall. As a consequence of lateral tumor extension, the patient’s ureters may be engulfed and obstructed. Cranial extension occurs into the body of the uterus, when the risk of developing lymph node metastases triples. Caudal extension is to the upper vagina and eventually the lower third of the

vagina. Finally, the tumor may extend into adjacent organs, particularly the bladder and rectum, but also occasionally to involve the pelvic floor or transgress the peritoneum to invade sigmoid colon or small bowel. Lymphatic spread occurs first to the paracervical and parametrial nodes. The obturator nodes are frequently the earliest pelvic sidewall lymph nodes to be involved, and presacral or perirectal nodes can be infiltrated in the posterior pelvis. Nodal disease may extend along the internal and external iliac chains, the common iliac chains or the upper retroperitoneal nodal stations, and there may be noncontiguous involvement of lymph node groups. Rarely, involved supraclavicular nodes are detected on clinical examination at presentation. With the exception of extrapelvic nodal disease, metastases are rare at presentation and usually occur in the lungs, liver, or skeleton. Clarification of Cervical Cancer TNM and FIGO Staging Using MRI It should be remembered that the FIGO staging system is clinically based, principally on surgical and pathological findings, but also on the results of physical examination and examination under anesthesia in patients with advanced tumors unsuitable for surgery. It is designed to be applicable worldwide, irrespective of imaging resources. The TNM system takes into account nodal and visceral metastases, often identified by imaging. When such systems are applied to imaging findings, areas of uncertainty arise. For example, MR evidence of bladder muscle layer invasion without involvement of the overlying mucosa might suggest stage TNM T4 or FIGO IVA disease, but it is important to remember that true stage T4 disease requires tumor infiltration of the mucosa as well as the muscle layer (Table 4.1). When patients have tumors which infiltrate through the pelvic floor, then they have tumor extension beyond the true pelvis and are stage TNM T4 or FIGO IVA. The N stage in cervical cancer only applies to pelvic lymph nodes. If there are upper retroperitoneal lymph node metastases, then the patient has TNM M1 or FIGO IVB disease, and inguinal lymph node metastases are treated similarly.

Prognostic Indicators The features that have been shown to correlate with an adverse prognosis include the following: l

l

Tumor volume; for example, in early stage disease (IB and IIA), when tumor diameter exceeds 3 cm then there is a 40% chance of lymph node involvement. Tumor stage; the five-year survival rate for stage IA is 98% and for stage IB1 is 90%. The survival rate drops as stage


CERVICAL CANCER

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Table 4.1 Cervical Cancer: TNM and FIGO Staging Classification 2010 TNM categories

FIGO stages

T – Primary tumor TX T0 Tis T1 T1a

0 I IA

T1a1

IA1

T1a2

IA2

T1b T1b1 T1b2 T2

IB IB1 IB2 II

T2a T2a1 T2a2 T2b T3

IIA IIA1 IIA2 IIB III

T3a T3b T4

IIIA IIIB IVA

N – Regional lymph nodes NX N0 N1 M – Distant metastasis M0 M1

l

l

l l

IIIB

IVB

The primary tumor cannot be assessed No evidence of primary tumor Carcinoma in situ (preinvasive carcinoma) Cervical carcinoma is confined to the uterus (extension to corpus should be disregarded) Invasive carcinoma diagnosed only by microscopy. Stromal invasion with a maximum depth of 5.0 mm measured from the base of the epithelium and a horizontal spread of 7.0 mm or less. Vascular space involvement, venous or lymphatic, does not affect classification Measured stromal invasion 3.0 mm or less in depth and 7.0 mm or less in horizontal spread Measured stromal invasion more than 3.0 mm and not more than 5.0 mm with a horizontal spread 7.0 mm or less Clinically visible lesion confined to the cervix or microscopic lesion greater than T1a2/IA2 Clinically visible lesion 4.0 cm or less in greatest dimension Clinically visible lesion more than 4 cm in greatest dimension Cervical carcinoma invades beyond uterus but not to the pelvic wall or to lower third of vagina Tumor without parametrial invasion Clinically visible lesion 4.0 cm or less in greatest dimension Clinically visible lesion more than 4.0 cm in greatest dimension Tumor with parametrial invasion Tumor extends to pelvic wall and/or involves the lower third of vagina and/or causes hydronephrosis or nonfunctioning kidney Tumor involves lower third of vagina, no extension to pelvic wall Tumor extends to pelvic wall and/or causes hydronephrosis or nonfunctioning kidney Tumor invades mucosa of bladder or rectum and/or extends beyond true pelvis (bullous edema is not sufficient to classify a tumor as T4) The regional lymph nodes cannot be assessed No regional lymph node metastasis Regional lymph node metastasis No distant metastasis Distant metastasis (including peritoneal spread, involvement of supraclavicular, mediastinal, or para-aortic lymph nodes, lung, liver or bone)

rises and is 15% to 20% for stage IV disease. Particularly important is the presence of lymph node metastases such that a patient with stage IB node-negative disease has a five-year survival of more than 90% but a woman with stage IB node-positive disease has a five-year survival of 50%. Poor tumor differentiation and small cell, neuroendocrine and clear cell types. Histological features including tumor vascularity and lymphatic permeation, deep cervical invasion, tumor extension into the body of the uterus, and mixed adenosquamous tumor histological type. Diagnosis during pregnancy or at a young age. Human immunodeficiency virus (HIV) positivity.

Treatment Surgery Patients are eligible for surgery only if their tumor stage is less than T2a and if they have no known nodal metastases. Radical hysterectomy involves resection of the upper third of the vagina, the body and cervix of the uterus, the pericervical tissues, including all ligaments, that is the cardinal, uterosacral and round ligaments, with bilateral salpingo-oophorectomy

and pelvic lymphadenectomy. Not all patients undergo a standard radical hysterectomy, and an ovary may be retained and either left in situ or transposed out of the true pelvis into the iliac fossa. Also, lymph node dissection can be extended to include upper retroperitoneal lymph nodes, or alternatively lymph node dissection may not be performed. Exceptionally, in young patients with early stage disease, local resection of the cervix (trachelectomy) can be contemplated to preserve the patient’s fertility. Patients who have positive surgical margins at the time of hysterectomy or who are lymph node positive may be referred for adjuvant radiotherapy. Radiotherapy Radiotherapy can be used to treat all stages of cervical cancer, although it is palliative in advanced disease (greater than T4). External beam radiotherapy, brachytherapy (internal placement of radioactive sources), conformal radiotherapy, and chemoradiotherapy are possible treatment methods. The current standard of care is that all patients should receive chemoradiotherapy except for those with reduced renal function, confirmed metastases, or poor performance status. There is strong evidence supporting its use with better local control of disease, a reduction in the rate of systemic metastases, and a five-year survival benefit of 6% compared to radiotherapy


40


alone, although with increased toxicity rates of approximately 10%. In advanced disease (T2 or greater) and in all nodepositive patients, the pelvic nodal stations are irradiated in addition to the primary tumor. Gynecological complications of radiotherapy include cervical or vaginal stenosis, hydrosalpinx, and fistula formation. Chemotherapy Neoadjuvant chemotherapy can be used in patients with advanced disease before they go on to receive standard chemoradiotherapy. When patients undergo radical hysterectomy and histopathology demonstrates poor prognostic factors such as lymphovascular invasion, then chemotherapy may be administered concurrently with postoperative radiotherapy. Chemotherapy alone is used palliatively for patients who present with metastatic disease, or in recurrence when salvage surgery is not possible.

MRI OF CERVICAL CANCER Technique When imaging the pelvis, injection of a smooth muscle relaxant such as hyoscine N-butylbromide (Buscopan1) is recommended in eligible patients to reduce or eliminate bowel peristaltic artifact and improve image quality. Turbo spin echo sequences and a phased array pelvic coil offer advantages over conventional spin echo sequences and the body coil in terms of an improved signal-to-noise ratio. This allows high-resolution (3 mm) sections with better spatial resolution and reduced movement artifacts because of faster scan times. In addition to orthogonal plane imaging, off-axis imaging may be useful to transect the cervical tumor at 908 and/or to scan perpendicular to the interface between cervix and rectum, or cervix and bladder. Fat-suppressed imaging can be used but offers no staging advantage over conventional T1- and T2-weighted turbo spin echo sequences in cervical cancer. Body coil imaging of the upper pelvis and retroperitoneum is advised to assess for noncontiguous lymph node involvement. Endoluminal coils may be used and have been shown to improve the detection of small tumors, but do not lead to a significant change in overall staging accuracy or accuracy in identifying parametrial invasion. Conventionally administered intravenous contrast enhancement has not been shown to improve the staging of cervical cancer, but dynamic contrast-enhanced imaging may improve detection of small tumors, determination of extent of stromal and parametrial invasion, and detection or confirmation of adjacent organ invasion. Dynamic contrast-enhanced imaging can be used to assess tumor perfusion and is thus an indirect method of assessing tumor hypoxia, which inversely correlates with tumor radiosensitivity and prognosis. Diffusion-weighted imaging is being investigated in cervical cancer and early studies have demonstrated restricted diffusion in the primary with lower apparent diffusion coefficients (ADCs) in squamous cell cancer than adenocarcinoma. The ADC has been shown to negatively correlate with tumor cell density and grade, and one study demonstrated that lymph nodes with low ADCs correlate with the most metabolically active (that is metastatic) lymph nodes on PET CT.

node metastases), tumor volume assessment, the identification of deep cervical extension, and uterine body involvement. It has also been shown to have a significant impact on management in up to 50% of patients undergoing MRI examinations. Dynamic contrast-enhanced MR may also be used to predict treatment response and survival after the first two to three weeks of chemoradiotherapy when the tumor mean signal intensity, signal intensity of the least enhancing tumor fraction, and residual tumor volume all correlate with long term survival. Magnetic resonance spectroscopy has been used in cervical cancer with variable results and does not have an established role. In some studies, excess choline was detected in the primary tumor, but in other studies it was identified in normal, CIN, and cancer patients with no significant differences between the groups. In a few studies, increased lipids have been detected in cervical tumors. After treatment, MRI may be used for surveillance to allow early detection of relapse. In proven recurrence, it is used to accurately document local tumor extent and involvement of adjacent viscera in any patient for whom salvage surgery or radical radiotherapy is contemplated, and to identify nodal and metastatic tumor. MRI is better than CT for the diagnosis of local recurrence and for the determination of local extent. 18 FDG PET-CT is also known to be accurate in detecting locoregional recurrent cervical cancer, although its spatial and contrast resolution is inferior to MRI in determining local visceral involvement. When patients are ineligible for curative therapy, imaging serves to document local and metastatic tumor burden as a baseline before chemotherapy, and can be used to monitor chemotherapy response.

MRI Staging Accuracy In cervical cancer, local staging accuracy of MRI ranges from 75% to 91%. This is better than conventional CT assessment, transrectal ultrasound imaging, or clinical evaluation. MRI is better than CT for evaluation of tumor size, and more sensitive for stromal invasion, and parametrial extension. A systematic review of MRI, CT, and PET in cervical cancer indicated a pooled MRI sensitivity of 72% and specificity of 96% for the detection of pelvic lymph node metastases compared to a CTpooled sensitivity of 47% (specificity was not available) and 18 FDG PET pooled sensitivity of 79% and specificity of 99%. A relatively recent large multicenter trial has reported more disappointing results with MR sensitivity of 53% and specificity of 85% for advanced disease, compared to 42% sensitivity and 82% specificity for CT and 29% sensitivity and 99% specificity for clinical FIGO staging. MR still performed better than CT in visualizing the primary tumor and detecting parametrial and uterine body extension.

Imaging Features Primary Tumor Usually, cervical cancer is of intermediate signal intensity on T1WI and higher signal intensity on T2-weighted turbo spin echo images, compared to the normal cervical stroma. Tumors may be solid or demonstrate central necrosis, sometimes with cavitation or ulceration.

Current Indications Magnetic resonance imaging (MRI) is the optimal method for locally staging cervical cancer because it is superior to clinical staging for overall tumor staging (including detection of lymph

Nodal Disease Local lymphatic spread to the paracervical and parametrial nodes is often not identified separate from the tumor proper.


CERVICAL CANCER

While the size of normal lymph nodes varies in different anatomical sites, the most robust measurement for normal nodal size is a short-axis diameter less than 1 cm. Other features suggestive of nodal involvement are round shape, an asymmetrical cluster of nodes on the pelvic sidewall, and nodal T2weighted signal intensity similar to the primary tumor. In patients with squamous cell tumors, central nodal necrosis is an accurate positive predictor of metastasis even in normalsized lymph nodes. Posttreatment: Surgery During radical hysterectomy, the vagina is oversewn and may appear bow tie shaped in the transaxial plane and may become of low signal intensity on T2WI due to fibrotic change. The bladder and bowel often adhere to its margins. The position of retained ovaries should be documented. The site of the surgical approach may be visible and lymphadenectomy clips may be identified as small areas of signal void on the pelvic sidewalls adjacent to the iliac vessels and in the upper retroperitoneum. It is important to recognize and avoid misinterpreting commonly occurring postsurgical complications such as lymphoceles, hematomata, and abscesses.

change or, occasionally, radiotherapy-induced telangiectasia can produce similar appearances. Dynamic contrast enhancement may help differentiate residual or recurrent disease from treatment effect. Currently, diffusion-weighted imaging is being investigated and may prove useful for the diagnosis of local recurrence in the future. Up to one-third of patients develop recurrent tumor in the pelvis by three years after treatment of their primary tumor. Central recurrence after hysterectomy manifests as a tumor mass arising from the vault of the vagina. All patients require assessment of locoregional nodal stations and the upper retroperitoneum. CT is necessary to assess the lungs.

Pitfalls of MRI Early-Stage Disease l

l

Posttreatment: Radiotherapy Metallic marker seeds placed in the cervix to provide a landmark for external beam therapy may be visualized on MRI as signal voids. After radiotherapy there is often rapid tumor resolution and cervical reconstitution, so that within weeks there is restoration of T2WI low–signal intensity fibrous stroma, whose signal intensity is often very low due to a fibrous reaction. Occasionally, when the primary tumor has been large, only a tiny, thinned cervical remnant reconstitutes, and this appears atrophied compared with the uterine body. The uterus of a postmenopausal woman may decrease in size following radiotherapy. A patient of reproductive age will demonstrate more profound changes with decrease in size of the uterus, loss of the junctional zone anatomy, low signal intensity of the uterine body, marked thinning of the endometrium, and low signal intensity of the cervix as it reconstitutes. The ovaries shrink, become lower in signal intensity, and no longer contain physiological cysts. The vaginal wall also demonstrates a decrease in signal intensity. Posttreatment: Chemoradiotherapy Chemoradiotherapy produces different local effects. The cervix may not become as fibrosed as with radiotherapy alone, and there are often residual islands of intermediate– to high–signal intensity tissue for the first six to nine months after therapy, which gradually decrease in signal intensity, usually over the course of a year. The vaginal vault often demonstrates patchy high signal intensity, particularly posteriorly. In younger patients, the uterine body occasionally demonstrates a T2weighted striped appearance with bands of intermediate and high signal intensity. Therapy effect in other pelvic tissues may be more severe, and there is nearly always small to moderate volume free pelvic fluid which may persist for months or years. These treatment effects may resolve and then flare up unpredictably. Residual/Recurrent Disease Residual disease should be considered when the cervix retains areas of high signal intensity more than six months after radiotherapy, but this finding is not specific since inflammatory

41

l

l

The identification of small tumors and differentiation from postbiopsy and inflammatory changes may be difficult. The biopsy may leave an ill-defined area of high signal intensity on T2WI, and if a cone biopsy has been performed, there may be a tissue defect present mimicking an ulcerating lesion. Nabothian cysts are cervical mucous retention cysts which may be misinterpreted as tumors. However, their typical site, spherical shape, fluid content, and thin wall differentiate them from a cancer. Early parametrial extension is sometimes difficult to identify. Preservation of hypointense fibrous stroma around the tumor has a high-negative predictive value for parametrial invasion, but, conversely, complete loss of the low– signal intensity fibrous stromal ring does not always indicate definite parametrial extension. Displacement and compression of the vaginal vault by a large exophytic cervical mass may mimic vaginal infiltration, or may be misinterpreted as preservation of the outer cervical stroma. It is important to review the images in multiple planes to determine whether the tumor is truly invading the vagina.

Late-Stage Disease l

l

l

l

Identification of stage T3a disease. Lower one-third vaginal infiltration may be difficult to diagnose because of uncertainty about the demarcation between the upper twothirds and the lower one-third of the vagina (arbitrarily the vagina distal to the bladder base). Laxity of the pelvic floor may alter the vaginal position, and large exophytic tumors may compress the vaginal wall and mimic vaginal involvement. Extension along the uterosacral ligaments may be difficult to define. The radiological signs of uterosacral ligament extension are thickening or lobularity of the uretosacral ligaments in continuity with the primary tumor, with signal intensity similar to that of the primary tumor on T2WI. Extension to the pelvic sidewall (stage IIIB) is problematic because of differences in radiological interpretation. Some authorities consider tumor extending to within 0.5 to 1.0 cm of the sidewall to indicate stage IIIB tumor; others only consider tumor actually making contact with the sidewall as stage IIIB. Bladder involvement (stage IVA) may be difficult to decide upon. While tumor can alter the signal intensity of the bladder muscle layer, it is only when the mucosa is of


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tumor signal intensity and/or there are tumor masses within the bladder lumen that stage IVA disease can be diagnosed. Pelvic floor invasion can be difficult to distinguish from tumor tethering or adherence. If there is no plane between the tumor and the levator ani, but the normal low signal

intensity of the muscle is preserved and differs from that of the tumor, then adherence is likely. If the tumor extends into or through the levator ani muscle then the normal low signal of the levator ani muscle is replaced by intermediate signal intensity similar to the tumor proper.

Figure 4.1 Normal cervical anatomy in a woman of reproductive age. T2WI in (A) the sagittal plane and (B) the coronal plane, the latter providing a true transaxial image through the cervix. The endocervical lumen can be seen as a high–signal intensity structure (black asterisk) surrounded by the cervical mucosa (white asterisk). The predominantly fibrous portion of the cervical stroma returns a low signal intensity and is discerned as a low–signal intensity ring immediately adjacent to the mucosa (long white arrow), while the outer cervix has an increased proportion of smooth muscle resulting in an intermediate signal intensity (short white arrow). The cervix is surrounded by parametrium laterally and anteriorly (P in B), which is composed of fat, connective tissue, numerous blood vessels, and lymphatics. The intraorgan anatomy of the uterus is well seen in A with the endometrial cavity (e), the junctional zone of the inner myometrium (j), and the outer myometrium (m).The pelvic floor formed by the levator ani muscular plate is well illustrated in (B) (black arrows). Abbreviations: B, bladder; U, urethra; IAF, ischioanal fossa; OI, obturator internus muscle.


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Figure 4.2 T1b cervical cancer. T2WI (A) sagittal and (B) transaxial images demonstrating a small predominantly endocervical tumor in a postmenopausal patient. The mass is of high signal intensity (arrows) but is of lower signal intensity than the endocervical secretions seen cranial to the lesion. There is slight distension of the endocervical canal. Note the preservation of normal cervical tissue around the tumor indicating that it is confined. After the menopause, the junctional anatomy of the uterus is lost and the cervix is often of low signal intensity throughout. The patient has a small nabothian cyst (asterisk in A). (C) Sagittal and (D) transaxial T2WI demonstrating a small confined intermediate signal cervical tumor (T) which has a rim of low signal intensity fibrous stroma around its margin (arrows).


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Figure 4.3 T1b1 N0/N1 M0 cervical cancer. (A) Sagittal and (B) off-axis coronal T2WI demonstrating a tumor (T) occupying the endocervical canal and protruding through the external os. The tumor measures more than 4 cm in its longest axis. In B a small right pelvic sidewall lymph node is noted (arrow), which is suspicious for a metastasis because of its round size and signal intensity, which is similar to that of the tumor.

Figure 4.4 T2a cervical cancer. (A) Sagittal T2WI demonstrating a T2a1 tumor (T) involving the superior aspect of the posterior vaginal fornix (arrows) with increased signal intensity of the vaginal wall compared to more caudally within the vagina (arrowheads). A smaller volume of disease (open arrow) is infiltrating the anterior vaginal fornix but has not breached the vaginal wall to involve the uterovesical ligament (curved arrow). A small amount of free pelvic fluid (asterisk) is noted. (B) Sagittal and (C) transaxial T2WI in another patient demonstrating an exophytic cervical tumor (T), which is infiltrating the posterior vaginal fornix (arrows) with loss of the normal low signal intensity of the vaginal muscle layer. In (C), the thinning and altered signal intensity of the vaginal wall can be appreciated in comparison to the normal lateral fornices (arrowheads). Note how the vaginal vault can form a pseudocapsule around the cervical tumor mimicking an intact fibrous stroma. A tampon (asterisk) is in the right anterior vaginal lumen.


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Figure 4.5 T2b N0/N1 cervical tumor with parametrial extension. Off-axis transaxial T2WI demonstrating a high–signal intensity tumor mass (T) involving the left cervix and extending from the endocervical canal throughout the entire cervical stroma with lobulated tumor extending beyond the lateral cervical margin and bulging into the parametrium (short arrows). There is also a left-sided posterior pelvic lymph node (long arrow) which, while small, is highly suspicious for an involved node because of its position and similar signal intensity to the tumor proper.

Figure 4.6 T2b cervical cancer with parametrial vascular engulfment. (A) Off-axis transaxial and (B) off-axis coronal T2WI demonstrating a cervical tumor (T) with bilateral parametrial extension and engulfment of right parametrial vessels (arrowheads). There is early lobular extension into the proximal uterosacral ligament (arrow in A).


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Figure 4.7 T2b cervical cancer with involvement of the uterovesical ligament, the anterior parametrium. (A) Sagittal T2WI demonstrating a large cervical tumor (T) with early breach of the anterior fibrous stroma and small volume extension into the inferior uterovesical ligament (arrowheads). The intact fat-filled uterovesical ligament can be seen superiorly (arrow). Note the marked endometrial distension due to obstruction of the endocervical canal by the large tumor mass. (B) Sagittal T2WI in a different patient demonstrating extensive uterovesical ligament involvement by a cervical tumor (T), which is inseparable from the low–signal intensity muscle layer of the posterior bladder wall. Small-volume pelvic ascites is present (asterisk).

Figure 4.8 T3a cervical cancer. Sagittal T2WI demonstrating a cervical tumor (T) with involvement of the anterior wall of the vagina (arrow) including the lower third (conventionally that portion of the vagina which is below the bladder). Note that the uterovesical ligament (arrowheads) is intact. There is some edema within the mucosa of the bladder, but the outer bladder wall is also intact. There is retention of fluid within the endometrial cavity due to tumor obstructing the endocervical canal.


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Figure 4.9 T3b cervical tumor with hydronephrosis. Transaxial T2WI demonstrating an extensive cervical tumor (T) invading the uterine body, extending into the parametrium, and obstructing the left ureter (arrow).

Figure 4.10 T3b cervical tumor with uterosacral extension to the pelvic sidewall. Transaxial T2WI demonstrating tumor (T) involving the entire cervix, infiltrating the left uterosacral ligament (arrows), which is thickened, and extending to within a centimeter of the left pelvic sidewall. Clinically, this tumor was fixed to the sidewall.


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Figure 4.11 T3b cervical tumor with uterosacral extension. Transaxial T2WI showing tumor extending along both uterosacral ligaments to within 0.5 cm of the sidewall on the right and to within a centimeter of the sidewall on the left. Note the lobular uterosacral tumor infiltration on the right side (arrow). Tumor extension to the pelvic sidewall is diagnosed variously by different authorities. Criteria include tumor extending to within 1 cm, tumor extending to within 0.5 cm, and tumor actually contacting the sidewall. Overall, however, early pelvic sidewall extension may be under identified.

Figure 4.12 T4 cervical cancer invading the bladder. Sagittal T2WI showing a large tumor (T) infiltrating the whole uterus and extending through the bladder into the mucosa (arrows). The mucosa should demonstrate the same signal intensity as the tumor proper to allow diagnosis of bladder infiltration. Note the normal low–signal intensity muscle layer of the bladder inferiorly (asterisk) and the presence of overlying mucosal bullous edema producing high signal intensity change within the mucosa (arrowheads), which should not be diagnosed as tumor infiltration.


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Figure 4.13 T4 cervical cancer invading the bladder. (A) Transaxial T2WI, (B) fat suppressed T2WI, and (C) sagittal T2WI. There is a large cervical tumor (T) invading the bladder in a left posterior location with a mass (arrow) of similar signal intensity to the tumor proper seen within the bladder lumen. Note that there is bladder mucosal edema (arrowheads) in B partially overlying the intravesical tumor but also extending over the posterior bladder wall. The central portion of the bladder wall in A and B is also abnormal but signal intensity is higher than the tumor proper and represents edema. (B) A portion of the bladder wall is shown to be partially infiltrated but to retain an intact though edematous inner muscle layer (small arrows), bladder muscle layer (M). In (C) the abnormal signal intensity of the posterior bladder muscle layer and its retraction toward the tumor can be appreciated. Note the apparent abnormal signal intensity at the dome of the bladder (asterisk) due to artifact from adjacent peristalsing small bowel. To overcome this, hyoscine butylbromide (Buscopan) could be administered if necessary.


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Figure 4.14 T3b cervical tumor with partial thickness rectal involvement. Transaxial T2WI showing a cervical tumor (T) extending through the perirectal fat to infiltrate the outer rectum on the left side (arrows). Disease extends around the left uterosacral ligament to the pelvic sidewall (open arrow). The overlying rectal mucosa (arrowheads) is intact but of high signal intensity indicating edema or hemorrhage and, because of this, although tumor is obviously invading the rectal wall, the stage is T3b by TNM criteria. Note a right adnexal mass (M) of similar signal intensity to the tumor proper due to involvement of the ovary by the primary cervical tumor.

Figure 4.15 T4 cervical cancer involving the bladder, rectum, urethra, and pelvic floor musculature. (A) Sagittal, (B, C) transaxial, and (D) coronal T2WI demonstrating a huge cervical tumor (T) involving the bladder (arrows in A and B), the rectum (open arrows in A and B), the urethra (curved arrows in A and C), and the puborectalis component of the left levator ani muscle (arrowheads in D). The mucosa of the bladder or rectum has to be involved to quality for stage T4 disease. Local extension beyond the pelvis, in this case into the ischioanal fossa, also makes the tumor stage T4.


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Figure 4.16 T4 cervical cancer. Sagittal T2WI demonstrating a large cervical tumor (T) extending into the uterovesical ligament (arrows) and incompletely involving the bladder muscle layer with overlying mucosal edema. Superoposteriorly the tumor breaches the peritoneum to involve an adjacent small bowel loop (arrowheads), making this a T4 tumor.


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Figure 4.17 Lymph node metastases. (A) Off-axis coronal T2WI demonstrating a small paracervical lymph node metastasis (arrow) adjacent to a cervical tumor (T), (B) sagittal, and (C, D) off-axis transaxial T2WI in a different patient demonstrating a large cervical tumor (T) invading the uterovesical ligament (arrows) and extending into the lower third of the vagina (asterisk). A large right parametrial lymph node metastasis (open arrow) is seen in C. Bilateral obturator (curved arrows) and perirectal lymph node metastases (arrowheads) are also present. Parametrial lymph node metastases are often small but are of similar signal intensity to the tumor proper and appear separate from it on all planes. They are infrequently seen because parametrial extension of the primary tumor often engulfs them. In this case, the perirectal and right obturator lymph nodes are small but are highly likely to be metastatic because they are of similar signal intensity to the primary tumor.


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Figure 4.18 Internal iliac and perirectal lymph node metastases. Transaxial T2WI demonstrating a high–signal intensity primary cervical tumor (T) with metastatic spread to a right internal iliac (arrow) and two perirectal lymph nodes (open arrows). The right internal iliac lymph node has undergone central nodal necrosis as shown by irregular very high signal intensity within its center, and it has an irregular anterior margin indicating extracapsular spread.

Figure 4.19 Presacral lymph node metastases in cervical cancer. Sagittal T2WI demonstrating a presacral node at S2 level (arrow), which has the same signal intensity as the tumor proper (T) and is likely to be involved by tumor. Overlooked presacral lymph nodes may be excluded from the radiotherapy field, particularly if they are situated in the sacral concavity below S3, because the posterior margin of the field is normally vertically aligned at the S2/ S3 junction.

Figure 4.20 External and common iliac lymph node metastases. (A) Coronal T1WI showing multiple enlarged right pelvic sidewall lymph nodes (arrows). (B) Transaxial T1WI in a different patient. There are left common iliac lymph node metastases (open arrows) replacing the fat posterior to the vessels, causing an asymmetrical appearance “filled in fat sign.” This site for lymph node metastases can be overlooked easily. There is a metastasis (M) in the right medial ilium and malignant infiltration of the left sacrum (arrowhead) directly underlying the metastatic lymph node mass. The left sacral infiltration could be due to hematogenous spread or direct bone erosion by the lymph node disease. Note the asymmetry of the iliopsoas muscles with increase in size on the left side. This is most likely to be due to edema arising from impaired lymphatic drainage.


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Figure 4.21 Pelvic metastatic lymph nodes. (A) Transaxial T2WI demonstrating a primary tumor (T) with a huge left external iliac lymph node mass (arrows) showing central necrosis (n) and extracapsular extension as well as encasing the left external iliac artery (arrowhead). The bladder (B) is displaced to the right. The patient also has bilateral adnexal cysts (asterisks). It is unusual to have such a large lymph node metastasis at presentation. (B) Transaxial T2WI showing a small right obturator lymph node (arrow) with central nodal necrosis exhibiting high signal intensity greater than pelvic fat. Histopathological analysis confirmed metastatic tumor in this node. In squamous cell carcinoma, T2weighted central nodal necrosis is a highly accurate predictor of metastatic nodal infiltration even if the lymph node is not enlarged by size criteria. If there is uncertainty whether T2-weighted high signal intensity in a node is fat or central nodal necrosis, the T1WI should be scrutinized for central high signal intensity, and, if there is persisting uncertainty, then fat-suppressed imaging (fat saturation or STIR sequences) may help. (C) Off-axis transaxial T2WI demonstrating a large cervical primary tumor (T) with parametrial extension and a left obturator lymph node (arrow) which is of normal size but of similar signal intensity to the tumor proper. This finding indicates likely metastatic infiltration.


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Figure 4.22 Metastases in cervical cancer. (A) Sagittal T2WI demonstrating a lower vaginal metastasis (M), which is separated from the primary cervical tumor (T). (B) Coronal T1WI demonstrating upper retroperitoneal lymph node metastases (arrows) in addition to left pelvic sidewall lymph node metastases (open arrow). (C) Off-axis coronal T1W fat-suppressed post contrast image in a different patient showing a large necrotic liver metastasis (M) with a satellite lesion (arrow). (D) Sagittal and (E) transaxial T2WI in another patient demonstrating a large ulcerating cervical tumor (T) invading the posterior bladder (arrows) and extending to the right pelvic sidewall (curved arrows) to abut the edematous piriformis muscle. Tumor is also infiltrating the peritoneum, which is thickened (arrowheads in D). There is a bladder catheter in situ. (Continued )


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Figure 4.23 Contrast-enhanced MRI and diffusion-weighted MRI in cervical cancer. (A) Sagittal and (B) transaxial T2WI demonstrating a small volume cervical tumor (T), which is thinning the outer cervix (arrowhead in B). There are multiple prominent parametrial veins producing tubular high signal intensity within the parametrium. (C) Diffusion-weighted image (b-value, 800) and (D) ADC map demonstrate restricted diffusion within the cervical tumor (asterisks) and a low ADC. Note the apparent restricted diffusion demonstrated by the parametrial vessels which are also extending into the presacral space. These areas show high signal on the ADC map (D) confirming that this is due to T2 shine through. Higher b-value imaging may have been useful to prevent this T2 shine through effect. (E) Signal enhancement curve of the cervical tumor demonstrating rapid early enhancement in keeping with a malignant lesion.


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Figure 4.24 Small tumors and postbiopsy change. (A) Off-axis coronal T2W and (B) transaxial T1WI in a patient who was imaged a week after biopsy. A focal lesion (arrows) was identified in the right inferior cervix which demonstrated some high signal intensity on the T1WI and corresponded to the cervical biopsy site. Without appropriate clinical information, this lesion could quite easily be mistaken for a small residual tumor.

Figure 4.25 Loss of cervical fibrous stroma. Transaxial T2WI demonstrating a tumor (T) with complete loss of the low–signal intensity fibrous stroma but with a smooth margin with the parametrial fat. Absence of the low–signal intensity fibrous stromal ring is not an absolute indicator of tumor extension into the parametrium, and this lesion is stage T1.


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Figure 4.26 The upper vagina mimicking the outer cervical stroma. (A, B) Off-axis transaxial T2WI with a cervical tumor (T) seen in A surrounded by a low–signal intensity rim (arrows), which was the vaginal wall. More cranially in B the tumor can be seen to extend into the parametrium (arrowheads). The left bladder wall is irregularly thickened and of altered signal intensity due to infiltration by a large left pelvic sidewall lymph node metastasis (out of plane on this image) and hemorrhage from this is producing the altered signal intensity of the urine and a fluid-fluid level (in A).

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Figure 4.27 Appearances postradical hysterectomy. Transaxial (A) and sagittal (B) T2WI demonstrating the oversewn vaginal vault (V), containing small signal voids (arrowheads) due to surgical clips, inseparable from the posterior wall of the bladder and the peritoneal reflection (arrows). The abdominal wall surgical scar is well seen (open arrows in A).


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Figure 4.28 Appearances after bilateral pelvic sidewall lymph node dissection. Transaxial T2WI showing low–signal intensity linear scarring (arrows) extending parallel to the pelvic sidewalls. There is also post laparotomy thickening of the pelvic peritoneum (arrowheads). The retained right ovary (open arrow) is adherent to the pelvic sidewall scarring.

Figure 4.29 Appearances after bilateral ovarian transposition. Transaxial (A) T1WI and (B) T2WI in a patient who underwent ovarian transposition at the time of radical hysterectomy. The ovaries (arrows) have been relocated to the iliac fossae. This procedure is performed to prevent the ovaries being included in a postoperative radiation field and thereby preserve ovarian function. The ovaries should not be confused with tumor masses.


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Figure 4.30 Central pelvic and subcutaneous hematoma complicating radical hysterectomy. (A) Transaxial T1WI, (B) transaxial T2WI, and (C) sagittal T2WI in which a central hematoma (H) is seen with characteristic high signal intensity on the T1WI, and T2-weighted heterogeneous appearance with a low–signal intensity rim and mixed high and intermediate signal intensity content. Compared to the central pelvic hematoma, the small subcutaneous hematoma (arrows) is of similar signal intensity. There is loculated ascites (A) above the hematoma in C. (D) Sagittal T2WI performed three months later demonstrates the small residuum of the hematoma (arrows) but persistent ascites (A). The appearance of hematomata varies with their age.


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Figure 4.31 Unilocular lymphocele after radical hysterectomy. Transaxial (A) T1WI and (B) T2WI showing a small left-sided unilocular lymphocele (arrow) in a common position adjacent to the external iliac vessels. Lymphoceles are extraretroperitoneal collections of lymph fluid caused by surgical disruption of lymphatic trunks. They demonstrate signal intensity characteristics similar to water on T1WI and T2WI, are usually unilocular and thin walled, and often resorb spontaneously. Occasionally, septations may be seen within larger lymphoceles.

Figure 4.32 Response of cervical tumor to radiotherapy. Sagittal T2WI (A) at presentation, (B) 2 months, and (C) 10 months after radiotherapy. The intermediate signal intensity cervical tumor (T) can be readily identified in A. (B) After two months there is only a small area of residual abnormal signal intensity (arrow) in the posterior lip of the cervix. The anterior lip of the cervix has reconstituted. The uterine body has lost its zonal differentiation but the outer myometrium (M) is still of normal signal intensity. (C) Ten months after radiotherapy, the cervix (arrows) and vagina (arrowheads) are of intense low signal intensity indicating a good treatment response. The uterus has atrophied and the uterine body (U) is of low signal intensity with loss of zonal anatomy.


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Figure 4.33 Evolution of chemoradiotherapy effect. (A) Sagittal and (B) transaxial T2WI pretreatment demonstrating a stage IIb cervical tumor (T), which is involving the vaginal vault (arrowhead). There is also adherence to the anterior mesorectal fascia (arrows). (C) sagittal T2WI three months post chemoradiotherapy, radiation therapy marker seeds are now in situ and producing a metallic bloom artifact, which is partially obscuring the cervical tissue on the sagittal view. There has been reduction in size and signal intensity of the cervix and uterine body. Note the development of more pelvic ascites (A) and treatment effect within the bladder where there is mucosal edema (arrowheads). High signal intensity of the rectal mucosa is also noted (open arrows). More generalized edematous change is also appreciated, most obviously in the retropubic space (asterisk). (D) Sagittal T2WI seven months post chemoradiotherapy. The cervix remains small and of slightly heterogeneous low signal intensity. The bladder mucosal edema which was present at 3 months has essentially resolved and apparent thinning of the superior bladder wall muscle layer (open arrows) is due to a treatment reaction within portions of the muscle. There is persisting abnormal signal intensity within the rectoanal mucosa. Note that the uterine body has increased in size and signal intensity, presumably reflecting an edematous/inflammatory reaction. There has been slight increase in volume of posterior ascites (A). The retropubic edema (asterisk) persists. (E) Sagittal T2WI 10 months after chemoradiotherapy. The cervix remains of heterogeneous low signal intensity. The uterine body junctional zone and inner myometrium are reduced in signal intensity compared to the seven months examination (asterisks). There is new mucosal edema of the bladder trigone (arrowheads). Rectal mucosal high signal intensity is again noted (curved arrows) but has improved. The volume of ascites (A) is little changed. The edematous change in the retropubic space has resolved. Note that the superior bladder wall muscle layer has reduced in signal intensity and appears more uniform. After chemoradiotherapy treatment effect can wax and wane. Because of uncertainty about residual altered cervical signal intensity, patients may have repeated MRI assessment or biopsy. 18FDG PET CT has been shown to be effective in the detection of post chemoradiotherapy recurrence. (Continued )


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Figure 4.34 Response of the ovaries to radiotherapy. Off-axis transaxial T2WI (A) before and (B) four months after radiotherapy. (A) The ovaries (arrows) have multiple follicular cysts present with high–signal intensity central stroma. (B) The ovaries (arrows) have shrunk, lost their follicular cysts, and the signal intensity of the central stroma has decreased.

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Figure 4.35 Radiotherapy-induced vesicouterine fistula. (A) and (B) sagittal T2WI. (A) There is a large necrotic cervical tumor (T) involving the uterine body and extending through the bladder wall to involve the mucosa (arrows). (B) Three months post treatment, a fistula (arrow) can be seen and the cervical cavity and vagina are fluid filled (open arrows). The uterus has decreased in size and the endometrial cavity is visualized (E). The posterior cervix has partially reconstituted (arrowheads).


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Figure 4.36 Severe chemoradiotherapy effect with a large vesicovaginal fistula. (A) Sagittal T2WI pretreatment demonstrating a cervical tumor (T) involving the anterior rectum (arrows) and the posterosuperior bladder (arrowheads) and superior vaginal vault. Sagittal (B) T2WI and (C) STIR images 12 months after chemoradiotherapy. The cervical tumor has completely responded, but there has been no reconstitution of the cervix or upper vagina, and there is a large vesicovaginal fistula (arrowheads) containing air anteriorly and fluid posteriorly. The residual bladder wall (arrows) demonstrates thickening and patchy high and low signal intensity. The anterior rectal wall is deficient and the posterior rectal wall is of abnormal high signal intensity (open arrows). Abnormal high signal intensity is seen within the residual vagina representing treatment effect (curved arrows in B), and there is air in the lower vagina. Extensive presacral fluid (F) is noted. This is a nonspecific finding and can occur as a treatment effect, particularly when there is inflammation or infection in the pelvis, but may also be identified in patients with disease relapse. Note small-volume ascites (A).


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Figure 4.37 Postradiotherapy cervical stenosis with hydrometria. Sagittal T2WI demonstrating a distended high–signal intensity endometrial cavity due to a stenotic internal os with the cervix demonstrating low signal intensity after radiotherapy. There is a metallic artifact from a radiotherapy marker seed (arrowheads). A fluid/debris level is noted posteriorly (arrows). The bladder (B) and urethra (curved arrows) are compressed and distorted by the hydrometria.


Figure 4.38 Postradiotherapy hematometria. (A, B) Transaxial T1WI and T2WI and (C) sagittal T2WI. The distended uterus (arrows) contains a hematometria (H) as shown by high signal intensity on T1WI and whorled intermediate and high signal intensity on T2WI. The apparent focal lesion (asterisk) in the left anterior uterine fundus represents hematoma of a different age to the rest of the uterine cavity. The patient went on to have a hysterectomy and the distension of the uterine cavity was confirmed to be due to altered blood. There was no evidence of malignancy.

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Figure 4.39 Postchemoradiotherapy hydrometria and hematocolpos with residual cervical cancer. (A) Sagittal T2WI pretreatment demonstrating a large cervical tumor (T) with extension into the uterovesical ligament (arrowheads). The vagina has been packed because of intractable PV bleeding and an admixture of packing material and hemorrhage is noted (asterisk). The urethral portion of a bladder catheter is seen (arrows). (B) Sagittal and (C) transaxial T2WI seven months after treatment demonstrating distension of the endometrial cavity due to stenosis of the internal os. There is also marked distension of the vagina with a fluid-fluid level within it (arrows) and a small amount of clot is adherent to the right anterior wall (arrowheads in C). There is residual tumor (T) in the cervix and the patient has developed a lower sacral bone metastasis (M).


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Figure 4.40 Residual cervical cancer. Sagittal T2WI (A) pretreatment and (B) six months post radiotherapy. (A) A cavitating high–signal intensity tumor (T) is present. Two metallic marker seeds (arrows) have been placed in the anterior and posterior lips of the cervix at examination under anesthesia to guide the external beam radiotherapy. These clips demonstrate the bloom susceptibility artifact associated with metal. (C) After treatment there remains a high–signal intensity mass (M) in the cervix, which shows no evidence of reconstituting. The rest of the uterus has atrophied. One marker seed remains in the posterior lip. The patient underwent salvage hysterectomy with cystectomy (anterior pelvic clearance) and residual adenocarcinoma was confirmed. Residual high signal intensity within the cervix more than six months after radiotherapy warrants investigation. The abnormality may be due to tumor or occasionally radiation-induced edema and telangiectasia. Dynamic contrast-enhanced MRI may help differentiate between the two conditions.


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Figure 4.41 Nonresponse of primary tumor and postchemoradiotherapy progression. Sagittal T2WI (A) immediately after chemoradiotherapy, (B) two months, and (C) six months later. The cervical tumor mass (T) remains after treatment and increases in size and extent to involve the posterior bladder wall (arrows in C) and extend through the uterine myometrium (arrowheads in C).


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Figure 4.42 Recurrent cervical cancer. Sagittal T2WI (A) six months and (B) eight months after chemoradiotherapy. There is irregular high–T2W signal intensity within the atrophied cervix (arrows), which was highly suspicious for recurrent tumor. Initial biopsy was inconclusive, and on reimaging the abnormal high signal intensity persisted although it appeared slightly smaller and well defined. A repeat biopsy confirmed recurrent tumor. Note the post treatment effect in the bladder with high signal intensity of the mucosa (arrowheads in A) and slight increase in signal intensity of the rectoanal mucosa (open arrows in A and B). A small amount of pelvic ascites (A) is present. Presacral fluid (F in A) was present at six months but had resolved by eight months.


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Figure 4.43 Parametrial recurrence. Transaxial T2WI (A) at presentation, (B) five months after chemoradiotherapy, (C) seven months after chemoradiotherapy and (D) nine months after chemoradiotherapy. The cervical tumor (T) is seen to be predominantly left sided and to extend into the parametrium at presentation. Five months after therapy, there is low signal intensity of the reconstituted cervix, although the left side remains smoothly expanded (arrows) compared to the right side. After seven months, there is alteration in signal intensity within the left cervix and parametrial region with patchy ill defined higher signal intensity (arrowheads) now noted together with some irregularity of the cervical/parametrial interface. By nine months the ill-defined high signal intensity has increased in extent and overall size with a posterior bulge into the mesorectal fascia (open arrow) and there is a more ragged interface with the parametrial fat. The recurrence does not extend to the pelvic sidewall. The patient underwent a PET CT which demonstrated high metabolic activity within this mass and no evidence of lymph node metastases. The patient therefore underwent salvage surgery.


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Figure 4.44 Recurrent cervical cancer with vesicovaginal and vesicorectal fistulae and involvement of the left sciatic nerve. (A, B) Sagittal, (C) transaxial, and (D) coronal T2WI demonstrating a necrotic thick-walled cervical tumor recurrence (arrows) with a tumor fistula between the recurrence and the rectosigmoid (arrowheads in A), and a vesicovaginal fistula (open arrow in B and C). Tumor is also involving the left lumbosacral plexus and sciatic nerve (curved arrows in D). The nerve involvement means that the patient is ineligible for salvage surgery.


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Figure 4.45 Recurrent common iliac lymph node metastasis. (A) Coronal and (B) transaxial T1WI showing a small left common iliac nodal mass (arrows), which was producing back pain. The patient had undergone radiotherapy to the primary tumor and pelvic nodal stations two years before. In these circumstances, nodal recurrences are often at or above the margin of the field, here at L5/S1 level. Note the high signal intensity of the pelvic marrow due to fat replacement, but preservation of hemopoietic marrow in L5 vertebral body. The metastatic nodes may erode into adjacent bone and produce severe pain.

Figure 4.46 Plaque-like tumor recurrence after salvage hysterectomy. (A) Sagittal and (B) transaxial T2WI in a patient who previously underwent salvage hysterectomy and a Hartman’s procedure for local cervical tumor recurrence. There is plaque-like tumor (T) extending posteriorly and involving the posterosuperior bladder (arrow in A), the vagina vault (arrowhead in A), the rectal stump (open arrow in A), and both ureters (curved arrows in B). The tumor is growing along the peritoneal reflection (hatched arrows) and there are adherent loops of small bowel. After a short interval, this patient developed complete small bowel obstruction.


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Figure 4.47 Anterior pelvic clearance. Sagittal T2WI. The bladder, urethra, uterus, and vagina have been removed and the levator ani muscles oversewn (arrows). The omentum (Om) has been placed in the surgical bed to prevent small bowel prolapsing inferiorly.

Figure 4.48 Anterior pelvic clearance with neovagina formation. (A) Sagittal and (B) transaxial T2WI demonstrating absence of the anterior pelvic organs, retention of the rectum (R), and formation of a neovagina (V) from colon. Omentum (Om) has been placed in the surgical bed.


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FURTHER READING Bipat S, Gln AFS, van der Velden J, et al. Computed tomography and magnetic resonance imaging in staging of uterine cervical carcinoma: a systematic review. Gynecol Oncol 2003; 91:59–66. Analysis of relative merits of CT and MRI. Booth SJ, Pickles MD, Turbull LW. In vivo magnetic resonance spectroscopy of gynaecological tumours at 3.0 Telsa. BJOG 2009; 116:300–303. This article reviews spectroscopic findings in a variety of gynecological lesions. Choi EK, Kim JK, Choi HJ, et al. Node-by-node correlation between MR and PET/CT in patients with uterine cervical cancer: diffusionweighted imaging versus size-based criteria on T2WI. Eur Radiol 2009; 19:2024–2032. This article compares diffusion-weighted MRI nodal findings in cervical cancer with 18FDG PET-CT and MR size criteria. Liu Y, Bai R, Sun H, et al. Diffusion-weighted magnetic resonance imaging of uterine cervical cancer. J Comput Assist Tomogr 2009; 33:858–862. This article describes the diffusion-weighted MRI findings in cervical cancer. Mitchell DG, Snyder B, Coakley F, et al. Early cervical cancer: tumour delineation by magnetic resonance imaging, computed tomography and clinical examination, verified by pathological results. J Clin Oncol 2006; 24:5687–5694. Recent multicenter study of cervical cancer staging.

Mitchell DG, Snyder B, Coakley F, et al. Early invasive cervical cancer: MRI predictors of lymphatic metastases in the ACRIN 6651/GOG 183 intergroup study. Gynecol Oncol 2009; 112:95–103. Further report by the multicenter study group on predicting lymph node status. Rockall AG, Reznek RH. Uterine and cervical tumours. In: Husband Janet ES, Reznek R, eds. Imaging in Oncology. 3rd ed. 2010:431– 470. Considers cross-sectional imaging of these tumors and puts MRI in context. Small W, Vern TZ, Rademaker A, et al. A prospective trial comparing lymphangiogram, cross-sectional imaging, and positron emission tomography scan in the detection of lymph node metastasis in locally advanced cervical cancer. Am J Clin Oncol 2010; 33:89–93. Interesting article with a small patient cohort which identifies the imaging predictors of one-year disease-free survival. Vale CL, Tierney JF, Davidson SE, et al. Substantial improvement in UK cervical cancer survival with chemoradiotherapy: results of a royal college of radiologists’ audit. Clin Oncol 2010; 22:590–601. Current U.K. cervical cancer chemoradiotherapy survival figures and toxicity. Yuh WTC, Mayr NA, Jarjoura D, et al. Predicting control of primary tumour and survival by DCE MRI during early therapy in cervical cancer. Invest Radiol 2009; 44:343–350. This article describes the DCE MRI features predicting response to chemoradiotherapy.


5 Endometrial cancer Maryna Brochwicz-Lewinski

BACKGROUND INFORMATION Epidemiology Endometrial cancer is the seventh most common cancer worldwide and accounts for 1% to 2% of deaths from cancer. It is the most common gynecological malignancy in North America and Western Europe, accounting for 7045 cases in the United Kingdom and 1659 deaths in 2006. Incidence in both the United States and Britain is similar at 23.5 and 22.8 per 100,000 population, and U.K. incidence has shown a 34% increase between 1993 and 2006, predominantly in those aged 60 to 79. Presentation is most commonly with postmenopausal bleeding or discharge. Endometrial cancer is associated with a “Western” lifestyle with a quoted incidence of only 3 per 100,000 in less developed countries. Etiological factors include unopposed estrogen exposure, hormone replacement therapy, polycystic ovary syndrome, and obesity. Long-term treatment for breast cancer with tamoxifen is also associated with an increased risk of endometrial malignancy as are women with hereditary nonpolyposis colorectal cancer (HNPCC) who may develop endometrial malignancy premenopausally.

endocervical canal or via myometrial invasion extending below the isthmus of the uterus into the cervical stroma. Lymphatic spread from the upper corpus and fundus is via the infundibulopelvic ligament to the common iliac and para-aortic lymph nodes. The lower corpus and cervix drain via parametrial, paracervical, and obturator nodes to the external and internal iliac nodal groups and thence to the common iliac and para-aortic nodes. Sentinel node studies suggest 10% to 30% of endometrial carcinoma metastases are located exclusively in the high para-aortic nodes. The presence of positive pelvic node metastases indicates a 50% probability of paraaortic metastases. Hematogenous metastases can occur to lungs, liver, or bones but are rare at presentation.

TNM and FIGO Classification Revised FIGO staging of 2008 altered the staging of uterine tumors and introduced new staging for sarcomatous lesions (Table 5.1).

Prognostic Indicators Histopathology Most endometrial tumors are of glandular epithelial origin and are adenocarcinomas of endometrioid type. Other types of tumors account for approximately 25% of endometrial cancers and include papillary serous and clear cell. Generally, these less common tumor types are associated with a poorer prognosis. Tumors are graded from 1 (well differentiated) to 3 (poorly differentiated), with all clear cell and papillary serous tumors regarded as grade 3. Uterine sarcomas of mesenchymal origin, including endometrial stromal sarcoma, adenosarcomas, carcinosarcomas (formerly mixed Mu¨llerian tumor), and leiomyosarcomas, are rare uterine malignancies accounting for less than 3% of uterine tumors.

Patterns of Tumor Spread Endometrial cancer arises within the glandular epithelium, often in a polypoidal or focal pattern and presents as a friable mass. Multifocal disease is well recognized with plaques of disease within the endometrial cavity. Tumor spreads as a result of direct invasion into the adjacent myometrium, initially at the base of the tumor, and then more extensively through the myometrium to the serosal surface. Once tumor has transgressed the serosa, direct peritoneal spread and invasion into adjacent organs, in particular the bladder, rectum or sigmoid may occur. Peritoneal spread is also seen in those tumors involving the uterine cornua, extending via the fallopian tubes to the adnexa and peritoneal cavity. Endometrial tumors may involve the cervix either by direct extension into the

Endometrial cancer is generally associated with a favorable outcome with an overall five-year survival rate of approximately 75%, with rates of up to 96% quoted for stage I disease. This is because abnormal bleeding in postmenopausal women is easily recognized and 70% of patients present with disease confined to the uterus. Advanced disease, however, has fiveyear survival rates of approximately 17%. Prognostic indicators include tumor type, tumor grade, and presence of deep myometrial invasion. Depth of myometrial invasion correlates with prevalence of lymph node metastatic disease, which increases from 3% with superficial myometrial invasion, to 46% with deep myometrial invasion. Patients considered in a high-risk group include all patients with papillary serous or clear cell histology and those with grade 3 morphology, deep myometrial invasion, and cervical stromal invasion. These features may be more important prognostically than nodal status in patients with disease confined to the corpus. Predictors for hematogenous relapse include high grade tumor, deep myometrial invasion, and lymphovascular space invasion.

Treatment Surgery Choice of treatment for endometrial cancer has hitherto been guided by patient variables and the preoperative assessment of risk of extrauterine disease, with low-risk patients (well-differentiated tumors grades 1 to 2, FIGO stage 1A) treated with hysterectomy and bilateral salpingo-oophorectomy and highrisk patients additionally treated with full-pelvic and paraaortic lymph node dissection in accordance with FIGO staging


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Table 5.1 FIGO and TNM Classification of Carcinoma of the Endometrium TNM classification TX T0 Tis T1 T1a T1b T2 T3a T3b T4 NX N0 N1 N2 M0 M1

FIGO stage

I IA IB II IIIA IIIB IVA

IIIC1 IIIC2

IVB

Description of tumor extent Cannot assess primary tumor No evidence of primary tumor Preinvasive carcinoma. Carcinoma in situ Tumor confined to the uterine corpus Tumor confined to the endometrium or invades less than one-half of the myometrium Tumor invasion into one-half or more of the myometrium Tumor invasion of stromal connective tissue of cervix but does not extend beyond uterus Involvement of the uterine serosa, or adnexae (direct extension or metastasis) Vaginal involvement (direct extension or metastasis) or involvement of the parametrium Invasion of bladder and/or bowel mucosa (bullous edema is not adequate to classify tumor as T4) Regional lymph nodes cannot be assessed No regional lymph node metastasis. Regional lymph node metastasis to pelvic lymph nodes. Regional lymph node metastasis to para-aortic lymph nodes, with or without positive pelvic lymph nodes No distant metastasis. Distant metastasis (includes metastasis to inguinal lymph nodes intraperitoneal disease or lung, liver, or bone. It omits metastasis to para-aortic lymph nodes, vagina, pelvic serosa, or adnexae)

(lymph node resection may be laparoscopic). However, two recent large randomized trials with nearly 2000 patients have not shown any survival benefit from surgical staging with pelvic lymph node resection but did show a significant increase in postoperative complications. Many centers in the United Kingdom have therefore discontinued routine lymph node resection unless there are enlarged nodes, but there remains variation in practice worldwide. Patients with papillary serous tumors require omentectomy and thorough examination of the peritoneum as they behave in a similar fashion to ovarian tumors. Selected low-risk cases may be treated laparoscopically where there is local expertise. Radiotherapy and Chemotherapy Adjuvant radiotherapy in the form of brachytherapy may be given to the vaginal vault in those with grade 2 or worse tumor, and external beam radiotherapy to patients with pelvic lymph node metastases to control locoregional disease. Recent large studies however have not shown overall survival benefit from radiotherapy and its role remains controversial. Overall relapse rates are quoted at 15% to 30% and therefore many patients will not recur and may not need radiotherapy. Most local recurrences are vaginal and 90% respond to brachytherapy at the time of recurrence. Even with pelvic radiotherapy, high-risk patients appear to show significant extrapelvic recurrence which is generally unsalvageable. There are ongoing trials to assess potential improvements in the delivery of radiotherapy and administration of systemic chemotherapy.

MRI OF ENDOMETRIAL CANCER Technique Patients should ideally be imaged using a phased array coil. An antispasmodic agent to reduce bowel peristalsis (20 mg hyoscine butylbromide) should be given either intravenously or intramuscularly. T2W imaging should be performed in at least two planes with one sequence at right angles to the long axis of the uterus to optimally assess myometrial invasion. If there is any suggestion of cervical involvement then a further sequence perpendicular to the axis of the cervix may be of benefit. As

direct nodal metastasis to the para-aortic region can occur, T1-weighted imaging of the upper abdomen should be performed. This also offers the advantage of visualizing the kidneys. Postcontrast imaging can be helpful in establishing depth of myometrial invasion; both dynamic contrast-enhanced imaging and high-resolution single acquisition at 2 minutes 30 seconds are described, with several studies showing improved accuracy. Ideally, imaging should be obtained in the plane best demonstrating the tumor/myometrial interface. Evidence is emerging of the usefulness of diffusion weighted imaging (DWI) in the staging of endometrial tumors as the mean apparent diffusion coefficient (ADC) value of endometrial cancer is lower than that of myometrium, but further research is needed.

Current Indications There is considerable debate regarding the usefulness of MRI in the work-up of endometrial cancer, which has intensified with the publication of studies questioning the benefit of lymph node resection. Lymph node resection, however, remains part of FIGO staging for all patients with grade 3 tumors or greater than 50% myometrial invasion. The main use of MRI is to select high-risk patients to plan adjuvant or alternative therapies and to identify those patients who would benefit from surgery in a specialist center with dedicated gynecological oncologists. Although some specialist centers now perform little MR for endometrial cancer, widely accepted indications include highgrade endometrioid and all papillary serous or clear cell tumors, those in whom advanced disease is suspected, patients with a contraindication to surgical staging, and those in whom cervical stenosis precludes curettage. Preoperative MR assessment of lymph nodes is limited as nodal size often shows no correlation with metastases, but MRI may help to guide selective lymph node sampling. Lymph node–specific contrast agents have shown some promise in pelvic tumors, but these are not commercially available at present. MR does not have a routine use in surveillance, but may be useful in selected patients where surgery has not been


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performed or where there is felt to be a high risk of recurrence. Where tumor recurrence is diagnosed, the role of MR is to establish its extent, particularly the involvement of pelvic organs and the pelvic sidewall to inform management decisions.

Staging Accuracy Compared to Other Imaging Techniques Overall staging accuracy for MR is 85% to 95%, with metaanalysis for deep myometrial invasion reporting sensitivities of 78% to 100% and specificities of 71% to 100%. Negative predictive value for cervical invasion is high (>90%), which is likely to reflect the low pretest probability of cervical involvement. A recent study has shown DWI to improve staging accuracy to 94% compared with 88% for contrast enhanced MR. MR remains superior to both ultrasound and CT in assessing myometrial invasion, and similar to CT in the assessment of distant disease and lymph node involvement. The value of F18 FDG PET-CT in staging has not been fully established.

Imaging Features Primary Tumor On unenhanced T1W images, endometrial cancer is isointense to the endometrium. Tumor results in diffuse or focal thickening of the endometrium, seen on T2W images as slightly lower signal intensity than the normal endometrium. Tumor is typically heterogeneous and can be differentiated from the inner myometrium or junctional zone which returns low signal. A regular endometrial/myometrial interface indicates tumor confined to the endometrium. In older patients, the junctional zone may be indistinct and the separation between tumor and myometrium difficult. Dynamic contrast administration can aid the detection of tumor invasion as there is early (1 minute) enhancement of the subendometrial zone. Preservation of the junctional zone and subendometrial enhancement exclude deep myometrial involvement. Contrast enhancement at two to three minutes (equilibrium phase) is better for evaluating deep myometrial involvement with maximum difference between tumor and myometrial enhancement. Stage 1B tumors with deep myometrial involvement (>50% depth) will show preservation of a thin stripe of myometrium. Late phase (4–5 minutes) contrast enhancement shows cervical mucosal enhancement and may be useful for evaluating cervical involvement. Tumor extending into the cervical canal does not constitute cervical involvement unless there is some disruption of the low–signal intensity ring of the normal cervical stroma (stage II disease). Stage III disease extends beyond the uterus but is confined to the pelvis. Full thickness involvement of the myometrium and disruption of the normal hypointense uterine serosa seen on T2W imaging identifies stage IIIA disease. The contour of the uterus may also be irregular. The presence of adnexal masses and parametrial involvement are also features of stage IIIA disease. Direct invasion or metastatic deposits to the vagina (stage IIIB) can be identified by loss of low signal intensity in the vaginal wall. Disruption of the low–signal intensity wall of the bladder or rectum by intermediate–signal intensity tumor as well as the presence of a mucosal or intraluminal mass signifies stage IV tumor. Contrast enhancement may help to identify tumor involving the mucosa.

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Mesenchymal Tumors Tumors of mesenchymal origin include carcinosarcomas, endometrial stromal sarcoma, and leiomyosarcoma. Carcinosarcoma is often indistinguishable from endometrioid adenocarcinoma and is staged identically, although it may show more avid enhancement following contrast. Endometrial stromal sarcoma arises in the endometrium and almost invariably shows myometrial involvement. Leiomyosarcoma is thought to arise predominantly de novo, rather than from an underlying leiomyoma, but MR does not provide a reliable means of differentiating malignant from degenerating fibroids. Lymph Node Disease Lymph nodes with a short-axis diameter greater than 8 mm in the pelvis and 10 mm in the retroperitoneum are taken to harbor metastatic disease. However, careful examination of all nodes greater than 5 mm for other signs that may suggest malignancy is suggested. These include round shape, heterogenous signal particularly if returned signal is isointense to the primary tumor, and an irregular margin. The stage and grade of the primary tumor will also affect the probability of nodal disease. Hematogenous Spread Patients with papillary serous and clear cell tumors should have CT imaging of the thorax, abdomen, and pelvis due to the risk of distant disease at presentation. Examination of the upper abdomen with MR in other tumor types will allow assessment of retroperitoneal lymph nodes and evaluation of bone marrow signal. Residual/Recurrent Disease Approximately 15% of patients will experience tumor recurrence. Twenty-five percent recur within six months, and 98% of recurrences occur within three years of treatment. Seventy percent of recurrences are within the vaginal cuff. Patients with high-risk disease treated with radiotherapy tend to recur in an extrapelvic location. Local recurrence at the vaginal vault, or indeed elsewhere within the pelvis, can be identified by the presence of a mass lesion which returns intermediate signal. This can be distinguished from postoperative change which tends to return low signal signifying fibrosis.

Pitfalls of MRI Early-Stage Disease l

l

l

l

Small tumors can be difficult to identify or differentiate from benign entities such as endometrial hyperplasia, but in practice this is of little importance as primary diagnosis is always histological. Loss of the junctional zone in older patients makes assessment of myometrial invasion difficult. A regular interface between the endometrium and myometrium may help in these cases, as may subendometrial enhancement following contrast administration, although this may only be seen in up to 60% of cases. Large polypoidal tumors can distend the endometrial cavity and thin the myometrium, making both the identification and quantification of myometrial invasion difficult. Coexisting benign myometrial disease such as leiomyomas and adenomyosis compress and distort the adjacent myometrium and may mimic deep tumor invasion. Contrast


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l

l

l

l


enhancement has been shown to improve accuracy in these situations, and there is emerging evidence that DWI may allow a clear differentiation of these pathologies, as the ADC value of endometrial cancer is reduced in comparison to both normal and benign myometrial conditions. Tumor growing within an area of adenomyosis is not considered to be invading the myometrium, regardless of its position. Endometrial tumors occasionally show a diffuse infiltrative pattern and in this situation can be very difficult to differentiate from normal myometrium even after contrast administration. DWI similarly shows promise in this area. Tumors sited at the cornua can be difficult to stage because of myometrial thinning in this location. Differentiation of tumor prolapsing into the cervical canal and early stromal invasion can be difficult. Assessment of the cervical stroma perpendicular to its long axis is helpful.

l

Tumor invading the cervical stroma by direct extension from the myometrium can be difficult to identify. Effort should be made to identify the isthmus and carefully examine the cervical stroma below this level.

Late-Stage Disease l

l

MR can be relatively insensitive in the detection of small peritoneal deposits, but these should be particularly sought out where there is high-grade disease, papillary serous disease, and sarcomatous tumors (leiomyosarcoma, carcinosarcoma, and endometrial sarcoma), which have a greater tendency for peritoneal dissemination. Tumor invading the bowel and bladder can be overstaged if careful attention is not paid to the presence of mucosal involvement, which is required for FIGO stage T4A.

Figure 5.1 Normal uterine zonal anatomy. Sagittal T2WI (A) in a premenopausal patient and (B) in a postmenopausal patient. The zonal anatomy of the uterus is appreciated in the premenopausal patient. There is a central high–signal intensity stripe (asterisk in A), which represents the endometrium and its secretions. The low–signal intensity junctional zone (arrowheads) represents the inner portion of the myometrium and blends inferiorly with the fibromuscular stroma of the cervix. The outer myometrium (arrows) is heterogeneous intermediate and high signal intensity. The junction between the uterine corpus and the cervix is marked by wasting of the contour of the uterus (open arrows). Ascites (A) from an incidental nongynecological cause. In the postmenopausal patient, the endometrial stripe is thin and the entire uterus is of low signal intensity with loss of the junctional anatomy. Abbreviation: B, bladder. Source: Image courtesy of Dr J Hawnaur, Central Manchester and Manchester Children’s Hospital.


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Figure 5.2 T1a N0 stage IA endometrial cancer. (A) Sagittal and (B) transaxial T2WI showing tumor (arrowheads) confined to the endometrium with minimal widening of the endometrial cavity, a smooth interface between the endometrium and the inner myometrium (M) and no sign of myometrial invasion. Source: Image courtesy of Dr J Hawnaur, Central Manchester and Manchester Children’s Hospital.

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Figure 5.3 T1a N0 stage IB—endometrial cancer. (A) Sagittal and (B) transaxial T2WI of an endometrial tumor (asterisk), which demonstrates irregularity of the endometrial/myometrial interface (arrowheads) indicating myometrial invasion confined to the inner half of the myometrium. Incidental note is made of cervical nabothian cysts (arrows in A).


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Figure 5.4 T1a N0 stage IA endometrial cancer—early myometrial invasion. Transaxial T2WI of endometrial tumor (T) invading the inner half of the myometrium along the left lateral aspect with thinning of the junctional zone (arrowheads).

Figure 5.6 T1a N0 stage IA endometrial cancer—inner myometrial involvement. Fundal tumor (T) on this sagittal T2WI is seen to invade the myometrium with only a thin layer of junctional zone confining the tumor to the superficial myometrium (arrows).

Figure 5.5 T1a N0 stage IA endometrial cancer—early myometrial invasion. Sagittal T2WI demonstrates small fundal tumor (arrow) outlined by fluid in the distended endometrial cavity (asterisk) secondary to cervical stenosis related to prior cervical radiotherapy. Zonal anatomy is not well defined in this postmenopausal patient, but the tumor involves the inner myometrium. Source: Image courtesy of Dr Sukumar, South Manchester University Hospital.

Figure 5.7 T1a N0 stage IA endometrial cancer—inner myometrial involvement. Coronal oblique T2WI of left lateral tumor (T) involving most of the inner half of the myometrium with a thin hypointense line of remaining junctional zone (arrowheads). Such tumors can be difficult to stage if the remaining junctional zone is attenuated. Abbreviation: F, fibroids.


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Figure 5.8 T1a N0 stage IA endometrial cancer—inner myometrial invasion confirmed with contrast enhancement. (A) Sagittal T2WI shows intermediate signal endometrial tumor (T) suspicious for outer myometrial involvement (arrows). (B) Sagittal dynamic contrast enhanced (DCE) THRIVE image of the same region shows that tumor is confined to the inner half of the myometrium (arrows). Pathology revealed coexistent adenomyosis. Contrast enhancement may be helpful for problem solving, although it is not required for all cases.

Figure 5.9 T1b N0 stage IB endometrial cancer—early deep myometrial involvement. Coronal oblique T2WI perpendicular to the axis of the uterus shows tumor (T) extending into the outer half of the myometrium (arrows). The junctional zone is discontinuous in this area. This plane of imaging may be helpful for examining the tumor/ myometrial interface.


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Figure 5.10 T1b N0 stage IB endometrial cancer—outer myometrial invasion. (A) Sagittal and (B) oblique transaxial T2WI showing a large endometrial tumor (T) invading the outer half of the myometrium on its anterior aspect (arrowheads). Note that the intact posterior myometrium is markedly stretched and thinned by the tumor but that the inner myometrial junctional zone retains its low signal intensity (arrows). Source: Image courtesy of Dr J Hawnaur, Central Manchester and Manchester Children’s Hospital.

Figure 5.11 T1b N0 stage IB endometrial cancer—extensive myometrial invasion. (A) Sagittal and (B) transaxial T2WI show bulky endometrial tumor (T) filling the cavity of a small postmenopausal uterus. A The tumor appears to extend to the serosal surface (arrows) with little myometrium visible. This perception is probably exacerbated by overfilling of the bladder. (C) Transaxial contrastenhanced T1 FS image shows good preservation of the myometrial layer around the tumor, excluding serosal involvement.


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Figure 5.12 T1b N0 stage IB endometrial tumor extending to serosal surface. (A) Coronal and (B) parasagittal T2WI show a heterogeneous bulky endometrial tumor (T), which appears to extend through the whole myometrial thickness superiorly (arrows). (C) Sagittal DCE THRIVE image confirms loss of normal myometrial enhancement at this site (open arrows). The contour of the uterus remains smooth as tumor has not penetrated the serosal surface. Abbreviations: F, fibroid; B, bladder.


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Figure 5.14 T2 N0 stage II endometrial cancer—carcinosarcoma. Sagittal T2WI shows tumor (T) obstructing the cervix and causing distension of the endometrial cavity (asterisk). Tumor involves the posterior and anterior portions of the cervix (arrows). There is a bladder catheter (C).

Figure 5.13 T2 N0 stage II endometrial cancer involving outer myometrium and cervix. (A) Sagittal T2WI and (B) DCE THRIVE image show carcinosarcoma filling the endometrial cavity with extensive myometrial penetration particularly along the anterior aspect (arrows), with cervical involvement (arrowheads). Normal low signal cervical stroma in A is shown to enhance in B (asterisk). Carcinosarcomas are often bulky tumors at presentation.

Figure 5.15 T3a N0 stage IIIA endometrial cancer with right adnexal involvement. Transaxial T2WI shows tumor (T) replacing most of the uterus. A small amount of normal myometrium is seen anteriorly (asterisk). Tumor has extended directly into the right adnexal region (arrows). The rectum (R) lies close to the tumor but is not involved.


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Figure 5.16 T3a N0 stage IIIA endometrial cancer with extraserosal extension. Sagittal T2WI demonstrates large endometrial tumor (T) arising from the anterior wall and extending beyond the serosal surface with an irregular margin. The cervix is not involved. Tumor comes close to the posterior bladder wall but a thin layer of fat separates the two (arrowhead). Abbreviation: F, fibroid.

Figure 5.17 T3a N0 stage IIIA endometrial cancer. (A) Transaxial and (B) coronal oblique T2WI showing a tumor (T) stretching the myometrium and penetrating the outer half along the superolateral aspect where it reaches the serosal surface (arrows) in A. There is cervical involvement (arrowheads) in B.


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Figure 5.18 T3b N0 stage IIIB endometrial cancer with extraserosal, cervical, and parametrial involvement. (A) Transaxial, (B) sagittal, and (C) oblique coronal T2WI. A large tumor (T) filling the endometrial cavity and invading the left adnexal structures (asterisk). A thin rim of stretched myometrium can be seen posteriorly (arrows in A). Trace of ascites (A). There is extraserosal extension (arrows in B) along the superolateral margin of the uterus. There is loss of normal low signal cervical stroma in a right lateral location (arrowheads in C). Tumor extends into the right parametrium (asterisk). (D) Sagittal DCE THRIVE demonstrates bladder wall enhancement and excludes bladder wall involvement which was suspected on the sagittal T2WI (open arrows in B and D). Abbreviation: F, fibroid.


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Figure 5.19 T3b N0 stage IIIB endometrial cancer with vaginal involvement. (A, B) Sagittal and (C) transaxial T2WI demonstrating a large endometrial tumor (T) distending the uterine cavity without evidence of myometrial or cervical invasion. There is a metastasis (M) in the right vagina which demonstrates similar signal intensity to the endometrial tumor proper. There is small volume pelvic ascites (A). Abbreviation: F, fibroid. Source: Image courtesy of Dr J Hawnaur, Central Manchester and Manchester Children’s Hospital.


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Figure 5.20 T4 N1 M1 stage IVB papillary serous endometrial tumor with bladder, vaginal, and omental involvement. (A) Sagittal, (B, C) transaxial T2WI. In A there is grossly abnormal uterus with distended endometrial cavity and blurring of zonal anatomy. Extensive infiltration of the cervix (C) and upper vagina is demonstrated (arrowheads). There is obliteration of the fat plane between the tumor and bladder (arrows) and tumor extension into the bladder lumen (open arrows). Gas within the bladder (asterisk) denotes fistulation. (B) There is left adnexal involvement (arrows) and right iliac lymph node metastasis (N). (C) At the level of the vagina, there is confirmed vaginal infiltration with circumferential wall thickening (V) and tumor involving the posterior bladder wall (crossed arrows). (D) Transaxial T2WI shows left-sided omental infiltration (arrow) and peritoneal disease (arrowhead). Enlarged bilateral iliac nodes are also seen (N). Patients with papillary serous tumors are at high risk of peritoneal dissemination and should have preoperative CT for staging and omentectomy at surgery.


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Figure 5.21 Central recurrence of endometrial cancer. (A) Transaxial and (B) sagittal T2WI demonstrating a large central pelvic tumor recurrence (T). The mass, which is arising from the vaginal vault, extends to involve the rectosigmoid colon (arrows) without extension to the pelvic sidewall. One small bowel loop (S) is seen to be adherent to the superior surface of the mass in B. The posterosuperior bladder wall is abnormal (arrowheads) due to small volume tumor infiltrating the remnant of the uterovesical ligament (asterisk). Source: Image courtesy of Dr Carrington, Christie Hospital.

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Figure 5.22 Recurrence of endometrial cancer. (A) Sagittal, (B) transaxial, and (C) coronal T2WI in a patient with lower vaginal recurrent tumor (T) extending up the anterior wall (asterisk). There is anterior extension to encircle the urethra (U) and infiltration of right levator ani (arrowheads) in B and C. Tumor reaches the right lateral pelvic sidewall (arrows) and posteriorly displaces but does not involve the anal canal (A). Abbreviations: B, bladder; U, urethra. Source: Image courtesy of Dr Bernadette M. Carrington, Christie Hospital. (Continued )


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Figure 5.23 T1b stage IB—adenosarcoma. (A) Sagittal T2WI, (B) transverse T2WI, and (C) sagittal DCE THRIVE images show a large prolapsing polypoidal tumor (T), which fills the endometrial cavity and prolapses through the cervix (C) but shows no evidence of stromal invasion. In these images, the junctional zone (arrows) appears preserved, but histologically there was focal inner myometrial penetration. Late-phase contrast images in C demonstrate enhancement of the cervical epithelium (arrowheads) and vaginal wall (open arrows). There is no contrast enhancement of the prolapsed tumor secondary to infarction. Trace of ascites (A).



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Figure 5.24 T1a N0 stage IA leiomyosarcoma. Transaxial T2WI demonstrates atypical appearing fibroid with a cystic component at the isthmus (T). Right hematosalpinx (Hs) from known endometriosis. Fluid within upper endocervix (asterisk). Cervical stroma (arrowheads). A diagnosis of leiomyosarcoma was made at surgery.

Figure 5.26 Nabothian cysts mimicking cervical invasion. (A) Coronal and (B) transaxial T2WI with tumor extending into the cervical canal (T). Multiple small nabothian cysts (arrowheads) should not be confused with tumor invading the cervical stroma.

Figure 5.25 T1b N1 stage IIIC leiomyosarcoma. Transaxial T2WI in patient with a rapidly enlarging abdominal mass shows a heterogeneous myometrial tumor (T) with a thin rim of surrounding myometrium (arrows) and a metastatic right common iliac lymph node (N) of similar signal intensity to the tumor and demonstrating extranodal extension medially.


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Figure 5.28 Adenomyosis and endometrial cancer. (A, B) sagittal and parasagittal T2WI of endometrial cancer (T) with coexistent adenomyosis (asterisk). The border between the adenomyosis and the tumor, and the depth of myometrial penetration is difficult to identify. (C) Sagittal DCE THRIVE contrast imaging is not helpful as the enhancement of tumor and adenomyosis is similar. Tumor in this case was thought radiologically to extend to the outer half (arrow), and this was confirmed histologically. DWI may be of use in this situation.

Figure 5.27 Pseudomyometrial invasion due to fibroids. (A) Coronal oblique T2WI of tumor (T) that appears to extend into the outer myometrium with an area of increased signal adjacent (asterisk) to a fibroid (F). (B) Sagittal DCE THRIVE image shows normal myometrial enhancement (asterisk) with tumor (T) confined to the inner half of the myometrium.


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Figure 5.29 Pseudoinvasion of cervix by endometrial cancer. (A) Sagittal T2WI and (B) coronal oblique T2WI of endometrial cancer (T) involving the outer myometrium along the fundal aspect (arrows), with adenomyosis adjacent (asterisk). Tumor extends directly into the upper endocervical canal (arrowheads) but in B there is preservation of circumferential low signal cervical stroma. Pathological examination showed tumor within the endocervical canal indicating the cervix is not involved. Figure 5.28 (Continued )


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FURTHER READING Endometrial Cancer. Diagnosis and pre-treatment staging and Endometrial Cancer Treatment. In: Guidance on Commissioning Cancer Services. Improving Outcomes in Gynaecological Cancers. The Research Evidence. NHS Executive, Department of Health publication, 1999. Review of research evidence for current management of endometrial cancer. Kinkel K, Forstner R, Danza FM, et al. Staging of endometrial cancer with MRI: guidelines of the European Society of Urogenital Imaging. Eur Radiol 2009; 19:1565–1574. Recent guidelines describing imaging technique. Published before new FIGO staging. Kinkel K, Kaji Y, Yu KK, et al. Radiologic staging in patients with endometrial cancer: a meta-analysis. Radiology 1999; 212:711–718. Meta-analysis of performance of MR, CT and ultrasound in the assessment of endometrial tumors.

May K, Bryant A, Dickinson HO, et al. Lymphadenectomy for the management of endometrial cancer (review). The Cochrane Library 2010; (1):1–42. Current Cochrane review of published randomized trials investigating the benefit of lymph node resection. Sala E, Wakely S, Senior E, et al. MRI of malignant neoplasms of the uterine corpus and cervix. Am J Roentgenol 2007; 188:1577–1587. Good recent overview, particularly of pitfalls. Takeuchi M, Matuzaki K, Nishitani H. Diffusion-weighted magnetic resonance imaging of endometrial cancer: differentiation from benign endometrial lesions and preoperative assessment of myometrial invasion. Acta Radiol 2009; 50(8):947–953. Description of potential additional use of DWI in staging endometrial tumors and differentiating from benign pathology such as adenomyosis.


6 Ovarian cancer Soo Y. S. K. Mak and Prakash Manoharan

BACKGROUND INFORMATION Epidemiology Ovarian carcinoma is the fifth most common cancer and fourth most common cause of cancer deaths in women in the Western world. There are approximately 7000 new cases per year in the United Kingdom and 20,000 new cases in the United States. Ovarian cancer accounts for 4% of all female cancers with a lifetime risk of developing this disease of 1 in 50. The peak incidence is over 65 years with about 80% diagnosed in women older than 50. There are several factors implicated in the etiology of ovarian cancer, including early menarche, nulliparity by 35 years, late menopause, taking hormone replacement therapy (HRT) for more than five years, smoking, endometriosis, obesity, and increasing age. The strongest risk factor is a family history of ovarian cancer. Risk is reduced by breast feeding, having a first child by 25 years of age, use of oral contraception, and sterilization by tubal ligation. Mutations in BRCA1 and BRCA2 genes and the autosomal dominant HNPCC/Lynch2 syndrome (colonic, endometrial, breast, and ovarian cancer) are associated with increased risk of ovarian cancer although only about 10% of ovarian cancer patients carry these genes. More recently, a genetic single nucleotide polymorphism (SNP) has been located on chromosome 9. Women with variation of this gene have a 40% increase in their lifetime risk of developing ovarian cancer. At present, screening for ovarian cancer is on a clinical trial basis only. Higher-risk women can be offered screening but they need counseling about the efficacy and false positive rates of such tests.

Histopathology Ovarian tumors are classified according to their tissue of origin (Fig. 6.1). Epithelial tumors account for almost 90% of malignant ovarian cancers. They arise from the surface epithelium or serosa of the ovary. The commonest are serous, followed by mucinous and endometrioid tumors. Histological grading is a more important prognostic indicator than cell type in early stage disease. Borderline tumors, also called epithelial ovarian tumors of low malignant potential (LMP), show some features of malignancy such as irregular architecture, nuclear stratification and polymorphism, and mitotic activity but no invasion into the

stroma. These demonstrate slow progression and occur in younger patients typically ranging from 39 to 45 years of age. Sex cord stromal tumors account for 5% to 10% of all ovarian tumors. They can differentiate into ovarian, testicular, or stromal tumors and often secrete steroids. Granulosa stromal cell tumors are the commonest type. About 1% of sex cord stromal tumors remain undifferentiated. Germ cell tumors arise from primitive ovarian germ cells and are commonest in women in their twenties. Their rapid growth often leads to presentations with pain due to torsion, hemorrhage, or necrosis. Metastases account for 5% to 10% of ovarian tumors, commonly from breast, endometrium, and gastrointestinal malignancy. Ovarian carcinomas are also graded histologically from 1 (well differentiated) to 4 (poorly differentiated) with grade 4 tumors having the poorest outcome.

Patterns of Tumor Spread Direct spread of ovarian cancer occurs along the fallopian tube to involve the broad ligaments and uterus. Direct invasion of the rectum, sigmoid colon, bladder, and pelvic sidewalls also occurs in late disease. Lymphatic spread occurs along the path of the ovarian vessels, on the right to precaval and lateral caval lymph nodes and on the left to para-aortic lymph nodes at the level of the renal hilum. Broad ligament lymphatics drain to the obturator, common and external iliac nodes and round ligament lymphatics drain to the inguinal nodes. Transcoelomic spread occurs by tumor surface shedding and intraperitoneal dissemination. Common sites of seeding include the undersurface of the diaphragm (preferentially on the right due to peritoneal fluid flow), the omentum, serosa of small and large bowel, the liver surface, and the pelvic cul-de-sac. Hematogenous spread occurs as a late feature in advanced disease to the liver, lungs, pleura, kidneys, and bone.

Prognostic Indicators l

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Tumor staging at diagnosis is important for prognosis as most of the improvement in survival has been in T1 or T2 disease. Currently, five-year survival for T1 disease at presentation is 73% and for T4 disease approximately 15%. Histological grade is also important, with high-grade tumors having a poorer prognosis. Histological cell type

[gajendra][8.511-Tight_Design][D:/informa_Publishing/Hulse-Mak_2400075/z_3B2_3D_files/978-1-8418-46767_CH0006_Oa.3d] [12/9/011/18:33:4] [97–117]

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Table 6.1 Epithelial Tumors: Make Up 90% of All Malignant Ovarian Tumors and 60% to 90% of All Ovarian Tumors Brenner

Clear cell

Mucinous

Endometrioid

Serous

Postmenopausal

Postmenopausal

Postmenopausal

Postmenopausal

Aggression

Any age. 50% over 50 yr Rarely malignant 6%

Incidence

1–2% of malignant tumors Solid and homogeneous. Occasionally cystic. Usually 1.0–2.0 cm. Extensive calcification is common

80% of benign 10% of malignant 5% of benign 20% of malignant 10% of malignant tumors Multilocular cysts containing hemorrhage or cellular debris

Mostly malignant

Bilateral

Mostly malignant, but 75% stage I 40%

60% of benign 25% of malignant 25% of benign 65% of malignant 20–50% of malignant tumors Predominantly cystic. Malignant lesions have more solid components. Psammoma bodies in 30%

Age

Typical features

6% of malignant tumors Usually unilocular cyst with few mural nodules protruding into the lumen

40% 20% of malignant tumors Variable cystic/solid components. Associated with endometrial hyperplasia and carcinoma

Table 6.2 Sex Cord Stromal Tumors: 5% of All Ovarian Malignancies Fibroma

Sertoli-Leydig cell

Granulosa cell

Thecoma

Age

40–50 yr

Reproductive years

Reproductive years

Aggression

Benign

Bilateral Incidence

Unilateral Rare Solid. Associated with pleural effusion. (Meig’s syndrome)

Unilateral in >95% 5–10% of all ovarian malignancies Multicystic. May be hemorrhagic or necrotic. Can secrete estrogen and is associated with abnormal vaginal bleeding, hyperplasia and carcinoma

Unilateral Commonest

Typical features

Depends on the degree of differentiation. 5-yr survival is 70% Unilateral 0.75) to 85%. Lymph nodes can be assessed on all sequences; the T1W sequences provide morphological information (size, shape, margin, presence of fatty hilum) and the T2W sequences provide a degree of tissue characterization (nodal signal intensity, presence of cystic areas). Long axis >21 mm, short axis >10 mm, short/long-axis ratio >0.75, irregular contour of nodes and cystic change are particularly helpful signs. An irregular contour suggests extranodal spread and cystic change suggests a squamous cell carcinoma deposit (Figs. 8.11 to 8.16). Residual/Recurrent Disease Assessment of the vulva for residual tumor is difficult in the early postoperative period due to inflammatory changes and

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anatomical distortion. Reactive changes may cause false-positive assessment of inguinal lymph nodes if imaging is carried out soon after significant vulval resection. Recurrent tumor usually arises in the residual vulval tissue or in the deep inguinal and femoral nodes as they may remain after inguinal lymph node dissection. Limited evidence suggests DWI may be helpful in the identification of recurrent tumor (Figs. 8.17 to 8.20).

Pitfalls of MRI Staging the Primary Vulval Tumor The superficial extent of the tumor is assessed clinically and MR has the advantage in identifying deep tumor extension. l l

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Stage I carcinoma may be too small to visualize on MR. Larger stage I or II tumors that are en plaque may be difficult to identify or distinguish from chronic inflammatory changes on the vulva. T2W fat-suppressed images may help. Early invasion of the urethral orifice, introitus, or anal margin can be difficult to exclude in tumors directly adjacent to these organs.

Imaging the Inguinal Lymph Nodes l

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For obese patients with a large fatty apron, surface coils may be a significant distance from the inguinal lymph node chains, reducing the signal to noise ratio. In obese patients, it may be difficult to judge the depth of lymph nodes from the surface, requiring careful positioning of the field of view (FOV) to ensure complete coverage of superficial and deep inguinal nodes. Hip replacements and other orthopedic hardware in the pelvic region may produce artifacts in the inguinal regions, reducing image quality. Lymph node enlargement can be secondary to inflammatory changes in the perineum or lower limb. Microscopic metastases are not visible on MRI.

Figure 8.1 Normal vulval anatomy. Coronal T2WI showing normal vulval anatomy. Symphysis pubis (arrow). B, bladder; C, clitoris; LM, labium majora; P, body of pubis; U, uterus.


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Figure 8.2 T1a vulval carcinoma. (A) Coronal T1WI, (B) transaxial, and (C) sagittal T2WI showing a small (2.0 cm with benign fat-containing ipsilateral lymph node (arrow).


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Figure 8.5 T1b vulval carcinoma—anterior tumor. (A) Transaxial and (B) sagittal T2WI showing tumor (T) exceeding 2.0 cm in diameter centered on the anterior aspect of the left side of the vulva.

Figure 8.6 T1b vulval carcinoma—central tumor. Transaxial T2WI demonstrating a bulky midline tumor (T) centered on the clitoris with a satellite nodule on the right labia superiorly (asterisk). Posteriorly the tumor involves the perineal body (arrow). Abbreviation: AC, anal canal.


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Figure 8.7 T2 vulval carcinoma—perineal and urethral involvement. (A) Transaxial T2WI at the level of the symphysis pubis (asterisk) shows a predominantly left-sided tumor which is involving the levator ani muscle (arrows). Posterior urethral invasion (open arrow) and early left anterolateral anal involvement with discontinuity of the hypointense muscular layer (arrowheads) are shown. (B) Sagittal T2WI in the same patient confirms posterior urethral involvement (arrow) and shows involvement of the lower vagina (asterisk) by centrally necrotic tumor (T).

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Figure 8.8 T2 vulval carcinoma—posterior tumor involving anal canal, lower vagina, and urethra. (A) Sagittal T2WI shows extensive posterior tumor (T) with a satellite nodule (asterisk) which involves the anal canal, lower third vagina, and urethra. The superior limit of the tumor may be difficult to identify on sagittal imaging if it is poorly defined and returns similar signal to the adjacent soft tissues. In these cases, orthogonal planes are helpful. (B) Coronal T2WI confirms involvement of the anal canal. The tumor (T) involves the right side of the anal canal (AC) but does not extend superiorly to the rectum.


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Figure 8.9 T3 vulval carcinoma involving the mid-third vagina. (A) Parasagittal T2WI of vulval tumor ( T ) extending cranially to the midthird of the vagina. A small amount of the hypointense muscular layer of the posterior margin of the vagina is evident on this image (open arrow). (B) Transaxial T2WI at a more caudal level shows tumor involving the anal canal posteriorly (arrows) and extending anteriorly into the right puborectalis muscle (arrowheads), displacing and partially encasing the urethra (U). An uninvolved fatty lymph node is seen in the left inguinal region (N).


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Figure 8.10 T3 vulval carcinoma involving vagina and rectum. (A) Transaxial, (B) coronal, and (C) sagittal T2WI showing extensive vulval carcinoma. The tumor (T) has extended through the vagina (arrows) to infiltrate the anal canal and rectum at the anorectal junction (arrowheads). With such large tumors, differentiation between those of vulval and vaginal origin can be difficult. Locating the epicenter of the lesion and review of the clinical history and examination findings are useful indicators.


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Figure 8.11 N1 vulval carcinoma. (A) Coronal T1WI and (B) transaxial T2WI showing a cystic metastasis in a right superficial inguinal lymph node (arrows). The T1WI shows that the metastatic node is not composed of fat. There are normal left inguinal lymph nodes (arrowheads).

Figure 8.12 N2c vulval carcinoma. (A) Coronal T1WI and (B) coronal T2W fat-suppressed images showing bilateral enlarged metastatic superficial inguinal lymph nodes (arrows). On the left side, there is extranodal spread (arrowheads) shown to advantage in B and a cystic area (asterisk) due to nodal necrosis.


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Figure 8.13 N2 vulval carcinoma—locally invasive tumor involving anal canal with inguinal lymph node metastases. (A) Transaxial T2WI at the level of the anal canal and (B) perineum show predominantly posterior tumor involving the anterior anal canal (arrowheads) and extending forward on to the right labia majora (arrows). On the right side, levator ani is replaced with tumor (open arrows), and the left side shows interruption of normal, low signal secondary to tumor infiltration (crossed arrows). Posteroinferiorly, the tumor shows central necrosis and local perineal invasion (T). (C) Coronal T2WI demonstrates bilateral inguinal lymph node metastases (N) with partially cystic mixed signal intensity.


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Figure 8.14 T2 N2c vulval carcinoma—inguinal lymph node metastases in tumor with urethral involvement. (A) Sagittal and (B) transaxial T2WI of anterior tumor with minimal involvement of the urethra inferiorly (arrows) in a patient with previous hysterectomy. Transverse imaging demonstrates bilateral inguinal lymph node metastases (N). Within the right groin, mild irregularity along the medial margin of the more laterally placed node is indicative of extranodal spread (arrowheads).

Figure 8.15 N2c M1 vulval carcinoma with inguinal and pelvic lymph node metastases. Transaxial T2WI (A, B) show a left vulval carcinoma involving the left bulbospongiosus muscle (asterisk). The isolated ipsilateral lymph node (N) has an irregular lateral margin (arrowheads) indicating extranodal spread. A left external iliac lymph node (N) is also identified in B. Nodes within the pelvis are classified as M1 in staging vulval carcinoma.


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Figure 8.16 N2 M1 vulval carcinoma with para-aortic lymph node metastases. (A, B) Coronal T1WI showing left inguinal (arrows), left external iliac (arrowheads), left common iliac (open arrowheads), and left para-aortic lymph node (asterisk) metastases.

Figure 8.17 Recurrent vulval carcinoma. (A, B) Transaxial T2WI, (C) coronal T2WI, and (D) sagittal T2WI showing recurrent vulval cancer following radiotherapy. The tumor (T) is centered on the right side of the natal cleft. It infiltrates the external anal sphincter (arrows) and vagina at the introitus (open arrowheads). Surgical treatment of this lesion would involve an extended radical vulvectomy and colonic stoma formation. Source: Image courtesy of Dr Paul Hulse, Christie Hospital. (Continued)


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Figure 8.18 Recurrent vulval carcinoma. (A) Sagittal, and (B, C) transaxial T2WI show local tumor recurrence (T) within the perineum, extending superficially with possible early infiltration of the external urethral orifice (arrow) and extending into the vagina (open arrow). The anatomy of this region is more clearly demonstrated on the transaxial images (B, C); B demonstrates the defect anteriorly relating to previous right hemivulvectomy (asterisk). In C, tumor (T) can be seen extending into the vaginal introitus (arrows). Patient has had previous hysterectomy.


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Figure 8.19 Recurrent vulval carcinoma. (A) Transaxial, (B) coronal, and (C) sagittal T2WI showing extensive recurrent vulval carcinoma, following radical vulvectomy. The vulvectomy void (asterisk) is evident in A and C. The tumor (T) has infiltrated the anus (arrows), posterior margin of the vagina (arrowheads), and the perineal aspect of the distal urethra (crossed arrow). (D) Coronal T2WI in the same patient showing a right inguinal lymph node metastasis (N), which has an irregular margin indicating extranodal extension of tumor. Source: Image courtesy of Dr Bernadette M. Carrington, Christie Hospital.


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Figure 8.20 Inguinal lymph node pitfall. (A) Coronal T1WI and (B) fat-suppressed T2WI in a patient who had a vulvectomy for vulval carcinoma a few weeks earlier. There is an enlarged right inguinal lymph node (arrows) which has a hyperintense focus in its lower pole (arrowheads) in B. This is an equivocal finding for a metastatic or hyperplastic node, although the high signal focus favors metastatic disease. On histology it was benign.


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FURTHER READING Bipat S, Fransen GA, Spijkerboer AM, et al. Is there a role for magnetic resonance imaging in the evaluation of inguinal lymph node metastases in patients with vulva carcinoma? Gynecol Oncol 2006; 103:1001–1006. One of only five papers examining the role of MR in assessing lymph nodes in vulval cancer. Grey AC, Carrington BM, Hulse PA, et al. Magnetic resonance appearance of normal inguinal nodes. Clin Radiol 2000; 55:124–130. Defines normal values for inguinal lymph node measurements on pelvic MRI. Hawnaur JM, Reynolds K, Wilson G, et al. Identification of inguinal lymph node metastases from vulval carcinoma by magnetic resonance imaging: an initial report. Clin Radiol 2002; 57:995–1000. Describes the technique and results of high-resolution MRI for staging the inguinal lymph nodes in vulval cancer. Kataoka MY, Sala E, Baldwin P, et al. The accuracy of magnetic resonance imaging in staging of vulvar cancer: a retrospective multi-center study. Gynecol Oncol 2010; 117:82–87. Contemporary review of vulval staging with MR. Does not include new FIGO staging. Retrospective data from three centers and is the largest series in the literature with 49 patients.

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NHS Executive. Vulval Cancer. In: Guidance on Commissioning Cancer Services: Improving Outcomes in Gynaecological Cancers—The Research Evidence. NHS Executive, Department of Health publication, 1999:131–133. Summary of the research evidence for current management of vulval carcinoma. Singh K, Orakwue CO, Honest H, et al. Accuracy of magnetic resonance imaging of inguinofemoral lymph nodes in vulval cancer. Int J Gynecol Cancer 2006; 16:1179–1183. Retrospective review of lymph node imaging with MRI in 39 patients. Sohaib SA, Richards PS, Ind T, et al. MR imaging of carcinoma of the vulva. Am J Roentgenol 2002; 178:373–377. Retrospective review of MR findings in 22 patients with vulval cancer. Zivanovic O, Khoury-Collado F, Abu-Rustum NR, et al. Sentinel lymph node biopsy in the management of vulval carcinoma, cervical cancer and endometrial cancer. Oncologist 2009; 14:695–705. Review of the technique of sentinel node imaging and its potential applications to gynecological tumors.


9 Rectal cancer Mike Dobson

INTRODUCTION Magnetic resonance imaging (MRI) plays an integral part in the staging of rectal cancer. The appearances on staging MR directly influence the initial management plan, which may include transanal endoscopic resection for small volume, superficial disease, or a “long course” of neoadjuvant chemotherapy prior to surgery for more advanced cases. MR is also central to the investigation of suspected recurrent pelvic disease.

l

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Protective factors against colorectal cancer include the following: l l l

BACKGROUND INFORMATION Epidemiology Colorectal cancer is the fourth most common cancer worldwide. There are over 38,000 new cases of bowel cancer diagnosed each year in the United Kingdom, with colorectal cancer the second commonest malignancy in women and the third commonest in men. Worldwide, there were 1.23 million new cases in 2008, with the highest incidence seen in North America, Europe, and Australasia. Over 30% of colorectal cancers arise in the rectum. The U.K. National Bowel Cancer Screening Programme commenced in 2006, in which patients between the ages of 60 and 69 years are invited to send a fecal sample for occult blood testing to a regional testing center. Of approximately 50% who return a sample, 2% of cases are positive, of whom approximately 10% are shown to have colorectal cancer at colonoscopy. There has been a notable increase in the number of early cancers detected, with a commensurate reduction in the proportion of more advanced disease. Other important outcomes such as stoma requirement and emergency admission have also shown a reduced frequency. A large trial has recently demonstrated that a single flexible sigmoidoscopy at the age of 50 can reduce mortality from colorectal cancer by 43%, compared with the 15% to 20% projected for the fecal blood testing program. This approach would not only detect existing cancers but also prevent future cancer in the left hemicolon by early detection and removal of adenomas. Etiological factors for colorectal cancer include the following: l

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Diet: genetically mediated susceptibility to dietary mutagens, for example, heterocyclic amines in cooked red meats; bile acids; low dietary folate in combination with high alcohol intake. Preexisting polyps: these may be sporadic (especially villous adenomas) or are part of hereditary polyposis syndromes. The familial polyposis gene on chromosome 21 and the p53 gene on chromosome 17 have been implicated in a substantial number of sporadic carcinomas Previous medical history of ovarian, endometrial, or breast cancer

A first-degree family history of colorectal cancer or colorectal adenomas Prolonged ulcerative colitis Smoking tobacco

l

Increased dietary fiber Reduced animal fat intake Supplements of vitamin D Folate and antioxidants such as vitamin E

Histopathology Most colorectal cancers are moderately well differentiated gland-forming adenocarcinomas. Less common cell types include signet ring adenocarcinoma (see “Linitis Plastica” in “Pitfalls of MRI” section), adenosquamous carcinoma, squamous cell carcinoma, small cell carcinoma, choriocarcinoma, and medullary cell carcinoma. Colorectal carcinoid tumors occasionally occur (more commonly in the rectum) and arise in the submucosa. Sarcomas (usually leiomyosarcoma) are rarer, comprising up to 0.3% of colorectal tumors. Genetic and immunological tumor profiling is becoming important. For example, in the context of immunotherapy targeting extracellular growth factor receptors (EGFRs), it has been shown that patients whose tumors express the so-called “wild type” of KRAS gene (a gene coding for a protein involved in signaling cell division) have a significantly higher treatment response rate than those patients whose tumors express mutant varieties of the gene.

Patterns of Tumor Spread Rectal cancers arise in the mucosa, usually in a preexisting adenomatous polyp. Tumors advance radially through the layers of the bowel wall; longitudinal spread is uncommon. Following breach of the bowel wall, spread occurs directly into the mesorectum (see the following text) and then progressively into adjacent pelvic structures. Locoregional lymphatic spread includes: mesorectal, presacral, superior, middle and inferior rectal, sigmoid and inferior mesenteric, and internal iliac sites. More advanced, nonregional nodes include the external iliac and paraaortic nodes and extraabdominal sites and these are denoted as metastases. Hematogenous spread is apparent in up to 15% of patients at presentation and occurs most commonly to the liver by the portal venous route and to the lungs via the systemic circulation. Spread to the lungs is more common from tumors of the lower rectum because of systemic drainage (middle and inferior rectal veins) compared with the upper


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TNM Staging Table (Table 9.1) Table 9.1 TNM System for Staging Rectal Cancer (2010) Primary tumor (T) TX Cannot assess primary tumour T0 No evidence of primary tumor Tis Carcinoma in situ (intraepithelial or invasion of the lamina propria) T1 Tumor invades the submucosa T2 Tumor invades the muscularis propria T3 Tumor invades through muscularis propria into the subserosa, or into the nonperitonealized perirectal tissues T4a Tumor penetrates to the surface of the visceral peritoneum T4b Tumor directly invades or is adherent to other organs or structures Regional lymph nodes (N) NX Cannot assess regional nodes N0 No regional lymph node metastasis N1 Metastasis in 1–3 regional nodes: N1a Metastasis in one regional node N1b Metastasis in 2–3 regional nodes N1c Tumor deposit(s) in the subserosa, mesentery or nonperitonealized perirectal tissues, without regional lymph node metastasis N2 Metastasis in 4 or more regional nodes N2a Metastasis in 4–6 regional nodes N2b Metastasis in 7 or more regional nodes Distant metastasis (M) M0 No distant metastasis M1 Distant metastasis: M1a Metastasis confined to one organ (e.g., lung, liver, ovary or nonregional lymph node) M1b Metastasis in more than one site/organ or the peritoneum

rectum, which drains into the portal system by the superior rectal vein. Metastases to the brain and skeleton occur less commonly. Discrete foci of mesorectal tumor, clearly separate from the primary lesion, in the absence of lymph node tissue, are termed “satellite nodules.” They may be due to extramural vascular infiltration, replaced lymph nodes or noncontiguous primary tumor spread and should be quantified as tumor deposits in the pathological dataset as prognostic indicators. The prefix “p” is used when the above staging is applied to the histological specimen, with further addition of the prefix “y” if the patient has had neoadjuvant chemo/radiotherapy. Adequate pathological lymph node staging requires that the pathologist examines at least 10 to 14 lymph nodes for a total mesorectal excision (TME) specimen in the absence of neoadjuvant therapy.

Prognostic Indicators The features that have been shown to correlate with an adverse prognosis include the following: l

Comparison Table of Dukes’ and TNM Systems (Table 9.2) Table 9.2 Combined Modified Dukes’ and TNM Systems for Staging Rectal Cancer TNM Tis T1, T2 T3, T4 Any T Any T a

Modified Dukes’ N0 N0 N0 N1, N2 Any N

M0 M0 M0 M0 M1

A B Ca D

Dukes’ C stage is divided into C1 and C2. C1 indicates peritumoral lymph node infiltration, but not up to the point of surgical ligation. C2 indicates nodal involvement at the highest point of ligation and has a significantly worse prognosis.

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Increasing tumor stage. Patients with tumor confined to the bowel wall have an approximately 80% five-year survival, falling to approximately 60% if there is transmural disease without lymph node involvement. It has been stated that it is important to subdivide T3 disease according to the radial diameter of extramural infiltration. This is because infiltration of 5 mm or greater carries a significantly worse prognosis than lesser degrees of extramural extension. Furthermore, infiltration of less than 2 mm carries a similar prognosis to stage T2 disease. Some authors suggest that there may, therefore, be a benefit in modifying the T3 stage to reflect varying depths of extramural tumor penetration. Five-year survival falls as low as 12% where there is lymph node involvement up to the point of surgical ligation (Dukes’ C2) and is less than 10% overall for M1 disease, although resection of limited liver or lung metastasis does carry a very significant survival advantage. Tumor involving the circumferential resection margin is associated with increased risk of local recurrence and a five-year survival of 15%. High tumor grade. KRAS gene mutation. Perineural, vascular, or lymphatic invasion. Increasing number of peritumoral deposits. Significant residual tumor after neoadjuvant therapy as graded histologically is an unfavorable prognostic factor,


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as opposed to complete or near complete histological remission which is likely to be favorable. Mucinous histology. Infiltrative (as opposed to well-defined) margin of extramural spread. Linitis plastica. Age below 40 years at presentation.

Treatment Chemotherapy There is clear evidence of a survival benefit for postoperative chemotherapy in patients with N1 or N2 (Dukes C) tumors of the colon, although there is, as yet, no definite evidence that this advantage extends to patients with rectal cancer, especially if they have already had neoadjuvant chemoradiotherapy. Research is ongoing in this regard. However, both patient groups have a similar beneficial response to chemotherapy in the presence of metastatic disease. Radiotherapy Short-course (5 days) neoadjuvant (preoperative) radiotherapy has been shown to reduce the rate of local recurrence for rectal cancer even if the patient has a TME performed by an experienced surgeon. Concern has been expressed, however, that treating all patients with early T3 or lesser stage disease may lead to unnecessary irradiation for a large number of patients. Research is ongoing into the development of evidence-based, stage-related therapeutic protocols. Patients with more advanced mesorectal infiltration or evidence of mesorectal lymph node involvement, especially if within 1 mm of the mesorectal fascia on MRI, are generally referred for a long course (typically 5 weeks) of neoadjuvant chemoradiotherapy. Such treatment significantly reduces the chances of local disease recurrence. French studies dating back to the 1950s have shown a 90% cure rate for early, lymph node negative rectal cancer treated with “contact” intraluminal brachytherapy alone. Encouraging results have also been reported for patients with T2 N0 tumors treated with preoperative contact brachytherapy and external beam radiotherapy followed by surgery. There may also be scope for treating frail patients who have T3 tumors with a combination of contact brachytherapy and external beam radiotherapy alone. Audit of recent experience with brachytherapy is ongoing to standardize protocols. The development of less invasive treatments with reduced associated morbidity is important, as the bowel cancer screening program is yielding a population with a larger proportion of early rectal cancers—29% of screening detected tumors are T stage 1 compared with 4% for patients presenting symptomatically. Surgery Best surgical practice for rectal cancer is TME—removal of the tumor en bloc with the surrounding mesorectum invested in the visceral mesorectal fascia. The mesorectum comprises the perirectal fat, containing the rectal vessels, extending from the region of the aortic bifurcation to the intersphincteric groove. The plane of resection lies between the inner (visceral) and outer (parietal) layers of the mesorectal fascia. Radial growth of tumor (or nodal disease) close to or into this plane greatly increases the risk of a positive circumferential resection margin at histology with associated increased risk of local recurrence,

and a reduced five-year survival. A positive circumferential tumor margin is defined as tumor involving or lying within 1 mm of the resected visceral mesorectal fascia. Patients with early rectal cancer (T1/2 N0 M0) whose tumors are mobile and less than 4 cm in size may be offered transanal resection, or, where the facility and expertise are available, transanal endoscopic microsurgery (TEM), with encouraging results. Accurate staging is crucial here to avoid under treatment. Improving outcomes guidance (IOG) recommends that the staging of such cases includes transanal ultrasound, which some studies have shown to be more accurate than MRI in the “T” staging of early rectal cancers.

MRI OF RECTAL CANCER Technique A pelvic phased array coil is required for images of suitable quality. Endorectal coils are not routinely required and may have inherent problems (see later in the chapter). Smooth muscle relaxants improve image quality, though not necessarily staging accuracy. Similarly, intravenous contrast enhancement and endorectal contrast agents may increase the conspicuity of the tumor though do not influence tumor staging. The tumor is localized using a T2-weighted turbo (or fast) spin echo (TSE or FSE) sequence in the sagittal plane. The presence of an accurate record of the endoscopic findings is very helpful at this stage of the examination. High-resolution (3 mm) T2-weighted images are then acquired perpendicular and parallel to the tumor to allow assessment of the circumferential extent of the lesion. T2-weighted images are also useful for assessing lymph node morphology. Lymph node heterogeneity and an irregular margin strongly suggest malignant infiltration. T1-weighted images may be useful for demonstrating benign fatty change within a lymph node and are also highly sensitive for identification of pelvic bone metastases. There is increasing evidence that diffusion-weighted imaging (DWI) increases the accuracy of tumor identification and may be useful in assessing the response of tumor to therapy. Rectal tumors demonstrate restricted diffusion and an apparent diffusion coefficient (ADC) which is significantly lower than benign tissues.

Current Indications Preoperative primary tumor staging of rectal cancer with pelvic phased array coil MRI is now standard practice. MR accurately defines earlier stages of disease, preventing unnecessary use of neoadjuvant radiotherapy in these patients. MR also accurately determines the proximity of tumor to the mesorectal fascia, allowing identification of those patients who may benefit from neoadjuvant chemoradiotherapy. Restaging MRI is indicated post long-course chemoradiotherapy to assess the degree of tumor response, and, where appropriate, facilitate surgical planning. MRI is also essential in evaluating suspected pelvic disease recurrence and for characterizing and quantifying liver metastases.

Staging Accuracy Staging accuracy of up to 82% has been reported for local rectal cancer staging. This, however, takes into account studies that used inherently low-resolution body coil techniques. One study quoted 100% correlation with histological staging using a pelvic phased array coil and a high-resolution technique, although


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this has not been reproduced in larger studies. Local staging accuracy of 84% has been quoted for endorectal coil techniques. However, acquisition of an image plane perpendicular to the tumor may not always be possible using endorectal MRI and technical difficulties may also arise with high rectal tumors or a tightly stenotic lesion. Near-field flaring may also occur with endorectal techniques, although most manufacturers have developed software to overcome this problem. Lymph node evaluation remains a challenge. Size criteria are notoriously inaccurate. The use of morphological criteria (signal heterogeneity and/or irregular lymph node margin) can achieve sensitivity and specificity of 85% and 97%, respectively, although these figures are not uniformly reproducible. MRI enhanced with ultrasmall paramagnetic iron oxide (USPIO) contrast agents has a reported sensitivity and specificity of 93% and 97% for other pelvic cancers, although this technique has yet to gain widespread popularity in the United Kingdom for rectal cancer staging. Initial reports suggest that DWI in combination with USPIO may be very accurate for lymph node evaluation, although this is still under evaluation and currently there is no availability of USPIOs. MRI, especially with liver-specific contrast agents, has been shown to be superior to CT for the identification and characterization of malignant liver lesions, in most reports comparing these techniques. This is important for patients with limited liver metastases who are being considered for hepatic metastatic resection, to ensure an accurate quantification of liver disease.

Imaging Features Primary Tumor There are five layers of the normal rectal wall, namely: mucosa (epithelium and lamina propria), muscularis mucosae, submucosa, muscularis propria (circular muscle and longitudinal muscle) and serosa/perirectal fat. Although all five layers may be seen on high-resolution T2WI, this is uncommon. In most cases, the mucosa and submucosa are seen as a single layer of high signal deep to the low signal muscularis propria. The normal rectal wall should be no more than 6 mm thick in the distended state, although this is variable and unreliable. Rectal tumors are usually of intermediate intensity compared with the muscularis propria of the bowel wall on T2WI. Mucinous tumors return a high signal due to their fluid content. Important features to be assessed are as follows: l l l l

l l l l l

l

Precise tumor location Approximate tumor length T stage Distance of the caudal aspect of the tumor from the dentate line Relation to the peritoneal reflection Radial depth of extramural tumor infiltration Proximity of tumor to the mesorectal fascia Proximity of tumor to the anal sphincter Presence and characterization of mesorectal nodes and perirectal tumor deposits and their proximity to the mesorectal fascia Extramural vascular infiltration

Lymph Node Disease Rectal cancer spreads initially to lymph nodes in the mesorectum, extending into the more proximal rectal mesentery, inter-

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nal iliac chain, and external and paraaortic groups with more progressive disease. In common with other primary tumors, enlarged nodes in the presence of rectal cancer may be simply inflammatory and nonenlarged nodes may contain tumor. Pointers toward malignancy include an overtly infiltrative or irregular gland margin, nodal necrosis, and signal intensity similar to the primary tumor (such as high signal nodes infiltrated by mucinous tumor). These features are best assessed on high-resolution T2-weighted sequences. Proximity of suspicious nodes to the mesorectal fascia should be noted as this may compromise the surgical plane and the patient may benefit from neoadjuvant radiotherapy. Hematogenous Spread MR is highly accurate at characterizing liver lesions, the commonest site of distant metastases, which are usually discovered on staging CT. Small simple cysts are usually readily definable as well demarcated high-signal lesions on T2W images. Hemangiomas are similarly hyperintense on T2W images with a long TE (>160 ms) (unlike metastases which are of lower signal) and have a characteristic pattern of centripetal, nodular enhancement. A large array of liver specific contrast agents is available to further improve lesion quantification and characterization. With most gadolinium-based agents, metastases typically demonstrate inhomogeneous enhancement, with central and/or peripheral “washout” relating to neovascularity. Delayed T1W images, using agents with significant hepatocyte 1 uptake (e.g., Primovist —Gd EOB-DTPA, Bayer Pharmaceuticals, U.S.) demonstrate metastases as foci of low signal contrasted against the hyperintense, enhanced hepatic parenchyma. USPIO particle agents are highly accurate at evaluating liver lesions, although they do have significant side effects. These agents are taken up by the hepatic reticuloendothelial system and cause marked parenchymal hypointensity on T2*W images. This contrasts against hyperintense metastases which do not demonstrate USPIO uptake. DWI is also very sensitive and specific in the evaluation of suspected spread of disease to the liver. MRI is also extremely useful in evaluating metastatic disease in the skeleton and central nervous system, which occurs less commonly. CT is the modality of choice for evaluating lung metastases. Synchronous Tumors There may be synchronous tumors in the rectum or colon. Careful review of the sagittal MR image should exclude the former, though the patient will also require formal colonic evaluation by colonoscopy (“virtual” or fiber-optic) or barium enema.

Posttreatment Appearances Surgery Both anterior resection TME and abdominoperineal resection (APR) TME may produce presacral and perirectal fibrotic change. This is usually more pronounced following an APR. Also, following APR, there may be a presacral “pseudomass” on CT and T1WI due to the uterus, prostate, or seminal vesicles occupying the void in the rectal bed. This should be readily discernible on T2WI. Radiotherapy The effects of rectal irradiation depend on the total radiation dose and will be more pronounced following a long (5 weeks)


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course of treatment compared with the shorter five-day regime. In the acute and subacute posttreatment phases (up to 12 months post therapy), changes on MRI reflect cell death and inflammation. Hence, there may be visceral mural thickening, increased mucosal and submucosal signal on T2WI, and mucosal enhancement with intravenous contrast agents. The chronic effects of radiotherapy reflect fibrosis, and there may still be visceral mural thickening, though this will usually return low signal on T1WI and T2WI and show little or no intravenous contrast enhancement. However, fibrosis can remain of intermediate signal intensity for an indefinite period. Other changes include perirectal fascial and peritoneal thickening, inflammation, and atrophy of adjacent pelvic muscles and fatty marrow change (high signal on T1WI) in irradiated bone. More severe changes may include strictures of bowel and fistulation (e.g., rectovaginal or rectovesical). In addition, atrophic change in the skeleton may lead to insufficiency fractures of the sacral ala and pubic bones. These are often associated with florid bone marrow edema and can be distinguished from bone metastases by visualization of a linear, low signal fracture line, of typical distribution, on the T1WI. Recurrent Disease Pelvic recurrence has been reported in up to 50% of patients with rectal cancer, although following TME with negative circumferential resection margins, this figure falls to less than 10%. Establishing the diagnosis of recurrent disease using imaging can be difficult. Recurrent tumor usually manifests as a mass returning intermediate signal intensity on T2WI compared with muscle. However, radiation fibrosis may also return intermediate signal especially within the first two years following irradiation. In addition, fibrotic tissue and desmoplastic foci of tumors can both return low signal on T1WI and T2WI. Dynamic intravenous contrast-enhanced MRI may add to the specificity of diagnosing recurrent disease. DWI is also showing encouraging results in discriminating recurrent tumor from fibrosis, although IOG recommends PET-CT imaging where there is any uncertainty over the status of possible local disease recurrence. PET-CT is also indicated prior to embarking on resection of pelvic recurrence or limited metastatic disease. This is to ensure as accurately as possible that there is no further occult metastasis which may render such major surgery futile. It is important to have a detailed surgical history and to review the PET-CT and MR images together as sepsis, recent postsurgical change and tumor may all cause avid 18FDG uptake on a PETCT scan. MRI is accurate in assessing the extent of proven, recurrent pelvic tumor and can significantly aid the planning of further “salvage” surgery.

Pitfalls of MRI Tumor Identification on the Planning T2-Weighted Sagittal View This may be difficult, though it is crucial to further imaging. Knowledge of the tumor site at sigmoidoscopy is very important and should be included in the clinical information. Tumor is usually of intermediate signal intensity relative to the muscularis propria and flatus/feces. At the site of tumor, there is often nonvisualization of the different layers of the rectal wall, which is thickened, except in the case of T1 lesions. Other useful pointers may be the presence of blood vessels entering

the tumor or, occasionally, bowel wall retraction at the tumor site. Smooth muscle relaxants, DWI, and intravenous contrast enhancement may increase tumor conspicuity, but, with experience, are seldom required for simple tumor identification. Overstaging due to Peritumoral Fibrosis This appears as linear, low signal stranding in the mesorectal fat, as opposed to tumor, which has a nodular interface with the mesorectum, and usually returns intermediate signal. Overstaging due to Partial Volume Artifact This should be minimized by meticulous attention to detail when planning the high-resolution sequence perpendicular to the tumor. Adjacent Visceral Infiltration This is clear evidence of the primary tumor extending into the adjacent viscera. Contiguity of the tumor with an adjacent organ does not necessarily indicate invasion and peritumoral fibrosis or inflammation may cause overstaging in these cases. Nodal Disease Standard MRI remains fairly inaccurate in the assessment of mesorectal lymph node metastasis, although there are some useful discriminating features such as round shape, irregular margin, or increased signal intensity on T2WI indicating central nodal necrosis or a mucinous tumor deposit. Increased accuracy is possible with the use of USPIO lymph node contrast agents. The accuracy of DWI alone or in combination with USPIO agents is under review. Recurrent Disease Radiation effect and/or surgical changes may give rise to an intermediate signal presacral mass, mimicking tumor recurrence. Recurrent disease may return low signal due to desmoplasia, mimicking simple fibrosis. PET-CT is recommended if there is diagnostic uncertainty, although this may occasionally yield a false positive result if there is pelvic sepsis. DWI may prove useful in this situation, though it is still under evaluation. Intussuscepted Tumor This makes it difficult to T stage the tumor precisely as the interface with adjacent fat is not evident. However, an intussuscepted tumor cannot be fixed and should be evident on the sagittal view. The key feature on the perpendicular image is the presence of several layers of muscularis propria. Hemorrhoids When hemorrhoids are extensive and internal, there is thickening of the lower rectal submucosa, which may return high or intermediate signal. This may cause some difficulty when planning the off-axis MR sequences. A review of the endoscopic detail is helpful in regard to the level of the tumor and the presence of hemorrhoids. Also, despite the presence of quite marked mucosal thickening, the mucosa remains intact in patients with hemorrhoids, as opposed to the mucosal disruption caused by tumor. Linitis Plastica This is a rare form of rectal cancer where malignant “signet ring” cells or undifferentiated carcinoma diffusely infiltrate the submucosa and muscularis propria, with relative sparing of the mucosa. This may be a primary rectal tumor or may be


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secondary to other pelvic cancers such as prostate, cervix, or bladder. On T1WI, there is marked thickening of the rectal wall and mesorectal fascia. On T2WI, there may be a ring pattern in the rectal wall due to a combination of tumor infiltration and fibrosis around intact layers of the muscularis propria. Early

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recognition is important as it may guide the physician to perform deep biopsies (if the mucosa is spared). Also, because the prognosis is very poor, the patient may be spared unnecessary major surgery.

Figure 9.1 Schematic diagram of the T-staging of rectal cancer.

Figure 9.2 Normal rectum.(A) Sagittal and (B) transaxial T2WI of normal rectum. Note the signal void due to gas in the rectal lumen (R), the high signal combination of mucosa and submucosa (arrowheads) and the low signal muscularis propria (arrows). Intermediate signal endometrial tumor (asterisk). Abbreviations: C, cervix; SP, symphysis pubis.


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Figure 9.3 Lateral view of a surgical specimen from an abdominoperineal TME. Note the peritoneal reflection (arrowheads) and the pouch of Douglas (asterisk), the uterus having been removed. Peritoneum covers the anterior and lateral aspects of the upper two thirds of the rectum. The lower third of rectum is circumferentially invested by mesorectal fascia, the visceral surface of which (arrow) invests the surgical specimen. Note the anus (A) and the ischioanal fossa fat (IAF).

Figure 9.4 T1 rectal cancer. Transaxial T2WI of the mid-third of rectum. Note the intact muscularis propria (arrow). The tumor (T) can be distinguished from fecal residue by the vessel entering the mass (arrowheads). Abbreviations: B, bladder; S, sacrum.


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Figure 9.5 T2 rectal cancer. T2WI perpendicular to an upper rectal tumor (T). Note the muscularis propria (arrow), which is focally infiltrated (asterisk) by the tumor. Note the peritoneal reflection (curved arrow) and piecemeal depiction of the mesorectal fascia (arrowheads). Right iliopsoas bursa (open arrow). Abbreviation: B, bladder.

Figure 9.6 T3 mid-third rectal cancer—margin uninvolved. (A) Sagittal and (B) T2WI perpendicular to a posterior, mid-third rectal tumor (T). Note the axis planned for the subsequent high-resolution off-axis sequence (line) in A. There is a broad front of infiltration into the mesorectal fat (arrowheads) making this a T3 lesion, although the mesorectal fascia (circumferential resection margin) is well clear (arrows) in B. Note the peritoneal reflection anteriorly (open arrows) in B, rectal lumen (L) obturator internus muscle (O), levator ani (curved arrow) in A. Abbreviations: B, bladder; PG, prostate gland; PS, pubic symphysis.


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Figure 9.7 T3 lower rectal cancer—margin involved. T2WI perpendicular to a tumor (T) of the anterior and right lateral rectal wall. The tumor demonstrates central ulceration (U) and is contiguous anteriorly with the retroprostatic or Denonvillier’s fascia (arrows) making this T-stage 3 with an involved anterior margin. This patient would benefit from a long course of preoperative radiotherapy to reduce the risk of a positive anterior resection margin. Note how little space there is between the rectal wall and the mesorectal fascia anteriorly compared with laterally, making anterior tumors at particular risk for resection margin involvement. Mesorectal fascia (arrowheads). Abbreviations: B, bladder; L, rectal lumen; O, obturator internus muscle; PCZ, hypertrophied prostate central zone.

Figure 9.8 T3 mucinous lower rectal cancer. (A) Sagittal and (B) T2WI perpendicular to a characteristically high signal mucinous tumor (asterisk) extending from the lower rectum into the upper part of the anus (A). There is focal extension (arrow) in B through the muscularis propria (curved arrows) into the lower left mesorectum/upper left intersphincteric plane, medial to the distal part of the levator ani muscle (arrowheads). Because of the narrow confines of the mesorectal space at this level, T3 tumors of the lower rectum are treated with longcourse chemoradiotherapy to reduce the risk of a positive surgical margin. Abbreviations: B, bladder; IAF, left ischioanal fossa.


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Figure 9.9 T3 mid-rectal cancer with mesorectal involvement. T2WI perpendicular to an extensive T3 mid-rectal tumor (T). There is a broad front of nodular tumor extending into the right side of the mesorectum with a satellite tumor nodule (arrow) infiltrating the right mesorectal fascia. This nodule may in fact reflect an infiltrated lymph node or discrete tumor deposit. The patient will require a long course of neoadjuvant radiotherapy to reduce the risk of a positive lateral resection margin. Note the normal mesorectal fascia elsewhere (arrowheads). An infiltrative tumor edge such as this carries a poorer prognosis than tumors with a better-defined margin such as in Figure 9.6. Abbreviations: B, bladder; O, obturator internus muscle; PCZ, prostate central zone.

Figure 9.10 T3 rectal cancer with extramural venous infiltration (EMVI). T2WI perpendicular to a mid third rectal tumor (T). Intact muscle is shown virtually around the tumor (closed arrowheads), though there is histologically proven extramural venous infiltration on the left side (open arrowheads) making this a stage T3 tumor. The venous infiltration causes tubular bulging of the involved vessel. Abbreviations: B, bladder; C, coccyx; O, obturator internus muscle; P, piriformis muscle; SV, right seminal vesicle.


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Figure 9.11 T3 rectal cancer contrasted against peritumoral fibrosis. (A) Sagittal T2WI planning image and (B) T2WI perpendicular to an upper and mid-third rectal tumor (T). Note focal infiltration dorsally into the mesorectum (arrowheads). There is quite extensive fine stranding (crossed arrows) extending into the dorsal mesorectal fat. This has been shown to represent peritumoral fibrotic change. Additionally, however, there is a nodular front of infiltrative tumor from the right and left walls (curved arrows) making this a stage T3 lesion. Note the anterior peritoneal reflection (straight arrows) and the mesorectal fascia (open arrows), which are not infiltrated. Levator ani muscle (curved black arrow) A. Abbreviations: AC, anal canal; B, bladder; P, piriformis muscle; PCZ, prostate central zone; PPZ, prostate peripheral zone; S, sacrum; SV, seminal vesicle.

Figure 9.12 T4a mid- and upper rectal cancer with peritoneal infiltration. (A) Sagittal T2WI through an extensive mid- and upper third rectal tumor (T) and (B) T2WI perpendicular to the mid-part of the tumor. The peritoneal reflection (arrowheads) is thickened with focal nodular peritoneal deposits (arrows) making this a stage T4a lesion. Note the enlarged mesorectal nodes (asterisk). Abbreviations: AC, anal canal; B, bladder; O, left obturator internus muscle; PG, prostate gland; SP, symphysis pubis.


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Figure 9.13 T4b lower rectal cancer infiltrating vagina. T2WI perpendicular to the long axis of a tumor (T) of the left side of lower rectum just above the anorectal junction. Tumor extends anteriorly to infiltrate the left posterior vaginal wall where the muscle layer is destroyed (arrows). Note the intact, low-signal posterior vaginal muscle on the right (arrowheads). This is therefore a T4b lesion. There is a broad base of contiguity with the left levator ani muscle (curved arrows), which was also infiltrated. Abbreviations: BN, bladder neck; IAF, ischioanal fossa; SPR, right superior pubic ramus.

Figure 9.14 T3/T4 lower rectal cancer abutting right levator ani muscle. Coronal T2WI of a large lower rectal tumor (T) that infiltrates through the right rectal wall (arrowheads) and is contiguous with the right levator ani muscle (curved arrow) that, however, retains its normal morphology and is not infiltrated. Adhesion to this structure, however, cannot be excluded. Left levator ani muscle (arrow). Abbreviation: IAF, left ischioanal fossa.


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Figure 9.15 T4b lower rectal cancer infiltrating levator ani muscle. Coronal T2WI showing a large lower rectal tumor (T) that clearly infiltrates the right levator ani muscle (curved arrow). Left levator ani muscle (straight arrow). Abbreviation: IAF, left ischioanal fossa.

Figure 9.16 T4b mucinous lower rectal cancer infiltrating the anus and vagina. (A) Sagittal and (B) T2WI perpendicular to the long axis of a large, mucinous lower rectal tumor (T) The tumor extends anteriorly into the vaginal lumen (long arrow) and, at introital level, extends into the left paravulval subcutaneous fat (curved arrows). Tumor abuts, but does not infiltrate the urethra (U) or levator ani muscle (short, open arrows). The external anal sphincter is diffusely attenuated with patchy focal infiltration (arrowheads). Inferior pubic rami (asterisk). Abbreviations: B, bladder; C, coccyx; IAF, left ischioanal fossa; SP, symphysis pubis.


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Figure 9.17 T4b mid-rectal cancer infiltrating a left sacral foramen and the posterior bladder wall. T2WI perpendicular to the long axis of a mucinous mid-rectal tumor (T). Note posterior extension into a lower left sacral foramen (curved arrow). Anteriorly, the tumor is contiguous with the posterior bladder wall (straight arrows), infiltrating the peritoneal reflection (arrowheads). There is gas in the bladder (asterisk) indicating rectovesical fistulation. Abbreviation: OIM, obturator internus muscle.

Figure 9.18 T4 lower rectal cancer infiltrating the prostate gland. (A) Transaxial T2WI demonstrating a large, ulcerating, anterior lower rectal tumor (T) extending into the prostate gland (P). Note the anterior displacement of the intraprostatic urinary catheter (curved arrow). There is tumor extension to the obturator internus muscle anteriorly (arrow). (B) DWI sequence (b-value 1000), the tumor returns high signal (asterisk), in keeping with restricted diffusion of water. (C) ADC Map. The lesion has a low ADC, with resultant low signal (arrows). Abbreviations: ADC, apparent diffusion coefficient; DWI, diffusion-weighted imaging; U, tumor ulceration. (Continued)


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Figure 9.19 Enlarged benign mesorectal lymph node. Transaxial T2WI through the mid-rectum (R) showing an enlarged left mesorectal lymph node (arrow). The node is homogeneous and has a smooth margin. This was benign on histology. Abbreviations: B, bladder; S, sacrum.


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Figure 9.20 N1 rectal cancer. T2 image perpendicular to the mesorectum in a patient with a mucinous rectal primary tumor (T). This demonstrates a high signal, enlarged mesorectal lymph node (curved arrow), the high signal mucinous change pathognomonic of nodal involvement when the primary lesion is mucinous. Such high signal change may persist within the primary lesion and lymph nodes, post chemo or radiotherapy, in which setting, such an appearance may simply represent residual, inert mucin, rather than residual tumour. Abbreviation: B, bladder.

Figure 9.21 N2 rectal cancer. Transaxial T2WI showing a leftsided mid rectal tumor (T). The muscularis propria (curved arrow) is poorly defined though there is no overt mesorectal infiltration. There are enlarged nodes in the left side of the mesorectum and right internal iliac territory (asterisk). The right internal iliac node demonstrates heterogeneous signal intensity similar to the tumor and both nodes demonstrate an irregular margin (arrowheads), both signs highly suggestive of lymph node infiltration with tumor, which was subsequently proven. Several other infiltrated mesorectal nodes were evident at final histology. Abbreviations: B, bladder; SV, right seminal vesicle.

Figure 9.22 Advanced local lymph node metastasis. Transaxial T1WI showing multiple enlarged lymph nodes (arrowheads) in the upper mesorectum in the distribution of the superior rectal vessels. Note the T3 rectal tumor (T), sacrum (S) and piriformis muscle (P).


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Figure 9.23 Intussuscepted tumor. (A) Sagittal and (B) T2WI perpendicular to an intussuscepted mid-rectal tumor (T). This was pathological stage T2 disease though the intussusception makes it very difficult to accurately define the stage on MRI. Note the multiple layers of muscularis propria (arrowheads) and intussuscepted mesorectal fat (asterisk). Abbreviations: AC, anal canal; B, bladder; C, coccyx; S, sacrum; Ur, urethra.


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Figure 9.24 Linitis plastica of the lower rectum. (A) Coronal T2WI parallel to and (B) T2WI perpendicular to the lower rectum. In A, there is mural thickening with a stratified appearance, and in B, a concentric mural ring pattern (arrowheads). There is a superficial resemblance to the intussusception shown in Figure 9.23. However, in this case, the ring pattern is due to undifferentiated tumor infiltrating between the different layers of the rectal wall, with the muscularis propria remaining essentially intact (MP). Also, a florid desmoplastic response causes low signal in the submucosa (SM). Levator ani muscle (arrows). Rectal lumen (asterisk). Abbreviations: B, bladder; IAF, ischioanal fossa; O, obturator internus muscle; P, piriformis muscle; S, sacrum.

Figure 9.25 Appearances following APR in males. (A) Sagittal, (B, C) transaxial T2WI in a male following APR. The bladder (B), prostate (P), and seminal vesicles (asterisk) prolapse into the pelvic void left by the excised rectum. A fibrotic band (arrows) binds the prostate and seminal vesicles to the pelvic floor. In A, note the high signal of the fatty marrow of the lower sacrococcygeal segments following radiotherapy (X) and the postsurgical changes in the anterior abdominal wall (S). The small area of high signal in the prostate (curved arrow) is secondary to needle biopsy. Source: Images courtesy of Dr. B M Carrington, Christie Hospital. (Continued)


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Figure 9.26 Appearances following APR in females. (A) Sagittal T2WI in a female following APR and (B, C) Transaxial T2WI in a different female following hysterectomy and APR. The bladder (B), uterus (U), and vagina (asterisk) prolapse into the void left by the excised rectum. A fibrotic band (arrows) binds the vagina and cervix in A and the vagina and bladder in B and C to the pelvic floor. Note the posterior angulation of the urethra (Ur) in A. Source: Images courtesy of Dr B M Carrington, Christie Hospital.


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Figure 9.27 Appearances following radiotherapy. (A) Sagittal T2WI in a female with an upper rectal tumor (T). Note the focus of extramural vascular invasion (EMVI) (arrowhead). (B) Sagittal T2WI in the same patient three months post long-course chemoradiotherapy. There is low-signal fibrotic change and structuring of the rectal wall at the level of the tumor (open curved arrow) with regression and fibrotic change at the site of EMVI. In the lower rectum, there is acute inflammatory postirradiation change, with high-signal change and thickening of the submucosa (asterisk). Note that the low signal mucosa remains intact (curved arrows). In addition, there is characteristic edema and stranding in the dorsal mesorectal fat (open arrowheads). (C) T2WI perpendicular to the lower rectum showing the same acute inflammatory change in the rectum. In addition, there is similar high-signal submucosal thickening within an anterior pelvic small bowel loop (open straight arrows). This loop would have been unavoidably within the treatment radiotherapy field. (D) Coronal T2WI in a different female previously treated with pelvic radiotherapy for cervical cancer, who has chronic radiation cystitis. There is thickening of the mucosa (arrowheads) and the high-signal submucosa (asterisk). A layer of low-signal muscle (arrows) is seen within the thickened bladder wall. Note the low signal fibrosis within a residual left pelvic sidewall nodal mass (curved arrows). Urethra (U). (E) Transaxial T1WI of the mid-pelvis in a patient with insufficiency fractures due to previous pelvic radiotherapy for cervical cancer. Note the low-signal edema in the sacral ala (asterisk) adjacent to low-signal fracture lines (arrows), characteristically running parallel to the sacroiliac joints (arrowheads), and the high-signal fatty marrow in the iliac bones (IL). (F) Sagittal T2WI demonstrating a large fistula (arrowheads) between the anterior wall of a rectal stump (RS) and the posterior vaginal wall (curved arrows) in a patient who had a previous Hartman’s procedure and radiotherapy for advanced rectosigmoid cancer. Note the intact anterior vaginal wall (arrows). Bladder (B). Abbreviations: B, bladder; O, obturator internus muscle; P, pyriformis muscle; S, Sacrum; SPR, superior pubic ramus; Ut, uterus. (Continued)


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Figure 9.28 Recurrent rectal tumor. T2WI perpendicular to the lower rectum. This patient previously had an anterior lower third rectal tumor resected, and there was clinical evidence of recurrent disease at the anastomotic site. Repeated biopsies through the left wall of the rectum revealed fibrotic tissue only, which characteristically returns low signal on T2-weighted imaging as shown here (F). This image, however, also shows an intermediate signal mass more anteriorly (asterisk) extending into the prostate gland (P) which is much more suggestive of recurrent tumor. This allowed accurate CT-guided biopsy, which confirmed the diagnosis of recurrent disease. Abbreviations: B, bladder; C, coccyx; L, rectal lumen; O, right obturator internus muscle.

Figure 9.29 Recurrent rectal cancer following Hartman’s procedure. (A) Sagittal T2WI demonstrating nodular, low to intermediate signal intensity mucosal tumor (arrowheads) within the rectal stump (S), after a previous emergency Hartman’s procedure for an obstructing rectosigmoid cancer. (B) Sagittal T2WI post radiotherapy, showing shrinkage of the rectal stump. Much of the tumor has resolved, apart from some intermediate signal tissue at the cranial end of the stump (closed arrows) which was biopsy-proven residual disease. (C) Sagittal T2WI three months following resection of the rectal stump. There is some nonspecific intermediate signal tissue within the wall of the anorectal bed (curved arrows) suspicious for tumor. (D) Avid FDG uptake (open arrows) within the anorectal bed reinforced the suspicion of residual disease, which was confirmed by progression on follow-up scans. Abbreviations: B, bladder; P, prostate; SPR, superior pubic ramus. (Continued)


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Figure 9.30 Recurrent rectal cancer following previous anterior resection. (A) Transaxial T2WI, (B) DWI (b-value 1000) images, and (C) ADC map showing extensive tumor recurrence infiltrating the parietal mesorectal fascia, presacral space, and posterior pelvic sidewalls in a male patient who had a previous anterior resection TME. Typically, the tumor returns intermediate signal intensity on the T2WI (arrows). The periphery of each tumor focus also returns high signal on the DWI (arrowheads), in keeping with restricted water diffusion. As expected, these areas are depicted as low-signal foci on the ADC map (curved arrows). Left seminal vesicle (asterisk). Abbreviations: ADC, apparent diffusion coefficient; B, bladder; DWI, diffusion-weighted imaging; S, sacrum.


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Figure 9.31 Recurrent mucinous tumor involving the cervix and left pelvic sidewall. (A) Sagittal and (B) transaxial T2WI in a patient who had a previous anterior resection for mucinous rectal cancer. There is a high-signal mass of recurrent mucinous tumor (asterisk) infiltrating the posterior lip of the uterine cervix (C). The recurrent tumor extends from the cervix, to infiltrate the internal iliac territory of the left pelvic side wall (arrows) in B. Levator ani muscle (arrowheads). Abbreviations: B, bladder; R, rectal lumen; S, sacrum.


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Figure 9.32 Hemorrhoids. (A) Sagittal T2WI in a female patient. There is high signal intensity thickening of the lower rectal submucosa (asterisk). Hemorrhoids can be quite florid and superficially resemble rectal tumor, which may lead to diagnostic error. The low-signal mucosa is, however, characteristically intact (curved arrows). If there is doubt, clinical and endoscopic review should confirm the diagnosis. (B) Sagittal T2WI in another female patient in whom there is prolapse of the posterior lower rectal wall secondary to submucosal hemorrhoids. Note the thickened submucosa (asterisk), and, within the prolapsed segment, the apposed double layer of intact, low-signal mucosa (arrowheads). Abbreviations: B, bladder; U, uterus.

Figure 9.33 Pelvic sepsis due to rectal anastomotic dehiscence. Transaxial T2WI demonstrating a large defect in the left side of the rectum at the level of the anastomosis, following anterior resection (curved arrow). Note the low-signal luminal gas extending into the perirectal tissue, which, more laterally, contains high-signal pus (asterisk). Abbreviations: B, bladder; O, left obturator internus muscle; P, left pyriformis muscle.


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FURTHER READING Atkin WS, Edwards R, Hines K-H, et al. Once-only flexible sigmoidoscopy screening in prevention of colorectal cancer: a multicentre randomised controlled trial. Lancet 2010; 375(9726):1624–1633. Beets-Tan RG, Beets GL, Vliegen RF. Accuracy of MR imaging in the prediction of tumour-free resection margins in rectal cancer surgery. Lancet 2001; 357:497–504. This paper demonstrates that the distance of tumor from the mesorectal fascia can be accurately predicted on pre-operative MR imaging, allowing identification of patients at risk for positive resection margins. Brown G, Richardson CJ, Newcombe RG, et al. Rectal carcinoma: thinsection MR imaging for staging in 28 patients. Radiology 1999; 211 (1):215–222. Seminal paper on the method and accuracy of high-resolution MR imaging in defining the stage and depth of extramural invasion of rectal cancer extent using surface phased array coils. Edge SB, Byrd DR, Compton CC, et al., eds. AJCC Cancer Staging Handbook. New York: Springer, 2010. The standard reference for TNM tumor staging. All new changes are clearly highlighted. There is also excellent background demographic and survival data. Heald RJ. Total mesorectal excision is optimal surgery for rectal cancer: a Scandinavian consensus. Br J Surg 1995; 82:1297–1299. This paper defines the best surgical practice for patients with operable rectal cancer. Kapiteijn E, Marijnen CAM, Nagstegaal ID, et al. Preoperative radiotherapy combined with total mesorectal excision for resectable

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rectal cancer. N Engl J Med 2001; 345(9):638–646. Large controlled trial proving that short-course pre-operative radiotherapy reduces the risk of local recurrence in patients with rectal cancer who have had a standardized TME. Kim HS, Lee JM, Hong SH, et al. Locally advanced rectal cancer: added value of diffusion-weighted MR imaging in the evaluation of tumour response to neoadjuvant chemo- and radiation therapy. Radiology 2009; 253(1):116–125. One of several small studies demonstrating that DWI improves diagnostic accuracy over conventional sequences in the evaluation of tumor response to neo-adjuvant chemotherapy for locally advanced rectal cancer. Kwok H, Bissett IP, Gill GL. Pre-operative staging of rectal cancer. Int J Colorectal Dis 2000; 15:9–20. A meta-analysis of almost 5000 patients in 83 studies comparing CT, MRI, and endoanal ultrasound for staging rectal cancer. Papillon J, Berard P. Endocavitary irradiation in the conservative management of adenocarcinoma of the low rectum. World J Surg 1992; 16:451–417. Groundbreaking work that is only recently being more widely explored in the United Kingdom. Skibber JM, Minsky BD, Hoff PM. Cancer of the colon. In: DeVita VT Jr., Hellman S, Rosenberg SA, eds. Cancer. Principles and Practice of Oncology. Vol 530, 7th ed. Walnut St., Philadelphia, PA: Lippincott, Williams and Wilkins, 2005. This is a definitive, comprehensive, and up-to-date text on all aspects of rectal cancer and it’s management.


10 Anal cancer Rohit Kochhar and Paul A. Hulse

BACKGROUND INFORMATION Epidemiology

Patterns of Tumor Spread

Cancers of the anal canal are rare, accounting for approximately 1.5% of gastrointestinal tract malignancies. In the United States, there were an estimated 5260 new cases in 2010. In the United Kingdom, about 930 new cases are diagnosed each year and the incidence has increased threefold since the early 1970s, especially in women. Anal cancer is found mainly in adults, with the peak age incidence being in the early 60s. The disease affects women more often than men. Anal cancer was initially thought to be associated with chronic irritation from hemorrhoids, fissures, fistulas, and inflammatory bowel disease. It is now well established that the majority of anal cancers in both sexes are due to infection with human papillomavirus, particularly HPV16. There is an increased risk of anal cancer in men and women who practice anal receptive intercourse, who have had more than 10 sexual partners, or who have sexually transmitted diseases such as genital warts, gonorrhea, or Chlamydia trachomatis. Other etiological risk factors are immunosuppression, HIV infection, and smoking. Women with anal cancer have a higher incidence of vulval, vaginal, cervical, and lung cancers.

Carcinoma of the anus is an indolent disease, which usually becomes locally extensive before distant metastases occur. Anatomical localization is important as it reflects the pattern of spread. According to the American Joint Committee on Cancer (AJCC), cancers are classified as anal tumors if their epicenter is less than or equal to 2 cm from the dentate line. They are rectal cancers if their epicenter is more than 2 cm proximal to the dentate line. Anal margin lesions are distal to the anal verge, where hair-bearing skin occurs. Anal canal cancers are of greater concern because they are more likely to invade the sphincters and spread deep into the pelvis via lymphatics and hemorrhoidal veins. The pattern of lymph node metastatic spread depends on the site of origin of the tumor within the anal canal. Above the dentate line, drainage is to the perirectal, internal iliac, and retroperitoneal nodes. Below the dentate line, drainage is to the inguinal nodes. The TNM staging classification for anal cancer remains unchanged in the seventh edition and is given in Table 10.1. At the time of presentation, approximately 50% of patients will have a T1 or T2 lesion and approximately 25% will have regional lymph node involvement.

Histopathology

Prognostic Indicators

The histology of tumors arising in the anus depends on their location with respect to the dentate line. The anal canal is divided by the dentate line into an upper part lined with transitional (urothelial type) or rectal glandular mucosa and a lower part lined by nonkeratinizing squamous epithelium. At the level of the dentate line there is a junctional area of squamous and nonsquamous mucosa. Cancers arising in the junctional zone at the level of and just above the dentate line are usually adenocarcinomas. Anal canal tumors below the dentate line are predominantly nonkeratinizing squamous cell carcinomas (SCCs). The anal margin is the pigmented skin surrounding the anus, extending laterally to a radius of approximately 5 cm from the anal orifice. Cancers arising from the anal margin are usually well-differentiated keratinizing SCCs. The previously employed subtype terms, basaloid, cloacogenic, and transitional, have now been abandoned because they are recognized as subgroups of nonkeratinizing SCC. Uncommonly, small cell carcinoma, undifferentiated carcinoma, and mucinous adenocarcinoma can arise within the anal canal to which the Tumor Node Metastasis (TNM) staging system applies. Melanoma, carcinoid tumors, and sarcomas rarely arise in the anal canal and are excluded from this staging system. Biological behavior, management strategies, and prognosis of the keratinizing and nonkeratinizing types of SCC are similar. Cancers arising in glandular mucosa of the upper anal canal behave like rectal cancers and are managed similarly.

Tumor size, location, and depth of penetration at presentation are the most important prognostic factors. Mobile lesions less than 2.0 cm in diameter are cured in approximately 80% of cases, whereas the cure rate for lesions greater than 5.0 cm in diameter is less than 50%. Skin ulceration and nodal disease are other poor prognostic factors. The likelihood of locoregional lymph node involvement is related to tumor size and location. Tumors at the anal verge are less likely to develop lymph node metastases than those at the anal canal, probably because of earlier clinical presentation. Women achieve better local control and longer survival.

Treatment Until the 1980s, the treatment of choice for cancer arising within the anal canal was an abdominoperineal resection (APR). In an attempt to reduce surgical failure rates, treatment with preoperative 5-fluorouracil (5-FU) and mitomycin, combined with radiotherapy, was introduced in the United States. The first three patients treated in this way were found to have no residual tumor in the excised anus following APR. This unexpected finding led to a change in management of anal cancer. Primary treatment now employs chemoradiation with APR reserved for patients with persistent tumor on postradiation biopsy or those with locally recurrent disease. Local excision can be considered for small well-differentiated carcinomas of


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dimension is the maximum diameter for tumors protruding beyond the anal verge.

Table 10.1 Anal Carcinoma Staging Systems Description of tumor extent Primary tumor (T) TX T0 Tis T1 T2 T3 T4

Lymph node (N) NX N0 N1 N2 N3

Distant metastasis (M) M0 M1 Stage grouping Stage 0 Stage I Stage II Stage IIIA

Stage IIIB

Stage IV

Cannot assess primary tumor No evidence of primary tumor Carcinoma in situ Tumor 2 cm but < 5 cm in greatest dimension Tumor > 5 cm in greatest dimension Tumor of any size invading adjacent structures, e.g., vagina, urethra, and bladder (involvement of sphincter muscle(s) alone is not classified as T4) Cannot assess regional lymph node No regional nodal metastasis Metastasis in perirectal lymph node(s) Metastasis in unilateral internal iliac and/or inguinal node(s) Metastasis in perirectal and inguinal nodes and/or bilateral internal iliac and/or inguinal nodes No distant metastasis Distant metastasis Tis T1 T2 T3 T1 T2 T3 T4 T4 Any T Any T Any T

N0 N0 N0 N0 N1 N1 N1 N0 N1 N2 N3 Any N

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M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M1

the anal margin (T1 N0), that is, less than 2 cm in diameter, without evidence of nodal spread and with no sphincter involvement. Multicenter studies in Europe (UKCCR and EORTC) have confirmed the benefit of chemoradiotherapy (CRT) over radiation therapy alone in reducing locoregional recurrence and death from anal cancer and producing a higher colostomyfree rate and improved progression-free survival. However, no overall survival benefit was demonstrated with CRT. A five-year survival rate of 67% has been achieved using combined radiotherapy, 5-FU, and mitomycin.

MRI Staging Accuracy There are no published results for the staging accuracy of primary or recurrent anal cancer using MRI.

Technique For local staging, MRI can be performed using phased array or endoluminal coils with no proven diagnostic advantage of either technique. However, endoluminal coil imaging is limited by a narrow field of view near field artifact and may not be tolerated by patients with anal cancer. A pelvic phased array coil is however easy to place and shows both the local spread of the disease as well as lymph node involvement. A standard technique is employed with body coil transaxial T1WI to cover the abdomen and pelvis and highresolution thin section T2WI in the three orthogonal planes. Fatsuppressed imaging can help to improve the conspicuity of the primary tumor mass and STIR sequences are used in cases with a suspected fistula. We have found no significant added advantage of contrast-enhanced MRI over standard T2-weighted sequences in primary staging. The role of diffusion-weighted imaging (DWI) in the diagnosis and staging of primary anal tumors has not been defined.

Imaging Features Usually anal cancer is of intermediate to low signal intensity on T1WI and intermediate to high signal intensity on T2WI and fat-suppressed imaging. Mucinous adenocarcinoma displays characteristic high signal intensity on T2WI. Tumor usually spreads circumferentially around the anal wall and may form a lobulated intraluminal or extramural mass. Primary anal cancers are staged based on the size of the cancer. The sphincter complex is the most commonly infiltrated structure, followed by the rectum. Invasion of adjacent organs such as the vagina, urethra, or bladder is required to establish stage T4 disease.

Nodal Disease Metastatic spread occurs to the inguinal, iliac, perirectal, and retroperitoneal nodes. As with other pelvic malignancy, lymph nodes with a short-axis diameter greater than 1.0 cm in the pelvis and 1.5 cm in the inguinal regions are considered pathological. Lymph nodes are not normally identified in the perirectal fat and should be regarded as pathological (hyperplastic or metastatic) when seen. Other radiological features of malignant nodes include signal intensity similar to the primary mass, extracapulsar infiltration, and central necrosis particularly when the primary mass is an SCC.

MRI OF ANAL CANCER Current Indications

Metastatic Disease

MRI has become the imaging modality of choice for locoregional staging and assessment of tumor regression following CRT. MRI displays high-resolution multiplanar images of the location, size, and circumferential and craniocaudal extent of the primary tumor and provides information regarding the involvement of adjacent structures. MRI is especially useful in staging large tumors particularly when the craniocaudal

Posttreatment—Chemoradiotherapy

In advanced disease, distant metastatic spread is primarily to the liver.

Posttreatment MRI is generally performed six to eight weeks after CRT. There is usually a reduction in size of the primary tumor with residual mixed, predominantly low signal intensity


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seen at the site of the original tumor. However, response to treatment can continue to occur for up to three to six months with resultant progressive fibrotic changes, and therefore a further follow-up MRI is advisable. In the United Kingdom Co-ordinating Committee on Cancer Research (UKCCCR) study, 70% of patients who had not achieved a complete response at the 6-week assessment demonstrated further tumor regression with longer follow-up. Changes in normal tissues are mainly attributable to radiotherapy. An acute reaction occurs up to three months following treatment and is characterized by mucosal edema and high signal on T2WI of the anal musculature. It is possible to mistake this appearance for disease, and correlation with pretreatment imaging is crucial to avoid this pitfall. Chronic changes occur up to five years following treatment and are predominantly fibrotic in nature, with low signal on T2WI and consequent morphological distortion of the pelvic viscera and soft tissues. Affected bone marrow shows fatty change seen as high signal on T1WI.

involvement is also different in distribution, with the inguinal nodes being less commonly involved and perirectal, presacral, and internal iliac nodes more commonly involved. Distant metastases are present in a large number of patients undergoing MRI for recurrence following surgery.

Pitfalls of MRI l

Posttreatment—Surgery Following APR, there are characteristic MRI appearances: l

l

l

A band of presacral fibrosis occurs, seen as intermediate signal on T1WI and low signal on T2WI. The levator ani muscles are sutured together with a consequent irregular contour to the central pelvic floor. The pelvic viscera prolapse posteriorly into the void left by the excised anorectum.

l

When radical pelvic surgery includes pelvic floor resection for advanced or recurrent tumors, reconstruction is performed using muscle grafts.

Residual/Recurrent Disease Following treatment, persistence of intermediate signal intensity on T2WI at the site of the original tumor, particularly if similar to the primary tumor, is suspicious of local residual disease and warrants biopsy assessment. Posttreatment high signal on T2WI usually signifies mucosal edema and low signal on T2WI represents fibrosis. Recurrent disease can occur at the site of the primary tumor mass, in the locoregional lymph nodes or outside of the radiation field, and can occur in up to 35% of anal cancer patients despite combined modality treatment. Recurrent anal cancer is often more extensive with involvement of adjacent organs and the pelvic skeleton. In recurrent as opposed to primary anal cancers, lymph node

l

Identifying the location and extent of the primary tumor can be problematic in anal cancer especially when the tumor is small. l Reference to the clinical findings and findings at examination under anesthetic can guide the radiologist to the site of the primary tumor. l Fat-suppressed imaging can increase tumor conspicuity. l Description of the relationship of the tumor to the anorectal junction, located at the indentation of the puborectalis muscle, helps differentiate between tumors of rectal and anal origin. l Measurement of tumor volume is difficult with infiltrative anal cancers that have circumferential spread. Measurement of the radial diameter of the anal canal wall at the site of tumor is useful for comparison with subsequent examinations. Prediction of metastatic disease in inguinal lymph nodes is particularly difficult. Inguinal nodes can normally measure up to 1.5 cm in short-axis diameter. However, the use of this measurement probably reduces sensitivity for the identification of metastatic disease. Features suggestive of metastatic disease in nonenlarged and enlarged nodes are as follows: l Round shape l Asymmetrical clustering in the groin or on the pelvic sidewall l Central nodal necrosis, which is a strong indicator of metastatic disease in squamous cell tumors Differentiation between residual/recurrent tumor and posttreatment effect can be difficult. l Reference to pretreatment MRI to establish the exact site of original tumor is recommended. l Posttreatment mucosal edema generally has a higher signal than the intermediate signal of residual/recurrent tumor. l Hemorrhoids can be difficult to recognize, as they are of variable signal on T2WI, depending on state of scarring/ fibrosis so that clinical examination may be required for confirmation when their presence is suspected.


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Figure 10.1 Normal anatomy of the anus. (A) Coronal, (B) sagittal, and (C) transaxial T2WI. The anorectal junction is depicted by a bold line in (A, B). In A, this is seen at the level of the transition of the puborectalis sling into the external sphincter (arrows). In B, this is at the level of a horizontal line drawn between the tip of the coccyx and the posterior margin of the pubis. The anal verge is at the mucocutaneous junction and marks the distal limit of the anal canal (hashed line in A and B). The anal margin (AM) in A and B extends for 5 cm circumferentially distal to the anal verge. The dentate line, although not visible on MRI, is seen macroscopically approximately 2.5 to 3 cm proximal to the anal verge (dashed and dotted line in A). The anal canal (AC) is shown in A, B, and C. The sphincter anatomy is depicted in C: internal sphincter (IS) longitudinal muscle layer in intersphincteric space (LM), external sphincter (ES), anococcygeal body (AB), perineal body (PB), and ischioanal fossa (IAF).


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Figure 10.2 T1 anal cancer. (A) Transaxial T2WI and (B) transaxial STIR image showing lobulated intermediate signal intensity tumor mass less than 2 cm in greatest dimension extending through anal wall (arrows). Abbreviation: V, vagina. Figure 10.3 T2 anal cancer. (A) Sagittal, (B) transaxial, and (C) coronal T2WI showing intermediate signal intensity mass (T) extending from the anal verge over a distance of 3 cm (arrowheads in A and C). The tumor infiltrates the internal sphincter from the 12 to 3 o’clock positions in the transaxial plane (arrows in B).


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Figure 10.4 T2 anal cancer. (A) Transaxial T2WI and (B) coronal T2WI showing intermediate signal intensity, non lobulated tumor (arrows) between 2 and 5 cm maximum diameter which extends to the anal verge. There is an incidental right adnexal cyst (asterisk).


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Figure 10.5 T2 anal cancer. (A) Transaxial T2W and (B) coronal T2W images demonstrate an intermediate signal intensity mass in the left anal canal from 12 to 6 o’clock positions (arrow in A and B) extending craniocaudally over approximately 4 cm to below the anorectal junction (arrowhead in B). Post-contrast T1W fat-suppressed transaxial (C) and coronal (D) images demonstrate moderate to intense enhancement of the mass differentiating it from the adjacent normal mucosa (arrows in C and D). Note is also made of incidental left ovarian teratodermoid (asterisk in B).


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Figure 10.6 T3 anal cancer. (A) Sagittal, (B) transaxial, and (C) coronal T2WI showing intermediate signal intensity tumor (T) extending from the anal verge over a distance of more than 5 cm (arrowheads in A and C). The tumor infiltrates the left puborectalis (arrow in B and C). Note a presacral lymph node (N) in A which represents a possible metastasis.


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Figure 10.7 T3 anal cancer. (A) Sagittal, (B) coronal, and (C) transaxial T2WI demonstrate an intermediate signal intensity anal mass extending inferiorly from the anal margin into the upper anal canal measuring >5 cm (arrows in A and B). The tumor infiltrates the external sphincter between 3 o’clock and 6 o’clock positions (arrowheads in C) and extends through it into the subcutaneous fat and ulcerates on to the skin surface (arrows in B and C). Note the small perirectal lymph nodes in B that represent possible metastatic nodes and a trace of ascites likely incidental (asterisk in A).


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Figure 10.8 T3 anal cancer. (A) Transaxial and (B) sagittal T2WI showing large lobulated high signal intensity mass (arrows) characteristic of a mucinous adenocarcinoma. Tumor has extended through the anal sphincter into the fat of the ischioanal fossa and buttock to abut onto the natal cleft; it also extends cranially into the lower rectum (asterisk). Abbreviations: IAF, ischioanal fossa; NC, natal cleft. Figure 10.9 T3 squamous cell anal cancer with rectal extension. (A) Sagittal, (B) coronal, and (C) transaxial T2WI demonstrate a heterogeneous anal canal mass extending beyond the anorectal junction into the lower rectum (arrows). The anorectal junction is best seen in B and is denoted by the dashed line labeled ARJ. The epicenter of the mass is less than 2 cm from the dentate line denoted by the dashed line labeled DL in B, making it a primary anal tumor. There is an extension beyond the left external sphincter to infiltrate the left levator sling at 5 o’clock (arrowhead in C). Note presacral lymph nodes (open arrowheads in A) which represent probable metastatic nodes with a similar signal intensity to the primary tumor. (Continued)


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Figure 10.10 T4 anal cancer with vaginal invasion. (A) Sagittal and (B) transaxial T2WI showing a lobulated intermediate signal intensity tumor (T) which has extended laterally through the sphincter complex into the ischioanal fossa (arrow in B) and anteriorly into the left side of the vagina (arrowheads in A and B).


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Figure 10.11 NI anal cancer. Transaxial T2WI showing lymph node metastases in the perirectal fat (arrows) and local spread of primary tumor to rectum (asterisk). Lymph nodes are not normally identified in the perirectal fat on MRI and should be regarded as pathological. Differentiation between malignant and hyperplastic nodes on the basis of size is not reliable in this location. Nodes with central necrosis or a similar signal characteristic to the primary tumor, as in this case, favor malignant disease.

Figure 10.12 NI anal cancer. Transaxial T2WI from mucinous anal cancer (T) shown in Figure 10.8. The perirectal lymph node (arrow) shows central high signal indicating a high probability of metastatic disease. Central lymph node high signal on T2WI occurs with metastatic mucin-secreting adenocarcinoma and central nodal necrosis in squamous cell carcinoma. A benign right inguinal node, with fat in the hilum (arrowheads), also returns high signal on T2WI. The eccentrically located fat usually indicates its benign significance, but uncertainty can be resolved with fat-suppressed (STIR) sequences.


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Figure 10.13 N2 anal cancer. Transaxial T2WI showing enlarged left inguinal lymph node with heterogeneous signal intensity (arrow) and the primary anal tumor (T).

Figure 10.15 N3 anal cancer. (A) Transaxial and (B) coronal T2WI showing bilateral inguinal lymph node metastases (arrows). Note intermediate signal intensity of the primary tumor (T). On the right side the node has a ragged margin (arrowheads) indicating extranodal tumor extension.

Figure 10.14 N3 anal cancer. Coronal T2WI showing bilateral surgical obturator (internal iliac) lymph node metastases (arrows). Note infiltrating anorectal tumor (T).


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Figure 10.16 Retroperitoneal, porta hepatis, and liver metastases in anal cancer. Transaxial T1WI showing enlarged interaortocaval lymph node (arrow), porta hepatis lymph node mass (arrowheads), and liver metastasis (asterisk). Note the intrahepatic bile duct dilatation secondary to the obstructing porta hepatis mass.

Figure 10.17 T3 anal cancer with fistula. (A) Transaxial and (B) coronal T2WI showing circumferential spread of an intermediate/high signal intensity tumor mass (arrows). There is transmural spread of tumor with a fluid and air containing fistula (open arrowheads) extending through the pubococcygeal portion of the levator ani muscle into the ischioanal fossa (IAF).


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Figure 10.18 T2 anal cancer with complete response to treatment. Transaxial T2WI performed (A) prior to treatment and (B) 8 weeks and (C) 20 weeks following completion of chemoradiotherapy. In A, there is a lobulated high-signal intensity tumor (T) centered on the anal verge with early infiltration of the right ischioanal fossa (arrows). In B, there has been response to treatment with virtual complete resolution of the tumor with a residual low signal intensity lesion (arrowheads) and some adjacent higher signal intensity cutaneous edema (crossed arrow). In C, there has been further organization with resolution of the mucosal edema and a residual band of low signal intensity fibrosis (arrowheads).


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Figure 10.19 T2 anal cancer with complete response to treatment and persistent mucosal edema (pseudotumor). (A) Transaxial T2WI, (B) transaxial fat-suppressed T1WI, and (C) coronal T2WI obtained prior to treatment demonstrate a lobulated intermediate signal intensity tumor (T) in the left anal canal. The boundary of the mass (arrows) is more conspicuous on the fat-suppressed image in B. (D) Transaxial T2WI, (E) fat-suppressed T1WI, and (F) coronal T2WI obtained 8 weeks following completion of chemoradiotherapy. There is a complete response with parallel bands of low signal intensity (arrows) representing fibrosis which enclose the reconstituted internal sphincter (arrowheads). There is mucosal edema (asterisk) in the anal canal attributable to the treatment. (G) Transaxial and (H) coronal T2WI obtained 20 weeks following completion of treatment. The treated tumor has not recurred (arrows). On the right side of the anal canal, mucosal edema persists and gives a polypoid (pseudotumor) appearance (asterisk) which should not be mistaken for recurrent disease. (Continued)


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Figure 10.20 Chronic radiation reaction. Transaxial T2WI showing changes in pelvic viscera four years following chemoradiotherapy for a T3 anal cancer. There is a mixed signal mass (M) fixed to the left piriformis muscle (P) stable in appearance over a one-year period indicating the lack of residual proliferating tumor. There is a band of presacral edema (arrows). The rectum and an adjacent loop of dependent small bowel show diffuse low signal, mural thickening, and minor serosal spiculation due to fibrosis (open arrowheads). Chronic radiation reactions can develop up to five years following treatment and persist indefinitely.

Figure 10.21 Residual anal cancer on diffusion-weighted imaging (DWI). (A) Transaxial and (B) coronal T2WI demonstrate the primary anal cancer seen as an area of intermediate signal intensity extending from the anal margin to just beyond the anal verge (arrows). (C) Transaxial and (D) coronal T2WI four months after completion of chemoradiotherapy demonstrate an increase in size of the mass in the left anal canal which now has heterogeneous signal intensity and extends to the lateral margin of the external sphincter (arrowhead). The inferior anal margin component has however responded. (E) High b-value (b = 1000) DWI and (F) corresponding ADC images demonstrate restricted diffusion in the periphery of the mass (curved arrow) with central necrosis. Abbreviation: ADC, apparent diffusion coefficient. (Continued)


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Figure 10.22 Locally extensive recurrent anal cancer following chemoradiotherapy and abdominoperineal resection. (A) Transaxial T1WI showing recurrent tumor (arrows) with substantial destruction of the left ischiopubic ramus and pubic bone. T1WIs are useful for indicating the extent of bone disease. (B) Transaxial, (C) coronal, and (D) sagittal T2W images showing extent of soft tissue infiltration in the pelvis by recurrent disease. Tumor has invaded the prostate and bladder with fistulation to a complex deep pelvic/perineal cavity (C). There is circumferential thickening of the bladder wall (crossed arrows in D). A separate gas-containing cavity is present in the involved pelvic floor and obturator muscles (arrowheads). A suprapubic catheter is in situ in the bladder (SP). Note the iliac lymph nodes (asterisk) in C which are equivocal for metastatic disease or hyperplasia secondary to pelvic sepsis. Multiplanar imaging is important in evaluating such complex cases and fistulas.

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Figure 10.23 Recurrent anal cancer following chemoradiotherapy. (A) Transaxial and (B) coronal T2WI showing a recurrent intermediate signal intensity tumor mass in the left anal canal and rectum (arrows). The rest of the anal wall is thickened and is of low signal intensity, representing radiation-induced fibrosis (open arrowheads). Note probable inguinal lymph node metastasis (asterisk) and definite perirectal lymph node metastasis (solid arrowheads).

Figure 10.24 Recurrent anal cancer following chemoradiotherapy. (A) Transaxial and (B) coronal T2WI showing recurrent tumor involving rectum (arrows), perirectal, right obturator and right internal iliac (asterisk), and bilateral common iliac lymph nodes (solid arrowheads). Note the dependent small bowel loop with mural thickening and mild serosal spiculation (open arrowheads) due to radiation change.


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Figure 10.25 Recurrence following total pelvic clearance. (A, C, D) Transaxial and (B, E) sagittal T2WI. A and B demonstrate the usual appearances following abdominoperineal resection of the rectum. There is posterior prolapse of the uterus (asterisk) into the void left by the excised rectum. There is descent of the bladder below the pubococcygeal line (dashed line in B) because of weakness of the pelvic floor. A recurrent tumor nodule is evident in the lower vagina (arrow in C). This necessitated a total pelvic clearance with pelvic floor flap reconstruction. Two years following this surgery, asymptomatic recurrent disease was identified on surveillance imaging. This is evident as a heterogeneous signal intensity mass (T) in D and E centered on and penetrating the reconstructed pelvic floor (arrowheads in D) to extend into the left ischiorectal fossa and infiltrating the fascia over the gluteus (crossed arrow in D). (Continued)


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FURTHER READING Das P, Bhatia S, Eng C, et al. Predictors and patterns of recurrence after definitive chemoradiation for anal cancer. Int J Radiat Oncol Biol Phys 2007; 68:794–800. Study of 167 patients with nonmetastatic squamous cell anal carcinoma demonstrates that the majority of locoregional failures involve the anus and rectum, whereas inguinal recurrences occur rarely. Glynne-Jones R, Northover J, Oliveira J. Anal cancer: ESMO clinical recommendations for diagnosis, treatment and follow-up. Ann Oncol 2009; 20(suppl 4):57–60. Internationally accepted recommendations for anal cancer. Indinnimco M, Cicchini C, Stazi A, et al. Magnetic resonance imaging using endoanal coil in anal canal tumours after radiochemotherapy or local excision. Int Surg 2000; 85:143–146. Study illustrating difficulty in differentiating tumor from benign change following treatment. Koh DM, Dzik-Jurasz A, O’Neill B, et al. Pelvic phased-array MR imaging of anal carcinoma before and after chemoradiation. Br J

Radiol 2008; 81:91–98. Review of MR appearances of anal carcinoma before and after chemoradiation. Raghunathan G, Mortele KJ. Magnetic resonance imaging of anorectal neoplasms. Clin Gastroenterol Hepatol 2009; 7:379–388. Primer for MR technique and appearances of anal cancer. Roach SC, Hulse PA, Moulding FJ, et al. Magnetic resonance imaging of anal cancer. Clin Radiol 2005; 60:1111–1119. Useful review in series of 27 patients, mainly with recurrent disease. Ryan DP, Compton CC, Mayer RJ. Carcinoma of the anal canal. N Engl J Med 2000; 342:792–800. Informative review. Stoker J, Rocio E, Wiersma TG, et al. Imaging of anorectal disease. Br J Surg 2000; 87:10–27. Useful review of anorectal imaging, but concentrating on benign disease of the anal canal and malignant disease of the rectum. Uronis HE, Bendell JC. Anal cancer: an overview. Oncologist 2007; 12:524–534. Good general review of clinical features and imaging of anal cancer.


11 Bladder cancer Suzanne Bonington

BACKGROUND INFORMATION Epidemiology Bladder cancer is the ninth most common malignancy worldwide and accounts for 3% of all new malignancies in the United Kingdom. The peak incidence is in the sixth and seventh decade, with the rate in elderly men being three times higher than that in elderly women. The U.K. age standardized incidence rate per 100,000 population is 18.9 for males and 5.3 for females. This incidence rate for men is low compared to the average for the European Union, which is 28/100,000 population. Smoking is the principal risk factor causing two-thirds of bladder cancers in males and one-third of bladder cancer in females. The risk is proportional to the duration of time smoking and the number of cigarettes smoked and decreases with time from cessation of smoking. There is also an increased risk of bladder cancer after exposure to various aromatic amines, causing an occupational hazard in the chemical, rubber, and paint industries. These industrial risk factors are well controlled in Europe but are seen as causes of bladder cancer in developing countries. Squamous cell carcinoma is associated with chronic urinary tract infections and prolonged schistosomiasis infection. This accounts for the high incidence rates in some areas of Africa. There is thought to be a hormonal association, with an increased incidence of bladder cancer in women who have undergone bilateral oophorectomy or an early menopause. There is also evidence of a racial difference in bladder cancer with a higher incidence in whites compared to nonwhites.

Histopathology In the United Kingdom, bladder tumors are predominantly epithelial in origin. Ninety percent are of transitional cell type with approximately 50% arising from the lateral bladder walls and 20% from the base/trigone. Squamous cell carcinoma, or mixed transitional cell and squamous cell carcinoma, accounts for 5% to 10% of malignancies. Adenocarcinoma, which accounts for 2% to 3% of malignancies, usually arises from the bladder urothelium but may also develop in the urachal remnant. Other cell types such as small cell are extremely rare, accounting for less than 1% of cases. At presentation about one-third of bladder tumors are multifocal in origin. Two to four percent of patients will also have lesions in the urothelium of the kidneys and ureter and, therefore, upper tract screening investigations are essential in patients presenting with bladder cancer. Approximately twothirds of bladder tumors are superficial and are usually papillary. These tumors have a good prognosis. One-third show infiltration into or beyond the bladder wall and have a worse prognosis.

Patterns of Tumor Spread Direct spread of tumor occurs into the perivesical fat, pelvic organs and to the pelvic sidewalls. Lymph node metastases are rare in superficial tumors but occur in 30% of patients when the deep muscle layer of the bladder is involved and in 60% of cases where there is extravesical tumor spread. The first lymph nodes involved are the anterior and lateral paravesical nodes and the presacral nodes. Subsequent nodal spread is to the internal iliac, obturator, and external iliac nodes and finally to the common iliac and para-aortic nodes. Para-aortic nodes are considered as distant metastases (M1) in the TNM staging system. Occasionally, metastatic lymph nodes may be identified above the diaphragm. Distant metastases to the liver, bones, lungs, adrenal glands, and brain are late features of bladder cancer. A summary of the TNM system is seen in Table 11.1, and illustrated in Diagram 1.

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Tumor stage: The depth of bladder wall invasion is the most important prognostic variable. Five-year survival decreases from approximately 80% to 90% for T1 disease to 50% for muscle invasive disease and to 5% to 10% for T4 disease. A major adverse feature is the presence of lymph node metastases. Tumor grade: Tumors are histologically graded as high or low grade. High-grade tumors are more likely to be infiltrative and to metastasize, irrespective of tumor stage at presentation. Multiple lesions: Multifocal tumor adversely affects survival. Multiple papillary recurrences in a short timescale worsens prognosis, as with each recurrence there is a 10% to 20% likelihood that the tumor will be of a higher grade. Lymph node metastases: Poor prognosis is associated with the number of positive lymph nodes and the ratio of positive lymph nodes to the number of nodes sampled. Poor prognosis is also associated with extracapsular tumor extension. Other factors: The following have been identified as adverse features: tumor size, vascular and lymphatic invasion, expression of epidermal growth factor receptors, mutation of P53, upregulation of Rb and other oncogene expression, hydronephrosis, and anemia.

Treatment Patients with superficial bladder tumors are treated with local endoscopic resection, often with a single postoperative dose of chemotherapy. Patients with frequent recurrences or high-


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Table 11.1 TNM Classification of Carcinoma of the Bladder, AJCC 2010 TNM classification

Description of tumor extent

TX T0 Ta Tis T1 T2 pT2a

Cannot assess primary tumor No evidence of primary tumor Noninvasive papillary carcinoma Flat tumor, carcinoma in situ Invasion of subepithelial connective tissues Invasion of muscularis propria Invasion of superficial muscularis propria (inner half) Invasion of deep muscularis propria (outer half) Invasion of perivesical tissue Microscopically Macroscopically (extravesical mass) Invasion of any of the following: prostatic stroma, seminal vesicles, uterus, vagina, pelvic wall, and abdominal wall Invasion of prostatic stroma, uterus, vagina Invasion of pelvic wall and abdominal wall Cannot assess lymph nodes No lymph node metastasis Single regional lymph node metastasis in the true pelvis (hypogastric, obturator, external or internal iliac, perivesical or presacral lymph node) Multiple regional lymph node metastasis in the true pelvis (hypogastric, obturator, external or internal iliac, perivesical or presacral lymph node) Metastasis to the common iliac nodes No distant metastasis Distant metastasis

pT2b T3 pT3a pT3b T4

T4a T4b NX N0 N1

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N3 M0 M1

Diagram 1 T Staging of bladder cancer

grade disease may require other intravesical treatment or a radical cystectomy, which involves removal of the bladder and adjacent organs. In a male this includes the prostate and seminal vesicles and in a female the uterus, cervix, ovaries, and anterior vagina. A urinary diversion or neobladder is then formed. Muscle invasive disease with minimal perivesical spread is most commonly treated by radical cystectomy and lymph node dissection or with radiotherapy. Both of these treatments are frequently preceded by chemotherapy (neoadjuvant therapy). Radiotherapy treatment with curative intent may be given concurrently with chemotherapies such as gemcitabine and cisplatin. These have been shown to be reasonably tolerated and have good local and distant disease control, with the advantage of bladder preservation. Advanced disease is palliated with either mitomycin-based chemotherapy or radiotherapy.

MRI OF BLADDER CANCER Technique The bladder should be moderately distended to separate the walls, but not too much so as to cause degradation of the images by motion artifact due to patient restlessness. This can usually be achieved by asking the patient to micturate two hours before the examination. Respiratory motion is limited by putting a band across the patient’s abdomen or more commonly by the use of a phased-array pelvic coil. Hyoscinen-butyl bromide (Buscopan1) or glucagon injection reduces artifact from bowel motion. A standard technique using T1W and high-resolution turbo/fast spin echo T2W sequences is used for staging. Imaging in multiple orthogonal planes is required. Sagittal and coronal planes are particularly useful for assessing tumors at the dome and trigone of the bladder. Fat-saturated/STIR sequences with intravenous contrast are sometimes used and studies suggest a 9% to 14% improvement in staging accuracy with contrast-enhanced imaging. Enhancement should appear earlier and be greater in the tumor compared to the normal bladder wall. Dynamic scanning of the whole bladder using a T1-weighted gradient echo sequence following administration of contrast allows the production of enhancement curves showing signal variation with time within selected regions of interest. Enhancement curves obtained from tumors demonstrate rapid enhancement which plateaus within a short period of time while nonmalignant tissues, such as fibrosis and postbiopsy inflammation, demonstrate more gradual enhancement which takes longer to peak. The normal bladder wall demonstrates a very low level of enhancement. Diffusion-weighted imaging (DWI) may be useful to identify bladder tumors. Early studies suggest that, when combined with T2W and contrast-enhanced examinations, this sequence may help to differentiate stage T1 from stage T2 tumors. If intravenous contrast has been given during the examination, a breath-hold T1-weighted MR angiographic sequence can produce a contrast urogram, which may be helpful to assess the pelvicalyceal systems and ureters for synchronous primaries.


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Current Indications Cystoscopic examination and biopsy remain the basis for evaluation of superficial tumors. MR is valuable in patients with invasive disease as clinical evaluation with bimanual palpation to assess adherence to local structures has an accuracy of only 50% to 75%.

Staging Accuracy The accuracy of MR in staging of bladder cancer varies between 73% and 96%. This is 10% to 30% higher than that achieved with CT. The improvement in accuracy is due to better visualization of the dome and trigone of the bladder and assessing adjacent organ invasion. MR, while still better than CT, is worse at staging low-stage tumors compared to high-stage disease due to the difficulty in differentiating between superficial and deep muscle invasion and early extravesical spread. MRI has been shown to be superior to clinical staging for patients treated with radiotherapy in that MR stage correlated better with risk of treatment failure and cancer-specific survival. Studies have assessed the use of 18F-fluorodeoxyglucose PET-CT in the staging of muscle invasive bladder cancer. They have indicated that there is a potential role for PET-CT to look for metastatic disease in patients prior to radical cystectomy. Assessment of the bladder and local lymph nodes is possible, with promising results but requires strategies such as diuresis and catheterization to reduce the confounding effects of FDG activity in the bladder.

Posttreatment and Recurrence After cystectomy, the bladder bed may demonstrate low-signal intensity fibrosis and bowel often prolapses into it or becomes adherent to the fibrotic tissue. The ileal loop diversion may be visualized, usually in the right iliac fossa. Local tumor recurrence following cystectomy is usually evident as a solid mass of intermediate to high signal in the bladder bed. Radiation therapy usually results in low-signal fibrotic change, but it can also cause generalized or focal bladder wall thickening of intermediate to high signal intensity on T2W images for up to 4 years after treatment, making differentiation from tumor difficult. Dynamic contrast-enhanced scans may be useful in differentiating recurrent tumor from posttreatment effects.

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Imaging Features Primary Tumor On T1W sequences, the perivesical fat appears high signal, the normal bladder wall intermediate signal, and urine in the bladder low signal. In general, the individual muscle layers of the bladder wall are not discriminated. This sequence is useful for assessing extravesical spread of tumor into the perivesical fat, lymph node enlargement, and bone metastases. T2W-weighted sequences are best at delineating intraorgan anatomy and are therefore used to assess bladder wall invasion and evaluate tumor extension into the prostate, uterus, or vagina. On T2W images, the bladder muscle layer is of low signal intensity and tumor is of intermediate signal intensity, slightly higher than that of the bladder wall. An intact low-signal muscle layer at the base of the tumor indicates a noninvasive tumor. Fullthickness wall invasion is difficult to see on MR but is implied by retraction of the outer bladder wall. A mass with an irregular shaggy outer border, perivesical nodules, or intermediate signal stranding of the fat is indicative of extravesical spread. Lymph Node Metastases/Spread Features suggestive of lymph node metastases include size, round shape, irregular margins, similar signal to the primary tumor, and presence of asymmetrical clusters of nodes. Lymph nodes are considered enlarged if they measure more than 8 mm in short axis if round, and 10 mm if oval shaped. In the seventh AJCC cancer staging manual (2010), the size of the nodes no longer alters the TNM stage. N2 disease involves multiple nodes, N3 the common iliac nodes, and disease is M1 if it involves retroperitoneal nodes above the level of the aortic bifurcation.

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Differentiation between T1, T2, and T3a tumors—It can be difficult to differentiate between the superficial and deep muscle layers of the bladder wall and to identify small volume extravesical extension on MR. In general, this is not a significant clinical problem as the differentiation between low-stage tumors does not affect management and is usually determined histologically. If required contrast and DWI may help in this differentiation and assist in evaluating prognosis. Bladder diverticula—Diverticula do not have a muscle layer and therefore direct spread of tumor from the superficial epithelium into the perivesical fat occurs early (T3). Over or under distension of the bladder—If the bladder is too full, images may be degraded by motion artifact. If the bladder is poorly distended the tumor and bladder wall may not be well visualized. Motion artifact can also degrade images at the dome of the bladder. Care in patient preparation and administration of smooth muscle relaxants may prevent these problems. Recent cystoscopic biopsy causing postoperative edema and inflammatory reaction can result in over staging. It is therefore imperative to have accurate information regarding the dates and depths of biopsies. In some circumstances, it may be necessary to rescan the patient at a later date or use dynamic contrast-enhanced imaging. Chemical shift artifact can potentially impair staging by affecting the perception of tumor depth of invasion. This is overcome by using orthogonal planes and altering the phase-encoding direction so that it is perpendicular to the tumor/bladder wall interface. Differentiation between late fibrosis, granulation tissue, and residual/recurrent tumor may be difficult. Tumor is more likely if there is a new or enlarging mass or new disease outside the treated area. Dynamic contrastenhanced sequences may be helpful when tumor should enhance earlier and more avidly than fibrosis. Differentiation between benign and malignant lymph nodes—Small nodes may contain malignant cells and enlarged nodes may be reactive to infection or inflammation. Lymph nodes of a similar signal intensity to the primary lesion are more likely to be malignant.


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Figure 11.1 Normal bladder—moderate distension. Transaxial T2WI through the bladder. The normal bladder muscle layer demonstrates low signal intensity (arrow), the mucosa intermediate signal (crossed arrow) with high signal urine within the bladder (B) and intermediate signal perivesical fat (F). (A) The normal high signal returned from the seminal vesicles (S) is seen. (B) A more cranial section, the distal ureters (U) are seen as they enter the bladder (B). The vas deferens (VD) are also clearly visualized.

Figure 11.2 Normal bladder—extreme distension. (A) Midline sagittal, (B) transaxial, and (C) coronal T2WI through the bladder, following injection of 20-mg hyoscine-n-butyl bromide. The normal bladder muscle is seen as a thin band of low signal intensity (arrows), the mucosa is a fine line of intermediate signal on the inner aspect of the muscle layer (crossed arrows) with high signal urine within the bladder. Urethral meatus (open arrow) bladder trigone (arrowheads).


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Figure 11.3 Bladder wall trabeculation. (A) Transaxial and (B) sagittal T2WI through the bladder. These images demonstrate circumferential low-signal thickening of the bladder wall (arrows) in keeping with detrusor muscle hypertrophy due to chronic bladder outlet obstruction.


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Figure 11.4 Polypoid T1 tumor. Coronal T2WI through the bladder. A large polypoid lesion (P) is seen arising from the left bladder wall. Note is made of the low-signal central vascular pedicle (arrow). The relatively low-signal muscle wall is intact, indicating that this is a nonmuscle invasive tumor (T1).

Figure 11.5 T2a bladder cancer. (A) Sagittal T2WI and (B) fat-saturated contrast-enhanced T1WI demonstrating an enhancing tumor invading the superficial bladder muscle (arrows). The intact outer bladder wall is demonstrated (open arrow). The patient has benign prostatic hypertrophy (asterisk). Source: Courtesy of Dr M Haider, Princess Margaret Hospital, Toronto.


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Figure 11.6 T3b bladder cancer. (A) Transaxial T1WI and (B) T2WI of a male patient with transitional cell carcinoma (T) of the bladder demonstrating transmural extension with stranding within the perivesical fat (arrows). There are also multiple serpiginous structures (open arrows) in the perivesical fat immediately adjacent to the tumor, which are of intermediate signal on T1W and high signal on T2W. These are perivesical vessels and could be confused with extravesical tumor if only the T1W sequence was assessed. The filling defect within the bladder represents benign prostatic hypertrophy (arrowheads).

Figure 11.7 T3b bladder cancer. Transaxial T2WI demonstrating extension of tumor (T) into the perivesical fat. Note the normal bladder wall demonstrates low signal intensity (open arrows) while the tumor demonstrates intermediate signal intensity, outlined by high-signal urine and intermediate to high-signal intensity perivesical fat. The tumor is involving the right ureteric orifice and causing a right-sided hydroureter (U). Uterus (open arrowhead), right external iliac node (N), rectum (R).


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Figure 11.8 T4a bladder cancer. Sagittal T2WI. There is a large bladder tumor arising from the bladder base and extending along the posterosuperior wall. The tumor is extending through the posterior bladder wall and perivesical fat and is invading the vagina (arrows) and lower cervix. Uterus (), rectum (R), symphysis pubis (S).

Figure 11.9 T4a bladder cancer. (A) Sagittal and (B) transaxial T2WI, demonstrating a small tumor (arrow ) arising from the posterior bladder wall extending into the vaginal vault. The patient had a previous hysterectomy for benign disease. Note is made of tethering of the peritoneum just superior to the mass (arrowhead ).


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Figure 11.10 T4a bladder cancer. Sagittal T2WI. A lobulated bladder base tumor (T) is invading the prostatic stroma. There is small volume anterior extravesical extension into the anterior perivesical fat (arrow), very close to the pubic symphysis. The tumor is stage 4a due to the prostatic involvement. Had the tumor involved the symphysis, this would have increased the stage to 4b.

Figure 11.11 T4b bladder cancer. Transaxial T2WI through the bladder. There is a large bladder tumor (T) extending to the rectus sheath anteriorly (arrows). Note the altered signal intensity of the rectus muscle which is different from the tumor and probably due to edema. There is also tumor arising in the posterior bladder (asterisks) which is not invading muscle (T2 or less) but is obstructing the left ureter (U).


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Figure 11.12 T4b bladder cancer. (A, B) Coronal T2WI. In A, a large bladder tumor (T) is seen extending into the perivesical fat and to the right posterior pelvic sidewall where it is starting to encase the right external iliac vessels (arrow). In B, tumor is seen to encase the roots of the sciatic nerve (open arrow).

Figure 11.13 T3bN1 bladder cancer. Transaxial T2WI through the bladder. There is a large intermediate signal intensity tumor (T) involving the right anterolateral bladder wall and extending into the perivesical fat. A left perivesical node is seen (arrowhead). This is of similar signal intensity to the main bladder tumor. A left obturator node (N) is seen with a similar signal intensity to the tumor proper making it more likely to be a metastatic node.


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Figure 11.14 T3b N2 bladder cancer. (A, B) Transaxial T2WI and (C) coronal T2WI. A bladder tumor (T) is extending into the perivesical fat (arrows) and obstructing the right ureter (arrowheads). There is a right obturator lymph node metastasis (N).


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Figure 11.15 N2 bladder cancer. Transaxial T2WI showing bilateral metastatic obturator nodes (N). The right obturator node has an irregular margin anteriorly (open arrowheads) indicating extracapsular extension.

Figure 11.16 T3b N2 bladder cancer. Coronal T2WI showing a large bladder tumor (T) extending into the perivesical fat (arrows). There is a large right obturator node (O) and small right external iliac node (E), of identical signal intensity to the primary tumor.


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Figure 11.17 M1 bladder cancer. Coronal T1WI showing multiple para-aortic (arrows) and aortocaval lymph node metastases (open arrow). Retroperitoneal nodes are considered to be distant metastases (M1) in the TNM staging of bladder carcinoma.

Figure 11.19 Post biopsy effect. (A, B) Sagittal T2WI through the bladder. In A, there is extensive abnormality of the bladder wall with intermediate signal thickening (open arrows), predominantly posteriorly with associated stranding of the perivesical fat (arrows), suggesting a stage T3b tumor. Thickening and irregularity of the bladder mucosa (open arrowhead) is also noted. B Three months later, these appearances have virtually resolved with no intervention and were due to biopsy-induced inflammation and edema. There is now some low signal intensity in this location, which is likely partly due to fibrosis (arrow).

Figure 11.18 M1 bladder cancer—bone metastasis. Coronal T1WI through the pelvis showing a left-sided bladder tumor (arrows). An intermediate signal lesion (M) is seen in left lesser trochanter of the femur due to a bony metastasis.


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Figure 11.20 Multifocal bladder cancer. Coronal T2WI. There are multiple nodules of intermediate signal tumor (arrows) involving the superficial bladder muscle. Some lesions show extension into the deep muscle layers (open arrow). Tumor (T) is also noted to extend into the defect (D) from a transurethral resection of the prostate performed for benign prostatic hyperplasia. This tumor also extends along the right levator ani muscle (arrowheads) which increases the T stage to T4b.

Figure 11.21 Multifocal bladder cancer. (A) Transaxial and (B) coronal T2WI showing multifocal intermediate signal intensity papillary tumors (arrows) involving the superficial bladder muscle. A low-signal stalk is noted (arrowhead). The low-signal bladder muscle layer is intact.


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Figure 11.22 Diffuse bladder cancer with layering. Coronal T2WI through the bladder. Extensive tumor (T) is seen spreading circumferentially around the bladder wall with components superficial and deep to the muscle layer, which appears intact between them (arrowheads). This is therefore T3b disease. This is an unusual appearance, but important as the deep component could easily be missed at biopsy. Small perivesical and pelvic sidewall nodes (N) are noted.

Figure 11.23 T3b bladder cancer with tumor extending into the left ureter. (A) Sagittal and (B) coronal T2WI through the bladder demonstrate a T3b tumor (T) involving the left bladder wall and base and extending into the lower left ureter. There is a left-sided hydroureter (H) with layering of urine and debris or hemorrhage seen in the ureter (arrow). Hydronephrosis and/or tumor extension into the ureter does not alter the tumor stage but is associated with a worse prognosis.


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Figure 11.24 Urachal cancer. (A) Sagittal and (B) transaxial T2WI showing tumor (T) extending along the obliterated urachus (median umbilical ligament) adjacent to the anterior bladder wall (arrow). This type of tumor is most commonly an adenocarcinoma. The uterus (U) contains multiple fibroids.

Figure 11.25 Treatment-related change following cystectomy and radiotherapy. Sagittal T2WI. A small postoperative fluid collection (asterisk) is seen in the bladder bed and there are low-signal fibrotic bands causing tethering of the sigmoid colon (arrow).


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Figure 11.26 Treatment-related change following localized radiotherapy. Transaxial T2WI showing low-signal thickening of the left posterolateral bladder wall (arrow) due to fibrosis and resulting in a left-sided hydronephrosis (asterisk). The bladder is tethered to the anterior vagina (open arrow).

Figure 11.27 Tumor recurrence post cystectomy. Transaxial T2WI in a patient who had a previous cystectomy for bladder cancer demonstrating an intermediate signal intensity tumor recurrence (R) in the urethral bed and also a bone metastasis in the left inferior pubic ramus (M).

Figure 11.28 DWI of primary tumor. (A) Transaxial T2WI, (B) transaxial b1000 DWI image, and (C) transaxial ADC image showing generalized thickening of the bladder wall (arrow) with more focal thickening posteriorly (open arrow) and stranding of the perivesical fat. This posterior area demonstrates restricted diffusion and a low ADC consistent with tumor. A right obturator node is seen (arrowhead).


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Figure 11.29 DWI and dynamic contrast imaging. (A) Transaxial T2WI through the bladder demonstrating an ill-defined lesion in the left anterolateral bladder wall (arrow) with stranding extending into the perivesical fat. It is difficult to be sure how much of the abnormality is due to tumor and how much is postbiopsy change. The diffusion-weighted images with increasing B values (B) with b = 600 msec and (C) with b = 1000 msec demonstrate a small region of restricted diffusion (open arrow) within the center of the lesion. This has a low ADC (D). These findings indicate that there is residual tumor within a larger area of biopsy-induced inflammation. (E) Enhancement curve for a region of interest over the area of thickening. This demonstrates very intense rapid enhancement, which plateaus quickly and is the typical profile for malignancy. (F) Transaxial T2WI through the same section of bladder after treatment with neoadjuvant chemotherapy. There is significant residual thickening in the region of the previous tumor (arrow), and on T2WI alone it is impossible to decide whether there is residual tumor at this site. Analysis of the enhancement curve for this region shows slow gradual enhancement which is typical of posttreatment effect, and this can easily be distinguished from the enhancement profile of the original tumor.


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FURTHER READING Barentsz JO, Jager GJ, Witjes JA. MR imaging of the urinary bladder. Magn Reson Imaging Clin N Am 2000; 8(4):853–867. Good description of technique. MacVicar D, ed. Contemporary issues in cancer imaging. Carcinoma of the Bladder. Cambridge, UK: Cambridge University Press, 2008. Comprehensive overview of bladder cancer imaging and treatment. Robinson P, Collins CD, Ryder WD, et al. Relationship of MRI and clinical staging to outcome in invasive bladder carcinoma treated

with radiotherapy. Clin Radiol 2000; 55(4):301–306. Identifies the most important findings on MR that alter prognosis. Takeuchi M, Sasaki S, Ito M, et al. Urinary bladder cancer: diffusionweighted MR imaging—accuracy for diagnosing T stage and estimating histologic grade. Radiology 2009; 251:112–121. This paper has good images and schema to help you in the practical use of DWI. Vikram R, Sandler CM, Ng CS. Imaging and staging of transitional cell carcinoma: part 1, lower urinary tract. AJR Am J Roentgenol 2009; 192(6):1481–1487. Good overview.


12 Prostate cancer Claire Barker

BACKGROUND INFORMATION Epidemiology Worldwide, over 670,000 men are diagnosed with prostate cancer each year. The highest rates are in North America, Australasia, and North West Europe. The incidence is rising, although much of this increase is due to increased detection through more prostate-specific antigen (PSA) testing. In the United Kingdom, prostate cancer is now the most common male cancer and is the second leading cause of male cancer deaths after lung cancer. Incidence statistics may be misleading, however, due to the high prevalence of occult disease. Age is the most important risk factor in developing prostate cancer with 60% of cases diagnosed in men over 70. Clinical disease is rare in men below 50. However, approximately 50% of men in their 50s are reported to have histological evidence of prostate cancer at postmortem.

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Histopathology Nearly all prostate cancers are adenocarcinomas. Rare tumors include squamous and transitional cell carcinomas and sarcomas. The most widely used classification system is the Gleason score. This is calculated as the sum of the two predominant cell types within the resected tumor tissue. The combined score can be further subgrouped into grades 2 to 4 (well differentiated), 5 to 7 (moderately differentiated), and 8 to 10 (poorly differentiated). Approximately 75% of tumors arise in the peripheral zone of the gland, 15% in the transition zone, and 10% in the central zone.

Patterns of Tumor Spread The outer prostatic “capsule” is strictly a pseudocapsule of fibromuscular tissue inseparable from the prostatic tissue. Prostate cancer spreads locally through the pseudocapsule to involve the periprostatic connective tissues, seminal vesicles, bladder base, and pelvic floor. The rectum is usually spared, as Denonvillier’s fascia forms a barrier to direct tumor extension. Regional lymphatic spread to nodes within the true pelvis occurs most frequently to the obturator nodes, with the pararectal, presacral and internal iliac nodal groups also commonly involved. Distant spread to lymph nodes outside the true pelvis may also occur. Hematogenous spread occurs through the periprostatic venous plexus, producing bone metastases particularly in the pelvic girdle and spine, via the spinal veins. Other common sites for metastatic disease are the liver and lung.

Treatment The management of prostate cancer continues to be the subject of much debate with no consensus on the best treatment for early prostate cancer. Watchful waiting with deferred treatment is a valid option, especially for well-differentiated low-risk localized tumors in elderly patients, who have a normal life expectancy of less than 10 years. This has to be weighed against an increased risk of interval disease progression and the potential complications of other treatments. l

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Prognostic Indicators Outcome/prognosis depends on: l

TNM stage. This is the most important prognostic variable. The five-year disease-specific survival for patients with

disease confined to the prostate (T2 or less) is over 90% but only approximately 30% for men with metastatic disease (M1) at presentation. The Gleason score. The 10-year disease-specific survival for clinically localized disease (managed conservatively) is 87% for well and moderately differentiated tumors, dropping to 34% for poorly differentiated tumors. PSA level. High levels correlate with advanced TNM stage at diagnosis, and a rising PSA post treatment is suggestive of tumor recurrence. Overlaps in PSA ranges, however, limit staging accuracy for individual patients. Newly diagnosed asymptomatic patients with a PSA less than 10 ng/L have a very low risk of skeletal metastases so that routine radionuclide bone imaging is not considered necessary. Tumor volume. Number of positive biopsies on transrectal ultrasound (TRUS). Tumor neovascularization and molecular tumor cell–specific markers are the subject of ongoing research.

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Active surveillance, in order to prevent overtreatment, is for men with low-risk localized tumors which are suitable for radical treatment if their disease progresses. Disease is monitored with regular PSA testing, digital rectal examination, and repeat biopsies as necessary. For men with intermediate risk disease, there is a choice of active surveillance or radical treatment with or without hormone therapy. There are choices for the radical treatment of high-risk patients dependent on the grade and stage of tumor and the prostate volume. Radical prostatectomy is a curative treatment option for patients with localized (T1-2N0M0) prostate cancer. Some centers restrict surgery to patients with a Gleason score less than 7 and PSA less than 20 ng/ mL due to increased risk of occult extracapsular disease at higher PSA levels. The main advantages of surgery are that definitive staging is possible, PSA levels are reliably suppressed following treatment and radiotherapy remains an option for locally recurrent disease. External beam radiotherapy (EBRT), including conformal radiotherapy, may also be offered with curative intent.


PROSTATE CANCER Table 12.1 Prostate cancer: TNM Staging Classification 2010 TNM classification

Description of tumor extent

TX T0 T1

Primary tumor cannot be assessed No evidence of primary tumor Tumor identified on histology but not apparent clinically or radiologically Tumor is an incidental finding in 5% resected tissue Tumor identified only on needle biopsy Tumor palpable or visible on imaging confined to the prostate Tumor involves one-half of one lobe or less Tumor involves more than one-half of one lobe Tumor involves both lobes Tumor extends through the prostatic pseudocapsule Extracapsular extension Invading the seminal vesicle(s) Tumor fixed or invading adjacent structures other than seminal vesicles: bladder neck, external sphincter, rectum, levator muscles, pelvic sidewall No lymph nodes involved Regional nodal metastases No distant metastases Distant metastases Nonregional lymph nodes Bone metastases Other sites involved þ/ bone metastases

T1a T1b T1c T2 T2a T2b T2c T3 T3a T3b T4

N0 N1 M0 M1 M1a M1b M1c

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field artifact although the latest scanners have software to overcome this problem. l

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Thin section T2-weighted turbo spin echo sequences are essential for differentiating normal internal zonal prostatic anatomy and pathology. The prostate and seminal vesicles must be covered in their entirety. Off-axis imaging, parallel to the prostate, can be helpful in evaluating extraprostatic extension. T1-weighted spin echo images are useful for detecting enlarged pelvic lymph nodes, bone metastases, and in identifying postbiopsy hemorrhage. Fat-suppressed imaging has no staging benefit over conventional T1- and T2weighted spin echo sequences. Dynamic gadoliniumenhanced imaging can improve tumor recognition and staging accuracy but is not widely used. In some centers, MRI is now supplemented with magnetic resonance spectroscopy (MRS) with an increase in the choline: citrate ratio seen in prostatic tumor. MRS, particularly when performed with an ERC, can been used to determine the presence and location of tumor within the prostate and regional lymph nodes and to improve the assessment of extraglandular extension. With experience, dynamic contrast-enhanced MRI and diffusion-weighted imaging (DWI) can significantly improve tumor localization in prostate cancer. DWI may also become a useful adjunct to MRI for differentiating recurrent tumor from posttreatment effect.

Current Indications

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Radical radiotherapy is suitable for patients with clinically localized disease (T1-2N0M0) and locally advanced tumors (T3N0M0) after “down staging” with hormonal therapy. Radiotherapy has similar results to surgery and can be administered on an outpatient basis without the need for a major operation. Brachytherapy, the implantation of radioactive seeds into the prostate, is gaining popularity but is only available in specialist centers. This technique delivers focal high-dose radiation to the prostate gland with relative sparing of the surrounding tissues. Criteria are more stringent than for EBRT and currently only small-volume, low-risk T2N0M0 tumors are considered. Metastatic disease is managed by a combination of hormone therapy and palliative radiotherapy. Radioactive strontium can be effective for diffuse bone metastases. Chemotherapy for hormone refractory disease is the subject of ongoing clinical trials.

The indications for MRI depend on local surgical and oncology practice, the availability of MRI and local radiological expertise. Many centers do not perform routine MRI, instead relying on clinical assessment (digital rectal examination) combined with PSA level and Gleason grade to predict tumor stage. l

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MRI OF PROSTATE CANCER Technique MRI evaluation of the prostate requires optimal technique using phased-array pelvic surface coils. Endorectal coils (ERCs) used either alone or in combination with pelvic phased-array coils have been shown to improve staging accuracy by better depiction of pseudocapsular penetration. ERCs have the potential drawbacks of causing patient discomfort with consequent movement artifact and also of producing near

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MRI can provide additional useful information in assessing for extracapsular tumor and seminal vesicle invasion. Decision analysis studies indicate MRI is most helpful in patients with an intermediate clinical risk of extracapsular extension (clinically localized at digital rectal exam (DRE), PSA level more than or equal to 10–20 ng/mL, Gleason score of 5–7). In these circumstances, MRI findings of extracapsular disease can stratify patients into low- and high-risk groups for disease progression, based on PSA levels at three years posttreatment. This information may influence the choice of treatment modality and the decision to offer adjuvant hormonal therapy. MRI is useful in the selection of patients for brachytherapy. Accurate staging information is essential, as disease must be contained within the prostatic pseudocapsule (T1-2 N0 M0). Despite the low positive predictive value of MRI, features suggestive of extracapsular extension are usually taken as a contraindication to treatment. MRI can also give an accurate assessment of prostatic volume, which ideally should be less than 60 cm3. MRI may assist radiotherapy planning for locally advanced disease. The greater soft tissue contrast and multiplanar capabilities of MRI provide a more accurate assessment of disease extent and involvement of adjacent organs. Fusion imaging systems are in development to facilitate radiotherapy planning using MRI data.


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alence in the population studied. Most published results give positive predictive values below 50%, indicating MRI usually overcalls extracapsular disease extension prior to radical prostatectomy. It is recognized that pathological stage is an imperfect gold standard, however, and selected histological sections may miss extracapsular disease extension if the gross specimen is not evaluated throughout.

MRI may also be useful in evaluating patients with a rising PSA following radical prostatectomy. Locally recurrent tumors or isolated lymph nodes may be suitable for salvage radiotherapy in the absence of more widespread disease.

Imaging Features Prostate cancer occurs in the peripheral zone in 75% of patients and usually has low signal intensity compared to the normal high signal of the peripheral zone on T2 weighted turbo spin echo images. Tumors outside of the peripheral zone may be indistinguishable from normal tissue or the heterogeneous signal of benign prostatic hyperplasia. The prostatic pseudocapsule is seen as a thin band of low signal between the peripheral zone and periprostatic connective tissue. In addition to frank extracapsular tumor, features suggestive of capsular penetration are capsular retraction, focal capsular bulging, periprostatic stranding, capsular thickening, and tumor contiguity with the pseudocapsule of more than 12 mm. Extension into the seminal vesicles is suggested by replacement of normal high signal with intermediate signal tumor in continuity with intraprostatic disease. This is often best seen on the coronal sequence. Following radiotherapy, the prostate gland shrinks and the peripheral zone becomes intermediate signal intensity on T2-weighted imaging. After radical prostatectomy, residual fibrosis in the prostatic bed has low signal intensity on all sequences. This may be differentiated from the intermediate signal intensity of recurrent tumor on T2-weighted images.

Staging Accuracy MRI offers the single most accurate imaging assessment of local disease and regional metastatic spread. The integration of MRI findings with standard clinical diagnostic tests has also been shown to improve the overall accuracy of prostate cancer staging. A meta-analysis of studies evaluating MRI staging accuracy in patients with clinically localized prostate cancer produced a maximum combined sensitivity and specificity on the receiver operating characteristic (ROC) curve of 74%, using pathological stage as the gold standard. At a specificity of 80% on the ROC curve, sensitivity was 69%. l

As with any diagnostic test, however, the positive and negative predictive values will vary according to the prev-

Pitfalls of MRI l

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Signal changes within the prostate should be interpreted with caution as other pathological processes may mimic prostate cancer. Infection, inflammation, and hemorrhage will all produce low-signal changes within the peripheral zone on T2-weighted imaging which can be confused with cancer. It is important to check for T1WI high signal within the prostate peripheral zone to exclude postbiopsy hemorrhage. The normal fibromuscular bands of the peripheral zone may also appear thickened as a normal variant and should not be confused with tumor. Staging accuracy is reduced following TRUS-guided biopsy. Evaluation of extracapsular extension is particularly difficult if the pseudocapsule or seminal vesicles have been subjected to multiple biopsies in an attempt to gain pathological evidence of locally advanced disease. Signal characteristics may be helpful as, unlike tumor, methemoglobin within hemorrhage is high signal on T1-weighted imaging. If equivocal findings are present, radical treatment can be deferred and the MRI repeated, as postbiopsy changes will resolve with time, although this may take several months. Similarly, signal changes within and around the seminal vesicles can be misinterpreted on MRI imaging. Hemorrhage, inflammatory scarring, stones, and amyloid can all produce focal abnormalities and tubular thickening. Normal fibrous tissue around the ejaculatory ducts and inferomedial tips of the seminal vesicles can also be misdiagnosed as tumor. Some published reports have disregarded signal changes in the seminal vesicles unless there is evidence of tumor within the adjacent prostate on TRUS biopsy. Post prostatectomy, the unresected tips of the seminal vesicles may be misinterpreted as residual or recurrent tumor.


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Figure 12.1 Normal prostate anatomy. (A) Transaxial T2WI. The normal zonal anatomy of the prostate is well demonstrated on T2WI. The central gland (C) is comprised of central and transition zones and encloses the urethra. These zones are low signal on T2WI and may thus mask any low-signal tumor within. Seventy-five percent of tumors arise in the peripheral zone (P) of the gland and are usually well demarcated from the high-signal glandular stroma. The pseudocapsule is seen as a thin surrounding low-signal band (arrowheads). Lateral to the pseudocapsule, the high-signal periprostatic venous plexus (V) can sometimes cause confusion as to the true margin of the gland. The neurovascular bundles supplying the corpora cavernosa are positioned at the 5 and 7 o’clock positions, (long arrows) just outside the pseudocapsule. The rectum (R) is closely applied to the prostate separated by the thin low-signal Denonvilliers’ fascia. The bladder (B) may be seen anteriorly on transaxial sections. (B) Coronal T2WI. The seminal vesicles (S) are high signal with regular thin-walled tubules. The prostate sits within the levator sling (L), laterally, the obturator internus muscles (O) form the pelvic sidewalls. There is a cyst in the midline (C).

Figure 12.2 Benign prostatic hyperplasia (BPH). Transaxial T2WI. BPH results in enlargement of the transition zone of the gland. The peripheral zone is thinned (short arrows), and the normal high signal intensity may diminish, although not usually to the extent seen with tumor infiltration. The hypertrophied transition zone (TZ) has heterogeneous signal on T2W.


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Figure 12.3 Stage T2a prostate cancer. Transaxial T2WI. Lowsignal tumor (arrow) is seen within the peripheral zone of the right lobe of the prostate. Changes of BPH are noted. The tumor occupies less than one-half of one lobe indicating stage T2a disease. There is no evidence of extension beyond the pseudocapsule. Abbreviation: BPH, benign prostatic hyperplasia.

Figure 12.4 Stage T2b prostate cancer. Transaxial T2WI. Lowsignal intensity tumor (arrow) is involving more than one-half of one lobe and is classified as T2b. The low signal is contiguous with the pseudocapsule for >12 mm, which increases the probability of microscopic extracapsular disease. This may influence patient selection for brachytherapy or other radical treatments.

Figure 12.5 Stage T2c prostate cancer. Transaxial T2WI. Tumor (arrows) involves both lobes, crossing the midline. Tumor is also seen within the central gland (T). There is no extracapsular extension.

Figure 12.6 Stage T3a prostate cancer. Transaxial T2WI. Extracapsular extension is most commonly seen from the posterior and lateral aspects of the prostate, often in the region of the neurovascular bundle. Here, small-volume, low-signal tumor (arrow) breaches the prostatic pseudocapsule on the right, indicating stage T3a disease.


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Figure 12.7 Stage T3a prostate cancer. Transaxial T2WI. Tumor in the central gland (arrows) can breach the anterior pseudocapsule extending into the fat deep to the symphysis pubis. Anterior extracapsular extension is not detectable clinically.

Figure 12.8 Stage T3b prostate cancer. (A) Sagittal and (B) transaxial T2WI. Low-signal tumor (T) within the peripheral zone is contiguous with tumor extending into base of the seminal vesicles (arrow). An enlarged presacral node is also present (arrowhead). Tumor is seen within the left seminal vesicle (arrow in B) replacing the normal high T2W signal as seen on the right. (C) Transaxial T2WI in a different patient. Low signal is seen in the right peripheral zone in keeping with tumor. There are indirect signs of extracapsular disease as the pseudocapsule is retracted and thickened (arrowheads), and there is contiguity with the tumor over a prolonged distance (>12 mm). Both seminal vesicles and ejaculatory ducts (arrows) are replaced with material of similar signal intensity indicating T3b disease. (Continued)


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Figure 12.9 Stage T3a/T4 prostate cancer. Transaxial T2WI. There is extracapsular tumor extension (arrows) into the right neurovascular bundle (arrowhead) and posteriorly to the right levator muscle (L). MR staging is equivocal and clinical correlation may be required to distinguish between stage T3a and stage T4 disease. In stage T4 disease, the tumor is “fixed” to the pelvic sidewall.


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Figure 12.10 Stage T4 prostate cancer. Transaxial T2WI. There is nodular extracapsular extension of tumor on the right extending to the right levator muscle and rectum (arrows). A right anatomical obturator node (arrowhead) is also present in the obturator foramen.

Figure 12.11 Stage T4 prostate cancer. (A) Transaxial and (B) coronal T2WI. Tumor (T) extends to the right pelvic sidewall (arrows). Bilateral hydroureters (arrowheads) are present due to invasion of the bladder trigone (crossed arrows). A trace of ascites (A) is seen in the rectovesical pouch. Several small perirectal nodes (N) are noted. In B, bilateral hydroureters (arrowheads) and further perirectal nodes (N) are demonstrated.


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Figure 12.13 Post prostatectomy tumor recurrence. Transaxial T2WI. Following radical prostatectomy, there is normally a ring of low signal representing postoperative fibrosis in the prostatic bed. Recurrent tumor usually shows as an area of intermediate signal intensity within the fibrotic tissue or adjacent periprostatic fat. In this example, the recurrent tumor (arrow) is present between the 7 and 9 o’clock positions within the fibrous ring.

Figure 12.12 Stage T4 prostate cancer. (A) Transaxial and (B) sagittal T2WI. There is an extensive tumor (T) infiltrating the bladder (arrowheads) and rectum (arrow). A catheter balloon (B) is in situ. Inferiorly, disease extends through the pelvic floor into the perineum (asterisk). Marrow hyperplasia due to anemia accounts for the signal change in the sacrum (S). Figure 12.14 Post radiotherapy tumor metastasis. Transaxial T2WI. Following radiotherapy, the prostate gland reduces in size and signal intensity decreases on T2WI, most obviously in the peripheral zone. Local tumor recurrence is usually heralded by a rise in PSA. This patient with a rising PSA had developed a bone metastasis (arrow) in the right ischium. Abbreviation: PSA, prostatespecific antigen


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Figure 12.15 Tumor recurrence. (A) Transaxial T2WI, (B) DWI b100, (C) DWI b1000, and (D) ADC. Tumor recurrence within the peripheral zone on the left (arrow) extends laterally to involve the levator ani muscle (arrowhead). There is restricted diffusion on DWI, especially at high b values (arrow) with a corresponding low ADC (arrow) in D. Abbreviations: ADC, apparent diffusion coefficient; DWI, diffusion-weighted imaging.


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Figure 12.16 Stage N1 prostate cancer. Coronal T2WI. There is a large left external iliac nodal metastasis (long arrow). A small right external iliac node has similar signal intensity and is also likely to be involved (short arrow). The obturator and iliac nodes are most commonly involved in prostate cancer. Local extracapsular tumor extension is seen from the right side of the prostate (arrowhead) abutting the levator ani muscle (L) on the right.

Figure 12.17 Stage N1 prostate cancer. Sagittal T2WI. Presacral lymph node metastasis (arrow) in a patient with a T4 prostatic tumor (T) involving the bladder base (arrowhead) and seminal vesicles (crossed arrow).


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Figure 12.18 Stage N1 prostate cancer. Transaxial T2WI. Bulky T4 prostate cancer (T) with extracapsular extension. There are extensive nodal metastases within right internal iliac (arrow), left external iliac (arrowhead), and perirectal (crossed arrow) nodes with extracapsular extension.

Figure 12.19 Stage M1a prostate cancer. Coronal T1WI. Multiple interaortocaval and para-aortic retroperitoneal lymph nodes are present (arrows), indicating stage M1a disease in addition to bilateral common and external iliac nodes (arrowheads). A transaxial upper T1W block of images may assist in equivocal cases.


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Figure 12.20 Stage M1b prostate cancer. Coronal T1WI. Prostate tumor (T) with multiple bone metastases involving the pelvis and lumbar spine (arrows) indicating stage M1b disease.

Figure 12.21 Stage M1c prostate cancer. (A) Transaxial T1WI. There are multiple hepatic metastases (arrows). Extraskeletal nonlymph node metastases are classified as stage M1c disease. (B) Transaxial T2WI in a different patient. An unusual metastasis is seen within the left spermatic cord (arrow). The metastasis is differentiated from an inguinal lymph node by its medial position, similar to the uninvolved right spermatic cord, and the compressed left spermatic cord structures (arrowheads) seen posteriorly. Note also a metastasis (asterisk) in the right pubic bone and other smaller bone metastases throughout the pelvis. Incidental left iliopsoas bursa (crossed arrow). (C) Sagittal T2WI in a different patient. There is a metastasis within the corpus spongiosum of the penis (arrow) in a patient who had previously undergone radical prostatectomy. Note the postsurgical fibrosis (open arrows) in the prostate bed. This is stage M1c disease. (Continued)


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Figure 12.22 Post-brachytherapy implantation. Transaxial T2WI. Multiple brachytherapy seeds (arrows) result in low-signal foci throughout the prostate gland. Low-signal areas may be seen within the prostate gland as a result of radiation effect.


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Figure 12.23 Fibromuscular bands. Transaxial T2WI. The fibromuscular bands traversing the peripheral zone may appear prominent, as a normal variant (arrows). These linear radial bands should be easily distinguished from the more amorphous mass-like, lowsignal change representing tumor infiltration.

Figure 12.25 Post biopsy hemorrhage. (A) Transaxial T1WI and (B) T2WI. There is post biopsy hemorrhage producing an asymmetric left-sided bulge to the prostate peripheral zone. Methemoglobin accounts for the high signal on the T1W and T2W images (arrows). Low signal in the right peripheral zone of the prostate is consistent with tumor (arrowheads). The signal changes associated with hemorrhage evolve over several weeks and, depending on the stage of evolution, hemorrhage may either mask or simulate tumor in the peripheral zone on T2-weighted images. Repeat imaging can help in equivocal cases, but, in our experience, changes can persist up to three months. Figure 12.24 Prostatitis. Transaxial T2WI. This patient had prostatitis producing diffuse low-signal change throughout the peripheral zone. Tumor and inflammation may be indistinguishable on MRI and prostatic biopsy is required to diagnose tumor in the absence of widespread metastatic disease. Abbreviation: MRI, magnetic resonance imaging.


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Figure 12.26 False positive seminal vesicle invasion. (A) Transaxial and (B) coronal T2WI. A localized increase in fibrous tissue (arrows) is normally found around the insertion of the vas deferens and origin of the ejaculatory ducts, which may encompass the medial portions of the seminal vesicles. This should not be interpreted as tumor invasion (stage T3b) unless there is contiguous tumor extending from the adjacent prostate.

FURTHER READING Hricak H, Choyke PL, Eberhardt SC, et al. Imaging prostate cancer: a multidisciplinary perspective. Radiology 2007; 243:28–53. An overview of prostate imaging. Huang Y, Isharwal S, Haese A, et al. Prediction of patient-specific risk and percentile cohort risk of pathological stage outcome using continuous prostate-specific antigen measurement, clinical stage and biopsy Gleason score. BJU Int 2010; 107:1562–1569. A recent online update based on Partin’s tables. An online computer program has been developed from the 2010 Partin Nomogram for predicting patient-specific pathological stage outcome at www.urology.jhu.edu/prostate/partintables.php. Kirby RS, Patel MJ. Fast Facts: Prostate Cancer. 6th ed. Oxford, UK: Health Press, 2009. Concise overview of the diagnosis and management of prostate cancer. Prostate cancer. Cancer Research UK, 2008. Background data and statistics relating to prostate cancer.

Qayyum A. Diffusion-weighted imaging in the abdomen and pelvis: concepts and applications. Radiographics 2009; 29:1797–1810. An overview of DWI in the abdomen and pelvis. Ramchandani P, ed. Preface. Radiol Clin N Am: Prostate Imaging, 2006; 44(5):xi. A further review of prostate imaging. Royal College of Radiologists Clinical Oncology Information Network and British Association of Urological Surgeons. Guidelines on the management of prostate cancer. Clin Oncol 1999; 11:55–81. Also known as the UK COIN guidelines. Zelefsky MJ, Eastham JA, Oliver OA. Cancer of the prostate. DeVita, Hellman and Rosenberg’s Cancer Principles and Practice of Oncology. 8th ed. In: DeVita VT, Lawrence TS, Rosenberg SA, eds. Philadelphia, USA: Lippincott Williams and Wilkins, 2008:1392– 1451. A comprehensive review of the management of prostate cancer. Zhang J, Hudolin T, Hricak H. Prostate cancer. In: Husband J, Resnick H, eds. Imaging in Oncology. 3rd ed. Colchester, UK: Informa Healthcare, 2010:348–370. Aimed at the clinical radiologist, this up-todate textbook has a detailed chapter reviewing prostate cancer imaging.


13 Penile cancer Rohit Kochhar and M. Ben Taylor

BACKGROUND INFORMATION Epidemiology Malignant lesions of the penis are rare in developed nations and constitute only 0.4% to 0.6% of all cancer types in males, compared with 10% to 22% in some developing countries. Around 470 men are diagnosed each year in the United Kingdom with penile cancer, compared to more than 36,000 cases of prostate cancer. Penile cancer is more common in the elderly and most cases are in men over 60. First-degree relatives of men with penile squamous cell cancer (SCC) have about eight times the risk of developing penile SCC compared to men without a family history. Genital wart infection with human papilloma virus (HPV) increases penile cancer risk, and around 5 out of 10 men with penile cancer have HPV infection. HPV 16 and HPV 18 are most frequently linked to penile cancer. Other risk factors include smoking and immunosuppression. Factors that lower risk include being circumcised and good personal hygiene.

Histopathology More than 90% of penile malignancies are SCC. SCC can develop anywhere on the penis, with the glans penis (48%) being the most common site. Other sites in decreasing order of frequency are the prepuce (21%), the glans together with the prepuce (9%), the coronal sulcus (6%), and the shaft (2%). Verrucous carcinoma is a rare type of squamous cell penile cancer with an exophytic, wart-like appearance, which is slow growing and rarely metastasizes. Approximately 5% of penile cancers are adenocarcinomas, which develop in the glandular cells that produce sweat in the skin of the penis. Other histological types reported include basal cell carcinoma (2%), melanoma (2%), and sarcoma (1%). Metastases to the penis are rare and usually occur in the setting of widespread metastatic disease. The most frequent primary cancers to metastasize to the penis are genitourinary tumors and rectosigmoid carcinoma, with prostate and bladder being the commonest primary sites.

Patterns of Tumor Spread SCC of the penis is usually an indolent disease, slowly growing over many years and becoming locally extensive before distant metastases occur. The TNM staging classification for penile cancer is given in Table 13.1 and the anatomical stage/prognostic groups in Table 13.2. The location of the primary determines the site of lymphatic spread. Lymphatic drainage from the skin and prepuce is to the superficial inguinal nodes, from the glans is to the deep inguinal and external iliac nodes and from the corpora and penile urethra is to the internal iliac nodes. Free communication

of lymphatics from side to side often results in bilateral lymph node metastases. Importantly, metastases to iliac nodes are rare in the absence of inguinal metastases. Between 30% and 60% of patients with penile carcinoma have palpable inguinal nodes at presentation, but nearly half of these are reactive. In addition, metastatic nodes may be nonpalpable, and 15% of patients without palpable nodes have positive nodal histology after standard groin dissection. Hematogenous metastases typically develop late in the course of the disease and occur most commonly in the lungs and liver.

Prognostic Indicators The overall prognosis of penile cancer depends on the stage and histological grade of the primary tumor and the presence or absence of lymph node metastases. For men with the very earliest stage, that is penile carcinoma in situ, over 90% will be alive at five years. The most important prognostic factor is the presence and degree of lymph node involvement. The prevalence of nodal disease is related to the stage of the primary lesion and occurs in 20% of T1 penile cancers and in 47% to 66% of T2–T4 tumors. For men who have metastases limited to one inguinal lymph node, just over 80% will live for at least five years. If more than two inguinal lymph nodes or lymph nodes in the abdomen are positive then around 40% live for at least five years. Distant metastases are uncommon at the time of clinical presentation, occurring in

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